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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
Q

epidemiology of parkinson’s

A

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

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26
Q

age of onset of Parkinson’s

A

typically between 40-70

  • avg is 60
  • 4-10% before 40
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27
Q

risk factors for Parkinson’s

A 
increasing age
family history
male gender
Caucasian
environmental (chemical based industries)
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28
Q

genetic causes of parkinsons

A

uncommon for parkinson’s to be an inherited form
a-synuclein
parkin
UCH-L1

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29
Q

autonomic manifestations of parkinson’s

A 
orthostatic hypotension
constipation
dysphagia
heartburn
excessive sweating, heat intolerance
urinary disturbances
male sexual dysfunction
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30
Q

cognitive manifestations of Parkinson’s

A

apathy
dysexecutive
dementia (15-40%)

31
Q

cortical targets of the basal ganglia

A

limbic channel - apathy
oculomotor channel - hypsometric saccades
prefrontal channel - dysexecutive
motor channel - akinesia

32
Q

current method of pharmacotherapy for Parkinson’s

A

repair the dopamine deficiency

33
Q

pharmacotherapeutic options

A

Levodopa
MAO-B inhibitors
dopamine agonists
COMT inhibitors

34
Q

how does levodopa work

A

crosses the BBB and is converted to dopamine in remaining neurons in the substantia nigra
can be stored as well

35
Q

combo therapy with levodopa

A

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
Q

efficacy of levodopa

A

most effective agent

if patients don’t improve, they probably don’t have parkinson’s

37
Q

pharmacokinetics of carbidopa/levodopa

A

half life is 90 min
5-10% enters brain w carbidopa
immediate and extended release options available

38
Q

long term complications of levodopa

A 
motor fluctuations
-wearing off phenomenon
-on/off phenomenon
dyskinesia (overshooting)
-chorea
-dystonia
39
Q

why are there long term complications of levodopa

A

short half life

decreasing ability of nigral neurons to store dopamine over time (remaining cells still dying away as time progresses)

40
Q

mechanism of action of MAO-B and COMT inhibitors

A

MAO-B and COMT break dopamine down into biproducts

inhibiting these makes dopamine’s effects last longer

41
Q

MAO-B inhibitors

A

selegiline & rasagiline

  • minimal effect when used alone
  • reduces motor fluctuations and increases on time as an adjunct to levodopa
42
Q

COMT inhibitors

A

entacapone & tolcapone
extends half life of levodopa from 1.5 to 2.5 hours
no role as monotherapy
no

43
Q

function of dopamine agonists in Parkinson’s

A

stimulate postsynaptic dopamine receptors directly
do not require metabolic conversion
half life longer than levodopa

44
Q

indication for dopamine agonists

A

initial monotherapy or as an adjunct to levodopa (after motor fluctuations begin)

45
Q

effectiveness of dopamine agonists

A

effective for tremor, bradykinesia, and rigidity

not as effective for motor symptoms as levodopa

46
Q

dopamine agonists

A

pramipexole

ropinirole

47
Q

targets of deep brain stimulation in parkinson’s

A

subthalamic nucleus or GPi

stimulation shuts off these areas briefly, decreasing inhibition of the thalamus and increasing movement

48
Q

effectiveness of deep brain stimulation in Parkinson’s

A

only effective in patients with Parkinson’s responsive to levodopa with motor fluctuations (well into course of disease)

49
Q

features suggesting non-Parkinson’s disease cause of parkinsonism

A 
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
Q

characterize multiple systems atrophy

A 
degeneration of cells in the striatum
parkinsonian features
early postural instability
early speech difficulties
pyramidal tract signs
cerebellar signs
peripheral neuropathy
51
Q

pathogenesis of multiple systems atrophy

A

pathology in striatum itself
INCREASES output from GPi
decreases movement

52
Q

characterize vascular parkinsonism

A

caused by ischemia / strokes to the striatum
history of HTN and strokes
MRI white matter changes

53
Q

agents causing drug induced parkinsonism

A

phenothiazines
metoclopramide
thioxanthenes

54
Q

characterize drug induced parkinsonism

A

postural tremor greater than resting tremor

reversible (may take 6 months)

55
Q

MPTP induced parkinsonism

A

causes death of substantia nigra neurons

signs and symptoms similar to Parkinson’s, but motor fluctuations occur right away

56
Q

characterize hyper kinetic movement disorders

A

heterogenous group of disorders
abnormal involuntary movements
classification based upon phenomenology
pathophysiology and etiology of most unknown
well established empiric treatments for most

57
Q

rhythmic involuntary movements

A

tremor

58
Q

tremor

A 
postural, action, rest
common disease
-essential tremor
-familial tremor
-Parkinson's
unknown cause
59
Q

treatment of tremor

A

essential: primidone, propranolol

PD associated: levodopa

60
Q

suppressible abnormal involuntary movements

A

tics

61
Q

tics

A

suppressible and associated with an urge to move
common disease
-Tourette’s
-adult onset tic disorder

62
Q

treatments for tics

A

neuroleptics

pimozide

63
Q

sustained abnormal involuntary movements

A

dystonia

64
Q

dystonia

A

common diseases
-focal dystonias (blepharospasm, torticollis, writer’s cramp)
-generalized
unknown cause, but due to a lack of reciprocal inhibition
segawa genetic variant

65
Q

treatment for dystonia

A 
focal: botulinum toxin
anticholinergics
levodopa (segawa variant)
neuroleptics
pimozide
66
Q

ballistic abnormal involuntary movements

A

chorea

67
Q

chorea

A 
ballistic movement: agonist, antagonist, agonist
common diseases
-hemi-ballismus
-essential chorea
-Huntingtons
-post-strep
68
Q

treatment of chorea

A

dopamine blockers

anticholinergics

69
Q

abnormal involuntary movements that are not rhythmic, suppressible, sustained, or ballistic

A

myoclonus

70
Q

myoclonus

A 
brief, shock like movements
common diseases
-idiopathic
-primary generalized epilepsies
-post anoxic
71
Q

treatment of myoclonus

A

anti-seizure meds (valproic acid)

long acting benzos

72
Q

tardive dyskinesia

A

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
Q

treatment of tardive dyskinesia

A

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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