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NEURO 210 > Movement Disorders > Flashcards

Movement Disorders Flashcards

1
Q

What is bradykinesia?

A

Slow movements.

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2
Q

What is rigidity?

A

Stiffness of limbs.

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3
Q

What is a rest tremor?

A

3Hz tremor during relaxation.

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4
Q

What are the (6) causes of Parkinsonism?

A
  1. Degeneration.
  2. Drugs.
  3. Vascular disorders.
  4. Infection.
  5. Toxins.
  6. Tumors.
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5
Q

When is PD most prevalent? When is the typical age of onset?

A

Incidence is rising slowly with age, the typical onset is 62 years. Occurrence is very rare before 30.

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6
Q

What are the typical features of early-onset PD?

A

Rest tremors, bradykinesia, tremor increases under stress, facial masking.

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7
Q

What are the diagnostic criteria for PD?

A 
Bradykinesia, rigidity, rest tremor.
Asymmetry of symptoms.
Absence of any autonomic dysfunction or any disease that would better explain dysfunction.
Absence of causal drug use.
Loss of dopamine detection.
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8
Q

What is the levodopa response? Why is this an important indicator of PD?

A

Loss of dopamine. Symptoms are typically reversed by the reintroduction of dopamine. When symptoms are relieved this way, the dysfunction is most definitely caused by PD.

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9
Q

What investigations do not provide any diagnosis for PD, but may be used to rule out other causes of mobile dysfunction?

A

CT, MRI scans that can detect abnormalities (strokes, tumors, etc).

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10
Q

What is the etiology of PD? (4)

A

Genetics, environmental toxins, other factors, aging.

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11
Q

What is the biggest risk/cause of developing PD?

A

Increase in age.

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12
Q

What are the genetic causes of PD? (No need for specifics, just list the heritability)

A

PD correlated genes are inherited both dominantly and recessively. Two loci exist as being high-risk for PD.

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13
Q

What environmental toxins cause parkinsonian disorders?

A

Manganese, MPTP, agricultural chemicals.

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14
Q

What are neuroprotective factors for PD?

A

Exercise, coffee, nicotine.

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15
Q

What are key characteristics present in the pathology of PD? (4)

A
  1. Degeneration of dopaminergic neurons in pars compacta of substantia nigra.
  2. Degeneration in the brainstem of pigmented nuclei, spinal cord, cortex, gut.
  3. Loss of dopamine, serotonin, noradrenaline.
  4. Lewy bodies.
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16
Q

Which pathway of the basal ganglia facilitates movement?

A

The direct pathway:
-Substantia nigra pars compacta modulates activity of the striatum, which will send inhibitory projections to the globulus palladus internal. This prevents the inhibition of activity in the thalamus and therefore promotes movement.

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17
Q

What pathway in the basal ganglia inhibits movements?

A

The indirect pathway:
-Pars compacta of the substantia nigra projects onto the striatum and inhibit the projection of inhibitory signals onto the GPe. The active GPe will then project inhibitory signals onto the STN. The inactivated STN can no longer inhibit the GPi, therefore majorly inhibitory signals are sent downstream to prevent excess movement.

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18
Q

What does a lesion in the indirect pathway cause?

A

Inability to inhibit thalamus; direct pathway occurs unopposed, hyperactivity of movements.

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19
Q

What is the Braak system Hypothesis?

A

Used to measure the degree of progression in PD by using stages.

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20
Q

What is stage 1 PD?

A

Deposition of alpha-synuclein in dorsal motor and olfactory areas.

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21
Q

What is stage 2 PD?

A

Synuclein clumps in coerulus, sub-ceruleus complex. Causes dysfunction in sleep and mood.

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22
Q

What is stage 3 PD?

A

Motor symptoms affected.

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23
Q

What is stage 4-6 PD?

A

Neurodegeneration of cortical areas, leads to dementa.

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24
Q

What is alpha-synuclein?

A

Protein in nerve cells that are required for normal function. They form clumps that are put into vesicles.

25
Q

How is de novo PDs treated pharmaceutically?

A

MAO B inhibitors prevent breakdown of dopamine.
Anti-cholinergics.
Dopamine agonists increase effect of dopamine.
Levodopa reintroduces dopamine.

26
Q

Why is dopamine administered as levodopa and not dopamine?

A

Dopamine cannot cross the blood brain barrier, but levodopa can and is metabolized into dopamine in the cortex.

27
Q

What are other treatments for PD?

A

Counseling, exercise, vitamin supplements.

28
Q

What is dysphagia?

A

Speech abnormalities.

29
Q

What is the subthalamic nucleus’ role in the basal ganglia?

A

The role of the STN is to turn the thalamus on or off based on previous projections from the cortex or globulus palladus.

30
Q

What is the pars compacta substantia nigra’s role in the basal ganglia?

A

The SNpc uses dopaminergic neurons to project onto the striatum, the first step in signalling movement.

31
Q

What is the globulus palladus? What is the function of its two components in the basal ganglia?

A

A structure in the basal ganglia composed of external and internal parts. The GPi and GPe both project inhibitory neurons onto the STN to prevent movement. They are controlled by the number of inhibitory signals relayed from the striatum.

32
Q

What surgeries are performed for PD?

A

Only used when the disease is advanced; deep brain stimulation of the STN.

33
Q

What is PD dementia? What are common co-symptoms?

A

Phenomenon that affects most advanced PD patients, cosymptomatic with hallucinations and loss of insight/multi-tasking and visuospatial abnormalities.

34
Q

What is ballism?

A

Larger unsustained movements/muscle contractions.

35
Q

What is chorea?

A

Distal, jerking movements of the limbs due to a sudden contraction of a muscle. Not sustained, but occurs with slower “flowing” contractions.

36
Q

What is dystonia?

A

Sustained contraction of the muscle group that causes abnormal posture.

37
Q

What is myoclonus?

A

Sudden, weak and unsustained movement/”jerk”.

38
Q

What is athetosis?

A

Slow writhing movement.

39
Q

What is the most common chronic/genetic cause of chorea? How is this inherited?

A

Huntington’s disease, autosomal dominant.

40
Q

How is Huntington’s disease caused?

A

Inherited repetitions of CAG sequence in gene, causes overproduction of glutamate, leads to toxicity and degeneration in basal ganglia.

41
Q

How many CAG repetitions must be present to declare a gene as Huntington’s positive?

A

40

42
Q

What symptoms are present in early-stage HD?

A

Restlessness, motor impersistence, slowing of eye movements.

43
Q

What symptoms are present at a mild-moderate stage HD?

A

Increased chorea, more disabling and apparent.

44
Q

What symptoms are present in late-stage HD?

A

Chorea lessens and rigidity/bradykinesia takes place.

45
Q

Why do basal ganglia diseases cause psychological and cognitive effects as well as weight effects?

A

The basal ganglia projects to any different structures that affect emotions, metabolism, and memory/learning.

46
Q

When is the typical adult-onset of HD?

A

45

47
Q

What are the three categories of dystonia?

A
  1. Primary.
  2. Dystonia-plus syndrome.
  3. Secondary dystonia
48
Q

What is primary dystonia?

A

Sporadic, inherited DYT1 dystonia.

49
Q

What is a dystonia-plus syndrome?

A

Inherited, responsive to dopamine. Includes HD.

50
Q

What is secondary dystonia?

A

Non-inherited dystonia.

51
Q

What is focal dystonia?

A

Adult-onset, non-progressive dystonia. Involuntary spasms caused by overactivity of motor pathways.

52
Q

How is focal dystonia treated?

A

DBS of GPi (inhibit STN, fewer movements)
Botox
Medication

53
Q

What are tics?

A

Brief, non-rhythmic semi-suppressible movements.

54
Q

What are the two classifications of tics?

A

Primary, secondary

55
Q

What are primary tics?

A

Transient, chronic tics, usually related to Tourette’s syndrome.

56
Q

What are secondary tics?

A

Caused by some sort of neurological damage.

57
Q

What is Tourette’s syndrome?

A

Syndrome in which an individual experiences multiple motor tics and 1+ vocal tics. Associated with OCD, ADHD, and behavioural problem.

58
Q

How is Tourette’s Syndrome treated?

A
  1. Counselling.
  2. Life modifications.
  3. Treatment for ADHD/Hyperactivity.
  4. Treatment for OCD (anti-anxiety medications)

NEURO 210 (13 decks)

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