PubMed Health⌕ Search

Biomedical subjects

C Hartard

Publications and source records attributed to C Hartard.

10 recordsLinked to original sources
PubMed1997

Prominent sensory ataxia in Guillain-Barré syndrome associated with IgG anti-GD1b antibody.

Sensitization with GD1b has been shown to cause sensory neuropathy in rabbit. A patient with chronic sensory-dominant polyneuropathy who had IgM antibody specifically to GD1b has been reported previously. This report describes the first patient with acute demyelinating polyneuropathy with prominent sensory symptoms who had a high titer of serum IgG anti-GD1b antibody. The serum reacted with neither GM1 nor with other b-series gangliosides (GD2, GD3, GT1b and GQ1b). Improvement in symptoms was coincident with decrease in IgG anti-GD1b antibody titer after plasmapheresis. This case supports the experimental results in rabbit suggesting that anti-GD1b antibody functions in the development of sensory ataxia.

Ataxia↗
PubMed1994

Seroreactivity to Campylobacter jejuni and gangliosides in patients with Guillain-Barré syndrome.

Seroreactivities to Campylobacter jejuni or Campylobacter coli and to the gangliosides GM1 and GD1b were studied by quantitative and immunoglobulin class-specific ELISAs in 42 patients with recent onset of acute Guillain-Barré syndrome (GBS), in 39 patients with positive Campylobacter serology but no neurologic disease, and in 52 healthy blood donors. GBS patients showed positive reactivities to C. jejuni in 57%, 26%, and 2% for IgG, IgA, and IgM, respectively, while blood donors had corresponding values of 6%, 2%, and 4%. IgG, IgA, and IgM reactivities to GM1 were 48%, 78%, and 56% for GBS patients and 4%, 2%, and 4% for blood donors, respectively. Reactivities to GD1b were 77%, 51%, and 15% for the GBS group and 2%, 8%, and 8% for the blood donors, respectively. Patients with positive Campylobacter serology but no neurologic disease also had antibodies to GM1 and GD1b in over half of the cases. Increased titers to C. jejuni closely correlated with increased titers to GM1 and GD1b.

Adolescent↗
PubMed1993

Wilson's disease with cerebral manifestation: monitoring therapy by CSF copper concentration.

The clinical courses, cerebrospinal fluid (CSF) and serum copper concentrations and urinary copper excretions under different schemes of drug treatment in four patients with cerebral manifestations of Wilson's disease were monitored over 6-11 years. CSF copper concentration measurements were performed from the beginning of therapy onwards in three patients and from 16 months after initial treatment onwards in the fourth. CSF copper levels decreased slowly over the years in parallel with clinical improvements, and increased in one patient who interrupted therapy for 2 years. These findings confirm our hypothesis that the concentration of copper in the CSF is a valuable quantitative parameter reflecting the normalization of copper in the brain. Copper measurements during phases of initial neurological deterioration in two patients receiving D-penicillamine, and in one patient receiving D-penicillamine and zinc sulphate, revealed decreased free serum copper and CSF copper levels.

Adult↗
PubMed1993

Treatment of multiple sclerosis with 15 +/- deoxyspergualin. Design of a controlled study with close MRI-monitoring.

The rationale and design of a prospective randomized double blind study of 15 +/- Deoxyspergualin in the treatment of Multiple Sclerosis are presented. The study was started in autumn 1992 and will include more than 200 patients who will be randomized either to DSG low dose or DSG high dose or placebo. Average number of contrast enhancing lesions in monthly cranial MRIs during the first six months of treatment and change in EDSS at the end of the two-year study period will be the main efficacy parameters.

Adolescent↗
PubMed1987

CSF copper concentration: a new parameter for diagnosis and monitoring therapy of Wilson's disease with cerebral manifestation.

In five patients with cerebral manifestation of Wilson's disease, copper was measured in CSF, serum, urine and liver, and ceruloplasmin was determined in CSF and serum. CSF copper was found to be elevated in all cases, especially in the four examined before therapy. Two patients were followed up for a period of 3 years, while undergoing therapy with chelating substances. In case 1, the data and the clinical course are presented in detail: prior to therapy, the daily urinary copper excretion had been elevated, and this increased during the initial treatment stages. The serum copper concentration, which was already low, decreased quickly the during the initial stages of therapy, and remained at a low level during further treatment. In contrast to its level in serum, the copper level in the CSF was up to 3-fold the normal range and fell only very slowly as clinical symptoms improved. These findings suggest transport of copper from the CNS to the CSF. The copper concentration in CSF appears to be a valuable parameter for diagnosis and monitoring therapy in patients with cerebral manifestation of Wilson's disease.

Adult↗
PubMed1986

Morphological and morphometric studies of cerebellar fissuration and myelination in mice with trisomy 19.

The fissuration and myelination in cerebella of trisomy 19 mice and of chromosomally balanced control animals on postnatal days (PD) 2, 5, 10, 12, and 15 were analyzed morphologically and morphometrically. In trisomy 19 mice, an increasing fissuration lag with a fissuration pattern and sequence identical to those of the control animals was found. The nuclear volume density of the trisomic glia cell in the neocerebellar commissure also developed like that of control mice, with an increase shortly before and parallel to the beginning of myelination and with a decrease in its further course. The trisomic axons and myelin sheaths were normally structured but axonal growth and myelination in the neocerebellar commissure were retarded. The quantitative relations of the assumed axon/glia interactions were similar to those of the control animals. The fissuration and myelination in the cerebellum of trisomy 19 mice did not seem to be pathologically changed but seemed to be differently retarded. On PD 15, a myelination lag of less than 5 days but a fissuration lag of nearly 10 days was found. This observation and the assumption of a differently retarded growth of the cerebellar cortex compared with cerebellar subcortical regions lead to the suggestion that the trisomy might result in a progressively asynchronous and disproportional development of different CNS structures.

Animals↗