CONTROL OF VOLUNTARY MOVEMENT

PLAN EXECUTION
Basal ganglia

IDEA Cerebral cortex- Premotor and

association areas MOVEMENT
motor cortices

Intermediate
Lateral Cerebellum cerebellum
CONTROL OF VOLUNTARY MOVEMENT
BASAL GANGLIA
 Basal ganglia - a group of subcortical nuclei

 Lies in the inferior part of the cerebral

hemisphere lateral to thalamus
LENTICULAR
NUCLEUS
 FOUR PRINCIPAL NUCLEI OF BASAL GANGLIA

Striatum Subthalamic nucleus

Globus pallidus Substantia nigra

External Internal
segment segment Pars Pars
compacta reticulata

caudate nucleus putamen

 Striatum - the major input nuclei of the basal
ganglia
 It receives inputs from

- cerebral cortex (corticostriate pathway)

- thalamus (thalamostriate pathway)

- brain stem (Raphe striate pathway)

 Output nuclei of the basal ganglia:

Globus pallidus internal segment and the

substantia nigra pars reticulata

 The principal output nucleus is the Globus

pallidus internal segment
 Cerebral
cortex

+
Globus - D1(+)
pallidus-ES Striatum
- D2 (-)
-
- Subs nigra- Subs nigra-
+ PR PC
Subthalamic + +
Globus pallidus-IS -
nucleus

- - +
Brain stem Thalamus
nuclei

Direct pathway INCREASE IN MOVEMENTS

Indirect pathway REDUCTION OF MOVEMENTS

Activation of direct pathway:
 Increased inhibition of the globus pallidus
internal segment (GP-IS) by the neurons in
the striatum.
 The tonically active neurons in the GP-IS fire
less, there is less inhibition of the
thalamocortical fibres.
 Net effect: Excitation of the motor cortex and
increased movements.
Activation of indirect pathway:
 There is increased inhibition of the globus pallidus
external segment (GP-ES) by the neurons in the
striatum
 subthalamic nucleus is excited.

 Increased firing of neurons in the GP-IS and the

thalamocortical fibres are inhibited more.
 Net effect: Inhibition of the motor cortex and
decreased movements.
Net effect of Dopamine on movements:
 Direct pathway is activated

 Indirect pathway is inhibited

 Decreased firing of neurons in the GP-IS,

thereby the thalamocortical fibres are
excited.
 The overall effect of dopamine is to increase
the movements.
Basal ganglia – Four circuits linking the thalamus
and cerebral cortex

-Skeletomotor circuit
-Occulomotor circuit
-Prefrontal circuit
-Limbic circuit

Control behaviours other than voluntary movement

Involves the putamen – SKELETOMOTOR CIRCUIT
PUTAMEN CIRCUIT

Begins and ends in

premotor, motor and PREMOTOR, MOTOR AND
supplementary motor
SUPPLEMENTARY MOTOR CORTICES
cortices

PUTAMEN

GLOBUS PALLIDUS GLOBUS PALLIDUS

- IS -ES
SUBSTANTIA NIGRA-PR
Modulated by
direct and indirect pathways

THALAMUS
 PREFRONTAL CIRCUIT (CAUDATE CIRCUIT)
Cognitive control of motor patterns – executive functions

Prefrontal lobe and cortical

association areas

Caudate nucleus

Globus pallidus Substantia nigra - PR

Thalamus
OCCULOMOTOR CIRCUIT (CAUDATE CIRCUIT)
Control of saccadic eye movements

FRONTAL AND SUPPLEMENTARY

MOTOR EYE FIELDS

Caudate nucleus

Substantia nigra - PR

Superior colliculus
LIMBIC CIRCUIT:

 Concerned with non motor aspects of

behaviour

 Originates from prefrontal and limbic cortex

 Cognition, mood and behaviour

 FRONTAL LOBE TARGETS OF
BASAL GANGLIA -THALAMO CORTICAL CIRCUITS
FUNCTIONS OF BASAL GANGLIA:
 Basal ganglia plays a role in planning and programming
of movements
 Initiates and ends movements
 Prevents unnecessary movements (suppression of
antagonistic movements by inhibition of thalamocortical
neurons to the opposing muscles)
 Has a role in establishing a normal level of muscle tone
 Role in ocular movements
 Has cognitive, emotional and linguistic functions
 DISORDERS OF BASAL GANGLIA
Imbalance in direct and indirect
pathway

Hypokinetic disorders Hyperkinetic disorders

•Huntington’s disease
PARKINSONISM •Hemiballism
•Involuntary movements –
Chorea, Athetosis, Ballism, Dystonia
PARKINSONISM/PARALYSIS AGITANS:
• Neurodegenerative disorder due to loss of
dopaminergic neurons in the substantia
nigra pars compacta.
• Overactivity of the indirect pathway

• Neurons in GP-IS fire more resulting in

inhibition of thalamocortical neurons and
decreased movements.
Causes:
 Idiopathic sporadic cause is the most
common cause of Parkinsonism
 Environmental-Drugs that block D2
receptors, toxins etc.
Features of Parkinsonism:
 Cardinal symptoms of the disease include a
paucity of spontaneous movement
 Bradykinesia –Decreased amplitude and
velocity of voluntary movements
 Akinesia – Impaired initiation of movement
 Expression-less or mask facies

 Resting tremor

 Flexed posture

 Festinant/Falling forward gait

 Cog wheel rigidity Co- contraction of both

agonists and
antagonists –
 Lead-pipe rigidity Hypertonia (Rigidity)
HYPERKINETIC DISORDERS

HUNTINGTON’S DISEASE:

 Trinucleotide repeat disorder involving the basal ganglia

 Loss of intra striatal GABAergic and cholinergic neurons

 Dysinhibition of GP-IS

 Hyperkinetic features

 Dyskinesia (Involuntary movements) and hypotonia

 Athetosis: Slow writhing movements of the
extremities

 Chorea: Jerky, rapid and random dancing movements

of limbs and orofacial structures

 Ballism: Involuntary, intense and violent large

amplitude proximal limb movements

 Dystonia: Co-contraction of agonists and antagonists

– sustained abnormal posture and slow movements