(e and f) Bilateral chorea and bilateral athetosis may be present in diplegia as in hemiplegia. In chorea the involuntary movements occur in the muscles of the face, the neck, back and extremities; the patients exhibit persistent, slow rotating and sinuous inovements, producing a striking and most alarming clinical picture. Owing to the extreme tension of the muscles of the neck the head is usually retracted. Speech is almost always slow and indistinct. The movements are greatly increased by excitement and when the child knows that it is being ob served. The muscular palsies are sometimes quite insignificant and the spasms are not very marked; sometimes there is muscular hyper trophy. As a rule the intelligence is not so much affected as the observer is led to suppose by the slowness of speech and the great inter ference with movements. Convulsions are absent.
Bilateral athetosis, which is not so conspicuous but none the less disturbing, affects only the muscles of the extremities. The athetosis resembles the above-described unilateral form, but with the difference that both arms anti legs are affected. Not infrequently the disturbance is more marked on one side than on the other. Unilateral athetosis may also be a.ssociated with bilateral hemiplegia, and in such a ease sympathetic movements sometimes occur on the side which is not affected by the athetosis.
Among symptoms referable to the cranial nerves, disturbances of the eye muscles are more frequent in cerebral diplegia than in hemi plegia. Strabismus is the most frequent disturbance: nystagmus is common. Atrophy of the optic nerve may also develop as the result of a neuritis during the original disease. Slowness and difficulty in learning to speak and dysarthria are common in cerebral diplegia; dis tinct aphasia is rare. Sometimes children vcith cerebral diplegia appear to be absolutely dumb; but, after a course of systematic speaking exercises, it is often found that inability to speak is due merely to neglect on the part of the child's parents to give it proper training. Apparent deafness inay also be due to the same causes. In some cases, however, the inability to hear or speak depends on a high grade of idiocy.
The bulbar symptoms, which occur in children with cerebral di plegia and w-hich have been carefully studied by Oppenheim and Peritz and described as infantile pseudobulbar paralysis, merit special atten tion. The condition is characterized by difficulty in speaking, swallow ing and chewing, interference with the finer movements of the lips: partial loss of facial expression; aphonia; and, rarely, by disturb ances of the respiration, the heart action, the movements of the eyes and the muscles of the neck. The disturbances manifest themselves only with voluntary movements, the involuntary movements of the affected muscles being preserved. There is no atrophy or fibrillar twitching. The masseter reflex IT exaggerated and the eating reflex is often present. In this form of pseudobulbar paralysis the muscles are normally flaccid and the usual muscular tone is preserved. But in addi tion to the paralytic form there is also a spastic variety in which all the above-mentioned muscle groups persist in a condition of spastic tension and undergo sPasmorlic distortion whenever a voluntary move ment is attempted. An observation of Oppenheim concerning a mother and daughter who both exhibited the same disturbance is frequently quoted. We also know of spurious forms (formes frustes) of pseudo
bulbar paralysis consisting only in slight disturbances of speech, and deglutition. The anatomical basis of this pseudobulbar palsy is not ft disease of the medulla oblongata but a cortical lesion involving the centres which innervate the corresponding muscles.
In contradistinction to this form of pseudobulbar paralysis the morbid process (congenital disturbance, inflammation) in genuine bulbar palsy affects the nuclei of the cranial nerves themselves, pro ducing a true picture of ophthalmoplegia or bulbar palsy. Congenital infantile nuclear atrophy is therefore analogous to a congenital defect of the cerebrum and belongs to the group of cerebral infantile palsies. In the same way acute inflam matory disease of the bulb, if it does not terminate fatally or subside completely, may result in recovery with symp toms of permanent loss of f unction of the bulbar nerves, which properly also belong to the group of cerebral infantile palsies.
The above-described symptoms of cerebral infantile palsy are in many cases asso ciated with two important conditions which are char acteristic of this disease, namely, epilepsy and demen tia or idiocy.
Epileptic convulsions may be unilateral, and are then always confined to the plegic half of the head; or they may be general. Both forms may alternate in the same dividual. The convulsions may occur at long intervals or may be quite frequent and dominate the clinical picture. In most cases they exhibit the typical character of epileptic attacks with the epileptic gait, loss of consciousness, general sions, biting of the tongue, etc. The attacks frequently terminate in a definite part of the body. In other cases the convulsions are less pronounced and often consist merely of short attacks of ness, the conditions described as petit Ina' or nocturnal epilepsy'. There is no constant relation between the intensity of the epileptic attacks and the severity, of the disease in the extremities. On the contrary, the cases vary from distinct paralysis or well-marked spasm and slight convulsions to frequent epileptic attacks and almost imperceptible remains of cerebral palsy. Even in the same individual hemiplegia may clear up all but a slight inequality of the tw-o facial nerves of a unilateral exaggeration of the reflexes, leaving only the epileptic con dition, which goes on increasing. Indeed, the original cerebral lesion may have been quite insignificant and the symptoms may disappear completely in the course of time while the epilepsy which is probably the re.sult of the irritation caused by the remaining scar persists. Such a condition of affairs is also possible when the primary disease is sit uated in a "silent" region of the brain where a lesion does not produce clinical manifestations although it is capable of leading to epileptic attacks. On this theory the domain of so-called symptomatic (Jack sonian) epilepsy, in which the convulsions are held to be the result of a circumscribed disease of the brain would be considerably enlarged as compared with that of genuine epilepsy, in whieh there is no local lesion. It is quite possible, and is strongly suggested by numerous observations, that most forms of epilepsy occurring in childhood belong to the group of symptomatic epilepsies.