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DPT 620: Neuro > Movement Disorders > Flashcards

Movement Disorders Flashcards

1
Q

what is the definition of a movement disorder?

A

neurological syndromes in which there’s excess movement (hyperkinesia) or a paucity of voluntary/involuntary movement (hypokinesia) unrelated to weakness or spasticity

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2
Q

movement disorders are typically linked to what two areas of the brain?

A

BG and cerebellum

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3
Q

what is the location of the BG?

A

subcortical

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4
Q

what is the location of the cerebellum?

A

subcortical

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5
Q

what is the role of the BG? what would a lesion cause?

A

the role of the BG is motor control

a lesion to the BG would cause movt disorder

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6
Q

what is the role of the cerebellum? what would a lesion cause?

A

the role of the cerebellum is motor control

a lesion to the cerebellum would cause movt disorder

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7
Q

the BG is part of the ____ system

A

motor

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8
Q

the cerebellum is part of the ____ system

A

motor

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9
Q

does the BG have any direct connections to the SC?

A

nope

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10
Q

does the cerebellum have any direct connections to the SC?

A

nope again

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11
Q

would a unilateral lesion to the BG cause contralateral or ipsilateral symptoms?

A

contralateral

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12
Q

would a unilateral lesion to the cerebellum cause contralateral or ipsilateral symptoms?

A

ipsilateral

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13
Q

what are the BG effects on tone?

A

rigidity

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14
Q

what are the cerebellar effects on tone?

A

hypotonia

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15
Q

what are the BG effects on movt?

A

decreased movt: bradykinesia, hypokinesia, akinesia

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16
Q

what are the cerebellar effects on movt?

A

increased movt: ataxia, dysmetria, dysdiadochokinesia

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17
Q

what is the umbrella term for hypokinetic conditions that present w/tremors, bradykinesia, postural instability, rigidity?

A

parkinsonism

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18
Q

what conditions are included under the umbrella term parkinsonism?

A

idiopathic PD

secondary parkinsonism

atypical Parkinson’s (PD+)

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19
Q

what conditions fall under PD+?

A

MSA (multiple systems atrophy)

PSP (progressive supranuclear palsy)

CBD (corticobasal degeneration)

LBD (Lewy body dementia)

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20
Q

what part of the brain is impacted by PD?

A

the BG, specifically the substantia nigra

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21
Q

what does TRAP stand for?

A

Tremors

Rigidity

Akinesia

Postural instability

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22
Q

how is PD often diagnosed?

A

through observation and response to Levodopa

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23
Q

what is the most common med to treat PD?

A

Sinemet (carbadopa/Levodopa)

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24
Q

what are the 3 motor loop pathways required for normal functioning?

A

hyperdirect (stop) pathway

“go” pathway

“no-go” pathway

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25
Q

which pathway DIRECTLY allows movt to occur?

A

the “go” pathway

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26
Q

which pathway INDIRECTLY stops unwanted movt from occuring?

A

the “no-go” pathway

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27
Q

t/f: normal movt requires normal activity in all 3 motor pathways

A

true

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28
Q

BG disorders affect the ____ of the fxn of the 3 motor pathways

A

balance

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29
Q

what are the consequences of degradation of the D1 receptor of the SNc?

A

loss of dopamine reduces the activity of the motor areas of the thalamus, resulting in decreased voluntary movt

increased inhibition of the PPN disinhibited the reticulospinal tracts, producing excessive contraction of postural muscles and rigidity

increased inhibition of the MLR reduces its activity and decreased out to the SPGs resulting in freezing and destination of gait

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30
Q

idiopathic PD is more common in males or females?

A

males

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31
Q

what is the fastest growing neurodegenerative disease?

A

idiopathic PD

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32
Q

what are the primary impairments in PD?

A

Tremor
Rigidity
Akinesia
Postural instability gait dysfunction (PIGD)

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33
Q

tremors occur in what % of those with PD?

A

70%

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34
Q

what is akathisia?

A

inability to remain still

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35
Q

what types of rigidity are common in PD?

A

cogwheel and lead pipe

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36
Q

what is rigidity?

A

involuntary increase in muscle tone to PROM

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37
Q

what is bradykinesia/hypokinesia/ akinesia?

A

decreased movt speed, amplitude leads to cessation/freezing of movt

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38
Q

what is the risk with postural instability gait dysfunction?

A

decreased postural stability can lead to falls

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39
Q

t/f: PD is usually a dx of exclusion

A

true

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40
Q

t/f: there is a diagnostic test that can ID PD w/o additional evaluation of medical hx and neuro exam

A

false

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41
Q

a formal dx of PD must include ____ as a notable symptom

A

bradykinesia

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42
Q

PD dx must include bradykinesia in addition to one or more of what 3 symptoms?

A

resting tremor

rigidity of arm, leg, or trunk

trouble with balance or falls

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43
Q

what tests can be included in PD dx?

A

DAT (dopamine transporter) scan

genetic testing

alpha-synuclein test

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44
Q

what is a dopamine transporter (DAT) scan?

A

an approved imaging technique for distinguishing essential tremor from PD

detects dopamine deficits w/in the substantia nigra

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45
Q

t/f: DAT scan is NOT commonly used in isolation for dx of PD

A

true

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46
Q

t/f: PD is linked to a gene that guarantees development of PD

A

false, PD is NOT linked to a single gene that guarantees development of PD s/s

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47
Q

t/f: genetic testing may help estimate risks of developing PD, however not diagnostics

A

true

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48
Q

what is alpha synuclein?

A

a presynaptic neuronal enzyme

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49
Q

what is an alpha synuclein test?

A

a test that can detect clumps of alpha-synuclein in the CSF to dx PD

can detect symptoms of PD b4 they appear

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50
Q

t/f: the alpha-synuclein test is diagnostic on its own

A

false

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51
Q

what is the UPDRS?

A

a tool for evaluation of interventions in PD that may be used at baseline during initial dx to evaluate progress and response to meds

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52
Q

what are the 4 subsections of the UPDRS?

A

1) mentation, behavior, mood

2) ADLs

3) motor manifestations

4) complications of therapy

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53
Q

the UPDRS is used in what settings primarily?

A

in the physicians office

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54
Q

what are the meds used to treat PD?

A

Levodopa and dopamine agonists (Sinemet and Pramipexol)

COMT inhibitor

MAO-B inhibitor (Rasagiline)

rescue meds (injection or inhalation powder)

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55
Q

what is the gold standard for treating PD?

A

Levodopa

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56
Q

t/f: Levodopa is a precursor to dopamine and can cross the blood barrier

A

true

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57
Q

what % of PWPD suffer from motor complications, fluctuation, and/or dyskinesias after 5 years of treatment

A

about 50%

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58
Q

long term use of Levodopa and/or progression of PD can lead to what?

A

“off” time at which symptoms occur most commonly bw doses

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59
Q

what are the side effects of levodopa?

A

motor complications

neuropsychiatric disturbances

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60
Q

what are the motor complications associated with Levodopa?

A

dyskinesias

dystonias

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61
Q

do dykinesias or dystonias result from too much meds?

A

dyskinesias

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62
Q

do dykinesias or dystonias result from not enough meds?

A

dystonias

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63
Q

what is dyskinesia?

A

faster, more rhythmic movts

uncontrolled involuntary movt that may be present as fidgeting, writhing, wriggling, head bobbing, or body swaying

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64
Q

what is dystonia?

A

painful involuntary muscle contractions that force the body into abnormal postures (ie toe curling)

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65
Q

what are the neuropsychiatric disturbances associated with Levodopa use?

A

hallucinations

psychosis

confusion

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66
Q

t/f: the longer someone is on Levodopa, the smaller the therapeutic window gets

A

true

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67
Q

what is an invasive treatment option for PD?

A

deep brain stimulation

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68
Q

what is a non-invasive treatment option for PD?

A

focused US

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69
Q

what is deep brain stimulation?

A

electrodes are placed in the subthalamic nucleus (STN) or globus pallidus internal (GPi) and connected to a neurostimulator inferior to the clavicle

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70
Q

t/f: DBS can reduce/control rigidity, bradykinesia, tremor, and dyskinesia

A

true

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71
Q

who are candidates for DBS?

A

those who respond to Levodopa/carbadopa

those with PD dx<5 years

those with severe motor impairments/fluctuations

those with significant issues of “off” times

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72
Q

t/f: pt satisfaction with DBS is high

A

true

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73
Q

are the effects of DBS fast or slow?

A

slow

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74
Q

t/f: the electrodes in DBS can be turned on/off

A

true

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75
Q

what is focused US?

A

MRI used to direct US to target brain location typically to decrease motor symptoms immediately

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76
Q

does focused US typically work fast or slow?

A

fast

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77
Q

t/f: DBS is irreversible and permanent

A

true

78
Q

is focused US used for one or both sides of the brain at a time?

A

one side at a time

79
Q

t/f: focused US only helps motor symptoms on one side of the body

A

true

80
Q

what are the side effects of focused US?

A

numbness/tingling, unsteadiness, gait dysfunctions, muscle weakness, speech abnormalities

81
Q

what is Hoehn and Yahr stage 1 PD?

A

one side of the body is effected

82
Q

what is Hoehn and Yahr stage 2 PD?

A

both sides affected but balance remains intact

83
Q

what is Hoehn and Yahr stage 3 PD?

A

impaired balance, fxning intact

84
Q

what is Hoehn and Yahr stage 4 PD?

A

walking and standing are difficult without help

85
Q

what is Hoehn and Yahr stage 5 PD?

A

WC bound or bed-ridden

86
Q

what are the motor impairments of PD?

A

bradykinesia

limited facial expressions (facial masking)

speech deficits (soft and monotone, slow/fast speech, poor awareness of volume)

tremor

micrographia (small writing)

visual impairments

swallowing deficits (often leads to drooling)

rigidity

dystonia

postural instability, ankle PF, toe curling

87
Q

t/f: the pt isn’t always aware of their deficits in PD

A

true

88
Q

when does facial rigidity usually start?

A

stage 4

89
Q

what are the 3 components of balance?

A

visual, vestibular, and somatosensory

90
Q

is anticipatory balance feedback or feedforward?

A

feedforward

91
Q

is reactive balance feedback or feedforward?

A

feedback

92
Q

what is a good test for reactive and anticipatory balance in PD?

A

miniBEST

93
Q

what are the balance deficits in PD?

A

decreased postural extension and awareness

decreased unconscious proprioception

decreased arm swing and trunk rotation

poor anticipatory and reactive postural responses

retropulsion

requires more steps to recover from a loss of balance

94
Q

why is there poor anticipatory and reactive postural control in PD?

A

inadequate “go” pathway

95
Q

what are the gait dysfunctions associated with PD?

A

freezing of gait (FoG)

destination of gait (FSG)

retropulsion

96
Q

what is freezing of gait (FoG)?

A

absence/marked reduction of forward progression despite intention to walk

difficulty adjusting the speed or size of steps quickly enough to changing environment

97
Q

t/f: FoG makes pts more likely to fall

A

true

98
Q

when does FoG typically occur?

A

doorways, crowds, small spaces, w/turns, w/distractions/dual-tasking

standing and trying to initiate steps immediately

trying to step with weight still on the forefoot

99
Q

what is festination of gait (FSG)?

A

gait with increased step cadence

100
Q

when does festination of gait (FSG) typically occur?

A

with complex motor tasks and dual tasking

when reaching too far outside of BOS

with increased flexed posture

after being told to “hurry up”

when reaching for a chair too soon b4 sitting

101
Q

what is retropulsion?

A

involuntary steps backwards

102
Q

what typically trigger retropulsion?

A

posterior weight shift or LOB (loss of balance)

103
Q

when does retropulsion have a tendency to occur?

A

during “off” times

104
Q

will neurogenic OH respond to hydration, position change, and muscle activation?

A

nope, you have to adjust meds

105
Q

what are the mental impairments associated with PD?

A

mood disorders, depression, anxiety, psychosis, dementia, apathy, impaired executive functioning and attention, bradyphrenia (slow processing)

106
Q

what are the sensory functions associated with PD?

A

olfactory impairments (anosmia)

pain

paresthesia

107
Q

why are olfactory functions effected in PD?

A

bc olfactory cells have dopaminergic neurons

108
Q

what is one of the most limiting non-motor effects of PD for PTs?

A

OH (CV or neurogenic)

109
Q

what are the genitourinary and reproductive problems associated with PD?

A

urinary problems and constipation

110
Q

what are the issues with functions of skin and related structures associated with PD?

A

restless leg syndrome

excessive sweating

sleep disturbances

111
Q

what are the clinical considerations for PD?

A

reduced ROM, endurance, and strength

poor posture

muscle atrophy

neurogenic orthostasis

on/off times

freezing

falls/fear of falls

112
Q

OH is drop in SBP > ___ mmHg or DBP >___ mmHg

A

20, 10

113
Q

t/f: progression of PD should be slow and fast progression is a sign of PD+

A

true

114
Q

what are the progression risks that make us think of PD+ rather than PD?

A

rapid progression of gait impairment, requiring WC w/in 5 years of onset

poor/absent response to dopaminergic therapy

early bulbar dysfunction (<5 years after onset)

inspiratory respiratory dysfxn (stridor, frequent sighs)

severe autonomic failure )<5 years after onset)

recurrent (>1/year) falls from imbalance w/in 3 yrs of onset

anterocollis (flexed forward head) or limb contractures within 10 years of onset

absences of common non-motor features (sleep dysfxn, RBD/PLMS, daytime somnelence, autonomic dysfxn, hyposmia, mood disturbances)

otherwise unexplained pyramidal tract signs (Babinski, hyperreflexia, hypertonia)

BL symmetric parkinsonism

115
Q

would PD or PD+ have limited response to dopamine therapy?

A

PD+

116
Q

is PD or PD+ more likely to start BL?

A

PD+

117
Q

is PD or PD+ more likely to have psych involvement?

A

PD+

118
Q

which has a more rapid progression, PD or PD+?

A

PD+

119
Q

what are the symptoms of Parkinson’s type MSA (MSA-P)?

A

bradykinesia

tremors

impaired balance

autonomic NS dysfxn

120
Q

what are the symptoms of cerebellar type MSA (MSA-C)?

A

nystagmus

trunk and limb ataxia

gait ataxia

ataxic dysarthria

dysphagia

respiratory impairment

121
Q

what are the corticospinal (pyramidal) signs of PD+?

A

pisa syndrome (excessive leaning to one side)

anterocollis (flexed forward head) or limb contractures

(+) Babinski sign

spasticity

stridor

122
Q

what are the autonomic dysfxns associated with PD+?

A

unexplained difficulty voiding and/or urge urinary incontinence

neurogenic OH

123
Q

what is MSA?

A

multiple systems atrophy

degradation of multiple areas of the brain

124
Q

what is the life expectancy of MSA following dx?

A

7-9 years

125
Q

when is the average age of onset of MSA?

A

40s-50s

126
Q

what is corticobasal ganglionic degeneration (CBD)?

A

frontotemporal disorder

tauopathy

127
Q

what is a frontotemporal disorder?

A

degeneration of the frontal and temporal lobes

128
Q

what is a tauopathy?

A

accumulation of Tau proteins in the brain

129
Q

what are the symptoms of CBD?

A

dystonias (UE>LE or cervical)

myoclonus

limb apraxia (ideomotor)

aphasia

alien limb syndrome

bradykinesia, limb rigidity, postural instability, tremors

personality changes and inappropriate behavior in later stages

130
Q

are males or females more affected by CBD?

A

females

131
Q

what is the average age of onset of CBD?

A

40-70 yo

132
Q

what is the life expectancy of CBD after dx?

A

6-8 years

133
Q

what is progressive supranuclear palsy (PSP)?

A

frontotemporal disorder

tauopathy

134
Q

what are the 4 fxnal domains of PSP?

A

1) oculomotor dysfxn

2) postural instability

3) akinesia

4) cognitive dysfxn

135
Q

what is the oculomotor dysfxn associated with PSP?

A

slow eye movt

vertical supranuclear gaze palsy

136
Q

bc pts with PSP can’t move their eyes themselves up/down what may we see?

A

compensation by moving the entire head

137
Q

what fxnal task is often difficult for pts with PSP?

A

stairs

138
Q

what are the postural instabilities associated with PSP?

A

spontaneous loss of balance and falls

retropulsion

139
Q

what are additional key symptoms of PSP?

A

blepharospasm (involuntary blinking/twitching of the eyelids) and eyelid opening apraxia

early onset of falling (PSP>MSA)

early onset dysphagia and dysarthria

140
Q

are more males or females affected by PSP?

A

males

141
Q

what is the life expectancy after onset of PSP?

A

6-9 years

142
Q

what is Lewy body dementia?

A

PD like symptoms following dementia symptoms

143
Q

what are the PD-like symptoms in Lewy body dementia?

A

bradykinesia, rigidity/stiffness, shuffling gait, tremors

144
Q

what are the cognitive changes in Lewy body dementia?

A

dementia (b4 onset of PD symptoms)

fluctuations w/concentration, alertness, attention, and wakefulness

145
Q

what are the autonomic dysnfxns associated with Lewy body dementia?

A

temp and BP irrregulation

urinary incontinence

constipation

sexual dysnfxn

146
Q

what are the behavioral changes associated with Lewy body dementia?

A

hallucinations

delusion

mood changes (anxiety, depression, apathy)

147
Q

what are the sleep disorder associated with Lewy body dementia?

A

REM sleep behavior disorders

excessive daytime sleepiness

insomnia

restless leg syndrome

148
Q

what are the chances associated with Lewy body dementia?

A

cognitive changes

movt changes

autonomic changes

behavioral changes

sleep disorders

149
Q

hallucinations, agitation, and dementia symptoms b4 PD symptoms are Hallmark signs of what?

A

Lewy body dementia

150
Q

what is the life expectancy of pts with Lewy body dementia after onset?

A

2-9 yrs

151
Q

what % of people with dementia have Lewy body dementia?

A

5%

152
Q

t/f: hyperkinetic disorders results from an overactive go pathway

A

true

153
Q

in hyperkinetic disorders the GPi is ….

A

less inhibited

154
Q

bc the GPi is less inhibited in hyperkinetic disorders, the motor thalamus is…

A

more facilitated

155
Q

what is the result of the GPi being less inhibited and the motor thalamus being more facilitated?

A

involuntary movt

156
Q

in hyperkinetic disorders, the corticospinal tracts are …

A

more facilitated

157
Q

what is the result of the corticospinal tracts being more facilitated?

A

increased involuntary movt (hyperkinesia like dyskinesia, chorea)

158
Q

in hyperkinetic disorders, the PPN is…

A

less inhibited

159
Q

in hyperkinetic disorders, bc the PPN is less inhibited, the reticulospinal tracts are …

A

more inhibited

160
Q

what is the result of inhibited reticulospinal tracts?

A

decreased activation (stability) or the trunk

161
Q

are dystonias intermittent or continuous?

A

can be either

162
Q

what are the types of dystonias?

A

focal

segmental

primary/isolated

secondary/acquired

paroxysmal

functional

163
Q

are dystonias often seen as a secondary incidence or an isolated/primary issue?

A

secondary

164
Q

what are common types of dyskinesias?

A

athetosis

chorea

myoclonus

Levodopa induced dyskinesia (LID)

ballism

165
Q

dyskinesias are often seen in what two diseases?

A

HD and MS

166
Q

what is Huntington’s disease (HD)?

A

an inherited autosomal dominant condition that results in degeneration of the caudate nucleus and putamen of the BG

167
Q

what are the motor symptoms of HD?

A

chorea

dystonia

bradykinesia/akinesia

motor impersistance (inability to stay still)

difficulty performing RAMs (rapid eye movts)

difficulty sequencing movt

168
Q

what are the psychiatric symptoms of HD?

A

depression

anxiety

169
Q

what are the cognitive symptoms of HD?

A

memory loss

executive fxn issues

verbal fluency issues

slowed info processing

170
Q

what are the cardiac symptoms of HD?

A

bradycardia

elevated BP

cardiac arrhythmias

HF

171
Q

is PD primarily a mobility or stability problem?

A

mobility problem

172
Q

is HD primarily a mobility or stability problem?

A

stability problem

173
Q

t/f: the UPDRS is a good way to document info and use the language of the neurologist so they will easily understand and quantify the severity of the disease

A

true

174
Q

individuals with HD have an average survival of how many years following onset of symptoms

A

15-20 years

175
Q

how old are pts usually when they are diagnosed with HD?

A

30-50 yo

176
Q

what is the prevalence of HD?

A

about 4.1-8.4 per 100,000 individuals in the US

177
Q

what are the 5 stages of HD?

A

preclinical stage

early stage

middle stage

late stage

end-of-life stage

178
Q

what stage of HD is characterized by mild symptoms, but no dx of HD from the doctor?

A

pre-clinical stage

179
Q

what stage of HD is characterized by symptoms becoming noticeable enough for diagnosis?

A

early stage

180
Q

what stage of HD is characterized by individuals being unable to carry out most activities on their own?

A

middle stage

181
Q

what stage of HD is characterized by pts requiring assistance in all areas of life and becoming bedridden?

A

late stage

182
Q

what stage of HD is characterized by pts becoming confined to bed completely and dependent on others for all their activities, needing help to live the last few months/years of their life peacefully and in the best way they can?

A

end-of-life stage

183
Q

what are the super 6 tests and measures?

A

6MWT

Berg

5xSTS

FGA

gait speed

ABC

184
Q

what is the MDC for the 6MWT?

A

82 m

185
Q

what is the MDC for the Berg?

A

5 points

186
Q

what is the MDC for the 5xSTS?

A

.6 sec

187
Q

what is the MDC for the FGA?

A

4 points

188
Q

what is the MDC for gait speed?

A

.18 m/s

189
Q

what is the MDC for the ABC?

A

13

190
Q

t/f: PD and HD have a multisystem presentation involving motor, non-motor, and secondary impairments

A

true

DPT 620: Neuro (12 decks)

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