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Biomedical subjects

J J Gilbert

Publications and source records attributed to J J Gilbert.

At least 55 records · Page 3Linked to original sources

Fatal intracranial arterial dissection: clinical pathological correlation.

The clinical pathological features of fatal arterial dissection confined to the intracranial vessels are described. Three patients with anterior circulation dissections presented with focal ischaemic neurological deficits and pathological examination of involved vessels revealed a dissection plane between internal elastic lamina and media accompanied by intravascular thrombosis. Three of four patients with posterior circulation dissections had clinical pathological features of subarachnoid haemorrhage and at necropsy had transmural dissections. In contrast to previous reports, primary vasculopathies either degenerative or inflammatory were not identified in affected vessels. The pathogenesis of intracranial arterial dissection is discussed and the clinical features are correlated with the pathological abnormalities.

Adolescent↗

The pathological basis of conduction block in human neuropathies.

Conduction block was detected in patients with neuropathy by measuring a decrease in the size of the compound muscle action potential of more than 20% on proximal versus distal stimulation of the peroneal, median or ulnar nerve in the absence of excess temporal dispersion of the potential. The teased fibre analyses of nerve biopsies from four patients with "definite" and six patients with "probable" conduction block and from seven patients with neuropathy but without conduction block were compared. All patients with conduction block had significant demyelination (X% demyelinated and remyelinated fibres = 50%) while those without conduction block did not (X = 5.0%). Demyelination is the pathological basis of conduction block in human neuropathies.

Adult↗

Oligoclonal bands in multiple sclerosis: clinical-pathologic correlation.

Although oligoclonal banding is a characteristic feature of MS spinal fluid, some patients do not show this abnormality. Four of 18 consecutive patients with autopsy-proven MS had no oligoclonal bands (OB) in CSF during life or at postmortem. Patients with OB had numerous plasma cells in meninges and plaques (confirmed in sections stained for cytoplasmic immunoglobulin). The four patients without bands had few or no identifiable plasma cells. Therefore, lack of OB correlates with both inactivity of plaques and absence of plasma cells in plaques or meninges. This is another form of heterogeneity in MS.

Adult↗

Lethal delayed radiation necrosis of the brain as a complication of radiotherapy for cancer in the head and neck.

Necrosis of the brain following irradiation of tumors adjacent to the cranial cavity is an insidious and often fatal complication. Three patients with this complication are reported. Recognition of the condition is often delayed due to the long time interval between irradiation and manifestation of first symptoms. Accurate shielding and limitation of irradiation to the brain may prevent this problem.

Aged↗

Radiographic-pathologic correlation in cerebral amyloid angiopathy. A review of 12 patients.

Twelve patients with pathologically proven cerebral amyloid angiopathy (CAA), causing intracerebral hemorrhage, were reviewed to determine the clinical and radiographic features. All 12 patients were 62 years of age or older and presented with acute neurological syndromes. The computed tomographic scan (CT) in each showed a relatively large intracerebral lobar hemorrhage located in a cortical and subcortical area. The finding of a lobar intracerebral hematoma in an elderly patient should suggest CAA as a cause.

Aged↗

Cerebellar norepinephrine in patients with Parkinson's disease and control subjects.

Norepinephrine was measured in postmortem cerebellar cortex of 22 non-neurological control subjects and nine patients with Parkinson's disease, using the high-performance liquid chromatography method with amperometric detection. In all control subjects, substantial amounts of norepinephrine was found in cerebellar cortex. There was a moderate negative correlation between age of control subjects and cerebellar norepinephrine concentration. In the patients with Parkinson's disease, the cerebellar cortical norepinephrine levels were significantly below normal. This is in accord with previously reported reduced norepinephrine levels in locus ceruleus and other regions of the parkinsonian brain. Although the main symptoms of Parkinson's disease are primarily caused by disturbed basal ganglia (dopamine) function, cerebellar dysfunction related to norepinephrine may contribute to some abnormalities of motor performance in this disorder.

Aged↗

Circulating lymphocyte subpopulations in experimental allergic neuritis.

T-cell subsets in the peripheral blood were analyzed using monoclonal antibodies during the development of experimental allergic neuritis in Lewis rats. Percentages of helper and suppressor cells and ratios of helper/suppressor cells did not exceed normal limits during the development of the disease.

Animals↗

Suppression of chronic-relapsing experimental allergic encephalomyelitis in strain-13 guinea pigs by administration of liposome-associated myelin basic protein.

Juvenile strain-13 guinea pigs were challenged with isologous spinal cord in CFA. After recovery from the first EAE episode the animals were treated with guinea pig MBP inserted into liposomes, with cytochrome-c-liposomes, with MBP in saline or with MBP in IFA. Guinea pigs treated with MBP-liposomes showed a striking reduction in clinical signs and in the number and intensity of relapses. They displayed virtually no demyelinating lesions, and had comparatively little parenchymal inflammation in the spinal cord. Early T rosette levels showed an inverse correlation with the severity of histological lesions in the spinal cord but correlation with the clinical status at the time of rosette assay was less well defined.

Animals↗

The role of myelin lipids in experimental allergic encephalomyelitis. Part 1. Influence on disease production by non-encephalitogenic doses of myelin basic protein.

Hartley guinea pig central nervous system (CNS) myelin has been purified and fractionated into its protein and lipid components. Experimental allergic encephalomyelitis (EAE) was induced in juvenile strain 13 guinea pigs with both lyophilized and fresh 'wet' myelin. However, a larger dose of lyophilized myelin was required to induce chronic EAE. Total myelin lipids, galactocerebrosides, gangliosides, phospholipids or proteolipids were combined with a non-encephalitogenic dose of myelin basic protein (MBP) and injected in juvenile Hartley guinea pigs. No clinical or histological manifestations of disease were observed. Parameters of immune functions indicated that the total myelin lipids augmented cell-mediated immune responses as measured by in vitro lymphocyte transformation and by a significant decrease in the percentage of peripheral early T cells. Only the proteolipids elicited delayed hypersensitivity reactions. Animals that received the phospholipid-MBP combination showed no changes when compared to animals injected with MBP alone. The results suggest that although the myelin lipids did not act synergistically with a non-encephalitogenic dose of MBP to induce EAE, they induced immunological changes and potentiated the immune response to MBP.

Animals↗

Body size and food size in freshwater zooplankton.

We used double-label liquid scintillation techniques to measure the efficiencies with which eight different-sized zooplankton species ingested four cell types relative to a standard cell type (Chlamydomonas). Efficiency ratios (ERs: clearance rate on cell type X / clearance rate on Chlamydomonas) on the three ultraplankton (<5 mum in diameter) cells (a coccoid bacterium and the algae Synechococcus and Nannochloris) varied greatly among zooplankton species but were not correlated with zooplankton body length. Variation in ERs on a much larger (17 x 14 mum) algal cell (Cryptomonas) was only partly explained by zooplankton body length. The eight zooplankton species were classified into three functional groups: (i) species having moderate to high ERs on all ultraplankton (0.4 < ER < 1.6) and ERs on Cryptomonas proportional to their body lengths (Conochilus, Diaphanosoma, and probably Keratella cochlearis and Ceriodaphnia); (ii) species having extremely low ERs on bacteria (mean ER < 0.05), higher but still low ERs on ultraphytoplankton (ER generally < 0.4), and ERs on Cryptomonas proportional to their body lengths (Bosmina, Diaptomus copepodites and adults); (iii) species having extremely low ERs on all ultraplankton (mean ER < 0.05) and ERs on Cryptomonas much higher than expected given their body lengths (Keratella crassa, Polyarthra, and Diaptomus nauplii). These functional groups follow neither taxonomic nor body-length groupings. We conclude that zooplankton body length may influence the maximal particle size a species can ingest but has little influence on the ingestion of smaller particles. Two frequently used models relating zooplankton body size and food size are unrealistic.

Journal Article↗

Polyneuropathy in critically ill patients.

Five patients developed a severe motor and sensory polyneuropathy at the peak of critical illness (sepsis and multiorgan dysfunction complicating a variety of primary illnesses). Difficulties in weaning from the ventilator as the critical illness subsided and the development of flaccid and areflexic limbs were early clinical signs. However, electrophysiological studies, especially needle electrode examination of skeletal muscle, provided the definite evidence of polyneuropathy. The cause is uncertain, but the electrophysiological and morphological features indicate a primary axonal polyneuropathy with sparing of the central nervous system. Nutritional factors may have played a role, since the polyneuropathy improved in all five patients after total parenteral nutrition had been started, including the three patients who later died of unrelated causes. The features allow diagnosis during life, and encourage continued intensive management since recovery from the polyneuropathy may occur.

Adult↗

Internuclear ophthalmoplegia and "optic neuritis": paraneoplastic effects of bronchial carcinoma.

A 56-year-old man developed bilateral internuclear ophthalmoplegia and "optic neuritis" as remote effects of a bronchial carcinoma. These clinical findings correlated pathologically with secondary demyelination of the medial longitudinal fasciculus and with round cell infiltration and adhesive arachnoiditis of the optic nerve. There was no evidence of CNS metastasis. "Optic neuritis" and internuclear ophthalmoplegia may be paraneoplastic effects of systemic cancer.

Carcinoma, Bronchogenic↗

Unsuspected multiple sclerosis.

Five patients known to have various medical problems were found unexpectedly at autopsy to have typical multiple sclerosis plaques. These were most often small and in a periventricular distribution in frontal, temporal, and occipital lobes. In two cases, small plaques were found in the thalamus and brain stem. The cerebellum was not involved.

Adolescent↗

Brief clinical report: short rib-polydactyly syndrome, Majewski type.

We describe a baby with external and internal anomalies of the Majewski form of the short rib-polydactyly (SRP) syndromes. Previously unreported abnormal vertebral bodies, delayed ossification of the sternum and fibulae, and a diencephalic hamartoma are noted. These abnormalities and minimal histologic abnormality at the chondro-osseous junction suggest that this syndrome may be heterogeneous or more variable than previously known.

Abnormalities, Multiple↗

Intraneural injection of lymphocytes in experimental allergic neuritis.

Passive transfer of experimental allergic neuritis (EAN) lymph node cells (LNC) by intraneural injection did not produce significant demyelination. EAN-LNC stimulated with myelin in vitro produced mild demyelination while those incubated with Concanavalin A had no effect. The lack of demyelination by unstimulated EAN-LNC is in contrast to the marked demyelination produced by intraneural injection of EAN serum. The mononuclear cell infiltration and demyelination of classical EAN seem to require both cellular and humoral immune responses.

Animals↗