cerebellum -connections and functions

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                                                                                                                                                                                           Connections and functions of the cerebellum

Keywords: Paleocerebellum, archi-cerebellum, neocerebellum, Stellate cells, basket cells, Purkinje mossy fibers, climbing fibers, knee heel test feedforward inhibition, negative feedback loop, dystaxia Finger nose test, dysarthria adiadochokinosis, rebound phenomenon, charcot's triad, asthenia, asynergia Friedreich's disease. Inferior vermis syndrome, superior vermis syndrome, intention tremor, and lalling speech.

Connections  of Cerebellum are:  Afferent, Internal processing, and Efferent

Afferents fibers are

1. Climbing fibers-originate from the inferior olivary nucleus, ascend to the cortex and connect with the deep cerebellar nuclei, then ascend to the molecular layer of the cortex and synapse with the Purkinje cells. Relation of the climbing fiber to the purkinje cell is one to one. The neurotransmitter is aspartate, and this is excitatory.

2. Mossy fibers: all afferent fibers of the cerebellum except climbing. Fibers are mossy fibers. They are spino cerebellar,vestibuo cerebellar, retticulo cerebellar, cuneo cerebellar etc. The mossy fibers, while ascending, connect with the deep cerebellar nuclei, then ascend to the granular layer of the cortex and synapse with granular cells. Axons of the granular cells synapse with the dendrites of stellate and basket cells. The connection is with multiple. The neurotransmitter is glutamic acid, and this is excitatory. The mossy fiber directly stimulates the golgi cell. In addition, the axon of the granule cell also stimulates th golgi cell. Then golgi cell will inhibit the granule cell.

connections of cerebellar neurons

All fibers of the cerebellar cortex converge on the purkinje cell. The axon of the purkinje cell is the only efferent of the cerebellar cortex. This final common pathway will synapse with the neurons of the deep nuclei and are inhibitory. The axon of the purkinje cell remains in the cerebellum. The neurotransmitter is gamma-aminobutyric acid (GABA).

The axon of the neuron of the deep nuclei leaves the cerebellum to the brain stem and the thalamus. The axon is excitatory, and the neurotransmitter is glutamic acid. In addition, some purkinje cell fiber may leave the cerebellum and synapse with vestibular nuclei, which is inhibitory.

So the stellate, basket, purkinji, and golgi cells are gabanergic and inhibitory.

On the other hand, the climbing and moss fibers, ganglion cells, and deep cerebellar nuclei neurons are excitatory. The neurotransmitter is aspartate in the climbing fibers, and in mossy and deep cerebellar nuclei, it is glutamic acid.

The climbing fiber goes up to the cerebellar molecular layer and the mossy fiber goes only up to the granular layer.

The climbing and mossy fibers stimulate the deep cerebellar nucleus. At the same time, the purkinji cell inhibits it. As a result, the axon of the deep cerebellar nuclei is excitatory to the thalamus and brain stem nucleus.

Negative feedback loop:

Granule cell stimulates golgi cell, which in turn inhibits the granule cell.

Feedforward inhibition:

Granule cell stimulates, basket, stellate cells which in turn inhibit —purkinji. In addition, however, granule cell stimulates purkinji cell. This inhibition limits the duration of the excitation produced by any stimulatory impulse.

Functions of the cerebellum:

1.    Control of balance and equilibrium.

2.    Control of muscle tone and the stretch reflex.

3.    Control of involuntary movements, and

4.    Coordination of voluntary activities.

Lesion of one hemisphere causes dysfunction of the same side. However, abnormalities of movements gradually disappear due to compensations.

Lesion of vermis causes bilateral dysfunction.

Lesion of deep cerebellar nuclei causes a persistent generalized defect.

The common site of the lesion is the neocerebellum.

Signs of cerebellar lesion:

1.    Ataxia or dystaxia: There is incoordination of movements. This is manifested as an unsteady gait, or drunken gait-patient cannot walk in a straight line and moves to the affected side due to hypotonia on the affected side.

2.    Dysmetria: In this condition, intended movement is poorly executed in direction, range, and force. Therefore movement overshoots the desired mark. The following tests test this:

3.    Finger nose test: The patient is asked to close his eyes and touch his nose with his index finger. He will fail to perform the act. It is past pointing.

4.    Heel knee test: The patient is asked to lie down on a bed, close his eyes, then be asked to touch his knee by the opposite heel, moving the heel along the tibia.

5.    Rebound phenomenon: the patient is unable to stop a movement. When he is pushed forward with little force, he will move forward. However, he can't stop himself. This rebound phenomenon may occur in any direction, forward, backward or lateral.

6.    Adiadochokinosis: The patient is asked to perform alternating movements rapidly, e.g., rapid supination and pronation of the forearm. He cannot perform these movements quickly and smoothly.

7.    Dysarthria: In this condition, speech is slow and lalling -like a baby. This is due to incoordination of movements of muscles of speech- tongue laryngeal muscles.

8.    Nystagmus: This is due to incoordination of movements of muscles of the eye. The eyeball moves to and fro slowly when the patient looks to the affected side and rapidly when he looks to the opposite side.

9.    Hypotonia occurs on the affected side:

The face is rotated away from the affected side as the face is pulled towards the healthy side.

The shoulder of the unaffected side is higher than that of the affected side.

The trunk is bent with concavity towards the affected side.

Spontaneous deviation: The patient is asked to stand with feet close to each other, close eyes, and extend arms straight and in front of the body. He will swing and may fall.

Intention tremor: When a patient is asked to pick up an object, his movements are jerky, and tremors occur that become more marked as his hand approaches the object.

Resting tremor occurs in parkinsonism

Fine tremor occurs in thyrotoxicosis.

Pendular knee jerk: deep reflexes become weak and pendular.

Asynergia lack of coordination.

Asthenia reduced muscle tone.

Charcot's triad: is a syndrome seen in disseminated sclerosis when there is a disturbance of cerebellar connections to the brain stem. The features are Intention tremor, nystagmus, and lalling speech.

Friedreich's disease: This is a hereditary disease that causes ataxia and other features of cerebellar dysfunctions.

Pan cerebellar syndrome: All features of bilateral lesion of the cerebellum-occurs seen in degenerative diseases like multiple sclerosis, acute alcoholic intoxications.

Cerebellar hemisphere syndrome: Dystonia or hypotonia is seen in neoplasm or infarction in the neocerebellum.

Superior vermis syndrome: dystaxia of the leg and trunk-upper limb is not involved, seen in alcoholism.

Inferior vermis syndrome: severe truncal dystaxia and nystagmus- occurs in tumors of the vermis.

 

Tag: Paleocerebellum, archi-cerebellum, neocerebellum, Stellate cells, basket cells, Purkinje mossy fibers, climbing fibers, knee heel test feedforward inhibition, negative feedback loop, dystaxia Finger nose test, dysarthria adiadochokinosis, rebound phenomenon, charcot's triad, asthenia, asynergia Friedreich's disease. Inferior vermis syndrome, superior vermis syndrome, intention tremor, and lalling speech.

 Internal link: https://blog.totalphysiology.com/2021/08/hypothalamus -connections and functions.

https://blog.totalphysiology.com/2021/08/hypothalamus

https://blog.totalphysiology.com/2021/08/thalamus -connections and functions

External link: en.m.wikipedia.org/wiki/cerebellum

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