Motor Pathways & Disorders Flashcards

1
Q

What are the two divisions of motor pathways?

A
  1. Lateral pathways (corticospinal, rubrospinal)
  2. Ventro-medial pathways (vestibulospinal, tectospinal, reticulospinal).
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2
Q

What is the main function of the corticospinal tract?

A

It provides direct cortical control of voluntary movements, especially fine movements of the limbs.

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3
Q

Which structures comprise the basal ganglia? (6)

A
  • caudate nucleus
  • putamen
  • globus pallidus (internal and external)
  • substantia nigra
  • subthalamic nucleus
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4
Q

What is the role of the basal ganglia in movement?

A

They regulate the initiation and control of voluntary movements, balancing the DIRECT and INDIRECT pathways to facilitate desired motor programs and supress competing ones.

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5
Q

Int the basal ganglia pathways, how does dopamine modulate activity? (3)

A
  • D1 receptors (direct pathway): Facilitates movement.
  • D2 receptors (indirect pathway): Inhibits movement.
  • Dopamine from the substantia nigra helps balance these pathways.
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6
Q

Which key motor roles does the cerebellum perform? (4)

A
  • Coordination of movement
  • Balance
  • Error correction
  • Motor Learning (fine-tuning and adjusting ongoing movement)
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7
Q

What is Parkinson’s Disease?

A

A hypokinetic motor disorder caused by degeneration of dopaminergic neurons in the substantia nigra, leading to reduced movement initiation.

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8
Q

List FOUR classic symptoms of Parkinson’s Disease

A
  1. Akinesia (difficulty initiating movement)
  2. Bradykinesia (slowness of movement).
  3. Rigidity
  4. Resting tremor (“pill-rolling” tremor)
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9
Q

What pathological hallmark is found in dying dopaminergic cells in Parkinson’s Disease?

A

Lewy bodies, which are intracellular aggregates of α-synuclein.

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10
Q

How does L-DOPA help in Parkinson’s Disease?

A

L-DOPA is converted to dopamine in the brain, temporarily replenishing DA levels and improving motor symptoms.

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11
Q

Name TWO adjunct therapies used alongside L-DOPA in Parkinson’s treatment.

A
  • MAO-B inhibitors (e.g., selegiline) to reduce DA breakdown.
  • COMT inhibitors (e.g., entacapone) to prolong DA effects.
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12
Q

What is Huntington’s Disease?

A

A hyperkinetic disorder characterised by chorea, caused by neuronal loss in the caudate/putamen (striatum) and a genetic mutation in the huntingtin gene.

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13
Q

Which symptoms define Huntington’s Disease? (3)

A
  • Chorea (involuntary jerking)
  • Impaired balance and gait
  • Cognitive decline and psychiatric disturbances
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14
Q

How does striatal degeneration in Huntington’s Disease affect movement?

A

Reduced inhibition of the thalamus leads to excessive thalamo-cortical activity, resulting in involuntary, hyperkinetic movements.

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15
Q

What pharmacological strategies exist for Huntington’s Disease? (3)

A

Symptomatic Treatments:

  • Antipsychotics or D2 receptor agonists for chorea
  • Baclofen (muscle relaxant)
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16
Q

What is the primary function of the cerbellum in motor control?

A

It coordinates and fine-tunes motor activity, ensuring smooth, accurate movements and adaptation through motor learning.

17
Q

Define cerebellar ataxia

A

A coordination disorder resulting from cerebellar dysfunction, leading to impaired balance, gair, and fine motor control.

18
Q

Mention TWO possible causes of cerebellar degeneration

A
  • Genetic (spinocerebellar ataxias).
  • Acquired (trauma, stroke, chronic alcohol use, certain drugs).
19
Q

How do lesions in the basal ganglia differ from cerebellar lesions in motor symptoms? (2)

A
  • Basal ganglia lesions: Lead to either reduced movement (Parkinson’s) or excessive movement (Huntington’s)
  • Cerebellar lesions: Lead to ataxia, poor coordination, and inability to correct motor errors.
20
Q

What is deep brain stimulation (DBS), and how is it used in Parkinson’s Disease?

A

An implanted device delivers electrical impulses to targets like the subthalamic nucleus, helping modulate basal ganglia output and improve motor symptoms.