Subcutaneous Phycomycosis

SIR,-In the past the aetiology of cerebral catastrophes in childhood has remained unsolved from the developmental point of view. This is epitomized in the facts that (1) neonates dying of convulsions have never demonstrated a lesion of the forebrain, such as cysts, though cysts are frequently found in infants dying of status epilepticus after six months; (2) acute hemiplegia occurs in a child apparently neurologically normal after birth ; (3) cerebral palsy does not reveal itself till approximately the sixth post-natal month. This time factor is the main stumblingblock to the acceptance of developmental theories in relation to epilepsy, acute hemiplegia (sic) in childhood, and cerebral palsy. It has led to the conclusion that cysts of the brain and other abnormalities cannot be developmental in origin but are due to degenerative processes precipitated by environmental factors operating after birth. Experimental evidence seems to support such a hypothesis, and all efforts are directed to the investigation of environmental causes ; however, not all cases can be explained in this way. One of the basic conclusions reached by me in 1961 was that the human brain develops functionally by definite stages and that the forebrain is inactive during the first six months of post-natal life. Under such circumstances maldevelopment of the forebrain would be masked until about the sixth month of post-natal life. Hence convulsions occurring before the sixth month would be related not to the forebrain but directly to the midbrain-that is, all fits or convulsions leading to unconsciousness (though often precipitated by conditions in the forebrain after the sixth month) are midbrain finally. True unconsciousness would only occur with spread to the midbrain. This helps in understanding the different forms of epilepsy and allows a clear-cut delineation between epilepsy and hysteria. If we apply the same basic reasoning to the aetiology of acute hemiplegia, the likely causative lesion is a developmental abnormality of the cerebral vessels which does not reveal itself until approximately the sixth month, when stress is put on the vascular supply. The lesion of the forebrain might be an established one such as cysts oratrophy, but the initial crisis might well be delayed until stress is put on the vascular supply. The condition would affect areas of the brain rather than specific centres and mental subnormality would therefore be a common finding. Gross abnormality of the vascular supply would lead to intrauterine death or obvious abnormality at birth. Angiography would be unlikely to reveal minor aberrations, and in the presence of the established syndrome the calibre of the vessel would not necessarily reflect the true position. Late atrophy of the hemisphere indicates increasing vascular inefficiency, and mental subnormality would be inevitable. There are, of course, other causes, but in these the aetiology would be obvious. Nevertheless, continued study and the accumulation of evidence over the years indicates that my explanation is undoubtedly correct. Much work still requires to be done, and we should be doing it.-I am, etc.,