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Clin Med-Neuro > Disorders of Extrapyramidal System > Flashcards

Disorders of Extrapyramidal System Flashcards

1
Q

function of extrapyramidal system

A

involuntary movement (dampens reflex arc)

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2
Q

hypo-kinetic disorder

A

dopamine

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3
Q

Hyperkinetic disorder

A

dopamine> Ach

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4
Q

epidemiology of PD

A

progressive neurodegenerative disorder

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5
Q

cause of primary PD

A

primary or idopathic

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6
Q

cause of secondary PD

A

damage to the basal ganglia

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7
Q

what is parkinsons PD

A

loss of dopaminergic cells in substantia nigra causes an imbalance between dopamine and Ach

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8
Q

cardinal symptoms of PD

A

bradkinesia
rigidity
postural instability (head tends to fall forward)
tremor (resting)

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9
Q

pathological hallmark of PD

A

lewey bodies

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10
Q

onset of PD

A

insidious and asymmetric

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11
Q

freezing

A

sudden interruption of movement

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12
Q

festination

A

tendency of gait to alternate between speeding up and slowing down

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13
Q

dysautonomia (PD)

A

associated with lewey bodes

  • sweating
  • ortho HTN
  • trouble with temperature ocontrol
  • drooling
  • insomnia
  • digestive problems (compounded by inactivity and use of anticholinergics)
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14
Q

when is a non-ergonline dopamine agonist used?

A

younger than 50

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15
Q

when is carbidopa/levodopa used?

A

older than 70

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16
Q

COMT inhibitors

A
  • Entacapone

- inhibits enzyme so that dopamine isn’t broken down = increase dopamine

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17
Q

Glutamate (NMDA) antagonists

A
  • Amantadine

- decreases ach levels by blocking glutamate receptors (good for treating tremor)

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18
Q

Levodopa

A
  • loses effectiveness after 5 years
  • pro drug
    combine with carbidopa ( a peripheral DOPA decarboxylase inhibitor) that does not cross BBB (reduces side effects)
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19
Q

treatment of on-off phenomenon

A

amantadine
addition of COMT or MAO-B inhibitor
addition of DA (decrease risk of dyskinesias)

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20
Q

risks of using ergot derivatives

A

valvular heart disease

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21
Q

MAO-B inhibitors

A
  • selegiline is commonly used
    inhibit oxidative metabolism of dopamine and doesn’t require dietary restrictions
    delay need for other parkinsons drugs
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22
Q

side effects of COMT inhibitors

A

liver dysfunction

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23
Q

side effects of MAO inhibitors

A

interactions with other drugs (anti-dep, tyramine food and opioids)

24
Q

side effects of amantadine

A

hallucinations

25
side effects of anticholinergics
hallucinations
26
side effects of DA
hallucinations, sleep attacks, orthostatic dizziness, compulsive behaviors
27
surgical treatment of PD
DBS - response to dopaminergic meds is the best predictor of success - patients less than 80 globus pallidus or subthalmic nucleus PD related dementia is a contraindication
28
benefits of DBS
reduces on-off | can reduce dose of levodopa
29
progressive supra-nuclear palsy (PSP)
- No tremor - poor response to L-dopa (+)lunging, fast walking, bumping, frontal lobe dementia
30
corticobasal degeneration
- no tremor - poor response to L-dopa (+) rest of PD signs
31
in general how does PD and parkinsons plus syndromes differ?
plus syndroms have a more rapid progression of symptoms
32
other name for Wilson's disease
hepato-lenticular degeneration
33
Wilson's disease
autosomal recessive disease onset during childhood treatable CU (overload in liver and CNS- basal ganglia)
34
findings in Wilson's disease
``` kayser-fleischer rings wing beating tremor risus sardonicus easy bruising anemia HSM ```
35
treatment of Wilson's disease
- removal of excess copper with chelators such as D-penicillamine - prevent Cu accumulation using oral zinc - liver transplant
36
dx of Wilson's disease
serum ceruloplasmic level 24 hours copper LFTs biopsy
37
huntingtons disease
- choreiform movement - psychiatric problems - autosomal dominant inheritance - dementia is inevitable w/ loss of executive function
38
when is memory loss seen in Huntington's dementia?
late
39
pathology of Huntington's disease
- accumulation of a mutant huntingtin protein--> reduction of GABA
40
treatment options in Huntington's disease
tetrabenazine is a dopamine depleter useful for treating the chorea causes depression, Parkinsonism, QT prolongation at higher doses
41
sydenhams chorea "st vitus dance"
autimmune destruction of basal ganglia results from childhood infection with group a beta hemolytic strep females younger than 18 most common
42
athetosis
writhing movements | mainly due to CP
43
dyskinesia
tardive dyskinesis due to drugs (exposure greater than 6 weeks to DA) tics on steroids
44
hemiballismus
throwing of the limbs on one side of the body | usually die to cva involving subthalmic nucleus
45
dystonia
- repeated patterned twisting and sustained movements that might be rapid or slow - start before 20 - children (distal) - adults (cranial-cervical) - primary: focal - secondary: generalized (wilsons, toxins)
46
monoclonus
simple jerky movements that are not coordinated or supressable
47
tics
go away at night - dopamine excess tx: DA
48
resting tremor
occurs at rest and improves with movement | - body is supported by gravity
49
action tremor
worsens as patient attempts to initate and continue activity
50
intention tremor
increase in amplitude as finger reaches the target
51
task-specific tremor
emerges during a specific activity
52
postural tremor
worsens when limbs held away from body
53
essential tremor
most common pathologic tremor - 50% cases autosomal dominant - bilateral, postural, action - most ob in hand and wrists (head, LE, voice can be affected)
54
cerebellar tremor
action (intention) tremor - seen w/ MS, trauma, stroke - caused by alcoholism
55
physiologic tremor
postural, action tremor not usually visible
56
parkinsonian tremor
pill rolling-> forarm (pron/supin)--> elbow flexion/extension - usually a combo of action and rest

Clin Med-Neuro (8 decks)

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