Basal ganglia

DR NILESH KATE
MBBS,MD
ASSOCIATE PROF
DEPT. OF PHYSIOLOGY
BASAL
GANGLIA.

OBJECTIVES
 Physiological
anatomy.
 Components.
 Corpus striatum.
 Connections.
 Functional neuronal
circuits.
 Functions of basal
ganglia.
 Disorders of basal
ganglia.
 Parkinson’s disease.
 Chorea & athetosis.
 Huntington’s disease.
 Wilson’s disease.
 Kernicterus.
Friday, March 4, 2016

Physiological Anatomy.
Components.
 Basal Ganglia ------ Group of
nuclei (mass of grey matter) in
the forebrain and
 upper part of the brain stem
that have motor function of
great importance --
Head ganglia of Motor control.

FIVE GREY NUCLEAR MASSESFIVE GREY NUCLEAR MASSES
At the base of the cerebral hemispheres.At the base of the cerebral hemispheres.
 Caudate nucleusCaudate nucleus
 Putamen (corpus striatum)Putamen (corpus striatum)
 Globus pallidusGlobus pallidus
 Substantia nigraSubstantia nigra
 Sub-thalamic body of LuysSub-thalamic body of Luys
 Red nucleusRed nucleus

CORPUS STRIATUM.
 Subcortical masses of
grey matter situated in
white core
 Divided into 2 parts by
internal capsule.
 Caudate nucleus
 Lenticular nucleus.
 Putamen
 Globus pallidus.

Salient Features of Nuclei of
Corpus Striatum.
 Caudate nucleus.
 Highly curved, comma
shaped band of grey
matter.
 Consists of Head, body
& Tail
 Separated from
lenticular nucleus by
internal capsule

Lenticular Nucleus.
 Biconvex lens.
 Triangular in both
coronal & horizontal
sections.
 Divided into 2 parts by
external lamina of
white matter.

Putamen
 Outer part of
lenticular nucleus.
 Dark in colour
 Quadrangular in
shape.

Globus Pallidus.
 Inner smaller part.
 Paler.
 Divided into 2 parts
 External segment.
 Internal segment.

Sub Thalamic Nucleus.
 Biconvex mass of grey
matter lateral to red
nucleus & dorsal to
substantia nigra.
 Separated from
thalamus by Zona
inserta.

Substantia Nigra.
 Made up of small unpigmented &
large pigmented nerve cells.
 Contains neuromelanin.
 Divided into 2 parts
 Pars compacta – contains
dopaminergic (75%) & cholinergic
(25%) neurons.
 Pars reticularis contains GABA
ergic neurons.

Connections.
 Main input – Corpus Striatum ( Caudate
Nucleus & Putamen)
 Main Output – Globus Pallidus.

Afferent or Inputs to Striatum.
 Corticostriate projections. – Glutamatergic.
 Thalamostriate fibre. – from Centromedian N
 Nigrostriate fibres.– Pars Compacta
(Dopaminergic)
 Raphe striate fibres. – Raphe N. in reticular
formation (Serotoninergic)
 Locus Coeruleus striate fibres. (Noradrenergic)

Projections from striatum.
 Striatum to Globus
pallidus. – GABAergic
inhibitory projections.
 Striatum to
Substantia Nigra. –to
Pars Reticulata
(GABA-ergic inhibitary
impulses)

Efferents or output from
Globus Pallidus.
 Thalamus– thalamic
Fasiculus or Ansa
Fasicularis – to VA, VL and
centromedian N.– to
Prefrontal & Premotor
cortex.
 Subthalamic nuclei – to
Substantia Nigra.
 Red nucleus – rubrospinal
tract pathway.
 Substantia nigra.
 3 routes
 Directly.
 Via Subthalamic N.
 Via Pedunculopontine
N.

Connections of Basal Ganglia.

Functional neuronal circuits or
loops.
 Corpus striatum does not have direct
connections to spinal cord.
 GPi & SNpr behaves as a lateral & medial part
of single functional unit.

Primary feedback loop or cortex
basal ganglia motor cortex circuit.
Cerebral cortex
(all parts)
Striatum
Globus Pallidus &
Substantia Nigra
Supplementary motor
cortex
Thalamus
Provide Negative Feedback Loop to Control Motor Cortex
Activity

Caudate Loop
Supplementary motor area & motor sensory area.
Caudate Nucleus.
GPi SNPr
Caudal part caudal part
VL (Thalamus) Pars VL Oralis VL(Thalamus) Pars Medialis
FUNCTION – Cognitive Control Of Motor Activity
-- Control Of EYE Movements

Putamen loop
Frontal Association Area.
Putamen Nucleus.
Gpi SNPr
VA (thalamus) VA (thalamus)
Parvocellular Magnocellular.
FUNCTION – For Motor Control Of Body Movements

Additional feedback loop.
Indirect Pathway via subthalamic N.
Cortex
Striatum
GPe
GPi SNPr
Subthalamic Nucleus
Supplementary Motor Cortex
Thalamus

Indirect Pathway Involving
Pars Compacta.
Cortex Supplementary
Motor Cortex.
Thalamus
Striatum
Ach D2 Dopamine
Ach D1 Dopamine
GPi SNPr
SNPc

Functions of basal ganglia.
 Control of voluntary motor activity.
 Control of reflex muscular activity.
 Control of muscle tone.
 Role in arousal mechanism.

Control of voluntary motor
activity.
 Cognitive control of
motor activity.
 Neural discharge in
Basal Ganglia begins
well before the
movement begins.

Control of voluntary motor
activity.
 Most of the motor actions
occur as a consequence of
thought process in mind.
 So basal ganglia is involved
in planning &
programming of
movements.
 It is executed through
functional neuronal
circuits.

Timing & scaling of intensity of
movements.
 How rapidly & how
much large the
movement should be.

Subconscious execution of
some movements.
 Swinging of arm while
walking.
 Crude movements of
facial expressions with
emotions.
 Movements of limbs
while swimming.
 Importance – cortex can
be free to plan its
actions.
 Pathway- Putamen
feedback circuits.

Control of reflex muscular
activity.
 Inhibitory effect on
spinal reflexes.
 Regulate muscle
which maintains
posture.
 Mainly visual &
Labyrinthine reflexes.

Control of muscle tone.
 Substantia Nigra of Basal
Ganglia control γ motor
neuron which maintain
muscle tone.
 Pathway – cortical inhibitory
area- striatum-pallidum-
substantia nigra-reticular
formation- spinal cord.
 Lesion – Lead pipe type
Rigidity in Parkinsonism.

Role in arousal mechanism.
 By connections of
Globus Pallidus & Red
Nucleus with Reticular
Formation.
 Lesion – drowsiness ,
sleep.

Disorders of Basal Ganglia.
 Parkinson’s disease.
 Chorea.
 Athetosis.
 Huntington’s disease.
 Hemiballism.
 Wilson’s disease.

Parkinson’s disease
 Paralysis agitans or
shaking palsy.
 Described by James
Parkinson in 1817.

Aetiopathogenesis.
 Primary idiopathic
condition.
 In elderly due to
Idiopathic
degeneration of
Nigrostriatal system
of Dopaminergic
Neurons.
 Secondary causes-
Parkinsonism nigra.
 Viral Encephalitis.
 Cerebral Arteriosclerosis.
 Drugs – Phenothiazines.
 Experimentally by
injecting MPTP (methyl-
phenyl-tetrahydro-
pyridine)

Pathogenesis.

Clinical features.
Akinesia or Hypokinesia.
 Unable to initiate
voluntary movements
or decreased
movements.
 Causes – Due to
Hypertonicity of
Muscle.

Clinical features
 C/F – Bradykinesia,
mask like face,
prolonged reaction
time,
 Absent associated
movements.
 Shuffling or
Festinant type gait.
 Retropulsion.

Rigidity
 Increased tone in the muscle.
 Cause – increase discharge of
γ Efferents to muscle spindle.
 Mechanism – striatum under
influence of both
Ach(excitatory) & Dopa
(Inhibitory)
 Degeneration of neurons of
SN – less Dopa & more Ach
activity – hyperkinetic
features.
 C/F – lead pipe & cog-
wheel type rigidity.
 Hypertone in
protagonists &
antagonists muscle.
 Statue like appearance.
 Posture – flexion
attitude.

Tremors
 Involuntary rhythmic
oscillatory movements of
distal parts of limb & head.
 Resting tremors.
 Absent at sleep & increased
by stress & excitement.
 4-6 times/sec.
 Frill rolling movements.
 Neural mechanism.
 Due to pacemaker
activity in nucleus
ventralis intermedius of
thalamus.

Treatment.
 L-Dopa
 As it crosses BBB.
 With Carbidopa as it
prevents its conversion
to dopamine in liver.
 Low dose – reduces
rigidity & high dose
reduces tremors.
 Surgical Destruction.
 Of Globus Pallidus or
VLN of thalamus.

Chorea.
 Rapid , jerky
involuntary
movements (dancing)
 Due to damage to
caudate N.
 Seen in children as a
complication of
Rheumatic fever.

Athetosis.
 Slow, rhythmic, twisting,
worm like , confluent
writhing movements of
the extremities
 Mainly fingers & wrist.
 Due to damage to
Putamen.
 Seen in children after
birth injuries.

Huntington’s disease.
 Genetic disease.
 Trinucleotide repeat
expansion.
 Autosomal Dominant
disorder.
 30-50 yrs of age.
 Abnormal gene at
short arm of chr-4.
 Lesion – damage to
GABAergic & cholinergic
neurons of striatum to
pallidum.
 Hyperkinetic features.
 C/F – hyperkinetic
chreiform movements,
Slurred speech, dementia,
jerky trajectory of hand.

Hemiballism.
 Cause – damage of
subthamic Nucleus
commonly haemorrhage.
 So reduce output from
GPiSNpc to thalamus.
 Disinhibition of thalamic
output – hyperkinetic
movements.
 C/F – spontaneous
attack of flail-like,
intense violent
movements of whole
opp of body.

Wilson’s disease.
 Hepatolenticular
degeneration by Cu
toxicity due to
impaired biliary
excretion of Cu.
 Changes more marked
in lenticular nucleus
mainly Putamen.
 C/F – Parkinsonism,
Akinesia, muscle
rigidity & tremors.
 Ceruloplasmin level
low & Cu content of
SN high.

Kernicterus.
 In Hemolytic diseases of
Newborn due to Rh
antibodies -- Raised
indirect bilirubin –
crosses BBB – damages
Globus Pallidus.
 C/F – Rigidity, Chorea,
Athetosis & Mental
Deficiency.

Basal ganglia

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