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Biomedical subjects

A G Kermode

Publications and source records attributed to A G Kermode.

At least 19 recordsLinked to original sources
PubMed2006

Leflunomide-induced peripheral neuropathy.

Two cases of leflunomide-induced peripheral neuropathy are described; in a 60-year-old woman with sero-negative polyarthralgia-myalgia syndrome and a 65-year-old man with sero-negative rheumatoid arthritis, both treated with leflunomide at 20mg/day. Nerve conduction studies and electromyogram showed sensorimotor axonal neuropathy in both cases. An alternative cause for the axonal neuropathy was excluded by extensive investigations, including cerebrospinal fluid examination and nerve biopsy in the second patient. Both patients stabilized symptomatically and electrophysiologically upon cessation of leflunomide. It is possible that leflunomide-induced peripheral neuropathy has been under-reported and under-recognized.

Adjuvants, Immunologic↗
PubMed2006

Cerebral amyloid angiopathy presenting with vasculitic pathology.

We present an elderly patient with an unusual extensive multifocal central nervous system mass lesion, with dramatic imaging changes but only minor disturbance of cerebral function. Cerebral biopsy revealed an unexpected finding of severe cerebral amyloid angiopathy with secondary florid vasculitic appearances, which is a very rare but recognised association. Immunosuppression has produced significant sustained clinical and radiological remission.

Aged↗
PubMed2005

Murray valley encephalitis mimicking herpes simplex encephalitis.

We describe a patient with serologically proven Murray Valley encephalitis (MVE), whose presentation was clinically and radiologically characteristic of Herpes simplex encephalitis (HSE). The reports of MRI abnormalities in MVE, and the closely related Japanese Encephalitis and West Nile virusii are mostly of bilateral thalamic or grey matter involvement. The MRI scan findings in this case instead showed the typical temporal lobe changes of HSE. Our case report highlights that MVE can mimic HSE, both clinically and radiologically. Therefore it is important to collect an accurate and detailed travel history from patients where there is a risk of exposure to MVE virus. If suspected, antibody testing of serum and CSF, and CSF for MVE-RNA if available, should be undertaken. This case also highlights the potential under-diagnosis of Murray Valley encephalitis.

Adult↗
PubMed1996

High activated and memory cytotoxic T-cell responses to HTLV-1 in healthy carriers and patients with tropical spastic paraparesis.

The cytotoxic T-lymphocyte (CTL) response to HTLV-1 is directed mainly against the Tax protein. Circulating, activated Tax-specific CTL can be found in a majority of healthy carriers and patients with the HTLV-1-associated disease tropical spastic paraparesis (HAM/TSP). In this study we present data on the Tax-specific CTL response of 26 HTLV-1 carriers, including 10 newly recruited subjects. Rex-specific CTL were not found in any subjects investigated. Activated and memory CTL responses were determined separately in 4 healthy carriers, 3 HAM/TSP patients, and 1 "seronegative HAM/TSP." In all subjects, the mean frequency of peptide-specific memory cells per epitope (1/1307) was high. There was no significant difference in mean memory CTL frequency per epitope or in the proportion of subjects with activated CTL between healthy carriers and HAM/TSP patients. One individual with HAM/TSP had an unusually high frequency response to two peptides, suggesting immunodominance of epitope recognition in this individual. We conclude that the magnitude and components of the HLTV-1-specific CTL response do not differ between healthy carriers and HAM/TSP patients. These data do not support a specific CTL-mediated component in the pathogenesis of HAM/TSP.

Amino Acid Sequence↗
PubMed1994

Demonstration of human T lymphotropic virus type I (HTLV-I)-specific T cell responses from seronegative and polymerase chain reaction-negative persons exposed to HTLV-I.

Human T lymphotropic virus type I (HTLV-I) is a human retrovirus etiologically linked to adult T cell leukemia and the progressive chronic neurologic disease HTLV-I-associated myelopathy/tropical spastic paraparesis. Described is a method that measures the production of interleukin-2 from HTLV-I synthetic peptide-stimulated peripheral blood lymphocytes (PBL) of HTLV-I-infected persons. The peptides correspond to immunogenic regions of the HTLV-I Env and Tax proteins. Significantly, this assay demonstrated T cell responses to these HTLV-I peptides from coded PBL samples in 7 of 19 HTLV-I-seronegative polymerase chain reaction-negative persons known to have been exposed to HTLV-I but in none of 16 matched controls without risk factors for exposure (P = .007). The implications of this finding are discussed.

Adult↗
PubMed1993

Seizures due to multiple sclerosis: seven patients with MRI correlations.

The MRI data of seven patients with clinically definite multiple sclerosis who developed epileptic seizures are presented. Six of these cases demonstrated new or enhancing lesions. Cerebral biopsy in one of these lesions confirmed inflammation with myelin breakdown products. Lesions implicated in the causation of seizures involved the cortex or subcortical area. In one patient, a new lesion was associated with EEG abnormalities which resolved as the lesion reduced in size. In three patients epileptic activity was the only clinical manifestation of disease. Large, unresolving lesions tended to be associated with continuing seizures.

Adult↗
PubMed1992

Symptomatic retrochiasmal lesions in multiple sclerosis: clinical features, visual evoked potentials, and magnetic resonance imaging.

We have studied 18 patients with relapsing-remitting multiple sclerosis (MS) who had symptomatic visual field defects due to retrochiasmal lesions. In 17, the lesion responsible was identified by magnetic resonance imaging (MRI), computed x-ray tomography (CT), or both. The lesion responsible involved the posterior optic radiations in eight cases, the optic tract and lateral geniculate nucleus in six, and the posterior limb of the internal capsule in three. The prognosis for recovery of the field defect was good; complete recovery occurred in 14 patients, and only two showed no recovery at all. The striking characteristic of the lesions was that most were unusually large; indeed, many were detectable on CT as well as MRI. Half-field asymmetries of either amplitude or latency of the visual evoked potentials (VEPs), consistent with a postchiasmal lesion, were present in only five out of 13 patients acutely. In only three of these did the abnormality persist at follow-up. We conclude that only large postchiasmal lesions are likely to cause symptomatic homonymous field defects in MS, usually characterized by rapid recovery. Hemifield VEPs have a low sensitivity for the detection of postchiasmal as compared with prechiasmal abnormalities.

Adult↗
PubMed1992

Late radiation associated neurological injury.

Late radiation-associated neurological injury is a recognised and often fatal complication of therapeutic ionising radiation. This retrospective study outlines its highly variable presentation, radiological findings and prognosis over a 6 year period in a major teaching hospital.

Acute Disease↗
PubMed1991

Major differences in the dynamics of primary and secondary progressive multiple sclerosis.

In patients with primary and secondary progressive multiple sclerosis (MS), major differences in the pattern and extent of abnormality on cerebral magnetic resonance imaging (MRI) between the two groups have recently been demonstrated. In the present study, 24 patients, matched for age, sex, duration of disease, and disability, had serial gadolinium diethylenetriaminepentaacetic acid-enhanced MRI over a 6-month period. The 12 patients in the secondary progressive group had a total of 109 new lesions over this time (18.2 lesions per patient per year) and 87% of these enhanced. Enhancement also occurred within and at the edge of preexisting lesions. In contrast, only 20 new lesions were seen in the primary progressive group (3.3 lesions per patient per year) and only one of these enhanced. There was no difference in the degree of clinical deterioration between the two groups over the 6-month period. These findings may indicate a difference in the dynamics of disease activity between the two forms of progressive MS, particularly in relation to the inflammatory component of the lesions, and have important implications for the selection of patients and the monitoring of disease activity in therapeutic trials.

Adult↗
PubMed1991

Measurement of the blood-brain barrier permeability and leakage space using dynamic MR imaging. 1. Fundamental concepts.

Leakage of Gd-DTPA through a defective blood-brain barrier is measured quantitatively using dynamic MRI scanning, in which repeated scans are made after a bolus injection. Image registration artifacts are minimized; a dose of 0.1 mM/kg and an IR sequence enable enhancement to be measured quantitatively. The triexponential enhancement curve is fitted to a theoretical model based on compartmental analysis. The transfer constant, or permeability surface area product per unit volume of tissue (k), and leakage space per unit volume of tissue (v1) are measured. Estimates for a quickly enhancing multiple sclerosis lesion are k = 0.050 min-1, v1 = 21%; for a slow one k = 0.013 min-1, v1 = 49%. This implies permeability in the range 4-17 x 10(-6) cm s-1, in broad agreement with other physiological methods. The method is noninvasive and can be used to make serial measurements in patients and in experimental animal models. The time course of pathological aspects of diseases with blood-brain barrier breakdown, such as multiple sclerosis, tumors, and infections (e.g., HIV) can be studied, along with their response to therapy. The measurements are of physiological variables and are therefore independent of imaging equipment and field.

Adult↗
PubMed1991

Destructive lesions in demyelinating disease.

Three cases are presented in which clinical and radiological features suggested the diagnosis of glioma but surgical biopsy revealed a demyelinating process, with tissue destruction and cyst formation in two. One patient had clinically definite multiple sclerosis. Two had probable acute disseminated encephalomyelitis. Treatment with high dose steroids is appropriate when there is clinical or investigative evidence to suggest the presence of demyelinating disease, before deciding on biopsy.

Adolescent↗