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This is a revised presentation of Basal Ganglia Anatomy function and clinical localization. Aug 2013
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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
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