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NPTE > Neuromuscular > Flashcards

Neuromuscular Flashcards

1
Q

MCA lesion characteristics

A

Contralateral Hemiplegia, Face, UE>LE
Contralateral Hemisensory loss UE>LE
Homonymous Hemianopsia

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2
Q

Superior division of MCA lesion

A

Expressive Aphasia (effects Broca’s area and frontal eye fields)

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3
Q

Inferior division of MCA lesion

A

Receptive aphasia (effects wernicke’s area and visual radiation )
Decreased graphesthesia, sterognosis on contralateral side, lack of awareness (hemineglect)

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4
Q

Homunculus ACA

A

Trunk, Leg Foot (motor), trunk, leg, foot, genitals, some arm sensory loss

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5
Q

MCA homunculus

A

Face, hand arm motor loss
Face, hand, tongue sensory loss (larger tongue sensory loss)

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6
Q

PCA stroke characteristics

A

Contralateral sensory loss with involuntary movements like choreoathetosis, tremor, hemibalismus, transient contralateral hemiparesis, homonymous hemianopsia

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7
Q

ACA-MCA watershed infarct

A

Trunk and proximal UE are affected !!! Severe drop in BP due to carotid stenosis or occlusion of the ICA

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8
Q

MCA-PCA watershed infarct:

A

Higher order visual processing is affected

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9
Q

ACA lesion characteristics

A

Contralateral paralysis and sensory loss affecting the LE, may lose control of micturition because bladder control involves frontal gyri and anterior cingulate gyrus

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10
Q

Why would an occlusion of the stem of MCA have leg involvement?

A

Gives off lenticulostriate arteries that go to BG and internal capsule (posterior limb of the IC gives off lower limb fibers)

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11
Q

Lesion of the posterior limb of internal capsule

A

Lower face weakness, hemi anesthesia, spastic hemiplegia (more severe distally) , Left homonymous hemianopia

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12
Q

Paracentral lobule lesion comes from what artery and what happens

A

Anterior cerebral artery, C/L hemiplegia and hemiparesis (lesion of the pre central and post central gyrus)

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13
Q

R MCA sup. Division lesion

A

Contralateral hemiparesis (face, arm hand), contralateral sensory loss , NO HOMONYMOUS HEMIANOPIA
Neglect variable

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14
Q

expressive aphasia typically found

A

in those with right hemiplegia

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15
Q

what is astereognosis

A

inability to recognize objects by touch alone

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16
Q

ideomotor apraxia

A

person cannot do a task on command but can do it spontaneously

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17
Q

ideation apraxia

A

person lo longer gets the idea of how to do a routine task

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18
Q

when does global aphasia occur

A

with occlusion to the main stem of the middle cerebral artery

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19
Q

what is conduction/associative aphasia:

A

damage to the arcuate fasciculus, patient struggles with repeating phrases and word finding

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20
Q

akinesia

A

hard to initiate movements

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21
Q

chorea

A

rapid involuntary jerky movements

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22
Q

what is a movement pattern seen in Huntington’s

A

chorea, rapid involuntary jerky movements

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23
Q

decorticate=

A

flexion contraction in upper extremities and extension in the lower extremitites , damage to red nucleus in the midbrain

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24
Q

decerebrate=

A

extension in UE and LE, injury to the brainstem above the vestibular nucleus an below the red nucleus

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25
Q

dysdiadochokinesia most often associated with

A

cerebellar disorders

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26
Q

what movements are common to both flexion and extension synergies

A

wrist/finger flexion, ankle inversion

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27
Q

what two strokes may cause homonymous hemianopsia

A

posterior cerebral and middle cerebral

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28
Q

what part of the brain functions to organize behaviors (executive functions, problem-solving, motivation)

A

the limbic circuit of the extrapyramidal tracts

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29
Q

what part of the brain functions to scale amplitude and velocity of movements and what are the other functions

A

putamen loops or motor loop of the basal ganglia
also reinforces selected movement patterns, suppresses conflicting patterns and preps for movement

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30
Q

_____ relays information from the cerebellum and globus pallidus to precentral motor cortex

A

motor nuclei of thalamus

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31
Q

what does the hypothalamus do

A

control ANS function and neuroendocrine system , HOMEOSTASIS

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32
Q

pineal gland helps with

A

circadian rhythms

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33
Q

injury to what part of the cerebellum may result in issues of muscle tone and synergistic actions, posture and voluntary movement control

A

spinocerebellum

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34
Q

issues of force, direction and extent of movement (coordination) may be a result of ____
May also have issues with cognitive function and mental imagery

A

posterior love of the cerebellum/neocerebellum,

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35
Q

where can you find lateral horns of spinal cord grey matter and what is the function

A

int he thoracic and upper lumbar segments for preganglionic fibers of the autonomic nervous system

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36
Q

what tract is responsible for deep and chronic pain

A

spinoreticular

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37
Q

high fall risk BERG balance score

A

<45

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38
Q

normal adults TUG norm

A

≤ 10 sec

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39
Q

normal TUG for frail elderly or disabled patients

A

11-20 seconds

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40
Q

increased fall risk for TUG

A

> 20 sec

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41
Q

high fall risk TUG

A

> 30 sec

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42
Q

balance efficacy scale low confidence

A

total score <50

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43
Q

tinetti /POMA high risk for falls

A

<19

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44
Q

tinetti/POMA moderate fall risk

A

19-24

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45
Q

DGI predictive of fall risk and for what population

A

<19/22
elderly

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46
Q

FGA strong evidence for what

A

acute and chronic neurological conditions

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47
Q

FGA moderate evidence for

A

for chronic progressive conditions

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48
Q

BERG balance strong evidence for what

A

sitting and standing balance for acute, chronic and chronic progressive conditions

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49
Q

Activities balance confidence scale has high evidence for what

A

acute, chronic and chronic progressive neurologic conditions

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50
Q

Walking tests with strong evidence for patients with chronic and chronic progressive neuro conditions

A

10 Meter walk and 6MWT

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51
Q

Functional reach test score indicating significant fall risk

A

≤6

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52
Q

Functional reach test score indicating moderate fall risk

A

score of 6-10

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53
Q

what is bitemporal hemianopsia and when does it happen

A

it is loss of vision to the lateral fields on R and L side, occurs with damage to the optic chiasm

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54
Q

apraxia correlates to damage where

A

prelateral frontal cortex and somatosensory association cortex

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55
Q

muscle fasciculations are indicative of

A

LMNL

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56
Q

what is opisthotonos

A

severe spasm of muscles, causing head back and heels to arch backward with arms and hands in rigid flexion

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57
Q

what might cause opisthotonos

A

meningitis, tetanus, epilepsy or strychnine poisoning

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58
Q

what is the abdominal reflex

A

scratching 4 quadrants of abdomen with lateral to medial strokes causes the umbilicus to deviate towards stimulus, absent with corticospinal lesions

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59
Q

cremaster reflex tests what levels

A

L1-L2

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60
Q

abdominal reflex tests what levels

A

T6-L1

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61
Q

cremaster reflex absent with what lesions

A

SCI and corticospinal lesions

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62
Q

Asymmetrical Tonic Neck reflex

A

rotation of head to one side produces flexion of the contralateral limb and extension ipsilateral limb

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63
Q

Symmetrical Tonic neck reflex

A

Flexion of the head produces flexion of the UEs with extension of lower extremities
Extension of the head produces extension of UEs and flexion of the LEs
Head=UEs, head is opposite of LEs

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64
Q

behaviors with lesions to Right hemisphere (L hemiplegia)

A

impulsive, quick, indifferent, poor judgment and safety, overestimating abilities

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65
Q

behaviors with lesions to L hemisphere (R sided hemiplegia)

A

slow, cautious, hesitant and insecure, often aware of impairments resulting in frustration

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66
Q

scissoring gait occurs with _____

A

spastic adductors

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67
Q

what does the stroke impact scale measure

A

biopsychosocial health and participation following stroke

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68
Q

what does the trunk impairment scale measure

A

motor impairment of trunk with static/dynamic sitting and coordination

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69
Q

perceptual deficits may be present from what strokes

A

with parietal lobe damage to non-dominent side (RMCA)

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70
Q

what should be avoided with a flaccid UE following stroke

A

pulleys, overhead activity, risk of sublux or dislocation

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71
Q

what should be emphasized for patients with sensory and perceptual losses

A

compensatory strategies in order to be safe

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72
Q

myopathies present with

A

pelvic girdle and proximal muscle weakness, resulting in hyperlordosis and compensated trandelenburg (hip hike on weight bearing)

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73
Q

which imaging has the most radiation

A

CT scan

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74
Q

what is CT scan most useful for

A

areas of acute bleeding (hemorrhage in developing stroke), cerebral edema (within 3 days post stroke), and cerebral infarction (3-5 days post stroke)

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75
Q

limitations of CT

A

decreased visualization of small/ischemic lesions and radiation

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76
Q

what is MRI imaging useful for

A

superior imaging, tissues and flow of blood within medium/larger arteries and veins, no radiation

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77
Q

what is more sensitive to diagnosis acute stroke

A

MRI, can detect cerebral edema within 30 min and infarction in 2-6 hours instead of 3-5 days)

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78
Q

what is primary imaging for tumors, demyelination, vascular abnormalities

A

MRI (MRA to see the vessels)

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79
Q

contraindications for MRI

A

metal implants, pacemakers

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80
Q

disadvantages of MRI

A

cost, time and movement artifact if the patient moves

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81
Q

Advantages of PET scan

A

allows physiological mapping for biochemical analysis, tool for imaging cerebral blood flow and brain metabolism

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82
Q

PET scan can help screen and diagnose what

A

tumors, dementia, stroke and seizure

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83
Q

which imaging might be useful to detect mild TBI, or disruption of projection fibers

A

diffuse tensor imaging (type of MRI)

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84
Q

what imaging can detect hematomas

A

CT

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85
Q

Normal CSF characteristics (following lumbar puncture)

A

crystal clear and colorless, 90-150ml volume for adult, 60-100 ml of volume for a child, 90-180 mm of pressure for adult or 10-100mm of pressure for child , protein in adult is 15-45 and 15-100 mg.dL for neonates

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86
Q

when might ICP pressure occur

A

intracranial tumors, abscesses, meningitis, inflammatory processes, subarachnoid hemorrhage, cerebral edema and thrombosis of venous sinus

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87
Q

when is insertional activity increased

A

acute denervated muscle and various muscle diseases

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88
Q

when is insertional muscle activity decreased

A

chronic neuropathies/myopathies with significant atrophy and fibrosis in the muscle

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89
Q

what correlates with Wallerian degeneration on nerve conduction studies

A

abnormal spontaneous EMG acticvty that occurs 7-21 days after peripheral nerve injury or compression

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90
Q

When might ICP be decreased

A

leaking CSF, subarachnoid block circulatory collapse, severe dehydration

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91
Q

mild TBI characteristics

A

0-30 min of LOC, brief; >24 hours of altered consciousness, post-trauma amnesia <1 day, GCS 13-15, normal imaging

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92
Q

Moderate TBI characteristics

A

> 30 min but <24 hours of LOC, >24 hours of altered consciousness, post-trauma amnesia >1 day <7 days, GCS 9-12, normal or abnormal imaging

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93
Q

Severe TBI

A

> 24 hours LOC, >24 hours altered consciousness, >7 days amnesia, <9 GCS, normal or abnormal imaging `

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94
Q

Ranchos Los amigos level I

A

no response, patient does not respond to external stimuli/appears asleep

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95
Q

Ranchos Los amigos level II

A

generalized response, reacts to external stimuli in nonspecific, inconsistent and non -purposeful manner with stereotpic and limited responses

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96
Q

Ranchos Los amigos level III

A

patient responds specifically and inconsistently with delays to stimuli, may follow simple commands for motor action

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97
Q

Ranchos Los amigos level IV

A

confused, agitated response, pt exhibits bizarre , non-purposeful, incoherent or inappropriate behaviors, has no short-term recall, attention is short and non-selective

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98
Q

Ranchos Los amigos level V

A

confused, inappropriate, non-agitated: pt gives random, fragmented and non-purposeful responses to complex or unstructured stimuli, simple commands followed consistently, memory and selective attention are impaired and new information not retained

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99
Q

Ranchos Los amigos level VI

A

confused, appropriate response: pt gives context appropriate, goal-directed responses, dependent upon external input for direction, shows carry over for re-learned but not NEW tasks, recent memory problems persist

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100
Q

Ranchos Los amigos level VII

A

automatic, appropriate: behaves appropriately in familiar settings, daily routines automatically performed, shows carry-over for new learning at lower than normal rates, pt initiates social interactions, judgment still impaired

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101
Q

Ranchos Los amigos level VIII

A

purposeful ,appropriate response: pt oriented and responds to environment but abstract reasoning abilities are decreased relative to pre-morbid levels

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102
Q

what is sympathetic storming

A

result of hypothalamic stimulation of the SNS with an increase in circulating corticoids and catecholamines (stress)
pts will exhibit minimal altertness, minimal awareness and reflexive motor responses to stimulation

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103
Q

PT goals for LOCF IV-VI

A

posted and written daily schedules, memory logs, pictures
clear feedback, written contracts, behavior modification techniques,
provide frequent orientation to time, place, name and task
emphasize safety, behavioral management techniques
calm and focused behavior

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104
Q

PT goals for LOCF (I-III)

A

prevent contractures and ulcers, reposition, keep HOB elevated if possible, structure environment to facilitate alertness and function

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105
Q

PT goals for LOCF VII-VIII

A

allow for increasing independence, wean patient from closed to open environments, allow for decision making, provide honest feedback and prepare for community, improve physical impairments,

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106
Q

common epileptic drugs

A

phenyotin (dilantin), cabamazepine (tegretol), pheobarbital

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107
Q

if there is a bump of head, what are the red flags

A

drowsiness or inability to wake up, pupils are different sizes, repeated vomiting or nausea, convulsions or seizures, LOC >30 sec, HA that is worsening, slurred speech, numbness or decreased coordination, changes in behavior; irritability, restlessness agitation, confusion , disorientation or amnesia

108
Q

mild concussion/grade I

A

symptoms last less than 15 min, no LOC

109
Q

moderate concussion/grade II

A

symptoms >15 min, no LOC

110
Q

post concussion syndrome =

A

persistent symptoms lasting ≥ 3 months, indicates severity, occurs more commonly with multiple concussions
may include seizures, depression and mild cognitive impairment later in life

111
Q

what is found in autopsy from CTE

A

brain changes of tau-positive neurofibrillary tangles (NFTs), neuropil threads and neocortical diffuse amyloid plaques with or without neoritic plaques

112
Q

typical signs and symptoms of CTE

A

recurrent HA and dizziness, cognitive impairments eventually progressing to dementia, mood or behavior disturbances, impaired judgement, impulsive, aggressive, irritable

113
Q

what electrolyte disorders may cause seizures

A

hypoglycemia, hypernatremia, hyponatremia, hypomagnesemia

114
Q

what is a generalized seizure

A

all areas of the brain are involved, sometimes referred to as grand mal

115
Q

symptoms of grand mal/generalized seizures

A

dramatic LOC, stiffening then rhytmic movements of arms and legs, eyes are generally open, breathing is altered, loss of urine common

116
Q

timing of grand mal seizures

A

typically 2-5 minutes

117
Q

what are absence or petit mal seizures

A

posture is maintained, repetitive blinking or other small movements, brief and last only a couple seconds but may occur multiple times a day

118
Q

what are partial or focal seizures

A

only one part of the brain involved so the symptoms are focal

119
Q

complex partial seizure=

A

person appears dazed and confused, not fully alert or unconscious

120
Q

temporal lobe seizure symptoms

A

episodic changes in behavior, complex hallucinations, automatisms (lip smacking, chewing, pulling on clothing), altered cog and emotional function , voilent

121
Q

what type of seizure is preceded by an aura

A

temporal lobe seizure

122
Q

secondarily generalized seizures

A

simple or complex partial seizures evolving to a generalized seizure

123
Q

status epilepticus

A

prolonged seizure or a series lasting >30 min, very little recovery in between attacks; may be life threatening, medical emergency

124
Q

what is arnold chairi syndrome

A

cerebellar symptoms due to cerebellum extending into spinal canal due to birth defect

125
Q

which cerebellar lesion is characterized by hypotonia, truncal and gait ataxia and disordered timing of movement

A

damage to paleocerebellum (spinocerebellum)

126
Q

which cerebellar lesion is characterized by dysmetria, intention tremor, dyssynergia, dysdiadochokinesia

A

neocerebellum

127
Q

a neocerebellar lesion will show ______ signs (ipsi or contra)?

A

ipsilateral

128
Q

what type of muscle test should be used for a patient with a cerebellar lesion

A

use a make test, some patients will have bursts of muscle activation

129
Q

what is common with dysmetric patients

A

fatigue

130
Q

where are MS lesions common

A

pyramidal tract, dorsal columns, optic tract, periventricular areas of cerebrum, cerebellar peduncles

131
Q

when should MS be a part of differential diagnosis

A

when patients have varying symptoms that do not fit a specific anatomical location

132
Q

most common type of MS

A

relapsing remitting 85%

133
Q

what are the diagnostic tests for MS

A

CT, MRI, myelogram, EEG, LP with CSF, elevated gamma globulin

134
Q

what is hyperpathia

A

hypersensitivity to sensory stimuli

135
Q

Lhermittes sign can be positive for

A

MS, or cervical myelopathy

136
Q

medical management of MS consists of

A

adrenocorticotropic hormone (ACTH) and steroids (prednisone, betamethasone, methylprednisone, dexamethasone), interferon drugs, spasticity meds, urinary anticholinergics

137
Q

when working with a patient with MS what should we monitor

A

UTIs and respiratory infection as respiratory infection may lead to death

138
Q

restorative rehab for MS

A

time limiting intensive designed to improve/stabilize patient status after a relapse

139
Q

functional maintenance rehab for MS

A

manage effects of progressive dx/ prevent/minimize indirect impairments like contractures, decubitis ulcers, sensation compensations, eye patching with diploplia, tone reduction techniques

140
Q

progression of MS interventions should increase ____ prior to _____

A

duration before intensity

141
Q

what happens with deficiency of dopamine

A

loss of inhibitory dopamine results in excessive excitatory output from cholinergic system (acetylcholine) of basal ganglia

142
Q

H &Y stage I

A

minimal or absent disability, unilateral

143
Q

H &Y stage II

A

minimal bilateral or midline involvement, no balance involvement

144
Q

H &Y stage III

A

impaired balance, some restrictions in activity

145
Q

H &Y stage IV

A

all symptoms present and severe; stands and walks only with assistance

146
Q

H &Y stage V

A

confined to bed or WC

147
Q

what contractures are common with PD

A

flexors and adductors,

148
Q

cause of blurred vision

A

gaze instability secondary to VOR dysfunction

149
Q

dizziness

A

sensation of disturbed or impaired spatial orientation without a false or distorted sense of motion

150
Q

sensation of self-motion when no self-motion is occurring or the sensation of distorted self-motion during an otherwise normal head movement

A

internal vertigo

151
Q

false sensation that the visual surround is spinning or flowing

A

external vertigo

152
Q

unsteadiness definition

A

feeling of being unsteady, standing or walking without a particular directional preference

153
Q

indicators of central nervous system pathology and need referral for imaging

A

direction changing gaze-evoked nystagmus and down-beating nystagmus

154
Q

what are the unilateral vestibular hypofunction disorders?

A

trauma, meiniere’s disease, vestibulo neuronitis/labyrinthitis, BPP, acoustic neuroma, brainstem or gliomas, cerebellar medulloblastoma

155
Q

meniere’s disease episode durations

A

20 min to 12 hours

156
Q

is recovery better in unilateral PVH or bilateral PVH

A

unilateral

157
Q

gaze stability exercises include

A

VORx1, VOR cancellation, do them on stable then unstable surfaces, with clear background to cluttered background

158
Q

roll test will test which canal?

A

horizontal canal

159
Q

what maneuver do you do for an anterior or posterior cupulolithiasis

A

semont manuever

160
Q

what maneuver do you use for horizontal canal cupulolithiasis

A

Gufoni maneuver, followed by the canalithiasis

161
Q

what is the most common mechanism of injury for lumbar SCIs

A

flexion

162
Q

what is the most common mechanis of injury for cervical is SCI

A

flexion-rotation

163
Q

most frequent spinal cord areas

A

C5, C7, T12, L1

164
Q

tetraplegia injury occurs between ____ and ____

A

C1 and C8

165
Q

paraplegia injury occurs between __ and __

A

T1 and T12-L1

166
Q

central cord syndrome

A

cavitation of central cord in cervical section
loss of spinothalamic tracts: bilateral loss of pain and temp
loss of ventral horn with bilateral loss of motor function: UE> LE
preservation of DCML

166
Q

Brown-sequard syndrome

A

hemi-section of spinal cord
ipsilateral loss of DCML so loss of tactile discrimination, pressure, vibration, proprioception
ipsilateral loss of cortico-spinal tracts (loss of motor function and spastic paralysis below lesion)
contralateral loss of pain and temp (spinothalamic), at the level of the lesion will have loss of pain and temp bilaterally

167
Q

anterior cord syndrome

A

bilateral loss of motor function and spastic paralysis below level of lesion (corticospinal tract)
loss of spinothalamic tracts= bilateral loss of pain and temp
preserved DCML function

167
Q

posterior cord syndrom

A

loss of DCML bilaterally
preservation of motor, pain and light touch

167
Q

cauda equina symptoms

A

flaccid paralysis with no spinal reflex activity
flaccid paralysis of bladder and bowel
potential for nerve regeneration, regeneration often incomplete, slows and stops after about a year

168
Q

how long can spinal shock last

A

several hours to 24 weeks

169
Q

signs of autonomic dysreflexia

A

HTN, bradycardia, severe headache, feeling anxious, constricted pupils, blurred vision, flushing and piloerection, increased spasticity/tone

170
Q

what do you do if autonomic dysreflexia is suspected

A

bring pt to upright if they are supine, loosen any tight or restrictive devices/clothes, reduce blockage of urinary drain, monitor blood pressure and HR, notify medical and/or nursing staff

171
Q

common complications of SCI recovery

A

heterotopic bone formation, DVT, spasticity/spasms, spinal shock

172
Q

appropriate wheelchair for C1-C4 SCI

A

tilt in space or reclining seat back, microswitch or puff and sip controls, portable respiratory may be attached

173
Q

appropriate wheelchair for C5 SCI

A

(have shoulder function) manual chair with propulsion aid, independent use for short/flat distances , electric for longer distances and energy conservation

174
Q

appropriate WC for C6 SCI

A

manual wheelchair with friction surface handrims

175
Q

appropriate WC for C7 SCI

A

increased propulsion with friction surface handrims

176
Q

appropriate WC for C8 SCI

A

manual/standard wheelchair and handrims

177
Q

locomotor equipment for T6-T9 injuries

A

supervised ambulation for short distances/limited household, physiological standing purposes: require bilateral KAFOs with crutches, swing-to pattern or a standing device

178
Q

locomotor equipment for T12-L3 injuries

A

independent in ambulation on all surfaces and stairs, using a swing through or four point gait pattern, bilateral KAFOs and crutches, may use RGO with or without FES system
independent household ambulation with wheelchair for community

179
Q

locomotor equipment for L4-L5 injuries

A

bilateral AFOs

180
Q

pts with high lesion paraplegia and tetraplegia, what should we monitor closely during exercise

A

bloop pressure and heart rate, looking for blunted tachycardia, lack of pressor response, low VO2 peak, higher variability

181
Q

what cells and tracts are involved in ALS

A

anterior horn cells, descending corticobulbar tracts and corticospinal tracts

182
Q

bulbar onset occurs in what ratio of ALS patients

A

1/3

183
Q

respiratory impairments in ALS

A

weakness> paralysis, nocturnal difficulty, exertional dyspnea, accessory muscle use, paradoxical breathing, ventilatory dependent, poor cough/clearance of secretions

184
Q

what cranial nerves are commonly involved in ALS

A

VII, IX, X, XI, XII

185
Q

bulbar palsy effects what nerves

A

IX, X

186
Q

bulbar palsy effects what muscles

A

face, tongue, larynx, pharynx

187
Q

triggering stimulus for trigeminal neuralgia

A

extremes of cold or heat, chewing, talking, brushing teeth, movement of air across the face

188
Q

trigger points for trigeminal neuralgia

A

light touch to face, lips or gums

189
Q

what divisions of the CN V are typically involved with trigeminal neuralgia

A

mandibular and maxillary

190
Q

treatments for trigeminal neuralgia

A

TENS for desensitization, medications like b12, anticonvulsants, alcohol injections, surgery or permanent anesthesia to the nerve

191
Q

what nerve is effected in bell’s palsy and what occurs

A

CN VII, facial dropp of one side of the face

192
Q

etiology of bell’s palsy

A

acute inflammatory process, immune or viral, compression of nerve within the temporal bone

193
Q

max severity of bell’s palsy occurs

A

in a few hours to days, preceded by a day or two of pain behind the ear

194
Q

full recovery of bell’s palsy occurs

A

several weeks or months

195
Q

facial nerve sensation distribution

A

taste to anterior 2/3 of tongue

196
Q

neuropraxia definition

A
197
Q

what is “screening for autonomic dysfunction”

A

vasodilation and loss of vasomotor tone (dryness, warm skin edema, orthostatic hypotension)

198
Q

nerve conduction studies can rule out ______

A

radiculopathy, spinal stenosis

199
Q

what can be used for the diagnosis of small fiber cutaneous (pain/temp) neuropathies

A

skin punch biopsy

200
Q

what is a focus of physical therapy with small fiber neuropathies

A

decrease pain

201
Q

rapid, nonsymmetric loss of myeline in nerve roots and peripheral nerves, with rapid muscle weakness progression

A

guillain-Barre

202
Q

etiology of guillian barre

A

unknown, autoimmune attack, usually occurs after recovery from an infectious illness (respiratory/GI)

203
Q

severe symptoms of guillian barre

A

dysarthria, dysphagia, diplopia, facial weakness, tetraplegia with respiratory failure

204
Q

recovery of guillain barre

A

6 months to 2 years, slow recovery, 10-20% of pts have severe disabilities and 5% mortality

205
Q

progression/evolvement of GB

A

over a few weeks or days

206
Q

medical management of GB

A

plasmapheresis, IVIG, analgesics for pain management, good nursing care

207
Q

important thing to note for GB therapy

A

teach energy conservation techniques and activity pacing, avoid overuse and fatigue cause it may prolong recovery

208
Q

_______ is unaffected by post polio syndrome

A

sensation

209
Q

primary symptom of post polio syndrome

A

fatigue, new muscle weakness

210
Q

patients with severe paresis, in post polio syndrome should avoid ____

A

muscle trainging

211
Q

most common neuromuscular junction disorder

A

myasthenia gravis (MG)`

212
Q

what is myashtenia gravis characterized by

A

progressive muscle weakness and fatigueability on exertion

213
Q

typical involvement in generalized myasthenia

A

bulbar (extraocular, facial, muscles of mastication) and proximal limb-girdle muscles

214
Q

myasthenic crisis

A

MG with respiratory failure, a medical emergency

215
Q

what is the ice pack test and what is it used for

A

aids in MG diagnosis, positive when ptosis of affected eye decreases following 2 min application of cold pack

216
Q

common difficulties in mobility with Myasthenia Gravis

A

climbing stairs rising from chair, lifting

217
Q

medical interventions for MG

A

acetylcholinesterase inhibitors; pyridostigmine, corticosteroids, IVIG, plasmapheresis, thymectomy

218
Q

goals of PT intervention for MG

A

teach energy conservation, promote independence in FMS and ADLS, monitor changes in condition (respiration, swallowing, vitals), psychological and emotional support

219
Q

Botulinum Toxin=

A

decreased release of ACh: botox will presynaptic binding to high-affinity recognition sites on cholinergic nerve terminals

220
Q

adverse events of botox

A

unintended muscle weakness, flaccidity, dysphagia, local hemotoma, general fatigue, dry mouth, pain and flu-like symptoms

221
Q

acquired myopathy s/sx

A

muscle cramps, exertional fatigue, weakness that progresses in proximal to distal direction, difficulty with overhead activity, stairs and getting in and out of chairs

222
Q

skin changes associated with dermatomyositis

A

butterfly rash= purple to reddish discoloration of the eyelids, cheeks and bridge of nose; scaling rash on the extensor surface of the fingers)

223
Q

typical finding in polymyositis

A

joint pain

224
Q

what lab tests confirm myopathy

A

elevated creatine phosphokinase (CPK), elevated aldolase, elevated lactate dehydrogenase (LDH), elevated liver enzymes

225
Q

____ might be normal in mild myopathies

A

MEG

226
Q

What should be done to identify etiology of the myopathy

A

metabolic panel, thyroid/parathyroid hormone, sedimentation rate and c-reactive protein

227
Q

a myopathic muscle defined by

A

random areas of CT and or lipid deposits

228
Q

muscle weakness in MG is worse with _____ contractions

A

repeated or prolonged

229
Q

Epstein barr virus is known best for causing

A

mononucleosis

230
Q

Sjogren’s syndrome common sx/sx

A

dry eyes and dry mouth

231
Q

prognosis for transverse myelties

A

partial recovery for most patients, occurs in first 3 months to 2 years, 1/3 of patients left with permanent disability, MS can be the cause and pt may experience relapse

232
Q

CRPS type I

A

no damage to peripheral nerve, example may be ankle sprain

233
Q

CRPS type II

A

specific damage to peripheral nerve

234
Q

what is acute flaccid myelitis

A

rare-polio like condition affecting motor neurons in gray matter of the SC< causing muscles and reflexes to become weak ; occurs in children; increasing frequency

235
Q

symptoms of acute flaccid myelitis

A

sudden onset of arm or leg weakness, loss of muscle tone and reflexes, may have difficulty with eye or eyelid movement, dysarthria and dysphagia some bladder and bowel issues potentially

236
Q

important education point with chronic fatigue syndrome/myalgic encephalomyelitis

A

avoid push and crash cycle, teach energy consercation techniques

237
Q

exercise recommendations for persons with chronic diseases/disabilites)

A

low to moderte intensity (RPE 9-12) with gradual progression, 3-5 days/wk, 5 min session initially and progress to 40-60 min; distrubuted, longer rest preaks, avoid overexertion

238
Q

allodynia=

A

pain response to stimulus that doesn’t usually provoke pain (light touch or brush)

239
Q

primary hyperalgesia

A

increased pain sensitivity to normally painful stimulus in the direct area of damage or inflammation

240
Q

secondary hyperalgesia

A

pain sensitivity that occurs in surrounding undamaged tissues

241
Q

symptoms of AIDS

A

one-third of patients exhibit CNS or PNS deficits, confusion and memory loss to disorientation, may have peripheral neuropathy, hypersensitivity, pain and sensory loss

242
Q

chronic pain persists for

A

> 6 months

243
Q

in distributed practice, rest time is ____ practice time

A

greater

244
Q

in massed practice, rest time is _____ than practice time

A

less

245
Q

variable feedback improves

A

learning and retention

246
Q

early in learning, feedback should be on

A

correct aspects of performance

247
Q

later in learning, feedback should focus on

A

errors as they become consistent

248
Q

feedback after every trial is useful during

A

early learning

249
Q

when should you use distributed practice

A

when superior performance is desired, when motivation is low, or when learner has short attention, poor concentration or fatigues easy

250
Q

retention=

A

ability to demonstrate the skill after a period of no practice

251
Q

what is required for task specific training

A

repetition and extensive practice

252
Q

pure motor lacunar stroke involves what structures

A

involvement of the posterior limb of the internal capsule, pons and pyramids

253
Q

pure sensory lacunar stroke involves what structures

A

involvement of the ventrolateral thalamus or thalamocortical projections

254
Q

dysarthria/clumsy hand syndrome is damage to what

A

pons, genu of anterior limn or the internal capsule

255
Q

ataxic hemiparesis involves what structures

A

involves pons, genu of internal capsule, corona radiata, cerebellum

256
Q

damage to what may cause lacunar sensory and motor stroke

A

junction of internal capsule and thalamus

257
Q

hemibalismus can be seen with damage to what structure

A

subthalamic nucleus

258
Q

dystonia/involuntary movements can be seen with damage to what structure

A

subthalamic nucleus, lacunar infarction of putamen or globus pallidus

259
Q

what deficits are not seen in lacunar strokes

A

consciousness, language or visual fields

260
Q

What is cheyne-stokes respiration

A

period of apnea lasting 10-60 seconds followed by gradually increasing depth and frequency of respirations

261
Q

what do cheyne stokes respirations accompany

A

frontal lobe depression and diencephalic dysfunction

262
Q

damage to upper pons may show what type of breathing pattern

A

apneustic breathing: abnormal respiration marked by prolonged inspiration

263
Q
A

NPTE (7 decks)

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