BASAL

GANGLIA.

DR NILESH KATE
MBBS,MD
ASSOCIATE PROF
DEPT. OF PHYSIOLOGY
 OBJECTIVES
 Physiological  Disorders of basal
anatomy.
 Components.
 Corpus striatum.
 Connections.
 Functional neuronal
circuits.
 Functions of basal
ganglia.
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.

Friday, March 4, 2016

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

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 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.

Friday, March 4, 2016

 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

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

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

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

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

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

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 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)

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

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

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Friday, March 4, 2016
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.

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 Primary feedback loop or cortex
basal ganglia motor cortex circuit.
Cerebral cortex Supplementary motor
(all parts) cortex

Striatum Thalamus

Globus Pallidus &

Substantia Nigra
Provide Negative Feedback Loop to Control Motor Cortex
Activity
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 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
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 Putamen loop
Frontal Association Area.

Putamen Nucleus.

Gpi SNPr

VA (thalamus) VA (thalamus)
Parvocellular Magnocellular.

FUNCTION – For Motor Control Of Body Movements

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 Additional feedback loop.
Indirect Pathway via subthalamic N.

Cortex
Supplementary Motor Cortex

Striatum

Thalamus
GPe
GPi SNPr

Subthalamic Nucleus
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 Indirect Pathway Involving
Pars Compacta.

Cortex Supplementary
Motor Cortex.

Ach D2 Dopamine
Striatum
Ach D1 Dopamine Thalamus

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

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

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

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 Subconscious execution of
some movements.
 Swinging of arm while
walking.
 Pathway- Putamen
feedback circuits.
 Crude movements of
facial expressions with
emotions.
 Movements of limbs
while swimming.
 Importance – cortex can
be free to plan its
actions.
Friday, March 4, 2016
 Control of reflex muscular
activity.
 Inhibitory effect on
spinal reflexes.
 Regulate muscle
which maintains
posture.
 Mainly visual &
Labyrinthine reflexes.

Friday, March 4, 2016

 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.

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

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

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

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

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

Friday, March 4, 2016

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

Friday, March 4, 2016

 Rigidity
 Increased tone in the muscle.  C/F – lead pipe & cog-
 Cause – increase discharge of wheel type rigidity.
γ Efferents to muscle spindle.  Hypertone in
 Mechanism – striatum under
protagonists &
influence of both
Ach(excitatory) & Dopa antagonists muscle.
(Inhibitory)  Statue like appearance.
 Degeneration of neurons of  Posture – flexion
SN – less Dopa & more Ach attitude.
activity – hyperkinetic
features.
Friday, March 4, 2016
 Tremors
 Involuntary rhythmic  Neural mechanism.
oscillatory movements of
distal parts of limb & head.
 Due to pacemaker
activity in nucleus
 Resting tremors.
ventralis intermedius of
 Absent at sleep & increased
by stress & excitement. thalamus.
 4-6 times/sec.
 Frill rolling movements.

Friday, March 4, 2016

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

Friday, March 4, 2016

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

Friday, March 4, 2016

 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.

Friday, March 4, 2016

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

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

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

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Friday, March 4, 2016
 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.

Friday, March 4, 2016

Thank
You