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Biomedical subjects

P Vermersch

Publications and source records attributed to P Vermersch.

At least 91 records · Page 5Linked to original sources

[Hearing loss in multiple sclerosis: clinical, electrophysiologic and radiological study].

Clinical presentation of multiple sclerosis (MS) is highly heterogeneous. Deafness is considered to be rare. The aim of this study was to determine the frequency of acute deafness in MS and to evaluate prognosis. The occurrence of acute deafness was systematically noted in a cohort of 400 consecutive clinically definite MS patients. Acute deafness was observed in 14 patients (3.5 p. cent) with a mean age of 28 years (15 to 48) and after a mean of 2.3 years (0 to 10) of disease duration. In all but two patients, deafness was associated with disease exacerbations, highly suggestive of infratentorial lesions. MRI showed hyperintensities in the pons or the midbrain in 11 cases. Deafness disappeared in all cases excepted for one patient. After a mean follow-up of 7.2 years (1 to 17), all the patients remain in the relapsing-remitting form of the disease with a mean EDSS of 2.4 (0 to 4.5). Acute deafness is observed in 3.5 p. cent of MS cases and occurs more frequently during the first years of the disease. Although follow-up of a larger cohort is necessary, deafness could be of good prognostic factor in MS.

Adolescent↗

Cardiac repolarization abnormalities in multiple sclerosis: spinal cord MRI correlates.

Ventricular repolarization dysfunction has recently been reported in multiple sclerosis (MS). We evaluated ventricular repolarization dysfunction in 52 MS patients and looked for a relationship between corrected QT (QTc) abnormalities (i.e., abnormalities of QT intervals corrected for rate) and spinal cord magnetic resonance imaging (MRI) findings. QTc intervals were increased in MS patients compared with controls (P < 0.01) and were correlated with a reduction of spinal cord area (P < 0.01). QTc abnormalities in MS were thus associated with axonal loss, reflected by spinal cord atrophy, rather than demyelination.

Adult↗

Visual evoked potentials study in chronic idiopathic inflammatory demyelinating polyneuropathy.

BACKGROUND: The frequency of the association between chronic demyelinating inflammatory polyneuropathy (CIDP) and central nervous system (CNS) demyelinating lesions is probably underestimated. OBJECTIVE: To investigate the occurrence of combined central and peripheral demyelination in CIDP patients and to correlate visual evoked potential (VEP) abnormalities with CNS demyelinating lesions, observed on brain magnetic resonance imaging, and antibodies against glycolipids. METHODS: Nerve conduction studies, brain MRI and antibodies against glycolipids were prospectively studied in 17 patients who fulfilled the diagnostic criteria proposed for CIDP (Cornblath DR, Asbury AK, Albers JW, Feasby TE, Hahn AF, McLeod JG, Mendell JR, Parry GJ, Pollard JD, Thomas PK. Ad Hoc Subcommittee of the American Academy of Neurology AIDS Task Force. Research criteria for diagnosis of chronic inflammatory demyelinating polyneuropathy. Neurology, 1991;41:617-618). VEPs were performed in each case before and after 6 months treatment with either intravenous immunoglobulins (IVIG) or steroids. RESULTS: Eight patients (47%) had increased latencies in at least one eye or showed increased interocular latency difference. Four patients (23%) presented a significant high signal intensity on T2-weighted brain MRI images. Of these 4 patients, 3 had prolonged VEP latency. Two patients with delayed VEP latency had antibodies against GM1, and SGLPG and anti-sulfatides, respectively. One patient with normal VEPs also had antibodies to GM1. VEP results were not significantly modified after treatment, either with steroids or IVIG. CONCLUSION: This study confirmed the high frequency of abnormal VEPs in CIDP patients, and found that they are poorly correlated with CNS demyelinating lesions and antibodies against glycolipids. The VEP abnormalities of these patients may be explained by the susceptibility to immune-mediated damage of both the peripheral nervous system and the optic nerve.

Adolescent↗

Multiple sclerosis with normal neuro-ophthalmological work-up: results of focal stimulations induced by a scanning laser ophthalmoscope.

OBJECTIVE: Visual evoked potentials (VEPs) are a very useful tool in diagnosis of multiple sclerosis (MS). Nevertheless, in some cases of the disease, VEPs are normal. The aim of this study was to evaluate the diagnostic value of focal checkerboard reversal stimulation based on opto-acoustic modulation generated by a scanning laser ophthalmoscope (SLO) in patients whose standard neuro-ophthalmological work-up was normal. METHODS: We prospectively studied 185 MS patients. In this cohort we found 30 patients with definite MS and normal neuroophthalmological work-up and we studied the diagnostic yield of focal visual stimulation in these patients. We performed focal SLO-elicited VEPs with two different spatial distributions: a central 8 x 8 degrees square field and a central 8 x 8 degrees exclusion square. The results were analysed in terms of age of the patient, course of the disease, and disability evaluated on the Expanded Disability Status Scale (EDSS). RESULTS: Mean latencies of focal VEPs were increased in MS patients compared to controls. In MS, focal stimulation allowed dysfunction of the visual system to be detected in 50% of patients who have been classified as normal according to conventional VEPs. VEP abnormalities were found to be correlated with the EDSS score (P<0.001) and the course of the disease (P<0.05). CONCLUSION: We have demonstrated the value of focal VEPs in MS diagnosis using SLO-based techniques. Further prospective work in patients with possible and probable MS should enable an evaluation of the sensitivity and specificity of this method in the early diagnosis of MS.

Adult↗

Atypical form of non-Langerhans histiocytosis with disseminated brain and leptomeningeal lesions.

An 18 year old girl presented with acute visual loss. T2 weighted brain MRI showed areas of hyperintensities in the thalamic nuclei, internal capsule, lentiform nuclei, the subarachnoidal spaces, and a retrobulbar infiltration. Analysis of CSF showed numerous foamy histiocytes without malignant cells, raised protein, and depressed glucose concentration. Biopsy of the right thalamus demonstrated aggregates of histiocytes with immunohistological and ultrastructural characteristics of non-Langerhans cell histiocytosis. The patient improved with chemotherapy and corticosteroids. After 3 months of treatment, CSF analysis showed no more histiocytes. Cytological examination of CSF can be helpful for the management of patients with extensive histiocytic infiltration.

Adolescent↗

Unusual MR findings of the brain stem in arterial hypertension.

MR imaging findings have been reported in only a few cases of severe arterial hypertension. We report two cases of severe paroxysmal arterial hypertension associated with unusual brain stem hyperintensity. The lesions improved dramatically after stabilization of blood pressure, suggesting that edema could be the main cause of the MR imaging-observed hyperintensity.

Adrenal Gland Neoplasms↗

[Spinal cord magnetic resonance imaging in multiple sclerosis: importance of determining degree of atrophy as a marker of disease course].

Spinal cord magnetic resonance imaging (MRI) is of particular interest in the management of multiple sclerosis (MS) especially in primary progressive forms. Most of the demyelinating lesions are located in the cervical or dorsal cord. Spinal cord area reduction has been recently correlated with the progression of disability (Losseff et al., 1996, Lycklama a Nijeholt et al., 1998). The aim of this study was to confirm this first result, to assess the reproducibility of this method and to correlate demyelinating lesions with spinal cord area reduction. Fifty two patients were included and compared with 15 controls (normal subjects). T2 Sagittal and axial plane images were performed to localized hypersignal lesions. Spinal cord area was obtained by a volume acquired inversion prepared fast spoiled gradient echo acquisition (MP-Rage) sequence. We compared the mean area value with clinical parameters (age, course of the disease, expanded disability status scale ¿EDSS) and with the number and location of demyelinating lesions. Demyelinating lesions were found in 82p.100 of MS patients and in none of controls. Mean spinal cord area was closely similar to Losseff et al. (1996) results and was reduced compared with controls (p<0.001). Spinal cord reduction was correlated with disability, studied by the EDSS. Furthermore, no correlation was found between demyelinating lesions and spinal cord area reduction. This study confirms the interest of spinal cord area mesurement in MS. Spinal cord atrophy is a reliable marker for axonal loss. This method should be of particular interest for the follow-up of axonal loss in thepeutic trials especially in primary progressive MS.

Adult↗

[Paraplegia episodes revealing tuberculous myelitis].

A 38 year-old woman, without previous medical history, presented, since 1993, several paraplegic fits carrying herself progressively through to a severe paraplegia. Diagnoses successively proposed were spinal cord compressions by slipped discs, spinal cord infarct and multiple sclerosis. In November 1998, the patient presented back pain and fever. Spinal cord magnetic resonance imaging (MRI) revealed a mildly enlarged dorsal cord with signal abnormalities. The lesions were isointense on T1-weighted images, hyperintense on T2-weighted images and showed a ringlike contrast enhancement. A lumbar puncture showed a trouble cerebrospinal fluid (CSF) with leucocytes 600/mm(3) (85 p.100 polynuclear), protein 6.7 g/l, glucose 0.26 g/l, chloride 109 mmol/l. The patient was first treated with parenteral unspecific antibiotherapy. Microbiological studies of blood and CSF were negative. CSF examination with polymerase chain reaction (PCR) was positive for Mycobacterium tuberculosis. Clinical (pain and fever) symptoms and CSF abnormalities decreased after antituberculous treatment. However, paraparesis remain severe. Spinal tuberculous localizations often lead to diagnostic and therapeutic errors. Improvement of spinal cord MRI sequences and using of PCR technics in CSF would contribute to reduce these difficulties.

Adult↗

[Adenovirus myelitis and Epstein-Barr myelitis: two unusual viral causes with similar presentations].

We report two cases of viral myelitis, one associated with adenovirus and the other with Epstein-Barr virus. The clinical presentation and course were similar, with viral illness, paraplegia with a D4 sensory level, and fever. Spinal magnetic resonance imaging showed a T2 cervico-dorsal high intensity signal. Cerebrospinal fluid examination showed pleocytosis without oligoclonal bands. Both patients recovered after treatment with high-dose methylprednisolone. These two cases suggest a similar clinical and paraclinical pattern in viral transverse myelitis. Moreover, treatment with corticosteroids seems to be useful in viral myelitis.

Adenoviridae Infections↗

[Clinical manifestations and therapeutic approach in neurosarcoidosis].

Neurological impairment is a frequent cause of morbidity and mortality in patients with sarcoidosis. The aim of this study was to evaluate the clinical manifestations of the disease, the response to corticosteroids and alternative treatments. During a 5 year period, diagnosis of neurosarcoidosis was performed in 40 patients. We retrospectively analyzed clinical, laboratory data and response to treatments. Mean age was 41.3 years (range 17-72). Mean time of follow-up was 46 months. Neurologic signs were the first symptom in 50 p. 100 of cases and an isolated manifestation in 12.5 p. 100. Central nervous system impairment was seen in 60.7 p. 100, meningitis in 27 p. 100. Other clinical manifestations were cranial nerve palsies (27 p. 100), peripheral neuropathy (33 p. 100), myopathy (16 p. 100). Eighty percent of the patients were treated by corticosteroids. Because of a lack of efficacy 40 p. 100 of patient required alternative treatment (including methotrexate, cyclophosphamide, azathioprin, cyclosporin). Complete recovery was observed in only 27.5 p. 100 of cases confirming the severity of neurosarcoidosis. Forty percent of patients were clinically stable and 10 p. 100 worsened. No patient died. This study confirms that intensive initial treatment is often necessary to prevent irreversible lesions. Alternative treatment should be rapidly initiated in resistant forms.

Adolescent↗

Tau and apo E in CSF: potential aid for discriminating Alzheimer's disease from other dementias.

To evaluate the usefulness of tau proteins as biological markers in the diagnosis of dementia of the Alzheimer type (DAT), we analyzed the concentration of tau proteins in 253 cerebrospinal fluid (CSF) samples from patients with or without neurological disorders. Our study showed a significant increase of the mean CSF tau concentration in DAT patients compared with that from non-DAT patients. Interestingly, a significative decrease of CSF tau in patients with frontotemporal dementia was found. We also observed a positive correlation between the CSF-tau concentration and the number of apoepsilon4 alleles. The CSF apolipoprotein E concentration was evaluated and revealed no variation between the groups, although we observed a significant correlation between CSF tau and apolipoprotein E in DAT patients.

Age Factors↗

The biochemical pathway of neurofibrillary degeneration in aging and Alzheimer's disease.

OBJECTIVE: To determine the spatiotemporal mapping of neurofibrillary degeneration (NFD) in normal aging and the different stages of AD. BACKGROUND: The pathophysiologic significance of AD lesions, namely amyloid plaques and neurofibrillary tangles, is still unclear, especially their interrelationship and their link with cognitive impairment. METHODS: The study included 130 patients of various ages and different cognitive statuses, from nondemented control subjects (n = 60, prospective study) to patients with severe definite AD. Paired helical filaments (PHF)-tau and Abeta were used as biochemical and histologic markers of NFD and amyloid plaques, respectively. RESULTS: NFD with PHF-tau was systematically present in variable amounts in the hippocampal region of nondemented patients age >75 years. When NFD was found in other brain areas, it was always along a stereotyped, sequential, hierarchical pathway. The progression was categorized into 10 stages according to the brain regions affected: transentorhinal cortex (S1), entorhinal (S2), hippocampus (S3), anterior temporal cortex (S4), inferior temporal cortex (S5), medium temporal cortex (S6), polymodal association areas (prefrontal, parietal inferior, temporal superior) (S7), unimodal areas (S8), primary motor (S9a) or sensory (S9b, S9c) areas, and all neocortical areas (S10). Up to stage 6, the disease could be asymptomatic. In all cases studied here, stage 7 individuals with two polymodal association areas affected by tau pathologic states were cognitively impaired. CONCLUSIONS: The relationship between NFD and Alzheimer-type dementia, and the criteria for a biochemical diagnosis of AD, are documented, and an association between AD and the extent of NFD in defined brain areas is shown.

Aged↗