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BMB Test 2 > B7.037 Motor Control Systems > Flashcards

B7.037 Motor Control Systems Flashcards

1
Q

major descending motor systems

A

corticospinal

corticobulbar

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2
Q

2 motor control systems

A 
basal ganglia (magnitude)
cerebellar (correction)
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3
Q

function of motor control systems

A

modulate outputs of corticospinal and corticobulbar systems
NO direct motor outputs
modulation via the thalamus

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4
Q

features of akinetic rigid syndrome

A 
slowness of movement (bradykinesia)
velocity independent increased tone (rigidity)
postural instability
rest tremor
bilateral, mildly asymmetrical
chronic
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5
Q

movement disorders

A

a group of disorders affecting the ability to produce and prevent movement
difficulty not caused by weakness

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6
Q

hypo-kinetic movement

A

move too little
akinetic-rigid syndromes
parkinsonism

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7
Q

hyperkinetic movement

A

move too much

abnormal involuntary movements

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8
Q

primary clinical signs of parkinsonism

A

bradykinesia/akinesia
increased tone: rigidity
postural instability

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9
Q

general orientation of basal ganglia system

A

follows lateral ventricles

subcortical gray structure (contains a lot of neurons)

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10
Q

components of the basal ganglia

A 
striatum:
-caudate
-putamen
globus pallidus
-interna
-externa
subthalamic nucleus
substantia nigra
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11
Q

major inputs of basal ganglia

A

cortico-striate

from cortex into either caudate or putamen portion of striatum (both work as one unit)

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12
Q

major output of basal ganglia

A

globus pallidus interna

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13
Q

direct path in basal ganglia

A

cortex > striatum > GPi > thalamus

inhibitory to thalamus (decreases magnitude of movement)

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14
Q

indirect path in basal ganglia

A

cortex > striatum > GPe > subthalamic nucleus > GPi > thalamus
path through subthalamic nucleus increases inhibitory effect even more (upregulates pathway which downregulates movement)

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15
Q

how is the basal ganglia system modulated

A

through the substantia nigra (dopaminergic)

input from the substantia nigra inhibits output from the GPi, leading to more movement

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16
Q

more dopaminergic activity

A

more modulation from substantia nigra
less output from GPi
more movement

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17
Q

less dopaminergic activity

A

less modulation from substantia nigra
more output from GPi
less movement

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18
Q

type of neurotransmission from GPi to thalamus

A

GABA = inhibitory

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19
Q

type of neurotransmission from subthalamic nucleus to GPi

A

glutamate = excitatory

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20
Q

hypokinetic movement disorders etiology

A

too much GPi activity (more inhibitory)

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21
Q

hyperkinetic movement disorders etiology

A

too little GPi activity (less inhibition)

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22
Q

types of conditions that cause parkinsonism

A 
Parkinson's Disease - most common 
drugs
vascular
encephalitis
multi systems atrophy
toxins (MPTP, MN, CO)
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23
Q

brain pathology of Parkinson’s disease

A

idiopathic neurodegenerative disease of the substantia nigra
less dopaminergic input to the striatum
more output from the GPi, more inhibition of the thalamus
not enough movement

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24
Q

clinical features of Parkinson’s

A

rest tremor, rigidity, bradykinesia and postural instability in later stages of disease
autonomic dysfunction
neuropsychiatric disturbances

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25
epidemiology of parkinson's
1 mil in US 0.3% of US population (3% of people over 65 and 10% over 80) 50,000-60,000 new diagnoses per year
26
age of onset of Parkinson's
typically between 40-70 - avg is 60 - 4-10% before 40
27
risk factors for Parkinson's
``` increasing age family history male gender Caucasian environmental (chemical based industries) ```
28
genetic causes of parkinsons
uncommon for parkinson's to be an inherited form a-synuclein parkin UCH-L1
29
autonomic manifestations of parkinson's
``` orthostatic hypotension constipation dysphagia heartburn excessive sweating, heat intolerance urinary disturbances male sexual dysfunction ```
30
cognitive manifestations of Parkinson's
apathy dysexecutive dementia (15-40%)
31
cortical targets of the basal ganglia
limbic channel - apathy oculomotor channel - hypsometric saccades prefrontal channel - dysexecutive motor channel - akinesia
32
current method of pharmacotherapy for Parkinson's
repair the dopamine deficiency
33
pharmacotherapeutic options
Levodopa MAO-B inhibitors dopamine agonists COMT inhibitors
34
how does levodopa work
crosses the BBB and is converted to dopamine in remaining neurons in the substantia nigra can be stored as well
35
combo therapy with levodopa
carbidopa used to block peripheral decarboxylase peripheral decarboxylase breaks down levodopa outside of CNS, blocking this allows levodopa to be used in smaller doses to decrease adverse effects (nausea and vomiting)
36
efficacy of levodopa
most effective agent | if patients don't improve, they probably don't have parkinson's
37
pharmacokinetics of carbidopa/levodopa
half life is 90 min 5-10% enters brain w carbidopa immediate and extended release options available
38
long term complications of levodopa
``` motor fluctuations -wearing off phenomenon -on/off phenomenon dyskinesia (overshooting) -chorea -dystonia ```
39
why are there long term complications of levodopa
short half life | decreasing ability of nigral neurons to store dopamine over time (remaining cells still dying away as time progresses)
40
mechanism of action of MAO-B and COMT inhibitors
MAO-B and COMT break dopamine down into biproducts | inhibiting these makes dopamine's effects last longer
41
MAO-B inhibitors
selegiline & rasagiline - minimal effect when used alone - reduces motor fluctuations and increases on time as an adjunct to levodopa
42
COMT inhibitors
entacapone & tolcapone extends half life of levodopa from 1.5 to 2.5 hours no role as monotherapy no
43
function of dopamine agonists in Parkinson's
stimulate postsynaptic dopamine receptors directly do not require metabolic conversion half life longer than levodopa
44
indication for dopamine agonists
initial monotherapy or as an adjunct to levodopa (after motor fluctuations begin)
45
effectiveness of dopamine agonists
effective for tremor, bradykinesia, and rigidity | not as effective for motor symptoms as levodopa
46
dopamine agonists
pramipexole | ropinirole
47
targets of deep brain stimulation in parkinson's
subthalamic nucleus or GPi | stimulation shuts off these areas briefly, decreasing inhibition of the thalamus and increasing movement
48
effectiveness of deep brain stimulation in Parkinson's
only effective in patients with Parkinson's responsive to levodopa with motor fluctuations (well into course of disease)
49
features suggesting non-Parkinson's disease cause of parkinsonism
``` symmetry at onset absence of rest tremor early dementia abrupt onset rapid progression supranuclear gaze palsy early or severe autonomic dysfunction UMN or cerebellar signs early falling **poor response to levodopa** ```
50
characterize multiple systems atrophy
``` degeneration of cells in the striatum parkinsonian features early postural instability early speech difficulties pyramidal tract signs cerebellar signs peripheral neuropathy ```
51
pathogenesis of multiple systems atrophy
pathology in striatum itself INCREASES output from GPi decreases movement
52
characterize vascular parkinsonism
caused by ischemia / strokes to the striatum history of HTN and strokes MRI white matter changes
53
agents causing drug induced parkinsonism
phenothiazines metoclopramide thioxanthenes
54
characterize drug induced parkinsonism
postural tremor greater than resting tremor | reversible (may take 6 months)
55
MPTP induced parkinsonism
causes death of substantia nigra neurons | signs and symptoms similar to Parkinson's, but motor fluctuations occur right away
56
characterize hyper kinetic movement disorders
heterogenous group of disorders abnormal involuntary movements classification based upon phenomenology pathophysiology and etiology of most unknown well established empiric treatments for most
57
rhythmic involuntary movements
tremor
58
tremor
``` postural, action, rest common disease -essential tremor -familial tremor -Parkinson's unknown cause ```
59
treatment of tremor
essential: primidone, propranolol | PD associated: levodopa
60
suppressible abnormal involuntary movements
tics
61
tics
suppressible and associated with an urge to move common disease -Tourette's -adult onset tic disorder
62
treatments for tics
neuroleptics | pimozide
63
sustained abnormal involuntary movements
dystonia
64
dystonia
common diseases -focal dystonias (blepharospasm, torticollis, writer's cramp) -generalized unknown cause, but due to a lack of reciprocal inhibition segawa genetic variant
65
treatment for dystonia
``` focal: botulinum toxin anticholinergics levodopa (segawa variant) neuroleptics pimozide ```
66
ballistic abnormal involuntary movements
chorea
67
chorea
``` ballistic movement: agonist, antagonist, agonist common diseases -hemi-ballismus -essential chorea -Huntingtons -post-strep ```
68
treatment of chorea
dopamine blockers | anticholinergics
69
abnormal involuntary movements that are not rhythmic, suppressible, sustained, or ballistic
myoclonus
70
myoclonus
``` brief, shock like movements common diseases -idiopathic -primary generalized epilepsies -post anoxic ```
71
treatment of myoclonus
anti-seizure meds (valproic acid) | long acting benzos
72
tardive dyskinesia
abnormal involuntary movements after use of dopamine blocking agents can result in any type of movement previously described -dystonia and chorea most common -typically oral, lingual, buccal
73
treatment of tardive dyskinesia
difficult most effective in short term: increase dopamine blocker, worsens in long term anticholinergics to prevent

BMB Test 2 (22 decks)

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