Transcript slide file for students(YYL)

Basal Ganglia
Principles of neural sciences 5th ed.
The human brain: an introduction to its functional anatomy 6th ed.
林永煬
國立陽明大學 腦科學研究所
Basal ganglia and surrounding structures, as seen in an axial section
Basal ganglia and surrounding structures, as seen in coronal sections
The compact (SNc) and reticular (SNr) parts of the substantia nigra
Terminology associated with the basal ganglia
Parasagittal section showing how the striatum got its name
Three-dimensional reconstruction of the striatum and globus pallidus
inside a translucent CNS
Striopallidal fibers: from putamen to globus pallidus (pallidum)
Corticostriate fibers: from cerebral cortex to putamen, caudate nucleus,
or nucleus accumbens
Pallidothalamic fibers: from globus pallidus to thalamus
Nigrostriatal fibers: from substantia nigra to striatum
Nigroreticular fibers: from substantia nigra to reticular formation
Thalamostriate fibers: from intralaminar nuclei to striatum
Basal ganglia circuitry
Corticostriate inputs:
Afferents from cortex to striatum and subthalamic nucleus
Excitatory (glutamate) connections
Output projections:
Efferents leaving from globus pallidus (GPi) and substantia nigra (SNr)
to thalamus
Inhibitory (r-aminobutyric acid [GABA]) connections
Thalamocortical projections:
Excitatory (glutamate) connections
Principal inputs to and outputs from the basal ganglia
Cortical functions related to basal ganglia circuitry
Movement
Cognition
Emotion
Motivation
Parallel loops through the basal ganglia
Cortical functions related to basal ganglia circuitry
Motor functions:
sensorimotor cortex  putamen  GP  thalamus
 motor/premotor/supplementary motor areas
Cognitive functions:
association cortex  caudate nucleus  GPi-SNr  thalamus
 prefrontal areas
Emotion/motivation:
amygdala/hippocampus/limbic cortex  ventral striatum (nucleus accumbens)
 ventral pallidum  thalamus (dorsomedial nucleus)
 temporal/ hippocampus/limbic cortex
Major connections of the striatum
Medial (A) and lateral (B) views of the left striatum showing the somatotopic
representation of body parts
Chemical compartmentalization of the striatum
*
*
CN
IC
P
A
P=putamen, CN=caudate nucleus,
IC=internal capsule,
A=nucleus accumbens
Acetylcholinesterase (AChE)-rich
background (matrix) with embedded
AChE-poor regions (striosomes *)
Caudate nucleus stained for
enkephalin
Caudate nucleus stained for AChE
High enkephalin levels are found in the
peripheries of striosomes.
Case presentation
A 25-year-old woman
with dramatic change in cognition, motivation, and self-care.
Contrast-enhanced computed tomography scans of a 25-year-old woman
with dramatic change in cognition, motivation, and self-care.
Acute stage
8 months later
Major connections of the external segment of the globus pallidus (GPe)
Afferents
to GPi and SNr
Efferents
from GPi and SNr
GPi and SNr receive inhibitory inputs from striatum,
and excitatory inputs from STN.
GPi and SNr provide output from basal ganglia.
Subthalamic fasciculus interconnecting STN and GPi
Major connections of STN
STN provides a powerful excitatory
input to GPi and SNr.
Major inputs to STN arise not only
from GP but also from cerebral cortex.
Different sectors of STN deal with
motor, cognitive, affective functions.
Abnormalities of movement due to basal ganglia disorders
Hyperkinetic disorders:
tremor, chorea, athetosis, ballismus, hemiballismus
Disturbance of muscle tone: dystonia
Huntington’s disease
Parkinson’s disease
Hemiballismus
Video show
s/s: wild flailing movements of one arm and leg
Lesion location in contralateral STN
Most often seen in older people with a stroke involving a ganglionic
branch of posterior cerebral artery
Contrast-enhanced mass in left STN of a 65 y/o
male HIV-positive patient with unintentional,
forceful flinging movements of right limbs.
Longitudinal slice of a normal brain
Huntington’s disease
s/s: involuntary choreiform movements,
alterations of mood or cognitive function
dementia and personality change
Symptom onset at age of 30 – 50 years
Inherited in an autosomal dominant pattern,
with a defective gene at short arm of chromosome 4
Pathomechanism:
striatal (esp. caudate nucleus) and cortical degeneration
Video show
MRI scan in a 29 y/o man
with Huntington's disease
MRI scan in a
normal individual
Dorsal-ventral degeneration
gradient (red > blue)
Parkinson’s disease
s/s: tremor
rigidity (increased muscle tone)
slow movements (bradykinesia, hypokinesia)
stooped posture
Pathomechanism:
degeneration of substantia nigra (esp. SNc, pigmented nigral cells)
The midbrain of a patient with Parkinson's disease, showing loss of
pigmentation in the compact part of the substantia nigra (*)
A model for movement control by basal ganglia
(through excitatory (green) and inhibitory (red) interactions)
Direct pathway
Loss of excitatory
STN projections
(e.g. hemiballismus)
Indirect pathway
Loss of dopamine neurons from
SNc causes a reduced thalamic
and cortical output. (e.g. PD)
Dopamine excites direct pathway,
but inhibits indirect pathway.
Increased blood flow in the supplementary motor area (S) and premotor cortex (P) of
Parkinson's disease patients during movement following treatment with levo-dopa
Parkinson’s disease following unilateral pallidotomy
Improvement in bradykinesia and rigidity
Increase in cerebral blood flow on PET