[Focal myositis of the leg in a woman with multiple sclerosis].
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Female↗
Biomedical subjects
M Baudrimont
Publications and source records attributed to M Baudrimont.
Acute varicella-zoster virus ventriculitis and meningo-myelo-radiculitis in acquired immunodeficiency syndrome.
A 30-year-old AIDS patient with no history of cutaneous eruption, presented with rapidly progressive flaccid paraplegia, hypoesthesia, urinary retention, moderate psychomotor slowing and fever (39.8 degrees C), leading to death within 1 week. CD4 count was 290/mm3. Cerebrospinal fluid contained 210 white blood cells and 238 mg/100 ml protein. Neuropathology revealed HIV encephalitis and diffuse ventriculitis with Cowdry type A inclusions in the ependymal cells. Extensive necrotic and hemorrhagic changes with marked recrotizing vasculitis involved the entire spinal cord and spinal roots. Immunocytochemistry revealed numerous inclusion bodies positive for varicella-zoster virus (VZV) and negative for cytomegalovirus (CMV) and herpes simplex virus type 1 and 2, in ependymal cells, subpial glial cells, endothelial cells and Schwann cells. Electron microscopy confirmed herpes virus-like particles. In situ hybridization confirmed VZV genome in leptomeninges, brain, spinal cord and spinal roots. Comparable neuropathological findings and numerous VZV inclusion bodies were also found in the brain, spinal cord, and spinal roots of a 40-year-old AIDS patient who died from a fulminant ascending myeloradiculopathy previously reported as "necrotizing vasculitis of the nervous system". Direct infection of the brain by VZV, in AIDS patients, has been shown to cause leukoencephalitis and cerebral non-inflammatory vasculopathies. Our observations demonstrate that, in AIDS patients, VZV infection of the central nervous system may also be responsible for meningo-myelo-radiculitis possibly secondary to ventriculitis as in CMV infection. The role of VZV in the pathogenesis of some AIDS-related vasculitides seems also very likely.
AIDS Dementia Complex↗
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy maps to chromosome 19q12.
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) has been recently reported as a cause of stroke. It is characterized, in the absence of hypertension, by recurrent subcortical ischaemic strokes, starting in early or midadulthood and leading in some patients to dementia. Magnetic resonance imaging and pathological examination show numerous small subcortical infarcts and a diffuse leukoencephalopathy underlaid by a non-arteriosclerotic, non-amyloid angiopathy. We performed genetic linkage analysis in two unrelated families and assigned the disease locus to chromosome 19q12. Multilocus analysis with the location scores method established the best estimate for the location of the affected gene within a 14 centimorgan interval bracketed by D19S221 and D19S222 loci.
Adult↗
Autosomal dominant leukoencephalopathy and subcortical ischemic stroke. A clinicopathological study.
BACKGROUND AND PURPOSE: We recently described an autosomal dominant syndrome characterized mainly by recurrent strokes and neuroimaging evidence of leukoencephalopathy. We now report the pathological findings in one of the affected subjects. CASE DESCRIPTION: A 40-year-old woman experienced her first grand mal seizure in 1971. From 1983 on she suffered recurrent strokes, seizures, and psychiatric disturbances with depressions, manic episodes, and dementia. In 1988, after her fourth stroke, she became tetraplegic with a severe pseudobulbar palsy, and she died in 1990. Pathological examination disclosed a recent capsulolenticular hematoma, multiple small deep infarcts, a diffuse myelin loss and pallor of the hemispheric white matter, and a widespread vasculopathy of the small arteries penetrating the white matter. The arterial wall was markedly thickened with an extensive nonamyloid eosinophilic deposit in the media and reduplication of the internal elastic lamella. CONCLUSIONS: The underlying lesion of this hereditary disorder is located in the small arteries and is of unknown etiology. It differs from arteriosclerotic and amyloid angiopathies but is similar to that described in some cases of hereditary multi-infarct dementia.
Adult↗
[Experimental use of liposomes carrying an antimetabolite (mitoxantrone) in filtering surgery].
Fibroblast proliferation plays a prominent role in closure of conjunctival filtering blebs and extensive investigations are being carried out to optimize antiproliferative pharmacotherapy in the prevention of filtering bleb failure in glaucomatous eyes with a poor prognosis undergoing surgery. Intercalating agents such as doxorubicin or daunorubicin have been shown to decrease fibroblast proliferation in tissue cultures. A liposomal delivery system was developed in an attempt to obtain a sustained release effect and to minimize ocular side effects of mitoxantrone (Novantrone, MITX), an antineoplastic agent with intercalating properties. The objectives of this study were to demonstrate the entrapment stability of MITX in multilamellar vesicles (reaching about 60% and remaining at this level for 8-weeks storage) and to investigate its activity in vitro (cell cultures) and in vivo (sclerectomy ab externo in rabbits). We showed that entrapped MITX inhibited in a dose-dependent manner subconjunctival fibroblast proliferation (ID50: 0.03 micrograms/l at D3 in cultures) and prolonged the success of filtration surgery in rabbits (decrease of intraocular pressure of 8 mm Hg in treated eyes versus 1.8 mm Hg in control eyes; p < 0.01). These results indicate the potential of MITX-entrapped liposomes in the control of conjunctival scarring in filtering bleb surgery.
Animals↗
Skeletal muscle toxoplasmosis in patients with acquired immunodeficiency syndrome: a clinical and pathological study.
The present article describes the clinical and pathological findings in 5 human immunodeficiency virus (HIV)-infected patients with muscle toxoplasmosis. The patients had marked lymphopenia (5/5), with less than five CD4+ cells/mm3 (3/3), when they developed fever (5/5), and multiorgan failure (5/5), including diffuse encephalitis, pneumonia, pancytopenia, and myopathy. Muscle involvement included weakness and wasting (4/5), myalgias (3/5), and high serum creatine kinase levels (3/3). Serology for toxoplasmosis showed high IgG titers in 3 patients (3/4). Anti-Toxoplasma therapy resulted in complete recovery in 2 patients. Muscle toxoplasmosis was detected by biopsy (3/5) or postmortem evaluation (2/5), and was identified using immunocytochemistry and electron microscopy. Toxoplasma cysts were detected in 0.5 to 4% of muscle fibers close to or remote from necrotic fibers and inflammatory infiltrates. Muscle fibers strongly expressed the major histocompatibility complex class I antigen (2/2) as in polymyositis. We suggest that Toxoplasma gondii should be sought by muscle biopsy in patients who have acquired immunodeficiency syndrome with fever, encephalitis, multiorgan dysfunction, and elevated serum creatine kinase levels of obscure origin.
Acquired Immunodeficiency Syndrome↗
Intrasplenic hepatocellular transplantation corrects hepatic encephalopathy in portacaval-shunted rats.
The aim of this work was to evaluate the effect of intrasplenic hepatocellular transplantation on hepatic encephalopathy in an experimental model of chronic liver failure induced by end-to-side portacaval shunt in the rat. Inbred male Wistar Furth rats were divided into three groups: rats subjected to portacaval shunt (n = 10), rats subjected to portacaval shunt and intrasplenic hepatocellular transplantation of 10(7) hepatocytes isolated from livers of syngeneic rats (n = 10) and sham-operated rats (n = 10). Behavior tests were performed in a blind fashion at 3 wk, at 2 mo and at 3 mo after surgery. Spontaneous activity and nose-poke exploration by individual rats were studied in automated open field boxes equipped with infrared cells. Each cell beam interruption was automatically recorded on a microcomputer and transformed into a score index (counts/hour). Plasma levels of amino acids, ammonia and total biliary acids were measured. Portacaval shunt rats showed reduced spontaneous activity and nose-poke exploration scores. Intrasplenic hepatocellular transplantation significantly increased spontaneous activity after 2 mo and improved nose-poke exploration after 3 wk. At 3 mo, spontaneous activity and nose-poke exploration in portacaval shunt/intrasplenic hepatocellular transplantation rats were not significantly different from those of sham rats. Increases in plasma ammonia levels after portacaval shunt were not corrected. Amino acid imbalance and bile acid concentration in plasma were partially corrected by intrasplenic hepatocellular transplantation. These data show that intrasplenic hepatocellular transplantation can correct the neurological symptoms of hepatic encephalopathy in an experimental model of chronic liver failure and suggest that intrasplenic hepatocellular transplantation might be of therapeutic interest in chronic liver failure.
Animals↗
Rapid detection of cytomegalovirus DNA in cerebrospinal fluid of AIDS patients with neurologic disorders.
A polymerase chain reaction (PCR)-based method was used to detect cytomegalovirus (CMV) DNA in 82 cerebrospinal fluid (CSF) samples from 67 patients infected by human immunodeficiency virus (HIV). The test was positive for 14 patients, 8 of whom had CMV-related neurologic disease proven by viral culture of CSF or histologic examination. Encephalitis was the most frequent manifestation in patients with positive PCR results, but CMV DNA was also present in some patients with peripheral neuropathy or polyradiculomyelitis. All patients with proven CMV neurologic disease were positive by PCR. In contrast, viral culture was negative for 4 of the 8 patients and pathologic studies were available only for 5. The specificity of the PCR-based assay could not be assessed precisely because of the lack of a reference standard, but the results correlated well with clinical course and results of the other methods. These findings suggest that the PCR-based method may be a useful noninvasive tool for the rapid diagnosis of CMV-related neurologic disease.
AIDS-Related Opportunistic Infections↗
Transesophageal echocardiographic detection of aortic arch disease in patients with cerebral infarction.
BACKGROUND AND PURPOSE: Ulcerated plaques in the aortic arch are frequent autopsy findings in patients with cerebral infarctions, particularly those of unknown cause. It has been suggested that they could be a source of cerebral emboli. Using transesophageal echocardiography, we prospectively studied 12 consecutive patients with cerebral infarction of undetermined cause after noninvasive workup to evaluate the frequency of aortic plaques or mural thrombi that could embolize in cerebral arteries. SUMMARY OF REVIEW: Six patients (50%) had an intraluminal echogenic mass of the aortic arch, mainly located at the junction of the ascending aorta and arch. This material was pedunculated (in one patient) or broad based (in five patients) with a markedly irregular surface and intraluminal extension from 3 to 15 mm. In addition, we found cholesterol emboli in two of the four patients who underwent quadriceps biopsy. CONCLUSIONS: These results show that transesophageal echocardiography has capabilities in detecting such lesions and point to the aortic arch as a possible source of cerebral emboli in patients with cerebral infarction of unknown cause.
Aged↗
Biopsy-proven myositis with microvasculitis in association with carbimazole.
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Adult↗
Zidovudine myopathy: a distinctive disorder associated with mitochondrial dysfunction.
Muscle biopsy specimens were obtained from 48 human immunodeficiency virus-infected patients suffering from various neuromuscular symptoms. Microscopic examination by conventional and electron microscopy revealed a characteristic structural myopathy associated with mitochondrial changes in 13 patients, all of whom had received long-term zidovudine therapy. The mean cumulative dose they had received (498 +/- 145 gm) was significantly higher than that of the other 14 zidovudine recipients of the study. They suffered from a progressive, usually painful, proximal myopathy with pronounced wasting, normal-to-moderately elevated creatine kinase levels, and a myopathic electromyographic pattern. The condition usually improved after withdrawal of the drug. Assay of mitochondrial enzymes, including succinate-cytochrome c reductase, cytochrome c oxidase, and citrate synthase, showed a decline in respiratory chain capacity. Southern blot analysis of mitochondrial DNA showed no abnormality. It is likely that mitochondrial dysfunction, probably resulting from drug-induced inhibition of the mitochondrial DNA polymerase, is implicated in the pathogenesis of this complication of zidovudine therapy.
Adult↗
Skeletal muscle involvement in human immunodeficiency virus infection.
In addition to muscle changes due to peripheral nervous system involvement, primary myopathic changes associated with the human immunodeficiency virus (HIV) have also been described. We studied seven cases: two had developed an acquired immunodeficiency syndrome (AIDS), four had seroconverted to HIV but were otherwise asymptomatic, one was HIV seronegative when the biopsy was performed and one was biopsied twice. Besides the HIV no other infectious agent was detected. Muscle biopsies showed: (a) muscle fiber necrosis and regeneration; (b) inflammatory changes with moderate perivascular infiltration; and (c) unusual myofibrillary disorganization. Immunocytochemical techniques using anti-HIV monoclonal antibodies showed the presence of the virus in one biopsy. HIV-RNA was detected by in situ hybridization in the same biopsy. With both techniques the HIV was detected in isolated mononuclear cells in the muscle endomysium and not within the muscle fibers. Muscle involvement associated with HIV infection may be related, at least in some cases, to the presence of the virus in interstitial cells.
Acquired Immunodeficiency Syndrome↗
Iron pigment deposits, small vessel vasculitis, and erythrophagocytosis in the muscle of human immunodeficiency virus-infected patients.
Hemosiderin deposition and vascular inflammation were evaluated in muscle specimens from 50 human immunodeficiency virus (HIV)-infected individuals with neuromuscular symptoms. Iron deposits were detected in 25 of 50 cases, and were found more frequently in the distal muscles of lower limbs than in proximal muscles (22 of 30 cases v three of 20 cases; P less than .001). The incidence was higher than in controls (P less than .01). Polyarteritis nodosa was observed in three cases and microvascular inflammation was observed in 27. Direct immunofluorescence showed deposits of both immunoglobulins (mainly immunoglobulin M) and complement in small vessel walls of 19 of 34 patients. The p17 and p24 HIV antigens were detected in three of 27 cases. Both T8 lymphocytes and macrophages were significantly more numerous in patients with Perls'-positive material; these patients also showed vascular inflammation more frequently. Other findings included noninflammatory microangiopathy (18 cases), tubuloreticular inclusions in endothelial cells (one case), and free and intracytoplasmic eosinophilic globules likely representing digested erythrocytes (seven cases). The present study shows that iron pigment deposition in skeletal muscle is a nonspecific finding, frequently observed in the lower extremities of HIV-infected individuals, where it reflects immunopathologic alterations of the microcirculation. Erythrophagocytosis, which may be observed in the muscle of some HIV-infected individuals, may also be implicated.
Adult↗
[POEMS cured by radical treatment of plasmacytoma].
A 53-year-old man presented with POEMS syndrome characterized by a solitary plasmocytoma and an angiofollicular lymph node hyperplasia similar to that observed in Castelmann's disease. Two features were prominent: first, a severe hypertriglyceridemia, which could have been related to autoimmune suppression of lipoprotein lipase activity; second, a marked immunostaining of myelin sheaths with occasional widening of myelin lamellae. These data, added to the complete regression of the neuropathy immediately following surgical removal of the plasmocytoma (with subsequent irradiation) suggested that the paraprotein was responsible for the neuropathy.
Castleman Disease↗
[Astrocytes: morphology and functional role].
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Astrocytes↗
NMDA receptors contribute to the resting discharge of vestibular neurons in the normal and hemilabyrinthectomized guinea pig.
Excitatory amino acids (EAA) like L-Glutamate or L-Aspartate have been suggested to be the neurotransmitters at the synapses between primary vestibular afferents and second-order vestibular neurons. In the first part of our work, we have tested the possibility that EAA receptors are implicated in the control of posture by vestibular nuclei. Normal guinea pigs were implanted with minipumps delivering EAA antagonists in the vestibular nuclei. Their resting posture was monitored during the perfusion by using an X-ray photographic method. Chronic infusion of D-L-2-amino-5-phosphonovaleric acid (APV), a specific antagonist of NMDA receptors, in the vestibular nuclei induced a postural and oculomotor syndrome similar to the one observed following acute vestibular deafferentation. Administration of 6-cyano-7-nitro-quinoxaline-2-3-dione (CNQX), a specific antagonist of kainate and quisqualate receptors, failed to induce any postural syndrome or eye deviation. These results suggest that, under physiological conditions, N-methyl-D-aspartate (NMDA) receptors, contrary to kainate and quisqualate receptors, are essential for the maintenance of a symmetric posture and of a normal eye position at rest. Previous electrophysiological studies have demonstrated that following unilateral labyrinthectomy the recovery of a resting discharge in the deafferented vestibular nuclei plays a key role in the compensation of postural disorders. In the second part of this study, we have tested whether NMDA receptors could be implicated in this postural recovery. APV mini-pumps were implanted in hemilabyrinthectomized guinea pigs after complete compensation. A postural decompensation was induced, which occurred after delivery of the same amount of APV which provoked a vestibular syndrome in intact guinea pigs.(ABSTRACT TRUNCATED AT 250 WORDS)
2-Amino-5-phosphonovalerate↗
A comparative experimental study of vascularized and nonvascularized nerve grafts.
In order to compare vascularized and nonvascularized nerve grafts in a normal bed, 96 median nerve grafts were performed in rabbits. The median nerves were grafted in situ bilaterally, whether vascularized or nonvascularized. The length of the grafts was 2 cm, 4 cm, or 6 cm. A morphometric study was performed eight weeks and 24 weeks after the operation. No significant differences were found between vascularized and nonvascularized grafts at the same levels of nerve grafts. However, significant differences between vascularized and nonvascularized grafts were found for 4-cm and 6-cm grafts at eight weeks, and for 6-cm grafts at 24 weeks postoperatively, comparing the proximal normal nerve segments with the nerve segments distal to the nerve grafts.
Animals↗
Giant gangliocytic paraganglioma of the filum terminale. Case report.
The clinical and pathological features of a giant cauda equina paraganglioma arising from the intradural filum terminale is described. Scattered mature large neurons characterized the tumor as a gangliocytic paraganglioma. Histologically, these neoplasms have considerable similarity with ependymoma and the diagnosis can be easily missed unless special techniques are employed.
Adult↗