Chapter 17: Alterations in Cognitive Systems, Cerebral Hemodynamics, and Motor Function
MU!"#$ CH%"C$
1. Cognitive operations cannot occur without the effective functioning of the brain’s: a. Pons c. Reticular activating system b. Medulla oblongata d. Cingulate gyrus A!: C
Cognitive cerebral functions re"uire a functioning reticular activating system #RA!$. Cognitive operations are not managed by any of the other options. P%!: 1
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). +hich intracerebral disease process is capable of producing diffuse dysfunction, a. Closed head trauma with bleeding c. eoplasm b. !ubdural pus collections d. -nfarct emboli A!:
isorders within the brain substance #intracerebral$/bleeding0 infarcts emboli0 and tumors/ primarily functioning as masses may cause diffuse diffuse dysfunction. !uch localied destructive processes directly impair functioning of the thalamic or hypothalamic activating activating systems. isorders outside the brain but within the cranial vault #e2tracerebral$0 including neoplasms0 closed3head trauma with subse"uent bleeding0 and subdural empyema #accumulation of pus$0 can cause similar dysfunction. P%!: 1
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4. +hat is the most common infratentorial brain disease process that results in the direct
destruction of the reticulating activation system #RA!$, a. Cerebrovascular disease c. eoplasms b. emyelinating disease d. Abscesses A!: A
Infratentorial disorders disorders produce produce a decline in arousal through a direct destruction of the RA! and its pathways. %he most common cause of direct destruction is cerebrovascular disease0 but demyelinating diseases0 neoplasms0 granulomas0 abscesses0 and head in5ury also may cause brainstem destruction by tissue compression. P%!: 1
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6. +hat stimulus causes cau ses posthyperventilation apnea ap nea #P78A$, #P78A$, a. Changes in PC9) levels c. amage to the forebrain b. Changes in PaC9) levels d. Any arrhythmic breathing pattern A!:
+ith normal breathing0 a neural center in the forebrain #cerebrum$ produces a rhythmic breathing pattern. +hen consciousness decreases0 lower brainstem centers regulate the breathing pattern by responding only to changes in PaC9) levels. %his irregular breathing pattern is called P78A P78A. %he other options are not responsible for P78A. P78A.
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(. Posthyperventilation apnea #P78A$ #P78A$ ceases and rhythmic breathing is resumed when levels of
arterial: a. Carbon dio2ide increase b. Carbon dio2ide become normal
c. 92ygen increase d. 92ygen decrease
A!:
Rhythmic breathing returns when the PC9) level returns to normal. one of the remaining options would affect normal rhythmic breathing after P78A. P78A. P%!: 1
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?. Cheyne3!to@es respirations are described as a: a. !ustained deep rapid but regular pattern of o f breathing b. Crescendo3decrescendo pattern of breathing0 followed by a period of apnea c. Prolonged inspiratory period0 gradually followed by a short e2piratory period d. Completely irregular breathing pattern with random shallow0 deep breaths and
irregular pauses A!:
Cheyne3!to@es respiration is an abnormal rhythm of breathing #periodic breathing$ that alternates between hyperventilation and apnea. Cheyne3!to@es respirations do not include a sustained deep respiratory rate. Altered inspiratory and e2piratory periods are not characteristic of Cheyne3!to@es respirations. Random0 irregular breathing patterns are not observed during Cheyne3!to@es respirations. P%!: 1
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>. 8omiting omiting is associated with central nervous system #C!$ in5uries that compress co mpress which of the
brain’s anatomic locations, a. 8estibular 8estibular nuclei in the lower brainstem b. 'loor of the third ventricle c. Any area in the midbrain d. iencephalon A!: A
8omiting0 omiting0 yawning0 and hiccups are comple2 refle2li@e motor responses that are integrated by neural mechanisms in the lower brainstem. 8om 8omiting iting often accompanies C! in5uries that involve the vestibular nuclei. %he remaining options will not trigger vomiting when compressed. P%!: 1
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*. +hich midbrain dysfunction causes pupils to be pinpoint sie and fi2ed in position, a. iencephalon dysfunction b. 9culomotor cranial nerve dysfunction c. ysfunction of the tectum d. Pontine dysfunction A!:
Pinpoint fi2ed pupils are a result of pontine dysfunction. %he diencephalon0 oculomotor cranial nerve0 and tectum are not involved in such a pupil reaction. P%!: 1
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;. +hat characteristic is a medical criterion of brain death, a. A@inetic mutism c. Apnea b. Coma d. oc@ed3in syndrome A!: C
Apnea is viewed as a criterion of brainstem death0 whereas the remaining options reflect cerebral death. P%!: 1
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1<. A clinical manifestation caused by damage to the lower pons includes an abnormal: a. 'le2ion with or without e2tensor response of the lower e2tremities b. &2tension response of the upper and lower e2tremities c. &2tension response of the upper e2tremities and fle2ion response of the lower
e2tremities d. 'laccid response in the upper and lower e2tremities A!:
A flaccid state with little or no motor response to stimuli is characteristic of damage to the pons. one of the other responses are considered a clinical manifestation of damage to the lower pons. P%!: 1
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11. +hich person is at the greatest ris@ for developing delirium, a. An individual with diabetes celebrating a >
|
elirium is associated with autonomic nervous system overactivity and typically develops in ) to 4 days0 most commonly in critical care units0 postsurgically0 or during withdrawal from C! depressants #e.g.0 alcohol0 narcotic agents$. Age0 gender0 and chronic illnesses are not generally associated with delirium triggers. P%!: 1
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1). A sudden0 e2plosive0 disorderly discharge of cerebral neurons is termed: a. Refle2 c. &pilepsy b. !eiure d. Convulsion A!:
A sudden0 e2plosive0 disorderly discharge of cerebral neurons describes a seiure. %his description is not accurate for the other options. P%!: 1
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14. A comple2 partial seiure is described as: a. Alternating of tonic and clonic movements b. -mpairment of both consciousness and the ability to reac t to e2ogenous stimuli c. 'ocal motor movement without loss of consciousness d. 9ne seiure followed by another in less than 1 minute A!:
A comple2 partial seiure results is impaired consciousness0 as well as the inability to respond to e2ogenous stimuli. one of the other options accurately describe a comple2 partial p artial seiure. P%!: 1
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16. !tatus epilepticus is considered a medical emergency because of the: a. oss of consciousness b. evelopment of cerebral hypo2ia c. Possibility of a head in5ury during seiures d. ecrease in brain metabolism A!:
!tatus epilepticus is a true medical emergency because a single seiure can last longer than 4< minutes0 resulting in hypo2ia of the brain. %he other options are not the criteria used to consider status epilepticus. P%!: 1
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1(. %he most critical aspect in correctly diagnosing a seiure disorder and establishing its cause is: a. Computed tomographic #C%$ scan c. !@ull 23ray studies b. Cerebrospinal fluid analysis d. 7ealth history A!:
Although the history may be supplemented with the remaining options0 it remains the pivotal tool for establishing the cause of a seiure disorder. P%!: 1
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1?. +hat type of seiure starts in the fingers and progressively spreads up the arm and e2tends to
the leg, a. Comple23psychomotor seiure b. 'ocal #partial$ ac@sonian seiure
c. Beneralied seiures d. Atonic3drop seiure
A!:
'ocal #partial$ ac@sonian seiures most often begin in the face and fingers and then progressively spread to other body parts. %he other options do not begin and spread in the fashion described. P%!: 1
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1>. +hat area of the brain mediates the e2ecutive attention functions, a. imbic c. Parietal b. Prefrontal d. 9ccipital A!:
%he prefrontal areas mediate several cognitive functions0 called executive attention functions (e.g., planning, problem solving, setting goals). %he goals). %he remaining options are not areas involved with the mediation of e2ecutive attention functions. P%!: 1
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1*. +hat term describes the loss of the comprehension or production of language, a. Agnosia c. A@inesia b. Aphasia d. ysphasia A!:
Aphasia is the loss of the comprehension or produc tion of language. %he remaining options are not terms used to describe this loss of function. P%!: 1
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1;. +ith receptive dysphasia #fluent$0 the individual is able to: a. Respond in writing0 but not in speech. b. Produce verbal speech0 but not comprehend language. c. Comprehend speech0 but not verbally respond. d. either respond verbally nor comprehend speech. A!: C
%he individual e2periencing receptive dysphasia may be able to produce verbal language0 but language is meaningless because of a disturbance in understanding all language. %he remaining options do not describe receptive dysphasia. P%!: 1
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)<. +hat is the normal intracranial pressure (in mm Hg), Hg), a. ( to 1( c. 1) to 16 b. > to )< d. *< to 1)< A!: A
-ntracranial pressure is normally ( to 1( mm 7g or ?< to 1*< cm water #7)9$. %he remaining options reflect increased intracranial pressure. P%!: 1
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)1. Cerebral edema is an increase in the fluid content of the brain’s: a. 8entricles c. eurons b. %issue d. Meninges A!:
Cerebral edema is an increase in the fluid content of brain tissueD that is0 a net accumulation of water within the brain. Cerebral edema is not noted in the brain’s ventricles0 neurons0 or meninges. P%!: 1
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occu rs when permeability of the capillary endothelium increases )). +hat type of cerebral edema occurs after in5ury to the vascular structure,
a. Cytoto2ic b. -nterstitial
c. 8asogenic d. -schemic
A!: C
-ncreased permeability of the capillary endothelium of the brain after in5ury to the vascular structure causes vasogenic edema. %he remaining options are not consistent with this description. P%!: 1
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)4. A communicating hydrocephalus is caused by an impairment of the: a. Cerebrospinal fluid flow between the ventricles b. Cerebrospinal fluid flow into the subarachnoid space c. lood flow to the arachnoid villi d. Absorption of cerebrospinal fluid A!:
7ydrocephalus from impaired absorption outside the ventricles is called communicating (extraventricular) hydrocephalus. hydrocephalus. %he other options do not accurately describe the cause of a communicating hydrocephalus. P%!: 1
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)6. +hich edema is most often observed with noncommunicating hydrocephalus, a. Metabolic c. 8asogenic b. -nterstitial d. -schemic A!:
-nterstitial edema is observed most often with noncommunicating hydrocephalus. oncommunicating hydrocephalus is not the cause of any of the other options. P%!: 1
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)(. +hich dys@inesia involves involuntary movements of the face0 trun@0 and e2tremities, a. Paro2ysmal c. 7yper@inesia b. %ardive d. Cardive A!:
%ardive %ardive dys@inesia is the involuntary movement of the face0 trun@0 and e2tremities. %he other terms do not describe involuntary movements of the face0 trun@0 and e2tremities. P%!: 1
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)?. Antipsychotic drugs cause tardive dys@inesia by mimic@ing the effects of increased: a. opamine c. orepinephrine b. Bamma3aminobutyric acid d. Acetylcholine A!: A
%he antipsychotic drugs cause cau se denervation hypersensitivity h ypersensitivity00 which mimics the effect of too much dopamine. one of the other options produce such an affect. P%!: 1
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)>. %he e2istence of regular0 deep0 and rapid respirations after a severe closed head in5ury is
indicative of neurologic in5ury to the: a. ower midbrain b. Pontine area
c. !upratentorial d. Cerebral area
A!: A
Central refle2 hyperpnea0 which is a sustained deep and rapid but regular respiratory pattern that is the result of central nervous system #C!$ damage or disease0 involves the lower midbrain and upper pons. %his neurologic in5ury is observed after increased intracranial pressure and blunt head trauma. amage to any of the other areas listed would not produce this breathing pattern. P%!: 1
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)*. +hat type of posturing e2ists when a person with a severe closed head in5ury has all four
e2tremities in rigid e2tension with the forearms in hyperpronation and the legs in plantar e2tension, a. ecorticate c. !pastic b. ecerebrate d. Cerebellar A!:
ecerebrate posturing includes opisthotonos #hypere2tension of the vertebral column$ with clenching of the teethD e2tension0 abduction0 and hyperpronation of the armsD and e2tension of the lower e2tremities including plantar e2tension. %he other options do not describe such posturing. P%!: 1
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);. !ince his cerebrovascular accident0 a man has been denying his left hemiplegia. +hat term is
used to describe this finding, a. 8isual agnosia b. Anosognosia
c. Amusia agnosia d. Agraphia agnosia
A!:
Anosognosia is ignorance or denial of the e2istence of disease. one of the remaining options describes such denial. P%!: 1
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4<. After a cerebrovascular accident0 a man is unable to either feel or identify a comb c omb with his
eyes closed. %his is an e2ample of: a. Agraphia b. %actile agnosia
c. Anosognosia d. Prosopagnosia
A!:
%actile %actile agnosia is the inability to recognie ob5ects b y touch. one of the other options o ptions define the inability to recognie ob5ects by touch. P%!: 1
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41. Most dysphasias are associated with cerebrovascular accidents involving which artery, a. Anterior communicating c. Circle of +illis
b. Posterior communicating
d. Middle cerebral
A!:
ysphasias are usually associated with a cerebrovascular accident involving the middle cerebral artery or one of its many branches. amage to or occlusion of any of the other options does not cause dysphasias. P%!: 1
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4). %actile agnosia is related to in5ury of which area of the brain, a. 'rontotemporal c. %emporal b. Parietal d. roca area A!:
%actile %actile agnosia #astereognosis$ is the inability to recognie ob5ects by touch as a result of damage to the parietal lobe. %actile agnosia is not related to an in5ury to any of the other options. P%!: 1
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44. eurofibrillary tangles characterie which neurologic disorder, a. ementia syndrome c. Alheimer disease b. elirium d. Par@inson disease A!: C
Amyloid pla"ues0 neurofibrillary tangles0 as well as neuronal and synaptic losses in the brain0 characterie Alheimer disease. P%!: 1
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46. %he body compensates for a rise in intracranial pressure by first by first displacing displacing the: a. Cerebrospinal fluid c. 8enous blood b. Arterial blood d. Cerebral cells A!: A
A rise in intracranial pressure necessitates an e"ual reduction in the volume of the other contents. %he most readily displaced content of the cranial vault is cerebrospinal fluid #C!'$0 not any of the other options. P%!: 1
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4(. !tage 1 intracranial hypertension is caused by the: a. oss of autoregulation that normally maintains constant blood flow during cha nges
in cerebral perfusion pressure b. isplacement of cerebrospinal fluid0 followed by compression of the cerebral venous system c. 8asoconstriction 8asoconstriction of the cerebral arterial system with reciprocal increase in systemic blood pressure d. Compression of the medulla oblongata in the brainstem by herniation of the cerebral corte2 A!:
-f intracranial pressure remains high after cerebrospinal fluid #C!'$ displacement out of the cranial vault0 then cerebral blood volume v olume is altered0 resulting in stage 1 intracranial hypertension. 8asoconstriction 8asoconstriction and e2ternal compression co mpression of the venous system occur in an attempt to further decrease the intracranial pressure. one of the remaining options accurately describe the cause of stage 1 intracranial hypertension. P%!: 1
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4?. ilated and sluggish pupils0 widening pulse pressure0 and bradycardia are clinical findings
evident of which stage of intracranial hypertension, h ypertension, a. 1 c. 4 b. ) d. 6 A!: C
!tage 4 intracranial hypertension e2hibits clinical manifestations that include decreasing levels of arousal0 Cheyne3!to@es respiration or central neurogenic h yperventilation0 pupils that become sluggish and constricted0 widened pulse pressure0 and bradycardia. %hese responses are not characteristic of any other stage. P%!: 1
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4>. ilation of the ipsilateral pupil0 following uncal herniation0 is the result of pressure on which
cranial nerve #C$, a. 9ptic #C -$ b. Abducens #C 8-$
c. 9culomotor #C ---$ d. %rochlear #C -8$
A!: C
%he oculomotor C #---$ is involved in this manifestation of pupil dilation. one of the other options would result in pupil dilation when sub5ected to pressure. P%!: 1
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4*. +hich characteristic is the most critical inde2 of nervous system dysfunction, a. !ie and reactivity of pupils c. Motor response b. Pattern of breathing d. evel of consciousness A!:
evel of consciousness is the most critical clinical inde2 of nervous system function or dysfunction. An alteration in consciousness indicates either improvement or deterioration of a person’s condition. o other option is used as the critical inde2 of nervous system. P%!: 1
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4;. iagnostic criteria for a persistent vegetative state include: a. Absence of eye opening b. ac@ of subcortical responses to pain stimuli c. Roving eye movements with visual trac@ing d. Return of autonomic functions such as gastrointestinal function A!:
iagnostic criteria for vegetative state #8!$ include the return of professed vegetative #autonomic$ functions0 including sleep3wa@e cycles and normaliation of respiratory and digestive system functions. 9nly the correct option appropriately describes the diagnostic criteria for a 8!. P%!: 1
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6<. Encal herniation occurs when: a. %he hippocampal gyrus shifts from the middle fossa through the tentorial notch into
the posterior fossa. b. %he diencephalon shifts from the middle fossa straight downward through the tentorial notch into the posterior fossa. c. %he cingulate gyrus shifts under the fal2 cerebri. d. A cerebellar tonsil shifts through the foramen magnu m. A!: A
Encal herniation #i.e.0 hippocampal herniation0 lateral mass herniation$ occurs when the uncus or hippocampal gyrus #or both$ shifts from the middle fossa through the tentorial notch into the posterior fossa. %his shift results in the compression of the ipsilateral third cranial nerve #C$0 impairing parasympathetic function. %his impairment is carried on in the periphery of the nerve0 then in the contralateral third C0 and finally in the mesencephalon0 inducing coma. %he other options do not appropriately describe when uncal herniation occurs. P%!: 1
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61. +hich assessment finding mar@s the end of spinal shoc@, a. Return of blood pressure and heart rate to normal b. Bradual return of spinal refle2es c. Return of bowel and bladder function d. &vidence of diminished deep tendon refle2es and flaccid paralysis A!:
A gradual return of spinal refle2es mar@s the end of spinal shoc@. %he other options are not an indication of the cessation of spinal shoc@. P%!: 1
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6). Characteristics of primary motor neuron atrophy include: a. oss of sensation in distal0 pro2imal0 or midline muscles b. 'asciculations and muscle cramps c. 'laccid paralysis with paresthesia d. !pastic paralysis with increased deep tendon refle2es A!:
'asciculations are particularly associated with primary motor neuron in5ury0 and muscle cramps are common. %he other options do not describe characteristics of primary motor neuron atrophy. P%!: 1
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64. %he wea@ness resulting from the segmental paresis and paralysis characteristic of anterior
horn cell in5ury is difficult to recognie because:
a. b. c. d.
Epper motor neurons are involved. %he in5ury is microscopic. %wo or more nerve roots supply each muscle. %he person is unable to feel the involved muscles.
A!: C
%he paresis and paralysis associated with anterior horn cell in5ury are segmentalD however0 because two or more roots supply each muscle0 the segmental character of the wea@ness may be difficult to recognie. %he reason this pathophysiologic pathophysiologic condition is difficult to recognie is not appropriately e2plained by any of the other options. P%!: 1
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66. Par@inson disease is a degenerative disorder of the brain’s: a. 7ypothalamus c. 'rontal lobe b. Anterior pituitary d. asal ganglia A!:
Par@inson disease is a commonly occurring degenerative disorder of the basal ganglia and not of any of the other brain structures. P%!: 1
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6(. Clinical manifestations of Par@inson disease are caused by a d eficit in which of the brain’s
neurotransmitters, a. Bamma3aminobutyric acid b. opamine
c. orepinephrine d. Acetylcholine
A!:
Par@inson disease is a commonly occurring degenerative disorder involving deficits of dopamine0 not of any of the other options. P%!: 1
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6?. %remors at rest0 rigidity0 a@inesia0 a@inesia0 and postural p ostural abnormalities are a result of the atrophy of
neurons in the brain’s: a. Caudate that produces serotonin b. Putamen that produces gamma3aminobutyric acid c. !ubstantia nigra that produces dopamine d. 7ypothalamus that produces acetylcholine A!: C
%he hallmar@ characteristics of Par@inson disease #P$ are a result of a loss of dopaminergic3 pigmented neurons in the substantia nigra pars compacta with dopaminergic deficiency in the putamen portion of the striatum #the striatum includes includes the putamen and caudate nucleus$. %he remaining options are not characteristics of P. P%!: 1 MU!"#$ &$S#%'S$
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6>. ementia is commonly characteried by the deterioration in which abilities, (Select all that
apply.) a. !ociability b. alance c. Memory d. !peech e. ecision ma@ing A!: C0 0 0 &
ementia is the progressive failure #an ac"uired deterioration$ of many c erebral functions that include impairment of intellectual function with a decrease in orienting0 memory0 language0 e2ecutive attentional functions0 and alterations in behavior. oss of the need for social conta ct and impaired balance are not associated with dementia0 although a person with such a diagnosis may e2hibit these deficiencies. P%!: 1
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6*. %he clinical manifestations of Par@inson disease include: (Select all that apply.) a. 'ragmented sleep b. rooping eyelids c. epression d. Muscle stiffness e. rady@inesia A!: A!: A0 C0 C0 0 0 &
%he classic motor manifestations of Par@inson disease #P$ are brady@inesia0 tremor at rest #resting tremor$0 rigidity #muscle stiffness$0 and postural abnormalities. onmotor symptoms associated with P include hyponosmia0 fatigue0 pain0 autonomic dysfunction0 sleep fragmentation0 depression0 and dementia with or without psychosis. rooping e yelids are not characteristics of P. P%!: 1
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6;. -n Par@inson disease the basal ganglia influence the hypothalamic function to produce which
clinical manifestations, (Select all that apply.) app ly.) a. -nappropriate diaphoresis b. Bastric retention c. 8omiting d. iarrhea e. Erinary retention A!: A0 0 0 &
%he basal ganglia influence hypothalamic function #autonomic and neuroendocrine$ through pathways connecting the hypothalamus with the basal ganglia and cerebral corte2. Common autonomic symptoms in Par@inson disease include inappropriate diaphoresis0 gastric retention0 constipation0 and urinary retention. either vomiting nor diarrhea would be clinical manifestation observed under these circumstances. P%!: 1
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