3.basal ganglia kjg

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BASAL GANGLIA Dr. K.Jaiganesh, MD Professor of Physiology MGMCRI

Transcript of 3.basal ganglia kjg

BASAL GANGLIA

Dr. K.Jaiganesh, MD

Professor of Physiology

MGMCRI

Basal ganglia and Cerebellum

•The basal ganglia and

cerebellum modify movement

on a minute-to-minute basis.

•Motor cortex sends

information to both, the output

of the cerebellum to cortex is

excitatory, while the basal

ganglia are inhibitory.

•The balance between these

two systems allows for smooth,

coordinated movement.

•Disturbance in either system

will show up as movement

disorders.Muscle

Execution of voluntary movements

Motor cortex

Spinal cord

CerebellumBasal ganglia

CerebellumBasal ganglia

Muscle receptors

Cortico spinal tract

Basal ganglia

• Objectives:

*Structure and Nuclei of Basal Ganglia

*Connections of Basal Ganglia

*Functions of Basal Ganglia

*Disorders of Basal ganglia

Basal Ganglia-Structure

STN

C R

ThalamusPutamen

Caudate

Corpus striatum

S.Nigra

Lenticular N

Basal ganglia connections

Connections of Basal Ganglia

• Afferent connections: terminate in (striatum)

Caudate nucleusPutamen

• Cortico striate projections from all parts of the cortex

• Projections from thalamus

• Efferent ( output from Basal Ganglia is from):

Internal segment of GLOBUS PALLIDUS

via thalamic fasciculus

Nuclei of Thalamus

Prefrontal and Premotor cortex

Afferent Connections to BG

1) Corticostriate fibers

Excitatory - Glutamate

2) Nigrostriate fibers

Dopamine

3) Thalamostriate fibers

4) Raphe striate fibers

Serotonin

5) Locus Cerulues striate fibers

Nor adrenaline

Efferent Connections from BG

1) Efferents to Thalamus

Ansa fascicularis – from

Internal segment of GP to

Thalamus - GABA

2) Efferents to Subthalamic

nucleus

3) Efferents to Substantia

Nigra

4) Efferents to Red nucleus

Neuro Transmitters - BG

•Glutamate

•GABA

•Acetylcholine

•Dopamine

Glutamatergic pathways - red,

Dopaminergic as magenta and

GABA pathways as blue.

Caudate circuit

•Concerned with

Cognitive control of

motor activity

•Initiating a motor

response

•Role in control of

eye movements

Putamen circuit

•Responsible for motor

control of body movements

•Concerned with skilled

movements

•Subconscious execution of

learned patterns of movement

Sub thalamic N of Luys – Function

• Controls posture of limbs

• Controls position & movement at shoulder & pelvic

girdles

• Effect of lesion

Hemiballismus: violent flinging movements of the

arm & leg on one side on attempting to make a

movement

Functions of basal ganglia

1. Control of voluntary motor activity

2. Control of reflex muscular activity

3. Control of muscle tone

4. Role in arousal mechanism

Functions of basal ganglia

• Control of voluntary motor activity

– Planning and Programming of movements –

Cognitive process – Caudate circuit

– Timing and scaling of movement: caudate circuit -

Lesion leads to Akinesia and Micrographia

– Production of automatic associated movements

• Swinging of arms while walking

– Subconscious execution of movements

– Prevents oscillations and after discharges in motor

system

Functions of basal ganglia

1. Control of Reflex muscular activity

– Has inhibitory effect on spinal reflexes

– Maintains posture

2. Control of muscle tone

– Through reticular formation –In BG lesion –rigidity occurs

3. Role in arousal mechanism

– Through its connections with reticular formation

4. Role in emotions and Learning

Disorders of Basal ganglia

Hypokinetic disorders (Lesion in Loop I)

Parkinsonism

Hyperkinetic disorders (Lesion in Loop II)

1. Athetosis

2. Ballismus

3. Chorea

4. Torsion spasm

Parkinsonism

• Described by James Parkinson in 1817 &

termed Paralysis agitans because of the

symptoms of weakness of muscle power

&tremor. Also known as Shaking palsy

Parkinsonism- Etiology

1. Infection - viral encephalitis

2. Degenerative - both due to aging & genetic predisposition

3. Drug induced parkinsonism

a) Phenothiazine group of drugs which Block Dopamine D2

Receptors eg.Chlorpromazine &promethazine

b) Reserpine which depletes Dopamine & prevents storage of

dopamine in nerve terminals

4. Ischemia- atherosclerotic

5. Toxin -- MPTP : 1 Methyl 4 Phenyl 1256 Tetra

hydropyridine that prevents synthesis of Dopamine

Parkinsonism- Patho physiology

• Degeneration of the

substantia nigra

• Loss of dopamine

• Increased inhibitory output of

the basal ganglia

• Hypokinetic movement

disorder (bradykinesia,

rigidity, etc.)

Parkinsonism- Patho physiology

• Decrease dopamine leads to imbalance in ratio of

cholinergic transmission & dopaminergic effect

• Nigrostriatal dopamine inhibits acetylcholine

secreting corticostriatal neurones; in absence of

dopaminergic inhibition there is increased cholinergic

transmission effects

Parkinsonism- Features

1. Rigidity

2. Akinesia

3. Tremor

4. Festinent gait

PARK - RAT- REST

Parkinsonism-Rigidity

• Rigidity may be cogwheel type of Rigidity or Plastic type or Lead pipe rigidity

1.COG WHEEL: intermittent change in tone to

passive movement of joint.

2.LEAD PIPE: Continuous resistance

Parkinsonism-Akinesia

• Poverty of movement seen as defects in fine

movement & speech

• Mask like face

• Difficulty in Initiating movement

• Micrographia: handwritten letters are small in

size & become progressively smaller

Parkinsonism-Resting Tremor

• Coarse Tremor at rest disappears during movement

• Fingers- Pill rolling movement

• Tremor disappears during movement

• Absent in sleep

• Tremor due to loss of inhibition of thalamus & relieved by lesion of VA&VL of thalamus

Parkinsonism- Festinant gait

• Festinant Gait : consists of short rapid

shuffling steps leaning forward as though to

catch centre of gravity

• Lack of associated movements such as

swinging of the arms

• Severe stage- retropulsion & propulsion ie.

Inability to stop

Parkinsonism-Treatment

1) L-DOPA because Dopamine does not cross the Blood-brain

barrier along with Carbidopa which inhibits extracerebral

DOPA decarboxylase to prevent formation of Dopamine in

circulation.

2) BROMOCRIPTINE- Dopamine Agonist

3) DEPRENYL- MAO inhibitor

4) ANTICHOLINERGICS which block action of

ACETYLCHOLINE leading to restoration of Ach/ dopamine

ratio

5) SURGERY: VA& VL OF THALAMUS -Electrocoagulation

relieves tremor.Globus pallidus externa lesions relieves

akinesia & rigidity &tremor

6) Transplantation of fetal neurons (dopaminergic)

Chorea

• Effects of Lesion of Caudate nucleus

• Involuntary semipurposive, Jerky, Dance Like movements of the Hands & Fingers

• Cause : Loss of GABAergic neurons action

• Types: – Sydenham Chorea (post Streptococcal infection sequelae)

– Senile chorea

– Huntington’s Chorea: Involuntary movement with dementia

Huntington’s disease

• Inherited as Autosomal Dominant

• Abnormal gene locus near end of short arm of

chromosome 4

• Hyperkinetic symptoms of choreiform

movements that gradually increase to

incapacitate the patient

• DEMENTIA is because of loss of Cholinergic

neurons

Athetosis

• Athetosis- Slow writhing purposeless movements of

the limbs &neck

• Lesion in Putamen

Other lesions of basal ganglia

• Hemiballismus: Due to destruction of

subthalamic nucleus. Flailing movements of

one arm and leg.

• Wilson’s Disease – Hepato Lenticular

degeneration – Copper toxicity.

• Kernicterus – Rh incompatibility.

Probable questions

• Essay

Describe the functional anatomy and connections

of Basal Ganglia . Enumerate the functions of

Basal ganglia . List the disorders of Basal ganglia.

• Short question:

Parkinsonism