We have seen that the maintenance of equilibrium, and of correct posture, is dependent on reflex arcs involving various centres including the spinal cord, the cerebellum, and the vestibular nuclei. Afferent impulses for these reflexes are carried by the posterior column tracts (fasciculus gracilis and fasciculus cuneatus), the spinocerebellar tracts, and others. Efferents reach neurons of the ventral grey column (anterior horn cells) through rubrospinal, vestibulospinal, and other ‘extrapyramidal’ tracts. Interruption of any of these pathways; or lesions in the cerebellum, the vestibular nuclei and other centres concerned; can result in various abnormalities involving maintenance of posture and coordination of movements.
Inability to maintain the equilibrium of the body, while standing, or while walking, is referred to as ataxia. This may occur as a result of the interruption of afferent proprioceptive pathways (sensory ataxia). Disease of the cerebellum itself, or of efferent pathways, results in more severe disability.Coordination of the activity of different groups of muscles is interfered with, leading to various defects. The person is unable to stand with his feet close together: the body sways from side to side and the person may fall. While walking, the patient staggers and is unable to maintain progression in the desired direction. Lack of proprioceptive information can be compensated to a considerable extent by information received through the eyes. The defects mentioned are, therefore, much more pronounced with the eyes closed (Romberg’s sign). Lack of coordination of muscles also interferes with purposeful movements (asynergia). Movements are jerky and lack precision. For example, the patient finds it difficult to touch his nose with a finger, or to move a finger along a line. There is difficulty in performing movements involving rapid alternating action of opposing groups of muscles (e.g., tapping one hand with the other; repeated pronation and supination of the forearm). This phenomenon is called dysdiadokokinesis. Incoordination of the muscles responsible for the articulation of words leads tocharacteristic speech defects (dysarthria). For the same reason, the eyes are unable to fix the gaze on an object for any length of time. Attempts to bring the gaze back to the same point result in repeated jerky movements of the eyes. This is called nystagmus.
Apart from incoordination, cerebellar disease is characterised by diminished muscle tone (hypotonia). The muscles are soft, and tire easily (asthenia). Joints may lack stability (flail joints). Tendon reflexes may be diminished. Alternatively, tapping a tendon may result in oscillating movements of the part concerned, like a pendulum.
Attempts have been made to correlate symptoms of cerbellar damage with different regions of the cerebellum, but without much success. Some correlations are as follows.
1. When the flocculus, nodule and uvula are damaged (flocculonodular syndrome) the mainsymptom is imbalance. Remember that the connections of the flocculonodular lobe are predominantly vestibular.
2. Small lesions in the cerebellar cortex may produce no effect. Extensive lesions are marked byhypotonia and incoordination (on the side of the lesion).
3. Intention tremor and staggering appear when the dentate nucleus or the superior cerebellarpeduncle (which carries fibres from the nucleus) is damaged.
The role of the cerebellum in the control of eye movements has been discussed.
This is a small triangle interval bounded by the pons (anteromedialy), and the cerebellum (posteromedially). A tumour in this space produces characteristic symptoms.
(a) Pressure on the spinal nucleus of the trigeminal nerve leads to loss of sensations of pain and temperature over the face.
(b) Pressure on fibres and nucleus of the facial nerve results in facial paralysis.
(c) Pressure on the middle cerebellar peduncle leads to ataxia.
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