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Biomedical subjects

G Saïd

Publications and source records attributed to G Saïd.

At least 19 recordsLinked to original sources
PubMed1998

Axonal regrowth through a collagen guidance channel bridging spinal cord to the avulsed C6 roots: functional recovery in primates with brachial plexus injury.

Intraspinal implantation of a collagen guidance channel (CGC) to promote axon regeneration was investigated in marmosets with brachial plexus injury. After avulsion of the right C5, C6 and C7 spinal roots, a CGC containing (group B) or not (group A) a nerve segment, or a nerve graft (group C), was ventro-laterally implanted into the cord to bridge the ventral horn and the avulsed C6 roots. No spinal cord dysfunction was observed following surgery. Two months later, the postoperative flaccid paralysis of the lesioned arm improved. In five months, a normal electromyogram of the affected biceps muscle was recorded in all repaired animals. Motor evoked potentials were obtained with a mean amplitude of 13.37 +/- 13.66 microV in group A, 13.21 +/- 5.16 microV in group B and 37.14 +/- 35.16 microV in group C. The force of biceps muscle contraction was 27.33 +/- 20.03 g (group A), 24.33 +/- 17.03 g (group B) and 37.38 +/- 21.70 g (group C). Retrograde tracing by horseradish peroxidase showed labelled motoneurons ipsilaterally located in the C5 and C6 ventral horn, nearby the implantation site. The mean labelled neurons was 32.33 +/- 21.13, 219.33 +/- 176.29 and 64.33 +/- 23.54 in group A, B and C respectively. Histological analysis presented numerous myelinated and unmyelinated regenerating axons in the implant of these animals. Statistical analysis did not show significant difference among the three repaired groups. Our results indicate that spinal neurons can regenerate through a CGC to avulsed nerve roots and induce motor recovery in primates.

Animals↗
PubMed1998

New transthyretin variants SER 91 and SER 116 associated with familial amyloidotic polyneuropathy. Mutations in brief no. 151. Online.

Mutations of the transthyretin (TTR) gene are associated with familial amyloidotic polyneuropathy (FAP). Two new mutations were detected in French patients with TTR amyloidosis. The first patient was a 72 year old man who presented with severe and rapidly evolving sensory motor polyneuropathy of the 4 limbs, a bilateral carpal tunnel syndrome and a restrictive cardiomyopathy. His father died after a clinical history suggestive in retrospect of TTR amyloidosis. The second patient was a 75 year old man who presented with axonal sensory neuropathy of the 4 limbs and a bilateral carpal tunnel syndrome. In both cases immunohistochemistry performed on a nerve biopsy reveled TTR positive amyloid. Direct genomic sequencing of the full TTR gene coding region indicated two heterozygous transversions encoding Ser for Ala 91 substitution in the third exon of the gene in patient 1 and Ser for Tyr 116 substitution in the fourth exon of the gene in patient 2. The mutations were confirmed by digesting PCR products with restriction enzymes and were not found in a control population of 100 unrelated individuals. The Ser 116 substitution was also detected in the daughter and the 70 year old sister of the proband. However the absence of symptomatology suggestive of TTR amyloidosis may be related to the late onset of the disease. The clinical immunohistochemical and molecular studies in both patients are highly suggestive of an association between the Ser 91 and Ser 116 TTR variants with amyloidosis.

Aged↗
PubMed1994

Cytomegalovirus multifocal neuropathy in AIDS: analysis of 15 consecutive cases.

A severe multifocal neuropathy caused by cytomegalovirus (CMV-MN) can occur in the late stage of human immunodeficiency virus (HIV) infection. In a retrospective study, we identified 15 consecutive HIV-positive patients with a diagnosis of CMV-MN based on (1) markedly asymmetric neuropathy, (2) fewer than 100 CD4+ cells per mm3, (3) exclusion of other causes of neuropathy, and (4) characteristic CMV cytopathic changes on neuromuscular biopsy (2 patients), positive CSF culture for CMV (2 patients), or clinical improvement on anti-CMV therapy given for concurrent extraneurologic CMV disease (8 patients) or neuropathy (3 patients). All patients were men and had severe immunosuppression (mean CD4+ cell count, 18 per mm3). The initial symptoms were numbness and painful paresthesias showing a patchy, multifocal distribution. After a mean of 11 weeks (range, 1 to 10 months), the patients developed moderate or severe sensorimotor asymmetric neuropathy. Extraneurologic CMV infection occurred in 10 patients before diagnosis. Electrophysiologic studies showed axonal neuropathy and CMV DNA was present in CSF by the polymerase chain reaction (PCR) technique in 90% of patients tested. Fourteen patients showed a marked improvement 1 to 4 weeks after starting ganciclovir or foscarnet therapy. During follow-up on maintenance therapy (13 patients), the neuropathy relapsed in three patients and probable or confirmed CMV encephalitis occurred in five. Twelve patients died during follow-up, at a mean interval of 9.5 months after their first symptoms. These results extend the clinical spectrum of CMV-MN and show that PCR detection of CMV DNA in CSF may be a useful diagnostic marker.

Acquired Immunodeficiency Syndrome↗
PubMed1993

[Sensitive polyneuropathy and diabetic cardiovascular dysautonomy].

We performed a clinical and physiological study in diabetic patients with distal symmetrical sensory neuropathy in an attempt to correlate the extension of sensory loss with alterations of cardiocirculatory tests. These tests included measurement of blood pressure and heart rate in the recumbent and upright positions, Valsalva's manoeuvre and respiratory variations of R-R intervals. We thus studied 56 patients with distal sensory neuropathy. We found that all three tests were impaired in all patients with sensory loss above the knee level. We found a highly significant correlation between the level of sensory loss and impairment of physiological tests (p < 0.001). We conclude that both sensory loss above the knee and impairment of all three cardiocirculatory tests result from a severe neuropathy, but this correlation may not be sufficient to assert that cardiocirculatory impairment that occurs in diabetic neuropathy is a length dependent phenomenon.

Adult↗
PubMed1992

[Postural hypotension with myoclonia in multisystemic atrophy].

Each time he stood up a 60-year old man experienced myoclonic jerks, quickly followed by a syncope due to major postural hypotension. Progressive autonomic failure was associated with pyramidal, extrapyramidal and cerebellar features in a pattern characteristic of Shy-Drager disease. Myoclonic jerks suggested seizures, but no electroencephalographic epileptiform activity was found. This case together with data from the literature suggest, that such involuntary movements may result from cerebral anoxia.

Blood Pressure Determination↗
PubMed1991

[Peripheral neuropathies in dysglobulinemia].

Peripheral neuropathies are frequently associated with different types of dysglobulinemia. These neuropathies may have different chemical features depending on the nature of the dysglobulinemia. Most frequently it is a picture of predominantly sensory polyneuropathy. The autoimmune origin of the neuropathies with demyelination, observed in "benign" monoclonal gammopathies or some Waldenström diseases, is strongly suggested by immunohistochemical studies. Neuropathies associated with multiple myeloma or amyloidosis, are generally due to compressions, infiltrations or hemorragic destructions. The neuropathy frequently reveals and preceeds the dysglobulinemia, which should be looked for in all neuropathy without any obvious cause.

Amyloidosis↗
PubMed1990

[Neurologic complications in hemodialysis patients].

Various neurological complications may occur in patients under haemodialysis for end-stage chronic renal failure. Their frequency has clearly been reduced by improvements in the modalities and techniques of dialysis. Some of these complications are related to uremia and/or to the accumulation of endogenous toxic substances the nature of which has not been elucidated (e.g. uraemic encephalopathy, polyneuropathy), while others are directly due to the haemodialysis itself (e.g. dialysis disequilibrium syndrome, aluminum encephalopathy).

Aluminum↗
PubMed1989

[Acute and reversible axonal polyneuropathy in post-leptospirosis].

A 53 year old woman presented, one month after an anicteric leptospirosis, an acute, asymmetrical, sensorimotor polyneuropathy involving the lower limbs. Electrophysiological study showed evidence of severe denervation, with normal motor nerve conduction velocities, indicating an axonal degeneration. Neuro-muscular biopsy showed signs of wallerian degeneration and perivascular infiltrates of epineural vessels. She received a corticosteroid therapy during 6 months and there was a nearly complete clinical recovery.

Acute Disease↗
PubMed1987

[Action of dihydroergotamine in severe orthostatic hypotension. 16 cases].

A cooperative study of dihydroergotamine in the treatment of severe postural hypotension was conducted in 16 patients. Postural hypotension was related to Shy-Drager syndrome in 9 and to diabetic neuropathy in one; it was idiopathic in 6 patients. With an average daily dose of 36 mg orally, the fall in systolic blood pressure when passing from supine to standing position was 39 mmHg versus 59 mmHg (mean values) before treatment. Standing and walking were made possible in 4 out of 6 and in 4 out of 7 patients respectively. The treatment was well tolerated. Dihydroergotamine was found worth trying in patients with symptomatic postural hypotension.

Adult↗
PubMed1984

Peripheral neuropathy in type A Niemann-Pick disease. A morphological study.

A black boy had a severe neuropathic form of Niemann-Pick disease (NPD) with a pronounced sphingomyelinase deficiency in the fibroblasts. Nerve conduction velocities were diminished, and a nerve biopsy was performed. Isolated fibers showed segmental demyelination and numerous dense bodies in the Schwann cells (SC). Electron microscopy revealed two categories of inclusions: the first was made up of lysosomal inclusions usually described in NPD. The second comprised myelin inclusions--sometimes still connected to the original myelin sheath--indicating severe myelinopathy. Both myelin debris and NPD inclusions were found in axoplasms and probably came from SC cytoplasm through axolemma lesions. NPD is a unique example of myelinopathy due to sphingomyelinase deficiency.

Humans↗
PubMed1981

[Progressive centripetal degeneration in polyneuropathies (author's transl)].

This is a clinicopathologic report on three patients with sensory polyneuropathies of different origin. Sensory loss involved all four limbs reaching the upper third of the thighs and the elbow level or higher, in all three patients. In addition to the limbs the central region of the anterior aspect of the trunk, from lower abdomen up to level T2, and on the top of the scalp were involved. There was minimal weakness. This pattern of sensory deficit can best be explained by a length dependent degeneration of fibers. Familial amyloidosis, Portugese type, was responsible for the neuropathy in the first patient, diabetes mellitus in the second and alcoholism in the third one. On teased nerve fiber study, single regenerating fibers were isolated on sural nerve biopsy specimens from patients 1 and 2. Segmental demyelination and/or remyelination occurred in 11 per cent of the fibres in patient 1, in 36 per cent in patient 2 and in 4 of the 19 fibres isolated in patient 3. On cross sections of nerve specimens embedded in Epon there was a striking loss of myelinated fibres which was less important and predominated on smaller fibres in patients 1 and 2. On electron microscopic examination loss of unmyelinated fibres was conspicuous in all three patients. On single fiber studies as well as on sections of embedded specimens, myelinated fibres occasionally showed demyelination in contact to amyloid deposits. The present study demonstrates that in this pattern of neuropathy degeneration of myelinated fibers begins in the distal part of longest axons and may be associated with axonal sprouting in more proximal parts of degenerating axons. As the neuropathy progresses axons of shorter and shorter length become involved.

Adult↗