Neurology High Yield ( http://www.neuroanatomy.ca/module_list.html )
Ischemic Brain Disease
IRREVERSIBLE DAMAGE after 5 minutes Most vulnerable Hippocampus pyramidal, cerebellum purkinjie cells, watershed areas Risks: diabetes, smoking, ATRIAL FIBRILLATION, cocaine Transient attack: less than 24 hours neurological deficit Types or stroke 1. Thrombotic/atherosclerotic: MOST COMMON -pale liquifactive necrosis (NO REFERFUSION) -causes reactive Gliosis cystic cavity -usually MCA therefore at periphery 2. Embolic -Hemorrhagic red infarct (DUE TO REPERFUSION) -usually atrial fibrillation or atherosclerotic plaques -MCA 3. Lacunar Infarct -small perforating vessels (at BASAL GANGLIA ) hyaline arteriosclerosis -Causes: diabetes, HTN 4. Hemorrhagic stroke -from aneurysm -CharcotBouchard microaneursym at basal ganglia of lenticulostriate arteries -from reperfusion of ischemic 5. Watershed Infarct -prolonged HYPOTENSION -damage usually bilateral deep cortical areas btw border of two vessels -ACA- MCA Top -MCA- PCA Bottom
Ischemic stroke Diminished blood flow Leads to Gliosis Watershed infarct Artery MCA
ACA
Hemorrhagic stroke Hemorrhage aneurysm Embolic Reperfusion
Deficient -Aphasia (Wernicke or brocas), -Neglect syndrome (if right parietal, so ignore left side) -hemiparesis weakness ( arm and face) -homonymous hemianopsia (temporal more common, so superior quadrant) -LEG paresis -hemiplegia (total paralysis)
PCA Basilar Lacunar stroke
urinary incontinence -homonymous hemianopsia with macular sparing (since MCA give blood) Affect pons ( cranial nerves, coma, apnea, vertigo) -Pure motor ( internal capsule) -Pure sensory (thalamus) but the smell intact (since only sensory that bypass) -dysarthria -Ataxic hemiparesis (ipsilateral clumpsy
Imaging: ACUTE do CT to see if hemorrhagic (dark on CT after 24 hours) MRI shows up bright in 3-30 min and remain bright 10 days Histology 12-24 H : RED neurons 24-72: necrosis + PMN 3 -5 day : macrophage 1-2 week : reactive gliosis + vascular proliferation >2 week: glial scar Treatment tPA for occlusive (give within 3 hours) warfarin/ aspirin for embolic once hemorrhage has been ruled out
Alzheimers
Diffuse cortical atrophy (widen sulci, narrow gyri, expand ventricles, ex vacuo hydrocephalus ) Nucleus basalis of Meynert ( low ACH) MOST COMMON cause of dementia ( 2nd is stroke) Causes 1. Apolipoprotein E 2protective ( “ 2 serve and protect”) 2. ‘’ E4 increases risk 3. Down Syndrome, chromosome 21 has APP (amyloid precursor protein) * will stain with Congo red -usually get it before 40 4. Presenilin -Presenilin 1 (chromosome 14) -‘’ 2 (chromosome 1) Clinical diagnosis (confirmed on autopsy) Histology Senile/ neuritic plaques : ABETA-amyloid (beta cleavage of APP) EXTRACELLULAR -normal cleavage if ALPHA Neurofibrillary tangles INTRACELLULAR in neurons -HYPER phosphorylated Tau proteins which are microtubule associated
-amount of tangles CORRELATED WITH DEGREE OF DEMENTIA Death: infection, penumonia
Diseases of myelination Guillain- Barre Syndrome/ Acute inflammation Demylinating polyradiculopathy (PNS and motor + autonomic) Endoneurium and Schwann cells attacked = autoimmune demyliantion 1-3 weeks post GI infection OR RESPIRATORY (campylobacter jejuni) or herpes SYMMETRIC Ascending paralysis MOTOR AND AUTONOMIC Physical exam: Decrease or absent reflex Facial paralysis if ascended to face Autonomic dysfunction : cardiac and blood pressure fluctuation Need to give respiratory support Lumbar puncture: high protein, normal cell count (albuminocytologic dissociation) -this high protein is also seen in intracranial cancer Progressive Multifocal Leukoencephalopathy( PML) (CNS ) Demylination by destruction of oligodendrocytes Associated with JC virus reactivation in AIDS patients (polyomavirus,ds DNA) Dementia and neurological deficits with RAPID PROGRESSION Typically fatal Histology: widespread demylination, astrogliosis, lymphohistiocytosis * associated with Natalizumab ( drug against alpha-integrin used in Crohns and MS) *MS also demylination oligodendrocytes Usually seen on one side more
Acute Disseminated /post infectious Encephalomyelitis Multifocal PERIVENULAR inflammation and demyelination immune activation -after infection : chickenpox, measles -Vaccination: rabies, smallpox Similar to Multiple Sclerosis + constitutional (fever etc) -mental status change, seizure coma *usually in children and adolescents (but anyone can get it) Metachromic Leukodystrophy ( CNS and PNS, myelin accumulate in lysosome) Autosomal recessive lysosomal disease due to ARYLSULFATASE A deficiency . cant metabolise sphingolipids Impaired myelin sheath Diverse psychiatric and neurological problems Presents at different times depends on the form inherited -infantile -juvenile -Adult Krabbe Disease A.R. lysosomal storage disease due to deficiency of GALACTOCEREBROSIDE See globoid cells Peripheral neuropathy, developmental delay, optic atrophy AdrenoLeukoDystrophy X linked disrupted metabolisim of VERY LONG chain Fatty acids Build up Fatty acids in adrenal gland, testes, nervous system Coma/ death, and adrenal crisis occur( not enough cortisol ) Charcot- Marie- Tooth Disease/ Hereditary motor and sensory neuropathy Defective protein for structure and function of peripheral nerves or myelin Onset less than 30 years old Slow progressive weakness of distal limbs with loss of proprioception and vibration Autosomal Dominant usually. Associated with Scoliosis and foot deformity (HGH ARCH OR FLAT) PRESENT FOOT DROP, and loss of foot and hands motor and sensory first Central Pontine Myelinolysis Demylination in the pons : loss of corticospinal and corticobulbar tracts Due to rapid correction of HYPONATREMIA Seen in malnourished or alcoholics Locked in presentation Often fatal
Sodium from low to high, pons will die” from high to low, brain will blow (edema/ herniation)
Multiple sclerosis destruction of oligodendrocytes by CD8 T cells anti-myelin Basic protein ( high protein IgG in CSF) white matter plaque form in brain and spinal cord in white women 20-40 onset in temperate climates. HLA-DR2 CN2 is the only cranial nerve that is mylinated by oligodendrocytes therefore affected in MS Presentation Optic neuritis (sudden loss vision) Marcus Gunn: swinging flashlight test . Affected CN2 -normal eye pupil reflex normal, -abnormal eye, both eyes dilate. Intranuclear opthalmoplegia (MLF) : ipsilateral MLF to the CN3 that cant Adduct . Nystagmus other eye when it Abducts . can be bilateral. CONVERGENCE INTACT Hemisensory symptoms Intention tremor Hemiparesis (weakness) Bladder/bowl incontinence SIN : Charcot classic triad of MS -Scanning speech -intention tremor, incontinence, intranuclear opthalmoplegia -nystagmus Evalutation MRI gold standard : PERIVENTRICULAR plaques Two demyelinating lesions separated in time and place Lumbar puncture: high Leukocytes, oligoclonal banding (high IgG), high Mylein basic protein, normal glucose Treatment IFN-beta : decreases the amount of inflammatory cells crossing BBB And thought to increase Nerve growth factor High dose steroids Natalizumab : humanized monoclonal antibody against Alpha-integrin a cell adhesion molecule
Neurophysiology Neuronal cells Astrocytes: GFAP stain, K+ metabolism, cause REACTIVE GLIOSIS, BBB, remove excess neurotransmitter Ependymal cells : line ventricles and maintain flow of CSF With cilia Microglia : from MESODERM migrate here -macrophages -not seen on Nissl stain -multinucleated with HIV infection -rods in neurosyphilis -perivascular in viral encephalitis Oligodendrocytes : fried egg appearance. CNS myelination -each mylinated up to 30 axons -Multiple sclerosis destroys these Schwann cells : peripheral myelination ( one axon/ Schwann) -Schwannoma bilateral in NF-2 , at internal acoustic meatus affect CN 7 and 8 -destroyed in Guillian Barre syndrome
Muscle Spindles/ Golgi Tendon Organs Muscle Spindle Ia Parallel to extrafusal muscle fibers Stimulates the A alpha to contract muscle Detect stretch
Golgi tendon Ib Series to intrafusal muscle Inhibits A alpha motor neurons to relax muscle Detect tension
GABA: accumbens : GRABA cucumber Raphe nucleus serotonin: RAP SIR Norepinephrin: Nor-mally LOOK SERIOUS
Blood Brain Barrier
Tight junctions btw endothelial cells + astrocyte foot processes Vasogenic edema: infarction destroy tight juntions Transport o Diffusion: water and nonpolar o Carrier transport: glucose, amino acids o Active transport: weak acids, K+ Areas without BBB because they have fenestrated capillaries -POSSuM Path (posterior pituitary, OVLT, Subforniceal organ, subcommissural, median eminence, Pineal gland) o Choroid plexus o Area Postrema : vomiting post chemo o OVLT ( organum vasculosum of lamina terminalis) :osmotic sensing o Neurohypophysis: ADH release from brain to circulation
CSF -Normal 0-4 lymphocytes or macrophage (PMN ALWAYS ABNORMAL) low protein (high in tumor, Guillain-Barre, and MS = albuminocytologic dissociation) equal NA+ to serum low PH since lower HCO3 higher Cl-, Mg2+ “ High Mg2+ Cleanse (causes diahrea)” lower K+, Ca2+, Hco3-, glucose -Made by Choroid plexus in all ventricles (lateral, 3rd , 4th ) -recycled 2-3 times/day Communicating hydrocephalus Made too much CSF (choroid plexus tumor) Low absorption (arachnoid granulations scar following meningitis) Noncommunication Blockage Normal Pressure Decrease reabsorption with ventricle dilation therefore no increase in pressure 3W : wet, wacky weird old people Ex Vacuo Decreased brain size (stroke, HIV, Alzheimers,, trauma) Venticles larger, but CSF pressure normal
Sleep
Suprachiasmatic nucleus Ne pineal gland melatonin Gaba agonist Alcohol, benzo, barbituates, NE decrease REM and delta Benzos are useful in night terror and sleep walking. Bed wetting treat with desmopressin
Stages BATS Drink Blood -Awake eyes open : beta ( highest frequency, lowest amplitude) -Awake eyes closed: alpha -Stage 1 NON-REM: Theta -Stage 2: Spindle and K complex * teeth grinding (Buxism) -Stage 3: delta (lowest frequency, highest amplitude) *sleep walking, night terror, bed wetting -REM: beta * dreams, and erection REM sleep dreaming, penile/clitoris erection loss motor tone memory processing function high O2 use brain, high and variable pulse and BP extraocular movements due to PPRF EEG beta (paradoxical sleep) Every 90 min and increase in duration every cycle Decrease with age Ach promote it, NE decrease it Narcolepsy : start off with REM sleep -Catplexy: loss all motor tone after strong emotional stimulus -treat with amphetamines Sleep Apnea Types Obstructive sleep apnea -Obesity, Craniofacial, nasal congestion, large tonsils Central sleep apnea : low CNS drive to breath Symptoms -excess daytime sleepiness (like narcolepsy) + unrestful sleep(narcolepsy is restful) -loud snoring -small jaw, large neck circumference -high EPO on labs, because chronic hypoxia Treatment
-Weight loss -Continuous positive airway pressure Complication -arrhythmia -pulmonary hypertension
Anatomy Head and neck Thoracic Outlet Subclavian vien and phrenic ON anterior scalene Btw Anterior and middle scalene above is subclavian artery and below is trunks brachial plexus -Thoracic outlet syndrome : compression of brachial plexus and subcleavian artery btw the anterior and middle scalene Causes -due to pancoast tumor -cervical rib -hypertophy of scalene muscles : body builders Symptoms -numbness and weakness on medial forearm and hand. -claw hand ( ulnar affected most) -decreased radial pulse -Horners syndrome, and recurrent laryngeal n. Pharyngeal apparatus Pharyngeal pouch (endoderm) 1,2,3,4,6 Pharyngeal arch (mesoderm and neural crest cells) Pharyngeal groove/ cleft (ectoderm) Pharyngeal groove btw 1 and 2 : external ear (only groove) Pharyngeal pouch 1 : middle ear 2nd pharyngeal arch grows over the other grooves ( if don’t fuse properly then pharyngeal/ lateral cervical/ brachial cyst on lateral part neck)
(skip 2) 579 , then 2 10 *DI George : 3rd pharyngeal POUCH (thymus and inferior calcitonin) + 4th fail to differentiate NEURAL crest cell involves. *thyroglossal cyst : remnant of thyroglossal duct that didn’t fuse. Midline cyst that moves on swallow and tongue protrusion * Cleft lip and palate : -develop from the mesoderm neural crest cells of 1st pharyngeal arch -Cleft lip : maxillary processes don’t fuse -cleft palate: palatine shelves fail to fuse First arch syndromes : abnormal formation of first arch (where mandible and maxilla from) with abnormal neural crest migration
-Treacher Collins : small jaw, eyes slanted down, malformed ears and hearing loss, colobomas -Pierre Robin sequence : very small jaw , cleft palate, posterior displaced tongue Pharyngeal fistula : 2nd groove and pouch persist, fistula on anterior border SCM
Nervous system development
Rostral neuropore close first ( 25 day) : high alpha feto protein + POLYHYDRAMINOS Caudal neuropore ( 27 day) : high alpha feto protein
Neural crest cells derivatives “ CAlifornia MOTEL PASS -craniofacial structure (1st arch maxilla and mandible) -Arachnoid, and pia (dura is mesoderm) -Melanocytes -Odontoblasts -Tracheal cartilage -Enterochromaffin cells (adrenal medulla) -Laryngeal cartilage -Parafollicular cells , psueounipolar -All ganglia, DRG, celiac -Schwann -Spiral septum (aorticopulomary septum) , also endocardial cushions
Neurons
Voluntary movement : 2 neuron system Sensory : 3 motor neuron Spinothalamic tracts always lateral in brainstem Costicospinal always medial and ventral in brainstem Medial lemniscus is medial in medullar and moves laterally in the midbrain bc need to join spinothalamic since going to thalamus together
Dural Venous Sinus
Reflection of DURA mater Cavernous sinus contains : CN 3,4, 5V1 and V2, 6, internal carotid -lateral to sella tunica -cavernous sinus thrombosis or carotid artery aneurysm affect CN6 first -drains eyes, nose, upperlip, Danger triangle
Return blood to INTERNAL jugular vien at JUGULAR FORAMEN -combo of sigmoid sinus and inferior petrosal sinus
Circle of Willis and arteries damage clinical Mnemonics: PICA and AICA are both lateral o Face and body pain and temp split o PIKA-CHEW : cant chew CN 9 and 10 o AICA is FACIAL : CN7 affected lower and upper face bc the nucleus Medial in medulla and pons : medial lemniscus = touch, vibration, proprioception opposite body o Medial medulla: anterior spinal o Paramedical branches of basilar artery Anterior spinal Artery = Medial Medullary syndrome (CN12) Medial lemniscus: contralateral touch, vibration, proprioception CN12 : ipsilateral tongue, and deviate to lesion “lick your wound Pyramid : lower extremity contralateral PICA = lateral Medullary / Wallenberg Syndrome ( CN 9 and 10) Dissociated pain and temp : ipsilateral face (spinal V), contralateral body (spinothalamic) Descending hypothalamics: ipsilateral HOrners (beside spinothalamic always) Nucleus Ambiguus (CN 9 and 10) : ipisilateral dysphagia, dysarthria, loss gag reflex, hoarsness voice Vestibular nuclei: vertigo, nausea, nystagmus Inferior cerebellar peduncle: ipsilateral limb ataxia Medial Pontine : paramedical branches of basilar artery ( CN6 and 7) **Corticospinal and medial lemniscus (LIKE MEDIAL MEDULLARY) BUT HAVE CN 6 AFFECTED ( 7 is more lateral so spared) AICA= Lateral Pontine
** same as PICA with the spinothalamic, dissociated pain and temp, and hypothalamic CN 7 and 8 Middle peduncle : ipsilateral aaxia Vestibular nuclei : vertigo, nausea, vomiting, nystagmus
Pontocerebellar Angle: is CN7 and 8 only! NO OTHER TRACTS. (unilateral loss of hearing) Medial Midbrain = PCA (posterior cerebellar artery) CN3 ipsilateral Corticospinal and corticobulbar tracts : contralateral body and lower face cn7 Dorsal Midbrain: Parinaud syndrome (pineal gland tumor) Superior colliculus : vertical conjugate gaze Pretectal : pupillary reflex Cerebral aqueduct : hydrocephalus non communicating PCA Middle cerebral
Anterior cerebral Posterior communicating Lenticlostriate (lentiform and stratum) Basilar Anterior communicating
Homonymous hemianopsia with macular sparing Contralateral face paralysis and sensory ‘’ arm ‘’ ‘’ aphasia if on the left side left side neglect if on right side (parietal lobe) Contralateral leg and foot motor and sensory CN3 down and out Pure motor ( internal capsule) Pure sensory (thalamus) Locked in Visual field
Spinal cord
Notochord nucleus pulposus -posterior lateral herniate due to posterior ligament 31 nerves , C1-7 exit above, others exit below spinal cord ends at L2, subarachnoid ends at S2 (children cord ends at L3-L4) -Lumbar puncture at L4-L5 *do my iliac crest L4 Cauda Equina: S2-S 5 affect o SADDLE SENSORY DISTURBANCE o Lower back pain o Lower extremity motor and sensory loss ( from sciatic) L4-S3 UNILATERAL ( therefore not much incontinence and impotence bc only one side) o Pelvic splanchnic
o Disk slip L4-L5 L5-S1, tumors, trauma Conus medullaris UMN and LMN ( cauda equine ONLY LMN) + BILATERAL SIGNS, INCONTINENCE, IMPOTENENCE
Basal Ganglia
Function : regulation of movements by modulation of cortical output The basal ganglia usually feedback on cortex DOPAMINE : o D1 CAUSES MOVEMENT by activating inhibited pathway: excitatory pathway (therefore Parkinsons decreases movement, bradykinesia etc) o D2 causes movement by INHIBITING inhibitory pathway -parkinsons no dopamine here, causes activation inhibitory pathway so low movement
Striatum : caudate and Putamen -Activated by cortex, -Direct: inhibit the internal Globus pallidus, so Thalamus activated -indirect (D2) : inhibits externus Globus pallidus so subthalamus activated activate internal globus pallidus inactivate thalamus - D1 activate direct, D2 inactivate indirect = BOTH promote move -Ach activate indirect therefore DECREASE MOVE * Lesion direct = decrease movement ( Parkinsons) * lesion indirect = chorea, athetosis, dystonia, tics ( EX: hemiballismus if subthalamus lesion) -Wilsons copper in basal ganglia (wing beating tremor) especially putamen ( lenticulo= putamen and globus pallidus)
Cerebellum -Input
- IPSILATERAL spinocerebellum via inferior -CONTRALATERAL Cortical middle cerebellar peduncles -Output -Purkinjie fibers deep cerebellar nuclei superior cerebellar peduncle contralateral cortex - Regions Region Function Input from Deep cerebellar nuclei Vermis Proximal muscles Input spinal cord Fastigial nucleus Intermediate Distal muscles Input spinal cord Eboliform and zone globose Lateral Planning and Cortex and inferior Dentate nucleus hemisphere coordination olivary nucleus thalamus VA, VL Flocculonodular Balance and eye CN8 vestibular FastigialLateral lobe movement vestibular -“don’t eat greasy foods” lateral to medial Pathology Damage vermis : truncal ataxia and dysarthria Damage cerebellar hemisphere : ipsilateral intention tremor and lImb ataxia -fall towards side lesion -DYSMETRIA, dysdiadochokinesia, dysarthria, nystagus, HYPOTONIA Anterior Vermis : alcohol leading to gait ataxia Posterior vermis: medulloblastoma, ependymomas causing truncal ataxia
Hypothalamus 1. Hunger
2. 3. 4. 5. 6. 7. 8.
-Lateral : makes hunger (inhibited by LEPTIN L=L) (destroy loss weight laterally first) -VentroMedial : satiety (damage cause expand from medial) Temperature -Anterior: A/C cools body (parasympathetics) -Posterior : heating (sympathetics) Suprachiasmatic nucleus Sex urge : septal nucleus Supraoptic : ADH Paraventicular: oxytocin AUTONOMIC send signal to sympathetic Arcuate nucleus : release dopamine to inhibit prolactin
Thalamus * SENSORY RELAY ( except olfactory bypass it ) 1. Lateral geniculate : visual ( Lateral= light) 2. Medial geniculate : auditory (medial= music) 3. VPL ( ventral posterior lateral) : all sensory body 4. VPM ( ventral posterior medial) : all sensory face 5. Ventral anterior/ lateral (VL and VL): MOTOR inform from basal ganglia and cerebellum Epithalamus: pineal gland Subthalamus lesion; hemiballismus
Limbic System “ 5 F’s : feeding, fight or flight, feelings, fuking,” Hunger Fight or flight Emotion Sex MEMORY -bilateral destroy Hippocampus : anterograde memory -bilateral destroy mammilary bodies: anterograde and retrograde Limbic contains : cingulate gyrus, fornix, mammillary, amygdala, hippocampus Kluver- Bucy Syndrome: bilateral lesion amygdala and hippocampus Anterograde amnesia, hypersexuality, oral behavior Decreased aggressiveness (they are passive) Objects in visual field treat inappropriate, human approach lion without fear
Cortex Prefrontal: organize and planning intellectual and emotional -cant concentrate, easily distracted, apathy, emergence infantile suckling and grasp reflex Premotor: planning motor activities -Lesion: APRAXIA cant do purposeful movements (even tho motor and desire there). Cant perform things in correct sequence Frontal eye field : cant move both eyes to contralateral side (deviate to side of lesion) Posterior parietal associated areas(left side): also APRAXIA , cant draw a circle. (bilateral) -Astereognosia : cant recognize objects in hand (contralateral) Internal capsule:
1. Anterior limb : thalamocortical 2. Genu: corticobulbar 3. Posterior: corticospinal, all somatosensory thalamocortical Aphasia 1. Brocas : “broken boca” : can understand, cant speak or write (frustrated) 2. Wernikes: Word salad. Speak but don’t make sense and don’t understand 3. Gerstmann Syndrome: (angular gyrus damage) : alexia( cant read) agraphia ( cant write) but understand spoken language 4. Conduction aphasia : ( arcuate fasiculus) : POOR REPITITION, can understand and speak 5. Transcortical apraxia: corpus callosum damaged so cant send signal. Understand command on left but cant move right arm (can move left) 6. Transcortical sensory: poor understanding, CAN SPEAK AND REPEAT 7. Transcortical motor: cant speak, CAN UNSERDTAND AND REPEAT Right Parietal Lobe: ASOMATOGNOSIA : awareness of body on left side is lost.
Cranial nerve muscle + exceptions
All tongue is hypoglossus ( EXCEPT palatoglossus CN 10) All palate is vagus ( except tensor veli palitini CN 5 V3) All pharyngeal muscles vagus (except stylopharyngeus , CN 9) Carotid sinus and body CN9 afferent, 10 efferent Aortic arch chemo and baroreceptos CN10 afferent and efferent Gag reflex lost = cn 9, cough reflex lost- CN 10
Eye -Lower retinal field lateral geniculate Dorsal optic radiation/ calicarine/parietal lobe SUPRA-calcarine (cuneus) -upper retinal fieldLG Meyers loop/ Temporal lobe INFRA-calcarine (lingual) Additional pathways Optic tract pretectal area ( light reflex) ‘’ superior colliculus ( vertical conjugate gaze) ‘’ suprachiasmatic nuclei ( circadian rhythm) Pupil Present in cortically blind and unconscious Constriction : CN2 pretectal bilateral Edinger westphal ciliary ganglion SHORT CILIARY nerves pupillary sphincter Dilation: T1 superior cervical ganglion LONG CILIARY * Adies: dilated pupil slow react light, lack knee jerk reflex (normal accom)
* Argyll Robertson : prostitute, accommodate but don’t react (syphilis) * Marcus Gunn : MS swinging flash light Conjugate Gaze Horizontal is by PPRF and MLF Vertical is superior colliculi
Vestibular System and Hearing
Utricle and saccule : linear acceleration and force of gravity Semicircular canals: angular acceleration/ deceleration Vestibular nuclei send info to flocculonodular lobe in cerebellum Endolymph has HIGH K+ , LOW Na+, like intracell fluid Nystagmus of vestibular damage - Vestibular system activates ipsilateral CN 3, contralateral CN6 so makes eyes GO OPPOSITE DIRECTION -Lesion causes the other side to over work, so the eyes deviate TOWARDS lesion (slow component) -the fast component back to normal position is by brain (called the nystagmus) - Caloric testing (COWS, Cold opposite, warm same) -cold water (mimicks lesion) slow component to ear with cold water, nystagmus opposite -warm water activates that ear, slow component away, nystagmus towards
Clinical 1. Otosclerosis: conductive hearing loss bc the ossicles don’t amplify sound 2. Hyperacusis: CN7 damage. 3. Presbycusis: loss of hair cell in the base of cochlea (therefore high frequency sound loss) OLD PEOPLE 4. Lesion at cochlear nucleus or pontomedullary junction= unilateral sensory hearing loss 5. Lesion anything higher up causes BILATERAL hearing DECREASED (not lost)
Nucleus + random areas Nucleus Solitaries: Visceral Sensory ( taste, baroreceptor, Gut distention) -CN 7, 9, 10 Nucleus AMbiguous : Motor pharynx, larynx, upper esophagus -CN 9 and 10 swallowing and palate elevation
Dorsal Motor Nucleus : Autonomic to heart, lungs, and upper GI CN10 Spinal nucleus of V: pain temp face Superior olivary nucleus: lower pons get auditory info Reticular formation -Raphe nuceli: Serotonin -Locus ceruleus : NE . invoved in cortical arousal -Periaqueductal grey: opiods Reticular activating system : in the midbrain. Responsible for arousal and wakefulness. Destruction causes coma Eyes above ears -Superior colliculi : conjugate vertical gaze -inferior colliculi : auditory pathway
MEDBULLETS KLM SOUNDS KUH: CN 10 LA-LA-LA : CN 12 MI-MI-MI : CN 7 Lumbar Puncture: Ends L2 adults, L3 neonates. Do puncture L4-L5 using iliac crest Aneurysm RBC in lumbar is acute, with turn yellow (xanthochromia) Give calcium channel blocker (nimodipine) to prevent secondary vasospasm which occurs 2-3 days post SUBARACHNOID hemorrhage Berry aneurysm at anterior communication ( ADPCK, marfan, Ehler danlos, artery vien malformation) o Subarachnoid (headache) Charcot Bouchard aneurysm is lenticostriate vessel at basal ganglia ( HTN chronic and diabetes) o Intraparenchimal (usually motor or sensory loss) Internal carotid In cavernous sinus In the foramen lacerum Parkinsons
Have Lewy Bodies/ alpha- synuclein eosinophilic inclusions ( but so does Lewy Body Dementia, therefore if dementia is present go with Lewy Body dementia) the Lewy body is the round pink dot the substantianiagra doesn’t send dopamine to striatum ( caudate and Putamen) Basal ganglia lewy body and late dementia = PARKINSONS Cortical lewy body and early dementia = Lewy Body Dementia
Huntington high Dopamine, low ACH and GABA high Dopamine in nigro-striatal = direct pathway activated so hyperkinesis high dopamine in meso-limbic = psychotic symptoms Alzheimers vs Pick’s Disease both have Tau protein aggregates intacellularly -Alzheimers is TANGLES -Picks disease is ROUND Poliomyelitis Fecal- oral infection: replicates in oropharynx and small intestine blood CNS Sore throat LMN symptoms WERDNIG-HOFFMAN DISEASE : autorecessive, destroy anterior horns like polio. FLOPPY BABY Friedreich Ataxia MITOCHONDRIAL FUNCTION INPAIRED GAA Macular degeneration ◦ Dry: fat deposits in macula, slow disease course ◦ Wet: neovascularization of the macula, fast disease course RANDOM Alpha- feto Protein
-High: neural tube defect, gastroschisis (lateral fold not fuse in gastralation), omphalocele (the GI doesn’t turn back in the 180 degree) -Low : Downs Syndrome Metastatic brain tumor if its located at junction grey and white matter Lesion surrounding MIDBRAIN (RED NUCLEUS ) -ABOVE: decorticate -Below : decerebrate UMN high reflexes ( except superficial abdominal and cremaster is lost) Fasciculus cuneatus is found about T5 only ( fasciculus gracilis at all levels) Spinocerebellar tracts destroyed in Friedreich ataxia Romberg sign 1. Eyes open and sway = cerebellum 2. Eyes closed and sway = dorsal column damage Bladder nerves 1. Spastic : lesion above sacral 2. Atonic : lesion at sacral ( overfill so continuous dribble) Endolymph is the only EXTRACELL fluid in body that has INTRACELL electrolytes Alcoholic thiamine deficiency cause deterioration of : dorsomedial nucleus thalamus, mammillary bodies, hippocampus, vermis of cerebellum Layer 4 cortex ( internal granular) : thalamus signals enter here (SENSORY) Layer 5 cortex ( internal pyramidal): Corticospinal and bulbar ( MOTOR) Aphasia also comes with AGRAPHIA ( they cant write)
FOOT ARCH IS HIGH OR FLAT Fredrich ataxia Charcot Marie tooth Fragile X
U WORLD Guillian Barre : segmental demylination , ENDONEURAL inflammation Werdnig- Hoffman syndrome: anterior horne degeneration in neonates inherited. FLOPPY BABY Craniopharyngioma is calcified cystic tumor ATM : Ataxia Telangiectasis Mutated -DNA breaks
-reccurent infections pulomary , ataxia, and distended capillaries on sun exposed areas. -IgA deficiency therefore sinopulomary infection Mitochondrial Diseases -Leber Hereditary optic neuropathy: bilateral vision loss -Myoclonic epilepsy with ragged red fibers: myoclonic seizures and myopathy with exercise. Muscle biopsy shows ragged red fibers -Mytochondrial encephalomyopathy with lactic acidosis and stroke like episodes (MELAS) Metabolic encephalopathy -hypoglycemia -hyperglycemia -hepatic encephalopathy (high ammonia levels) Rabies -to DRG brain -killed vaccine give as prophylactic to people who are at high risk of rabies like veternarians, cave exploerers, lab workers, rabies dog countries) Heroin -Withdrawal: nausea, vomit, abdominal pain, muscle ache -flu like : dilated pupils, yawn, lacrimation, piloerection, hyperactibe bowl sounds Stimulants (cocain, amphetamines) withdrawal -increased appetite, hypersomnia -psychomotor retardation severe depression “crash” Alcohol and benzos: seizure, tachycardia, palpitations Lysosomal alpha 1-4 glucosidase = maltase 47, XXX is clinically silent. May have a little lower IQ 47, XYY is aggressive, criminal, lower IQ, tall, severe acne Congenital toxoplasmosis: hydrocephalus, intracranial calcification, chorioretinitis. They are infected in utero across the placenta . avoid cat feces if pregnant Sciatic nerve is L4 S3 Spinal cord sections Look if has the dorsal cuneaus ( above T5) Look for lateral horn T1-L2 Look for large anterior horn in cervical and lumbosacral More proximal has more white mater and more ovoid Nisseria meningitis: from respiratory droplets. -Pharyn blood choroid meningies Meniere: tinittus (ringing), vertigo, hearing loss, episodic! Bi polar: lithium, valproate, carbamazepine and atypical antipsychotics Screening tests need a high sensitivity (SNOUT) HSV-1 most common teens and young adults for SPORADIC ENXEPHALITIS,
-reactivation latent virus -Temporal lobe involved bilaterally. -fever, headache, mental status changes, Cranial nerves, seizures, aphasia (temporal) , olfactory hallucination (temporal), personality (amygdala) -Cowdry A bodies eosinophilic + multinucleated cells Neurology Vascular malformation o Causes hemorrhage intraventricular o Seen on microscope as dilated, tortuous worm like channels and can cause seizure disorder This is tuberous sclerosis, an autosomal dominant condition characterized by intellectual disability and seizures beginning early in life. The characteristic feature is the presence of "tubers" which are enlarged and firm, whitened gyri.
The small petechial hemorrhages in the mammillary bodies seen here are characteristic for Wernicke disease, another complication of chronic alcoholism
