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Neurological Systems I > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Coma

A
  • complete paralysis of cerebral function; a state of unresponsiveness
  • eyes are closed; no response to painful stimuli;
  • reflexes may be present depending on the site of the lesion
  • 2-4 weeks, nearly all patients begin to awaken
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2
Q

Consciousness

A
  • alert wakefulness
  • clearly appreciates environment
  • responds quickly and appropriately to visual, auditory, other sensory stimuli
  • gradual recovery of orientation and recent memory
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3
Q

Minimally Conscious State

A

definite evidence of environmental awareness

characterized by inconsistent behavior but reproducible and localized rather than generalized

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4
Q

PT for patients in a minimally conscious state includes:

A
  • disorders of consciousness program

- structured stimulation and recording of responses to document emergence

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5
Q

Persistent Vegetative State

A
  • wakeful, reduced responsiveness
  • no evident cerebral function
  • eye tracking, minimal motor
  • no speaking or response to verbal stimuli
  • non-purposeful movement
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6
Q

JFK Coma Recovery Scale

A

a research tool used for studying recovery of patient’s in a coma; 23 items that comprise six subscales addressing:

  1. auditory
  2. visual
  3. motor
  4. oral motor
  5. communication
  6. arousal functions
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7
Q

What are the two most commonly used clinical rating scales for patients s/p TBI?

A
  1. Rancho Los Amigos Hospital Level of Cognitive Functioning Scale (LOCF)
  2. Glasgow Coma Scale
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8
Q

Rancho Los Amigos LOCF

A
  • consists of 10 levels
  • describes pt. during recovery
  • not always clearly in one level
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9
Q

Rancho Los Amigos LOCF: Levels 1-3

A

total assistance

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10
Q

Rancho Los Amigos LOCF: Levels 4-5

A

maximal assistance

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11
Q

Rancho Los Amigos LOCF: Levels 6

A

moderate assistance

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12
Q

Rancho Los Amigos LOCF: Levels 7-10

A

progressively less assistance

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13
Q

Glasgow Coma Scale

A
  • quantify degree of coma at time of injury, and every 2-3 days
  • three categories (EMV score): Eye opening, best Motor response, and Verbal response
  • 3-15 point range; 3 = coma
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14
Q

Functional Assessment Measure

A

an adjunct to the FIM to specifically address major functional area less emphasized in the FIM including:

  • cognitive
  • behavioral
  • communication
  • community functioning
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15
Q

Mortality after TBI

A

over 1600 subjects surviving 1 year after injury, with increased risk of death from:

  • aspiration pneumonia
  • seizures
  • pneumonia
  • suicide
  • digestive conditions
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16
Q

Postural changes following TBI:

A
  • decorticate posture - UE flexed, LE extended
  • decerebrate posture - UE and LE extended

both indicate low brain function and absence of selective movement

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17
Q

Sensory changes following TBI:

A
  • light touch
  • deep pressure
  • pain
  • temperature
  • proprioception
  • kinesthesia
  • cranial nerve involvement
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18
Q

Motor changes following TBI:

A
  • monoparesis
  • hemiparesis
  • tetraparesis
  • coordination, timing, sequencing deficits

*Highly variable between patients

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19
Q

Perceptual changes following TBI:

A
  • unilateral visuospatial neglect

- hemispatial neglect, hemiagnosia, and contralateral neglect

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20
Q

Input vs. Output Neglect

A

input neglect or “inattention” includes ignoring contralesional sights, sounds, smells, or tactile stimuli; output neglect includes motor and pre-motor deficits. A person with motor neglect does not use a contralesional limb despite the neuromuscular ability to do so.

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21
Q

The presence of neglect w/in the first ten days following TBI is a strong predictor of ____ __________ ________ after 1 year than several other variables

A

poor functional recovery

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22
Q

Perception

A

integration of sensory info into meaningful psychological info, including prior information; more complex than sensation

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23
Q

Cognitive impairments following TBI:

A
  • memory deficits

- attention deficits

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24
Q

Memory deficits

A

post-traumatic amnesia - time between the injury and the time patient remembers ongoing events (short-term); declarative (habit) vs. declarative (facts)

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25
Q

Retrograde vs. Anterograde amnesia

A

retrograde amnesia is the inability to recall memories of prior events, while anterograde amnesia is the inability to make new memories

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26
Q

Attention deficits

A
  • decreased attention span
  • impulsiveness/lack of safety awareness
  • distractibility
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27
Q

Emotional/behavioral changes

A

most enduring and socially disabling of any sequelae

  • disinhibition
  • lability
  • aggression
  • low frustration tolerance
  • inpatient
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28
Q

Secondary body function/structure impairments

A
  • soft tissue contractures
  • altered muscle tone/spasticity
  • pressure sores
  • DVT
  • heterotopic ossification
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29
Q

Factors in predicting outcomes following TBI

A
  • severity of injury
  • duration of coma
  • duration of post-traumatic amnesia (≥12 wks = poor; ≤4 wks = good prognosis)
  • low Glasgow Coma Scale
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30
Q

Predicting outcomes

A

motor disturbances generally have GOOD prognosis, but cranial nerve injury - hearing, smell, vestibular sense are rarely fully recovered

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31
Q

Care Manager/Case Manager

A

coordination of care, seeking appropriate services, conducting team meetings, family liaison, etc.

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32
Q

Physical Therapist

A

mobility skills, transfers, walking, balance, attention, memory, community reintegration

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33
Q

Occupational Therapist

A

self-care, gross and fine motor skills, emphasis on UE, memory, attention, organization, community reintegration

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34
Q

Speech Language Pathologist

A

communication: rehabilitation of dysarthria, aphasia, swallowing (dysphagia), along with memory, attention, community reintegration

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35
Q

Physician

A

medical management; medication, imaging, testing

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36
Q

Nurse

A

personal care and carrying out medical plan, follow-up care consistent with rehab team

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37
Q

Neuropsychologist

A

assessment of cognition and behavior through testing; psychological, personal, interpersonal, and wider contextual circumstances

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38
Q

Precautions during examination of pts. following a TBI

A
  • cervical ROM caution: shunts, head should be elevated in acute phase
  • passive ROM: LOCF I-III
  • position changes: confirm status of fracture before standing, sitting contraindicated if unstable ICP or BP, tube/line management
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39
Q

Essential outcome measures during examination of pts. following a TBI

A
  • FIM
  • Modified Ashworth Scale
  • Balance assessments
  • Timed walking tests (2 min, 3 min)
  • Functional reach balance test
  • Single-limb stance
  • activity limitations
  • bed mobility
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40
Q

In which two ways should you classify patients following a TBI?

A
  1. Sahrmann & Scheets model

2. Rancho Los Amigos LOCF

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41
Q

In which two ways should you classify patients following a TBI?

A
  1. Sahrmann & Scheets model

2. Rancho Los Amigos LOCF

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42
Q

Behavioral Treatment Strategies

A
  • assumption: cognitive recovery can be inferred from progressive behavioral changes
  • LOCF is determined by observation throughout the day
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43
Q

What are client factors to consider when discharge planning?

A
  1. previous living/social environment
  2. family/caregiver availability and competence
  3. patient/family wishes/goals

*with current abilities, progression, and safety at the core

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44
Q

Prognosis factors

A
  • severity of health condition
  • predicted improvement
  • self and family care capabilities
  • less certainty = more conservative decision
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45
Q

What are the options for discharge?

A
  • home with family care
  • home with home health care
  • home with OP care
  • subacute/LTC
  • acute rehab center
  • assisted living
  • nursing home
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46
Q

Who decides the discharge location?

A
  • discharge planner/case manager
  • the team: PT/OT/nursing/MD/psychology
  • family
  • admission professionals from outside facilities
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47
Q

Who coordinates arrangements?

A

D/C planner/care manager

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48
Q

Patient factors that may indicate the need for subacute care:

A
  • ongoing physical therapy consult required
  • specialized devices (catheters, IV use, etc.)
  • wound care required
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49
Q

Poor discharge outcomes may result from:

A
  • lack of family/social support
  • multiple hospitalizations
  • hx of depression
  • significant co-morbidities/activity limitations
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50
Q

PT contributions to the rehab process:

A
  • ongoing rehab needs
  • opinion on progress, safety and prognosis
  • equipment recommendations
  • exercise programs
  • communication with the next rehab site/professionals
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51
Q

What equipment with medicare/medicaid cover?

A
  • hospital bed rental
  • oxygen
  • walker OR wheelchair
  • bedside commode if bathroom is inaccessible
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52
Q

What are the specific recommendations to make regarding ramps?

A

1” rise per 1 foot of length; pay attention to neighborhood zoning problems

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53
Q

Multiple Sclerosis

A

MS causes the body’s immune system to mistakenly attack and destroy the myelin that surrounds the axons of nerves in the CNS (brain, spinal column, and/or optic n.)

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54
Q

Gliosis

A

the damaged myelin forms scar tissue (sclerosis). This scarring along the myelin sheath interferes with the transmission of nerve impulses, which produces the symptoms of MS.

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55
Q

T/F: Multiple Sclerosis is considered an auto-immune disease

A

true; it is also considered an immune-mediated disease

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56
Q

Epidemiology of MS

A
  • most common neurological disorder in young people, typically diagnosed between ages 20-50
  • more common in women, but more progressive in men
  • more frequent in caucasians, especially those of northern European ancestry
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57
Q

What are the three types of multiple sclerosis?

A
  1. relapsing-remitting
  2. primary-progressive
  3. secondary-progressive
58
Q

Relapsing Remitting MS (RRMS)

A
  • most common (85% of diagnoses)

- clearly defined acute attacks with either full recovery, or with residual deficit upon recovery

59
Q

Secondary Progressive MS

A
  • follows the RRMS course
  • most of the 85% with RRMS will transition to SPMS, in which the disease will begin to progress more steadily, with or without any relapses and minor remissions and plateus
60
Q

Primary Progressive MS (PPMS)

A
  • characterized by progression of disability from onset, without any distinct relapses or periods of remission
  • the progression is continuous, although the rate of progression may vary over time, with periods of occasional plateaus or temporary improvements
  • less prevalent, ~10% of people initially diagnosed with PPMS
61
Q

RRMS vs. progressive types of MS

A
  • people with RRMS have more lesions in the brain and more inflammatory cells, while progressive MS have more lesions on the spinal cord and contain less inflammatory cells
  • with RRMS, women are affected 2-3x as often as men
  • with PPMS, woman and men affected equally

most people with RRMS are diagnosed in their 20s and 30s, whereas the onset of PPMS is in the 40s and 50s

62
Q

Clinically Isolated Syndrome

A

a first occurrence of a neurological episode of inflammation or demyelination that lasts at least 24 hours; can involve one or multiple areas

  • may or may not be an early sign of MS
  • 60-80% likely to develop MS if lesions consistent with MS per MRI
  • 20% likely to develop MS if brain scan is normal
63
Q

How is MS diagnosed?

A

no single clinical test, rather a combination of diagnostic tools:

  • medical hx
  • physical exam
  • MRI
  • spinal tap
64
Q

A definitive diagnosis of MS can be made when:

A
  • evidence of plaques or lesions in 2 distinct areas of the nervous system
  • evidence that these plaques occurred at different points in time
  • there are no other explanations than MS for the plaques in the white matter of the CNS
65
Q

McDonald Criteria

A

Review on pg. 4 of the MS lecture

66
Q

“Dawson’s Fingers”

A

demyelinating plaques through the corpus callosum; relatively specific to MS

67
Q

Oligoclonal bands indicate:

A

inflammation of the CNS, and may be a sign of MS

68
Q

MS symptoms may vary due to issues, including:

A
  • side effects of medicines
  • fatigue
  • UTI
  • elevated core body temp
  • stress
  • affective disorders (ie depression)
  • other medical conditions
69
Q

MS Symptoms

A
  • fatigue = 88%
  • ataxia
  • visual disturbances = 58%
  • cognitive problems = 44%
  • spasticity
  • sensory impairments
  • muscular weakness or paralysis
  • balance deficits
  • ambulation problems = 87%
  • bowel and bladder problems = 65%
  • tremor = 41%
  • movement problems in the arms = 41%
70
Q

Factors that predict a favorable outcome for pts. with MS:

A
  • female
  • onset prior to age 35
  • single area of CNS involvement
  • complete recovery after exacerbation, with little or no residual impairment
71
Q

Factors that predict a less favorable outcome for pts. with MS:

A
  • male
  • onset after age 35
  • brainstem symptoms (ataxia, nystagmus, tremor, dysarthria)
  • poor recovery after exacerbations
  • frequent attacks
72
Q

Treatment of multiple sclerosis

A
  1. treatment of acute exacerbations
  2. symptom management
  3. disease modification
  4. rehabilitation
  5. psychosocial support
73
Q

Multiple Sclerosis Functional Composite (MSFC)

A
  • 25’ walk test
  • 9 hole peg test
  • paced auditory serial addition test (PASAT)

*may also include a Berg balance test and symbols digit modality test

74
Q

Outcome measures for fatigue/cognition with MS pts.

A
  • visual analog scale
  • modified fatigue impact scale
  • fatigue scale for motor and cognitive function
75
Q

Outcome measures for pain with MS pts.

A
  • Visual Analog Scale
  • Wong Baker FACES Pain Rating Scale
  • 24-hour pain report
76
Q

Outcome measures for vision

A
  • tracking
  • visual field cut assessment

*vestibular screen if indicated by symptoms

77
Q

What are the three main motor symptoms of Parkinsonism?

A

shakiness, stiffness/rigidity, and bradykinesia

78
Q

Secondary Parkinsonism

A
  • drug-induced Parkinsonism
  • vascular Parkinsonism
  • essential tremor
  • normal pressure hydrocephalus
  • progressive supranuclear palsy
  • multiple system atrophy
  • corticobasal degeneration
  • dementia and lewy bodies
79
Q

Braak’s Hypothesis

A

states that alpha-synuclein aggregation could begin in the nervous system of the gastrointestinal tract and migrate from there to the CNS; evidence of non-motor symptoms may detect PD, such as:

  • loss of sense of smell
  • sleep disorders
  • constipation
80
Q

When approximately ______ of dopamine-producing neurons are damaged, motor symptoms begin to appear

A

60-80%

81
Q

Motor signs of PD

A
  • shakiness/tremor
  • stiffness
  • slow movements/bradykinesia/akinesia
  • postural instability
82
Q

Tremor

A

can be resting or postural; tremor-dominant patients generally follow a more benign disease course than non-tremor patients; tremor is linked to altered activity in not one, but two distinct circuits: the basal ganglia and the cerebello-thalamo-cortical circuit

83
Q

Tremor is increased by:

A
  • stress
  • fatigue
  • excitation
84
Q

Tremor is decreased by:

A
  • relaxation
  • during voluntary movement
  • disappears during sleep
85
Q

Treatment for bradykinesia

A
  • LSVT BIG
  • LSVT LOUD
  • PWR!
  • visual cues
  • auditory cues
  • counting steps
86
Q

Strategies when akinesia or freezing of movement occurs?

A
  • STOP moving
  • stand tall (or sit tall)
  • weight shift/rocking
  • take a step backwards or to the side
  • aim next step at a specific spot on the floor
  • counting (out loud or in your head)
  • sing/hum rhythmic tune
87
Q

Rigidity

A

increased resistance to passive motion throughout the range of motion; present in >90% of people with PD

lead pipe rigidity - resistance to passive movement throughout the entire ROM w/o fluctuation

cogwheel rigidity - combination of lead pipe rigidity and tremor and presents as jerky resistance to passive movement

88
Q

Non-motor symptoms of Parkinson’s disease

A
  • depression
  • cognitive problems (memory loss and concentration)
  • sense of smell
  • sleep disturbance
89
Q

Hoen and Yarh: Stage 1

A

unilateral involvement only; minimal or no functional disability

90
Q

Hoen and Yarh: Stage 2

A

bilateral or midline involvement without impairment of balance

91
Q

Hoen and Yarh: Stage 3

A

bilateral disease; mild to moderate disability with impaired postural reflexes; physically independent

92
Q

Hoen and Yarh: Stage 4

A

severely disabling disease; still able to walk or stand unassisted

93
Q

Hoen and Yarh: Stage 5

A

confinement to bed or wheelchair unless aided

94
Q

Pallidotomy

A

permanently destroys the overactive globus palladis to decrease PD symptoms and can include reduction of rigidity, reduction of tremor, bradykinesia, and balance problems.

95
Q

Thalamotomy

A

destroys part of the thalamus to block the abnormal brain activity from reaching the muscles and causing tremors

96
Q

Deep Brain Stimulation

A

surgical procedure used to treat the motor symptoms of PD, such as tremor, rigidity, bradykinesia, and walking problems. Also used to treat essential tremor and dystonia.

97
Q

Outcome measures for the PD population

A
  • Berg Balance test
  • Mini-BESTest
  • FGA
  • 10 meter walk test
  • TUG test
  • Four Square Step test
98
Q

Movement limitations in PD

A
  • difficulty with initiation of movements
  • difficulty with ADLs
  • balance/postural instability
  • walking, esp. turns and in tight spaces
  • transitional movements
  • activities that require dual/multi-tasking
99
Q

Gait abnormalities

A
  • short shuffling steps
  • freezing episodes
  • difficulty with turns
  • difficulty with initiation of movement and/or stopping a movement
  • festinating gait pattern
  • decreased arm swing
  • decreased trunk rotation
  • dual task attention during gait
100
Q

LSVT BIG

A

applies the principles of LSVT LOUD to limb movement, developed by Becky Farley and Cynthia Fox; most beneficial to patients in stages 1-3/4 of the Hoen and Yarh

101
Q

Principles of neuroplasticity used in LSVT LOUD & BIG

A
  • forced use
  • intensive practice
  • repetition
  • challenging
  • motivating
102
Q

LSVT BIG must be:

A
  • high effort: 7-8/10 for effort each exercise
  • repetitive: 10 reps each exercise
  • dosage: exercises must be done 2x/day every day
103
Q

What are factors that affect resource allocation?

A
  1. task demand
  2. performance criteria
  3. long-term predispositions
  4. arousal
104
Q

What are factors that affect resource allocation?

A
  1. task demand
  2. performance criteria
  3. long-term predispositions
  4. arousal
105
Q

What are the cortical structures commonly implicated in executive functions network?

A
  • orbitofrontal
  • ventromedial
  • dorsolateral
106
Q

What is the SLP’s role in acute care for cognition?

A
  • manage distractability
  • monitor post-traumatic amnesia
  • awareness training
  • family training
107
Q

What is the SLP’s role in acute care for cognition?

A
  • manage distractability
  • monitor post-traumatic amnesia
  • awareness training
  • family training
108
Q

Communication recommendations in acute setting

A
  • ALWAYS try to leave sessions on a positive note
  • engage eye contact
  • speak in simple sentences, active voice
  • pause between ideas
  • clearly identify topic shifts
  • don’t quiz patients
  • never leave sessions without ensuring all their questions have been answered to their satisfaction
  • always make sure the patient has their memory book with them
109
Q

What are the principles of group practice?

A
  1. topic limit and structure
  2. group composition
  3. task selection
  4. mediator style
110
Q

What are the three types of attention?

A
  • sustained
  • selective
  • alternating
111
Q

What are the two types of memory?

A

working and new learning (encoding)

112
Q

What are the two types of social cognition?

A
  • emotion recognition

- theory of mind

113
Q

Guillain-Barre’ Syndrome

A
  • a polyradiculoneuropathy
  • a primary demyelinating disease
  • immune-mediated inflammatory disorder
  • typically appears days or weeks after an infection (upper respiratory or GI)
114
Q

Auto-immune vs. Immune-mediated

A

autoimmune is a well-defined disease process in which the exact cause is known; immune-mediated is not well known

115
Q

Primary impairments of GBS

A
  • abnormal sensation
  • muscle weakness
  • combination of the two
  • pain
116
Q

How is GBS diagnosed?

A
  • clinical presentation
  • elevated proteins in the CSF
  • nerve conduction/velocity/EMG
117
Q

Chronic Inflammatory Demyelinating Polyneuropathy

A
  • a chronic variation of GBS
  • more rare
  • develops more slowly
  • symptoms persist and are less likely to completely resolve
118
Q

Medical treatment options for GBS

A
  • intravenous immunoglobulin therapy (IVIg) - immunoglobulins are injected intravenously 1x/day for 5 days; act as antibodies
  • plasma exchange (plasmapheresis) - plasma cells are removed; RBC, WBC, platelets are returned; administered every other day for 2 weeks
119
Q

Progression of GBS General Timeframe

A
  • 50% of cases-weakness peaks in 1st week
  • 80% of cases-within first 3 weeks
  • few cases weakness progresses over 1-2 mos.
120
Q

Recovery of GBS General Timeframe

A
  • usually begins 2 wks - 2 mos after disease plateaus
  • 80% ambulatory within 6 mos of onset
  • 30% have residual distal weakness (ant. tib., hand intrinsics, quads, and glutes)
121
Q

What are the primary impairments of GBS?

A
  • force production deficit
  • sensory impairments
  • pain syndromes
  • autonomic dysfunction
122
Q

Force production deficit in GBS

A
  • progressive
  • rapid onset
  • symmetrical
  • distal to proximal
  • self-limiting
123
Q

Sensory impairments

A
  • tend to be mild
  • 75% of patients have paresthesia/hyperesthesia)
  • stocking/glove pattern
  • dysesthesia
124
Q

Pain syndromes (three types)

A
  1. back and leg pain - deep throbbing/aching back pain with radiation into lower extremities
  2. Dysethetic extremity pain - burning, tingling, shock-like
  3. Myalgic - rheumatic extremity pain (achy or cramping sometimes associated with joint stiffness)
125
Q

Autonomic dysfunction

A
  • tachycardia
  • arrhythmia
  • blood pressure fluctuation
  • hyperhydrosis
  • persistent goose bumps
126
Q

Secondary complications of GBS

A
  • DVT
  • contracture
  • muscle atrophy
  • hypercalcemia of immobilization
  • pressure sores
  • respiratory complications
127
Q

What are important considerations during the examination of a patient with GBS?

A
  • skin inspection
  • respiration
  • autonomic nervous system
  • DVT
  • avoid overexertion
  • be alert for autonomic dysreflexia, orthostatic hypotension, and DVT
128
Q

Treatment of a pt. with GBS in the ICU should consist of:

A
  • PROM exercises
  • transfer by lift to w/c gradually tilted to upright
  • monitor VS throughout
  • sitting edge of bed
  • progressive rolling, transfer-movement organized around functional goals
129
Q

Treatment of a pt. with GBS in the acute phase should consist of:

A
  • breathing strategies/intervention
  • skin integrity
  • pain relief - positioning
  • contracture prevention
  • exercise while monitoring overuse/fatigue
130
Q

What factor in patients with GBS is strongly predictive of the need for extended LOS in inpatient rehab?

A

prior ventilator support

131
Q

Significant factors for a longer LOS in acute rehab

A
  • muscle belly tenderness
  • severe LE weakness
  • lower FIM mobility score upon admission and d/c (1-2 on admission & 4-5 on discharge)
132
Q

Outcome measures used in pts. with GBS

A
  • Guillain-Barre disability index (0 = best; 6 = death)
  • FIM
  • Pain intensity numerical rating scale
  • Manual muscle testing
133
Q

Exercise precautions in patients with GBS

A
  • avoid exacerbation in acute phase
  • allow frequent rest periods
  • assess overwork during rest intervals through objective strength tests and evaluation of complaints of soreness
134
Q

Exercise guidelines in patients with GBS

A
  • submaximal strength training
  • allow for 24 hours of recovery
  • monitor appropriate physiological responses during aerobic training
  • recruit/train a variety of muscle fibers - slow/fast twitch (i.e. isometrics, then eccentrics)
135
Q

Amyotrophic Lateral Sclerosis (ALS)

A
  • demyelination and gliosis in the corticospinal tracts and corticobulbar tracts d/t degeneration and drop out of Betz cells (UMN) in motor cortex
  • degeneration of the anterior horn cells r/in muscle atrophy
  • affects spinal cord and motor cranial nerve nuclei in the lower brainstem (bulbar area)
  • lower motor neurons show massive cell loss
  • atrophy seen after loss of 30% of cells
136
Q

Cell death in pts. with ALS can happen in which three places?

A
  • cell body dies via apoptosis
  • axon via another mechanism
  • synapse via a different mechanism

*All do not die simultaneously, so signs may differ between patients

137
Q

What are the two types of ALS?

A
  • sporadic: 85-90% of patients

- familial: 10-15% of patients (autosomal dominant)

138
Q

ALS Clinical Features

A
  • requires both UMN and LMN signs for definitive diagnosis
  • UMN: weakness, spasticity, hyperreflexia
  • LMN: weakness, atrophy, fasciculations, hypotonia, areflexia
  • generally have bulbar and spinal muscle involvement
139
Q

Clinical features of variations of motor neuron disease

A
  • bulbar muscle weakness (speech and swallowing) -> progressive bulbar palsy
  • if pure LMN -> progressive muscular atrophy
  • if pure UMN -> primary lateral sclerosis
140
Q

ALS Diagnosis

A
  • combination of clinical exam and diagnostic tests
  • EMG, NCV
  • blood and urine studies
  • thyroid/parathyroid hormone levels
  • spinal tap
  • MRI
  • muscle and nerve biopsy
141
Q

ALS functional problems

A
  • head control
  • poor gait posture
  • weakness in proximal muscles of gait
  • sitting posture which affects speaking swallowing, writing, eating, reading, socialization
  • contractures (shoulder/neck)

Neurological Systems I (3 decks)

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