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Biomedical subjects

J H Deck

Publications and source records attributed to J H Deck.

At least 37 records · Page 2Linked to original sources
PubMed1989

T2 values in the human brain: comparison with quantitative assays of iron and ferritin.

Magnetic resonance (MR) imaging with a whole-body imager was performed in 10 fresh, unfixed whole human brains selected randomly from cadavers. All subjects were neurologically intact before death. T2 time constants were measured within the caudate nucleus, putamen, globus pallidus, cortical gray matter, subcortical white matter, and optic radiation. These regions were then excised, and T2 values were measured again with a 1.5-T MR spectrometer. Quantitative assays of iron, ferritin, and protein from these areas were then performed. Iron concentration varied significantly among brain regions, whereas ferritin and protein concentrations were constant among brain regions and among individuals. Neither iron nor ferritin concentration showed any consistent correlation with T2 values. Histologic examination of brain micro-sections with iron- and ferritin-specific stains of demonstrated poor correlation with biochemical assays of ferritin and iron concentrations. Results indicate that T2 values correlate poorly with iron and ferritin concentrations found in neurologically intact brains.

Adolescent↗
PubMed1989

Phrenic involvement in Charcot-Marie-Tooth disease. A pathologic documentation.

A 69-year-old woman diagnosed as having Charcot-Marie-Tooth disease (CMT) for 30 years' duration died of respiratory failure secondary to diaphragmatic weakness. At autopsy, identical neuropathic changes were found in phrenic and other affected somatic peripheral nerves. We conclude that the phrenic nerve may be involved by the neuropathy of at least some forms of CMT.

Aged↗
PubMed1989

Directed embolization is an alternate cause of cerebral watershed infarction.

Selective embolization of thrombotic material to the borderzone territories between major cerebral arteries was found to be the cause of watershed cerebral infarction in three reported cases. The embolic source was cardiac in two cases and carotid artery in one. The findings in these cases support the hypothesis that small thromboemboli may not be randomly distributed in the cerebral arterial supply but may be preferentially distributed to the small terminal arterial branches in the borderzones between major arterial territories. Previous reports of this phenomenon laid emphasis on the sharp angle at which small penetrating arteries branched from parent arteries as the mechanism underlying this preferential distribution. We propose that the unequal size of the branches at the majority of bifurcations of subarachnoid arteries is a more important anatomic feature leading to this pattern of infarction.

Aged↗
PubMed1988

Delayed myelopathy following lightning strike: a demyelinating process.

Although the clinical findings in over 30 cases of delayed myelopathy after electrical injury have been described, there are scanty reports of the pathology of the spinal cord in such cases. We report a case in which progressive myelopathy presented 1 month after electrical injury by lightning strike and death occurred 4 months after injury. The spinal cord showed widespread demyelination of white matter from the medulla to just above the conus medullaris. This consisted of selective degeneration of myelin sheaths without inflammation or injury to axons, other cord components, or nerve roots. Infarction of more circumscribed segments of the thoracic cord where demyelination was greatest was probably due to edema associated with myelin degeneration, causing cord swelling limited by the pia mater. Raised pressure within the cord then resulted in secondary infarction.

Adult↗
PubMed1988

Jakob-Creutzfeldt disease associated with Wernicke encephalopathy.

Wernicke disease (WD) is a complication of alcoholism and malnutrition and usually presents acutely and is characterized by disturbances of consciousness, paralysis of the external ocular muscles, and ataxia. The disease results from deficiency of vitamin B 1, or thiamine, an essential coenzyme in intermediate carbohydrate metabolism. On the other hand, Jakob-Creutzfeldt disease (J-C) results from infection with an unconventional agent with a long incubation period and is characterized by a rapidly progressive dementia and histologically by a spongiform encephalopathy associated with neuronal destruction and pronounced astrogliosis. Combination of both diseases has not been reported in the literature previously and their relationship is uncertain. We present 3 cases with this interesting association and consider their relationship.

Aged↗
PubMed1987

Wernicke's encephalopathy in patients on peritoneal dialysis or hemodialysis.

Although the occurrence of Wernicke's encephalopathy (WE) in patients on dialysis is frequently alluded to, review of the literature reveals only 3 described cases. We describe 5 patients on dialysis who developed WE in the absence of alcoholism or other predisposing factors. The clinical diagnoses included uremic encephalopathy (2 patients), dysequilibrium syndrome (1), dialysis dementia (1), and brainstem hemorrhage (1). At postmortem examination, classic findings of WE were evident. The rarity of WE in patients on dialysis may in part be explained by studies indicating a genetic defect in transketolase activity. Patients on dialysis are also potentially at risk for thiamine deficiency because of anorexia, vomiting, and intravenous alimentation. Other factors altering thiamine requirements, such as glucose load or infections, may also contribute. Preventable and potentially curable, WE should be suspected in all patients on dialysis who have an unexplained neurological picture.

Adult↗
PubMed1987

Massive cerebral edema associated with meningioma.

Cerebral edema is a well-known complication of malignant astrocytoma and metastatic brain tumour. Though far less frequent, the association of cerebral edema with meningioma is also recognized; this is unpredictable and sometimes out of proportion to tumour size. We describe three cases where the mass effect was due to severe edema, rather than the tumour itself and was responsible for a catastrophic clinical presentation. The mechanisms responsible for the development of severe edema with meningioma which have been previously proposed are reviewed. They include tumour size, location, histologic subtype, cellularity, mitotic activity, vascularity and the presence of excretory-secretory activity. None of these consistently correlate with cerebral edema. Our cases suggest that spontaneous hemorrhage into the tumour may be the common factor responsible for severe cerebral edema. It is stressed that though a decidedly rare complication, cerebral edema secondary to meningioma should be entertained in the differential diagnosis of acute neurologic deterioration of these patients.

Adult↗
PubMed1987

Pathology of spontaneous dissection of intracranial arteries.

Spontaneous dissection of a major subarachnoid artery is an uncommon cause of stroke in young and apparently healthy individuals. Such dissection does not correlate well with systemic conditions such as emboli, thrombotic or hemorrhagic tendencies or hypertension, nor with disease of blood vessels such as atherosclerosis, fibromuscular dysplasia, cystic medial necrosis or Moya-Moya disease. Unusual exertion has been implicated as a factor in some cases. Gap defects were found in the internal elastic lamina near the site of dissection in three of four cases of spontaneous dissection reported here. It is suggested that such defects, because of their unusual size or number, may be responsible for initiating dissection in susceptible individuals. A detailed study of the major cerebral arteries in cases of dissection and control cases to document the size and frequency of such defects could shed light on the pathogenesis of spontaneous dissection. The subsequent course of events tends to differ in the internal carotid and vertebro-basilar systems. In most cases, the dissection in the internal carotid system is sub-intimal leading to thrombosis and cerebral infarction, while in the vertebrobasilar system dissection lies between the media and adventitia leading to subarachnoid hemorrhage. It is not known what structural differences of the two arterial systems may underlie this difference in the pattern of arterial dissection.

Adult↗
PubMed1986

Fatal subarachnoid hemorrhage due to traumatic rupture of the vertebral artery.

Massive fatal subarachnoid hemorrhage maximal in the posterior fossa following minor trauma to the head and neck was first attributed to rupture of a vertebral artery (VA) in 1971. Typically, a young, healthy, but intoxicated man receives a minor blow and immediately collapses and dies within minutes. Early reports suggested an extracranial site of rupture with upward tracking of blood into the subarachnoid space. In few cases has this site of rupture been histologically verified, and more recent reports have drawn attention to intracranial rupture of the VA. We describe herein six cases in which the intracranial segment of the VA was the site of traumatic rupture, a site which can be demonstrated by careful examination of the most proximal segment of the VA attached to the brain in the course of routine brain removal.

Adolescent↗
PubMed1984

Cerebral hyperperfusion after carotid endarterectomy: a cause of cerebral hemorrhage.

Correction of a very high grade carotid stenosis by endarterectomy in a normotensive man was followed by the development of severe unilateral head, eye, and face pain, seizures, and on the 6th day a fatal intracerebral hemorrhage. Autopsy revealed changes in the cerebral hemisphere ipsilateral to the endarterectomy that resembled the changes seen in malignant hypertension, whereas the opposite hemisphere was normal. These changes included hypercellularity and edema of arterial and arteriolar walls, with necrosis, extravasation of erythrocytes, and exudation of fibrin. We propose that the clinical and pathological features in this case were due to relative hyperperfusion of a cerebral hemisphere in which autoregulation had been impaired because of preoperative chronic hypoperfusion with chronic maximal dilatation of its blood vessels. This state of relative hyperperfusion is probably similar to the normal perfusion pressure breakthrough that occasionally occurs after the resection of cerebral arteriovenous malformations. It is similar to the breakthrough perfusion that occurs in severely hypertensive patients and results in hypertensive encephalopathy.

Arterioles↗
PubMed1983

Central nervous system toxicity of high-dose cytosine arabinoside.

Ten patients with refractory acute leukemia were treated with high-dose cytosine arabinoside (Ara-C) infusions. Nine patients had previously achieved at least one complete remission using standard chemotherapy protocols that include cytosine arabinoside. Eight of the ten had been on maintenance therapy. Twelve courses of treatment were given, with the cytosine arabinoside infused over 1-2 hours in a dose of 3 gm/m2. Each course consisted of 12 to 16 doses given at 12-hour intervals. The drug was generally well tolerated but five patients developed central nervous system symptoms characterized by ataxia, dysphasia, nystagmus, dysdiadochokinesis, and a decreased level of consciousness. These changes began 3 to 34 days after the initiation of therapy and were severe at the time of death in two of the patients. One complete and one partial remission, lasting 2.5 months and 1 month, respectively, were documented. This experience suggests that high-dose Ara-C is of limited usefulness in refractory acute leukemia and may be frequently associated with significant neurotoxicity.

Acute Disease↗
PubMed1983

Fluspirilene neuroleptic depot injections and indurations.

Local reactions at injection sites have limited the use of depot fluspirilene, an otherwise effective treatment for chronic schizophrenia. Thirty-nine reports of fluspirilene-treated patients were analyzed and the patients were examined for indurations. It was found that patients with indurations were given significantly higher doses and volumes of the drug. The mean number of high volume injections (over 3ml) at each site was the most significant differentiating factor between the two groups: 19 such injections over a twelve month period for those with indurations, as compared to 3 for those without. None of the following variables were significant; age, sex, allergies, or total length of time on the drug. Previous administration of other forms of depot neuroleptics did not differentiate the two groups. Biopsy showed serous atrophy of subcutaneous fat, prominent blood vessels and hemosiderin laden macrophages.

Adult↗
PubMed1981

Glial fibrillary acidic protein in stromal cells of some capillary hemangioblastomas: significance and possible implications of an immunoperoxidase study.

Thirty-nine hemangioblastomas from 26 patients were studied by the immunoperoxidase method for GFA protein. Reactive gliosis in the form of trapped GFA protein-positive astrocytes or astrocytic cell processes penetrated the margins of all the neuraxial tumors and none of those occurring on nerve roots or in the tumor explants maintained in an organ culture system. Gliosis was especially prominent in tumors recurring after surgical excision or in patients with a long history of tumor. In six tumors, representing both the reticular and the cellular variants of hemangioblastoma, GFA protein-positive stromal cells were also found, chiefly in the periphery of the neoplasma: all these tumors were surrounded by dense reactive gliosis. Four hypotheses accounting for the presence of GFA protein-positive stromal cells are considered: (1) The tumors are astrocytomas. (2) The GFA protein-positive cells are not neoplastic but lipidized or altered reactive astrocytes. (3) The tumors are mixed and partly composed of neoplastic astrocytes. (4) The stromal cells are capable of taking up extracellular GFA protein derived from the adjacent reactive astrocytes. The last of these hypotheses is the most consistent with the collective evidence derived from the histological findings. It implies that the presence of GFA protein in the cytoplasm of a cell does not necessarily establish that the cell is glial. The possibility of uptake of GFA protein by non-glial cells must be considered if dense gliosis is present in the vicinity.

Adolescent↗
PubMed1981

Nodular regenerative hyperplasia of the liver associated with macroglobulinemia. A clue to the pathogenesis.

Nodular regenerative hyperplasia of the liver is an infrequent condition characterized by transformation of the hepatic parenchyma into nodules with only mild fibrosis. Little is known about the etiology except that there is usually an underlying chronic disease, such as Felty's syndrome, which antedates the development of clinical liver disease. It is poorly understood how the associated diseases contribute to the pathogenesis of nodular regenerative hyperplasia. Presented are four cases of nodular regenerative hyperplasia in which macroglobulinemia was also present. This new association suggests to us a hypothesis for the pathogenesis of nodular regenerative hyperplasia. Histologic examination of the livers in these and other cases of nodular regenerative hyperplasia reveals widespread obliteration of the small portal veins. Postmortem angiography of one liver in the present series demonstrated that the nodules were well perfused and that the atrophic areas were poorly perfused with portal blood. This supports the view that atrophy of lobules results from a lack of portal blood supply and that nodules develop from lobules well supplied with portal blood. In each of the clinical conditions associated with nodular regenerative hyperplasia, including macroglobulinemia, inflammatory or thrombotic vascular lesions are found in many organs. Therefore, nodular regenerative hyperplasia may be the hepatic expression of a more widespread vascular disease.

Adult↗
PubMed1980

Cerebral blindness and oculomotor nerve palsies in toxoplasmosis.

We studied the clinicopathologic and neuro-ophthalmic manifestations of central nervous system toxoplasmosis in two patients who were being treated with immunosuppressive chemotherapy, one for renal transplantation and the other for systemic lupus erythematosis. Both pateints had oculomotor nerve palsies and later developed visual loss from cerebral involvement. Multifocal central nervous system toxoplasmosis appeared as a complication of their systemic diseases.

Adult↗
PubMed1980

Interhemispheric cyst of neuroepithelial origin in association with partial agenesis of the corpus callosum. Case report and review of the literature.

The authors report an adult patient with a symptomatic interhemispheric cyst demonstrated by computerized tomography (CT), angiography, and at surgery. Choroid plexus epithelium was identified arising from the inner aspect of the cyst wall. Partial agenesis of the corpus callosum is postulated on the basis of the CT findings and the presence of choroid plexus in the interhemispheric cyst.

Agenesis of Corpus Callosum↗