Neurocutaneous melanosis and Dandy-Walker malformation are both forms of rare congenital neurodysplasia. Interestingly, 8 to 10% of patients with neurocutaneous melanosis also harbor an associated Dandy-Walker malformation, indicating that these developmental abnormalities share a common origin. The authors describe a case of neurocutaneous melanosis associated with Dandy-Walker malformation and an occipital meningohydroencephalocele with a giant melanotic nevus. Multiple congenital liver masses were also observed in the infant. The occipital nevus was totally excised, and ventriculoperitoneal and cyst-peritoneal shunts were created to prevent subsequent hydrocephalus. Findings in this case support the possibility that excessive melanocytes hinder normal mesenchymal development, causing Dandy-Walker malformation and an occipital meningocele.
A systematic radiological and pathological study of the cerebral arteries was made in an autopsy case of meningitis associated with three phases of cerebral arteriopathy. The latter consisted of vasospasm, vasodilatation, and organic stenosis. A marked change in the caliber of the cerebral arteries was demonstrated 3 times. Vasospasm, the stimulus phenomenon, was produced by the surrounding purulent material. Vasodilatation, the paralytic phenomenon, was presumably due to decreased contractile energy in association with myonecrosis. Organic stenosis, the repair process, was due to the organization of subendothelial edema with resultant intimal thickening. Evidence of increased endothelial permeability, subendothelial proliferation of smooth muscle cells, and necrosis of the latter in the media is presented in both light and electron micrographs.
A systematic radiological and pathological study of the cerebral arteries was made in an autopsy case of meningitis associated with three phases of cerebral arteriopathy. The latter consisted of vasospasm, vasodilatation, and organic stenosis. A marked change in the caliber of the cerebral arteries was demonstrated 3 times. Vasospasm, the stimulus phenomenon, was produced by the surrounding purulent material. Vasodilatation, the paralytic phenomenon, was presumably due to decreased contractile energy in association with myonecrosis. Organic stenosis, the repair process, was due to the organization of subendothelial edema with resultant intimal thickening. Evidence of increased endothelial permeability, subendothelial proliferation of smooth muscle cells, and necrosis of the latter in the media is presented in both light and electron micrographs.
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