cerebral palsy causes

Cerebral palsy causes : The cerebral palsies of childhood comprise a group of conditions which may be either of intra-uterine onset, or which are acquired during parturition or at a still later period. Cases of intra-uterine origin are usually developmental in character, and to this group belong porencephalia, agenesis corticalis and other defects, although evidences of hæmorrhage and sclerotic changes, as a result of traumatism, fœtal meningo-encephalitis and syphilis, have been observed in rare instances. The cerebral palsies encountered later in child-life are the result of either hæmorrhage, embolism or thrombosis.
A cerebral abscess or tumor may likewise cause definite paralytic manifestations, but in their etiology and clinical course they differ distinctly from the foregoing conditions. Hæmorrhage at this period of life is more frequently meningeal than cerebral. It may result from traumatism, arteritis, or from a sudden and severe venous congestion of the brain occurring during a convulsion or during a paroxysm of whooping-cough. I have seen two cases resulting directly from whooping-cough. The convulsion is probably the result of the hæmorrhage, and not vice versa. Birth-palsies are usually bilateral, that is, diplegic or paraplegic, while the later palsies are most frequently hemiplegic. Sometimes hemiplegia attacks an infant in apparently perfect health, the symptoms coming on with fever, followed by convulsions and hemiparalysis. Strumpell advanced the theory that these cases were infectious, and that an acute inflammatory process in the cortical gray matter of the motor area was the primary lesion. Pathologically and etiologically it was supposedly similar to poliomyelitis, for which reason he named it "Acute Polioencephalitis of Infants." Osler and Sachs from a study of a number of these cases, question the correctness of this view, claiming that the lesions are probably always hæmorrhagic. In spite of the opinion of the high authorities just quoted, I believe with Mills, Holt and others that we do encounter cases whose mode of onset and clinical coarse certainly appear to bear out Strumpell's theory of an inflammatory lesion of infectious origin. Again, I believe that in some cases the symptoms are purely toxic, and we know that in adults apoplectiform attacks without hæmorrhage frequently occur as a phase of uræmia. In such cases we are surprised to find no gross lesion at the autopsy. Recently a colored child, two years old, previously perfectly healthy, was brought to my clinic for convulsions occurring daily and confined to the left side of the body. There was hemiplegia, although considerable improvement was manifest. The condition developed suddenly six weeks previous, the child being seized with these one-sided convulsions and temporary loss of consciousness, followed by hemiplegia. There was also fever continuing for several days. Why hæmorrhage should occur in such a case is hard to explain, but an encephalitis is quite conceivable.
Cure : Massage and faradization of the extensor muscles, and mechanical contrivances to overcome contractures, are generally useful later on. Arnica, Kali hydrojod and Sulphur are aids in absorbing the hæmorrhagic extravasations, while Causticum, Cocculus and Cuprum frequently exert a beneficial influence upon the paralytic symptoms.     Dr.L.Mukherjee