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Neuromuscular Conditions I > Exam 1 Info > Flashcards

Exam 1 Info Flashcards

1
Q

stroke

A

sudden loss of neurological function caused by a lack of blood flow to the brain
-signs/symptoms > 24 hours

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2
Q

transient ischemic attack

A

temporary impairment of blood flow

-signs/symptoms < 24 hours [usually minutes to hours]

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3
Q

causes of an ischemic stroke

A
  • thrombus (blood clot)
  • embolus (blood, plaque, or other matter)
  • hypotension
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4
Q

Which artery is normally involved with the ischemic stroke?

A

MCA

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5
Q

lacunar stroke

A
  • small vessels involved, can be purely motor or purely sensory
  • tends to have better outcome (b/c small artery)
  • deep in the white matter of the brain
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6
Q

hemorrhagic stroke

A
  • blood vessel rupture leading to decreased blood to downstream structures & pressure on nearby structures
  • can be intra-cerebral or subarachnoic
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7
Q

potential causes for hemorrhagic stroke

A
  • aneurysm

- arterial-venous malformation

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8
Q

aneurysm

A

-dilation in a blood vessel

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9
Q

list of general risk factors for stroke

A
  • exercise
  • diet
  • blood pressure
  • cholesterol
  • diabetes
  • smoking
  • atrial fibrillation
  • family history
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10
Q

arteriovenous malformation

A

abnormal collection of small arteries

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11
Q

time frame of being able to use t-PA

A

if stroke occurred less than 3 hours previously

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12
Q

signs/symptoms of stroke

A
  • focal weakness

- speech impairments

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13
Q

intracerebral hemorrhage signs/symptoms

A

progressive worsening of signs and symptoms with loss of consciousness

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14
Q

angiogram

A
  • invasive test (requires insertion of catheter & dye)
  • used to image blood vessels
  • not good for acute strokes due to the time it takes to administer
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15
Q

CT

A
  • computed tomography
  • generally good for imaging mass lesions
  • best choice for detecting subarachnoid hemorrhage
  • not as sensitive for detecting ischemic strokes
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16
Q

MRI

A
  • magnetic resonance imaging

- T2 best for detecting pathologies (more water present)

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17
Q

Which imaging is preferred for detecting ischemic strokes?

A

MRI

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18
Q

diffusion weighted MRI

A
  • can detect ischemia within minutes of inclusion

- highly sensitive & specific in diagnosing ischemic stroke

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19
Q

multi-infarct dementia

A
  • multiple small strokes deep in white matter
  • associated with advancing age and HTN
  • cause dementia
  • chronic
  • neuronal tissue decreasing
  • motor function is fine but generally more confused state of mind
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20
Q

thrombolysis

A
  • is the breakdown (lysis) of blood clots by pharmacological means, and commonly called clot busting
  • t-PA
  • indicated for patients with an ischemic stroke within 3 hours of onset
  • does not affect mortality but does help with reduction of disability/mobility months later
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21
Q

ischemic stroke cascade

A

circulatory arrest -> focal infarction -> release of neurotransmitters -> altered metabolism with depolarization -> brain cells cease to produce energy -> influx of calcium -> free radical formation -> release of nitric oxide & cytokines -> further damage to brain cells

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22
Q

ACA syndrome

A
  • contralateral hemiparesis & sensory loss
  • LE more involved (due to homunculus)
  • personality & behavioral changes
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23
Q

MCA syndrome

A
  • contralateral hemiparesis & sensory loss
  • UE more involved
  • speech/language impairments OR perceptual problems [determined by which side of the brain is dominant]
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24
Q

internal carotid artery syndrome

A
  • produces massive infarct of MCA & can impact ACA
  • significant edema is common & can result in herniation, coma & death
  • massive infarct & with an entire hemisphere affected there is not big opportunity for neuroplasticity [which is why the edema can easily come in]
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25
Q

PCA syndrome

A
  • signs/sx depend on location of occlusion
  • if proximal to PCA = minimal deficits
  • if distal to PCA = sensory loss, thalamic pain, homonymous hemianopsia, certain agnosias, cortical blindness, memory loss
  • big sign/sx is pain & visual problems
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26
Q

vertebrobasilar artery syndrome

A
  • vertebral arteries: cerebellum & medulla
  • basilar artery: pons & cerebellum
  • highly complex b/c of arteries coming off of basilar, etc.
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27
Q

locked-in syndrome

A
  • complete paralysis w/ some preservation of eye movement

- full blown stroke of the basilar artery

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28
Q

positive symptoms

A
  • “release” of abnormal behaviors

- brainstem does not receive inhibition messages & therefore does whatever it wants

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29
Q

What do positive symptoms lead to?

A
  1. presence of abnormal reflexes
  2. increased DTRs
  3. spasticity
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30
Q

negative symptoms

A

-a loss of normal behaviors

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31
Q

What do negative symptoms lead to?

A

-weakness (plegia vs. paresis; hemi, tetra, para, incomplete or complete etc.)

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32
Q

primary impairments

A
  • those due directly to the CNS insult

- largely dependent on lesion location so highly variable

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33
Q

list of motor system impairments

A

-weakness, abnormal synergies, abnormalities of tone, co-activation, poor coordination, hypokinetic & hyperkinetic disorders

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34
Q

list of non-motor impairments

A

-sensation (including vestibular function), perception, vision, cognition & behavior

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35
Q

motor control impairments & CNS involvement with cerebral cortex

A
  • hemiplegia
  • tonal abnormalities
  • loss of selective movement
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36
Q

motor control impairments & CNS involvement with basal ganglia

A
  • movement disorders
  • rigidity
  • athetosis
  • chorea
  • dystonia
  • hemiballismus
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37
Q

athetosis

A

a condition in which abnormal muscle contractions cause involuntary writhing movements. It affects some people with cerebral palsy, impairing speech and use of the hands

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38
Q

hemiballismus

A

violent writhing and muscle spasms involving one side of the body, usually caused by a lesion of the subthalamic nucleus of the opposite side of the brain

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39
Q

motor control impairments & CNS involvement with cerebellum

A

-ataxia

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40
Q

hemiplegia

A
  • weakness on one side of the body
  • pts with UMN lesions
  • loss of input from descending tracts
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41
Q

strength

A
  • ability to generate sufficient tension in a muscle

- number & type of motor units recruited & firing frequency

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42
Q

weakness

A
  • inability to generate sufficient levels of force
  • due to loss of input from descending motor pathways -> decreases excitatory drive to motor units -> decreased ability to recruit & modulate motor neurons
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43
Q

muscle tone

A

-characterized by a muscle’s resistance to passive stretch

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44
Q

How is muscle tone assessed?

A

-through PROM, observation (posturing), & DTRs

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45
Q

flaccidity

A
  • abnormality of muscle tone
  • limb feels heavy & limp
  • weak
  • present immediately post stroke due to cerebral shock & can last days to weeks (could persist esp in pts with cerebellar lesions)
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46
Q

visual/perceptual sensory abnormalities

A
  • neglect

- homonymous hemianopsia

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47
Q

spasticity

A

velocity dependent increase in muscle tone/tonic stretch reflexes

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48
Q

synergistic movement

A

problem in activating & sequencing appropriate muscles = production of unwanted stereotypical movements
-reflects the lack of fractionation & loss of selective movement

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49
Q

list of 7 ways to characterize spasticity

A
  1. hyperactive DTRs
  2. abnormal posturing
  3. excessive coactivation
  4. associated movements
  5. clonus
  6. stereotypical/synergistic movement
  7. clasp-knife response
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50
Q

UE flexor synergy pattern

A
  1. scapular elevation/retraction
  2. shoulder abd & ER
  3. elbow flex
  4. forearm supination
  5. wrist & finger flex
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51
Q

UE extensor synergy pattern

A
  1. scapular protraction
  2. shoulder add & IR
  3. elbow ext
  4. forearm pronation
  5. wrist & finger flexion
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52
Q

LE flexor synergy pattern

A
  1. hip flex, abd, ER
  2. knee flex
  3. ankle DF & inv.
  4. toe ext.
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53
Q

LE extensor synergy pattern

A
  1. hip ext, add, IR
  2. knee ext
  3. ankle PF & inv.
  4. toe flex
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54
Q

Brunnstrom’s Stages of Recovery

A
  1. flaccid paralysis
  2. minimal movement in synergy
  3. voluntary movement - synergistic
  4. some movement out of synergy
  5. movement almost independent of synergy
  6. normal movement
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55
Q

impairments of secondary progressive MS

A
  • weakness
  • mild hypotonia
  • fatigue
  • poor coordination
  • ataxia
  • intention tremor
  • short term memory loss
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56
Q

dysmetria

A

-errors in range & direction of movement

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57
Q

decomposition

A

-altered movement trajectories with tendency to move one joint at a time

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58
Q

dysdiadochokinesia

A

-inability to sustain rhythmic movements

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59
Q

impairments of Parkinson’s Disease

A
  • hypokinesia = bradykinesia, resting tremor, rigidity
  • postural abnormalities
  • oral motor impairments
  • slightly slowed cognitive thinking
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60
Q

bradykinesia

A
  • slowed movement time

- decreased amplitude

61
Q

two types of rigidity (hypertonicity)

A
  1. lead pipe

2. cog wheel

62
Q

athetosis

A
  • slow, involuntary, writhing or twisting movements
  • accompanies cerebral palsy
  • can have fluctuations in tone & movement patterns
  • may occur with spasticity, chorea, or tonic spasms
  • any body part but mostly seen in UEs
63
Q

chorea

A

involuntary, rapid, irregular, jerky movements

64
Q

dystonia

A

-sustained muscle contraction; twisting & repetitive

65
Q

ballismus

A

-large violent proximal limb movements

66
Q

3 levels of task oriented approach to the examination

A
  1. functional: ability to perform given tasks [interview-based, performance-based]
  2. strategy [movement patterns used, organization of sensory & perceptual information]
  3. impairment [motor, sensory, cognitive, perceptual; multi-system impairments such as gait, balance, posture]
67
Q

MDC

A
  • smallest amount of change that can be considered above the threshold for error in the measurement
  • minimal detectable change
68
Q

MCID

A
  • smallest change in an OM that is perceived as beneficial by the patient & that would not lead to a change in the patient’s medical management
  • minimal clinically important difference
69
Q

responsiveness

A

-ability of a test to measure change (minimal detectable change and minimally important difference or minimal clinically important difference)

70
Q

multiple sclerosis defined

A

-chronic inflammatory, demyelinating disease of the central nervous system

71
Q

Charcot’s triad

A

-paralysis & cardinal symptoms of MS including intention tremor, scanning speech, and nystagmus

72
Q

onset of MS

A

-typically occurs between ages of 15-50 years with peak at age 30

73
Q

Is MS more common in men or women?

A

-women by a 2:1 ratio

74
Q

Which ethnicity has highest reported rates of MS developing?

A

-white populations

75
Q

etiology of MS

A

-precise etiology is unknown BUT thought to be an autoimmune disease induced by a viral or other infectious agent

76
Q

pathophysiology of MS

A

-normal immune response to a virus up to a point where the T-lymphocytes (that are myelin-sensitive) go through the blood-brain barrier & attack the myelin

77
Q

myelin

A
  • insulator that speeds up the conduction along nerve fibers from one node of Ranvier to another
  • also serves to conserve energy for the nerve b/c depolarization occurs only at the nodes
78
Q

mass effect

A
  • abnormally high pressures

- in MS this is caused by local inflammation, edema, & infiltrates that surround the acute lesion

79
Q

oligodendrocytes

A

-myelin-producing cells

80
Q

Which type of MS (of the 4 types discussed in class) appears to be associated exclusively with disease of the oligodendrocytes?

A

-primary-progressive MS

81
Q

gliosis

A

-proliferation of neurological tissue within the CNS & results in plaques or glial scars

82
Q

retrograde degeneration

A

-stage of degeneration where the axon itself becomes interrupted & begins to die

83
Q

primary place in CNS that is affected by MS

A

-primarily white matter

84
Q

list of areas of involvement in CNS with MS

A
  • white matter
  • optic nerves
  • periventricular areas
  • cerebellar peduncles
  • spinal cord [corticospinal tracts & posterior columns]
85
Q

relapsing-remitting MS (RRMS)

A
  • most common course affecting approximately 70% of patients with MS
  • characterized by clearly defined disease relapses (periods of acute worsening of neurological function) followed by remissions (periods w/o disease progression & partial or complete abatement of signs/symptoms)
86
Q

secondary progressive MS (SPMS)

A

-begins with a relapsing-remitting course followed by progression with or without occasional relapses, minor remissions, & plateaus

87
Q

progressive-relapsing MS (PRMS)

A
  • begins with progressive disease course from onset, with clear, acute relapses that may or may not resolve with full recovery
  • intervals between relapses are marked by continuing disease progression
88
Q

primary progressive MS (PPMS)

A
  • rare form occurring in about 10% of cases
  • characterized by a nearly continuous worsening of the disease from onset without distinct relapses
  • typically later onset, usually after age 40
89
Q

benign MS

A

-characterized by mild disease in which patients remain fully functional in all neurological systems 15 years after disease onset

90
Q

malignant MS (Marburg’s variant)

A

-characterized by rapid progression leading to significant disability of death within a relatively short time after onset

91
Q

exacerbations (MS relapses)

A

-defined by new & recurring MS symptoms that last at least 24 hours & are unrelated to another etiology

92
Q

pseudoexacerbation

A
  • refers to temporary worsening of MS symptoms

- typically comes & goes quickly, usually within 24 hours

93
Q

Uthoff’s symptom

A
  • adverse reaction to heat that a majority of individuals with MS demonstrate
  • anything that raises the body temperature can bring on an attack
94
Q

clinically isolated syndrome (CIS)

A

-first clinical episode indicating possible demyelinating disease

95
Q

characteristics of CIS

A
  1. involves young individuals (25-40 yrs)
  2. acute to sub-acute onset with peak reached within 2-3 weeks
  3. isolated in time
  4. typically monofocal signs indicating lesion in optic nerve, SC, brainstem, or cerebellum
  5. 50-70% have multiple brain lesions on MRI
96
Q

MS related impairments (most common to least common)

A
  • poor balance & mobility
  • LE weakness
  • fatigue
  • poor bladder control
  • poor concentration or forgetfulness
  • bowel irregularity
  • pain
  • depression
  • visual impairment
97
Q

What is the most common problem reported in MS?

A

-fatigue (overwhelming sense of tiredness, lack of energy, feelings of exhaustion)

98
Q

peripheral fatigue in MS

A
  • muscle fatigue
  • Secondary to exertion
  • not present at rest
  • late in disease course
99
Q

central fatigue in MS

A
  • progressive decline in ability to drive muscles maximally
  • affects arousal & attention
  • feeling of constant exhaustion
  • not related to changes in sensory & motor pathways
100
Q

pathophysiology of fatigue

A
  • BG or widespread axonal damage
  • impairment of volitional drive to motor pathways
  • over-activation of frontal cortical areas during movement preparation [supplementary motor area, dysfunction between thalamic-BG-frontal cortex circuits, increases perception of effort even with submax exercise]
101
Q

weakness & MS

A
  • common impairment with MS
  • more severe in LEs
  • affects both generation force & muscle endurance
  • related to corticospinal tract abnormalities
  • patients with UMN lesions: weakness more a problem than spasticity
102
Q

spasticity & MS

A
  • due to combination of neural & muscular changes
  • causes velocity dependent increase in resistance to stretch
  • secondary impairment: decreased ROM due to reduced muscle fiber length & decreased number & length of sarcomeres
  • changes in fiber type also occur: may affect muscle recruitment
103
Q

ataxia & MS

A

-incoordination of movement due to sensory or cerebellar involvement

104
Q

patients with cerebellar lesions

A
  • difficulty with predicting movement

- problems with adapting movement to new circumstances

105
Q

prognosis of MS

A
  • life expectancy typically unchanged
  • yet, functional decline is expected over time
  • 10 years: majority of pts able to work
  • 15 years: 50% need assistive device to walk
  • 20 years: 50% require wheelchair
106
Q

positive prognostic indicators influencing short-term prognosis for MS

A
  • mild to moderate impairment
  • intact cognition: increases probability of improving on RMI
  • intact sphincter control
107
Q

negative prognostic indicators influencing short-term prognosis for MS

A
  • more severe disease - 10% improvement
  • cognitive impairment
  • disease duration
108
Q

factors influencing long-term prognosis for MS

A
  • male gender
  • older age (> 40) at onset
  • motor, cerebellar, sphincter problems at disease onset
  • multifocal disease at onset
  • frequent attacks within first 5 years
  • short interval between first 2 attacks
  • shorter time to reach EDSS = 4
  • progressive course
109
Q

requirements to confirm MS

A
  • dissemination in space: 2 lesions in CNS
  • dissemination in time: evidence showing lesions occurred at different times, > or equal to one month apart
  • rule out other diagnoses
110
Q

interferons as medication for MS

A
  • slow immune system by reducing inflammation, swelling & T & B cell proliferation -> reduce frequency & severity of exacerbations
  • block T cells from crossing blood-brain barrier
111
Q

Which type of MS would benefit most from using interferons for medication?

A

-relapsing-remitting to reduce the number & frequency of exacerbations

112
Q

Parkinson’s Disease Defined

A

chronic, progressive CNS disorder

113
Q

Cardinal Signs of PD

A

Bradykinesia
Rigidity
Tremor
Postural Instability

114
Q

Parkinson’s Population

A

Affects >/=2% of population >65yo

Average onset=40-60

115
Q

Parkinsonism

A

group of disorders related to abnormal basal ganglia function

116
Q

3 Classifications of Parkinsonism

A
  • Ideopathic PD (most common)
  • Parkinson’s due to known causes (tumor, infection, virus, toxins, drugs)
  • Parkinson’s Plus Syndromes
117
Q

Striatum Made up of:

A

Caudate

Putamen

118
Q

Basal Ganglia Inhibits the:

A

Brainstem (reticular formation)

119
Q

Basal ganglia excites the:

A

Motor cortex

120
Q

Basal ganglia loops

A
  • Direct

- Indirect

121
Q

Direct Loop

A

Excitatory–increases movement

122
Q

Indirect Loop

A

Inhibitory–decreases movement

123
Q

Basal Ganglia Function

A

initiation and modulation of movement

124
Q

Substantia Nigra

A

Part of BG that produces dopamine for movement

125
Q

Damage to substantia nigra–>

A

Increased inhibition to cortex–>bradykinesia

Decreased inhibition to brainstem–>increased postural tone=rigidity

126
Q

PD Clinical Presentation

A
  • Insidious onset
  • Gradual progression
  • 2 subgroups (postural instability/gait dysfunction and Tremor predominant)
127
Q

Rigidity

A
  • Hypertonia (increased resistance to stretch) due to co-contractions on agonist/antagonist
  • usually bilateral (asymmetrical early on)
  • non-velocity dependent
  • proximal>distal (lots in trunk)
  • 2 Types (cog wheel/lead pipe)
128
Q

Bradykinesia

A
  • Reduced movement (speed, amplitude, range)
  • Hypokinesia–>akinesia
  • Freezing
129
Q

Freezing

A
  • Sudden break or block of movement

- giving pt targets or visual cues work well

130
Q

resting tremor

A
  • Rhythmic oscillations (4-6Hz)
  • Diminishes with movement of that body part
  • Increases with stress, anxiety, fatigue
131
Q

Postural Instability

A
  • One of most common Sx of PD

- Decreases QOL

132
Q

Factors Contributing to Postural Instability

A
  • Rigidity
  • Poor anticipatory control
  • inflexible motor responses to pertrubations
  • decreased muscle torque and speed of contraction
  • problems with dual-tasking
  • visuospatial impairment
133
Q

PD Cognition/Perception impairments

A
  • mild to severe
  • slowed processing/thining
  • loss executive function
  • impaired vertical perception
  • impaired topographical orientation
  • impaired body scheme and spatial relations
134
Q

PD Behavior impairments

A
  • Hallucinations
  • Delusions
  • Mood disorders
  • Anxiety
  • Social withdrawal
  • depression
135
Q

Other PD Impairments

A
  • Paresthesias
  • pain
  • speech/swallowing
  • ANS dysfunctin (thermoreg, seborrhea, slowed pupillary response, bowel/bladder, sexual dysfunction)
  • Cardiopulm (orthostatic hypotension, pneumonia)
136
Q

Motor Planning Problems

A
  • Prolonged movement start times
  • Freezing
  • difficulty performing complex, sequential movements
  • poor control with learned motor skills
  • freezing
137
Q

Motor Learning problems

A
  • Procedural learning (especially complex)
  • random practice
  • Dual tasking
138
Q

PD type with worse prognosis

A

Postural instability/gait disorder

139
Q

Hoehn & Yahr

A

Track PD progression

140
Q

PD Diagnosis

A
  • based on history and clinical S/Sx
  • 2 of 4 cardinal signs
  • no diagnostic test
141
Q

Goals of PD management

A
  • Slow disease progression (neuroprotective agents)
  • Symptom management
  • Prevention of compications
142
Q

PD drug classifications

A
  • Neuro-protective
  • Anticholinergic
  • Dopamine Replacement
  • Dopamine Agonist
143
Q

Sinemet

A
  • PD drug
  • Dopamine Replacement
  • Decrease bradykinesia and rigidity
  • Side effects
  • Loss of effectiveness after 5-7years
  • on/off phenomena
144
Q

Surgical Management of PD

A
  • Thalamotomy/Pallidotomy

- deep brain stimulation

145
Q

Diagnostic Tests for MS

A
  • MRI
  • CSF Analysis (increased immunoglobulin)
  • Evoked Potentials (slow NCV)
146
Q

Best Test for Ischemic Stroke

A

-Diffusion Weighted MRI

147
Q

Best Test for Hemorrhagic Stroke

A

-CT

148
Q

Best Test for TBI

A

-MRI better resolution than CT

Neuromuscular Conditions I (11 decks)

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