Basal Ganglia Flashcards

1
Q

Generally, what is the basal ganglia and what does it do?

A
  • It is a collection of gray matter nuclei located deep within the white matter of the cerebral hemispheres
  • It influences the descending motor systems without directly projecting to the periphery
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2
Q

What structures make up the basal ganglia?

A
  • Caudate nucleus
  • Putamen
  • Globus pallidus internal segment
  • Globus pallidus external segment
  • Subthalamic nuclei
  • Substantia nigra
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3
Q

What makes up the striatum?

A

The caudate nucleus and the putamen which are separated by the internal capsule but connected via cellular bridges

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4
Q

What makes up the lentiform nucleus?

A

The globus pallidus (both internal and external segments) and the putamen

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5
Q

Describe the anatomy of the subthalamic nucleus

A
  • Cigar-like structure inferior to the thalamus
  • Derived from the midbrain
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6
Q

Describe the anatomy of the substantia nigra

A
  • Lies just dorsal/posterior to the cerebral peduncles
  • Substantia nigra pars reticulata: ventral anterior portion, cells are similar to globus pallidus internal segment
  • Substantia nigra pars compacta: dorsal/posterior portion, neurons that produce dopamine
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7
Q

What arteries supply blood to the basal ganglia?

A
  • Lenticulostriate artery (from MCA)
  • Anterior choroidal artery (from ICA)
  • Recurrent artery of Huebner (from ACA)

A single stroke cannot “take out” the entire basal ganglia because of the redundancy

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8
Q

Describe the motor channel of the basal ganglia

A

Function: general motor control
Thalamic relay nuclei: VL nucleus, VA nucleus
Cortical output targets: supplementary motor area, premotor cortex, primary motor cortex

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9
Q

Describe the oculomotor channel of the basal ganglia

A

Function: regulation of eye movement
Thalamic relay nuclei: VA nuclei, MD nuclei
Cortical output targets: frontal eye fields, supplemental eye fields

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10
Q

Describe the prefrontal channel of the basal ganglia

A

Function: cognitive functions
Thalamic relay nuclei: VA nuclei, MD nuclei
Cortical output targets: prefrontal cortex

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11
Q

Describe the limbic channel of the basal ganglia

A

Function: regulation of emotions and motivational drives
Thalamic relay nuclei: VA nuclei, MD nuclei
Cortical output targets: anterior cingulate gyrus, orbital frontal cortex

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12
Q

What are the thalamic relay nuclei involved in basal ganglia channels?

A
  • Ventral lateral nucleus
  • Ventral anterior nucleus
  • Mediodorsal nucleus
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13
Q

What are the inputs to the basal ganglia?

A
  • Cerebral cortex sends excitatory glutamate
  • Substantia nigra pars compacta sends dopamine which can be excitatory and inhibitory
  • Intralaminar nuclei of the thalamus sends excitatory glutamate
  • Subcortical systems can send modulatory inputs of acetylcholine, serotonin, norepinephrine, histamine
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14
Q

Which basal ganglia nuclei are input nuclei and which are output nuclei?

A

Input: caudate nucleus, putamen
Output: globus pallidus internal segment (motor control of body), substantia nigra pars reticulata (motor control of head and neck)

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15
Q

What are the two intrinsic pathways within the basal ganglia?

A
  • Direct pathway: direct connection between input and output nuclei
  • Indirect pathway: pathway between input and out put nuclei with additional steps
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16
Q

Describe the anatomy of the direct pathway

A
  • Input from cortex to the striatum
  • Striatum connects directly to the globus pallidus internal segment and substantia nigra pars reticulata
  • GPi and SNr send output to thalamic nuclei which will relay signals to cortical motor areas
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17
Q

What happens when the direct pathway is turned on (go through the pathway)?

A
  • Glutamate from the cortex excites the striatum
  • Striatal neurons release inhibitory GABA on the GPi and SNr
  • GPi and SNr activity is decreased due to inhibition by striatum
  • GPi and SNr release less GABA onto thalamic nuclei which decreases inhibition
  • Thalamic nuclei becomes more active and releases more excitatory glutamate onto cortical motor areas
  • Wanted movement is now able to occur
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18
Q

What happens when the direct pathway is turned off/at rest?

A
  • The striatum is not being excited, so it does not send inhibitory signals to the GPi and SNr
  • GPi and SNr remains active/excited and releases inhibitory GABA on to thalamic nuclei
  • Allows us to be still
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19
Q

Describe the anatomy of the indirect pathway

A
  • Input from cortex to striatum
  • The striatum indirectly connects to the GPi and SNr via the globus pallidus external segment and subthalamic nuclei
  • The GPi and SNr send output to the thalamic nuclei which will relay to cortical motor areas
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20
Q

What happens in the indirect pathway when an individual is at rest?

A
  • There is no signal between the cortex and striatum, so the striatum is not inhibiting GPe
  • The GPe is active and releasing inhibitory GABA on the STN, so the STN is not active
  • Even though the GPi and SNr are not being excited by the STN, they still release some inhibitory GABA onto the thalamus
  • Decreased glutamate signals from the thalamic nuclei to cortical motor areas
  • Inhibits unwanted movements while at rest
21
Q

What happens in the indirect pathway with cortical excitation?

A
  • The cortex releases excitatory glutamate onto the striatum
  • The striatum sends inhibitory GABA to the GPe, so it is unable to inhibit STN activity
  • The STN releases excitatory glutamate onto the GPi and SNr
  • The GPI and SNr now release an increased amount of inhibitory GABA onto the thalamic nuclei
  • No signals from the thalamic nuclei to cortical motor areas
  • Inhibits unwanted movements when active/volitional movements
22
Q

How does dopamine impact the direct pathway?

A
  • Dopamine is released from the substantia nigra pars compacta to the striatum
  • The dopamine is excitatory when it binds the D1 receptors in the striatum
  • Dopamine increases activity of the direct pathway to promote movement
23
Q

How does dopamine impact the indirect pathway?

A
  • Dopamine is released from the substantia nigra pars compacta to the striatum
  • The dopamine is inhibitory when it binds to D2 receptors in the striatum
  • Dopamine inhibits activity of the indirect pathway to decrease movement inhibition in order to promote movement
24
Q

Movement disorders are caused by what?

A

Lesions or damage to basal ganglia that leads to abnormal movement patterns

25
Describe the type of movement that can be observed in a patient with a hyperkinetic movement disorders
Excessive, uncontrolled, involuntary movements
26
Describe the type of movement that can be observed in a patient with a hypokinetic movement disorder
Rigidity, slowness, and difficulty with initiating movements
27
True or False If a patient has a unilateral lesion to the basal ganglia, symptoms would present contralaterally
True
28
What are the characteristics of movement disorders?
- Focal vs general - Unilateral vs bilateral - Motor symptoms, poor eye control, cognitive symptoms, impaired emotional regulation
29
What is bradykinesia?
Slow movements
30
What is hypokinesia?
Small movements or decreased amount of movements
31
What is akinesia?
The absence of movement
32
What causes bradykinesia/hypokinesia/akinesia?
- Caused by an increased inhibitory outflow from the basal ganglia to the thalamus - May result from lesion is various regions - Associated with parkinson's
33
What is rigidity associated with?
Rigidity is associated with movement disorders and is different from spasticity because it is not dependent on velocity or change in position
34
What are the two types of rigidity?
Lead pipe rigidity: continuous resistance through range Cogwheel rigidity: ratchet-like interruptions in tone felt throughout the range
35
Describe the characteristics of dystonia
- Co-contraction of agonist and antagonist muscles resulting in abnormal distorted positioning of the trunk, limbs, or face - Slow and sustained - Can be generalized, unilateral, or focal - Can occur in disorders of the basal ganglia
36
What is athetosis?
Slow, writhing movements of the limbs, face, and trunk
37
What is chorea?
- Nearly continuous involuntary movements of extremities, trunk, neck, face, and respiratory muscles - Low amplitude: can be concealed with voluntary movement - Large amplitude: can interrupt voluntary movement
38
What is ballismus?
Larger amplitude of proximal limb movements with a rotary or flinging quality
39
What is a tremor?
Rhythmic or semi-rhythmic oscillating movements
40
What are the three types of tremors?
Resting tremor: most prominent when limbs are relaxed, common with parkinson's disease Postural tremor: seen when holding limbs active but still (isometric contraction) Intention tremor: occurs when moving limb towards a target
41
What is Parkinson's disease?
- Idiopathic neurodegenerative disorder, hypokinetic movement disorder - Loss of dopaminergic neurons in the substantia nigra pars compacta - Symptoms: resting tremor, bradykinesia, rigidity, postural instability, gait disturbance - Symptoms improve with Levodopa
42
How does Parkinson's disease impact the direct pathway?
- Less dopamine, less excitation of D1 receptors - Less activation of pathway - Less disinhibition (more inhibition from the basal ganglia to the thalamus) - Less movement
43
How does Parkinson's disease impact the indirect pathway?
- Less dopamine, less inhibition of D2 receptors - Less inhibition of pathway - More inhibitory outflow from basal ganglia to thalamus - Less movement
44
What characteristics can help distinguish Parkinson's disease from other hypokinetic movement disorders?
NOT found in Parkinson's disease: Symmetrical presentation, rapid progression, little response to dopamine
45
What is Huntington's disease?
- Autosomal dominant neurodegenerative condition - Progressive atrophy of striatum - Degeneration of only enkephalin-containing striatal neurons progressing to degeneration of all striatal neurons - Symptoms: chorea, abnormal eye movements, dementia, emotional distrubances
46
Describe early stage Huntington's disease
- Degeneration of enkephalin containing neurons in indirect pathway on striatum - Striatum cannot inhibit GPe, so GPe inhibits STN - STN unable to excite output nuclei - Less inhibition of unwanted movement
47
Describe late stage Huntington's disease
- Indirect pathway: reduced inhibition of unwanted movement - Direct pathway: increased inhibition of movement - Advanced stages begin to show signs of rigidity
48
What are two ways to surgically manage movement disorders?
Stereostatic Neurosurgery: creating lesions at specific locations in the brain using therapeutic ablation and CT or MRI to see brain tissue, this is irreversible Deep Brain Stimulation: electrodes are placed in deep brain structures to "stimulate" the area and cause a depolarization block leading to dysfunction of target neurons, this is reversible
49
Where would electrodes be placed in a Parkinson's patient during deep brain stimulation?
Subthalamic nucleus and globus pallidus internal segment