The mineralization and biodegradation of cerebrospinal fluid shunting systems were studied using material from 25 shunts that had been implanted for between 6 days and 10 years. New unused materials were also examined for comparison. Surface changes in six systems could be observed under an operating microscope. Substantial quantities of a white deposit had adhered to the tubing in four of the shunts. These changes were most advanced in the galeal penetrative portion of the shunts and are believed to have been caused by mechanical stress. Scanning electron microscopic analysis revealed surface wrinkles, microscopic holes, and tiny particles, suggesting deterioration of the material itself. An energy-dispersive analysis using x-rays demonstrated that the surface deposits were due to mineralization of calcium phosphate and that the tiny particle growth was aluminum. These changes may be a consequence of the degradation of silicone rubber. A discriminant analysis of the mineralization was carried out; thus, the age of the host and the duration of system implantation could be correlated with the incidence of mineralization (p less than 0.1). A measurement of the physical properties showed progressive change with a remarkable deterioration in systems implanted for more than 5 years.
A 55-year-old male suffered sudden onset of dysarthria and mild left hemiparesis due to a right in tracerebral small hemorrhage. On admission, six subcutaneous elastic hard lumps were found on the scalp with painless and regular pulsation. The lumps were located along the course of the bilateral su perficial temporal arteries (5 locations) and the occipital artery. The patient did not have symptoms of headache or blurred vision associated with temporal arteritis. The largest lump was removed for cosmet ic reasons and definitive diagnosis. Histological examination demonstrated many infiltrating inflam matory cells along the entire vascular wall but without giant cells or fibrinoid necrosis. These multiple scalp aneurysms were probably caused by atypical temporal arteritis.
The authors report two cases of bitemporal compression injury caused by a static loading mechanism. These head injuries resulted from gradual bitemporal compression of the head. Plain skull films showed multiple skull fractures, and carotid angiography revealed internal carotid artery obstruction at the base of the skull. Neurological examination disclosed a slight disturbance of consciousness, hemiparesis, multiple cranial nerve injuries, and Horner's syndrome. In comparison with impact head injury, the energy from this type of trauma tends to be transmitted to the foramina and hiati of the middle cranial fossa and results in multiple injuries to the cranial nerves, sympathetic nerves, and blood vessels.
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