basal ganglia clinical anatomy physiology

BASAL GANGLIA

SUBDIVISION OF BG

A. Neostriatum or Striatum

PutamenCaudate nucleus

B. Pallio striatum or Pallidum

Globus pallidus

C. Lentiform nucleusPutamenGlobus Pallidus

D. ArchistiatumAmygdela

E. Substantia nigraF. Subthalamic nucleus

NERUONS AND CIRCUITS OF BG

DYSINHIBITION

MOTOR COMPONENT OF BASAL GANGLIA

STRIATAL PARALLEL PATHWAY

BG EFFERENTS

CONNECTIONS OF THE NEOSTRIATUM WITH THE SUBSTANTIA NIGRA

CORTICAL LOOP

Cortex: 4,6,temporo, parietal and occipital glutamate

Striatum spiky GABA Pallidum medial

GABA Thalamus VL, VA

BG: SUBCORTICAL LOOPS

In the case of all sub-cortical loops the position of the thalamic relay is on the input side of the loop

Red – Excitatory Blue - Inhibitory

INTERNAL CONNECTIONS OF THE BASAL GANGLIA: DIRECT PATHWAY

PROJECTIONS FROM THE BASAL GANGLIA TO OTHER BRAIN REGIONS

FUNCTION OF BG

Voluntary movement Initiation of movement Control of ramp movement Change from one pattern to other Programming and correcting movement while in

progress (thalamocortical circuts) Postural control

Righting reflex Automatic associated movement (walking)

Control of muscle tone Reticulospinal Vestibulospinal

ABLATION STUDY Unilateral lesion minimal effect Denny Brown – Bilateral lesion → Akinesia + Flexion

dystonia Brook – Cooling of GP → Contralateral cocontraction of

antagoniastic muscle → Flexion, alternate and amplitude of movement

Bilateral striatal ablation → Overactive, does not respond to visual cue – walk to wall

Bilateral pallidal ablation → Hypoactive akinetic Human sterotactic Gpi lesion → tremor >rigidity Subthalamic Nucleus ablation → Hemibalismus Bilateral CN ablation → immobile animal VL thalamic cooling → Ia discharge to stretch reflex →

rigidity by y tone

STIMULATION STUDIES

CN stimulation → head and body turn to opposite site, circling movement, or mild hypertonia, late tremor, changes tonic to clonic phase of epilepsy

Neostriatal stimulation → arrest of motion in progress

MICROELECTRODE RECORDING Activity seen during initiation of internally generated

movement but not to stimulus triggered movement Activity seen during co-contraction of agonist (stimulus

triggered thus control amplitude and velocity of movement

Preparation of motor act or programming as MC and SMA React

Spontaneous movement of individual body part Alternating movement Visually and kinesthetically triggered movement Postural adjustment to body tilt Rapid ballistic movement Slow ramp movement Isometric muscle contraction

SNc – tonic discharge -> postural control SNr - phasic discharge change with limb movement

Cortex

DISCHARGE OF MOTOR CIRCUIT

No spontaneous discharge, only during limb movement

increased phasic activity

High spontaneous discharge, inhibit tonically thalamus

Phasic reduction of activity during movement due to disinhibition by striatum

Phasic activity during movement

Striatum

GPi SNr

Thalamus

1

2

3

4

5

BG AND EYE MOVEMENT

REINFORCEMENT LEARNING

POSSIBLE ROLE OF INTRINSIC CIRCUITS

DISORDER OF BASAL GANGLIA

Disorder of voluntary movement Bradykinesia Rapid alternating movement Intension spasm

Postural abnormalities Gait disorder Tone changes Involuntary movement Phonation, articulation

AKINESIA AND BRADYKINESIA Akinesia is disorder characterized by poverty and

slowness of initiation and execution of willed and associated movement and difficulty in changing one motor patter to another, in absence of paralysis.

Disinclination to use a part Bradykinesia: Slow execution of movement due to

failure of development of initial burst (low amplitude agonist burst) during ballistic movement.

Selection of muscles and agonist : antagonist relationship is retained.

The final position is often achieved by a repetitive series of small agonist burst → sequence of incremental steps

MECHANISM OF BRADYKINESIA

Putamen → Globus pallidus internus encodes amplitude information during movement

Increased reaction time for initiation of movement and correcting or stopping movement

Velocity of movement reduced due to defective programming of movement both ramp and ballistic and disorderly recruitment of motor unit by pyramidal tract (thalamo-cortical circuit ↓)

Not due to rigidity Defect in message from basal galngia to SMA

→MC

MECHANISM OF BRADYKINESIA CONT… Difficulty in generating smooth continuous

movement of all kind due to failure of generator function

Changes in cerebral cortex secondary to basal ganglia

Impairment of nigro-striatal dopaminergic system, improved by L-dopa

Caudate n. stimulation → inactivation syndrome Globus pallidus cooling → akinesia Meso-limbic dopaminergic pathway abnormality of

ventral tegmental tract → nucleus accumbence may be responsible

Pre-movement potential reduced proportional to akinesia

MECHANISM OF BRADYKINESIA CONT…

Tegmental dopamine lesion → continuous synchronized burst of Gpi. Reduced by Dopamine or Apomorphine

Also disturbance of phasic changes in discharge → un-modifiable inhibition of thalamic neuron due to sustained unchanging discharge of Gpi.

Normal motor plan but inaccurate in-exact specification and initiation of agonist activity and running smooth sequence of motor programes

HASTENING PHENOMENON

Proportional to akinesia but not to tremor and rigidity

Defective checking Not controlled by L-dopa, or thalamotomy

FREEZING PHENOMENON

Not related to akinesia Appears 5-6 years after L-dopa therapy Due to ↓ NA in frontal cortices –striatal

complex Dopamine beta hydroxylase in CSF reduced L-threo-DOPS (L-threo -3-4 dihydroxyphenyl

serine) precursor of NA improve Can walk up and down (visual and auditory

modality) Related to frontal apraxia

POSTURAL ABNORMALITY

Involuntary flexion of trunk limb and head Inability to correct while turning limb and

head Inability to correct while turning /falling Anticipatory postural reflex that precede shift

of center of gravity are abnormal due to GP lesion → failure of compensatory righting reflex

Whether GP or more diffuse abnormality ?

ALTERATION OF MUSCLE TONE

Hypertonia Gamma loop over activity - ↑ long loop tonic

stretch reflex activity release by basal ganglia brain stem and cord

αγ co-contraction → rigidity Relived by Thalamotomy or Gpi lesion

Hypotonia Degeneration of micro-neuron of thalamus with

chorea

THE END