Parkinsonian Disorders Flashcards

1
Q

Parksinsons: Large loss of __ neurons in the nucleus accumbens and substantia nigra

Higher levels of __ are suggested to cause the dyskinesia — uncontrolled, involuntary movements — observed in Parkinson’s patients under long-term dopamine therapy

Tissue concentrations of ___ (NE) are markedly decreased in various regions of the Parkinson’s disease (PD) brain. As in the substantia nigra pars compacta, neuronal dropout and Lewy bodies are prominent changes affecting the locus coeruleus, which is the source of ascending NErgic projections

A

Parksinsons: Large loss of dopaminergic neurons in the nucleus accumbens and substantia nigra

Higher levels of acetylcholine are suggested to cause the dyskinesia — uncontrolled, involuntary movements — observed in Parkinson’s patients under long-term dopamine therapy

Tissue concentrations of norepinephrine (NE) are markedly decreased in various regions of the Parkinson’s disease (PD) brain. As in the substantia nigra pars compacta, neuronal dropout and Lewy bodies are prominent changes affecting the locus coeruleus, which is the source of ascending NErgic projections

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2
Q

TRAP features of PD

A

T= tremor

R= rigidity

A= akinesia/bradykinesia

P= postural inability

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3
Q

etiology, risk factors and protective factors for parkinsons

A

Etiology: sporadic, familial (10% of cases), exposure to MPTP neurotoxin

  • Risk factors: family history, male, head injury, rural living, exposure to neurotoxins
  • Protective factors: coffee, smoking, NSAID use, estrogen replacement in post-menopausal F Epi: 1% of pt over 60yo Stages:
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4
Q

mechanism of Parkinson’s disease

___ accumulates in ___ bodies → neurotoxicity of substantia nigra–>loss of ___ neurons in SNc→ decreased dopamine in striatum→ disinhibition of indirect pathway + decrease activation of direct pathway→ increased ___ of cortical motor areas

A

Alpha-synuclein accumulates in Lewy bodies → neurotoxicity of substantia nigra–>loss of dopaminergic neurons in SNc→ decreased dopamine in striatum→ disinhibition of indirect pathway + decrease activation of direct pathway→ increased inhibition of cortical motor areas

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5
Q

early non motor symptoms of parkinsons

A

Early non motor symptom can predate the motor symptoms; acting out your dreams, anosmia. Later on; drooling, incontinence, dementia, depression and anxiety. Quiet voice.

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6
Q

diagnosis of Parkinsonian Syndrome

A

Early non motor symptom can predate the motor symptoms; acting out your dreams, anosmia. Later on; drooling, incontinence, dementia, depression and anxiety. Quiet voice.

a. bradykinesia (the slowness of initiation of voluntary movement with progressive reduction in speed and amplitude of repetitive actions)
b. AND either
i. muscular rigidity, or
ii. 4-6Hz rest tremor, or
iii. postural instability not caused by primary visual, vestibular, cerebellar or proprioceptive dysfunction

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7
Q

exclusion criteria for Parkinson’s Disease (for ordinary idiopathic PD– does not rule out Parkinson’s plus)

A
  • poor response to levodopa,
  • abrupt onset of symptoms,
  • rapid progression,
  • early falls,
  • early autonomic dysfunction,
  • symmetric symptoms at onset,
  • <50yo, early cognitive impairment, family hx of psychiatric/dementing disorders, recent diagnosis of psychiatric disease,
  • toxic exposure, Babinski sign (would indicate vascular parkinsons or stroke- multiple small vessel ischemic events that have affected the basal ganglia– more symmetrical and lower limb focussed) … there are lots
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8
Q

Supportive (non diagnostic) criteria for PD

A
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9
Q

Management for PD

A

• Levodopa: decreases motor and non-motor symptoms but NOT disease modifying

o Neuropsychiatric: depression, anxiety, apathy, impulse control disorder, psychosis, anhedonia, hallucination, panic attacks, ADD

o Cognitive: executive dysfunction, memory loss, dementia

o Sleep: insomnia, somnolence, EDS, RLS, sleep attacks, vivid dreams, REM sleep behaviour disorder

o Autonomic: orthostatic HTN, constipation, fecal/urinary incontinence, N/V, ­sweating, GI dysfunction

o Sensory: anosmia, pain, ageusia, numbness, paresthesia

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10
Q

Motor features of atypical parkinsonism

A
  • rapid disease progression
  • early inability and falls
  • absent, poor or not maintained repsonse to levodopa
  • myoclonus
  • cerebellar/pyramidal signs
  • early dysarthria or dysphagia
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11
Q

autonomic features of atypical parkinsonism

A
  • impotence
  • early orthostatic hypotension unrelated to treatmnet
  • early and/or severe urinary symptoms
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12
Q

oculomotor features of atypical parkinsonism

A

marked slowing of saccades; difficulties initiating saccades

  • supranuclear gaze palsy
  • nystagmus
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13
Q

cognitive and behavioural features of atypical parkinsonism

A
  • early and severe cortical or frontal dementia
  • visual hallucinations not induced by treatment
  • ideomotor apraxia
  • sensory or visual neglect/cortical disturbances.
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14
Q

definition of atypical parkinsonism

A

Definition: a primary Parkinsonism disease that has atypical features

Etiology: sporadic (PSP, MSA, DLB, CBD) or genetic

Symptoms: Parkinsonism + atypical features

  • Motor: rapid progression, early instability, myoclonus, cerebellar/pyramidal signs, early dysarthria/dysphagia, poor levodopa response
  • Autonomic features: impotence, early orthostatic hypotension, early/severe urinary symptoms
  • Oculomotor: marked slowing of saccades, difficulty initiating saccades, supranuclear gaze palsy, nystagmus
  • Cognitive/Behavioural: cortical/frontal dementia, visual hallucination, ideomotor apraxia, neglect

Parkinson’s Plus Definition: a group of disorders characterized by Parkinson’s + evidence of more widespread degeneration of other system. Will respond to levodopa but less robustly.

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15
Q

definining feature of dementia with lew body (parkinson’s plus)

A

hallucination

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16
Q

Multiple System Atrophy (MSA) (type of Parkinson’s Plus) Defining features

A

Actually a form of parkinsonism but also has cerebellar signs.

Two forms: MSA-P (Parksinsonian) or MSA-C (Cerebellar)

Moderate to rapid rate of progression– most become wheelchair bound within the first few years.

Dysarthria, dysphadia, pseudobulbar affect, early autonomic dysfunction, LMN, cerebellar defects–> defining features

Slurring of speech, swallowing difficulties.

Pyramidal signs (cortical spasticity) in addition to the rigidity, and systemic symptoms as well– marked constipation and bladder dysfunction, cardiology and sleep problems.

Cross bun sign on MRI.

17
Q

key features of progressive supranuclear palsy (atypical parkinsons)

A

vertical gaze, axial dystonia

18
Q
A