Neuro Flashcards

1
Q

What are the three types of impairments?

A

Direct/1’- direct result of pathology e.g. lesion
Indirect/2’- complication of direct impairments e.g. oedema
Composite- multiple underlying causes, both primary and secondary

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2
Q

What are the eight direct impairments?

A

Weakness
Sensation
Proprioception
Coordination
Tone
Perception
Vision
Vestibular function

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3
Q

What are the three stages of motor skill learning?

A

Cognitive- understanding and learning, frequent errors
Associative- refining practice, minor errors
Autonomous- less conscious attention, smooth/efficient

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4
Q

What is the difference between open and closed skill?

A

Open- unpredictable environment, performer has to react e.g. soccer
Closed- predictable e.g. golf

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5
Q

What is the difference between discrete, continuous and serial skills?

A

Discrete- distinct start and end e.g. kicking football
Continuous- no obvious beginning or end e.g. running
Serial- discrete skills linked by a movement sequence e.g. dribbling basketball

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6
Q

What does V1, V3, R1 and R2 mean?

A

V1- as slow as possible
V3- as fast as possible
R2- end range
R1- range measured at catch or point of clonus

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7
Q

What are some risk factors for stroke?

A

Age, hypertension, smoking, low physical activity and obesity

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8
Q

What is an ischaemic stroke?

A

Infarction is cerebral, spinal or retinal cell death attributable to ischaemia causing neurological dysfunction. May result from thrombosis, embolism

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9
Q

What is a subarachnoid stroke?

A

Haemorrhagic stroke with rapid onset due to bleeding in subarachnoid space

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10
Q

What are intracerebral and intraventricular strokes?

A

Non-traumatic bleeding into brain or ventricles, increasing ICP

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11
Q

What are some impairments following stroke?

A

Decreased AMC
Loss of proprioception
Loss of sensation
Neglect
Pushing Syndrome, altered perception of vertical
Language, Cognition, Memory
Pain

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12
Q

What impairments arise with anterior, middle and posterior cerebral strokes?

A

Ant- lower limb sensation/motor
Middle- upper limb sensation/motor
Post- hemianaesthesia, hemiparesis

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13
Q

How is ischaemic stroke from thrombosis treated?

A

Intravenous rt-PA to cause thrombolysis

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14
Q

What are gait kinematics?

A

Amount and type of movement seen at various joints during gait

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15
Q

What are the 3 key muscles of gait?

A

Ankle PF for push off
Hip extensor in early stance
Hip flexor in late stance

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16
Q

What is drop foot gait?

A

Increase hip and knee flexion to allow clearance of the foot due to drop foot

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17
Q

What are the immediate effects of trauma?

A

Cerebral haemorrhage and diffuse axonal injury (shearing of axons)

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18
Q

What are the 2’ implications of trauma?

A

Cerebral oedema, increased ICP, infection, cardioresp compromise

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19
Q

What is CPP?

A

Central perfusion pressure= MAP- ICP
After trauma the autonomic system can drop BP, risking no perfusion of the brain

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20
Q

What is PTA?

A

Post traumatic amnesia, inability to store new information and impaired learning, correlated with GCS, distractable and agitated

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21
Q

How is PTA severity classified?

A

<5min- very mild
>4 weeks- extremely severe

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22
Q

How is PTA managed?

A

Minimal stimulation, keep routine, integrate familiar people/environment

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23
Q

What is a heterotopic ossification?

A

Palpable bony mass that often occurs after CNS injury

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24
Q

What are the complications of heterotopic ossification?

A

Appear 4-12 weeks post surgery with sudden reduced ROM. oedema, fever

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25
Q

How is the STS phases classified?

A

Flexion Momentum- initiation of movement
Momentum Transfer- buttocks off to max DF
Extension- after max DF, to end hip E
Stabilization-

OR

Pre-extension- feet backwards, upper body forward, knee F and DF
Extension- extend pelvis, spine, head

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26
Q

What factors affect STS performance in the elderly?

A

Strength
Tactile sensitivity
Proprioception
Reaction Time
Sway
Pain

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27
Q

What are some deviations of sit to stand in stroke?

A

Hemiplegic leg positioned backwards in PE phase
Trunk not brought far enough forward
Pause between phases
Slow
Hands for balance

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28
Q

What are some deviations in stand to sit in stroke?

A

Reduced F at ankle, knee, hip

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29
Q

What are some alterations to make progress and regress treatment for STS?

A

Change height
Active UL
Scales under feet for symmetry
Change foot position

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30
Q

What are the consequences of falls?

A

Injury
Fear of falling restricts activities

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31
Q

What are some intrinsic RF’s for falls

A

Age
Falls history
Cognitive impairment
Sensory loss
Postural hypotension

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32
Q

What is proactive and reactive postural control?

A

PPC- response in anticipation of a destabilizing force (prior experience)
RPC- feedback to correct response reaction due to external force

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33
Q

How do postural control strategies manifest?

A

Ankle- small disturbance of COG
Hip- larger disturbance of COG
Step- final defence

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34
Q

What are some extrinsic RFs for falls?

A

Gait aids
Bed height
Footwear
Clutter

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35
Q

What are some ways to assess falls risk?

A

Functional reach test
Step test
Four square step test
TUG
Pastor’s- ensures patient can perform postural response
Clinical Test of Sensory Integration of Balance (CTSIB)- multiple criteria, changes vision and surface

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36
Q

What is the 6-pack program for hospital fall intervention?

A

Falls alert sign
Low-low bed
Walking aid in reach
Bed chair alarm
Toilet regime
Bathroom supervision

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37
Q

What is a functional neurological disorder?

A

Motor and sensory symptoms related to functional rather than structural disorder, software rather than hardware problem

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38
Q

What is Hoover’s sign as what disorder does it indicate?

A

FND, asked to lift one leg, the other leg will extend

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39
Q

What is the pathophysiology of MS?

A

Dysregulation of immune system, CNS infiltrated by T and B cells, inflammation -> demyelination -> axon damage -> degeneration

Develop plaques, decreased nerve conduction, atrophy of axons from 2’ damage

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40
Q

What is the aetiology of MS?

A

Epstein-Barr virus, necessary but not sufficient
Genetic susceptibility
RF’s- childhood obesity, smoking, concussion

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41
Q

How is MS diagnosed?

A

MRI
Lumbar puncture to assess CSF
Neurological exam- McDonald criteria disseminated in time, disseminated in space, oligoclonal bands in CSF

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42
Q

What is radiologically isolated syndrome vs clinically isolated syndrome?

A

RIS- lesions found when imaged for other reasons, may be asymptomatic
CIS- 1st episode of lesion, diagnosed with MS

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43
Q

What is relapsing remitting MS?

A

Lasting >24 hours without other cause, interspersed by periods of stability

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44
Q

What is 2’ progressive MS?

A

Progression independent of relapse activity

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45
Q

What is primary progressive MS?

A

Slow disability progression

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46
Q

What are some symptoms of MS?

A

Depends on lesion location
- Weakness
- Ataxia
- Tremor
- Speech, swallowing
- Numbness
- Bowel, bladder
- Thinking, memory

Pain, fatigue, vestibular dysfunction

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47
Q

How is MS managed and how does it change recovery?

A
  • Anti-inflammatories and immunosuppressants
  • Exercise, slows disability and encourages neurogenesis and neuroplasticity
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48
Q

What are some considerations for exercise in MS?

A
  • Low intensity may be better tolerated
  • Strength less adhered than aerobic
  • Bladder dysfunction
  • Resp. m. weakness (Borg)
  • Sensitivity to cold, painful in winter, vests to keep cool in summer
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49
Q

What is the function of the vestibulocerebellum?

A

Eye movement, visual fixaiton and adapts postural muscles

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50
Q

What is the function of the spinocerebellum?

A

Somatosensory information, compares ongoing movement with intended movement

Dysfunction can cause hypotonia, reduced balance, ataxic gait

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51
Q

What is the function of the cerebrocerebellum?

A

Motor planning, coordinating and planning voluntary movements

Dysfunction incoordinated arm movements

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52
Q

How is ataxia treated?

A

Exercise, incl. hydrotherapy
Balance
Gait aids
Treadmill training

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53
Q

What are the recommendations for physical activity?

A

150 min of moderate or 75 min of vigorous intensity exercise/week
Break up prolonged sitting

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54
Q

How can circuit class therapy improve stroke patients in rehab?

A

Improve walking ability, speed and endurance
Balance confidence
Monitor falls risk

55
Q

What are common observations in stroke pts?

A

Forward trunk F
Poor AMC, speed, smoothness and trajectory
Less accurate and excessive grasp
Poor anticipatory modulation of grip

56
Q

What are typical adaptive patterns in stroke?

A

When reaching, flex trunk instead of shoulder
(Sh elevation, abd, IR, LF of spine, elbow F, wrist pronation)
Excessive opening of hand to grasp

57
Q

What are some general outcome measures for stroke?

A

Fugel Meyer Assessment- criteria rated 0-66 test motor Fx, sensory, balance, ROM
ARAT- box with 19 items
Wolf Motor Function Test (WMFT)- rating Fx ability 1-5, e.g. arm to table, extend elbow, grip
Motor Assessment Scale- for UL, e.g. pick up jelly bean and put it in a cup

58
Q

What are some outcome measures for dexterity in stroke?

A

Purdue Peg Test- time unimanual and bimanual fine dexterity
Box and block test- timed gross unimanual dexterity

59
Q

What are some outcome measures for sensation in stroke?

A

Wrist position sense test for proprioception
Functional Tactile Object Recognition

60
Q

How do you assess shoulder pain in stroke?

A

Ritchie Articular Index, 0-3 when in ER

61
Q

What are some considerations in treatment of UL in stroke?

A

Subluxation prevention
Initiate voluntary muscle, FES can help stimulate
Prevent loss of muscle length with positioning
Resistance Training
Functional Training
Constraint of non-affected limb
Mirror therapy

62
Q

What is neglect?

A

Failure to respond to anything on opposite side of brain lesion

63
Q

Give an example of the difference between personal, peripersonal and extrapersonal neglect?

A

P- failure to groom contralesional side or don’t use contralesional limb
PP- failure to eat food on contralesional side or don’t read words at start or end of sentence
EP= failure to observe objects on contralesional side

64
Q

How can neglect can be divided into 3 categories, what are they?

A

Sensory- visual, auditory etc.
Motor- akinesia, bradykinesia
Other domains- representational (e.g. drawing half a house), mental images

65
Q

How can neglect be assessed?

A

Extrapersonal- describe 10 objects in room
Peripersonal- bisecting line test, circling all the stars
Personal- Comb and Razor test

66
Q

How can neglect be treated?

A

Encourage recognition of affected side
Mirror therapy
Up against wall to limit stimuli on good side

67
Q

What is pusher syndrome?

A

Active pushing of body across towards affected side due to skewed perceived midline

68
Q

What are some Fx problems with pusher syndrome?

A

Difficult indep. sitting and standing
Falls risk
Impaired reactive balance

69
Q

What is the aetiology of pusher syndrome?

A

Unknown but associated with lesions in posterolateral thalamus

70
Q

How is pusher syndrome assessed?

A

4 point pusher score 0-3, no pushing to severe
Scale of Contraversive Pushing, measure posture, extension and resistance in sitting and standing
Burke Lateropulsion scale, examines rolling, sitting, standing, transfers, walking

71
Q

How is pusher syndrome treated?

A

Keep vertical with feedback (visual, wall)
Reach beyond BOS

72
Q

What is apraxia?

A

Cognitive perceptual disorder with an inability to perform movement in response to verbal command,

73
Q

What are the two types of apraxia?

A

Ideomotor- problem in producing movement despite understanding motor programme
Ideational- recognize objects but cannot explain how to use them e.g. use object incorrectly

74
Q

What is the aetiology of apraxia?

A

Left hemisphere lesions

75
Q

How is apraxia treated?

A

Errorless training-elimination of incorrect or inappropriate responses

76
Q

What are some examples of behavioural interventions?

A
  • Operant conditioning, positive reinforcement
  • Focus on lifestyle change to prevent behaviours
77
Q

What is parkinsons disease?

A

Chronic neurodegenerative disease characterized by rigidity, hypokinesia and resting tremor, with a loss of dopamine producing cells

78
Q

How is PD commonly presented early on?

A

Resting tremor early clinical sign
Starts unilateral before progresses to bilateral

79
Q

What are some RFs for PD?

A

Age, history, head injury, exposure e.g. pesticides

80
Q

What is the role of the basal ganglia?

A

Automatic execution of motor programs
Simultaneous and complex movement
Planning and organizing movement

81
Q

What is the pathophysiology of PD?

A

Gradual loss of dopaminergic neurotransmitters in the substantia nigra, causing an imbalance in neurotransmitters

82
Q

What are the symptoms of PD?

A
  • Tremor
  • Rigidity
  • All kinesia (Hypo, Brady, A, Dys)
  • Postural Instability
83
Q

What is the difference between the kinesias of PD?

A

A- freezing
Hypo- reduced movement
Brady- slow movement
Dys- aberrant movements

84
Q

When does resting tremor change?

A

Stops with initiation of movement
Increases with emotion, stress, fatigue

85
Q

How is rigidity different from spasticity?

A

No clonus
Not velocity dependent

86
Q

How does levadopa dose affect falls risk?

A

Increased risk with increased dose

87
Q

What is characteristic of a PD pt gait?

A

Overall lack of movement
Reduced step length
Normal or increased cadence
Freezing especially at initiation

88
Q

How is PD most commonly pharmacologically treated?

A

Dopamine Replacement Therapy, Levadopa agents

89
Q

What are some outcome measures for PD?

A

TUG
10MWT
6MWT
Dynamic Gait Test
Berg Balance Test
Functional Reach
MiniBESTest

90
Q

How is PD often assessed?

A
  • Unified PD Rating Scale- impairments and activity lim
  • Hoen & Yahr Scale- staging scale, 1-5
  • Modified Parkinsons Activity Scale (M-PAS)- 18 activities incl. balance, gait, transfers
91
Q

How can falls self-efficacy be measured?

A

Falls Efficacy Scale
Activities specific Balance Confidence Scale

92
Q

What are some treatments for PD?

A
  • Resistance Training
  • Core Training
  • Education on falls, PA
  • Motor Skill Learning
  • Gait Training, cuing with floor markers, large arcs, clock turn
93
Q

What is the utricle and saccule?

A

Part of peripheral vestibular apparatus
U: detects horizontal movements
S: detects vertical movements

94
Q

What is the vestibuloocular reflex?

A

VOR, semicircular canals detect movement, sent to medial and lateral rectus muscles to stabilize on target

95
Q

What is VOR gain?

A

Ratio of eye movement to head movement
Velocity of eyes should be exactly opposite to velocity of head

96
Q

What happens when VOR gain is less than 1 (eyes slower than head)?

A

Patient complains of blurring

97
Q

What is the vestibulospinal reflex?

A

Protective extension of the limbs in response to head position changes

98
Q

What is the vestibulocolic reflex?

A

Acts on neck musculature to stabilize the head

99
Q

What are some secondary symptoms of vestibular dysfunction?

A

Fatigue
Concentration issues
Anxiety, depression, frustration
Reduced confidence

100
Q

What are the key questions of a vestibular subjective?

A
  • Characteristics of sensation
  • Onset
  • Duration of attacks
  • Associated symptoms
  • Exacerbating factors e.g. movement, diet
101
Q

What does nystagmus direction suggest about problem area?

A

Eyes beat to more neurally active side, left ear problem, right beating

102
Q

What is abnormal saccadic movement?

A

Cannot move eyes quickly from one point to another or accurately

103
Q

What are contraindications for Dix-Hallpike?

A
  • Neck surgery/trauma
  • RA
  • Myelopathy/radiculopathy
104
Q

How is BPPV diagnosed?

A

Positive Dix-Hallpike, upbeat torsional nystagmus and vertigo

105
Q

What is vestibular neuritis and its presentation?

A
  • Inflammation of vestibular nerve
  • Acute onset lasting hours to days
  • Hearing loss
  • Spontaneous horizontal nystagmus
  • Positive HIT, negative Dix-Hallpike
106
Q

How do you perform a skew deviation test?

A

Cover eye and have pt focus on nose
Uncover eye, see how eye realigns

107
Q

What HINTS results suggest central problem (e.g. stroke)

A
  • Direction changing nystagmus
  • Abnormal skew
  • Normal HIT
108
Q

How is Vestibular Neuritis treated?

A

Bed rest 24-48 h
Corticosteroids
Vestibular rehab

109
Q

What is Menieres Disease and how does it present?

A

Backed up fluid leads to swelling and pressure
- Episodic vertigo
- Hearing loss and tinnitus

110
Q

How is Meniere’s treated?

A

Diuretics and low salt intake to reduce fluid retention
Vestibular rehab

111
Q

What is acoustic neuroma and how does it present?

A

Benign tumour on vestibular nerve
- Unilateral hearing loss
- Tinnitus
- Disequilibrium

112
Q

How is acoustic neuroma treated?

A
  • Surgery
  • Vestibular rehab postsurge
113
Q

What is vestibular migraine and how does it present?

A

Migraine causing vertigo symptoms
- Episodic vertigo
- Photophobia

114
Q

What does vestibular rehab entail?

A

Gaze stability, habituation and balance and gait training to:
- Enhance gaze stability
- Enhance postural and gait stability
- Improve ADLs, fitness and feelings of dizziness

115
Q

What is the difference between gaze stability and habituation exercises?

A

GS: retrain VOR
H: Controlled exposure to provocative movement

116
Q

How does the sensory and motor tracts ascend/descend?

A

Dorsal Light Touch- ascend ipsilaterally
Spinothalamic Pain/Temp- ascend contralaterally
Lateral corticospinal Motor- descend ipsilaterally

117
Q

How does central cord syndrome present?

A
  • Incomplete injury
  • Compression, hypoxia and haemorrhage of central cord
  • UL > LL
  • Commonly hyperextension injury in fall
118
Q

How does Brown Sequard syndrome present?

A
  • Hemisection of cord
  • Ipsi motor/light touch
  • Contra pain and temp
  • Penetrating injury
119
Q

How does anterior cord syndrome present?

A
  • Often flexion injury
  • Altered motor, pain/temp, intact light touch
120
Q

How does cauda equina syndrome present?

A
  • Below L1
  • Flaccid paralysis
121
Q

What are the benefits and limitations of the ISNCSCI (ASIA)?

A

+ Predict outcomes, helps develop individualized rehab
- Exhaust pts, sensory is ordinal rather than quantitative

122
Q

How is ASIA scale measured?

A

A= complete, no sensory or motor in S4-5
B= Sensory incomplete, incomplete with sensory but not motor below neurological level
C= Motor incomplete, incomplete with motor function preserved below neurological level
D= Motor Incomplete, half of muscle function below neurological level being >3
E= Normal

123
Q

What is the zone of partial preservation?

A

ZPP- Only in complete injuries (S4-5), dermatomes and myotomes caudal to levels that remain partially innervated

124
Q

What is the difference between neurogenic and spinal shock?

A

NS- disruption to sympathetic activity and unopposed vagal tone (vasodilation, hypotension, bradycardia)
SS- temporary loss of reflexes, strength and sensation below lesion level

125
Q

What are some hospital considerations for SCI?

A
  • Respiratory muscle weakness (IMT, ventilation, abdominal binders)
  • Secretion clearance (manual assisted cough)
  • Supine to prevent paradoxical breathing
  • Pressure care
  • Bladder/bowel control
  • Pain management
126
Q

How does autonomic dysreflexia present?

A
  • Sudden hypertension
  • Headache
  • Bradycardia
  • Flushing
  • SOB
  • Blurred vision
127
Q

What does the literature say about interventions in paraplegic pts?

A
  • Weak for strength
  • Strong for cycling, sports and combined arm cranking/leg cycling for fitness
  • Strong for functional training
128
Q

What is the pathophysiology of GBS and its presentation?

A
  • Inflammatory demyelination and antibody mediated axonal damage
  • Ascending weakness, paraesthesia, pain
129
Q

What is drug therapy for GBS?

A

Plasmaphoresis- Blood removed and plasma substituted
IVIg

130
Q

How do you manage GBS?

A
  • Prevent cardioresp (NIV, ACT)
  • Maintain muscle length
  • Strength training, aerobic exercise
131
Q

What is the pathophysiology of MND?

A

Progressive degeneration of motor neurons

132
Q

What are the three phenotypes of MND?

A

ALS- Upper and lower, dysarthria, dysphagia, fatigue, asymmetrical weakness
Flail- only LMN signs, hyporeflexia, fasiculations (vibrate), weakness, atrophy
PLS- UMN, weakness, spasticity, hyperreflexia

133
Q

How is MND diagnosed?

A

UMN, LMN signs
Neurological tests to differentially diagnose

134
Q

How is MND managed?

A
  • Drugs for symptom management, cramps, pain, spasticity
  • Some evidence that exercise improves ALS function, prevents secondary impairments