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Neurobiology > Basal Ganglia > Flashcards

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
Q

Describe the type of movement that can be observed in a patient with a hyperkinetic movement disorders

A

Excessive, uncontrolled, involuntary movements

26
Q

Describe the type of movement that can be observed in a patient with a hypokinetic movement disorder

A

Rigidity, slowness, and difficulty with initiating movements

27
Q

True or False
If a patient has a unilateral lesion to the basal ganglia, symptoms would present contralaterally

A

True

28
Q

What are the characteristics of movement disorders?

A
  • Focal vs general
  • Unilateral vs bilateral
  • Motor symptoms, poor eye control, cognitive symptoms, impaired emotional regulation
29
Q

What is bradykinesia?

A

Slow movements

30
Q

What is hypokinesia?

A

Small movements or decreased amount of movements

31
Q

What is akinesia?

A

The absence of movement

32
Q

What causes bradykinesia/hypokinesia/akinesia?

A
  • 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
Q

What is rigidity associated with?

A

Rigidity is associated with movement disorders and is different from spasticity because it is not dependent on velocity or change in position

34
Q

What are the two types of rigidity?

A

Lead pipe rigidity: continuous resistance through range
Cogwheel rigidity: ratchet-like interruptions in tone felt throughout the range

35
Q

Describe the characteristics of dystonia

A
  • 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
Q

What is athetosis?

A

Slow, writhing movements of the limbs, face, and trunk

37
Q

What is chorea?

A
  • 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
Q

What is ballismus?

A

Larger amplitude of proximal limb movements with a rotary or flinging quality

39
Q

What is a tremor?

A

Rhythmic or semi-rhythmic oscillating movements

40
Q

What are the three types of tremors?

A

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
Q

What is Parkinson’s disease?

A
  • 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
Q

How does Parkinson’s disease impact the direct pathway?

A
  • 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
Q

How does Parkinson’s disease impact the indirect pathway?

A
  • Less dopamine, less inhibition of D2 receptors
  • Less inhibition of pathway
  • More inhibitory outflow from basal ganglia to thalamus
  • Less movement
44
Q

What characteristics can help distinguish Parkinson’s disease from other hypokinetic movement disorders?

A

NOT found in Parkinson’s disease: Symmetrical presentation, rapid progression, little response to dopamine

45
Q

What is Huntington’s disease?

A
  • 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
Q

Describe early stage Huntington’s disease

A
  • 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
Q

Describe late stage Huntington’s disease

A
  • Indirect pathway: reduced inhibition of unwanted movement
  • Direct pathway: increased inhibition of movement
  • Advanced stages begin to show signs of rigidity
48
Q

What are two ways to surgically manage movement disorders?

A

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
Q

Where would electrodes be placed in a Parkinson’s patient during deep brain stimulation?

A

Subthalamic nucleus and globus pallidus internal segment

Neurobiology (15 decks)

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