Search PubMed⌕ Search

Biomedical subjects

C Vital

Publications and source records attributed to C Vital.

At least 163 records · Page 9Linked to original sources
PubMed1987

[Divry-Van Bogaert cortico-meningeal angiomatosis and Sneddon's syndrome. Nosological study. Apropos of 4 cases].

Four patients with idiopathic livedo reticularis and multiple cerebral ischemic events leading to a severe dementia are reported. Imaging (CT, MRI, angiograms) and pathological features (in one case) are presented. Similar clinical features have been described previously in Divry-van Bogaert's disease and Sneddon's syndrome. Data from our cases and a review of the literature did not find distinctive characteristic between these entities. Thus, for practical purposes, considering them as one group appears at present warranted.

Adult↗
PubMed1987

[Neurogenic muscular hypertrophy. Association with abnormal electrophysiological activities].

Muscle hypertrophy in neurogenic disorders is an uncommon phenomenon which has been reported in various conditions: hereditary or acquired anterior horn cell diseases, essentially S1 radicular compressions, and polyneuritis generally of a demyelinating type. We report two cases of denervating disease with muscle hypertrophy. The first was an S1 radiculopathy, and the second a compression with ischemia of the spinal cord by herniation of the D11-D12 disc, and showing partial improvement after surgery. In both cases, electrophysiological examination of the hypertrophic muscles revealed abnormal activities identified as complex repetitive discharges. In the second case they were associated with a syndrome of continuous motor unit activity. Such activities are rare in peripheral nerve involvement. However they have quite often been recorded in cases of neurogenic muscle hypertrophy and may therefore be partly responsible for the development of the hypertrophy.

Adult↗
PubMed1986

Relapsing inflammatory demyelinating polyneuropathy in a diabetic patient.

Inflammatory demyelinating polyradiculoneuropathies exhibit well-known ultrastructural lesions of the peripheral nerve, both in acute cases, i.e., Guillain-Barré syndrome, and in relapsing, sub-acute and chronic cases. We present a case of relapsing inflammatory demyelinating polyradiculoneuropathy in a diabetic patient with a biopsy exhibiting these lesions, as well as a widening of the outermost myelin lamellae in some fibers. Such associated lesions are classic in experimental inflammatory demyelinating polyradiculoneuropathies, but have not been reported in human pathology.

Animals↗
PubMed1985

Acute inflammatory demyelinating polyneuropathy in a diabetic patient: predominance of vesicular disruption in myelin sheaths.

A diabetic woman underwent an incision of the right big toe for an abscess and developed a typical Guillain-Barré syndrome 48 h later. A biopsy of a peripheral nerve, performed 10 days later, showed modifications usually seen in diabetic patients, as well as the characteristic ultrastructural modifications of the Guillain-Barré syndrome (GBS). Moreover, 22% of myelinated fibers exhibited vesicular disruption of the myelin sheaths. This lesion is rarely encountered on the biopsies of peripheral nerve in GBS and concerns only a few myelinated fibers. Such a prominence of myelinic vesicular disruption and its occurrence in a diabetic patient are discussed.

Acute Disease↗
PubMed1985

Polyarteritis nodosa and peripheral neuropathy. Ultrastructural study of 13 cases.

Peripheral nerves from 13 patients suffering from polyarteritis nodosa with multiple mononeuropathy were studied by light and electron microscopy. In the majority of cases, the vascular lesions were associated with Wallerian-like degeneration. Myelinated fibers presenting a normal axon with a disproportionately thin myelin sheath were less numerous. Unusual abnormalities consisted of swollen axons with an accumulation of organelles. Unmyelinated fibers were also damaged. A quantitative estimation of myelinated fibers loss did not show any selective vulnerability of either the large or the small diameter group.

Adult↗
PubMed1985

Histologic and non-histologic factors correlated with survival time in supratentorial astrocytic tumors.

One hundred and ninety-two cases of supratentorial astrocytic tumors are classified in 4 groups according to the presence or absence in the pathological material of simple morphological criteria: abnormal cellular density, nuclear pleomorphism, neovascularization, necrosis. Each one of these criteria is strongly correlated with prognosis. Nevertheless only a simple classification in low and high grade lesions has a definite predictive value. A multivariate analysis utilizing Cox's hazard function confronts these histological findings with a number of clinical and etiological possible factors of prognosis. Age and performance status at the time of diagnosis are the best predictors of survival time. The clinical use of a predictive model derived from Cox's function analysis is discussed.

Adult↗
PubMed1985

[Tomaculous neuropathy. Electrophysiologic study].

In two cases with recurrent palsies, the results of electrophysiological studies led to nerve biopsy showing typical tomacula. The first case was an inherited neuropathy with liability to pressure palsies. The second case was an apparently sporadic painless recurrent brachial neuropathy. Electrophysiological alterations were diffuse and sensory fibres of the median nerve between index and wrist were the most involved. Conduction blocks were observed without palsy in narrow anatomical passageways where nerve compressions are frequent (ulnar nerve at the elbow, peroneal nerve at the fibula). A compression by a neighbouring anatomical structure could make the prognosis worse and justify nerve decompression. The nerves with slowest conduction have the most important risk of palsy and the patients should be given advice to avoid their compression.

Adolescent↗
PubMed1985

Waldenström's macroglobulinemia and peripheral neuropathy: deposition of M-component and kappa light chain in the endoneurium.

Some cases of peripheral neuropathy associated with benign IgM monoclonal gammopathy, or Waldenström's macroglobulinemia, are probably of autoimmune origin; in some cases, anti-IgM serum reacts with the myelin sheaths of peripheral nerves. However, mechanisms may differ in other cases. In one case of neuropathy with macroglobulinemia, we found deposits of IgM immunoglobulin in the endoneurium. On ultrastructural examination, the deposits had erased the basement membrane of some nerve fibers that showed damage of both myelin and axon.

Humans↗
PubMed1985

[Hypermyelination in a case of peripheral neuropathy with benign IgM monoclonal gammopathy].

A 65 year-old man presented with a 8 months history of ataxia and weakness of the lower limbs. Acroparesthesias had been present for ten years in all four limbs. Serum protein electrophoresis showed a monoclonal IgM kappa spike. Bone marrow showed no increase in plasma cells. Motor conduction velocities were reduced. A biopsy from the right superficial peroneal nerve revealed several enlarged myelin sheaths in each fascicle on semi-thin sections. Under electron microscopy these large myelin sheaths were either regularly arrayed around the axon or formed several large additional loops. The outer lamellae of these abnormal myelin sheaths and of the additional loops were frequently widened. Other fibers showed a widening of some myelin lamellae (W.M.L.) with a myelin sheath of varying thickness, and these widened lamellae were frequently joined together. A direct immunopathological study could not be made. The widening of some myelin lamellae is present in most cases of peripheral neuropathy with IgM monoclonal gammopathy and a fixation of anti IgM serum on some myelin sheaths may be demonstrated by direct immunopathology. Hypermyelination has been reported in a few cases. In this patient hypermyelination was as developed as in typical cases of tomaculous neuropathy. An association in some myelin sheaths of hypermyelination and W.M.L. has been noted in serum induced myelin aberrations in peripheral nervous system cultures.

Aged↗
PubMed1985

[Cerebral lesions in a case of Degos' disease].

The central nervous system may be involved in Degos disease, but neuropathologic observations are still few. We report a typical case with cerebral involvement. The diagnosis was suggested by the characteristic skin lesions and vascular damage. In the central nervous system, occlusive changes of small arteries were responsible for areas of ischaemic necrosis. These foci of infarction were of varying size, age and distribution. Intestinal lesions were discrete and death was due to several cerebral infarcts.

Adult↗
PubMed1985

[Peritoneal gliomatosis associated with a mature teratoma of the ovary].

Peritoneal or/and omental implants composed of mature glial tissue is a rare complication of ovarian teratomas. A few cases have been previously reported, and one more case is described. The glial nature of the implants is proved by the presence of glial fibrillary acidic protein. The previous reports of long survival indicate that occurrence of this peritoneal gliomatosis does not alter the prognosis and that therapy directed at the peritoneal implants of mature glia is not required for cure.

Child↗
PubMed1984

IgM demyelinative neuropathy with amyloidosis and biclonal gammopathy.

A 59-year-old man developed a sensorimotor neuropathy of the upper and lower limbs, associated with a biclonal gammopathy, within the space of a few months. Each of two paraproteins was coupled with a distinct IgM kappa IgG lambda light chain. Examination of a nerve biopsy specimen by electron microscopy revealed a demyelinative process with a widening of the interlaminar space in the myelin sheath, as well as deposits of amyloid substance between nerve fibers. Direct immunofluorescence revealed the presence of IgM and of the kappa light chain in certain Schwann cells, while the lambda IgG was fixed to the amyloid deposits. Immunoperoxidase histochemistry showed a positive reaction in normal human nerve tissue to the immune serum IgM and kappa light chain. The findings suggest that the widening of the interlaminar space of the diseased myelin corresponds to an active fixation of immunoglobulin on the sheath of the Schwann cell. The presence of two light chains in this patient's gammopathy caused a dual pathology: the kappa chain, a demyelinative neuropathy, and the lambda chain, a primary amyloidosis, with deposits in the peripheral nerve and in the kidney.

Amyloidosis↗
PubMed1984

Chronic demyelinating neuropathy with IgM-producing lymphocytes in peripheral nerve and delayed appearance of "benign" monoclonal gammopathy.

A chronic demyelinating neuropathy with "benign" IgM gammopathy was followed for 6 years in a 63-year-old man. The clinical, biologic, and EMG aspects were similar to those already reported, but a lymphoplasmocytic infiltrate in the nerve connective tissue of this patient has only rarely been observed in benign IgM gammopathy. The paraprotein was not evident in the serum until 5 years after symptoms of the neuropathy started.

Demyelinating Diseases↗
PubMed1984

Amyloid neuropathy: relationship between amyloid fibrils and macrophages.

A case of amyloid neuropathy associated with a multiple myeloma IgG light chain is reported. Under light microscopy the peripheral nerve exhibited several amyloid deposits. Electron microscopy revealed numerous amyloid deposits; at their periphery, macrophagic histiocytes were observed, containing a few tufts of parallel fibrils in their cytoplasm. A few plasma cells were scattered in the endoneurium and did not exhibit such a relationship. These findings resemble those recently observed in stem-cell cultures of IgG lambda chain human myeloma.

Amyloid↗