Biomedical subjects
Publications and source records attributed to J W Schmidley.
Brain metastases from prostate adenocarcinoma are rare; spread to brain as the only site of metastasis is even rarer. We present a patient with a large, cystic, solitary intracerebral metastasis from prostate adenocarcinoma. The pertinent literature is reviewed.
OBJECTIVE: To test the hypothesis that in patients under age 50, with a first, arterial, ischemic cerebral infarct, whose family history and medical history do not suggest an inherited coagulation inhibitor deficiency, the yield of a laboratory search for these disorders will be low. MATERIALS AND METHODS: In 55 such patients under age 50, we systematically searched for deficiencies of protein C, protein S, and antithrombin III. RESULTS: No abnormalities of protein C or antithrombin III were found. One patient had a deficiency of protein S, which was most likely acquired rather than inherited. CONCLUSIONS: In patients who lack clinical features of a prothrombotic state, the yield of testing for protein C, S and AT III deficiency is likely to be low.
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We report a patient with delayed postanoxic demyelination who had pseudodeficiency of arylsulfatase A, reducing his enzyme activity to 10 to 30% of normal. This may have implications regarding the pathogenesis of postanoxic demyelination.
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Transient neurologic deficits are an unusual presentation of chronic subdural hematoma. Presented herein are three patients with transient aphasia and right-sided sensory-motor abnormalities caused by subdural hematoma. Review of the literature revealed 32 cases similar to ours. Presenting complaints were aphasia (77%), sensory symptoms (57%), headache (48%), hemiparesis (50%), and visual disturbance (3%). Fifteen patients underwent cerebral angiography; only three showed significant carotid atherosclerosis. Electroencephalograms were performed in seven patients; five revealed lateralized slowing, but none showed epileptiform activity. Drainage of the hematoma was uniformly curative, although six patients had transient postoperative symptoms. Patients presenting with transient deficits require imaging to rule out the presence of a chronic subdural hematoma.
The hypothesis that the accumulation of prostaglandin (PG)E2 during reperfusion of severely ischemic tissue contributes to a breakdown in the blood-brain barrier (BBB) was expanded to include a parallel role for levuglandins(LGs), gamma-ketoaldehydes produced by rearrangement of PGH2. LGE2 was shown to be more potent than PGE2 in causing breakdown of the BBB when injected intrahemispherically. Brain tissue necrosis was clearly evident with total doses of levuglandin as low as 100 nmole.
Poisoning with tropine alkaloids from cultivated plants and pharmaceuticals is an uncommon cause of delirium and coma. We report a patient with a toxic delirium following ingestion of the tropine alkaloid-containing root of Datura innoxia. Thin-layer chromatography and gas chromatography/mass spectrometry confirmed the presence of atropine and scopolamine in samples of the ingested root. Routine clinical toxin screens may not include an assay for tropine alkaloids. A specific tropine alkaloid assay may provide supporting evidence. The clinical, electroencephalographic, and therapeutic aspects of anticholinergic poisoning are discussed.
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Using the critical electrolyte concentration technique, with ruthenium red as a strain for polyanionic macromolecules, we examined the basement membranes of the rat choroid plexus. Concentrations of Na+ exceeding 3.0 M were required to reversibly inhibit discrete staining of endothelial and epithelial basement membranes by ruthenium red, whereas 2.5 M Na+ inhibited staining of renal pertitubular capillary basement membranes. The findings are consistent with recent evidence that basement membranes underlying fenestrated capillaries are more polyanionic that those underlying continuous capillaries, and suggest that basement membranes of the choroid plexus are more polyanionic than those of peritubular capillaries.
The greater mitochondrial density found in blood-brain barrier endothelium has been attributed to greater utilization of energy, for tasks such as maintaining ionic homeostasis of brain extracellular fluids. To examine whether endothelial mitochondrial density changes in parallel with neural activity, we studied capillaries in rat optic nerves rendered functionless by enucleation. We found no change in endothelial mitochondrial density compared with that in contralateral control nerves. Perhaps endothelial mitochondrial density may not change in capillaries in white matter tracts, or may not ever drop below a baseline level.
We identified and characterized the glucose transporter in the human cerebral cortex, cerebral microvessels, and choroid plexus by specific D-glucose-displaceable [3H]cytochalasin B binding. The binding was saturable, with a dissociation constant less than 1 microM. Maximal binding capacity was approximately 7 pmol/mg protein in the cerebral cortex, approximately 42 pmol/mg protein in brain microvessels, and approximately 27 pmol/mg protein in the choroid plexus. Several hexoses displaced specific [3H]cytochalasin B binding to microvessels in a rank-order that correlated well with their known ability to cross the blood-brain barrier; the only exception was 2-deoxy-D-glucose, which had much higher affinity for the glucose transporter than the natural substrate, D-glucose. Irreversible photoaffinity labeling of the glucose transporter of microvessels with [3H]cytochalasin B, followed by solubilization and polyacrylamide gel electrophoresis, labeled a protein band with an average molecular weight of approximately 55,000. Monoclonal and polyclonal antibodies specific to the human erythrocyte glucose transporter immunocytochemically stained brain blood vessels and the few trapped erythrocytes in situ, with minimal staining of the neuropil. In the choroid plexus, blood vessels did not stain, but the epithelium reacted positively. We conclude that human brain microvessels are richly endowed with a glucose transport moiety similar in molecular weight and antigenic characteristics to that of human erythrocytes and brain microvessels of other mammalian species.
Although the core protein of a heparan sulfate proteoglycan has been detected in brain microvessel basement membranes by immunoperoxidase staining, cytochemical evidence of a glycosaminoglycan component, in the form of discrete staining with ruthenium red, is not found. To resolve this discrepancy, we examined the glycosaminoglycan content of this basement membrane directly. Microvessels were isolated from pig cerebral cortex, and basement membranes freed from cellular elements. Following digestion with papain and Pronase, the glycosaminoglycans were precipitated with cetyl pyridinium chloride and ethanol. The resulting extract contained uronic acid, and after electrophoresis on Super Sepraphore revealed 2 bands: One co-migrated with heparan sulfate standard, the other with chondroitin sulfate A and C. The first was completely eliminated by nitrous acid and heparitinase, but not by hyaluronidase or chondroitinase ABC and was therefore confirmed as heparan sulfate; the other band was eliminated by chondroitinase ABC but not by the other three treatments. The findings suggest that basement membrane of brain microvessels, like other vascular basement membranes, contains heparan sulfate and chondroitin sulfate A and/or C. The failure of staining with ruthenium red is probably a result of unique structural features of this basement membrane, rather than an absence of glycosaminoglycan.
We report a case of syphilitic lumbosacral polyradiculopathy in an HIV-positive, 22-year-old bisexual man with a recent history of secondary syphilis treated with intramuscular penicillin. He presented with rapidly progressive pain and weakness, and muscle wasting in the legs. CSF was under increased pressure and showed a marked pleocytosis (1,130 cells/mm3), hypoglycorrhachia (19 mg/dl), and very elevated protein (1,000 mg/dl). Serum and CSF VDRL serologies were positive. In the legs, nerve conduction studies and needle EMG were consistent with an asymmetric lumbosacral polyradiculopathy with active denervation. His clinical state, CSF, and electrophysiologic studies all improved promptly and markedly after intravenous penicillin. This report documents an uncharacteristically aggressive case of neurosyphilis accompanied by marked changes in the CSF in an HIV-positive patient. While the immunologic effects of HIV and syphilis in combination are not yet fully understood, the cellular immunity defect associated with HIV may alter the natural history of syphilis in patients with concomitant infection, producing unusually aggressive forms or atypical presentations of neurosyphilis.
Our recent observation that the basement membranes of brain microvessels do not stain with the cationic dye ruthenium red has raised the question of whether the basement membranes of this and other vascular beds functioning as barriers between blood and neural tissues are deficient in the polyanionic macromolecules, such as glycosaminoglycans, which are responsible for the ruthenium red staining of other vascular basement membranes. We therefore attempted to produce staining in the only barrier-type microvascular basement membrane known to contain heparan sulfate. Bovine retinas were fixed by immersion in aldehyde fixatives containing ruthenium red, buffered with either 10 mM or 100 mM sodium cacodylate. We found discrete, electron-dense deposits of ruthenium red in vascular basement membranes, quite similar to those seen in vascular basement membranes of nonneural tissues after exposure to ruthenium red. These deposits were more distinct and more frequent in tissue exposed to ruthenium red-aldehyde solutions buffered with 10 mM cacodylate. They were not seen if ruthenium red was omitted from the fixative. The results demonstrate that anionic macromolecules in basement membranes of barrier-type microvessels can be stained with cationic dyes, and suggest that the failure of brain microvessels to stain with ruthenium red may be the result of a relative or total lack of polyanion in this basement membrane, or of other unique properties.
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