A pathological survey of 41 cases of acute intrinsic spinal cord disease.
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Biomedical subjects
Publications and source records attributed to A M Whiteley.
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We describe a patient who developed topographical memory loss after a closed head injury. His symptoms and the psychological test results indicate a selective deficit of topographical memory, his perceptual and spatial skills being relatively unimpaired.
Two patients are described in whom computerised tomography revealed contrast-enhanced lesions in the early stages of multiple sclerosis. Such lesions may be differentiated from tumours by their transient nature, lack of space-occupying effect, and localisation in the white matter. Contrast enhancement in demyelinating disease is probably related to local breakdown of the blood-brain barrier.
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A study has been made of facial pigmentation resulting from industrial inorganic mercury exposure. Electron microscopy has shown electron-dense 400--900 nm aggregates of 12 nm particles in dermal macrophages and free in the dermis. Use of the analytical electron microscope has enabled direct confirmation of the presence of mercury in these aggregates. The unexpected finding of coexistent selenium is discussed.
Three patients with prosopagnosia are described of whom two had right occipital lesions. An analysis of visual and perceptual functions demonstrated a defect in perceptual classification which appeared to be stimulus-specific. A special mechanism for facial recognition is postulated, and the importance of the right sided posterior lesion is stressed.
Two cases of encephalomyelitis are described in which the major clinical manifestation was muscular rigidity and stimulus-sensitive muscular spasms. It is suggested, from pathological evidence, that this rigidity was of spinal origin, and that this disorder is a rare but recognizable entity. Comparison is made with previously reported cases of rigidity of spinal origin, including encephalitis lethargica, and with 'subacute myoclonic spinal neuronitis' and the 'stiff man syndrome.'
Two brothers with congenital myasthenia gravis are described. In both, ptosis and ophthalmoplegia responded poorly to oral anticholinesterase therapy and to thymectomy. The brothers had two different HLA haplotypes and neither had the HLA-A1-B8-DW3 haplotypes which are commonly associated with myathenia gravis in adult-onset cases.
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