Basal Ganglia

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Neuro-anatomy & localization of

the Basal Ganglia

Mesfin Efrem (MSc in


ICCMH)
Outlines of presentation
 Introduction
 Embryonic Development
 Basal Ganglia
 Anatomy
 Physiology
 Pathophysiology of BG lesions
Introduction
 Basal “ganglia” is a misnomer
 No clear consensus on which structures
should be included in the basal ganglia
 Those structures in the striatopallidal circuits involved in
modulation of the thalamocortical projection

 The basal ganglia don’t originate on


separate motor pathway
 Influence and modulate the activity of motor
cortex and descending motor pathway
Embryonic Development of the
Basal Ganglia
Contd
 Striatum- telencephalon
 GPi & GPe – telencephalon
 SN - mesencephalen
 STN - diencephalon
Basal Ganglia

Putamen
Globus Pallidus
Basal Ganglia

 Striatum
 Caudate nucleus
 Putamen
 Nucleus accumbens
 GP
 Globus pallidus
external (GPe)
 Globus pallidus internal
(GPi)
 Substantia Nigra
 Pars compacta (SNc)
 Pars reticulata (SNr)
 Subthalamic nucleus (STN)
The basal ganglia and surrounding
structures
The basal ganglia and surrounding
structures
On Imaging(MRI)
Caudate nucleus

 C-shaped mass of gray


matter.
 The head, located deep
 Within the frontal lobe
 The body, located deep
 In the parietal lobe
 The tail, which goes in
to
 The temporal lobe
 The caudate is continuous with the
putamen at the head and tail.
 caudate + putamen = the striatum,
the major target for projections from the cerebral
cortex and the SN
Lentiform nucleus
(putamen,GP)

 Wedge-shaped
mass of gray
matter .
 Latin’ lens-
shaped’
 Medially
 The internal
capsule
 Laterally
 The external
Nucleus accumbens

 IS a Component of
the striatum
 Receives input from
 The limbic system
 Process
Emotional aspects of
movement
SN (black substance)

Composed of two
parts:
 Deep pars or
zona compacta
(SNc)
Melanin-containing,
dopaminergic.

Superficial zona
reticulata (SNr) The substantia nigra (SN), a
 Nonpigmented, melanin-containing (pigmented)
GABAergic. nucleus, normally contains about
500,000 dopaminergic neurons
Subthalamic nucleus

 Small ,lens-shaped
Gray mass
component of the
subthalamus.
 Lateral to the
hypothalamus
 Medial to the internal
capsule
STN
 subthalamic
nucleus exerts an
inhibitory or
regulating
influence on the
globus pallidus and
ventral thalamus
Arterial Supply of the Basal Ganglia
Arterial Supply of basal ganglia
Basal ganglia circuits
 Five parallel and separate closed circuits
through the basal ganglia have been
proposed. Motor, oculomotor,
dorsolateral prefrontal, lateral
orbitofrontal, and limbic loops

 These loops form three major divisions—


 Sensorimotor  motor function
 Associative cognitive function
 Limbic emotional functions
Physiology
 The basal ganglia exert a dual control on the
initiation and execution of movement:
 1) they facilitate the initiation of a particular motor
program by transiently interrupting the output.

 2) Inhibit the initiation of competing motor


programs by increasing the tonic inhibitory output .

 This dual effect is regulated by two opposing


influences:
 Tonic excitation by the subthalamic nucleus and
 Transient (phasic) inhibition by the striatum.
Neurotransmiters
 Most excitatory synapses of the basal
ganglia and its connections
 From the cerebral cortex to the striatum
 STN to the GPi glutamat
 e
Thalamocortical projections

 Projections from the striatum to the GPe and


GPi, from the GPe to the STN, and from the GPi
to the thalamus are inhibitory and employ
GABA
Neurotransmitters
Basal ganglia input and output nuclei

24
Intrinsic pathway
Efferent pathway
 The GPi & SNr are the major output
structures
 GABAergic inhibitory connection
 Gpi to number of thalamic
structures(VL,VA)
 The Ansa reticularis
 Lenticular fasiculus
 SNr projects to the superior colliculus
which is invoved in eye movts as well as
the thalamic nuclei
Two pathway signals in the Basal
Ganglia
1. Direct pathway:

♦ Inhibition of internal GP DIRECT


so no longer keeps
thalamus from exciting
cortex

♦ Facilitate the ongoing


movement.

Cortex(Stimulates)striatum(inhibits)”SNr-Gpi”complex (less inhibition


of
thalamus)Thalamus(stimulates)Cortex(stimulates)muscle,etc(hyperk
inetic state)
2. Indirect PW:

♦ Causes subthalamus INDIRECT


to activate internal
GP, suppressing
thalamic activation

♦ Suppressing
unwanted movements

Cortex(Stimulates)striatum(inhibits)”GPe (less inhibition of


STN)STN(stimulates)”SNr-Gpi”complex(inhibits)Thalamus(is
stimulating less)Cortex(is stimulating less)muscle,etc
(hypokinetic state)
Nigrostriatal pathway
 Important in the
modulation of
the Direct &
Indirect pathway

 Direct pathway
neurons have D1
dopamine
receptor

 Indirect pathway
neurons have D2
dopamine
receptor
Basal Ganglia functions

 Motor function
 Ocular motor function
 Cognitive function
 Affective function
Motor function

 Planning the
sequence of
actions in order to
execute learned
motor activities.
Ocular motor function
SNr neurons are tonically active suppressing
the output of collicular neurons

Excitation of the direct striatal neurons by


cortical frontal eye fields

momentarly inhibit SNr neurons releasing


collicular neurons from inhibition

Allows the appropriate collicular neuron to


signal the target of the eye movt allowinjg to
change gaze
Cognitive function
 Cognitive functions
are largely mediated
by the associative
striatum.

 Involved in our
ability to
subconsciously learn
the probability of
predicting outcomes
associated with
particular stimuli
Affective function
 Functions in the
emotional and
motivational aspects
of movement.
 Manifested as
various facial
expressions or other
body movements
Clinical Correlations

Pathophysiology of Movement
Disorders
 According to the “dual model” of the

basal ganglia circuits, shifts in the


balance between the activity in the direct
and indirect pathways underlies several
movement disorders.
Hypokinetic movement
disorders
 Parkinson’s
Disease

 MSA
(multisystem
atrophy)

 Wilson disease

(hepatolenticul
ar
degeneration)
Hyperkinetic movement
disorders

 Chorea
 Huntington’s
chorea
 Secondary chorea
 Tremor Disorders
 Tardive dyskinesia
 Ballismus
 Athetosis
 Dystonias
 Tic Disorders
REFERENCES
 FUNCTIONAL
NEUROANATOMY, ATLAS &
TEXT, 2ND EDITION
 Adams & Victor`s
principle of
Thank
neurology, 9th edt.

You
Thank You

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