BASAL GANGLIA

Dr Raghuveer Choudhary

5/4/2012

1

Basal Ganglia

OBJECTIVES
• Define basal ganglia and describe the parts • Describe the main connections and functions • Describe the function and the disorders of basal ganglia such as Parkinsonism and tremors

Basal Ganglia
Anatomic considerationsGroup of subcortical Grey nuclear masses at base of cerebral hemisphere, on each side of brain. play an essential role in control of movements.

Where are the basal ganglia?

• Caudate nucleus + putamen=Neo Striatum(major input center). • Putamen +Globus pallidus = Lenticular nucleus.
– Caudate nucleus- comma shaped band of gray
matter,head, body & tail.Head continuous with putamin, tail ends with close relation of amygdaloid body.

– Putamen - outer part of lenticular nucleus, seperated
from pallidum by white fibrous band, it is dark in color compared to pale pallidum.

– Globus pallidus- Inner region of lenticular nucleus,
divided into GP externa & GP interna by internal lamina of white matter.

Subthalamic body of Luys- biconvex mass of grey matter located in midbrain, just below the thalamus.

Substantia nigra- sheet of neurons containing dark pigment neoromelanin present ventral to the crus cerebri in midbrain,divided into – Pars compacta- dopaminergic and cholinergic neurons. Pars reticulata GABAergic neurons.
Globus pallidus referred as- palaeostriatum, Caudate N & Putamin- neostriatum.

The internal capsule lies within borders formed by the thalamus, caudate N & lenticular nucleus(P+G.P=lens shaped). This is a crucial area for passage way for all nerve fibers connecting cerebrum with rest of CNS.

BG dysfxn Slow, inefficient actions, rigidity, bradykinesia, unwanted movement

Connections
• BG has multiple connections with other parts of CNS- cerebral cortex, cerebellum, thalamus,reticular formation, mid brain. • They are imp. Centres of coordination, in control of automatic associated movements. • Corpus striatum(C+P) is responsible for initiation and inhibition of gross intentional body movements that are unconsciously performed in normal person. • Also provide muscle tone – so that exact movements can be performed,hand work- requiring coordinated effort of entire arm & trunk for hand to be able to perform.

Connections
• Caudate nucleus • Putamen

receive input

• Globus pallidus –

output leaves

Connections
• Connections of striatum
– Caudate nucleus & putamen – input – Receive afferent cerebral cortex, intralaminar thalamic nuclei, subs nigra – Efferent – globus pallidus, subs nigra

• Connections of globus pallidus
– 2 segments – GPi & GPe – GPi& subs nigra – output – Receive afferent – striatum, subthalamic nucleus – Efferent
• GPe – subthalamic N • GPi– thalamus (VA,VL,CM) – motor areas

• The corticostriatal projections arise from neurons from in layer V of cortex& appear to use glutamate as its excitatory NT. • The striatum then influences neurons in VL, VA nucleui of thalamus by- 2 pathways.

Basic Circuit of Basal Ganglia
Cerebral Cortex

Neostriatum

+

+ Gpi/SNpr Gpe

+ VA/VL thalamus Subth

Direct and Indirect- fig.
In direct pathway- striatum projects-i segment of GP & pars R of SN. This projection is inhibitory, NT are GABA,subatance P. Gpi +SNr project to VA/VL of thalamus, this is also inhibitory(GABA). The VA /VL send excitatory connection to prefronatal, premotor & supplementary area of cortex.

• This input to cortex influences motor planning, affects discharge of corticospinal, corticobulbar neurons. • Pars reticulata also influences eye movementsby projection to superior colliculus. • Direct pathway appears to function as follows– Neurons in striatum have little background activity,activated from input of cortex. – In contrast Gpi has high level of background activity. – Striatum is inhibitory to Gpi, but pallidial neurons themselves are inhibitory to VA,VL N , therefore activation of striatum disinhibits the thalamusi.e excites these neurons and their target neurons in MOTOR CORTEX .

Indirect pathway

Striatum –to exter. Segment of GP which projects to SN- this inturn projects back to Gpi. In this pathway pallidial neurons in Gpe are inhibited by- GABA& enkephalin. GABA & enkephalin disinhibit neurons neurons of STN. The STN neurons become more active as disinhibition. Release Glutamate in int. seg of GP. This transmitter excites neurons of VA/VL Thalamic N. The pallidal action is inhibitory, activity of thalamic N decreases, as does that of cortical neurons.

• Thus the direct & indirect pathways have opposing actions. • An increase in either one of these pathways – leads to imbalance in motor control. • It influences increase/ decrease in motor output of cortex. • Neurons of SN (pc)- project to striatum • (3rd circuit)Dopamine is the neurotransmitter. • This has an excitatory effect on Direct and • Inhibitory action on indirect pathway. – Both actions facilitate activity in C.Cortex. – This circuit is imp. Functionally.

Forebrain: Basal Motor Nuclei
Motor cortical areas

+
CST

Motor cortical areas

loop

-

+ contra

loop

+

E I +

E

I
DIRECT PATHWAY

-

Nolte 13-6

•Motor loop: ipsilateral

INDIRECT PATHWAY

•M. cort. areasstriatumGpithalamus (VA/VL)M. cort areas
•Substantia nigra interconnected with striatum (e.g., nigrostriatal proj.) •Subthalamus reciprocally interconnected with GP

•Gpi: major lentiform output (-) to motor thalamus
• Basal-motor nuclei (-) tonic (spont.) activity of motor thalamus, and thus modulate CST outputs: BMN modulate contra movement
34

Direct

Indirect

Pathway

Striatum  (-) GPi, SNr

Striatum  (-) GPe  (-) STN  (+) GPi GPi stimulated Inhibited
Inhibited
Huntington’s
Chorea

Effect on BG output Effect on Thalamus
Effect on movement Malfxning

GPi, SNr inhibited Stimulated
Initiated Parkinson’s
bradykinesia

Putamin circuit-execution of movements
• Principal role of BG in motor activity is – skilled movements performed subconsciously• Writing letters of alphabet • Cutting paper with scissor • Hammering nails, shooting basketball. • Passing throwball, shoveling dirt • Vocalisation, controlled movements of eyes. – Damage in putamin circuit• Damage in GP-ATHETOSIS(writhing movements). • Lesion in subthalamus- HEMIBALLISMUS(flialing of whole limb) • Lesion in putamin- CHOREA(flicking movmet in hand,face) • Damage in SN- PARKINSONISM(TRA/D).

Caudate circuit-cognitive control

• Thinking process using sensory input & memory in information (stored). • Motor activity occur as result of – thoughts generated. • Efferents end in accessory motor regions in premotor & supplementary areas-concerned in putting together
sequential patterns of movement lasting for seconds/ don’t excite muscle movements. For e.g person seeing a lion. • Without thinking for long, respond immediately to achieve complex goal.

• Another imp. Function is change timing & scale the intensity of movements. – How rapidly movement is to be performed. – How large the movement will be. • In patients of severe lesion in BG- timing & scaling is lost. • Example is – writing alphabet ‘a’. • This is function of BG along with cerebral cortex. • In lesion of post. Parietal cortex– Centre for spatial coordination for motor control of all parts of body & relation of body its parts with surrounding.

Fig showsperson lacking lt.post.parietal cortex draw the face of human being, proper proportion for rt. Side ignoring lt. side(rt. Field of vision), avoid using rt.hand, arm not aware of existance.

•Circuit of connections
–cortex to basal ganglia to thalamus to cortex –Helps to program automatic movement sequences (walking and arm swinging or laughing at a joke)

Basal Ganglia Connections

•Output from basal ganglia to reticular formation –reduces muscle tone –damage produces rigidity of Parkinson’s disease

• The general effect of BG excitation is of inhibitory (-) signals to bulboreticular facilitatory(+), • and excitatory(+) signals to bulboreticular inhibitory(-) areas. • When BG are not functioning adequately– Facilitatory areas(+) become overactive. – Inhibitory areas(-) become underactive. – Resulting in Rigidity throughout body.

Metabolic considerations
• Metabolism is unique.
– The structures have a high O2 consumption. – Copper content of substantia nigra & locus ceruleus is particularly High. – In Wilson’s disease, genetic autosomal recessive disorder, plasma level of copper binding protein ceruloplasmin is- LOW. – Chronic copper intoxication and severe degeneration of Lenticular nucleus take place.

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