Clinical Skills Additional Notes 2009
CLINICAL SKILLS
Medical History Taking
CLINICAL SKILLS
Medical History Taking
CLINICAL COACHING:
TAKING A HISTORY
“The most important part if a medical consultation is the gathering of information. A good history is all a diagnostician needs to formulate a hypothesis. The examination is then used to test the hypot hesis” hesis” i) History taking ii) Examination iii) Investigations
HISTORY TAKING Introduce yourself e.g. “Hello “Hello Mr Smith, my name is Rachel and I am a first year medical student. I have been asked to chat with you about why you’re in hospital, and your medical history . history . Is that OK with you?” you ?” “Could you tell me a little but about yourself?” –patient’s –patient’s age, birth date, address, address, occupation, marital and family status etc…
PC (Presenting Complaint) “What concern brought you in here today?”
HPC (History of the Presenting Complaint) Nature Intensity Location Duration Onset Contributing Aggravating Alleviating Radiating Features Impact Attribute (What do you think is causing this Problem?) Treatment (Taking anything for it?) Associated
symptoms (e.g. if cough – cough – sputum?; sputum?; “Is there anything else you can think to
tell me?”
PMH (Past Medical History) -Medical, Surgical, Trauma, Obstetric (female) “ Apart from this illness, please please tell me about any other illnesses, accidents accidents or operations you have had” “Have you ever been in hospital for anything?” “Have you ever been pregnant? Tell me about your pregnancies.” pregnancies .”
Drugs and Allergies -current medications, dosages, and why taking it, (ask for contraceptive pill and asthma inhaler!!!) - over the counter meds -recently stopped meds and why -adverse drug reactions -vaccinations -herbal, vitamin and nutritional supplements -recreational drug use -allergies?
FH (Family History) “Are your parents still alive? How is their health?” -brothers, sisters, children , “How are they” “Any disease/ conditions that run in the family?”
SH (Social History ) - age, race, sex, religion, partner, education -Occupation (where, what?) -Lifestyle - cigarettes # pack years (1 pack year = 20 cig/ day/ year) - alcohol, caffeine, recreational drugs -diet, exercise, hobbies -living conditions
ROS (Review of Systems) “ Apart from the ‘presenting complaint’, how is your health?”
Conclusion: “Is there anything else you’d like to take about today?” “That has given me a pretty clear history of your ‘presenting problem’. Is there anything you would like to add at all? Any other concerns? Thank you very much for you time Mr Smith.” -a follow up arrangement should be arranges (and the patient should be encouraged to make contact sooner if symptoms worsen or they have further concerns.
EXAMPLE OF PATIENT HISTORY TEMPLATE (blank template on next page...) Name: _____________________
INTRODUCTION
Age: _____
Date:________
PP (Patient Particulars) -name, age, DOB, occupation?
PC (Presenting Complaint) HPC
“What concern brought you in here today?”
(History of Presenting Complaint)
*Also associated symptoms and ROS can be done here
-Associated symptoms? ROS can be done here.
N ature I ntensity Location “What concern brought you in here today?” Duration Onset C ontributing Aggravating Alleviating Radiating F eatures I mpact Attribute (What do you think is causing this Problem?) -Anyone around with similar symptoms? T reatment (Taking anything for it?) -Psych impact? *Psych impact?
SUMMARY of PC
PMH (Past Medical History)
“Apart from this can you tell me about any other illnesses/ surgeries you’ve had?”
-medical, surgical, trauma, obstetrics -drugs/ allergies -asthma meds, OCP, vaccinations, supplements? -asthma meds, OCP, vaccinations, supplements?
(Family History) FH -Home life? -stressed? Over-worked? -How is home life? -stressed? Overwhelmed?
SH (Social History)
“Are your parents still alive? How is there health?” “How about brothers or sisters? “Any diseases or conditions that run in the family?”
e.g. Smoking
How many packs a day? What sized packs? When did you start smoking? Has the amount you have smoked changed over time?
-age, race, sex, religion, partners, education -occupation QUANITIFY -lifestyle (cigarettes, alcohol, caffeine, recreational drugs, diet, exercise, travel) (QUANTIFY)
ROS (System Review) SUMMARY of IMPORTANT POINTS “Is there anything else you want t o tell me?” CONCLUSION “That’s given me a pretty clear history of your ‘PC’. Is there anything you would like to add at all? Any other concerns? Thank-you for your time.”
INTRODUCTION
Name: ___________________________
Age: _____
Date:__________
PP (Patient Particulars) -name, age, DOB, occupation?
PC (Presenting Complaint) HPC
(History of Presenting Complaint)
*Also associated symptoms and ROS can be done here
-Associated symptoms? ROS can be done here.
N ature I ntensity Location Duration Onset C ontributing Aggravating Alleviating Radiating F eatures I mpact Attribute (What do you think is causing this Problem?) -Anyone around with similar symptoms? T reatment (Taking anything for it?) -Psych impact? *Psych impact?
SUMMARY of PC
PMH (Past Medical History) -medical, surgical, trauma, obstetrics -drugs/ allergies -asthma meds, OCP, vaccinations, supplements? -asthma meds, OCP, vaccinations, supplements?
(Family History) FH -Home life? -stressed? Over-worked? -How is home life? -stressed? Overwhelmed?
SH (Social History) -age, race, sex, religion, partners, education -occupation QUANITIFY -lifestyle (cigarettes, alcohol, caffeine, recreational drugs, diet, exercise, travel) (QUANTIFY)
ROS (System Review) SUMMARY of IMPORTANT POINTS CONCLUSION
ASSOCIATED SYMPTOMS/ ROS CARDIO-VASCULAR Pain, shortness of breath, heart beating irregularly, pain in legs or feet, high blood pressure, ever had blue hands or feet?
RESPIRATORY Short of breath, cough- sputum/ phlegm (colour? blood? etc), wheeze, fever, recent chest xray?
GASTRO-INTESTINAL Indigestion, heart-burn, difficulty swallowing, nausea/ vomiting (blood?), pain, bloating, bowel habits/ stool (blood?), weight loss, yellow skin or eyes, blood transfusions?
MUSCKULO-SKELETAL Pain, skin rash, swelling, eyes dry or red, back/ neck pain
ENDOCRINE Unusually thirsty, sweating, appetite or weight changes, lethargy, hair distribution, polyuria, menstruation?
REPRODUCTIVE History of high blood pressure or diabetes with pregnancy, miscarriage?
MEDICAL INTERVIEW: CLINICAL COMMUNICATION SKILLS SHEET STUDENT’S NAME: __________________________________ GROUP No. ____ DATE OF ASSESSMENT: _______________TUTOR’S NAME: _______________ Code: 1=not acceptable, 2=not quite good enough, 3=OK, 4=good, 5=excellent MICRO SKILLS INTRODUCTION introduces self explains purpose of interview enquiries if patient is comfortable with the situation LANGUAGE avoids ambiguous and technical jargon avoids repetition. ACTIVE LISTENING listens with minimal interruptions unless necessary paraphrases facilitates the discussion gives verbal and non-verbal encouragement encourages interaction, receptivity uses transition statements QUESTIONS shows good use of open questions avoids excessive use of leading, loaded or closed questions avoids double-barrelled and multiple questions avoids irrelevant questions EYE CONTACT, BODY POSTURE, MANNERISMS natural, regular, attentive and direct eye contact (without staring) relaxed but attentive body posture - not rigid, symmetrical, slouched or bored no awkward, excessive or intrusive mannerisms, verbal or non-verbal behaviour which occurs repetitively VERBAL FLUENCY, VOICE PROJECTION average to slightly slower than average speech rate, not too fast, impatient, slow or hesitant clearly audible voice volume – not too loud or too soft SELF ASSURANCE confident, open and relaxed – not shy or embarrassed WARMTH AND EMPATHY voice tone warm and expressive, smiling where appropriate positive regard for the patient caring, attentive and non-judgemental concern APPROPRIATE NOTE-TAKING took notes does not intrude or interfere with the interview May use paper-and-pen or laptop CLOSING gives clear concluding statement – summarises main points enquires if patient has anything to add or ask
CODE
Comments
thanks the patient (B)HIGHER ORDER SKILLS CUE IDENTIFICATION AND INTERPRETATION appropriate response to, and understanding of patient’s statements follows up on verbal leads sensitive to patient’s non-verbal cues CONCENTRATES ON PATIENT RATHER THAN THE MECHANICS OF THE INTERVIEW not preoccupied with “What will I say next”. CONTROL controls and gives some direction to the interview but does not dominate the interview keeps patient relevant without overriding the patient’s free flow of information
*HANDLES EXPLICIT QUESTIONS APPROPRIATELY HANDLES PATIENT’S FEELINGS AND CONCERNS elicits patient’s feelings, fears, apprehensions, expectations and acknowledges patient’s feelings appropriately (e.g. reflects patient’s feelings non-judgmentally) HISTORY TAKING uses the bio-psychosocial approach elicits course, duration and current treatment of the problem encourages patient to be precise about dates of onset of illness, major events and recent events establishes patient’s past illnesses operations family history medications establishes lifestyle diet exercise smoking alcohol marital status/family responsibilities occupation
SYSTEMATIC APPROACH logical sequence and structure to the interview HYPOTHESIS GENERATION AND TESTING appears to generate and test hypotheses about the nature of the patient’s problem/s. TIME MANAGEMENT manages time in the interview appropriately. *Patient may not always ask questions (score N/A )
CLINICAL SKILLS
Introduction to Physical Examination
NOTE: Leave distressing/ uncomfortable examinations LAST! It is tradition to examine from the RIGHT SIDE of the patient. “Tell me if you feel uncomfortable of in pain at any time.”
These are the lymph nodes that can be palpated when performing a physical examination. LYMPH NODES: LYMPHADENOPATHY: swollen, enlarged lymph nodes
CLINICAL SKILLS
Gastro-intestinal System Exam
G ASTRO-I NTESTINAL EXAMINATION
The Gastro-intestinal History Red flags to look for: -Change in appetite -Unintentional weight loss/ gain -Dysphagia (difficulty swallowing) -Indigestion/ heart-burn -Nausea or vomiting -Haematemesis (vomiting blood) (is blood fresh (red), or is i t like ‘coffee grounds’) -Abdominal pain -Jaundice (yellowish tinge to eyes and skin) -Change in bowel motions -Blood in stool?- obvious red blood- lower GIT (e.g. haemorrhoids, cancer) -mixed blood (e.g. inflammatory bowel) -malaena – upper GIT – black digested blood (e.g. gastric ulcer)
The Gastro-intestinal Examination 2
BMI (body mass index) = mass (kg)/ height (m) <18: very underweight 18-20: underweight NOTE 20-25: acceptable Waste-to-hip ratio is a better predictor 26-29: overweight of heart attack than BMI 30-39: obese >40: morbidly obese Hepatic Flap (asterixis): Asterixis describes a motor disturbance characterised by intermittent lapses of an assumed posture. It is commonly associated with liver failure where it produces the flapping tremor of hepatic encephalopathy characterised by jerky, irregular flexion-extension movements at the wrist and metacarpophalangeal joints, often accompanied by lateral movements of the fingers. The motor disturbance may rarely involve the arms, neck, tongue, jaw and eyelids. It is usually bilateral, absent at rest, and asynchronous on each side. The mechanism is attributed to interference with the inflow of joint position sense to the reticular formation in the brainstem.
Bruising: Petechiae (small red dots), Purpura (bruises), Ecchymoses (very large bruises) -can be caused by aspirin, steroids, in elderly, malignancy with platelets, problems with clotting factors (synthesized in LIVER)
Petechiae: red or purple spot caused by minor haemorrhage (<0.3cm)
Purpura: (0.3-1cm)
Ecchymosis: larger size than petechia, but more diffuse border than purpure (>1cm)
Linea nigra: A dark vertical line that appears on the abdomen during about three quarters of all pregnancies. The brownish streak is usually about a centimeter in width. The line runs vertically along the midline of the abdomen from the pubis to the xiphoid process. It is a type of hyperpigmentation resulting from increased production of the pigment melanin thought to be caused by increased estrogen, the same process that causes the areolas to darken
Divarication of the Recti (hernia): The rectus abdominis muscles should meet in the midline at the linea alba. Superior to the umbilicus, some people have a congenital defect that results in a wider gap between them. As a result, when a patient flexes the abdominal muscles as when doing a sit-up, the rectus muscles spread apart (divaricate), and causes a bulge (slight hernia). The divarication is made more obvious when the patient lifts their head or legs off the bed when supine. Divarication is common in obese men, and those with poor muscle tone. It can be surgically corrected, although such an operation would be almost entirely for cosmetic purposes and not of any functional value.
Palpation: check for pain/ tenderness, shape (are borders smooth?), size, texture or organs (firm?), pulsations is a mass part of or
behind abdominal wall? Tense abdomen (lift/ raise head) and if you can still feel the mass it’s part of the abdominal wall)
Murphy’s sign: Pain -sub-costal, upper-right quadrant semi-lunaris = GALLBLADDER pathology sign
Splenomegaly: Splenomegaly is usually associated with increased workload (such as in hemolytic anemias), which suggests that it is a response to hyperfunction. Splenomegaly is associated with any disease process that involves abnormal red blood cells being destroyed in the spleen. Other common causes include congestion due to portal hypertension and infiltration by leukaemias and lymphomas. The finding of an enlarged spleen; along with caput medusa; is an important sign of portal hypertension. Percussion in last intercostals space on left side, breath in and out, Δ in resonance?- if becomes dull- indication of splenomegaly
Bruit: Any of several generally abnormal sounds heard on auscultation
Oedema: An abnormal excess accumulation of serous fluid in connective tissue or in a serous cavity. Can indicate diabetes or alcoholism. If bed bound- oedema will be sacral and not in t he legs. Five factors can contribute to the formation of edema: i) It may be facilitated by increased hydrostatic pressure or, ii) reduced oncotic pressure within blood vessels; iii) by increased blood vessel wall permeability as in inflammation; iv) by obstruction of fluid clearance via the lymphatic; or, v) by changes in the water retaining properties of the tissues themselves. Raised hydrostatic pressure often reflects retention of water and sodium by the kidney.
Ascites: is an accumulation of fluid in the peritoneal cavity. Although most commonly due to cirrhosis and severe liver disease, its presence can portend other significant medical problems
Finding Direction of Venous Blood Flow Examiner’s fingers
If fills, blood flow → Push blood away
Let go of finger
Vein X filling, blood flow ←
Hereditary haemochromatosis is associated with bronzing/ hyperpigmentation of the skin (excess iron deposition in the liver, heart and pancreas leads to fibrosis and organ failure, if untreated)
Leukonychia- white nail bed, typically of thumb index finger Koilonychia: spoon-shaped nails due to iron deficiency
Palmar erythema: reddening of thenar (thumb)/ hypothenar (pinky) eminences; suggestive of liver disease (disturbed [hormones], or alcohol)
Dupuytren’s Contracture: thickeing of palmar fascia, esp ring finger (associated with alcoholism, diabetes mellitus, epilepsy and smoking) -feel for it as well
Clubbing: ~1/3 cirrhosis patients, angle between plate and proximal nail fold >180° (also respiratory disorders and inflammatory bowel disease)
Xanthelasma: yellowish periorbital plaques, associated with hyperlipidaemia
Spider naevi: small angiomata on surface of skin, particularly on face, neck, shoulders. Thorax, arms, hands (~[hormones], eg. Oestrogen (males 2-3, females 5-6)
Bruises (purpura): -petechiae (1-2mm); small, red dots -ecchymoses; very large bruises NB. Can be due to problem with clotting factors, .: liver problem, & VitK deficiency)
Jaundice: (scleral icterus) yellowing of skin and eyes due to bilirubin (sign of liver disease)
Hepatic Flap (asterixis): bilateral asynchronous flapping of outstretched dorsiflexed hands seen in patients with hepatic encephalopathy (aka flapping tremor, liver flap)
Iritis: a form of anterior uveitis, and refers to inflammation of the iris (acute and chronic), can get with Crohn’s Disease
Telangiectasia: small dilated blood vessels near surface of skin or mucous membranes Geographic tongue (benign migratory glossitis) Papillae missing from some areas and over-crowded in others
Gingivitis: erythema and oedema of gingival margins (with blunting and hypertrophy of the interdental papillae)
Oral candidiasis: creamy, white curdlike patches, caused by Candida albicans, can be scraped away leaving bleeding surface
Glossitis: infection/ inflammation of tongue (smoothened appearance- loss of papillae) (IF & VitB deficiency~ one cause)
Leukoplakia: white thickened patched on mucosa, gums or tongue Aphthous stomatitis: single or multiple painful ulcerations of the buccal mucosa (immune reaction to oral bacteria?)
Striae: Caused by stretching due to growth and also hormonal changes
Gynaecomastia: hormone-induces swelling of male breast (hyperoestrogenism?)- seen frequently with cirrhosis
Caput Medusae with ascites
Ascites: fluid in peritoneal cavity, abdominal flanks and wall appear tense, shallow or everted umbilicus facing downwards (gross ascites umbilical hernia?)
Caput Medusae: rare sign of porto-systemic shunting (engorged para-umbilical veins radiating fro umbilicus to join systemic vein) severe portal hypertension (flows to legs) (check direction of venous blood flow) VS Inferior Vena Cava Obstruction: Abdominal collateral veins develop to bypass the blocked IVC and flows to head
CLINICAL SKILLS
Respiratory System Exam
R ESPIRATORY EXAMINATION Bronchiectasis: a chronic inflammatory or degenerative condition of one or more bronchi or bronchioles marked by dilatation and loss of elasticity of the walls Bronchitis: acute or chronic inflammation of the bronchial tubes Displaced Septum : deviation of the nasal septum from its normal position that results from a developmental abnormality or trauma and may be asymptomatic or cause nasal obstruction and predispose to sinusitis and nosebleed (nasal obstruction?? – Talley and O’Connor) Engorged Turbinates (nasal chonchae): can be caused by various allergic conditions Flapping Tremor: (asterixis) may occur with severe carbon dioxide retention, usually due to severe chronic obstructive pulmonary disease, however this is a late and unreliable sign Haemoptysis: expectoration of blood from some part of the respiratory tract Horner’s syndrome : a syndrome marked by sinking in of the eyeball, contraction of the pupil, drooping of the upper eyelid, and vasodilation and anhidrosis of the face, and caused by paralysis of the cervical sympathetic nerve fibers on the affected side PND (postnasal drip) : occurs when excessive mucus is produced by the sinuses. The excess mucus accumulates in the throat or back of the nose. It can be caused by rhinitis (allergic or non-allergic), sinusitis (acute or chronic), laryngopharyngeal acid reflux (with or without heartburn), o r by a disorder of swallowing (such as an esophageal motility disorder). Pulsus paradoxus: a pulse that weakens abnormally during inspiration and is symptomatic of various abnormalities (as in pericarditis) Rhinitis: inflammation of the mucous membrane of the nose marked especially by rhinorrhea, nasal congestion and itching, and sneezing Sinusitis: sinuses are tender on palpation Stridor: a harsh vibrating sound heard during respiration in cases of obstruction of the air passages -high ptch sound from turbulent air flow Urticaria: (hives) an allergic disorder marked by raised oedematous red patches of skin or mucous membrane and usually by intense itching and caused by contact with a specific precipitating factor (as a food, drug, or inhalant) either externally or internally
Dyspnoea: difficult or laboured respiration, ~breathlessness Class I: disease present but no dyspnoea or dyspnoea only on heavy exertion Class II: dyspnoea on moderate exertion Class III: dyspnoea on minimal exertion Class IV: dyspnoea at rest
Clubbing: patient with carcinoma of the lung has clubbing and hypertrophic pulmonary osteroarthopathy. Clubbing may be caused by platelet-derived growth factor, which activates fibroblasts and other connective tissue cells when platelet precursors lodge in the digitis.
Yellow Nail Syndrome: rare condition caused by hypoplasia of the lymphatic system. The nails are thickened and yellow, and there is separation of the distal nail plate from the nail bed (onchyolysis). It may be associated with pleural effusion and bronchiectasis, and usually lymphoedema of the legs.
Clubbing of the fingers of a HIV- positive 11 year old child due to chronic hypoxia. Pulmonary complications are common in HIV-infected children in the first decade of life and may progress to bronchiectasis.
Horner’s Syndrome: (left) The pupil of the affected eye is smaller (miotic), due to unbalanced sympathetic action; there is a partial ptosis of the upper eyelid, since sympathetic fibres supply the smooth muscle of the eyelid, and perhaps loss of sweating on the left forehead. The meiotic pupil responds briskly to light and near effort. This may be caused by a carcinoma in the apex of the left lung compressing the brachial plexus. If this is the case, the patient may also show weakness of finger abduction, and clubbing. Disruption of the sympathetic innervations to the eye anywhere along its path from the brain can result in an ipsilateral Horner’s syndrome.
Nasal Polyp: a projecting mass of swollen and hypertrophied or tumorous membrane of the nose or para-nasal sinuses. They are overgrowths of the mucosa that frequently accompany allergic rhinitis. They are freely moveable and non-tender. Associated with asthma (Talley and O’Connor).
Oral/ pharyngeal thrush: due to candida infection
Exudative tonsillitis: caused by the Epstein Barr virus. It may be mistaken for a bacterial tonsillitis, although glandular fever may be accompanied by tender enlargement of the liver and spleen, fevers and fatigue. If a penicillin, especially amoxicillin, is prescribed to a patient with glandular fever, the patient develops a rash.
Ulceration: The oral lesions of hand, foot and mouth disease are various-sized erosions and ulcerations on a surrounding erythematous base. Coxsackie virus A16 is the most common cause. Hand, foot and mouth disease most commonly occurs in children under the age of ten, and is also associated with lesions on the hands, palms and soles.
Pharyngitis (Streptococcal): Typically affects school-aged children, although adults may also be susceptible. This slide illustrates pharyngeal erythema, exudates and lymphoid enlargement. There is a right peritonsillar abscess, displacing the tonsil to the midline.
Barrel-Chest: when AP diameter is increased compared to lateral diameter beyond 0.9 is abnormal, and is seen in patients with sever asthma or emphysema
Pectus excavatum: ‘funnel-chest’. Concurrent respiratory diseases may occur in association with pectus excavatum, including bronchiectasis, asthma and chronic bronchitis.
Pectus carinatum: ‘pigeon chest’, involving anterior displacement of the sternum and costal cartilage. May be manifestation of childhood respiratory illness, in which case it is thought to result from repeated strong contraction of diaphragm while thorax is still pliable. Also occurs in rickets.
Chest X-ray Checklist
Kyphoscoliosis: backward and lateral curvature of the spine. Kyphoscoliosis may be idiopathic (80%), secondary to poliomyelitis, or associated with Marfan’s syndrome. Severe thoracic kyphoscoliosis may reduce lung capacity and increase work of breathing.
Normal Chest X-Ray
A- Airway (midline, no obvious deformities, no paratracheal masses) B- Bones and soft tissue (no fractures, subcutaneous emphysema) C- Cardiac size, silhouette and retrocardiac density normal D- Diaphragms (right above left by 1cm to 3cm, costophrenic angles sharp, diaphragmatic contrast with lung sharp) E- Equal volume (count ribs, look for m ediastinal shift) F- Fine detail (pleura and lung parenchyma) G- gastric bubble (above the air bubble one shouldn’t see an opacity of more than 0.5cm width) H- Hilum (left normally above right by up to 3cm, no larger than a thumb), hardware (in the intensive care unit: endotracheal tube, central venous catheters).
Bilateral lower lobe consolidations: (in a HIV patient). Clinically, we would expect reduced lung expansion, dullness to percussion, bronchial breath sounds, crackles, increased vocal resonance, and perhaps pleural rubs. The blood cultures were positive for Haemophilus influenza. This illness followed a rapidly fulminating course, and the patient died. Consolidations: due to bacterial lobar pneumonia, but a central bronchostenotic lesion should be considered.
Pneumothorax: (right-side) a condition in which air or other gas is present in the pleural cavity and which occurs spontaneously as a result of disease or injury of lung tissue, rupture of air-filled pulmonary cysts, or puncture of the chest wall or is induced as a therapeutic measure to collapse the lung
Chronic Obstructive Pulmonary Disease: This chest X-ray of a heavy smoker shows hyperinflated lungs, a flattened diaphragm, and a long narrow cardiac silhouette. Clinically, there may be the use of accessory muscles during inspiration, pursed lips during expiration, a barrel-shaped chest with reduced lung expansion, hyper-resonant percussion, decreased liver dullness, decreased breath sounds and early inspiratory crackles.
Pleural Effusion: This chest x-ray shows moderate-sized right side pleural effusion. This patient presented with a fever, cough and dyspnoea. Clinically, we would expect reduced lung expansion on the right, stony dullness to percussion, reduced or absent breath sounds, and reduced vocal resonance. Chlamydia pneumonia was isolated from the pleural fluid and nasopharyngeal culture. NB: the upper margin of the effusion is curved ‘meniscus sign’ (Talley).
Right Lower Lobe Pneumonia: This Xray shows a density in the right lower lobe. Clinically you may find reduced expansion on the affected side, dullness (but not stony dullness) to percussion, bronchial breath sounds, inspiratory crackles, increased vocal resonance, and perhaps a pleural rub.
NOTES FROM CLINICAL COACHING ~ RESPIRATORY EXAMINATION
th
-mitral valve – 5 intercostals space
inside
the mid-clavicular line on the left side
GENERAL OBSERVATIONS -barrel-chest can be normal body shape (esp if excess weight), or due to asthma or smoking (i.e. emphysema) HAND & UPPER LIMB - look for anaemia- pallor of the palmar creases -check for peripheral cyanosis (bluish tinge) NOTE: If ↓RBCs – cyanosis occurs later on (as low O 2 saturation occurs later on) Vs ↑RBCs (e.g. due to ‘ polycythemia’ , if hypoxic more RBCs flushed and really pink skin but becomes cyanosed easily) – cyanosis earlier Peripheral cyanosis:- sludging of blood in the periphery/ vascular shunting (e.g. due to cold); but oxygenation of blood near heart is normal Central cyanosis: -deoxygenated arterial blood around heart ~watch out for ‘pulse oximetry’- do on hand
without BP
cuff
-look for muscle wasting (esp of hands and fingers chronic hypoxia) -look for asterixis (flapping tremor) –can be caused by respiratory acidosis
Respiratory Rate: (chronic anaemia can also cause ↑RR) -average for adult ~18-20 breaths per minute, for accuracy take over 30secs to 1 min (if slower RR take for 1 min over longer period) -must be taken when patient is UNAWARE (.: take when checking patient’s radial pulse) -patient should not be talking Look for: chest moving, back moving, hearing (only if laboured breathing) etc… Axillary Lymph Nodes (can be taken at end of examination) -(i) apex of axilla, lateral chest wall (arm of patient can be resting down on your hand?) -(ii) turn hand around (palm – superior), up against medial/ inner side of arm
Apex
Medial arm
Lateral chest wall
HEAD/ FACE
(ii) Hand (palm towards (i) Hand medial arm) (palm towards lat chest wall)
To check axillary lymph nodes: press hand into all 4 walls of the axilla (anterior, posterior, medial, lateral) and then up into apex
NOSE: -look for object in nose – can interfere with breathing sounds (e.g. can sound like stridor) -check septum – especially the antero-inferior part known as Little’s Area or Kiesselback’s plexus major blood vessels – where you get nose bleeds
-check turbinates (chonchae)- inflamed?? -check for nasal polyps- ‘red pearls/ grapes’ in nose, usually covered with mucous
Infection/ allergy situation
MOUTH: -check under tongue for bluish tinge indicative of central cyanosis -tonsils? –inflamed, exudative?; scarred, white nothingness = tonsils removed -adenoids nose – itchy? Blocked? -check for Koplik’s spots Koplik’s spots: Little spots inside the mouth that are highly characteristic of the early phase of measles (rubeola). The spots look like a tiny grains of white sand, each surrounded by a red ring. They are found especially on the inside of the cheek (the buccal mucosa) opposite the 1st and 2nd upper molars. Koplik's spots. Bright erythema of buccal mucosa with pinpoint white macules in rubeola.
FACE -inflamed sinuses? = inflamed face percuss sinuses by tapping with single finger (not onto another finger), and not too hard -ethmoid and frontal (frontal headaches?) and maxillary sinuses -NB many children and some adults don’t have frontal sinuses -if painful = sinusitis? -transillumination? –torch into inflammatory cavity and then sinuses light up like lantern
NECK: -palpation of trachea in sternal notch (warn patient first!!!) -extend head back slightly - check windpipe is equal distance from strap muscles -watch out- may cause coughing fit- don’t do too deeply or for too long Neck
strap muscles trachea
fingers
-also look for tracheal tug
IMPORTANT LANDMARKS Ribs (12 pairs) -7 true -5 false (2 floating)
Jugular notch manubrium n
2 rib
Sternal angle
-C6/C7 – most prominent spinous process of neck vertebrae (at back) -spinous process of T2 ~ spine of scapula
Body of sternum
Xiphoid process of sternum NOTE inferior spine of scapula has ↑ muscle attachments muffles sound .: patient ‘hugs’ chest to move scapula laterally out of the way
CHEST MOVEMENT - look for symmetry (COMPARE LEFT AND RIGHT SIDES) - quiet respiration & ask to take deep breath in - pleural rub/ pneumonia/ broken rib = less movement on affected side -FRONT? Look for use of accessory muscles (e.g. sternocleido-mastoid muscles – strap muscles) - bracing against object/ hips??
PALPATION
look
for symmetry (difference between sides??)
Apex of lungs
1 2 3
cm expansion? – around nipples 1 2 3
Costal margin and fingers on lower ribs (max flare)
Note expansion -diaphragmatic excursion should be ~3-5cm (4) -can also do on lateral side of chest under arms (lateral to (3))
Compare Left/ Right (i) expansion (ii) vocal fremitus (palpable vibration) – say ‘99’ (the more inferior, the further from the voice box, the less strong the vocal fremitis) (iii) may be able to feel a wheeze (can sometimes transmit through
PERCUSSION -hit enough areas to cover all lobes and determine dullness/ resonance -fingers should be positioned parallel to ribs - L/R comparative percussion at same level
How many levels?? – (7) -in pneumothorax
hyper-resonance
at apex
Patient: mouth slightly open, and deep breath, but not too deep (just slightly more than normal)
Normal breath sounds: -heard over near all parts of chest -ask to breathe through mouth so sounds form nasopharynx does not interfere -louder and longer on inspiration vs expiration, and there is no gap between inspiratory and expiratory sounds
Normal bronchial breathing
apex
Bronchial breath sounds: -hollow, blowing quality -they are audible throughout expiration and there is often a gap between inspiration and expiration -expiratory sound has a higher intensity and pitch than the inspiratory sound -heard over areas of consolidation
1 2 3 4
7 6
Added (adventitious) sounds: (i) continuous wheezing (ii) interrupted crackles NOTE when sound occurs, Beginning of inspiration? Throughout?
5
If long chest...
can
also percuss clavicles
AT EVERY POINT (1) Percussion (resonance?) (2) breath sounds (3) vocal sounds (say ‘99’)
Percussion Notes and Their Meaning Flat or Dull
Pleural Effusion or Lobar Pneumonia
Normal
Healthy Lung or Bronchitis
Hyperresonant Emphysema or Pneumothorax
Adventitious (Extra) Lung Sounds Crackles
These are high pitched, discontinuous sounds similar to the sound produced by rubbing your hair between your fingers. (Also known as Rales)
Wheezes
These are generally high pitched and "musical" in quality. Stridor is an inspiratory wheeze associated with upper airway obstruction (croup).
Rhonchi
These often have a "snoring" or "gurgling" quality. Any extra sound t hat is not a crackle or a wheeze is probably a rhonchi.
CORRELATION OF PHYSICAL SIGNS & DISEASE
CONSOLIDATION (lobar pneumonia) Pneumonia = inflammation of the lung with exudation into alveoli Expansion: reduced on affected side Vocal fremitus: increased on affected side Percussion: dull, but not stony dull Breath Sounds: bronchial Additional Sounds: medium, late or pan-inspirational crackles as pneumonia resolves Vocal Resonance: increased Pleural Rub: may be present
COLLAPSE e.g. bronchus obstructed by tumour mass, foreign body Trachea: displaced towards collapsed side Expansion: reduced on affected side with flattening of chest on same side Percussion: dull over the collapsed area Breath Sounds: reduced, with or without bronchial breathing above area of collapse Note: there may be no signs with complete lobar collapse, the early changes after inhalation of a foreign body may be over-inflation of the affected side.
PLEURAL EFFUSION Collection of fluid in pleural space (blood = haemothorax, chyle = chylothorax, pus = empyema) (cardiac failure, hypothyroidism, pneumonia, neoplasm, TB, pulmonary infarction etc) Trachea and apex beat: displaced away from a massive effusion Expansion: reduced on the affected side Percussion: stony dullness over the fluid Breath Sounds: reduced or absent, there may be an area of bronchial breathing audible above the effusion due to compression of overlying lung Vocal Resonance: reduced
PNEUMOTHORAX Leakage of air from the lung or a chest wall puncture into the pleural space causes pneumothorax; spontaneous or traumatic Expansion: reduced on affected side Percussion: hyper-resonance if the pneumothorax is large Breath Sounds: greatly reduced of absent There may be subcutaneous emphysema. There may be no signs if the pneumothorax is small (less than 30%).
TENSION PNEUMOTHORAX This occurs when there is communication between the lung and the pleural space, with a flap of tissue acting as a valve, allowing air to enter the pleural space during inspiration and preventing it from leaving during expiration. Air accumulates under increasing pressure in pleural space, causing considerable displacement of mediastinum with obstruction and kinking of great vessels. Trachea and apex beat: displaced away from the affected side
Expansion: reduced or absent on affected side Percussion: hyper-resonant over affected side Breath sounds: absent Vocal resonance: absent The patient is often tachypnoeic and cyanosed, and may be hypotensive.
BRONCHIECTASIS Pathological dilation of the bronchi, resulting in impaired clearance of mucus, and chronic infection. A history of chronic cough and purulent sputum since childhood is virtually diagnostic. Systemic signs: fever, cachexia, sinusitis (70%0 Clubbing and cyanosis Sputum: voluminous, purulent, foul-smelling, sometimes bloodstained Coarse pan-inspiratory or late inspiratory crackles over the lobe Signs of severe bronchiecstasis: copious sputum, haemoptysis, clubbing, widespread crackles, signs of airway obstruction, signs of respiratory failure, signs of secondary amyloidosis
BRONCHIAL ASTHMA This may be defined as paroxysmal recurrent attacks of wheezing (or in childhood of cough) due to airways narrowing which changes in severity over short periods of time. Wheezing, tachypnoea, dry or productive cough, tachycardia, prolonged expiration, prolonged forced expiratory time, use of accessory muscles of respiration, hyperinflated chest, inspiratory and expiratory wheezes Signs of severe asthma: appearance of exhaustion and fear, breathlessness, drowsiness, cyanosis, tachycardia, pulsus paradoxus, reduced breath sounds
CHRONIC OBSTRUCTIVE PULMONARY DISEASE- chronic airflow limitation (From predominantly emphysema) Diagnosis on basis of three findings (i) History of heavy smoking (more than 70 pack years) (ii) Previous diagnosis of emphysema or COPD (iii) Reduced breath sounds.
EMPHYSEMA Hyperinflation, patients are usually not cyanosed but are dyspnoeic and are sometimes called ‘pink puffers’ , usually caused by smoking Barrel shaped chest, increased AP diameter Pursed lip breathing Use of accessory muscles of respiration Palpation: reduced expansion and a hyper-inflated chest Percussion: hyper-resonant with decreased liver dullness Breath Sounds: decreased, early inspiratory crackles Wheeze is often absent Signs of right heart failure may occur, but only in late course of disease
CHRONIC BRONCHITIS Defined clinically as the daily production of sputum from three months of the year for at least two consecutive years. Loose cough and sputum (mucoid or muco-purulent) Cyanosis: present in latter stages, and associated oedema from right ventricular failure
Palpation: hyper-inflated chest with reduced expansion Percussion: increased resonance Breath Sounds: reduced with end-expiratory high or low pitched wheezes and early inspiratory crackles Signs of right ventricular failure (Smoking is major cause, but recurrent bronchial infection may cause progression)
PULMONARY FIBROSIS: Diffuse fibrosis of lung parenchyma impairs gas transfer and causes ventilation-perfusion mismatching. Can result from inhalation of mineral dusts (focal fibrosis), replacement of lung tissue following disease which damages the lungs (e.g. TB), or interstitial disease (fibrosing alveolitis). General: dyspnoea, cyanosis and clubbing may be present Palpation: expansion is slightly reduced Auscultation: fine (Velcro-like) late inspiratory or pan-inspiratory crackles heard over the affected lobes Signs of associated connective tissue disease: rheumatoid arthritis, systemic lupus erythrematosus, scleroderma, Sjögren’s syndrome, polymyositis and dermatomyositis
TUBERCULOSIS: Primary: Usually no abnormal chest signs, but segmental collapse, due to bronchial obstruction by the hilar lymph nodes, occasionally occurs. Post-primary TB: Often no chest signs. The clues to the diagnosis are the classical symptoms of cough, haemoptysis, weight loss, night sweats and malaise. Miliary TB: Fever, anaemia and cachexia are the general signs. The patient may also be dyspnoeic, and pleural effusions, lymphadenopathy, hepatosplenomegaly or signs of meningitis may be present.
MEDIASTINAL COMPRESSION Mediastinal structures may be compressed by a variety of pathological masses, including carcinoma of the lung (90%), other tumours (lymphoma, thyroma, dermoid cyst), a large retrosternal goitre or rarely an aortic aneurism. Superior vena cava obstruction Tracheal compression: stride, usually accompanied by respiratory distress Recurrent laryngeal nerve involvement: hoarseness of voice Horner’s syndrome Paralysis of the phrenic nerve
CARCINOMA OF THE LUNG NOTE many patients have no signs Haemoptysis Clubbing Lobar collapse or volume loss Pneumonia Pleural effusion Fixed inspiratory wheeze Tender ribs (secondary deposits of tumour in ribs) Mediastinal compression, including signs of nerve involvement Supraclavicular or axillary lymphadenopathy Distant metastases brain, liver and bone most commonly affected organs Non metastatic extrapulmonary manifestations:
-anorexia, weight loss, cachexia, fever -endocrine changes -neurological manifestations -haematological manifestations -skin and renal effects
SARCOIDOSIS Systemic disease characterised by the presence of non-caseating granulomas which commonly affect the lungs, skin, eyes, lymph nodes, liver and spleen and the nervous system. The aetiology is unknown. Pulmonary signs: Lungs: no signs usually, although 80% of patients have lung involvement. In severe disease there may be signs of pulmonary fibrosis. NOTE: there are many other extrapulmonary signs
PULMONARY EMBOLISM Embolism to the lungs often occurs without symptoms. One should always entertain this diagnosis if there has been a sudden and unexplained dyspnoea. Pleuritic chest pain and haemoptysis occur only when there is an infarction. Syncope or the sudden onset of sever substernal pain can occur with massive embolism. NB a firm diagnosis cannot be made from signs and symptoms alone. General signs: tachycardia, tachypnoea, fever (with infarction) Lungs: pleural friction rub if infarction has occurred Massive Embolism: elevated jugular venous pressure, right ventricular gallop, right ventricular heave, tricuspid regurgitation murmur, increased pulmonary component of the second heart sound Signs of deep venous thrombosis: fewer than 50% of patients have clinical evidence of a source
CLINICAL SKILLS
Cardio-vascular System Exam
Look for evidence for oedema/ ascites This patient with cor pulmonale has marked peripheral cyanosis, increased venous filling pressure with hepatomegaly, abdominal distension secondary to ascites, severe peripheral oedema, and elevated jugular venous pressure. Cor pulmonale may be caused by primary or secondary pulmonary hypertension with associated right ventricular failure. Cor pulmonale is the effect of a chronic respiratory disease (e.g. COPD) on the heart. RV failure ↑JVP, enlarged liver and peripheral oedema
Cyanosis: This shows a 17 year old male with an unrepaired ventricular septal defect, and secondary pulmonary hypertension. Cold weather alone can cause peripheral cyanosis of the fingertips and lips. Central cyanosis, caused by abnormal amounts of arterial deoxygenated haemoglobin, is best noted in parts of the body with good circulation, e.g. the tongue.
Hands and Upper Limbs: Tendon xanthomata: yellow orange deposits of lipid in the tendons that o ccur in type II hyperlipidaemia. These can be seen over the tendons of the hand and arm.
C, Achilles tendon xanthomas. Note the marked thickening of the tendons. D, Tendon xanthomas.
Palmar xanthomata and tuboeruptive xanthomata : over the elbows and knees are characteristics of type III hyperlipidaemia.
E, Tuberous xanthomas. F, Palmar xanthomas. G, Eruptive xanthomas
Raynaud’s phenomenon: is an abnormal response of the fingers and toes to cold, due to spasm of the distal arteries. The fingers turn white, then blue, and finally red after exposure to cold. It is during the red phase that the pain is most sever. Females are more likely to be affected.
Peripheral cyanosis and clubbing in a 36 year old woman sue to a complete atriovenrticular canal defect, and advanced pulmonary hypertension.
Signs of infective endocarditis: Splinter haemorrhages (of the nail beds): linear haemorrhages lying parallel to the long axis of the nail. They are most often due to trauma, particularly in manual workers. However, an important cause is infective endocarditis, which is bacterial or other infection of the heart valves or part of the endocardium. Other rare causes of plinter haemorrhages include vasculitis, sepsis anywhere else in the body, haematological malignancy or profound anaemia.
Check every nail bed!!!
Janeway lesions: are non-tender erythematous maulopapular lesions containing bacteria, which occur very rarely on the pals or pulps of the fingers in patients with infective endocarditis.
Osler’s nodes: are rare manifestations of infective endocarditis. These re red, raised tender nodules on the pulps of fingers (or toes), or on the thenar or hypothenar eminences. They are seen in fewer than 5% of patients.
Mouth Xanthelasma is characterised by soft yellowish plaques of the eyelids. Xanthelasma is the most common form of xanthomatosis. In xanthomatosis, lipid-laden histioncytes are deposited in the skin, due to hyperlipidaemia.
Check mouth and teeth as potential source of endocarditis. Although many bacteria can cause endocarditis, one type that lives in the mouth, called Streptococcus viridans, is responsible for half of all cases, which is why dental procedures are the most common cause of endocarditis. Therefore children with congenital heart disease should take antibiotics before undergoing dental procedures.
Neck
Inspect the neck for a visible jugular venous pulse with the patient lying at 45o. Estimate the JVP (measured vertically from the sternal angle), and it should be less than 3cm.
Assessing Pulse Character: Rate: normal for adults is between 60 and 80 beats per minute. Bradycardia <60. Tachycardia >100. An athlete may have a resting pulse rate of 40-50. Rhythm: regular (intervals between beats is constant) or irregular (interval is not constant) Pulse force: A full pulse is felt as if a strong wave had passed beneath fingertips. When a pulse feels weak and thin, the pulse is described as thready. A bounding pulse is a strong and forceful pul se often associated with high blood pressure or fluid overload. Radial Pulse
Carotid pulse: (common carotid artery) beneath the angle of the mandible, medial to sterno-cleido mastoid muscle. Palpate only one at a time. Check for rate, rhythm and character.
Chest: Palpation:
(i) find apex beat (ii) describe location and note if it is displaced (>2cm lateral to mid-clavicular line) – indicates hypertrophy, cardiomegaly, mediastinal shift…
Auscultation:
Apex beat: most distal and lateral palpable beat of heart, take heart rate
-listen to all areas with diaphragm, then use the bell to auscultate the mitral (M) area. While holding the bell against M, turn the patient over into the left lateral position. Next, auscultate the A and P areas while the patient is sitting up and leaning forward, after a full expiration and holding their breath. *Mechanical murmur (patent ductus arteriosus)listen posteriorly between scapula
Left lateral position
ALSO do auscultation of the back between the two scapulae (while the patient is holding their breath) and listen for a ‘machinery mumur’: he long “continuous” rumbling murmur of patent ductus arteriosus
Abdomen Liver palpation: (i) is the liver edge palpable? (ii) is it tender? (iii) is it pulsatile ( suggesting tricuspid regurgitation)
MEASURING BLOOD PRESSURE: Take 2 readings for each arm and then staning. If readings don’t correlate, take until 2 similar readings achieved.
Lower Limbs: Peripheral arterial disease: Other findings commonly noted in inspection include ulcerations, petechiae, infarcted areas and various trophic skin changes. Trophic changes include thinning or thickening of the skin in response to chronically inadequate blood flow, changes in hair growth, callus formation etc.
Pitting oedema: a mark persists on this patient’s foot after pressure has been applied by the thumb for at least 15 seconds. The skin indentation only slowly refills. Pitting oedema occurs in a range of conditions, including cardiac failure. It is important to assess the upper level of the oedema (e.g. “pitting oedema to mid-thigh”).
Neuropathic ulcer: on the right hallux has developed in a pressure points with diminished sensation due to diabetes. Surrounding skin is usually calloused. There is no pain, which sometimes results in the ulcer going unnoticed. Associated signs include decreased sensation and absent ankle jerks.
This picture shows an ischaemic toe due to peripheral arterial disease. The peripheral pulses will be decreased, with foot pallor on elevation, and dusky rubor on dependency. The patient may experience intermittent claudication when walking (i.e. painful ischaemia of the lower leg which is relieved by rest). Gangrene may develop. Ischaemic skin ulceration is most likely to occur on the heel, the lateral malleoli, or at the base of the toes, since these sites are subjected to repeated trauma during ambulation. Skin surrounding the ulcer shows no callous or excess pigment.
Varicose veins: are dilated tortuous and elongated superficial veins in the leg. The veins are dilated because of incompetence of the valves in the superficial veins, or in the perforating veins between the deep and superficial systems. Inspect for varicosities of the long saphenous vein (below the femoral vein in the groin to the medial side of the lower leg), as shown here, then inspect the back of the calf dor varicosities of the short saphenous vein (from the popliteal fossa to the back of the calf and lateral malleolus).
Chronic venous insufficiency . Due to venous occlusion or incompetence of the venous valves, may result in ulceration on the inner or sometimes outer ankle. This ulceration is associated with pigmentation, sub-cutaneous oedema (induration) and varicose eczema (or “stasis dermatitis”). There may be diffuse aching of the leg. Get
patient to stand to check for varicose veins
Buerger's test is used to assess the adequacy of t he arterial supply to the leg. It is performed in t wo stages. With the patient supine, elevate bot h legs to an angle of 45 degrees and hold for one to two minutes. Observe the color of the feet. Pallor indicates ischaemia. It occurs when the peripheral arterial pressure is inadequate to overcome the effects of gravity. The poorer the arterial supply, the less the angle to which the legs have to be raised for them to become pale. Then sit the patient up a nd ask them to hang their legs down over the side of the bed at an angle of 90 degrees. Gravity aids blood flow and colour returns in the ischaemic leg. The skin at first becomes blue, as blood is deoxygenated in its p assage through the ischaemic tissue, and then red, due to reactive hyperaemia from post-hypoxic vasodilatation. Both legs are examined simultaneously as the changes are most obvious when one leg has a normal circulation.
This test is not very sensitive (~50%), but it is specific
LOWER LIMB PULSES Femoral Pulse: Locate the superior border of the pubis in the mid line of the body; this is the uppermost part of the pubic symphysis. Feel the anterior limit of the iliac crest. The femoral pulse can be found midway between these two bony points (the mid-inguinal point)
Dorsalis Pedis Pulse The dorsalis pedis artery pulse can be palpated readily lateral to the extensor hallucis longus tendon (or medially to the extensor digitorum tendons) on the dorsal surface of the foot. Place your fingers half way down the dorsum of the foot on the bony area in the line between the first and second toes. The bones you can feel are the dorsal aspect of the navicular and the intermediate cuneiform bones. It is absent, unilaterally or bilaterally, in 2-3 % of young healthy individuals.
Posterior Tibial Pulse: Locate the medial malleolus. 2-3cm below and behind it you should fi nd the posterior tibial pulse. when taking the pulse on your own foot it is easier to use the thumb. In clinical practice the pulse is palpated using the pulps of the index and middle fingers. The artery is slightly deeper placed than the dorsalis pedis and therefore more concentration is often required to feel its pulsations.
Popliteal pulse: Ask the subject to bend the knee so that it is flexed to about 90 degrees. Sit on the ri ght hand edge of the bed close to the subject right foot. As before gently clasp the sides of the knee (of either limb) and press the pulps of your fingers into the popliteal fossa.
Heart sounds and murmurs:
http://depts.washington.edu/physdx/heart/tech.html
S1: First heart sound (M & T) Check for – loud heart sound (hyperdynamic (fever, exercise), mitral stenosis, atrial myxoma (rare) soft first sound (low cardiac output, tachycardia, severe mitral reflux) variable intensity (atrial fibrillation, complete heart block) S2: second heart sound (A & P) Check for – loud aortic component (systemic hypertension, dilated aortic root) soft aortic component (calcific aortic stenosis) loud pulmonary component (pulmonary hypertension) SPLITTING (see below) Splitting of S2 Audible expiratory splitting means > 30 msec difference in the timing of the aortic (A2) and pulmonic (P2) components of the second heart sound. -Splitting of S2 is best heard over the 2nd left intercostal space -The normal P2 is often softer than A 2 and rarely audible at apex Differential Diagnosis of P 2 audible at apex = Significant pulmonary hypertension, Atrial septal defect Findings should be present in both upright and supine positions: normal subjects may have expiratory splitting when recumbent that disappears when upright.
Extra Heart Sounds (S3 & S4) A triple rhythm in diastole is called a gallop and results from the presence of a S3, S4 or both. Description: Both sounds are low frequency and thus best heard with the bell of the stethoscope. Location: If originating from LV -Usually best heard over apex with patient in the left lateral position -Softer during inspiration If originating from RV -Usually best heard over left lower sternal border -Louder during inspiration S3: third heart sound -Low frequency sound in early diastole, 120 to 180 ms after S2 -Lub du bub S1S3S2 cadence similar to "Kentucky" -Results from increased atrial pressure leading to increased flow rates, as seen in congestive heart failure, which is the most common cause of a S3. Less commonly, valvular regurgitation and left to right shunts may also result in a S3 due to increased flow. May be normal physiological finding in patients less than age 40. S4: fourth heart sound -Low frequency sound in presystolic portion of diastole, -Belub dup S1S4S2 cadence similar to "Tennessee" -Seen in patients with stiffened left ventricles, resulting from conditions such as hy pertension, aortic stenosis, ischemic or hypertrophic cardiomyopathy. In patient with mitral regurgitation, suggestive of acute onset of regurgitation due to the rupture of the chorda tendinae that anchor the Valvular leaflets.
Clicks and Snaps Ejection click: Most common early systolic sound; Results from abrupt halting of semilunar valves Aortic : loud high frequency, does not vary with inspiration, best heard at apex, Causes associated with aortic valve with decreased but some residual mobility: i.e., aortic stenosis, bicuspid aortic valves and dilated aortic root; not generally heard with calcific aortic stenosis due to non-mobile valve Pulmonary : early systolic ejection sound with associated murmur, often diminishes on inspiration, sterna edge 2 or 3 ICS, Causes associated with pulmonic valve: pulmonic stenosis, pulmonary hypertension and dilated pulmonary trunk Opening snap Description: High-frequency early diastolic sound (occurs 50-100 msec after A2) associated with mitral stenosis; sound due to abrupt deceleration of mitral leaflets sound with associated murmur. Often diminishes with inspiration' accentuated in left lateral position. Location: Between apex and left lower sternal border Sounds like:RUP bu Dup rrrrrrRup Bu Dup Correlating to s1, s2, OS, murmur of mitral stenosis, Clinical significance: The OS plus typical murmur indicates the murmur is due to mitral stenosis and not a flow rumble across a non-stenotic valve. The timing of the OS has been suggested as a gauge of the severity of the stenosis but has not been found to be reliable for this. Mid-systolic click (plus late systolic murmur of mitral valve prolapse) Others: Prosthetic valves Prosthetic mitral valve sounds: (opening sound analogous to opening snap, closing sound coincides with S1 ) Prosthetic aortic valve sounds: (opening sound analogous to ejection click, closing sound coincides with S2)
Murmurs: Cardiac murmurs can be divided into three categories based on where they occur in the cardiac cycle; systolic, diastolic and continuous. Analyse the murmur for Intensity (Grade) Where it occurs in systole Where it is best heard and where it radiates to What it sounds like What happens during special maneuvers Note: Short, quiet systolic murmurs are generally benign. Long systolic murmurs, diastolic murmurs and continuous murmurs are generally pathologic. (Two continuous murmurs that are benign are mammary soufflé and cervical venous hum.)
Systolic Causes -Blood flow through a structure normally closed during systole (mitral or tricuspid valves or the interventricular septum). -Blood flow through a valve normally open in systole but abnormally narrowed (e.g. aortic or pulmonary stenosis). -Increased blood flow through a normal valve (a flow murmur).
CLINICAL SKILLS
Musculoskeletal System Exam
MUSCULO-SKELETAL SYSTEM:
CLINICAL EXAMINATION
HISTORY TAKING
*
- Chronic > 6 weeks (if <6 weeks- still acute phase) Systems Review - Does it involve the muscle, bone or joint? or is there another association? - vasculitis of skin, liver, kidney - inflammatory bowel (Δ bowel habits? Loose? B lood?) -if 1° problem is related to - neisseria gonorrhoea joint pain (with urinary burning) joints ask about specific - iritis (red eyes)- found in types of arthritis conditions - smokey urine, kidney pain??
PAIN is a common presenting problem Stiffness, deformity, functional impairment -What joints are involved? -Level of impairment? -Characteristics? e.g. psoriatic arthritis – have you ever had skin rashes? Where is the pain?
-In the joint? Bone? Or muscles around it? (You can’t move because joint is sore or are the muscles weak?) When do you get the pain? And how long does the pain last?
-claudication (ischaemic pain) dissipates in minutes vs arthritic pain that takes 30min to hours to dissipate -can you walk normally afterwards? Yes for claudication, but stiff and sore for arthritis. -Do you have pain at rest? Does it get worse or better as you go along? -arthritis: bad better bad again with movement -inflammation: exercise = bad for ~30min, then settles down, but pain at rest
BACK PAIN a lot of limb pain can be referred to the pain -sciatic pain: ‘sciatica’ is nerve pain arising from the sciatic nerve. It can be produced by pressure on the nerve, where it passes through the buttock. -also visceral referred pain to shoulder (e.g. gallbladder), jaw etc...
*Degree of pain? How much pain relief do you need? Paracetamol, NSAIDs, narcotics (opiates)? *How does it interfere in your daily living? – how aggressive does treatment need to be? What are the patient’s lifestyle requirements: sitting all day (.: only control) vs athlete (‘level of commitment’?- if you have a full reconstruction you need to adhere to post op)
DISTIBUTION? – one joint vs multiple One joint: -have you injured this joint before, and did it involve the joint surface (e.g. tibial plateau fracture). -suggestive of acute condition (~injury) or infection (septic arthritis) Multiple: - is it symmetrical? -suggestive of generalised inflammatory disorders i) Rheumatoid arthritis: symmetrical, small joints ii) Psoriatic arthritis: can be a asymmetrical
AGGRAVATING and RELIEVING Factors -Degenerative – rest eases pain -Inflammation- no change (pain won’t go away though it might ease) STIFFNESS- all diseases of the joints cause stiffness - Inflammatory- long time to wear off (hour or more)m nay be diurnal, improves with exercise - Degenerative- settles quite quickly (<1 hour), mechanical (worse with exercise) SWELLING: in joint or in surrounding tissue e.g. oedema; (distinguish by palpation) -boggy ? Around joint – reactive swelling (infective, inflammatory process)
Baker’s cyst (popliteal cyst): benign swelling of the semimembranous bursa found behind the knee joint that usually arise from almost any form of knee arthritis and cartilage (particularly the meniscus) tear calf soreness (need to exclude DVT)
TENDERNESS: is it the joint, bone or muscle? -bone tenderness is fairly constant – wakes you at night (malignancy related? Acute osteomyelitis) FAMILY HISTORY? -psoriasis, rheumatoid arthritis, Crohn’s disease RED FLAGS 1. Multitude of diseases- AIDs, inflammatory joint disorders, haematological malignancies (multiple myeloma) 2. Weight loss- malignancy or thyroid? 3. Bone scan: multiple myeloma, bone tumour, abscess (e.g. extra dural abscess of spine) 4. <20yo: juvenile onset of destructive joint disease? >50yo – secondary malignancy (does patient have history of breast cancer? –bony metastases) -osteoporotic crush fracture (impacted fracture?)- post menopausal women and men >70yo 5. IV drug use- increase risk of infection 6. cauda equina –pressure on sacral/ lumbar spinal nerves IF back pain?- do you have control or urine (urinary incontinence) and bowels (toneless anus?) = orthopaedic emergency YELLOW FLAGS - Will maximise their condition -Sleep disturbance – classic depression: sleep in the afternoon, but wake early in the morning and can’t get back to sleep.
Nature Intensity Location Duration Onset Characteristics Aggravating factors Relieving factors Features Impact Attribute- what do you think caused it? Treatment Inflammatory
Non-Inflammatory
-present at rest, many joints -long lasting stiffness, >1 hour -haphazard variance of pain, rest and stiff next day, X related to meds -affected by weather (cold/ rain?) -swelling- intermittent and often not related to pain and can move between joints -e.g. Reiter’s syndrome/ reactive arthritis: autoimmune condition that develops in response to an infection in another part of the body. Coming into contact with bacteria and developing an infection can trigger reactive arthritis -chlamydia can also cause reactive arthritis
-pain when start moving joint, better with rest -stiffness is short lasting -improves with periods of rest -busy one day, stiff next day, related to med use -swelling- usually localised (no systemic associated symptoms usually) -e.g. osteoarthritis
THE CERVICAL SPINE EXAMINATION
*
Positioning and Exposure: the patient should be sitting down and exposed from the waist up Look: 1. 2. 3.
You can do spinal examinations in isolation, or do all three at once.
Look at the patient’s posture, and whether they are in any discomfit Inspect the whole spine and shoulders and assess symmetry Inspect for: spinal scoliosis, lordosis, flatt ening of the chin, scars, wasting, spasm, rashes, deformities of any other joint
Kyphosis: ‘Kyphosis is the extreme curvature of the upper
Lordosis- chin sticks out
back also known as a hunchback; The upper back bone (thoracic region), is normally curved forward. If the curve exceeds 50° it is considered abnormal (kyphotic).
Lordosis: describes an inward curvature of a portion of the vertebral column. Excessive lordotic curvature is also called hollow back, saddle back, and swayback. Common causes of excessive lordosis including tight low back muscles, excessive visceral fat, and pregnancy. Although lordosis gives an impression of a stronger back, ironically it can lead to moderate to severe lower back pain. Loss of lordosis is sometimes seen with painful spinal conditions.
Scoliosis: side-to-side curvature of the spine. While a small
Scoliosis
degree of lateral curvature does not cause any medical problems, larger curves can cause postural imbalance and lead to muscle fatigue and pain. More severe scoliosis can interfere with breathing and lead to arthritis of the spine (spondylosis).
*ask patient ‘any tenderness?’
Feel:
*any headaches?- feel occipital insertion of trapezius (muscle tension = cause of band-like headache?)
1. Muscles noting tenderness, spasm, bulk, wasting:
2. 3.
a. Anteriorly: sternocleidomastoid muscles, scalene, levator scapulae, rhomboids b. Posteriorly: trapezius, semispinalis capitus, splenius capitus, levator scapulae, rhomboids Spinous processes and along the interspinous ligaments for t enderness and stiffness Facet joints for stiffness and pain.
Semispinalis capitis
Splenius capitis Trapezius Splenius cervicis Levator scapulae Rhomboid minor (cut)
Move: active movement only, passive movement is for the skilled examiner 1. 2. 3. 4.
Flexion Extension Left and right lateral flexion Left and right rotation
NOTE
limitation of movement, and any pain If the neck is very painful, it is useful to lie the patient down and roll them into supine position to complete the exam.
***TEST: bend forward in flexion to look for scoliosis (one side has hump due to muscle imbalance)
THE THORACIC SPINE EXAMINATION
*
Positioning and Exposure: standing, sitting, and lying down; preferably undressed except for underwear Look: Look at the patient from behind: 1. Height of the shoulders 2. Scoliosis 3. Spasm of intervertabral muscles 4. Wasting: paraspinal muscles, gluteal muscles 5. Symmetry: inferior angle of scapulae, You can palpate using the pulp of your thumb posterior superior iliac crests, or the hook of your gluteal folds, popliteal creases hamate on your thenar 6. Foot posture eminence
Paraspinal muscles
Look from the side: 1. Thoracic kyphosis 2. Lumbar lordosis
Feel: Lie patient face-down and palpate: Tenderness? Spasm? 1. Paraspinal muscles 2. Spinous processes and interspinous ligaments for stiffness and t enderness 3. Costovertebral articulation Should be firm Roll the patient over: 1. Feel the costochondral joints for tenderness (between ribs and costal cartilage)
Move: Sit the patient up, preferably on a stool this position locks the patient’s pelvis, but if you are worried that they may fall off, stand them up and hold the pelvis steady during rotation. 1. Rotation left and right (60°) To isolate rotation : hold both sides of pelvis as Pt cross arms over onto -rotation is the major thoracic spine movement Pt touches knee and shoulders and turns left and right 2. Flex the patient forwards until their fingers touch their knees tucks chin in- is arch even??? - look for one side of the thorax higher than the other – scoliosis X much extension of thoracic spine
THE LUMBAR SPINE EXAMINATION
*
Positioning and Exposure: The patient should be undressed except for underwear. Shoes and socks should be off.
Look & Feel: as per ‘Thoracic Spine Examination’ Move: Ask the patient to actively move in the following directio ns: 1. 2. 3. 4.
Extension: 20° to 30° Flexion: 75° to 90° Lateral flexion: 30° (left and right) Rotation minimal at lumbar spine.
*Ask Pt to put hands on side and slide down leg towards their knee
SPECIAL TESTS: the following are neurodynamic tests. If positive, perform a neurological exam. 1. Femoral nerve stretch -With the knee prone, place a palm on the hamstrings of the limb to be examined and fl ex knee gently -Pain should be reproduced in distribution o f femoral nerve -This test is positive is almost all patients with high lumbar disk lesions Do with patient PRONE
2. Straight leg raise -With the patient supine, raise the leg slowly until pain in the posterior aspect is elicited -The leg must remain straight and not bent at knee. -The test is positive when pain is reproduced in the range of 30 ° to 40° Tests for SCIATICA (sciatic nerve impingement)- more commone that femoral nerve, do SUPINE
THE HIP EXAMINATION
*
Positioning and Exposure: The patient should be in their underwear. Start the exam with the patient standing. GAIT: any hops, jumps, limps, swaying???
Look:
ASIS (ant. superior iliac spine)
Inspect: deformity Posture: inspect the patient’s spinal, leg and foot posture Gait: observe how they walk over 10 paces, get into/out of a chair, use of aids (walker?) 4. Spine: look for scoliosis, paravertebral spasm 5. Hip: inspect gluteal folds, popliteal creases 6. Leg length: measure for leg length discrepancy (measure supine) i. True leg length = ASIS to medial malleolus Top edge of ASIS to distal ii. Apparent leg length = umbilicus to medial malleolus edge of medial malleolus iii. Note the best measure of leg length is standing X-ray 1. 2. 3.
Look
at the bulk of the gluteus maximus. If uneven bulk ~congenital hip dislocation? - Leg length inequality can cause scoliosis. -Also assess equality of popliteal creases and muscle bulk.
Medial malleolus
‘True Leg Length’
Feel: Invite the patient to lie down supine for the remainder of the examination. The hip joint is difficult to palpate. -Try at about 2cm distal to the midpoint of the inguinal ligament (this is a sensitive area) 1. Note any swellings 2. Feel the pubic symphysis, adductor muscles, iliopsoas, greater trochanter of the femur (+) Tighten both rectus femoris muscles and compare bulk of both sides. A torn muscle will bruise 2448 hours post injury. Also note any bruises on the posterior, at the gluteal fold. This can occur with a torn hamstring, and the bruise can track inferiorly to the popliteal fossa. NOTE: there is too much muscle bulk to feel for minor swelling or heat of the hip joint. You can feel laterally, but mostly you are just feeling the greater trochanter of the femur, and bursa.
Move: (you can do both active and passive movement for each move and then go on to the next move) NOTE: Degree of movement varies with changing body habitus; values are only an average. BUT compare left and right sides, and at different times (e.g. pre - and post-injury) 1.
2.
Ask the patient to actively make the following movements a. Flexion 90° (with knee extended) or 135° (with knee flexed) b. Abduction 50° c. Adduction 45° d. Internal rotation 45° (with knee/hip flexed 90°) e. External rotation 45° (with knee/hip flexed 90°) Repeat passively, noting any crepitus and watching for signs of discomfort. CREPITUS: a peculiar crackling, crinkly, or grating feeling or sound under the skin, around the lungs, or in the joints. Crepitus in a joint can represent cartilage wear in the joint space.
3. 4.
Roll the patient onto the unaffected side, stabilise the pelvis and test extension (should be 15°). Roll the patient supine to perform the Thomas test. *Examiner can fix Pt ASIS to hold pelvis
Flexion (knee extended) 90°
Flexion (knee flexed) 135°
Extension 15° *Do this one last, as it requires Pt to be rolled over
Abduction 50°
Adduction (cross-over) 45°
External rotation 45°
Internal rotation 45°
Function: assessed at the beginning of the examination when observing gait Special Tests:
THOMAS TEST- a test for fixed flexion deformity inflammation
(e.g. septic arthritis of hip) or structural deformity of hip if checking the left hip joint, raise the right leg
*Under hip side, not leg side
The patient lies supine and the examiner flexes one of the hips (one hand can be placed under patients back to check for lumbar lordosis), bringing the knee to the chest to flatten out the lumbar spine.
If there is NO flexion contracture, the hip being tested (the straight leg) remains flat on the examination couch.
If there is CONTRACTURE, the leg rises off the couch. The angle of contracture can be measured.
TRENDELENBERG TEST – a test for hip instability due to gluteus medius weakness or tear, short femoral neck or unstable hip due to dysplasia, (e.g. congenital dislocation of the hip) Traditionally, this test is performed with the examiner viewing the patient from behind, however, it may be safer to test facing the patient (aiding with balance).
1. Hold the patient’s hands with the patient facing you.
2. Ask the patient to stand on the (R) foot by lifting the (L) foot off the ground, keeping the (L) thigh is position and bending the knee so that the foot is lifted behind the patient.
3. The iliac crest on the side with the foot off the ground (in this case the left) should rise or stay level.
4. The test is abnormal if t he hemipelvis falls, refecting gluteal weakness or inhibition from hip pain on the contralateral side.
gait:
‘sag’ into step and swing leg around
THE KNEE EXAMINATION
*
Positioning and Exposure: Begin with the patient in a standing position. Your patient should be in exercise shorts or underwear. Tibial tuberosity (in children- growing fat- stretching growth plate) -growing pain of knee
Look: 1. 2. 3.
Osgood Shlatter
Inspect for: swelling, wasting, spasm, scars, erythema, deformities (e.g. t he ‘knock-knees’ of genu valgum and the ‘bow-legs’ of genu varum) Posture: inspect the posture of the foot NOTE: medial injuries are more common (note whether walking Gait with ‘genu varum’ posture eases pressure on medial side of knee a. Observe the patient walk 10 steps b. Watch the patient getting in/out of a chair and taking shoes and socks on/off.
SCARS
Modern ‘arthroscopic surgery’ of the knee, only leaves slight scars at the outer corners of the knee joint.
Older scars are larger, are more easily seen.
Genu valgum: ‘knock knees’ is a condition in which the lower legs are positioned at an outward angle. When the knees are touching, the ankles are separated. Most children develop slight knock-knees by 2-3yo, that often persists through age 56. Causes of genu valgum include osteomalacia, Marfan’s sundrome, Ehlers-Danlos syndrome, osterogenesis imperfecta and pseudochonroplasia. Genu varum: ‘bowlegs’ is a condition in whi ch the knees remain wide apart when a person stands with the feet and ankles together. Infants are born bowlegged, with normal appearance attained ~3yo. Severely bowed legs can be a sign of rickets. Other causes of bowleggedness include Blount's disease, bone dysplasias, and lead or fluoride intoxication.
Feel: 1. 2. 3. 4. 5. 6. 7. 8. 9.
Skin: temperature (use back of the hand) Quadriceps: loss of tone/bulk, spasm, tenderness, signs of tear/rupture Patella: mobility, thickenings Patellar ligament: tenderness (esp where ligament inserts to tibia and patella), thickening, gaps Medial condyle/ epicondyle of femur: attachment of medial ligament Lateral condyle of femur and head of fibula: attachment of lateral ligaments Joint line: feel for tenderness (suggests a meniscal tear) and swelling Bursae: supra- and prepatellar, assess temperature, colour, fluctuance, and tenderness Effusion: test for effusion using patella tap and bulge test.
Congenital dislocation of the patella?
Patella slips out of femoral groove and dislocation occurs.
Can be due to either: i) flattened femoral groove OR ii) flattened posterior surface of patella bone
- Check evenness of L and R patella, and compare bulk. Any bul ges? Is an effusion obscuring the outl ine of the patella bone? - Feel for heat; check both sides at the same time. *Place rolled towel under knee to examine knee slightly flexed (to o pen up joint lin e)
CHECKING STRUCTURE (when possible you can do L and R sides at the same time) Note
pain at any time (look for toe curl, grimacing), does it feel boggy? bruising?
i)
Feel quadriceps (relaxed and tense; if injury- one side feels floppy and can’t sustain tension properly due to pain) ii) Feel the medial thigh and then the lateral thigh (if one side is painful, do that side last) iii) Feel around the knee as follows...
9
1
2
10 3
8 5
12
11 4
7 6
13
Behind the knee
*Also check bursae
1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13.
Upper pole of the patella Medial femoral condyle (superior attachment of the medial collateral ligament) Medial collateral ligament (MCL) Tibial condyle (medial), inferior attachment of the MCL Inferior pole of the patella Tibial tuberosity (move superiorly and feel patellar ligament for tenderness) Tibio-fibular articulation (inf. attachment of LCL) Lateral collateral ligament (LCL), tends to lie more posterior than MCL, don’t confuse with ilio-tibial band Lateral femoral condyle (superior attachment of LCL) Patella (feel for tenderness)* Lateral meniscus: from the lower pole feel laterally along the joint line, where the cartilage attaches, if there is a meniscal injury = tender Medial meniscus, medially from lower pole of patella Popliteal fossa: check for the posterior of the knee for cystic swelling (e.g. Baker’s cysts)
*NOTE when the muscles of the leg are relaxed the patella should move a little, and if it has never had a dislocation, it should not be painful.
PATELLAR TAP – will only occur when there is effusion Slide one hand down the thigh towards the knee to empty the suprapatellar pouch. When you reach the upper edge of the patella, keep your hand in place. With your other examining hand, push down gently on the patella. 1
If effusion is present, the patella will press down on the effusion before hitting (tap) the femur.
2 3
Tap??
BULGE TEST – test for effusion
*Can be caused by mechanical injury/ inflammation
-If there is no obvious patellar tap, stroke the medial side of the knee upwards (towards the suprapatellar border) to empty the medial compartment. -Then stroke the lateral side downwards (towards feet). -A mild effusion may refill the medial compartment producing a bulge.
Move:
Lateral
Medial
2
3
1 4
Is there a bulge???
*Also test KNEE ROTATION (one hand holds thigh, the other holds the lower leg above the ankle and TWIST
Active and passive movements 1. Flexion: 135° 2. Extension: 0 - 10° of hyperextension is acceptable Observe tracking of patellar and palpate for crepitus during passive movement.
Pathophysiology : Between 0° and 30° of flexion, the patella
Function: (assessed at the beginning of the examination) Special Tests:
is at its highest point in the trochlea. Pressure from the medial side will push the patella in a lateral direction, causing it to dislocate from the trochlear groove. This will cause not only pain, but apprehen apprehension sion on the part of the patient.
Patellar Apprehension Test: this is a test for patellar dislocation 1. The patient must be supine with the test knee flexed to 30°. 2. The examiner places a thumb along the medial patellar border and applies a laterally directed force. 3. The test is positive if the patient becomes apprehensive about the patella dislocating and the quadriceps contract. NOTE NOTE
knee caps tend to dislocate laterally
Medial and Lateral Collateral Ligament Stress Test Bracing side opposite to ligament being tested.
Applying lateral lateral force to distal tibia.
MCL Stress Test
1. With the patient lying supine, flex the knee to 15 30°. 2. Alternatively stress medial and collateral ligaments by bracing the opposite side of the j oint line to the ligament you are testing and applying varus (medial) or valgus (lateral) force to the distal tibia. 3. Repeat both movements in full extension. If ligament is torn? = big movement If
Anterior Draw Test: -this is a test for anterior cruciate ligament integrity. This test is positive if there is evident laxity or pain 1. Place both hands around the upper tibia with thumbs over the tibial tuberosity and index fingers tucked behind the hamstrings to grasp the leg. 2. Feel with fingers to detect if hamstring spasm is present. 3. Stabilise lower tibia by carefully sitting on patient’s foot. 4. Gently pull the upper tibia forward.
Lachman’s Test -This is a test of anterior cruciate ligament integrity. The test is positive if there is evident laxity or pain. 1. The patient lies on their back with their knee held between full extension and 15° flexion. 2. The femur is stabilised with one hand, while pressure is applies to the posterior aspect of the proximal tibia in an attempt to move it anteriorly. The The
posterior cruciate ligament can also be tested by pushing down, while supporting the femur.
*Can hold Pt’s anterior knee along meniscal line (joint line)
McMurray’s Test for Medial/ Lateral Meniscal Tear 1. The patient lies on their back, the knee is flexed and the foot is held by the heel. 2. The ankle held by the examiner is rotated causing relative internal and external tibial rotation (this tests the posterior cartilage). 3. Variations of this test include addition of abduction-adduction forces and gradual extension of the knee.
APLEY TEST: alternative to McMurray’s test If the examiner is not strong enough for the McMurray test, the Apley test can be performed, which is easier on the examiner.
The test is performed with the patient pati ent in the prone position. 1. The examiner pushes down on the heel (applying axial pressure), rotating the tibia on the femur (~‘grinding’ test). 2. Anchor the femur and rotate the leg at the heel, this time holding the tibia up off the femur. If it is a meniscal injury this will lessen the pain, but if it is a collateral ligament injury, the pain will be uncharged.
Additional Test: The Test: The Sag Sign -Tests the integrity of the posterior cruciate ligament The sag sign reveals posterior displacement of t he tibial tuberosity as the knee is flexed at 90°. Ask patient to fully extend leg, raising it off the examination couch. Ask the patient to slowly drop their foot back into the couch and the relax. The sign is positive if the proximal tibia drops in relation to the end of the femur.
THE ANKLE AND FOOT EXAMINATION
*
Positioning and Exposure: both lower limbs should be completely exposed Look: 1. 2. 3.
Footwear: abnormal/ asymmetrical wearing, poor fit, special insoles Gait: observe normal cycle of heel strike, stance and toe-off, toe in/ toe out? Standing (weight bearing): toe alignment, midfoot arch position, swelling, redness, bruising, scars, foot posture (pronated/ supinated), wasting of calf, fibular muscles, hamstrings, calcaneal tendon thickening, varus/ valgus deformity Check for xanthomata Sit patient on couch with feet hanging over end (pillow under knees). th 4. Ankles: anterior joint swelling, medial and lateral malleoli (swelling/ bruising/ deformity), 5 metatarsal bases (swelling/ bruising/ deformity), tibialis posterior, flexor digitorum longus, flexor hallucis longus 5. Feet: nail changes (psoriasis), skin colour, rashes, ulcers, infection, callus formation, joint swelling, look at plantar surface st 6. Toes: alignment (straight, hammer, claw, mallet), swelling/ redness of 1 MTP joint, hallux valgus
ANATOMY OF THE LOWER LEG:
*Can easily miss tarsal fractures with X-ray .: CT
GAIT: normal gait cycle and common gait abnormalities
-Heel-toe gait? -skipping gait?
MIDFOOT ARCH POSITION AND FOOT POSTURE Pes cavus (high arch)
Normal arch
Pes planus (flatfoot)
-Is the foot splayed outwards? -Pidgeon toed? -Look at wear on soles of Pt’s shoes
?? What is the line of the calcaneal (Achilles) tendon from the posterior view?
- Is weight bearing uniform (same time spent on both R and L legs), if not uniform = limp - Is gait heel toe -Is there a rolling in (eversion) of the trailing foot when taking a step? ]- gives knee/ ankle problems -Is there inversion of leading foot when stepping down? NOTE
lateral/ collateral ligament injuries are more common for ankles, as inversion is more common
SKIN & NAIL CHANGES with PSORIATIC ARTHRITIS Psoriatic arthritis: Psoriatic arthritis is a chronic disease characterized by inflammation of the skin ( psoriasis) and joints (arthritis). Psoriasis is a common skin condition affecting 2% of the Caucasian population in the United States. It features patchy, raised, red areas of skin inflammation with scaling. Psoriasis often affects the tips of the elbows and knees, the scalp, the navel, and around the genital areas or anus. Approximately 10% of patients who have psoriasis also develop an associated inflammation of their joints. Patients who have inflammatory arthritis and psoriasis are diagnosed as having psoriatic arthritis
Psoriatic nail: pitting (small depressions in nail), onycholysis and, less commonly, hyperkeratosis (thickening of the nail), ridging and discolouration. The presence of vascular changes around nailfolds, implies active disease (black to brown 1-2mm lesions due to sk in infarction and occur typically in Rheumatoid arthritis).
Psoriasis: is a chronic, non-contagious autoimmune disease which affects the skin and joints. It commonly causes red scaly patches to appear on the skin. The scaly patches caused by psoriasis, called psoriatic plaques, are areas of inflammation and excessive skin production. Skin rapidly accumulates at these sites and takes on a silvery-white appearance. Plaques frequently occur on the skin of the elbows and knees, but can affect any area including the scalp and genitals. In contrast to eczema, psoriasis is more likely to be found on the extensor aspect of the joint.
C o r n s a n d c a l lu s e s form
on the skin because of repeated pressure or friction. A corn is a small, tender area of thickened skin that occurs on the top or side of a toe. A callus is a rough, thickened area of skin that appears because of repeated irritation or pressure to an area of skin. Calluses usually develop on the palms of the hand and soles of the feet.
ALIGNMENT OF THE TOES Hammer Toe A hammer toe occurs when the middle of the t oe points upwards abnormally. This most often occurs in the second toe, and is often the result of a big toe bunion pushing on the second toe. A painful callous often forms on to on the first joint in the toe. Claw Toe Claw toes appear as the name would describe--like a clenched fist. While most other toe deformities are the result of footwear, claw toes are the result of muscle imbalance. The cau se of the imbalance may be rheumatoid arthritis, neuromuscular disorders, a stroke, or other conditions. Mallet Toe The mallet toe is the deformity where the most distant joint points downward. This is most common in the second toe in patients whose second toe is the longest toe. A painful callous can form at the tip of a mallet toe.
Hammer toe
Claw toe
Mallet toe
Hallux valgus (bunion): A bunion or hallux val gus is a prominence on the inner border of t he foot effecting the big toe and at the level of the 1st metatarso-phalangeal (MTP) joint. The bunion prominence which is seen and felt on the inner border of the foot is not due to any growth of bone but is due to the 1st metatarsal bone. With a bunion this ha s become more prominent than normal because the 1st metatarsal has moved away from its immediate neighbour the 2nd metatarsal. This widens the forefoot thus producing the bunion. The tendons have an off-centre pull with the first metatarsal moving away from the second.
Hallux varus: A deformity of the great toe joint where the hallux is deviated medially (towards the midline of the body) away from the first metatarsal bone. Hallux varus has variable degrees of severity, symptomatology, and etiology. Causes range from the most common iatr ogenic postoperative variety to idiopathic, rheumatic, and posttraumatic (tear of the hallux lateral collateral ligament) forms. Flexible hallux varus is a common finding in newborn children and usually corrects to valgus in early childhood when walking begins
Feel: 1. 2.
3.
Temperature over the ankle and forefoot Ankle a. Distal 1/3 of fibula (deformity, tenderness, swelling)- especially posterior aspect b. Media and lateral malleoli c. Medial and lateral ligaments d. Fibular tendons th e. Base of 5 metatarsal f. Talus and anterior joint line of the ankle g. Posterior tibialis pulse Foot th a. Base and shaft of the 5 metatarsal (common fracture) b. Gently squeeze across metatarsal heads (watch the patient’s face for discomfort (neuromas, stress fractures)
c. Feel the MTP and interphalangeal joints d. Medial tuberosity of the navicular bone e. Tendons of tibialis anterior, extensor hallucis extensor digitorum f. Plantar surface- the medial tubercle of the calcaneus (this is tender in plantar fasciitits) g. Dorsalis pedis pulse Turn patient supine: 4. Feel the calcaneal tenden for tenderness or deformity and perform the Thompsons test.
1
Palpation of the ankle and foot:
7 2 5
4
3
6 9
8
*Also feel posteriorly for CALCANEAL TENDON integrity.
-common avulsion injury with
1. 2. 3.
Distal 1/3 of the tibia eversion Medial malleolus Talo-navicular joint (and medial ligaments) bulges, effusions, boggy? 4. Anterior joint line (usually ca n feel extensor digitorum longus and extensor hallucis longus) 5. Lateral malleolus (+ fibular tendons) 6. Lateral ligaments (it is usually the anterior talofibular ligament that is damaged with an inversion injury- check with anterior draw test ) 7. Distal 1/3 of the fibula th 8. Base and shaft of 5 metatarsal 9. Gently squeeze across the metatarsal heads 10. Tendons, plantar surface, dorsal surface
THOMPSON’S TEST: test of the integrity of the calcaneal tendon 1.
2.
3.
Anterior drawer test: to assess the integrity of the anterior talofibular ligament . If the ligament is torn, the talus will subluxate anteriorly compared with the unaffected ankle.
The patient should be prone with the foot extending over the end of the examination couch. The calf muscles are then squeezed in the middle one-third below the widest girth Passive plantar flexion of the foot is normal, and a positive test is the absence of passive plantar foot flexion. This indicates a rupture of the calcaneal tendon.
Morton's neuroma: is a benign neuroma of an intermetatarsal plantar nerve, most commonly of the third and fourth intermetatarsal spaces. This probl em is characterised by numbness and pain, relieved by removing footwear. The thickening, or enlargement, of the nerve that defines a neuroma is the result of compression and irritation of the nerve. This compression creates swelling of the nerve, eventually leading to permanent nerve damage.
Move: Active movement 1. Dorsiflexion: 20° 2. Plantar flexion: 30° 3. Inversion: 25-30° 4. Eversion: 5-10° 5. Dorsiflexion of the toes 6. Plantar flexion of the toes Passive movement 1. Fix heel in one hand, and using the other, passively invert / evert forefoot.
-Plantar surface of foot is medial
Function: assessed at the beginning of the examination
-Plantar surface of foot is lateral
THE SHOULDER EXAMINATION
*
Positioning and Exposure: ideally standing (so that the patient can move their shoulder in all directions unimpeded). Both shoulders should be fully exposed. -Bare from waist up (males) or with bra or sports top (females) -Watch the patient undress to assess functional impairment
Look: 1. 2. 3. 4.
General: skin changes, muscle wasting, muscle spasm, swelling, deformity, a symmetry, posture Front: muscle wasting (esp. deltoid) Side: position of shoulders in sagittal plane, posture of spine and limbs Behind: supraspinatus, infraspinatus, trapezius, rhomboids, scapula winging, scoliosis
Winged scapula (scapula alata) is a condition in which the medial border (the side nearest the spine) of a person's scapula is abnormally positioned outward and backward. The resulting appearance of the upper back is said to be wing-like because the inferior angle of the shoulder blade protrudes backward rather than lying mostly flat like in people without the condition. A winged scapula is associated with damage or a contusion to the long thoracic nerve of the shoulder and / or weakness in the serratus anterior muscle. If the long thoracic nerv e is damaged or bruised it can cause paralysis of the serratus anterior muscle and winging of the scapular or shoulder blade.
Normal Shoulder
Ear, shoulder, elbow, knee and ankle should be approximately aligned.
Dislocated Shoulder
The deltoid is responsible for the cur ved outline of the normal shoulder. However, with dislocation, the angle of the shoulder is much sharper.
Feel: 1. 2.
3.
Temperature over anterior of shoulders (use back of hand) Assess bony landmarks for tenderness, swelling and deformity a. Sternoclavicular joint b. Clavicle c. Acromioclavicular joint d. Coracoid and acromion process e. Spine and borders of scapula Deltoid muscle, biceps, triceps (& pectoralis major) assess tone and muscle bulk
d
c
b
a
Superior border
e
Medial border
Inferior angle
Anterior
Posterior
Move: Active movement: ask the patient to mimic you as you perform the following movements: 1. Abduction to 90°- abduction through to elevation is 180° 2. Flexion to 90°- flexion through to elevation is 180° 3. Internal rotation to 70° 4. External rotation to 90° 5. Extension to 60° 6. Adduction to 30° (humerus passes in front of trunk) 7. Look from behind for scapulohumeral rhythm (abduct both arms) and painful arc 180° 120° Glenohumeral joint
120°
Painful arc is observed during abduction form 60° to 120° and is the result of pinching of inflamed or tender structures under acromion process.
Painful arc 60° 60° 0° scapulothoracic joint
Scapulohumeral rhythm is observed during abductionthere should be 120° of movement occurring at the glenohumeral joint and 60° occurring at the scapulothoracic joint.
Passive movement: 1. Sit or lie the patient down and repeat the movements passively. 2. Note any discrepancy. Note
total range of movement and sequencing. E.g. for abduction, normal movement is straight out to side keeping the shoulders back and down, vs hitching your shoulders first, throwing the arms forward to start movement (problem with supraspinatus to originate movement). Compare
PASSIVE to ACTIVE movement. Active movements will stop when motor-unit stops due to pain or nerve/ muscle problem. i) If passive movement in normal (suggesting joint is O K), but active movement is not = neural or muscle problem ii) If passive movement = active movement = less t han normal, this suggests a joint pr oblem.
outward rotation (external) abduction flexion
adduction
0°
extension
0°
inward rotation (internal)
Function: Ask the patient about washing, grooming and dressing. Observe if possible.
Special Tests:
APLEY’s SCRATCH TEST : this is a quick, non-specific assessment of active function The patient is instructed to reach and ‘scratch’ at three points on the body: 1. Reach over the opposite shoulder (adduction) 2. Reach behind the neck (adduction, external rotation) 3. Reach behind the back (internal rotation)
HAWKINS-KENNEDY TEST: this is a test of impingement 1. 2.
Flex the patient’s elbow and shoulder to 90°. The examiner supports the shoulder with one hand and uses the other to forcibly internally rotate the shoulder.
The test is positive if pain is reproduced. This suggests supraspinatus impingement (supraspinatus tear = most common rotator cuff injury).
APPREHENSION TEST: this is a test of anterior stability 1. 2.
3.
Any
The patient may be standing or is a supine position. The examiner passively abducts the arm to 90° and externally rotates the arm with one hand while also applying posterior pressure to humerus. Ensure you watch the patient for signs of distress. The test is positive if the patient experiences apprehension about impending subluxation/ dislocation. pain, sliding, patient resistance?
ROTATOR CUFF TEST 1: DROP ARM TEST: this is a test for supraspinatus (rotator cuff) injury Patient raises arm to 90° out to the side and holds that position. Patient slowly lowers arm. If the arm drops quickly and not smoothly = sign of rotator cuff tear. A gently applied pressure to the abducted arm may force arm to give way. Examiner can also place hands on forearm and ask patient to ‘push up against’ them.
~ PASSIVE ABDUCTION (perform passive abduction whilst supporting the arm.
ROTATOR CUFF TEST 2: EMPTY CAN TEST Abduct the arm to 90° in neutral position and test abduction strength. Then internally rotate the arm and to adduct 30° and test again. The test is positive if t here is pain and suggests a supraspinatus tear.
*With thumb facing up, Pt pushes arm up against Dr, and with Pt’s thumb facing down repeat
WINGED SCAPULA To accentuate winging of a scapula stand the patient about arms length facing a wall. Ask the patient to push with both hands against the wall. Observe from behind the patient.
THE ELBOW EXAMINATION
*
Positioning and Exposure: Patient standing with both upper limbs completely exposed. Watch patient undress to assess functional impairment.
Look: 5. 6. 7.
General: swelling, deformity, erythema, nodules, rashes Effusion: usually seen on the lateral aspect in the triangle between epicondyle, head of the radius, and olecranon process Carrying angle: 5-10° (slightly greater in females than males)
Rheumatoid Nodules: As part of the rheumatoid process, firm, nontender, subcutaneous nodules develop in about 25 percent of rheumatoid arthritis patients. These are commonly found at pressure points like the elbow, back of the fo rearm, and metacarpophalangeal joint. Nodules usually occur in chronic active cases of rheumatoid arthritis, and are commonly associated with more joint deformity and serious extra-articular manifestations including those in the lungs, eyes, and blood vessels.
NB Should also be same on both sides.
5-10°
*Ulnar nerve around medial epicondyle
coronoid fossa capitullem
humerus trochlear
lateral epicondyle
medial epicondyle
head of radius
coronoid process
olecranon fossa olecranon process
lateral epicondyle
ulna radius
radius bicipital tuberosity
Carrying Angle If
increased carrying angle on one side = fracture of lateral epicondyle as child???
Ulnar (medial) collateral ligament
Radial (lateral) collateral ligament Annular ligament
ANTERIOR VIEW
POSTERIOR VIEW
Feel: 1. 2. 3. 4. 5.
Olecranon process and bursa if palpable Tendon of triceps Lateral and medial epicondyles Head of radius, biceps tendon Bulk of the flexor and extensor muscle groups
NOTE: nerve around medial epicondyle = ‘funny’ bone fingers fingers th tingling especially 5 digit
Move: Active movement: ask the patient to mimic you as you perform the following movements: 1. Flexion to 140° (depends on muscle bulk) 2. Extension to 0° 3. Pronation to ~70° 4. Supination to ~85° Passive movement: repeat the same movement passively noting any discrepancy
Flexion
Supination Pronation Extension
Function: ask the patient about functional activities such as eating, brushing teeth and dressing (also lifting up a cup of coffee, eating, cutting up food) Assess if possible
Special Tests:
GRIP STRENGTH 1. Ask the patient to make a fist and squeeze tightly This
will be painful at the elbow if epicondylitis -The examiner can place a finger in both fists of the patient and compare grip strength.
VARUS & VALGUS STRESS TEST: this is a test of the integrity of the medial & lateral ligamentous complexes 1.
The patient’s arm is flexed to 20° at the elbow and and supinated.
2.
The examiner supports the humerus with one hand and gently stresses the medial or lateral side of the elbow joint with the other hand.
Valgus Varus
~ Valgus movement tests the medial ligaments, while varus movement tests the lateral ligaments.
LATERAL EPICONDYLITIS (Tennis Elbow) With the elbow extended, extending the wrist against resistance will elicit pain.
MEDIAL EPICONDYLITIS (Golfer’s Elbow) With the elbow flexed, flexing the wrist against resistance will elicit pain.
ENTRAPMENT Entrapment of radial, median and ulnar nerves may occur. Refer to the neurological examination of the upper limb.
THE WRIST & HAND EXAMINATION
*
Positioning and Exposure: The patient and examiner should be seated, ideally across the corner of a table. The whole of both upper limbs should be exposed.
Look: 1. 2.
Observe how the wrist / hand is held Look for: scars, deformities, swelling, wasting, colour ( erythema, pallor, cyanosis), skin changes (e.g. rashes), wounds (especially seemingly minor puncture wounds)
~ulnar deviation
Heberden's nodes: are hard or bony swellings that can develop in the distal interphalangeal joints. They are a sign of osteoarthritis and are caused by formation of osteophytes (calcific spurs) of the articular cartilage in response to repeated trauma at the joint. Heberden's nodes typically develop in middle age, beginning either with a chronic swelling of the affected joints or the sudden painful onset of redness, numbness, and loss of manual dexterity. This initial inflammation and pain eventually subsides, and the patient is left with a permanent bony outgrowth that often skews the fingertip sideways.
Bouchard's nodes may also be present; these are similar bony growths in the proximal interphalangeal (PIP) joints (middle joints of the fingers), and are also associated with osteoarthritis.
Typical hand deformities in rheumatoid arthritis
Heberden's nodes are more common in women than in men, and there seems to be a genetic component involved in predisposition to the condition.
Feel: 1.
2. 3.
Palpate the dorsal aspect of the wrist Distal forearm Snuff box tenderness Styloid process scaphoid bone injury?? Ulna Radius Snuff box Base of metacarpals Lunate Any swelling along the extensor tendon sheaths, ganglia, joint swelling, warmth Palpate the palmar aspect of the wrist Feel for the pisiform and hook of hamate Palpate the hand Assess for swelling, tenderness, warmth, nodules, thickening and contracture of fascia. Feel the distal carpal, metacarpal and interphalangeal joints these are bedt felt from the lateral sides, squeezing gently between your fingers
Move the Wrist: Active movement: ask the patient to actively mimic your movements at the wrist 1. Flexion 80° *You can get Pt to hold pen in fist while 2. Extension 70° pronating and supinating to check range 3. Ulnar deviation 60° of movement pen 4. Redial Deviation 20° Passive movement: repeat these movements passively, feeling for crepitus fist
Flexion 80°
Radial Deviation 20°
Neutral position
Extension 70° Ulnar Deviation 60°
Move the Hand: Active movement followed by passive movement 1. Flexion: a. Ask the patient to actively make a fist b. Note any decreased ranger of finger flexion c. All fingers should point towards scaphoid d. Metacarpal heads should have normal aligment e. Feel for creptis 2. Extension: -Note any decreased range, suggestive of tendon avulsion. It may be useful to resist finger movements to elicit tendon integrity. 3. Thumb opposition, abduction and adduction -Test with grip strength, OK sign, key grip, and opposition of thumb to little finger *Piece of paper between ‘OK’ grip- try to pull out
th
5 Metacarpal Fracture (Boxer’s Fracture): is the term for a pinky-side hand fracture, most often at the neck of the pinky’s metacarpal bone. As the name indicates, the condition is generally a punching injury, occurring in such sports as boxing, kickboxing, karate, and mixed martial arts.
An Avulsion fracture is a bone fracture which occurs when a fragment of bone tears away from the main mass of bone as a result of physical trauma. This can occur at the ligament due to the application forces external to the body (such as a fall or pull) or at the tendon due to a muscular contraction that is stronger than the forces holding the bone together. Generally muscular avulsion is p revented due to the neurological limitations placed on muscle contractions
Adduction
Abduction
Opposition
Function: Assess the patient’s limitation by as king them to open a jar, and tie their shoelaces. Special Tests:
PHALEN’S TEST: this is a test for medial nerve compression/ entrapment 3.
The patient flexes both wrists and pushes the dorsal aspect of their hands together, in a ‘reverse prayer sign’ for 1 minute.
4.
The test is positive if paraesthesia is evident on the palmar surface of the thumb, index, middle and lateral half of the ring finger.
Carpal tunnel syndrome (CTS), or
median neuropathy at the wrist, is a medical condition in which the median nerve is compressed at the wrist,
TINEL’S SIGN: this is a test for CTS
ANATOMICAL SNUFF BOX:
Position the patients wrists in supination and tap over the flexor retinaculum at the proximal part of the palm.
Pressure in the middle of the anatomical snuff box can elicit a fracture of the scaphoid, but can also be tender in sprain.
This
Check with pressure over the scaphoid tubercle.
test is positive if this reproduces the paraesthesia and is suggestive of carpal tunnel syndrome.
Other causes of Hand Disease: -
Seropositive and seronegative arthritidis are systemic diseases, so think systematically An apical lung tumour can cause wasting of the hand muscles Also remember the many hand, nail and finger signs from CVS / RESP / GIT
DIAGNOSTIC IMAGING FOR THE MUSCULO SKELETAL SYSTEM 1. X-ray
2. Ultrasound
3. Computed Tomography
4. Magnetic Resonance Imaging
*
CLINICAL SKILLS
Neurological System Exam
NEUROLOGICAL SYSTEM:
CLINICAL EXAMINATION
NEUROLOGICAL SURFACE ANATOMY
*
Dermatomes: the lateral wall of a somite from which the dermis is produced NOTE: that the domains of the dermatomes (spinal nerve roots) differs from that of indiv idual nerves. Radicular pain is pain that radiates along a dermatome, corresponding to a spinal root injury.
Key Sensory Points:
C4: ~ necklace C5: ~ tip of shoulder
T4: nipples
T10: umbilicus
S6: thumb S7: middle digit
L1: ~ underwear
You sit on S3/S4
S5: anus L3: knee
You stand on L5 (medial) and
Anterior and posterior views of the dermatomes. Each segment is named for the principal spinal nerve serving it. V, trigeminal segments; C, cervical segments; T, thoracic segments; L, lumbar segments; S, sacral segments.
OVERVIEW OF THE NERVOUS SYSTEM
*
CENTRAL NERVOUS SYSTEM DISORDERS : Lesions in the two components of the central nervous system (CNS)—the brain and the spinal cord—typically cause paresis, sensory loss, and visual deficits. In addition, lesions in the cerebral hemispheres (the cerebrum) cause neuro-psychologic disorders. Symptoms and signs of CNS di sorders must be contrasted to those resulting from peripheral nervous system (PNS) and psychogenic disorders.
Signs of Cerebral Hemisphere Lesions Of the various signs of cerebral hemisphere injury, the most prominent is usually… Contralateral hemiparesis: weakness of the lower face, trunk, arm, and leg opposite to the side of the lesion. It results from damage to the
corticospinal tract, which is also called the pyramidal tract . During the corticospinal tract's entire path from the cerebral cortex to the anterior horn cells of the spinal cord, it is considered the upper motor neuron (UMN). The anterior horn cells, which are part of the PNS, are the beginning of the lower motor neuron (LMN). The division of the motor system into upper and lower motor neurons is a basic tenet of clinical neurology.
Each corticospinal tract originates in the cerebral cortex, passes through the internal capsule, and descends into the brainstem. It crosses in the pyramids, which are long protuberances on the inferior portion of the medulla, to descend in the spinal cord as the lateral corticospinal tract. It terminates by forming a synapse with the anterior horn cells of the spinal cord, which give rise to peripheral nerves. The corticospinal tract is sometimes called the pyramidal tract because it crosses in the pyramids. A complementary tract, which originates in the basal ganglia, is called the
UPPER MOTOR NEURONE(UMN) vs LOWER MOTOR NEURONE (LMN) DISEASE: Characteristics of lower motor neurone disease include: weakness and wasting, hypotonicity, decreased reflexes, fasciculation. Characteristics of upper motor neurone disease include : weakness, spasticity, increased tendon reflexes with clonus, extensor plantar response.
Cerebral lesions that damage the corticospinal tract are characterized by
signs of UMN injury
Signs of UMN injury: - Paresis with muscle spasticity (muscular hypertonicity) - Hyperactive deep tendon reflexes (DTRs) - Babinski signs
HEMIPARESIS (UMN) Severe right hemiparesis typically has weakness of the right arm, leg, and lower face. The right-sided facial weakness causes the widened palpebral fissure and flat nasolabial fold; however, the forehead muscles are normal. The right arm is limp, and the elbow, wrist, and fingers are flexed. The right hemiparesis also causes the right leg to be externally rotated and the hip and knee to be flexed. When the patient stands up, his weakened arm retains its flexed posture. His right leg remains externally rotated, but he can walk by swinging it in a circular path. This manoeuvre is effective but results in circumduction or a hemiparetic gait.
Mild hemiparesis may not be obvious. To exaggerate a subtle hemiparesis, the physician has asked this patient to extend both arms with his palms held upright, as though each outstretched hand were holding a water glass or both hands were supporting a pizza box (the “pizza test”). After a minute, a weakened arm slowly sinks (drifts), and the palm turns inward (pronates). The imaginary glass in the right hand would spill the water inward and the imaginary pizza would slide to the right. This arm's drift and pronation represent a forme fruste of the posture seen with severe paresis.
In contrast, peripheral nerve lesions, including a nterior horn cell or motor neuron diseases, are associated with signs
of LMN injury:
-Paresis with muscle flaccidity and atrophy -Hypoactive DTRs -No Babinski Signs
Deep Tendon Reflex in UMN and LMN Disease:
Normal
UMN Lesion
LMN Lesion
A , Normally, when the quadriceps tendon is struck with the percussion hammer, a deep tendon reflex (DTR) is elicited. In addition, when the sole of the foot is stroked to elicit a plantar reflex, the big toe bends downward (flexes).
B , When brain or spinal cord lesions involve the corticospinal tract and cause upper motor neuron (UMN) damage, the DTR is hyperactive, and the plantar reflex is extensor (i.e., a Babinski sign is present).
C , When peripheral nerve injury causes lower motor neuron (LMN) damage, the DTR is hypoactive and the plantar reflex is absent.
Cerebral lesions are not the only cause of hemiparesis. Because the corticospinal tract has such a long course, lesions in the brainstem and spinal cord as well as t he cerebrum may produce hemiparesis and other signs of UMN damage. Signs pointing to injury in various regions of the CNS can help identify the origin of hemiparesis, that is, localize the lesion.
LOCALISING LESIONS in the CEREBRUM (e.g. APHASIA)
Wernicke Aphasia (Receptive aphasia): Speech is preserved, but language content is incorrect. This may vary from the insertion of a few incorrect or nonexistent words to a profuse outpouring of jargon. Grammar, syntax, rate, intonation and stress are normal. Substitutions of one word for another (paraphasias) are common. Comprehension and repetition are poor.
Broca’s Aphasia: Sufferers of this form of aphasia exhibit the common problem of agrammatism. For them, speech is difficult to initiate, non-fluent, labored, and halting. Similarly, writing is difficult as well. Intonation and stress patterns are deficient. Language is reduced to disjointed words and sentence construction is poor, omitting function words and inflections (bound morphemes).
Signs of Basal Ganglia Lesions The basal ganglia, located subcortically in the cerebrum, are composed of the globus pallidus and the putamen (the striatum), the substantia nigra, and the subthalamic nucleus (corpus of Luysii). They give rise to the extrapyramidal tract, which modulates the corticospinal (pyramidal) tract. The extrapyramidal tract controls muscle tone, regulates motor activity, and generates the postural reflexes through its efferent fibers that play on the cerebral cortex, thalamus, and other CNS structures. However, the extrapyramidal tract's efferent fibers are confined to the brain and do not act directly on the spinal cord or LMNs.
Signs of basal ganglia injury include a group of fascinating, often dramatic, involuntary movement disorders:
▪
Parkinsonism is the combination of resting tremor, rigidity, bradykinesia (slowness of movement) or akinesia (absence of movement), and postural abnormalit ies. Minor features include micrographia and festinating gait. Parkinsonism usually results from substantia nigra degeneration (Parkinson's disease and related illnesses), dopamine-blocking antipsychotic medications, or toxins.
▪
Athetosis is the slow, continuous, writhi ng movement of the fingers, hands, face, and throa t. Kernicterus or other perinatal basal ganglia injury usually causes it.
▪
Chorea is intermittent, randomly located, jerking of limbs and the trunk. The best-known example occurs in Huntington's disease (previously called “Huntington's chorea”), in which the caudate nuclei characteristically atrophy.
▪
Hemiballismus is the intermittent flinging of the arm and leg on one side of the body. It is classically associated with small infarctions of the contralateral subthalamic nucleus, but similar lesions in other basal ganglia may be responsible.
Signs of Brainstem Lesions: IF appropriate, attribute lesion to one of three divisions of the brainstem:
Midbrain, Pons or Medulla. The brainstem contains the cranial nerve nuclei, the corticospinal tracts and other “long tracts” that travel between the cerebral hemispheres and the limbs, cerebellar afferent (inflow) and efferent (outflow) tracts, and several largely self-contained systems. Combinations of cranial nerve and long tract signs indicate the presence and location of a brainstem lesion. The localization should be supported by the absence of signs of cerebral injury, such as visual field cuts and neuropsychologic deficits. For example, brainstem injuries cause diplopia (double vision) because of cranial nerve impairment, but visual acuity and visual fields remain normal because the visual pathways, which pass from the optic chiasm to the cerebral hemispheres, do not travel within the brainstem. Massive
brainstem injuries, such as extensive infarctions or barbiturate overdoses, cause coma, but otherwise brainstem injuries do not impair consciousness or mentation. With the exception of MS and metastatic tumors, few illnesses simultaneously damage the brainstem and the cerebrum. Although these particular brainstem syndromes are distincti ve, the most frequently observed sign of brainstem dysfunction is nystagmus (repetitive jerk-like eye movements, usually simultaneously of both eyes). Resulting from any type of injury of the brainstem's large vestibular nuclei, nystagmus can be a manifestation of various disorders, including intoxication with alcohol, phenytoin (Dilantin), or barbiturates; ischemia of the vertebrobasilar artery system; MS; Wernicke-Korsakoff syndrome; or viral labyrinthitis.
Signs of Cerebellar Lesions: The cerebellum (Latin, diminutive of cerebrum) is composed of two hemispheres and a central portion, the vermis. Each hemisphere controls coordination of the ipsilateral limbs, and the vermis controls coordination of “midline structures”: the head, neck, a nd trunk. Because the cerebellum controls coordination of the limbs on the same side of the body, it is unique—a quality captured by the aphorism, “Everything in the
brain, except for the cerebellum, is contralateral.” Another unique feature of the cer ebellum is that when one hemisphere is damaged, the other will eventually assume the functions for both. Thus, alt hough loss of one cerebellar hemisphere will cause incapacitating ipsilateral incoordination, the disability improves as the remaining hemisphere compensates almost entirely. For example, patients who lo se one cerebellar hemisphere to a stroke or trauma typically regain their ability to walk, although they may never dance or perform other activities requiring both cerebellar hemispheres. Young children who sustain such an inju ry are more resilient and often can learn to ride a bicycle, dance, and perform various athletic activities. In addition to incoordination, cerebellar lesions cause subtle motor changes, such as muscle hypotonia and pendular DTRs. However, they do not cause paresis, hyperactive DTRs, or Babinski signs.
GAIT ATAXIA: Damage to either the entire cerebellum or the vermis alone causes incoordination of the trunk (truncal ataxia). It forces patients to place their feet widely apart when standing and leads to a lurching, unsteady, and widebased pattern of walking (gait ataxia). A common example is the staggering and reeling of people intoxicated by alcohol or phenytoin. SCANNING SPEECH: Extensive damage of the cerebellum also causes scanning speech, a variety of dysarthria. Scanning speech, which reflects incoordination of speech production, is characterized by poor modulation, irregular cadence, and inability to separate adjacent sounds. Dysarthria—whether from cerebellar injury, bulbar or pseudobulbar palsy, or other neurologic conditions—should be distinguishable from aphasia, which is a language disorder that stems from dominant cerebral hemisphere injury. NOTE: Age related change of the cerebellum. Before considering the illnesses that damage the cerebellum, physicians must appreciate that the cerebellum undergoes age-related changes that appear between a ges 50 and 65 years in the form of mildly impaired functional ability and abnormal neurologic test results. For example, as people age beyond 50 years, they walk less rapidly and less sure-footedly. They begin to lose their ability to ride a bicycle and to stand on one foot while putting on socks. During a neurologic examination they routinely tend to topple when walking heel-to-toe, that is, performing the “tandem gait” test
ILLNESSES THAT AFFECT THE CERBELLUM: The illnesses that are responsible for most cerebral lesions—strokes, tumors, trauma, AIDS, and MS—also cause most cerebellar lesions. The cerebellum is also particularly vulnerable to toxins, such as alcohol, toluene, and organic mercury; medications, such as phenytoin; and deficiencies of certain vitamins, such as thiamine and vitamin E. Some conditions damage the cerebrum as well as the cerebellum and may cause a combination of cognitive impairment and incoordination
Signs of Spinal Cord Lesions:
SPINAL TRACTS
In this sketch of the spinal cord, the centrally located gray matter is stippled. The surrounding white matter contains myelin-coated tracts that ascend and descend within the spinal cord.
Clinically important ascending tracts are the -spinocerebellar tracts (SC) (light blue), -lateral spinothalamic tract (ST) (light blue), -the posterior column ( fasciculus cuneatus [FC ], from the upper limbs, and fasciculus gracilis [FG], from the lower limbs
ra .
The major descending pathway is the lateral corticospinal tract. The major ascending pathways, which are vir tually all sensory, include the following:
▪
Posterior columns, composed of the fasciculi cuneatus and gracilis, carry position and vibration sensations to the thalamus.
▪
Lateral spinothalamic tracts carry temperature and pain sensations to the thalamus.
▪
Anterior spinothalamic tracts carry light touch sensation to the thalamus.
▪
Spinocerebellar tracts carry joint position and movement sensations to the cerebellum.
Conditions that affect the spinal cord: Discrete Injuries: The site of a spinal cord injury—cervical, thoracic, or lumbosacral—determines the nature and distribution of the motor and sensory deficits. In general, all spinal cord injuries disrupt bladder control and sexual function, which rely on delicate, intricate systems
Neurlogical Diseases: MS, the most common CNS demyelinating illness, typicall y causes myelopathy alone or in combination with cerebellar, optic nerve, or brainstem damage. Tumours of the lung, breast, and other organs that spread to the vertebral bodies often compress the spinal cord and cause myelopathy. Similarly, regions of degenerative spine disease, such as cervical spondylosis, can narrow the spinal canal enough to compress the spinal cord. There are also several illnesses damage only specific spinal cord tracts (e.g. tabes dorsalis (syphilis), Friedreich’s ataxia etc).
NEURAXIS LOCALISATION: Neuraxis Level Cortex/ hemisphere
e n v i o t i i t n c g n o u C F
+
e r u z i e S
+
e ) g a a i s u a g h n p a ( L a
+
a i r h t r a s y D
d l e i s F l s a o L u s i V
+
+
Brainstem
+
Cerebellum
+
e t a g u j e z n a o G c s y D
+
Cord
r e d e c d n a e l n B i t / l n e o w c n o I B
s n i e o t l a c s l u u c M i c s a F
a i x e l f e r r e p y H
i g k s n n i i o b g a p B u
+
+
+
+
+
+
+
+
+
+
+
+
+
+
s e s l e c n s k u a M e w
y e h l c s p u o r M t a
s s o L y r o s n e S
e r e v e S n i a P
Anterior Horn Cell
+
+
+
Root
+
+
+
+
+
Plexus
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
Nerve
+
NMJ Muscle
+
+
Aphasia: loss or impairment of the power to use or comprehend words usually resulting from brain damage Dysarthria: difficulty in articulating words due to disease of the central nervous system Dysconjugate Gaze: failure of the eyes to turn together in the same direction Fasciculations: muscular twitching involving the simultaneous contraction of contiguous groups of muscle fibers NMJ: Neuromuscluar junction
WHERE is the lesion? -cortex/ hemisphere -brainstem -cerebellum -spinal cord -anterior horn cell -nerve root -plexus -peripheral nerve -neuromuscular junction -muscle
WHAT is the lesion? CITTEN DVM -Congenital -Inflammatory (autoImmune, Infectious) -Toxic -Trauma -Endocrine -Neoplastic and Nutritional -Degenerative or Drugs -Drugs -Metabolic
What is the TEMPORAL profile? -Acute -Subacute -Chronic -Progressive -Paroxysmal/ relapsing
Age-Related Special Sense Impairments (more degeneration of sensory organ than of cranial nerve) Smell
Some degree of anosmia in 75% of individuals older than 80 years
Vision
Presbyopia: mostly inability to accommodate to see closely held or small o bjects; cataracts
Taste
Loss of taste sensitivity and discrimination, as well as anosmia for aroma
Hearing Presbycusis: loss of speech discrimination, especially for consonants; poor high-pitched sound detection, tinnitus
Mini-mental state examination “The mini -mental state examination (MMSE) is a brief 30-point questionnaire test that is used to screen for cognitive impairment. It is commonly used in medicine to screen for dementia. It is also used to estimate the severity of cognitive impairment at a given point in time and to follow the course of cognitive changes in an individual over time, thus making it an effective way to document an individual’s response to treatment.”
Mini-Mental State
Write in the points for each correct response. A total of 30 points is possible. Score Points Orientation
1. What is the:
2. Where are we?
Year?
_____ 1
Season?
_____ 1
Date?
_____ 1
Day?
_____ 1
Month?
_____ 1
State?
_____ 1
Country?
_____ 1
Town or city?
_____ 1
Hospital?
_____ 1
Floor?
_____ 1
Registration 3. Name three objects, taking 1 second to say each. Then ask the patient to repeat all three names after you have said them. (Give one p oint for each correct answer.) Repeat the answers until the patient learns all three. _____ 3 Attention and calculation Serial sevens. Have the patient count backward from 100 by 7's. (Stop after five answers: 93, 86, 79, 72, 65. Give one point for each correct answer.) Alternatively, have the patient spell WORLD backwards.
_____ 5
Recall 5. Ask for the names of the three objects learned in question 3. (Give one point for each correct answer.) _____ 3 Language 6. Point to a pencil and a watch. Have the patient name them as you point.
_____ 2
7. Have the patient repeat "No ifs, ands or buts."
_____ 1
8. Have the patient follow a three-stage command: "Take a paper in your hand. Fold the paper in half. Put the paper on the floor."
_____ 3
9. Have the patient read and obey the following: "CLOSE YOUR EYES." (Write the words in large letters.)
_____ 1
10. Have the patient write a sentence of his or her choice. (The sentence should contain a subject and an object, and it should make sense. Ignore spelling errors when scoring.)
_____ 1
11. Have the patient copy the following design. (Give one point if all sides and angles are preserved and if the intersecting sides form a quadrangle.)
_____ 1
Total
_____
THE CRANIAL NERVE EXAMINATION
*
Positioning and Exposure: the patient should be sitting on the edge of the bed General Inspection: 4. 5. 6. 7. 8. 9.
Craniotomy scars Neurofibromas Facial asymmetry Ptosis Proptosis Deviation of the eyes or unequal pupils
Neurofibromatosis (type 1, affecting peripheral nerves) is characterised by more than five face-au-lait spots (discoloured patched of skin), and soft, sometimes pedunculated neurofibromas
This patient has a right-sided occulomotor nerve
( fibrous tumours or nodules
palsy, due to a large pituitary adenoma invading
growing from the peripheral
the cavernous sinus. He has paralysis of the right
nerve sheath). Associated
levator palpebral superioris muscle (complete
abnormalities may include
ptosis), and a dilated right pupil (mydriasis).
Proptosis ( or exopthalmos). Proptosis is a forward displacement o f the eyeball from the orbit, associated with eyelid retraction, so that the sclera is visible above the iris. Unilateral proptosis may be a sign of an orbital tumour, haemorrhage, or infiltration, and requires prompt treatment to avoid damage to the optic nerve. This patient has Proptosis may be difficult to detect if the eyeball protrusion is subtle. If suspicious, view from above the seated patient. Draw the upper eyelids gently upward, then compare protrusion of the eyeballs.
This congenital right-sided occulomotor nerve palsy is characterised by potosis, divergent strabismus (eye “down and out”) and a dilated pupil, which is unreactive to direct light and accommodation. Consensual reaction in the opposite normal eye is intact. Third nerve lesions may also be caused by trauma.
This patient’s abducens palsy results in an abduction deficit of the left eye, convergent strabismus (“cross eye”) and diplopia (double vision). Sixth nerve lesions may be caused by vascular lesions, tumour, trauma, raised intracranial pressure, or diabetes.
THE CRANIAL NERVES CN I II III
Name Olfactory Optic Oculomotor
Nerve Type * S Special Sensory S Special Sensory M Motor
Autonomic IV V
Trochlear Trigeminal
M B
Motor Motor Sensory
VI VII
Abducens Facial
M B
Motor Motor Autonomic Sensory
VIII IX
Vestibulocochlear (Auditory) Glossopharyngeal
S B
Special Sensory Special Sensory Motor Autonomic Motor Autonomic Sensory Sensory
X
Vagus
B
XI
Accessory
M
Special Sensory Motor Autonomic Motor Sensory Motor
XII
Hypoglossal
M
Motor
Functions Smell- direct extension from the brain Vision- direct extension from the brain Moves muscles of eye and eyelid (superior, inferior and medial recti; levator palpebrae superioris) Parasympathetic (ciliaris and sphincter papillae) Moves eye (superior oblique) Muscles of mastication (masseters, temporalis) Face and neck, sinuses, meninges and external tympanic membrane Moves eye (lateral rectus) Muscles of facial expression Parasympathetic (salivary glands except parotid and lacrimal) Sensory around ear and external tympanic membrane Taste anterior 2/3 tongue Hearing Balance Moves pharynx upwards (Stylopharageus) Parasympathetic (parotid gland) Carotid body Sensory posterior 1/3 tongue and internal surface of tympanic membrane Taste posterior surface of tongue Muscles of pharynx & larynx swallow & speech Parasympathetic to neck, thorax, abdomen Sensory from pharynx, larynx, viscera Trapezius and sternocleidomastoid (shrugs ans turns head) Muscles of tongue movement
* S: sensory / M: motor / B: both pneumonic for remembering the nerve type for the cranial nerves: “Some Say Money Matters But My Brother Says Big Boobs Matter More”
OLFACTORY NERVE (I)
*
“ From the olfactory receptors located deep in the nasal cavity, branches of the pair of olfactory nerves pass upward through the multiple holes in the cribriform plate of the skull to several areas of the brain. Some terminate on the undersurface of the frontal cortex, home of the olfactory sensory areas. Others terminate deep in the hypothalamus and amygdala—cornerstones of the limbic system. The olfactory nerves' input into the limbic system, at least in part, accounts for the influence of smell on psychosexual behaviour and memory.”
Smell 1.
Ask the patient if they can smell normally -If they answer ‘YES’ this is usually sufficient and you may proceed to CNII.
2.
If altered olfaction is suspected -Inspect nares with light and speculum -Ask the patient to close his/her eyes -Test one nostril at a time by offering a variety of materials with common smells -Either use materials close at hand with an aroma (fruit, soap, coffee, perfume) or specially prepared materials -Ask the patient if they can identify the smell -Ask the patient if the smell is the same on both sides
NB: Volatile and irritative substances, such as ammonia and alcohol, are not suitable because they may trigger intranasal trigeminal nerve receptors and bypass a possibly damaged olfactory nerve.
anosmia, cannot perceive smells One-sided anosmia may result from tumors adjacent to the olfactory nerve, such an olfactory groove meningioma. In the classic Foster-Kennedy syndrome, a meningioma compresses the olfactory nerve and the nearby optic nerve. The damage to those two nerves causes the combination of unilateral blindness and anosmia. If the tumor grows into the frontal lobe, it can also produce personality changes, dementia, or seizures. In most cases of bilateral anosmia, the underlying disturbance is mundane. Anosmia is routine in anyone with nasal congestion and those who regularly smoke cigarettes. Head trauma, even from minor injuries, can shear off the olfactory nerves as they pass through the cribriform plate and cause anosmia Olfactory hallucinations may represent the first phase or aura (Latin, breeze) of partial complex seizures that originate in the medial-inferior surface of the temporal lobe.
OPTIC NERVE (II)
Visual Acuity 1. Test visual acuity with the patient wearing his/ her spectacles 2. Each eye is tested separately with a Snellen chart, while the other is covered with a small card. (record last full line; 6/3 (good), 6/6 (normal), 6/9 ( ↓acuity)) -also COMPARE eyes (and can you improve with pin hole?- glasses will then help. Ishihara dot chart for assessing red/ green colour blindness:
*
Visual Fields 1.
2.
Examine the visual fields by confrontation using a hat pin or pen a. Ask the patient to remove their spectacles b. The examiners eyes should be level with the patient’s eyes, and the patient should be at arm’s length c. Ask the patient to cover one eye and mirror them by covering whichever of your eyes is opposite. Both you and the patient need to stare straight ahead and not move the eye from its neutral position d. With an outstretched arm, position the pin halfway between you and the patient and gradually bring the pin diagonally into the visual field and towards the centre of vision e. Ask the patient to report when they first sight the pin i n their peripheral vision and if it disappears while travelling to the centre of their vision f. Test each eye separately and compare to your own visual fields. If visual acuity is poor, map the fields with a finger.
Patient closes one eye (or covers with card) and doctor 1
2
Centre of vision 3
closes mirroring eye.
“When can you see it and does it ever disappear?” 4
Visual inattention: test fields by wriggling two fingers in front of Pt and coming in peripherally.
Fundi 1.
Use an opthalmoscope to examine the fundi Check optic disc for papillodema (normal vision vs vision loss with oedema for MS), optic neuritis (X vision and blurry disc)
This is a normal fundus of the left eye. The field of view is much wider here than in direct opthalmoscopy. Look for the pale yellow optic disc (where the optic nerve exits from the back of the eye), the four retinal vascular ‘arcades’ radiating out from the optic disc, the orange light-sensitive retina, and the dark red of the macula (the most sensitive area of the retina, located centrally).
Visual defect is dependent on location of lesion. e.g. pituitary adenoma, push up against optic chiasm, affecting medial tracts
Papilloedema may be caused by raised intracranial pressure, optic nerve or vascular disease. This patient has a brain tumour, resulting in raised ICP. Vascular congestion and axonal swelling within the optic nerve causes fuzziness and heaping up of the disc margins, loss of pulsation of the retinal veins, and obliteration of the physiological cup. Initially there are few visual symptoms, but as the oedema progress, the blind spot enlarges and vision blurs. Finally, arterial blood flow falls, and infarction of the optic nerve occurs, with sudden,
In this diabetic, frond-like
This fundus demonstrates retinopathy
proliferations of new vessels
due to severe acute hypertension. There
appear on the (yellow) optic disc.
are flame-shaped and blot retinal
Such neovascularisation is typical of early proliferative
diabetic retinopathy, and places the patient at risk of visual
In optic atrophy, the disc is flat, white and has sharp margins due to axonal death and decreased vascularity. Optic atrophy may
haemorrhages, and hard
result from papilloedema, or from various
exudates, caused by leakage of lipids
other processed including thromboembolism.
and proteins in this instance around the
A total optic nerve lesion causes unilateral
macular.
blindness with loss of direct and consensual
OCULOMOTR, TROCHLEAR & ABDUCENS NERVES (III, IV, VI)
*
The oculomotor, trochlear, and abducens nerves constitute the “ extraocular muscle system” because, acting in unison, they move the eyes in parallel to provide normal conjugate gaze. Damage of any of these nerves causes dysconjugate gaze, which results in diplopia (double vision). Extraocular muscle nerve damage leads to characteristic patterns of diplopia. In addition, with oculomotor nerve damage, patients also lose their pupillary constriction to light and strength of the eyelid muscle.
Diplopia is most often attributable to a lesion in the oculomotor nerve on one side or the abducens nerve on the other. For example, if a patient has diplopia when looking to the left, then either the left abducens nerve or the right oculomotor nerve is paretic.
Inspect the pupils: shape, relative sizes, associated ptosis Reaction to light 1. 2. 3.
Use a pocket torch and shine the light from the side to gauge the reaction of the pupils to light Assess both the direct and consensual responses Look for an afferent papillary defect by moving the torch in an arc from pupil to pupil (swinging torch reflex)
The light reflex, which is more complex than a deep tendon reflex, begins with its afferent limb in the optic nerve (cranial nerve II). 1. The optic nerve transmits light impulses from the retinas to two neighboring midbrain structures: (1) In conveying vision, axons synapse on the lateral geniculate body. Then postsynaptic tracts convey visual information to the occipital lobe's visual cortex. (2) In conveying the light reflex, optic nerve axons also synapse in the pretectal region. 2. Postsynaptic neurons travel a short distance to both the ipsilateral and contralateral Edinger-Westphal nuclei, which are the parasympathetic divisions of the oculomotor (third cranial nerve) nuclei. Those nuclei give rise to parasympathetic oculomotor nerve fibres, which constitute to the reflex's efferent limb. Their fibres synapse in the ciliary ganglia and postsynaptic fibres terminate in the iris constrictor (sphincter) muscles. Thus, light shone in one eye constricts the pupil of that eye ( the “direct” *ipsilateral+ light reflex) and the contralateral eye ( the “consensual” *indirect or contralateral+ light reflex).
Conjugate gaze: the normal movement of the two eyes simultaneously in the same direction to bring something into view. Dysconjugate gaze: failure of the eyes to turn together in the same direction Binocular vision: vision with a single image, by both eyes simultaneously Monocular vision: vision with one eye
Accommodation 1.
Test accommodation by asking the patient to look into the distance and then at the hat pin placed about 30cm from the nose Normally both pupils will constrict (accommodate) and eyes converge Focus on point, move close (constrict) and away (dilate)
Eye movements 1. 2. 3. 4.
Ask the patient to keep their head still and to fo llow the hat pin with their eyes only Assess both eyes first and as they follow the hat pin in an ‘H’ pattern (do it slowly) Look for failure of movement and for nystagmus Ask the patient to report diplopia (double vision) in any direction Dr should say: ‘Keep looking... is it double???’
*Nystagmus: Rapid rhythmic repetitious involuntary (unwilled) eye movements. Nystagmus can be horizontal, vertical or rotary.
Doctor holds patient’s head, slowly moves hatpin, stopping at each point asking “can you see double?”. Watch for nystagmus.
Superior rectus
Inferior oblique UP
NOSE SIDE
G Lateral
Medial
A
rectus
rectus
DOWN Inferior rectus
Superior oblique
TRIGEMINAL NERVE (V)
*
The trigeminal (Latin, threefold) nerves convey sensation from the face and innervate the large, powerful muscles that protrude and close the jaw. Because these muscles' main function is to chew, they are often called the “muscles of mastication.” NB: tongue (sensory) is also part of CNV-3, but usually not tested
Corneal Reflex 1. 2. 3.
Gently touch the cornea with a piece of cotton wool brought form the side (just inside iris) Ask the patient if they felt the touch (sensory component via CNV) The normal response is reflex blinking (motor component via CNVII) Contact lens: ↓reflex; NB- don’t let cotton touch eyelashes
Assessing the corneal reflex is useful, especially in examining patients whose sensory loss does not conform to neurologic expectations. The corneal reflex is a “superficial reflex” that is essentially indepe ndent of upper motor neuron (UMN) status. It begins with stimulation of the cornea by a wisp of cotton or a breath of air that triggers the trigeminal nerve's V 1 division, which forms the reflex's afferent limb. A brainstem synapse stimulus innervates both facial (seventh cranial) nerves, which form the efferent limb. The synapse innervates both sets of orbicularis oculi muscles. Normally, because of the synapse, stimulating one cornea will provoke bilateral blinking. However, if the cotton tip is first applied to the right cornea and neither eye blinks, and then to the left cornea and both eyes blink, the right trigeminal nerve (afferent limb) is impaired. On the other hand, if cotton stimulation on the right cornea fails to provide a right eye blink but succeeds in provoking a left eye blink, the right facial nerve (efferent limb) is impaired.
Facial Sensation 1. 2. 3.
Test facial sensation in the ophthalmic, maxillary and mandibular divisions of CNV Test pain sensation with the pin first and map any areas of sensory loss from dull to sharp (sharp: use point of paper clip, soft: cotton wool) Test light touch as well so that sensory dissociation can be detected if present
R
L Patient closes their eyes:
Forehead
Testing the three branches of the trigeminal nerve.
L R
Cheek
forehead cheek chin
sharp soft
Chin
Hypalgesia : areas of reduced sensation, should conform to anatomic outlines -The first division (V1) supplies the forehead, the cornea, and the scalp up to the vertex; -the second (V2) supplies the malar area; -the third (V3) supplies the lower jaw, except for the angle. These distributions have more than academic importance. These dermatomes may be mapped by herpes zoster infections (shingles), trigeminal neuralgia, and facial angioma in the Sturge-Weber syndrome
Herpes zoster (or shingles) commonly affects the ophthalmic division of the trigeminal nerve.
Muscles of mastication 1. 2.
Examine the motor division of CNV by asking the patient to clench their teeth while you feel the masseter muscles Ask the patient to open the mouth while you attempt to force it closed
Jaw Jerk 1. 2.
Ask the patient to relax their jaw Place a finger tip on the midline of the jaw and strike t his lightly with a tendon hammer Normal reflex response is slight elevation of the mandible (close the mouth) -Stretch reflex, an increased jerk is abnormal
Abnormalities are mostly a ma tter of rapidity and strength.
In a hypoactive reflex, as found in bulbar palsy and other lower motor neuron (LMN) injuries, there is little or no rebound. In a hyperactive reflex, as in pseudobulbar palsy and other upper motor neuron (UMN) (corticobulbar tract) lesions, there is a quick and forceful rebound.
FACIAL NERVE (VII)
*
Muscles of Facial Expression (first LOOK- is face symmetrical???- PALSY???) Palsy: In medicine, palsy is the paralysis of a body part, often accompanied by loss of sensation and by uncontrolled body movements, such as shaking. Medical conditions involving palsy include cerebral palsy (caused by certain intracranial lesions) , brachial palsy (the paralysis of an arm), and Bell's palsy (the paralysis of half the face due to inflammation of the facial nerves). -Test the muscles of facial expression by asking the patient to mimic your facial expressions 1.
Raise your eyebrows and wrinkle your forehead As the patient mimics your expression, look for loss of wrinkling and feel their muscle strength by pushing down on each side 2. Ask the patient to shut their eyes as tight as they can, and keep them closed as you try to open them (compare two sides) 3. Smile- compare the patient’s nasolabial grooves 4. Puff out your cheeks, as if you are holding a mouthful of water – check the patient’s cheeks for symmetry *If muscle wasting- flattening of nasolabial fold and can’t keep eyes closed (CNVII- obicularis oris) To test POWER i) ii) iii)
Dr pokes puffed cheeks Pt keep eyebrows up while Dr pushed them down Pt keeps eyes closed by Dr tries to open them
**In the classic portrayal, corticobulbar tracts originating in the ipsilateral, as well as in the contralateral, cerebral hemisphere supply each facial nerve nucleus. Each facial nerve supplies the ipsilateral muscles of facial expression. Because the upper half of the face receives cortical innervation from both hemispheres, cerebral injuries lead to paresis only of the lower half of the contralateral face. In contrast, facial nerve injuries lead to paresis of both the upper and lower half of the ipsilateral side of the face. **
If there are herpes zoster vesicles found in the ear or the palate, unilateral LMN 7th nerve palsy is known as Ramsay Hunt syndrome (shown here). An UM 7th nerve palsy, most commonly caused by vascular lesions or tumours, spares the muscles of the forehead. The muscles of the upper face are controlled by pathways from both sides of the cerebral cortex.
VESTIBULOCOCHLEAR NERVE (VIII)
*
“The cochlear nerve, one of the two divisions, transmits auditory impulses from the middle and inner ear mechanisms to the superior temporal gyri of both cerebral hemispheres The other division of the acoustic nerve, the vestibular nerve, transmits impulses from the labyrinth governing equilibrium, orientation, and change in position. The most characteristic symptom of vestibular nerve damage is vertigo, a sensation that one is spinning within the environment or that the environment itself is spinning.” -Test hearing first and then vestibular.
Auditory Acuity 1.
2.
Softly whisper a number 60cm away from each ear -Cover the external acoustic meatus of the opposite ear with your finger (or whisper 3 letters from behind, ask the Pt to block other ear with finger) Ask the patient to repeat the number back to you.
Weber’s Test 1. 2.
Strike a 256Hz tuning fork and place the base on the centre of the patient’s forehead Ask the patient where they hear the ringing fork -Ringing should normally be heard in the midline or e qually in both ears -If ringing is reported to be louder in one ear, this may indicate a conductive loss of that ear, or a sensorineural loss of the opposite ear
Rhinne’s Test 1. 2.
3.
Strike a 256Hz tuning fork and place the base of the fork on the patient’s mastoid process Ask the patient to report when they can no longer hear the tuning fork ringing -At this point, position the prongs of the fork in front of the auditory canal -The test is positive if the patient can hear ringing again Repeat for other side
Rhinne positive: Rhinne negative:
Air conduction > Bone conduction Bone conduction > Air conduction
(Normal or sensorineural deadness) (Conduction deafness)
Otoscopy 1.
Examine the external auditory canals and the eardrum with an otoscope if this is indicated. Wax build up or middle ear infection?
Other Questions: Have you had an ear infection lately? Any buzzing in ears? Occupations? When you fly is it hard to equalize pressure? (Eustachian tube problem?)
This right sided view shows: (1) the umbo (where the ear-drum meets the tip of the malleolus) (2), the light reflex (3,4,5), the malleolus (8), and a healthy tympanic membrane, which is translucent, pearly grey and with little vascularity.
Acute otitis media may be suspected in the presence of otalgia (ear ache), an upper respiratory tract infection, and fever. The tympanic membrane is dull, opaque, and bulging, with obscured landmarks and increased vascularity. The light reflex is absent.
TESTING VESTIBULAR COMPONENT by Dix- Hallpike manoeuvre for testing vertigo
The Dix-Hallpike test: determines whether vertigo is triggered by certain head movements. Your doctor will carefully observe any involuntary eye movements (nystagmus) that may occur during this test to determine if the cause of your vertigo is central or peripheral. Central vertigo is caused by a problem inside the brain, and peripheral vertigo is caused by a problem with the inner ear or the nerve leaving the inner ear. The Dix-Hallpike test also can help determine which ear is likely affected.
During the test: 1.
2.
3.
You sit with your legs extended on the examination table. Your doctor turns your head 30º to 45º toward on e side and helps you quickly lie back so your head hangs over the end of the table. Your doctor watches your eyes for involuntary eye movements (called nystagmus). The timing and appearance of the eye movements will identify the cause of vertigo as either the inner ear or the brain. After you sit upright for a few minutes to recover from the vertigo, the procedure is repeated with your head turned in the opposite direction.
-Not for those with neck problems
GLOSSOPHARYNGEAL & VAGUS NERVES (IX, X)
*
Inspect the Soft Palate 1. 2.
Note any uvular displacement Ask the patient to say ‘Ah’ and look for symmetrical movement of the soft palate (straight up = normal) If uvular removed (e.g. sleep apnoea)- also, puff out cheeks and if can’t or air goes out through the nose = problem)
Gag Reflex- this test is unpleasant and is not indicated if the soft palate rises symmetrically (drugs also stop this) 1.
Illicit the gag reflex by gently touching the palate with a tongue depressor (touch around tonsillar pillar) i) The sensory component of the reflex is mediated by CN IX ii) The motor component is mediated via CN X X Gag = aspiration pneumonia
Hoarseness and Cough (Vagus closes vocal cords) -Conversation with the patient may already have alerted you to a hoarse voice -To assess hoarseness further, ask the patient to cough -A bovine cough suggests bilateral recurrent laryngeal nerve lesions “Bovine cough" is used to describe the non- explosive cough of someone unable to close their glottis. It is seen vagus nerve lesions, and may be associated with dysphonia.
Bulbar Palsy (bulbar nerves= CN IX, CN X) Bulbar cranial nerve injury within the brainstem or along the course of the nerves leads to bulbar palsy. This commonly occurring disorder is characterized by dysarthria (speech impairment), dysphagia (swallowing impairment), and hypoactive jaw and gag reflexes.
A, The soft palate normally forms an arch from which the uvula seems to hang.
B, When the pharynx is stimulated, the gag reflex elicits pharyngeal muscle contraction; the soft palate rises with the uvula remaining in the midline. With bulbar nerve injury (bulbar palsy)—lower motor neuron (LMN) injury—the palate has little, no, or asymmetric movement. With corticobulbar tract injury (pseudobulbar palsy)—upper motor neuron (UMN) injury —the reaction is brisk and forceful. Unfortunately, it often precipitates retching, coughing, or crying. (If the purpose of the examination is to assess the patient's ability to swallow, a more reliable decision can be reached by simply observing the patient attempt to swallow a few sips of water.)
Unilateral vagus nerve paralysis may cause difficulty in initiating swallowing of solids and liquids and hoarseness. This picture demonstrates the clinical findings on examination. The tenth nerve received sensory fibres from the pharynx and larynx, and innervates muscles of the pharynx, larynx and palate. Uvular movement towards unaffected side
HYPOGLOSSAL NERVE (XII) The hypoglossal nerves originate from paired nuclei near the midline of the medulla and descend through the base of the medulla (see Fig. 2-9). They pass through the base of the skull and travel through the neck to innervate the tongue muscles. Each nerve innervates the ipsilateral tongue muscles. These muscles move the tongue within the mouth, protrude it when people eat and speak, and push it to the contralateral side. Because of the muscle contractions, each side is balanced, and the tongue protrudes in the midline.
Tongue 1. 2.
Inspect the tongue for wasting and fasciculation while examining the mouth Ask the patient to protrude the tongue a. If the tongue deviates to one side, this is suggestive of a CN XII lesion (to test strength ask Pt to push tongue against inside of cheek) b. The tongue will deviate towards the side of the lesion
Fasciculation: A fasciculation is a small, local, involuntary muscle contraction (twitching) visible under the skin arising from the spontaneous discharge of a bundle of skeletal muscle fibres
If one hypoglossal nerve is injured, that side of the tongue will become weak and, with time, atrophic. When protruded, the partly weakened tongue deviates toward the weakened side which illustrates the adage, “the tongue points toward the side of
the lesion.” If both nerves are injured, as in bulbar palsy, the tongue will become immobile. Patients with hypoglossal LMN dysfunction from ALS have tongue fasciculations, as well as atrophy.
*
When a patient with a
right hypoglossal nerve palsy is asked to poke out the tongue, it deviates towards her weaker, affected right side, demonstrating unilateral lower motor neuron lesion of CN XII. The tongue has a bilateral UMN innervations, so a unilateral UMN lesion causes no deviation.
The hypoglossal nerve is the motor nerve for the tongue. Wasting and fasciculations (fine irregular non-rhythmical muscle fibre contractions) of the tongue are signs of CN XII LMN lesion. This patient had motor neurone disease.
ACCESSORY NERVE (XI) 1. 2. 3.
Inspect for torticollis Ask the patient to shrug their shoulders a. Assess the strength of the tapezius as you push the shoulders down Ask the patient to turn their head against resistance a. Assess the bulk and strength of the sternocleidomastoid mucle
Torticollis, or wry neck, is a condition in which the head is tilted toward one side (cervical rotation), and the chin is elevated and turned toward the opposite side (cervical extension).
*
EXAMINATION OF THE PERIPHERAL NERVOUS SYSTEM
*
The peripheral nervous system (PNS) resides or extends outside the central nervous system (CNS), which consists of the brain and spinal cord. The main function of the PNS is to c onnect the CNS to the limbs and organs. Unlike the central nervous system, the PNS is not protected by bone or by the blood-brain barrier, leaving it exposed to toxins and mechanical injuries. The peripheral nervous system is divided into the somatic nervous system, the autonomic nervous system, and the sensory system. The somatic nervous system is responsible for coordinating the body movements, and also for receiving external stimuli. It is the system that regulates activities that are under conscious control. The autonomic nervous system is then split into the sympathetic division, parasympathetic division, and enteric division. The sympathetic nervous system responds to impending danger or stress, and is responsible for the increase of one's heartbeat and blood pressure, among other physiological changes, along with the sense of excitement one feels due to the increase of adrenaline in the system. The parasympathetic nervous system, on the other hand, is ev ident when a person is resting and feels relaxed, and is responsible for such things as the constriction of the pupil, the slowing of the heart, the dilation of the blood vessels, and the stimulation of the digestive and genitourinary systems. The role of the enteric nervous system is to manage every aspect of digestion, from the esophagus to the stomach, small intestine and colon.
NEUROLOGICAL EXAMINATION OF THE UPPER LIMB
Upper limb peripheral nerve innervation with the arm supinated on an arm board
*
Ant Post Dermatomes Test each dermatome *Pain testing: sharp (tip of paperclip) & dull (end of pen/ curve of paperclip) *Light touch (cotton wool)
Upper limb peripheral nerve innervation with the arm pronated on an a rm board
Mononeuropathies: Disorders of single peripheral nerves, mononeuropathies, are characterized by flaccid paresis, deep tendon reflex loss (areflexia), and reduced sensation, particularly for pain (hypalgesia or analgesia). Paradoxically, mononeuropathies and other peripheral nerve injuries sometimes lead to spontaneously occurring sensations,paresthesias that may be painful, dysesthesias. They also convert stimuli that ordinarily do not cause pain, such as a light touch or cool air, into painful sensations, allodynia; exaggerate painful responses to mildly noxious stimuli, such as the point of a pin, hyperalgesia; or delay but then exaggerate and prolong pain from noxious stimuli, hyperpathia. Major Mononeuropathies Nerve
Motor Paresis
DTR Lost
Pain or Sensory Loss
Examples
Median
Thumb abduction with thenar atrophy
None
Thumb, 2nd and 3rd fingers, and lateral ½ of 4th
Carpal tunnel syndrome
Ulnar
Finger and thumb adduction (“claw hand”)
None
5th and medial ½ of 4th fingers
Radial
Wrist, thumb, and finger extensors (“wrist drop”)
Brachioradialis*
Dorsum of hand
Femoral
Knee extensors
Quadriceps (knee)
Anterior thigh, medial calf
Sciatic
Ankle dorsi flexors and plantar flexors (“flail ankle”)
Achilles (ankle)
Buttock, lateral calf, and most of foot
Sciatica from a herniated disk
Peroneal
Ankle dorsiflexors and evertors (“foot drop”)
None
Dorsum of foot and lateral calf
Foot drop from lower knee injury
Saturday night palsy
DTR, deep tendon reflex. * When radial nerve is damaged by compression in the spiral groove of the humerus, the triceps DTR is spared.
CARPAL TUNNEL SYNDROME: The median nerve passes through the carpal tunnel, which is a relatively tight compartment. The usual sensory distribution of the median nerve is the palm, thenar eminence (thumb base), thumb, and adjacent two fingers. In carpal tunnel syndrome, pain that spontaneously shoots distally from the wrist is superimposed on this area. The Tinel's sign, a reliable indication of carpal tunnel syndrome, can be elicited by a physician's tapping the palmar wrist surface and producing pain or paresthesias in the median nerve distribution.
ULNAR NERVE INJURIES: With ulnar nerve injuries, the palmar view shows that intrinsic muscles of the hand, particularly those of the hypothenar eminence (fifth finger base), undergo atrophy. The fourth and fifth fingers are flexed and abducted. When raised, the hand and fingers assume the “benediction sign.” In addition, the medial two fingers and palm are anesthetic. Right, Ulnar nerve injuries also produce a “claw hand” because of atrophy of the muscles between the thumb and adjacent finger (first dorsal interosseous and adductor pollicis), as well as of those of the hypothenar eminence. WRIST DROP (RADIAL INJURY): As the radial nerve winds around the humerus, it is vulnerable to compression and other forms of trauma. Radial nerve damage leads to the readily recognizable wrist drop that results from paresis of the extensor muscles of the wrist, finger, and thumb. “Saturday night palsy”alcohol induced stupor who lean against upper arm.
POLYNEUROPATHIES The most frequently occurring PNS disorder, polyneuropathy or, for short, neuropathy, is generalized, symmetric involvement—to either a greater or lesser extent—of all peripheral nerves. In polyneuropathy, pain and o ther sensations are typically lost symmetrically, more severely in the distal than proximal portions of the limbs, and more severely in the legs than the arms. This pattern of sensory loss is termed stocking-glove hypalgesia.
LOOK for: - movement of limb (any abnormal movement?) -Parkinsonian movement? -Huntington’s chorea -fasciculations (involuntary muscle tremors) -skin changes, herpes virus changes -autonomic nervous system signs (rare; e.g. diabetes) sweating in certain areas, too dry (cracking?)
Positional Drift (with eyes closed): especially with cerebellar disease (toxins- most common = alcohol)
Tone: (ask patient to ‘go limp’) Spasticity: tone and resistance of muscle lengthening in one group of muscles is greater than another Cogwheel Rigidity (Parkinsonian): basal ganglia disease will cause a cog or interruption of tone in the examined extremity Leadpipe Rigidity: if it is equally difficult to extend and flex t he arm against resistance Clasp Knife: the patient may have an increased tone on extension o f the arm that suddenly because of 1b fibre inhibition from tendons that project to inhibitory interneurons or the anterior horn cells themselves and the tone suddenly lessens -Shaking the hands gently as if you are drying them often demonstrates hypotonicity
Loss of tone: occurs by breaking the reflex arc (no input to anterior horn cells) of the firing from anterior horn cells is decreased which occurs with cerebellar disease, spinal or cerebral shock (decrease of facilitation of anterior horn cells which decrease the drive of the gamma loop). The gamma loop controls the muscle spindle. When activated, the intrafusal muscle fibres of the spindle contract which in turn brings the anterior horn cells closer to depolarisation and discharges some with consequent muscle contraction. Not enough muscle fibres to move the joint, but muscle tone is increased.
CLONUS: Sudden stretching of a disinhibited muscle induces repetitive reflex contractions which are often caused by a supranuclear lesion of the pyramidal tract. It may be evident in any muscle but is most easily seen in the legs. The ankle is suddenly or rhythmically extended, which induces the repetitive contractures. It may be easily seen in the quadriceps muscle by displacing the patella sharply downward. Extremely nervous patients may demonstrate the sign. It is associated with weakness, poor fractionated movement and hyperactive reflexes. Spasticity and Babinski’s or Hoffman’s signs are often associated.
Method for eliciting ankle clonus
Reflexes: (Absence of reflexes can occur in normal patients (or with LMN lesion). It is really only important if the reflex is strong (indicates an UMN lesion). NOTE reflex alone does not rule in/out a disease, need other signs.
Diagram illustrating the pathways responsible for the stretch reflex and the inverse stretch reflex. Stretch reflex: Stretch stimulates the muscle spindle, which activates Ia fibers that excite the motor neuron. Inverse stretch reflex ( golgi apparatus): Stretch also stimulates the Golgi tendon organ, which activates Ib fibers that excite an interneuron that releases the inhibitory mediator glycine. With strong stretch, the resulting hyperpolarization of the motor neuron is so great that it stops discharging.
Block diagram of peripheral motor control system. The dashed line indicates the nonneural feedback from muscle that limits length and velocity via the inherent mechanical properties of muscle. d, dynamic -motor neurons; s, static -motor neurons.
BICEPS JERK TRICEPS JERK (three methods)
SUPINATOR JERK FINGER JERK
3/5
5/5
5/5
5/5 4/5
POWER MAP (compare symmetry)
5/5
COODINATION: FINGER-TO-NOSE MOVEMENTS: This patient, who has a multiple sclerosis (MS) plaque in the right cerebellar hemisphere, has a right-sided intention tremor. During repetitive finger-to-nose movements, as his right index finger approaches his own nose and then the examiner's finger, it develops a coarse and irregular path. This irregular rhythm is called dysmetria. Another sign of a cerebellar lesion that reflects incoordination of the limbs is impaired ability to perform rapid alternating movements, dysdiadochokinesia. When asked to slap the palm and t hen the back of the hand rapidly and alternately on his or her own knee, for example, a patient with dysdiadochokinesia will use uneven force, move irregularly, and lose the alternating pattern.
Pain testing: Patient closes eyes and says whether they are feeling sharp or dull and point with other hand to where they are feeling it. Areas of dullness (where sharp feels dull)- map out and tell me when it feels sharp (dermatome distribution or peripheral nerve distribution.
Area of dullness Map out!
Sensory testing (upper limb): (Light touch and pain sites routine)
1 2 3 4 5 6 7 8
Location Supraclavicular fossa Shoulder AC joint Lateral elbow Thumb Middle finger Little finger Medial elbow Axilla
Dermatome C3 C4 C5 C6 C7 C8 T1 T2
E.g. L6, R2, L3, R8, R7, L1, L8, R6, L2, L5, R4, L3, R5, R1, L4, R3
Vibration and Proprioception (Joint) Sense Clinical examination of joint position sense and vibration sense can provide important information concerning specific cutaneous sensory receptors, peripheral nerves, dorsal roots, and central nervous system pathways and should be included as a regular component of the neurological examination. Although these sensory modalities share a spinal cord and brainstem pathway (dorsal column-medial lemniscus pathway ), they arise in different receptors and terminate in separate distributions within the thalamus and cerebral cortex. Consequently, both modalities should be tested as part of the neurological examination. Clinical testing of these modalities requires simultaneous stimulation of tactile receptors; hence this review will include information about the receptors and pathways responsible for tactile sensation. Note: test vibration sense most distally first. If sensation is present, there is no need to test the more proximal sites.
Motor Testing Segmental innervations of muscles s implified: UPPER LIMB
Reflexes UPPER LIMB
C5 Elbow flexors (biceps, brachialis) and shoulder abductionsupraspinatus and deltoid) C6 Wrist extensors (ext carpi radialis –longus brevis) C7 Elbow extensors (triceps) C8 Finger flexors (flex digitorum profundus- middle finger) T1 Small finger abductors (abductor digiti minimi) Brachioradialis (wrist flick) – Radial nerve – C5/6 Biceps – Musculoskeletal nerve – C5/6 Triceps – Radial nerve – C7/8
NEUROLOGICAL EXAMINATION OF THE LOWER LIMB
*
Sensory testing (lower limb): (Light touch and pain sites routine)
1 2 3 4 5 6 7 8 9 10 11
Location Umbilicus Mid-inguinal ligament Upper 1/3 thigh Mid front thigh Medial knee Medial malleolus Base dorsum middle toe Lateral heel Popliteal fossa Ischial tuberosity Perianal skin
Dermatome T10 T12 L1 L2 L3 L4 L5 S1 S2 S3 S4/5
Ant Post Dermatomes
Peripheral Subcutaneous Nerves
KNEE JERK
ANKLE JERK
COODINATION: In the heel-to-shin test, the patient with the right-sided cerebellar lesion in Figure 2-11 displays limb ataxia as his right heel wobbles when he pushes it along the crest of his left shin.
Gait Abnormalities Associated with CNS Disorders Gait
Associated Illness
Apraxic
Normal pressure hydrocephalus
Astasia-Abasia
Psychogenic disorders
Ataxic
Cerebellar damage
Festinating (marche à petits pas) Parkinson's disease Hemiparetic Circumduction
Cerebrovascular accidents
Spastic hemiparesis Tabes dorsalis (CNS syphilis) Steppage* Peripheral neuropathies Waddling
Duchenne's dystrophy and other myopathies
CNS, central nervous system. *The steppage gait consists of each knee being excessively raised when walking. This maneuver compensates for a loss of position sense by elevating the feet to ensure that they will clear the ground, stairs, and other obstacles. It is a classic sign of posterior column spinal cord damage from tabes dorsalis. However, peripheral neuropathies more co mmonly impair position sense and lead to this gait abnormality.
Motor Testing Segmental innervations of muscles simplified: LOWER LIMB
Reflexes LOWER LIMB
L2 L3 L4 L5 S2
Hip flexors (iliopsoas) Knee extensors (quadriceps) Ankle dorsiflexion (tib ant) Long toe extensors (ext hallucis longus) Ankle plantar flexors (gastrocnemius, soleus)
Patellar –Femoral nerve – L2, L4 Ankle – Tibial nerve – S1
Differences between CNS & PNS Differences Between Central (CNS) and Peripheral Nervous System (P NS) Signs CNS
PNS
Motor system Upper motor neuron Lower motor neuron Paresis
Patterns*
Distal
Tone
Spasticˆ
Flaccid
Bulk
Normal
Atrophic
Fasciculations No
Sometimes
Reflexes [+]
DTRs
Hyperactive
Hypoactive
Plantar
Babinski sign(s)
Absent
Sensory loss
Patterns*
Hands and feet
*
Examples: motor and sensory loss of one side or lower half of the body (e.g., hemiparesis or paraparesis), and hemisensory loss. May be flaccid initially.
+
May be absent initially.
Another contrast arises from the difference between demyelinating diseases of the CNS and PNS. Despite performing a similar insulating function, CNS and PNS myelin differ in chemical composition, antigenicity, and cells of origin. -Oligodendrocytes produce CNS myelin, and Schwann cells produce PNS myelin. Also, each oligodendrocyte produces myelin that covers many nearby CNS axons, but each Schwann cell produces myelin than covers only one portion of a single PNS axon. From a clinical viewpoint, Schwann cells regenerate damaged PNS myelin and Guillain-Barré patients usually recover. In contrast, because oligodendrocytes do not regenerat e damaged CNS myelin, impairments are permanent in patients who have lost CNS myelin to toxins and infections. For example, the CNS demyelination that results from toluene use represents a permanent loss. -Multiple sclerosis (MS) appears to be an exception. In this illness, episodes of demyelination of several CNS areas, including the optic nerves, partially or even completely resolve. However, the improvement results from resolution of myelin inflammation rather than regeneration. When MS finally encompasses large areas o f cerebral CNS myelin, it often results in dementia and other mental status changes.
SOME NEUROLOGICAL DISORDERS Diabetic neuropathies are a family of nerve disorders caused by diabetes. People with diabetes can, over time, develop nerve damage throughout the body. Some people with nerve damage have no symptoms. Others may have symptoms such as pain, tingling, or numbness—loss of feeling—in the hands, arms, feet, and legs. Nerve problems can occur in every organ system, including the digestive tract, heart, and sex organs. There are four factors thought to be involved in the development of diabetic neuropathy. i) microvascular disease, ii) advanced glycated end products, iii) protein kinase C and iv) polyol pathway.
Parkinson's disease (also known as Parkinson disease or PD) is a degenerative disorder of the central nervous system that often impairs the sufferer's motor skills, speech, and other functions. It is characterized by muscle rigidity, tremor, a slowing of physical movement (bradykinesia) and, in extreme case s, a loss of physical movement (akinesia). The primary symptoms are the results of decreased stimulation of the motor cortex by the basal ganglia, normally caused by the insufficient formation and action of dopamine, which is produced in the dopaminergic neurons of the brain. Secondary symptoms may include high level cognitive dysfunction and su btle language problems. PD is both chronic and progressive.
Huntington's disease or chorea (HD) is an incurable neurodegenerative genetic disorder that affects muscle coordination and some cognitive functions, typically becoming noticeable in middle age. It is the most common genetic cause of abnormal involuntary writhing movements called chorea. It is much more common in people of Western Europe descent than in people from Asia or Africa. The disease is caused by a dominant mutation on either of the two copies of a specific
gene, located on an autosomal chromosome. Physical symptoms of Huntington's disease can begin at any age from infancy to old age, but usually begin between 35 and 44 years of age. The exact way HD affects an individual varies, and can differ even between members of the same family, but the symptoms progress predictably for most individuals. The earliest symptoms are a general lack of coordination and an unsteady gait. As the disease advances, uncoordinated, jerky body movements become more apparent, along with a decline in mental abilities and behavioural and psychiatric problems. Physical abilities are gradually impeded until coordinated movement becomes very difficult, and mental abilities generally decline into dementia.
Multiple sclerosis is an autoimmune disease in which the body's immune response attacks a person's central nervous system (brain and spinal cord), leading to demyelination. Almost any neurological symptom can appear with the disease, and often progresses to physical and cognitive disability and neuropsychiatric disorder. MS takes several fo rms, with new symptoms occurring either in discrete attacks (relapsing forms) or slowly accumulating over time (progressive forms). Between attacks, symptoms may go away completely, but permanent neurological problems often occur, especially as t he disease advances.
Vertigo is a specific type of dizziness, a major symptom of a balance disorder. It is the sensation of spinning or swaying while the body is actually stationary with respect to the surroundings. The effects of vertigo may be slight. It can cause nausea and vomiting and, in severe cases, it may give rise to difficulties with standing and walking. Vertigo is typically classified into one of two categories depending on the location of the damaged vestibular pathway. These are peripheral (arising from inner ear’s vestibular system) or central vertigo (affected cerebellum).
