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7 Neuro Dysfunction > L5 Movement Disorders > Flashcards

L5 Movement Disorders Flashcards

1
Q

Movement Disorders

A

neurological conditions characterized by an excess of movement or paucity of voluntary movement unrelated weakness or spasticity

fall into hyperkinetic and hypokinetic

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2
Q

Dyskinesia

A

uncontrolled, involuntary movement that occur in pts with movement disorders

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3
Q

Types of dyskinesia

A

dystonia
athetosis
chorea
ballismus
tic
myoclonus
tremor

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4
Q

Hypokinetic movement disorders

A
  • movement are difficult to initiate
  • slow and rigid
  • ex: parkinson’s disease
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5
Q

Hyperkinetic Movement Disorders

A
  • movements are dancelike and involuntary
  • includes huntington’s disease, hemiballismus
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6
Q

Athetosis

A
  • writhing, twisting movements of limbs, face, trunk
  • caused by basal ganglia diseases and stroke
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7
Q

Chorea

A
  • nearly continuous involuntary movements that are fluid or jerky
  • can be small or large amplitude
  • caused by huntington’s disease, side effect of levodopa
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8
Q

Choreoathetosis

A

blend of athetosis and chorea

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9
Q

Ballismus

A
  • large amplitude, more rotatory, or flinging quality than chorea
  • most common type is hemballismus/unilateral
  • caused by infarct of subthalamic nucleus/basal ganglia
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10
Q

Tic

A
  • sudden brief action that is usually preceded by an urge to perform it and is followed by sense of relief
  • includes motor and vocal tics
  • example: tourette’s syndrome
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11
Q

Myoclonus

A
  • sudden, rapid, muscular jerk
  • can be focal, unilateral, bilateral
  • caused by anoxic brain injury, encephalitis, toxic or metabolic encephalopathies in severely ill patients
  • common in end stage renal or liver disease
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12
Q

Tremor

A
  • rhythmic or semirhythmic oscillating movements
  • both agonist and antagonist muscles are activated resulting in bidirectional movements
  • can be slow or fast
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13
Q

Types of tremors

A
  • resting tremor (PD)
  • postural tremor (PD, cerebellar, metabolic)
  • intention tremor (cerebellar)
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14
Q

Dystonia

A
  • co-contraction of agonist and antagonist muscles causing distorted positions of the affected body part during voluntary movement
  • can be generalized, unilateral, focal
  • exact pahtophys is unknown, current hypothesis is disorder of brain networks
  • multiple causes, adult onset
  • examples includes torticollis, writer’s cramp, musician’s cramp
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15
Q

Types of dystonia

A
  • cervical (most common)
  • blepharospasm (eye twitch)
  • limb
  • musician’s
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16
Q

Medical treatment for dystonia

A
  • focal dystonia treated with botox
  • general dystonia treated with anticholinergic medications
  • DBS
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17
Q

Outcome measures for Dystonia

A
  • unified dystonia rating scale
  • global dystonia scale
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18
Q

Huntington’s Disease prevalence

A
  • inherited autosomal dominant neurodegenerative disease
  • caused by huntington gene mutation
  • 4-5 cases/100,000
  • average onset is 30-50 yo
  • no cure, medial survival is 15 years
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19
Q

Huntington’s overview

A
  • gradual onset of defects in behavior, cognition, movement beginning in 4th to 5th decade
  • presents as alteration in mood or change in personality like impulsive behavior, irritability, suspiciousness
  • hallmark is movement disorder consisting of rapid, jerky, no clear purpose
20
Q

Huntington’s Disease Pathophys

A
  • selective atrophy in caudate and putamen, atrophy in frontal and temporal cortex
  • degeneration of spiny neurons
  • decreased inhibition to GPe leads to greater inhibition of GPe on STN
  • inhibition on STN makes it less able to excite GPi, resulting in less tonic inhibition from GPi
21
Q

CP of Huntington’s

A

Abnormalities of
* motor s/s
* oculomotor s/s
* mood dysfunction
* cognition

22
Q

Motor s/s of HD

A
  • early in disease clumsiness, mild jerking, fidgety movements
  • as disease progresses, movements become more dance-like
  • no weakness, ataxia, or deficit of sensory function
23
Q

Oculomotor S/S of HD

A

slow saccades
impaired smooth pursuit

24
Q

Mood dysfunction S/S of HD

A

depression
irritability or aggression

25
Q

Cognition S/S of HD

A

depression and anxiety
OCD
impulsive, manic behavior
late stage severe dementia

26
Q

Presymptomatic/early stage of HD

A
  • presents with chorea, impaired balance, fine motor problems, unsteady gait
  • PTs should do exercise, balance training, environmental mods
  • main goal of PT is to delay onset of mobility problems
27
Q

Middle Stage of HD

A
  • presents as chorea, joint ROM limitations, weak stabilizers, falls
  • PTs should do strengthening, ROM, functional training, fall prevention
  • main goal of PT is maintain function and delay decline
28
Q

Late Stage of HD

A
  • presents as postural changes, respiratory limitations, risk for pneumonia
  • PTs should do exercises for ROM, postural alignment, chest PT, seating systems
  • main goal of PT is limit impact of complications
29
Q

Functional Neurologic Disorder

A
  • involuntary but learnt habitual movement pattern driven by abnormal self-directed attention
  • triggered by physical or pyscho events
  • brain prioritizes excessively strong predictions based on what the brain expects to see or be able to do over the actual incoming sensory input
30
Q

Pathophys and etiology of FND

A

not only the occurrence of stressful events and elevation of biological stress markers, but addition of greater perceived stress and/or lack of awareness of this stress that appears to contribute to and result from the underlying pathophys

31
Q

5 constructs affected in FND

A
  • emotion processing, such as salience
  • agency
  • attention
  • interoception
  • predictive processing/interference
32
Q

Emotion Processing in FND

A
  • one of the core features
  • evidence supports increased emotional reactivity, heightened arousal and avoidance, impaired top-down emotion regulation, deficits in emotional awareness, errant activation of learned/innate defensive responses
33
Q

Agency

A
  • two events must occur for agency : person must have the sense of willing the movement, movement has to happen
  • feedforward has to meet feedback
  • this matching of signals occurs in the right TPJ.
  • TPJ becomes activated when tehre is a mistmatch between wiling and movement
34
Q

Attention

A
  • impairment in attention has been characterized in FND
  • manifests as attentional perservation, which is tendency to focus on a partciular physiological system to neglect of other systems and impaired ability to adaptively, volitionally shift attentionIn
35
Q

Interoception

A
  • process by which nervous system senses, interprets, integrates internal bodily signals, providing a moment by moment mapping of body’s internal landscape across conscious and unconscious levels
  • FND may preferentially influence the weighting of top-down or bottom-up information streams in the CNS
  • leads to abnormally enhanced or diminished sensory perceptions or movements
36
Q

Perceptual Inference and Predictive Processing

A
  • the process by which a person generates beliefs or explanations about the causes and effects of events occurring within and outside the body
  • potential overutilization of the prediction rather than reliance on sensory information to update predictive model
37
Q

How is FND diagnosed?

A

Hoover’s sign
Hip abductor sign
distraction or entrainment of a tremor

38
Q

Hoover’s sign

A

weakness of hip extension which returns to normal with contralateral hip flexion against resistance

39
Q

Hip abductor sign

A

weakness of hip abduction which returns to normal with contralateral hip abduction against resistance

40
Q

Distraction or entrainment of a tremor

A

abolishing tremor by asking the patient to copy rhythmical movements or generate ballistic movements with contralateral limb

41
Q

Subjective exam for FND

A
  • ask to know full range of symptoms
  • describe a typical day
  • ask about onset and disease course
  • ask about triggers
  • patient’s understanding of disease
  • functional outcome measure
42
Q

Treatment for FND

A
  • neurologist
  • OT
  • PT
  • SLP
  • psychiatry
43
Q

PT for FND

A

PT has an important role in normalizing illness beliefs reducing abnormal self-directed attention and breaking down learnt patterns of abnormal movement. use:

  1. education
  2. demonstration that normal movement can occur
  3. retraining movement with diverted attention
  4. changing maladaptive behaviors related to s/s
44
Q

Critical outcomes of explanation which appear to facilitate PT for FND patients…

A
  • an understanding by pt that their treating health professionals accept that they have genuine problem
  • understanding by pt that they have a problem which has potential for reversibility and thus PT can help
45
Q

Who can benefit from PT with FND

A
  1. unambiguous diagnosis of FMD
  2. pt has confidence or openness to diagnosis of FMD
  3. pt desires improvement and can identify treatment goals
46
Q

Treatment for FND in PT

A
  • retraining movement w/diverted attention
  • minimize self-focused attention through distraction
  • non-specific and graded exercise
  • visualization or external focus of attention, mirrors
  • graded sensory stimulation
  • introducing role of PT in retraining in nervous system
  • explanation that wide variety of factors may be involved in triggering s/s
  • explanation of diagnosis
  • explanation of possible improvement
  • acknowledging s/s are real, build trust
47
Q

Best to do PT in…

A
  • optimum setting
  • treatment duration and parameters are unknown, will vary on intensity on pts s/s and ability to limit environmental triggers

7 Neuro Dysfunction (7 decks)

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