basal ganglia 14
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The Basal Ganglia
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I. Functional anatomy
A. Input and output components
cerebral cortex BG thalamus (VA) frontal lobe.
B. Parallel circuits
C. Neurotransmitters
D. Intrinsic circuitry of the basal ganglia and movement
without.
II. Regional anatomy
A. Internal capsule and striatumB. Series of coronal sections revealing anatomy and
relationships of the nuclei.
C. Midbrain sections showing substantia nigra.
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I. Functional anatomy
Introduction: Basal ganglia are subcortical
structures that are part of cerebralhemispheres. They receive input from and
send regulatory signals back to the cortex
(frontal lobes).Regulation of movement, cognitive,
motivation, and emotion.
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A. Input and Output Components of the Basal Ganglia
VL
Know this figure!!
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The Striatum shown in relation to ventricles
Note that caudate n. and putamen are connected by cell bridges
(spanning internal capsule)
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B. Parallel circuitsanatomical loops
subserve the various functions.
Input-output nuclei specifically assigned to
these jobs are outlined and specific frontal
cortical projection areas are illustrated in
Fig. 14-3.
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Parallel circuits Fig. 14-3
Skeletomotor loop:
Control of skel muscle
Oculomotor loop:
Control of extraocular muscles
Association loop:
Role in cognition
Limbic loop:
Maturation/emotions
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Fig. 14-3 - Loops
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C. BG Neurotransmittersused in the various BG
circuits and outlined (Fig. 14-4)
Glu/Asp: excitatory
GABA: inhibitory (major neurotransmitter of the BG)Important neuromodulators:
dopamine (from SN pc to striatum)
acetylcholine (connect within striatum)
enkephalin, substance P (out of striatum direct + indirect pathways
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D. Intrinsic circuitry of the basal gangliaandmovement disorders.
Refer to Box 14-1.
Direct and indirect striatal output pathways:
direct excitatory to thalamus (VA)
indirect inhibitory to thalamic target neurons.
Direct path: what happens when you inhibit an
inhibitory signal (disinhibition = doublenegative)?
Indirect path: opposite effect on thalamus (-) (and
ultimately, cerebral cortex.
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Double negative (disinhibition) excites the
output of the STN, which will drive
inhibitory output from Gpi
SNr Thalamus
{Internal segment of globus pallidus and SN pc}Therefore, the inhibition is increased inhibitory output.
This model helps us understand the mechanism of
hypokinetic disorders (e.g.,Parkinsons Disease) and
hyperkinetic disorders (e.g., Huntingtons Disease andhemiballism).
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Parkinsons Disease: decreased dopamine fromSN decreased inhibition of the inhibition
excessive inhibitory output classic signs of PD(hypokinesia, bradykinesia)via decreased
thalamic signals to cortex decreased
corticospinal outflow.
Huntingtons Disease: decreased striatal(enkephalin) output and decreased inhibition of
Gpo enhanced excitatory effects of indirect path
decreased inhibition via direct path
hyperkinesis.
Hemiballism: similar mechanism (subthalamic n.lesion).
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Parkinsons: increased indirect
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Most modern therapies for PD have
involved lesions without the circuit in an
effect to re-established the balance (e.g.,STN lesion)
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Hyperkinesis: increased direct
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II. Regional Anatomy
A. Internal capsule and striatumrecall how the
striatum is divided into caudate n. and putamen
by the anterior limb of the internal capsule and
that cellular bridges (visible in horizontal
section) exist between these (Fig. 14-6).
Note also that internal and external segments of
globus pallidus, posterior limb, and the thalamic
nuclei below (Fig. 14-8).
B. Series of coronal sections revealing anatomy ofthe nuclei and their spatial relationships.
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Horizontal Section Through Basal Ganglia (Fig. 14-6)
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Anterior section (Fig. 14-8)
Note: head of caudate, nucleus accumbens, and
cell bridges are prominent here.
The head of caudate is often used as a radioligand landmarknormally
buldges into anterior horn of lateral ventricles.
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Head of caudate = radiological landmark (Fig. 14-10)
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Fig. 14-11
The globus pallidus and ventral pallidum are beneath the anterior
commissure.
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Subthalamic nucleus (Fig. 14-14)
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Mid-section
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Midbrain through the substantia nigra (Fig. 14-16).
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