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At least 163 records · Page 9Linked to original sources
PubMed1993

The R-(+)isomer of O-n-hexyl S-methyl phosphorothioamidate causes delayed neuropathy in hens after generation of a form of inhibited neuropathy target esterase (NTE) which can be reactivated ex vivo.

To initiate delayed neuropathy (DN) in adult hens organophosphates and phosphonates must inhibit most neural NTE and the inhibited NTE must undergo an 'aging' reaction. Phosphinates and those chiral isomers of phosphonates which produce non-aging NTE do not cause DN but act as prophylactic agents. Some racemic phosphoramidates cause DN although the inhibited NTE in autopsy samples can be reactivated in vitro (Johnson, Read and Vilanova, 1991, Arch. Toxicol., 65, 618-624). We now report that pure R(+)isomer of O-n-hexyl S-methyl phosphorothioamidate (5-20 mg/kg per os) caused slight acute effects but typical DN associated with high inhibition of NTE in brain, spinal cord and sciatic nerve (maximum by 6-24 h): the inhibited NTE was easily reactivated by KF (presumed not aged). For each dose the average residual NTE activity in the three tissues 24 h after dosing and the clinical ataxia severity on peak days 15-17 (score out of 4) was: 5 mg/kg: 13, 14, 27% (2,2,2,1); 10 mg/kg: 10, 14, 12%, (4,3,2); 15 mg/kg: 10,11,17%, (3,3,4); 20 mg/kg: 6, 10, 8% (3,3,3,2). The ability of this isomer and of other racemic phosphoramidates to initiate DN by covalent reaction at the active site of NTE (inhibition) without subsequent aging suggests that the chemistry (? charge distribution) in the region of the phosphorus atom determines that disturbance in the molecular environment of NTE which initiates DN.

Animals↗
PubMed1990

MR imaging in hypertrophic neuropathy: a case of hereditary motor and sensory neuropathy, type I (Charcot-Marie-Tooth).

We describe findings of Charcot-Marie-Tooth disease in magnetic resonance imaging (MRI). The MRI examination of the lumbar spine with and without gadolinium DTPA showed diffusely enlarged cauda equina, nerve roots, and ganglia. In the setting of appropriate family history and clinical presentation, the findings of diffusely enlarged nerve roots support the diagnosis of hereditary motor and sensory neuropathy, Type I (HMSN I, Charcot-Marie-Tooth).

Adult↗
PubMed1993

Relative frequency of nerve conduction abnormalities at carpal tunnel and cubital tunnel in France and the United States: importance of silent neuropathies and role of ulnar neuropathy after unsuccessful carpal tunnel syndrome release.

The two most frequently diagnosed nerve compression syndromes of the upper extremities are carpal tunnel syndrome and cubital tunnel syndrome. In order to determine the relative frequencies of nerve conduction abnormalities at the carpal tunnel and cubital tunnel in France and the United States, we evaluated all patients (nFR = 882 and nUS = 818) who had nerve conduction studies of the upper extremities over a six-yearFR or three-yearUS interval. In both France and the United States, the risk of electrophysiological abnormalities was 2 to 1 for the wrist relative to the elbow. Abnormal median nerves were twice as likely to be symptomatic as were abnormal ulnar nerves (silent ulnar neuropathy). Thus, the clinical risk for carpal tunnel syndrome relative to cubital tunnel syndrome was approximately 4 to 1. In many cases of persistent hand symptoms following carpal tunnel release, the problem may actually be related to an undiagnosed ulnar nerve lesion. Thus, a complete neurophysiological evaluation of the upper extremity necessitates both median and ulnar studies.

Adolescent↗
PubMedDate not supplied

Triphenyl phosphite neuropathy differs from organophosphorus-induced delayed neuropathy in rats.

The topographies of neuropathic damage produced by triphenyl phosphite (TPP) and tri-ortho-cresyl phosphate (TOCP) are contrasted in the present study. Long-Evans, male rats were exposed (sc) to single (0.1 ml kg-1; 1.0 ml kg-1) or multiple (2 X 1.0 ml kg-1; 3 X 1.0 ml kg-1) doses of TPP, and sampled 1-3 weeks after exposure. Additional animals were dosed acutely with TOCP (1160 mg kg-1, p.o.) alone or in combination with multiple doses of TPP (2 X 1 ml kg-1). Functional changes, seen in multiple-dosed TPP-rats included tail-kinking, circling, and ataxia. Neuropathological damage seen in all but the 0.1 ml kg-1 treated animals consisted of degeneration of the ventrolateral and ventral columns of the spinal cord at all levels, and moderate peripheral nerve fibre damage. Medullary brainstem involvement consisted of axonal swellings and fragmented axons in the medial longitudinal fasciculus, the reticular formation, and the inferior cerebellar peduncles. Tissues examined from TOCP-treated rats displayed severe degeneration of the fasciculus gracilis at the cervical level, mild involvement of the dorsolateral columns at the lumbar levels and a sparing of all other cord and brainstem regions. Rats treated with neuropathic doses of both TPP and TOCP showed a composite pattern of degeneration that included damaged sites characteristic of the individual neurotoxicants. These data indicate that the neuropathic profile of TPP differs markedly from the delayed neuropathy (OPIDN) associated with exposure to model organophosphorus compounds such as TOCP.

Animals↗
PubMed2003

[Two patients with different types of vasculitic neuropathy--a comparison between cutaneous polyarteritis nodosa and nonsystemic vasculitic neuropathy].

We describe a patient with cutaneous polyarteritis nodosa (CPN) and a patient with nonsystemic vasculitic neuropathy (NSVN), both presenting mononeuritis multiplex. Patient 1 was a 50 year-old woman. She developed livedo reticularis, palpable purpura, and sensory disturbance of lower extremities. Laboratory examinations showed no abnormal findings except for slight elevation of ESR, CRP, and anti-nuclear antibody. Skin biopsy revealed vasculitis of small to medium sized arterioles in dermis and subcutaneous adipose tissue. Sural nerve biopsy revealed axonal degeneration of myelinated fibers and infiltration of polymorphonuclear cells and mononuclear cells around feeding arteries. From these findings, she was diagnosed as having CPN. She was treated with intravenous injections of methylprednisolone (1,000 mg/day) followed by oral prednisolone (40 mg/day), which had a limited effect. Addition of an immunosuppressive agent (azathioprine 50 mg/day) produced marked improvement in her clinical symptoms. However, azathioprine was discontinued because of liver injury. Then, we added cyclophosphamide which was as effective as azathioprine. Patient 2 was a 57 year-old man. He developed weakness of legs and sensory disturbance of lower extremities and trunk. Laboratory examinations showed no abnormal findings except for slight elevation of CRP and anti-nuclear antibody. Sural nerve biopsy revealed infiltration of inflammatory cells mainly consisting of mononuclear cells around small sized arterioles in the epineurium and severe loss of myelinated fibers. From these findings, he was diagnosed as having NSVN. Treatment with oral prednisolone (60 mg/day) and azathioprine (50 mg/day) improved his clinical symptoms. CPN is differentiated from NSVN by the existence of skin lesions and the type of inflammatory cells involved. However, these two diseases share common clinical features such as mononeuritis multiplex, absence of systemic organ involvement, no specific abnormal laboratory data, effectiveness of immunosuppressive therapy, and relatively good prognosis. We suggest that CPN and NSVN are included in the same category of nonsystemic vasculitis that can involve peripheral nerves and/or skin.

Diagnosis, Differential↗
PubMedDate not supplied

[Familial peripheral neuropathy caused by susceptibility to entrapment (tomaculous neuropathy)].

The authors describe a case of hereditary neuropathy with liability to pressure palsies (entrapment), and compare it to reports from literature. The main characteristics are: autosomal dominant inheritance, recurrent mononeuropathies (ulnar, median, peroneal, brachial plexus), and specific features at nerve biopsy. The sensory nerve reveals predominantly demyelinating alterations, having the remaining myelin fibres focal thickenings, the so called tomaculous, and shows numerous subperineural structures named Renaut Bodies. The EMG findings show a slowing of the nerve conduction velocities and an increase of distal latencies.

Adult↗
PubMed1998

Pachymeningitis with multiple cranial neuropathies and unilateral optic neuropathy secondary to Pseudomonas aeruginosa: case report and review.

Hypertrophic cranial pachymeningitis is a rare disorder that frequently presents with multiple cranial neuropathies. This disorder, which is characterized by thickening and infiltration of the cranial dura, can result from a variety of inflammatory and infectious conditions. A patient with hypertrophic cranial pachymeningitis is described in whom meningeal biopsy and bacterial cultures of the biopsy specimen revealed Pseudomonas aeruginosa. The authors believe this to be the first documented case of pachymeningitis secondary to this organism.

Ceftazidime↗
PubMed1999

[Hereditary motor-sensory neuropathies (Charcot-Marie-Tooth syndrome) and related neuropathies. Current classification and genotype-phenotype correlation].

Charcot-Marie-Tooth (CMT) disease is the most common inherited disorder of the peripheral nervous system with an incidence of 40:100,000. Clinically, it is characterized by distal muscle weakness and wasting, primarily of the legs and later of the arms, foot deformity, diminished or absent tendon reflexes, and mild-to-moderate sensory loss. Molecular genetic studies over the past 2 decades have revealed the genetic heterogeneity of this disorder and the identification of different genes or gene loci, respectively. Therefore, a current CMT classification though constantly changing due to ongoing detection of further genetic defects must take into consideration both phenotypic and genotypic criteria. Since certain clinical features appear to be associated with specific genetic subtypes, we provide a detailed description of characteristic phenotypic variants to facilitate differential diagnosis and allow more precise referral to subsequent genetic investigations.

Charcot-Marie-Tooth Disease↗