Irritative lesions of the sensory mechanism cause numbness and tingling (paræsthesia); more extensive paralytic lesions produce anæsthesia, astereognosis, loss of muscle sense, loss of pain, or inability to distinguish temperature, according to the tracts that are affected.

Lesions of the Upper Motor Neurone may occur in any part of its course. Localised lesions of the motor cortex of an irritative kind, for example, a patch of meningitis, a tumour, meningeal hæmorrhage, or a spicule of bone, produce spasms in those groups of muscles on the opposite side of the body that are supplied by the centres implicated—Jacksonian epilepsy. The cortical discharge may overflow into neighbouring centres and cause more widespread convulsive movements, or, if strong and long-continued, may even lead to general convulsions. Consciousness is usually lost before the whole of one side becomes implicated in the spasms; always before they spread to the opposite side. Contracture may occur in the muscles affected after the spasms cease.

If an area of the cortex is destroyed by the lesion, paralysis is produced of the corresponding muscles on the opposite side of the body. At first the paralysed muscles are flaccid, but spasticity soon develops. In some cortical lesions, for reasons not yet understood, the paralysis remains of the flaccid type. The seat and extent of the paralysis depend upon the area of the cortex destroyed. In rare cases the whole motor area is destroyed—cortical hemiplegia; more generally the lesion affects one or more groups of muscles, and occasionally all the muscles of one limb are paralysed—cortical monoplegia. Lesions are often both irritative and destructive, and lead to paralysis of one or more groups of muscles associated with spasms and convulsions of the muscles governed by neighbouring areas of the cortex. Irritation or destruction of the sensory centres may also exist, giving rise to areas of paræsthesia and anæsthesia.

Lesions in the centrum ovale, which destroy the fibres proceeding from the overlying cortex, produce a corresponding spastic paralysis on the opposite side of the body. No irritative phenomena are associated with such a sub-cortical lesion.

Lesions in the region of the internal capsule often produce complete spastic hemiplegia of the opposite side of the body. When the posterior part of the capsule is involved, there are, in addition, hemianæsthesia and hemianopia, and sometimes disturbances of hearing, smell, and taste.

A lesion of the crus may in like manner produce spastic hemiplegia and hemianæsthesia of the opposite side, often associated with a lower neurone paralysis of the third and fourth nerves of the same side (crossed paralysis). The optic tract, which crosses the crus, may also be affected, and hemianopia result.

Lesions of the corpora quadrigemina cause interference with the reaction of the pupil, disturbance of the functions of the oculo-motor nerve and of mastication, ataxia, and inco-ordination of the movements of the limbs.

The symptoms produced by lesions of the pons and medulla vary according to the position of the lesion. If it is unilateral, there may be spastic hemiplegia and hemianæsthesia of the opposite side; if it is situated in the lower part of the pons or in the medulla, there is often also a lower neurone paralysis of one or more of the cranial nerves on the same side as the lesion (crossed paralysis). Paralysis of the external rectus of one eye and of the internal rectus of the other (conjugate paralysis) is frequently found in pontine, and in cortical and internal capsule lesions.

Cerebellar lesions are associated with special symptoms. In ataxia, there is inco-ordination of muscular movements, especially of the coarse movements, such as walking. The gait becomes irregular and staggering, with a tendency to fall, sometimes to the side on which the lesion is situated, sometimes to the opposite side. In patients who cannot walk, ataxia may be tested by ordering repeated pronation and supination of the forearm. Paresis or asthenia may be found in the trunk muscles, or evidenced by weakness of the grip, or drooping of the head to one side. Changes in muscle tone may arise and lead to exaggerated or decreased reflexes, often varying from day to day. Vertigo and nystagmus may also be present, in addition to occipital headache and tenderness on percussion. When one lateral lobe is implicated, the symptoms are referred to the same side; when the median lobe is involved, they are bilateral, and there may be retraction of the neck with extension of the legs, probably as the result of the associated internal hydrocephalus.

A unilateral lesion of the spinal cord causes a lower neurone paralysis of the muscles supplied from the cord at the level of the lesion, with spastic paralysis of the muscles of the same side of the body supplied from a lower level of the cord. The sensory symptoms are variable. Typically there is some anæsthesia in the structures supplied from the damaged section of the cord—incomplete owing to the overlapping by other sensory nerves. Just above the lesion there is irritation of spinal nerves, and hyperæsthesia and pain referred to their distribution. On the same side below the lesion, there is a loss of epicritic, stereognostic and deep sensibility, and on the opposite side below the lesion, loss of the sense of pain and the discrimination between heat and cold. Ordinary tactile sensibility, which is governed by a double path, may or may not be lost on either side below the lesion.