“…In the temporal lobes the boundary zone between the middle and posterior cerebral arteries was also selectively involved. Calcification of the second frontal gyrus has been previously noted in other cases of symmetrical cerebral calcification (Beyme, 1945-46;Chavany, van Bogaert, and Houdart, 1949), but its significance has not been discussed. Even in more widely calcified brains, as in that illustrated by Erbsloh and Bochnik (1958), this site of predilection has shown an evident accentuation of the deposits.…”
Calcification of cerebral capillaries and smaller blood vessels appears to be a response on the part of the tissues to a wide range of pathological influences. Various forms of encephalitis and endocrine anomalies, particularly hypoparathyroidism, together account for the greatest number of cases to which a definite aetiology may be assigned, while familial instances, often associated with oligophrenia or microcephaly, are well known. Irrespective of aetiology and in the large group of cryptogenic cases, the localization of the calcifications is singularly uniform. The putamina and central parts of the cerebellar hemispheres usually show dense deposits which by confluence often form "brain stones" of massive size. The globus pallidus, thalamus, parts of the cerebral cortex and centrum semiovale are also bilaterally implicated though the complete pattern is not always present.These favoured sites for calcification have been recognized for many years but little attention has been paid to their finer topographical features. In the present case we have been struck by the fact that the site of the calcifications is remarkably similar to that of ischaemic lesions often found in cases of birth injury or associated with circulatory disturbances in later life. This is particularly apparent in the involvement of the deeper parts of the gyral walls and of the boundary zones between major cortical arterial territories. Moreover, the distribution of the calcifications in the basal ganglia has much in common with that of status marmoratus. Our purpose in this paper is to develop this comparison more fully, for we believe that the exposure of a vascular factor sheds light on the pathogenesis of cerebral calcification.Case Report Clinical History.-J.P., a man, died at the age of 49 years. His parents were dead at the time he came under supervision and nothing is known about the family history or his early childhood except that he suffered from epilepsy and had been admitted to a hospital at the age of 3 years for "paralysis of the legs".From the age of 5 years, however, he was able to attend an ordinary elementary school but at 11 years he was transferred to a special school. On leaving he worked as an errand boy for four years and then in a factory for two years until discharged for incompetence. When 28 years old he was certified as a feeble-minded person. A year before his death he was transferred to Stoke Park Hospital for mental defectives. His mental age as estimated by the Terman-Merrill scale was then only 4 years 8 months (I.Q. 30). He had preserved traces of verbal ability well above his apparent level at the time of testing and in the psychologist's opinion he was an imbecile who had deteriorated considerably. The impression was given of psychosis superimposed on mental defect. No abnormality was found on neurological examination. The blood Wassermann reaction was negative. During the last few months of life, however, there ensued a rapid physical and mental deterioration. He developed increasing flexion rigidity of ...
“…In the temporal lobes the boundary zone between the middle and posterior cerebral arteries was also selectively involved. Calcification of the second frontal gyrus has been previously noted in other cases of symmetrical cerebral calcification (Beyme, 1945-46;Chavany, van Bogaert, and Houdart, 1949), but its significance has not been discussed. Even in more widely calcified brains, as in that illustrated by Erbsloh and Bochnik (1958), this site of predilection has shown an evident accentuation of the deposits.…”
Calcification of cerebral capillaries and smaller blood vessels appears to be a response on the part of the tissues to a wide range of pathological influences. Various forms of encephalitis and endocrine anomalies, particularly hypoparathyroidism, together account for the greatest number of cases to which a definite aetiology may be assigned, while familial instances, often associated with oligophrenia or microcephaly, are well known. Irrespective of aetiology and in the large group of cryptogenic cases, the localization of the calcifications is singularly uniform. The putamina and central parts of the cerebellar hemispheres usually show dense deposits which by confluence often form "brain stones" of massive size. The globus pallidus, thalamus, parts of the cerebral cortex and centrum semiovale are also bilaterally implicated though the complete pattern is not always present.These favoured sites for calcification have been recognized for many years but little attention has been paid to their finer topographical features. In the present case we have been struck by the fact that the site of the calcifications is remarkably similar to that of ischaemic lesions often found in cases of birth injury or associated with circulatory disturbances in later life. This is particularly apparent in the involvement of the deeper parts of the gyral walls and of the boundary zones between major cortical arterial territories. Moreover, the distribution of the calcifications in the basal ganglia has much in common with that of status marmoratus. Our purpose in this paper is to develop this comparison more fully, for we believe that the exposure of a vascular factor sheds light on the pathogenesis of cerebral calcification.Case Report Clinical History.-J.P., a man, died at the age of 49 years. His parents were dead at the time he came under supervision and nothing is known about the family history or his early childhood except that he suffered from epilepsy and had been admitted to a hospital at the age of 3 years for "paralysis of the legs".From the age of 5 years, however, he was able to attend an ordinary elementary school but at 11 years he was transferred to a special school. On leaving he worked as an errand boy for four years and then in a factory for two years until discharged for incompetence. When 28 years old he was certified as a feeble-minded person. A year before his death he was transferred to Stoke Park Hospital for mental defectives. His mental age as estimated by the Terman-Merrill scale was then only 4 years 8 months (I.Q. 30). He had preserved traces of verbal ability well above his apparent level at the time of testing and in the psychologist's opinion he was an imbecile who had deteriorated considerably. The impression was given of psychosis superimposed on mental defect. No abnormality was found on neurological examination. The blood Wassermann reaction was negative. During the last few months of life, however, there ensued a rapid physical and mental deterioration. He developed increasing flexion rigidity of ...
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