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IMS: Neuroanatomy > Basal Ganglia > Flashcards

Basal Ganglia Flashcards

1
Q

Basal Ganglia

Overview

A

Motor control center for regulation of movement.

Does not generate motor commands.

Provides gain control by ∆ combinations, directions, and sequences of movements via indirect connections:

BG → thalamus → cortex → spinal cord

BG → reticular formation → PRST & MRST

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2
Q

Basal Ganglia

Functions

A
  1. initiation and termination of movement
  2. context switching between patterns of movement
  3. sequence learning
  4. reinforcement learning
  5. combining limbic drive with motor action

Also involved in cognitive functions.

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3
Q

Basal Ganglia

Dysfunction

A

Results in progressive motor symptoms of excessive or deficient movement, or both.

Includes:

  • rigidity involving active contractions
  • slowed or absent ability to initiate movements
  • loss of postural reflexes
  • involuntary and inappropriate movements
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4
Q

Basal Ganglia

Structures

A

Group of 5 main forebrain structures:

  1. Caudate nucleus
  2. Putamen
  3. Globus pallidus
    • internal segment (GPi)
    • external segment (GPe)
  4. Subthalamic nucleus (STN)
  5. Substantia nigra (SN)
    • pars compacta (pC or SNc)
    • pars reticulata (pR or SNr)

Caudate + putamen = striatum (STR)

Putamen + globus pallidus = lenticular nucleus

Nucleus accumbens and ventral pallidum sometimes considered part of the basal ganglia.

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5
Q

Blood Supply

A

Supplied mainly by perforating branches of 3 arteries:

Caudate nucleus:

ACA, MCA, and anterior choroidal artery (AChA)

Putamen:

ACA and MCA

Globus pallidus:

anterior choroidal and MCA

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6
Q

Striatum

Characteristics

A

Caudate + Putamen

  • Similar cell types, afferents, and efferents
  • Extent and pattern of cortical projections produces functional differences
  • Afferents from 3 major inputs converge onto the same striatal cells.
    • Cortical and thalamic inputs ⟾ distally on dendrites of striatal spiny neurons
    • SNc DA inputs ⟾ proximally
      • able to modulate effects of other inputs
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7
Q

Striatum

Inputs

A
  1. Cortical input:
    • Glutamatergic → ⊕ distal spiny neurons
    • Significant input from all cortical areas
      • Cognitive and affective areas → caudate n.
      • Primary motor and sensory areas → putamen
    • Primarily ipsilateral
    • Topographically organized
      • maintained throughout BG
  2. Thalamic input:
    • Mainly from intralaminar nuclei
      • CM thalamus → caudate n.
      • Parafascicular n. → putamen
    • Thalamic n. receive convergent input from many sources and sensory modalities
  3. SNc input:
    • Sign. input from dopaminergic neurons
    • Modulates effects of other inputs
    • Destroyed in Parkinson’s disease and by MPTP neurotoxin
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8
Q

Striatum

Outputs

A
  • Projects to globus pallidus and substantia nigra
    • Mainly GABAergic → inhibitory
    • Also uses enkephalin, dynorphin, and substance P
  • Topographic organization received from cortex perserved in projections
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9
Q

Globus Pallidus

A

Globus pallidus externa (GPe)

  • GABA/enkepalin striatal input
  • Projects mainly to STN
    • GABAergic → inhibitory

Globus pallidus interna (GPi)

  • GABA/Substance P striatal input
  • One of two major BG output pathways
  • GABAergic → inhibitory
  1. Thalamic projection (VA >>> VL and CM)
    • Pallidothalamic projections forms 2 fiber bundles
      • Ansa lenticularis
        • originates from GPi areas receiving caudate n. input
        • projects to VA thalamus
      • Lenticular fasciculus
        • originates from GPi areas receiving putamen input
        • projects to VL and CM
  2. Mesencephalic reticular formation
  3. Pedunculopontine nucleus
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10
Q

Subthalamic Nucleus

(STN)

A

Contains glutamatergic neurons.

Only basal ganglia n. with pure excitatory function.

GPe → STN → GPi

Cortex & SNc → STN → SNr

Unilateral STN lesion ⟾ contralateral hemiballism.

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11
Q

Substantia Nigra

A

Pars compacta (SNc)

  • pigmented cells contain melanin
  • dendrites extend into SNr
    • affected by SNr inputs
  • Dopaminergic neurons project mainly to striatum ⟾ nigrostriatal pathway
  • Lost in Parkinson’s disease

Pars reticulata (SNr)

  • Inputs:
    • striatal neurons ⟾ GABA
    • subthalamic neurons ⟾ Glu
  • Major output n. of basal ganglia (GABAergic)
    1. Nigro-thalamic → VA
    2. Nigro-tectal → superior colliculus
      • control of eye movements
    3. Mesencephalic reticular formation
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12
Q

Basal Ganglia

Circuits Overview

A

Basal ganglia inputs and outputs organized into two circuits ⟾ direct and indirect.

  • Both activated by excitatory inputs from cortex.
    • Functions to disinhibit thalamic/RF targets of BG
  • Both with inhibitory output mainly to:
    • VA thalamus
      • ⊕ ⟾ premotor & supplementary motor
      • involved in generation of movements
    • Pediculopontine nucleus (PPN) of RF
      • ⊖ ⟾ spinal cord circuits
      • involved in postural control
  • Direct path:
    • disinhibition of VA and PPN
    • faciliates motor synergies
    • suppresion of postural control
  • Indirect path
    • increased inhibition of VA and PPN
    • promotes inhibition of motor synergies
    • faciliates postural control
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13
Q

Modular Loops

A

Circuits show tight somatotopic organization within striatum, globus pallidum, STN, and corticothalamic loops.

Specific areas of each component projects to a specific area of the next.

Eventually projects back to original cortex area.

Establishes a modular organization within corticothalamic and basal ganglia loops.

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14
Q

Direct Pathway

A

Cortical activation of direct path inhibits spontaneous activity of Gpi/SNr cells

⟾ disinhibition of VA and PPN

⟾ increases activation of motor cortices

⟾ promotes initiation and facilitation of movements (VA)

⟾ suppresses postural control (PPN)

Mechanism

  1. Motor plan from cortex to striatum.
    • Glu → ⊕ GABA/substance P neurons of direct path.
  2. ↑ GABA/substance P → ⊖ GPi/Snr
  3. ↓ GPi/Snr inhibits less VA thalamus
  4. Disinhibited VA → ⊕ Glu → activates more the premotor and supplementary motor cortices
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15
Q

Indirect Pathway

A

Cortical activation of indirect path inhibits GPe neurons.

⟾ disinhibition of STN

⟾ ↑ STN activation of GPi/SNr

⟾ ↑ inhibition of VA/PPN

⟾ promotes inhibition of movement (VA)

⟾ facilitation of postural control (PPN)

Mechanism

  1. Motor plan from cortex → striatum (indirect path)
    • Glu → ⊕ GABA/enkephalin neurons
  2. ↑ [GABA/enkephalin] → ⊖ GPe
  3. Inhibited GPe inhibites less STN
  4. Disinhibited STN via Glu activates more GPi/SNr
  5. Activated GPi/SNr via GABA inhibites more VA/PPN
  6. Inhibited VA activates less motor cortices.
  7. Inhibited PPN inhibites less spinal cord pathways.
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16
Q

Effects of Dopamine

A

Dopamine released by SNc acts on STR and STN.

⊕ direct path via D1 receptors

⊖ indirect path via D2 receptors

Net effect of DA to facilitate movement.

Modulates how systems process information.

Affects how quickly they switch on and off movement.

Loss of modulation causes direct and indirect circuits to ‘jam’.

17
Q

Direct Path

Altered Activity

A
  • Overactivity
    • ↓ GPi/SNr
    • ↑ VA/PPN
    • Excessive movement
    • Decreased postural control
  • Underactivity
    • ↑ GPi/SNr
    • ↓ VA/PPN
    • Voluntary movement difficult and slow
    • Increased postural control = rigidity
18
Q

Indirect Path

Altered Activity

A
  • Overactivity
    • ↑ GPi/SNr
    • ↓ VA/PPN
    • Voluntary movement difficult and slow
    • Increased postural control = rigidity
  • Underactivity
    • ↓ GPi/SNr
    • ↑ VA/PPN
    • Involuntary movement
    • Decreased postural control
19
Q

Parkinson’s Disease

Mechanism

A

Caused by loss of dopaminergic neurons within SNc.

  • Direct pathway becomes underactive (D1)
    • generation of movement difficult and slow
    • postural control increased
  • Indirect path becomes overactive (D2)
    • difficult to initiate movement
    • rigidity
20
Q

Parkinson’s

Symptoms & Treatment

A
  • Positive motor symptoms
    • Tremor at rest
      • “pill-rolling”
      • postural tremor
    • Cogwheel or lead pipe rigidity
    • Involuntary movements (akathesia)
  • Negative motor symptoms:
    • Bradykinesia
      • shuffling gait (marcher a petit pas)
      • expressionless face (masked facies)
      • povery of blinking
      • lack of spontaneous speech
    • Postural disturbances
      • head droop
      • stooped posture
      • impaired righting
  • Treatments:
    • L-Dopa
    • Grafting of DA containing cells (fetal mesencephalon)
    • Lesion in/around VA/VL nucleus, pallidum, or STN.
    • Deep brain stimulation (DBS)
      • likely functions by unjamming or functional lesion of STN action on movement
21
Q

Huntington’s Corea

Mechanism

A

Efferent neurons of striatum progressively destroyed.

Starts in caudate n. and progresses to putamen.

Early Phase

GABAergic/Enkephalin & cholinergic cell degeneration.

  • Indirect path becomes underactive
    • ↑ GPe → ↓ STN → ↓ GPi/SNr → ↑ VA/PPN
    • Excessive and involuntary movements
    • Decreased postural control

Late Phase

GABA/substance P cells also degenerate.

  • Direct path becomes underactive
    • failure to initiate normal movements
    • akinesia
    • rigidity
22
Q

Huntington Chorea

Symptoms and Treatment

A
  • Symptoms
    • chorea
    • cognitive impairment (dementia)
    • psychiatric disturbances
    • death 15-20 years after onset
  • Treatment
    • Palliation of motor and affective sx
23
Q

Hemiballismus

A

Due to lesion in STN.

  • ↓ GPi/SNr → ↑ VA/PPN
    • Reduced input from GPi allows thalamocortical neurons to respond in exagerated manner
    • inc. tendency to discharge spontaneously
  • Results in involuntary violent movements of contralateral limbs
24
Q

Tardive Dyskinesias

A
  • Caused by certain medications including neuroleptics and anti-psychotics.
  • Temporarily alters or permanently damages basal ganglia function.
  • May be caused by denervation hypersensitivity of dopamine receptors.
  • Sx. include involuntary tongue protrusion and grimacing.
25
Q

Striatum

Histological Organization

A

Composed of striosomes (islands) embedded in matrix.

Areas have different afferent and efferent projections.

  • Striosomes
    • continuous tortuous columns of cells
    • low ACh content
    • enriched in enkephalin, SP, somatostatin, opiate, and DA receptors
    • mostly limbic input from cortex
    • projects to SNc
  • Matrix cells
    • enriched in ACh
    • low in neuropeptide receptors
    • mostly sensorimotor input from cortex
    • projects to SNr and GP

Combines limbic with motor programming and sequencing control to generate appropriate goal directed and cognitive behaviors.

26
Q

Basal Ganglia Dysfunction

Symptoms and Causes

A
  1. Involuntary movements
    1. Resting tremor ⟾ lesion in SNc
    2. Athetosis ⟾ lesion in putamen - partial caudate
      • disturbance in posture with involuntary movements which are slow and writhing
    3. Chorea ⟾ lesion in caudate + partial putamen
    4. Hemiballismus ⟾ lesion in STN
  2. Rigidity ⟾ lesion in any BG nuclei
  3. Akinesia ⟾ lesion in SNc and others
  4. Dystonia ⟾ lesion in globus pallidus
    • exaggerated tone or posture, torticollis
27
Q

Cognitive Functions

A

Cognitive functions of the prefrontal cortex involves projections to BG.

Dorsolateral prefrontal cortex (BA 9 & 10) ⟾ head of caudate n. ⟾ GPi/SNr ⟾ MD thalamus ⟾ dorsolateral prefrontal cortex

Pathway modulated by dopamine via mesocortical projections from VTA.

28
Q

Mood Functions

A

Mood functions involves BG structures.

limbic cortex/hippocampus/amygdala ⟾ nucleus accumbens ⟾ ventral pallidum ⟾ MD thalamus ⟾ anterior cingulate gyrus and orbitofrontal regions

Pathway modulated by DA via mesolimbic projections from VTA.

29
Q

Basal Ganglia

Behavioral Disorders

A

Hypothesized that neural mechanisms for behavioral disorders analogus to those of motor.

Ex.

Schizophrenia ⟾ disorder of thought

OCD ⟾ hyperactivity

30
Q

Basal Ganglia

Pathways

A

Ansa Lenticularis​

GPi → VA thalamus

Fibers pass under internal capsule to reach thalamus.

Lenticular fasciculus

GPi → VA thalamus

Fibers go through internal capsule, dorsal to subthalamus, then reach thalamus.

Thalamic fasciculus

Receives fibers from ansa lenticularis and lenticular fasciculs.

Projects to thalamus

Subthalamic fasciculus

GPe ↔ STN

IMS: Neuroanatomy (23 decks)

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