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O Gout

Publications and source records attributed to O Gout.

At least 37 records · Page 2Linked to original sources

[The first episode of central nervous system demyelinization and hepatitis B virus vaccination].

BACKGROUND: Central nervous system (CNS) demyelinating episodes have been described following numerous vaccines but there is no definite conclusion about a causal relationship. Recently, in France, in the context of an Expanded Program on Immunization, several cases of CNS demyelination have been observed following injection of recombinant hepatitis B (HB) vaccine, leading to great concern. METHODS: We performed a hospital-based case-control study of 121 patients with a first episode of CNS demyelination occuring between July 1993 and December 1995 and 121 age and sex matched controls seen in the same period. Data on vaccinations history of cases and controls were collected by a postal questionnaire and confirmed by a phone interview. RESULTS: Adjusted odds ratio (OR) obtained from conditional logistic regression between a first episode of CNS demyelination and any vaccination were equal to 1.4 (95 p. 100 CI 0. 5-4.3) for an exposure within the 60 previous days and 2.1 (95 p. 100 CI 0.7-6.0) for an exposure within the 61-180 previous days. Similar results were found for HB vaccine exposure within the 60 previous days (adjusted OR=1.7, 95 p. 100 CI 0.5-6.3) or within the 61 to 180 previous days (adjusted OR= 1.5, 95 p. 100 CI 0.5-5.3). CONCLUSION: These findings did not permit to exclude confidently an association between HB vaccine and the occurrence of a first CNS demyelinating episode.

Adult↗

[Susac's syndrome: improvement with combined cyclophosphamide and intravenous immunoglobulin therapy].

We report a case of Susac's syndrome characterized by subacute encephalopathy, bilateral hearing loss and multiple bilateral branch retinal artery occlusions in a forty-year-old-white-woman. Brain Magnetic Resonance Imaging showed on T2-weighted images multiple, punctate areas of increased signal intensity in periventricular white matter, gray matter and brainstem most of them being enhanced by gadolinium. Cerebrospinal fluid was acellular but with an increased protein level (1.66 g/l). Treatment with cyclophosphamid and intravenous immmunoglobulin resulted in dramatic improvement of the clinical status over the following months and CSF normalization.

Adult↗

Localized proton magnetic resonance spectroscopy in relapsing remitting versus secondary progressive multiple sclerosis.

OBJECTIVE: To determine the efficacy of MRS in discriminating between relapsing remitting (RR) and secondary progressive (SP) MS. METHODS: MRS at long and short echo times was carried out in 104 patients with MS stratified for clinical course (RR or SP), and the results were compared with those of 15 control subjects. Normal-appearing white matter (NAWM) was studied in 55 patients, and a high-T2-signal area on MRI in 49 others. RESULTS: At long echo times, there was a highly significant decrease in the ratios N-acetyl-aspartate/creatine (NAA/Cr) and NAA/ choline (Cho) in high-T2-signal areas and in the NAWM in patients with an SP course compared with control subjects and patients with an RR course. There was a significant negative correlation between these ratios and clinical disability measured by Expanded Disability Status Scale score, which was independent of disease duration. Discriminant values between patients with RR and SP courses were found in the NAWM (NAA/Cr = 1.75 and NAA/Cho = 1.5), but not in high-T2-signal areas. At short echo times, there was a significant increase in the ratio myoinositol/Cr in high-signal areas of patients with an SP course compared with control subjects, and the presence of abnormal resonances in the lesions and NAWM for free amino acids and lipids (in 30% and 8%, respectively) and GLX complex (glutamine, glutamate, gamma-aminobutyric acid; 16% and 20%, respectively). CONCLUSIONS: Studying normal-appearing white matter on MRI with MRS allows discrimination between relapsing remitting and secondary progressive patients. In the NAWM of patients with MS and an SP course, severe axonal loss/dysfunction is negatively correlated to clinical disability and independent of the duration of the disease.

Adolescent↗

Encephalitis after hepatitis B vaccination: recurrent disseminated encephalitis or MS?

OBJECTIVE: To describe clinical and MRI features of patients with a disease suggestive of CNS inflammation after hepatitis B vaccination. METHODS: Eight patients with confirmed CNS inflammation occurring less than 10 weeks after hepatitis B vaccination are described. They received follow-up clinically and on MRI for a mean period of 18 months. RESULTS: Clinical and MRI findings were compatible with acute disseminated encephalomyelitis. However, clinical follow-up, repeated MRI, or both showed the persistence of inflammatory activity, which makes this encephalitis more suggestive of MS than of acute disseminated encephalomyelitis. CONCLUSION: The persistent inflammatory activity observed clinically and on MRI in these patients is comparable with that usually observed in MS. Epidemiologic studies are currently testing the hypothesis of a triggering role of hepatitis B vaccination in CNS demyelination.

Adult↗

Facial diplegia complicating a bilateral internal carotid artery dissection.

BACKGROUND AND PURPOSE: We report a case of facial diplegia complicating a bilateral internal carotid artery dissection. CASE DESCRIPTION: A 49-year-old patient presented with unilateral headache and oculosympathetic paresis. Cerebral angiography revealed a bilateral internal carotid artery dissection. A few days later, the patient developed a facial diplegia that regressed after arterial recanalization. An arterial anatomic variation may explain this ischemic complication of carotid dissection. CONCLUSIONS: Double carotid dissection should be included among the causes of bilateral seventh nerve palsy.

Aortic Dissection↗

Persistent oligoclonal expansion of human T-cell leukemia virus type 1-infected circulating cells in patients with Tropical spastic paraparesis/HTLV-1 associated myelopathy.

The pattern of HTLV-1 replication was assessed through PCR amplification of the 3' proviral integration sites in patients with TSP/HAM at different times. Integration sites were sequenced and oligonucleotides specific for the flanking sequences were synthesized. Together with HTLV-1 LTR specific primers, clonotypic nested PCR was performed on peripheral blood from two patients. The frequencies of five clones studied ranged from 1/300 to 1/1500 PBMCs while four clones persisted for more than 1-5 years. It would seem that Tax driven expansion of T cells may persist for considerable periods of time in TSP/HAM despite strong cellular immunity. This may provide a background for the accumulation of subsequent mutations leading to malignancy.

Adult↗

Systemic autoimmune features and multiple sclerosis: a 5-year follow-up study.

OBJECTIVES: To evaluate in patients with multiple sclerosis (MS) the occurrence of clinical systemic signs and biological autoimmune abnormalities, including positive titers of antinuclear antibodies and antiphospholipid antibodies, suggestive of autoimmune diseases that may affect the central nervous system. Also, to compare the clinical and magnetic resonance imaging features and evolution of MS in patients with and without autoimmune abnormalities. DESIGN AND PATIENTS: Prospective study of 161 patients fulfilling the criteria of having probable or definite MS hospitalized in our institution between November 1990 and June 1992. RESULTS: Among the 161 patients, 84 (52.1%) had at least 1 clinical and/or biological general sign suggestive of an autoimmune disease; 64 were followed up for 4 to 5 years. The diagnosis of MS was confirmed in 50 patients and is still pending in 14 of them. No significant difference was found between patients with MS who were free of autoimmune features and those with autoimmune abnormalities (MS plus) concerning the age of disease onset, the presenting symptoms and signs, symptoms found on neurologic examination, and the course of the disease. For all patients with confirmed MS, general signs were found in 13.3%, positive titers of antinuclear antibodies in 26%, and positive titers of antiphospholipid antibodies in 6.2%. CONCLUSIONS: Patients with MS with autoimmune features, including those with titers of antinuclear antibodies of 1:100 or less and/or antiphospholipid antibodies, are not different than others with MS, and therefore should not be excluded from clinical trials.

Adolescent↗

Tropical spastic paraparesis/HTLV-I-associated myelopathy in Europe and in Africa: clinical and epidemiologic aspects.

We review here the epidemiologic and clinical aspects of tropical spastic paraparesis, human T-cell lymphotropic virus type I (HTLV-I)-associated myelopathy (TSP/HAM) as observed in Europe and in Africa. Europe is not an endemic region for HTLV-I (seroprevalence in blood donors, < 0.03%), and TSP/HAM is thus rarely observed in European countries. Most of the few patients suffering from TSP/HAM are first- or second-generation immigrants from HTLV-I endemic areas (mostly the West Indies), and the clinicoepidemiologic aspects of these patients are similar to those seen in endemic areas. However, rare cases occur in European-born subjects with or without risk factors for HTLV-I infection, which raises the possibility of limited foci areas in Europe. Although Africa is considered as a primary HTLV-I endemic area, with at least a few million infected inhabitants, epidemiologic data on the situation of TSP/HAM in Africa remain scarce. Relatively few cases of patients with TSP/HAM have been reported in Africa, including some clusters in Zaire (prevalence, 50/100,000) and in South Africa and sporadically in the main cities of some Western, Central, and Eastern African countries. The paucity of clinical and epidemiologic data on TSP/HAM may be linked to several factors, including the paucity of neurologists, the lack of laboratory and radiologic facilities, and the chronicity of the disease, along with the limited number of field epidemiologic studies performed on this topic and the wide diversity of causes (toxic, nutritional, and infectious) of chronic myelopathies as seen on the African continent.

Adolescent↗

Interaction of mouse hepatitis virus (MHV) spike glycoprotein with receptor glycoprotein MHVR is required for infection with an MHV strain that expresses the hemagglutinin-esterase glycoprotein.

In addition to the spike (S) glycoprotein that binds to carcinoembryonic antigen-related receptors on the host cell membrane, some strains of mouse coronavirus (mouse hepatitis virus [MHV]) express a hemagglutinin esterase (HE) glycoprotein with hemagglutinating and acetylesterase activity. Virions of strains that do not express HE, such as MHV-A59, can infect mouse fibroblasts in vitro, showing that the HE glycoprotein is not required for infection of these cells. The present work was done to study whether interaction of the HE glycoprotein with carbohydrate moieties could lead to virus entry and infection in the absence of interaction of the S glycoprotein with its receptor glycoprotein, MHVR. The DVIM strain of MHV expresses large amounts of HE glycoprotein, as shown by hemadsorption, acetylesterase activity, and immunoreactivity with antibodies directed against the HE glycoprotein of bovine coronavirus. A monoclonal anti-MHVR antibody, MAb-CC1, blocks binding of virus S glycoprotein to MHVR and blocks infection of MHV strains that do not express HE. MAb-CC1 also prevented MHV-DVIM infection of mouse DBT cells and primary mouse glial cell cultures. Although MDCK-I cells express O-acetylated sialic acid residues on their plasma membranes, these canine cells were resistant to infection with MHV-A59 and MHV-DVIM. Transfection of MDCK-I cells with MHVR cDNA made them susceptible to infection with MHV-A59 and MHV-DVIM. Thus, the HE glycoprotein of an MHV strain did not lead to infection of cultured murine neural cells or of nonmurine cells that express the carbohydrate ligand of the HE glycoprotein. Therefore, interaction of the spike glycoprotein of MHV with its carcinoembryonic antigen-related receptor glycoprotein is required for infectivity of MHV strains whether or not they express the HE glycoprotein.

Animals↗

Transplantation of oligodendrocyte precursors in the adult demyelinated spinal cord: migration and remyelination.

A demyelinating lesion induced by an injection of lysolecithin into the spinal cord can be partly repaired by oligodendrocyte precursors transplanted at a distance of 6-8 mm from the lesion. Using a non-toxic fluorescent dye (Hoechst 33342) as a cell marker, we demonstrate that transplanted oligodendrocyte precursors from different origins (periventricular zone fragments from newborn mouse and cultured rat oligodendrocyte progenitor cells) can migrate along specific pathways (i.e. white matter fasciculi, ependymal wall, meninges and blood vessels). These cells can be attracted when passing at the vicinity of the lesion as well as differentiate and remyelinate axons with the lesion. Myelin repair thus appears to be the result of distinct successive events: migration, specific attraction, differentiation and myelination. This can occur in both shiverer and normal adult hosts.

Animals↗

Directed migration of transplanted glial cells toward a spinal cord demyelinating lesion.

To investigate the migration of transplanted glial cells in normal adult mice with a focal demyelinating lesion, we have used A2G mice which have the autosomal dominant Mx-1 allele as donor. Mx-1 protein expression is inducible by interferon and is detected in a dotted pattern in the nucleus of A2G cells. A/J mice were used as recipient animals as they express the same major histocompatibility antigens as A2G but cannot express the Mx-1 protein. An acute demyelinating lesion was produced in the A/J spinal cord by intraspinal injection of lysolecithin. Mixed glial cultures derived from newborn A2G brain were treated with alpha/beta interferon for 24 hr. These Mx-1 expressing glial cells were then transplanted two intervertebral spaces away from the demyelinating lesion. The fate of the grafted cells was followed over the next 13 days, during which the induced Mx-1 protein can still be detected by immunocytochemistry. Grafted cells were found between the transplantation site and the lesion at 24 hr and some of the Mx-1+ cells reached the lesion at 4 days. The majority of the Mx-1+ migrating cells expressed GFAP and were located in the myelinated white matter and around the blood vessels. Scattered MBP+, Mx-1+ cells were detected in the lesion indicating that some of the transplanted cells may participate in the repair process. The Mx-1 is a useful marker to follow the migration events in the days after grafting and to determined what factors may attract transplanted cells toward a demyelinating lesion.

Animals↗

[Symptomatic heterozygotic adrenoleukodystrophy in adults. 10 cases].

Adult adrenoleukodystrophy is a X-linked peroxisomal disease associated with the accumulation of very long chain fatty acids (VLCFA) in tissues and body fluids. The diagnosis is established on the demonstration of elevated VLCFA in blood and cultured skin fibroblasts. Women are affected in nearly 15% of cases and neurological symptoms and/or signs develop in 53% of them. Identifying these women is important because of genetic counseling and a possible therapeutic approach. Ten cases of symptomatic heterozygous adult adrenoleukodystrophy are reported. Mean age at the time of diagnosis was 44.6 +/- 9.3 years. All patients presented with spastic paraparesis with inconstant and mild sensory or bladder disturbances. Cognitive impairment was present in 1 case. Cerebrospinal fluid was normal. Adrenal function in response to tetracosactide injection was abnormal in 1/7 cases. Electromyography detected a peripheral neuropathy in 1 case. Somatosensory evoked responses were abnormal in all cases, visual and auditory evoked responses in respectively 3/6 cases and 3/4 cases. Brain MRI detected non specific abnormalities in 3/7 cases; spinal cord MRI was normal in 3/3 cases. The familial history was helpful for the diagnosis in 3/10 cases. Examination of pedigrees detected 5 hemizygous and 1 asymptomatic heterozygous cases. All the patients were enrolled in a dietary study which adret with low VLCFA is currently under evaluation.

Adrenoleukodystrophy↗

Chronic myelopathy associated with human T-lymphotropic virus type I (HTLV-I).

PURPOSE: To review the clinical, epidemiologic, immunologic, and virologic aspects of the chronic myelopathy associated with human T-cell leukemia/lymphoma virus type I (HTLV-I), currently called tropical spastic paraparesis/HTLV-I-associated myelopathy (TSP/HAM). DATA IDENTIFICATION: Studies done after 1985, when TSP/HAM was first recognized, were identified by a computer search using MEDLARS II and CANCERLIT. Additional information was acquired from personal files and bibliographies of existing literature. STUDY SELECTION: A total of 400 articles, 90 book chapters, and 150 abstracts from meetings covering all aspects of HTLV-I and neurologic diseases were critically analyzed, and information from 250 publications was included. RESULTS OF DATA ANALYSIS: TSP/HAM is present in most HTLV-I endemic areas, with a prevalence ranging from 5.1 to 128 per 100,000 inhabitants. Up to 20% of patients develop TSP/HAM after transfusion of HTLV-I contaminated blood. Pathologic characteristics indicate a chronic meningomyelitis. The clinical features consist of a chronic progressive spastic paraparesis or paraplegia, sphincter disturbances, and minimal sensory loss. Supraspinal and peripheral nerve involvement is sometimes observed. High titers of HTLV-I-specific antibodies are present in the serum and cerebrospinal fluid. The high level of humoral and cellular immunologic response and the association of TSP/HAM with other immunologic diseases suggest an immune-mediated process. Corticosteroids and immunosuppressor treatment usually result in only short-term improvement. CONCLUSION: TSP/HAM is a common neurologic disease in many parts of the world. All patients with chronic progressive myelopathies should be tested for serum and cerebrospinal fluid HTLV-I-specific antibodies. Systematic screening of blood donors for HTLV-I is necessary to help prevent the dissemination of the virus and the occurrence of post-transfusional cases.

Adolescent↗