Biomedical subjects
Publications and source records attributed to J N Angelo.
Although increased skeletal blood flow in the bone involved by Paget's disease is well described, spinal hemorrhage in association with that disease has not previously been reported. We report a patient with Paget's disease of bone who developed a subacute epidural hematoma of the lumbar spine.
The morphologic description and measurements of endarterectomy specimens are usually believed to be accurate and are used as the gold standard against which the findings of diagnostic procedures are judged. Pathology data on 289 endarterectomy specimens from five participating centers and the corresponding angiography and B-mode ultrasonography data provided a basis for scrutinizing the validity of using the morphologic measurements as a standard. Discrepancies of greater than 1 mm between pathology and angiography measurements of minimum residual lumen occurred in 35% of the cases and between pathology and B-mode ultrasonography measurements in 64% of the cases. Discrepancies of greater than 1 mm between pathology- and angiography-measured lesion width occurred in 81% of the cases and between pathology and B-mode ultrasonography measurements in 64% of the cases. The cases representing mismatches of greater than 1 mm at one participating center were subjected to a rigorous review, with remeasurement of all morphologic features, in an attempt to explain the discrepancies. Various types of artifactual distortion of the specimens, the presence of slit-like and occluded lumens that were likely related to loss of perfusion pressure, and an inability to match planes of interrogation used in angiography and B-mode ultrasonography with pathology planes contributed significantly to the existence of mismatches. On the other hand, fixation and decalcification produced minimal and insignificant distortional changes. We conclude that the acquisition of quantitative data from endarterectomy specimens and the acceptance of morphologic data as a standard are limited by a number of problems that can be defined but have been difficult to resolve.
Subependymomas are relatively unusual tumors with a distinctive histological appearance. They are generally considered to be benign, and they are often found incidentally at autopsy. Most are located intracranially, and the most common site of origin is the fourth ventricle. Only two cases of subependymoma of the spinal cord have been reported previously. The authors present two additional cases of subependymoma of the cervical cord; both were symptomatic, and both were treated by microsurgical removal.
Brain and cervical spinal cord removed at autopsy from hypertensive humans have been subjected to 4 levels of microscopic study, 3 being first histochemically prepared so as to stain the arterial and capillary system. Thick (100 microns) sections for light microscopy and thicker (500-1000 microns) for x-ray microscopy facilitate the study of long, complex anatomic units. Arterial and arteriolar microaneurysms have not been found. In addition to the usual age related vascular changes in normal people we have found: moniliform capillary dilatations, focal segments of arteriolar narrowing, état pre-criblé, and lacunar infarcts. Few changes have been encountered in the corpus callosum. While the segmental arteriolar narrowing occurs in the cortex as well as deep white matter, the effects of resultant poor perfusion might be expected to be more profound in the deep white matter.
A case of neuromyelitis optica had strikingly increased numbers of thickened, hyalinized small blood vessels, which were associated with cystic degeneration in the cervical spinal cord and the optic chiasm. These findings support the contention that neuromyelitis optica is a clinical syndrome rather than a distinct nosologic entity.
A 3-month-old infant had hypernatremia, neurologic dysfunction, and an unusually high level of cerebrospinal fluid protein. The autopsy findings included cerebral edema, intravascular coagulation, and bilateral choroid plexus hematomas. Extensive destruction of the choroid plexus, in combination with diffuse intravascular coagulation may explain the much greater elevation of CSF protein than previously described with hypernatremia.
Two episodes of severe, relapsing sensorimotor polyneuropathy closely paralleled the course of systemic illness in a patient with immunoblastic lymphadenopathy. A review of the literature shows three other cases, although none with documented pathologic changes in muscles and nerves. Based on the pathologic findings in this patient, the peripheral neuropathy associated with immunoblastic lymphadenopathy can be classified under the group of relapsing inflammatory polyneuropathies associated with systemic disorders. Whether prednisone therapy helped this condition is uncertain.
The pathologic changes in the brain of a five and a half month old male child who died of propionic acidemia are presented. Although previous pathologic reports of this disorder describe either no involvement of the central nervous system or focal myelin sheath vacuolization, the present case exhibited different pathology, namely, spongy degeneration of the white matter of Van Bogaert and Bertrand's type. Thus this case illustrates that the pathologic changes in the brain in propionic acidemia are variable. In addition, the cerebellum in this patient showed marked diffuse atrophy and early loss of the external granular layer, two changes that have not been emphasized by previous authors.
Lhermitte-Duclos disease is a rare, benign cerebellar condition that mimics a posterior fossa mass and has never been diagnosed preoperatively. Grossly, the diseased cerebellar tissue is tough and poorly demarcated; microscopically, the cortex has a thick outer layer of nerve fibers, an inner layer of abnormal ganglion cells, and the absence of normal Purkinje cells. The prognosis, based on cases treated surgically since 1955, is good. A case is reported in which cranial computerized tomography performed 5 years after the partial removal of abnormal tissue showed neither enhancement nor radiolucency.
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The transmission and serial propagation of Creutzfeldt-Jakob disease from man to guinea pigs are reported. The latency, symptomatology, and morphology of the infection during the first four passages are presented. The incubation period between the first and subsequent passages was halved. One hundred percent take, morbidity, and mortality were achieved in all inoculated animals. All guinea pigs developed a subacute spongiform virus encephalopathy with marked neuronal destruction in the cerebral cortex and subcortical grey structures. The neuronal loss resulted in cerebral atrophy and hydrocephalus ex vacuo.