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NEURO 210 > Lecture 7: Movement Disorders > Flashcards

Lecture 7: Movement Disorders Flashcards

1
Q

What are the characteristics of hypokinetic movement disorders?

A

decreased or slow movement

loss of direct pathway in basal ganglia

loss of dopamine

Parkinsonism

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2
Q

What are the characteristics of hyperkinetic movement?

A

excessive movement

loss of direct pathway

loss of inhibition of thalamus

chorea, dystonia

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3
Q

What is the direct pathway of movement in the basal ganglia?

A

facilitates movement

fueled by dopamine (Parkinson’s)

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4
Q

What is the indirect pathway of movement in the basal ganglia?

A

inhibits movement

slows down movement (Huntington’s)

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5
Q

What other systems is the basal ganglia connected to through the caudate?

A

limbic
visual
oculomotor
motor cortex
frontal cortex

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6
Q

What are some characteristics of Parkinsonism?

A

bradykinesia

rigidity

rest tremor

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7
Q

What are the causes of Parkinsonism?

A

degenerative (PD)
drugs (neuroleptics)
vascular
infectious (HIV)
toxins (CO)
tumors

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8
Q

What injury in the basal ganglia causes Parkinson’s?

A

decreased action of the direct pathway

indirect system is active so it inhibits the thalamus so motor cortex can’t be active

no gas pedal, all break

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9
Q

What is the process of diagnosis of Parkinson’s disease?

A

remains a clinical diagnosis (stiffness, rest tremor)

investigations (such as CT, MRI) not proven to be useful for diagnosis on evidence based review but rule out other causes

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10
Q

What are the stats of the incidence of Parkinson’s disease?

A

5-24/10,000 worldwide

incidence of PD rising slowly with aging population

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11
Q

What are the stats of the prevalence of Parkinson’s disease?

A

57-371/10,000 worldwide (USA/Canada, 300/10,000)

40% of cases undiagnosed at any time

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12
Q

What are the stats of the prevalence of Parkinson’s disease?

A

mean 62 years

rare before age 30

10% cases before age 50

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13
Q

What are the risk factors of Parkinson’s disease?

A

genetic factors: more in younger people

environmental toxins: greater risk in rural area (exposure to pesticides, MPTP)

other factors: aging, older we get more dopamine we loose

biggest risk factor is aging

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14
Q

What are the environmental risk factors of Parkinson’s disease?

A

manganese (or CO2)

MPTP

epidemiologic studies suggest that agricultural chemicals may play a role

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15
Q

What risk factors cause Parkinson’s disease in younger people?

A

more likely to be caused by genetic factors

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16
Q

What risk factors cause Parkinson’s disease in older people?

A

combination to genetic predisposure and environmental or other factors

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17
Q

What are neuroprotective factors against Parkinson’s disease?

A

exercise, coffee, nicotine

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18
Q

What is the pathology of Parkinson’s disease?

A

deposition of alpha-synuclein in Lewy bodies (becomes misfolded, clumps up, and get deposited in Lewy body)

degeneration of dopaminergic neurons in pars compacta of substantia nigra

degeneration in brainstem of pigmented nuclei, spinal cord, cortex, gut

Parkinson’s is not just limited to dopamine in substantia nigra, gets deposited in other NS areas as well

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19
Q

What does the substantia nigra look like with Parkinson’s disease and without?

A

without: makes lots of dopamine so lots of melanin

with: no dopamine so no melanin

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20
Q

What is the Braak system of Parkinson’s disease?

A

Parkinson’s starts in the gut

Stage 1 of PD: dorsal motor, olfactory, start in the nose or gut then moves to the brain to cause depression, anxiety, and sleep problems (dorsal motor, olfactory, then marches UP brainstem)

Stage 2: coeruleus, sub-coeruleus complex (function in sleep, mood)

Stage 3: motor symptoms

Stages 4-6: cortical involvement, dementia, etc.

so, other signs before motor

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21
Q

What is the pharmacology of treating Parkinson’s disease?

A

dopamine can’t cross blood-brain barrier, so can’t ingest it

have to give supplements to make sure it doesn’t turn into dopamine entry

LD is a neutral amino acid that gets into the brain, brain makes it into dopamine

22
Q

What are the drugs involved in the replacement of dopamine?

A

MAO B inhibitors (rasagiline, selegiline)

anti-cholinergics

amantadine

dopamine agonists (pramipexole, ropinirole, rotigotine)

levodopa (short-acting and long-acting)

23
Q

What are the non-motor problems associated with Parkinson’s disease?

A

fatigue, apathy

psychiatric (anxiety and depression)

sleep disturbances

autonomic nervous system (bladder, bowel, sexual dysfunction and hypotension)

cognitive dysfunction

24
Q

What are other treatments of Parkinson’s disease?

A

counseling: referral to support society groups

alternative treatments: exercise, calcium, Vitamin D

neuroprotection: none proven to date, studies ongoing

25
What is the management of moderate disease?
multiple medications needed in combination gait problems (physio, gait assessment, risk of falls) dysphagia, speech abnormalities
26
What are the surgeries of Parkinson's disease?
advanced disease GPi vs. STN, DBS vs. lesion helps all motor symptoms of PD meds can be decreased with STN DBS
27
What is the treatment of advanced disease?
treatment of motor symptoms (adjustment of meds often limited by side effects) non-motor symptoms (dementia, depression) planning for care (placement, caregiver burden)
28
What is Parkinson's disease dementia?
up to 70% of PD patients affected onset heralded by visual hallucinations loss of insight and multi-tasking, visuospatial abnormalities Montreal Cognitive Assessment vs. MMSE
29
What are the three types of choreaform disorders?
ballism (more proximal, violent) athetosis (more sinuous) chorea (distal, irregular, non-stereotypical movement)
30
What are the acute causes of chorea?
medications vascular immune-mediated hormonal infectious metabolic disorders toxins/substance abuse
31
What are the chronic causes of chorea?
genetic Huntington disease SCA 2, 3, 17 DRPLA Wilson disease mitochondrial dopaminergic blockers infectious nutritional endocrine
32
What is Huntington disease?
autosomal dominant CAG repeat age of onset (and progression) dependent on size of triplet repeat 50% of AOO dependent on other genes slow progression (15-30 years)
33
What is juvenile-onset HD (JHD)?
symptom onset before the age of 21 years childhood onset (<10 years) adolescent onset (10-20 years)
34
What is pediatric HD?
patients with manifest disease who are still below the age of 18 years
35
What are the motor features of early stage Huntington's disease?
restlessness motor impersistence slowing of eye movement
36
What are the motor features of mild-moderate stage Huntington's disease?
chorea gradually becomes more apparent and disabling
37
What are the motor features of late stage Huntington's disease?
chorea lessens significant rigidity and bradykinesia, gait and balance problems
38
What are the clinical features of Huntington's disease?
motor (chorea, dystonia, rigidity/bradykinesia, myoclonus, gait disorder, dysphagia/dysarthria, eye movement abnormalities) psychiatric (personality changes, behavioral disorders, depression, irritability/anxiety, obsessive compulsive, psychosis (rare), suicidal ideation) cognitive (executive dysfunction, dementia) weight loss apathy
39
What is the treatment of Huntington's disease?
interdisciplinary management ongoing psychosocial support genetic counseling research
40
What is the definition of dystonia?
abnormal sustained muscle contraction and postures may be associated with tremor may be alleviated by sensory tricks
41
What is the classification of dystonia?
age of onset (early vs. late) distribution (focal, segmental, generalized)
42
What is the pathophysiology and etiology of dystonia?
pathophysiology poorly understood multiple causes: brain injury, toxic, genetic (particularly in children) some forms may be related to decreased dopamine (usually children)
43
What is primary generalized dystonia?
childhood onset, progressive legs --> trunk --> arms DYT 1 mutation most common (autosomal dominant with variable penetrance and expressivity)
44
What is focal dystonia?
adult onset, non-progressive blepharospasm (eyes) oromandibular (mouth and jaw) occupational (writing, playing instruments) cervical (neck)
45
What is the treatment of focal dystonia?
botulinum toxin injections (botox was created to treat dystonia, most effective treatment) medications surgery (DBS of GPi)
46
What are tics?
brief, non-rhythmic semi-suppressible movements
47
What are types of tics?
simple motor clonic tonic dystonic simple vocal sensory complex motor complex vocal
48
What are the primary diagnoses of tics?
transient tics of childhood chronic tics (motor or vocal) Tourette syndrome
49
What are the secondary diagnoses of tics?
infections post-infectious neurodegenerative chromosomal disorders drug induced toxic - metabolic head injury stroke neuropsychiatric
50
What is needed for a diagnosis of Tourette's syndrome?
multiple motor + > 1 vocal tics duration greater than 1 year
51
What are associated features of Tourette's syndrome?
obsessive-compulsive symptoms ADHD behavior problems
52
What are treatments of Tourette's syndrome?
education and counselling modification of home/school/work environment hyperactivity/ADHD (clonidine, CNS stimulants) obsessive-compulsive behavior (SSRIs, clomipramine, venlafaxine, atypical antipsychotics)

NEURO 210 (23 decks)

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