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Biomedical subjects

Vinay Chaudhry

Publications and source records attributed to Vinay Chaudhry.

13 recordsLinked to original sources
PubMed2006

Practice Advisory: utility of surgical decompression for treatment of diabetic neuropathy: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology.

Surgical decompression at the site of anatomic narrowing has been promoted as an alternative treatment for patients with symptomatic diabetic neuropathy. Systematic review of the literature revealed only Class IV studies concerning the utility of this therapeutic approach. Given the current evidence available, this treatment alternative should be considered unproven (Level U). Prospective randomized controlled trials with standard definitions and outcome measures are necessary to determine the value of this therapeutic intervention.

Clinical Trials as Topic↗
PubMed2005

Rhabdomyolysis: an evaluation of 475 hospitalized patients.

Rhabdomyolysis is a common and potentially lethal clinical syndrome that results from acute muscle fiber necrosis with leakage of muscle constituents into blood. Myoglobinuria is the most significant consequence, leading to acute renal failure (ARF) in 15%-33% of patients with rhabdomyolysis. Rhabdomyolysis occurs from inherited diseases, toxins, muscle compression or overexertion, or inflammatory processes, among other disorders. In some cases, no cause is found. We describe 475 patients from the Johns Hopkins Hospital inpatient records between January 1993 and December 2001 for the following discharge diagnosis codes: myoglobinuria, rhabdomyolysis, myopathy, toxic myopathy, malignant hyperthermia, neuroleptic malignant syndrome, and polymyositis. Of 1362 patients, 475 patients with an acute neuromuscular illness with serum creatine kinase (CK) more than 5 times the upper limit of normal (>975 IU/L) were included. Patients with recent myocardial infarction or stroke were excluded. The etiology was assigned by chart review. For all, the highest values of serum CK, serum creatinine and urine myoglobin, hemoglobin, and red blood cells were recorded. Forty-one patients had muscle biopsy within at least 2 months from the onset of rhabdomyolysis.Of the 475 patients, 151 were female and 324 were male (median age, 47 yr; range, 4-95 yr). Exogenous toxins were the most common cause of rhabdomyolysis, with illicit drugs, alcohol, and prescribed drugs responsible for 46%. Among the medical drugs, antipsychotics, statins, zidovudine, colchicine, selective serotonin reuptake inhibitors, and lithium were the most frequently involved. In 60% of all cases, multiple factors were present. In 11% of all cases, rhabdomyolysis was recurrent. Underlying myopathy or muscle metabolic defects were responsible for 10% of cases, in which there was a high percentage of recurrence, only 1 etiologic factor, and a low incidence of ARF. In 7%, no cause was found. ARF was present in 218 (46%) patients, and 16 died (3.4%). A linear correlation was found between CK and creatinine and between multiple factors and ARF, but there was no correlation between ARF and death or between multiple factors and death. Urine myoglobin detected by dipstick/ultrafiltration was positive in only 19%. Toxins are the most frequent cause of rhabdomyolysis, but in most cases more than 1 etiologic factor was present. Patients using illicit drugs or on prescribed polytherapy are at risk for rhabdomyolysis. The absence of urine myoglobin, by qualitative assay, does not exclude rhabdomyolysis. With appropriate care, death is rare.

Acute Disease↗
PubMed2005

Toxic neuropathy.

PURPOSE OF REVIEW: This paper examines recent research on toxic neuropathy and potential therapeutic developments. It also summarizes reports of new agents reported to cause peripheral neuropathy. RECENT FINDINGS: Gene therapy with vasoactive endothelial growth factor, neurotrophic substances such as nerve growth factor and neurotrophin-3 are reported to reverse or protect against neurotoxicity in animal models. The neuroprotective effects of more established therapeutic agents like vitamin E, tacrolimus (FK 506) and erythropoietin hold promise for the immediate future. Cisplatin and high-dose pyridoxine are used more frequently to produce robust models of peripheral neuropathy in animals. Statins do appear to cause peripheral neuropathy. The incidence is low, however, and compared to its benefits in terms of cardiovascular protection, relatively innocuous. The profile of thalidomide neuropathy is becoming clearer as the indications for this drug increases. The incidence of thalidomide neuropathy is high, up to three quarters in some series, and although the information on dose dependency is variable, lower cumulative doses appear to be less toxic. Like thalidomide bortezomib, a novel proteosome inhibitor, is reportedly effective in the treatment of multiple myeloma and is associated with peripheral neuropathy. Oxaliplatin and epothilone are emerging anticancer drugs with neurotoxic potential. Similarly, leflunomide, a new disease modifying-agent approved for the treatment of rheumatoid arthritis, is reported to cause neuropathy. SUMMARY: The study of toxic neuropathy is not only enhancing our knowledge of the mechanisms of neurotoxicity but also the neurobiology of peripheral neuropathy in general; and is likely to reveal avenues for therapeutics.

Animals↗
PubMed2004

Clinical comparison of muscle-specific tyrosine kinase (MuSK) antibody-positive and -negative myasthenic patients.

We assayed cryopreserved sera from 38 acetylcholine receptor (AChR) antibody-negative patients with myasthenia gravis (MG) who were followed clinically for muscle-specific tyrosine kinase (MuSK) antibodies and analyzed and compared their clinical characteristics. None of 13 sera from patients with purely ocular MG were positive. Sera from 10 of 25 patients (40%) with generalized MG were positive for MuSK antibodies. The age at onset of myasthenic symptoms was significantly earlier in MuSK antibody-positive patients (P = 0.02). MuSK antibodies were present in AChR antibody-negative patients of either gender, with virtually identical prevalence in women (41.2%) and men (37.5%). The distribution of weakness more commonly involved neck muscles in MuSK antibody-positive patients, and limb muscles in MuSK antibody-negative patients. Patients responded to immunosuppressive treatment regardless of whether MuSK antibody was present. We conclude that MuSK antibodies are present and diagnostically useful in a subset of myasthenic patients without AChR antibodies. Although the distribution of weakness differs somewhat depending on whether MuSK antibodies are present, responses to anticholinesterase and immunosuppressive treatments are similar.

Adult↗
PubMed2004

Role of magnetic resonance neurography in brachial plexus lesions.

Magnetic resonance neurography (MRN) is a relatively new imaging technique that is highly sensitive in detecting lesions in the peripheral nerves. We studied six cases of brachial plexopathies in which MRN played a pivotal role in making the correct diagnoses. All patients had clinical, nerve conduction, and electromyographic findings consistent with brachial plexus lesions. Four patients had brachial plexitis and two had multifocal demyelinating neuropathy presenting as brachial plexopathies. MRN in all patients showed edema, thickening, and T2 hyperintensities localized to the brachial plexus region. We conclude that MRN is a useful technique in evaluating patients with brachial plexus lesions, particularly in cases of brachial plexitis, where conventional magnetic resonance imaging is generally normal.

Adolescent↗
PubMed2003

Literature review: nervepace digital electroneurometer in the diagnosis of carpal tunnel syndrome.

Over the last two decades, several diagnostic devices have been developed to assess patients with suspected carpal tunnel syndrome (CTS). One such device is the Nervepace Digital Electroneurometer (NDE). At this time, however, the AAEM concludes that the current literature does not support the substitution of the NDE for standard electrodiagnostic studies in the clinical evaluation of patients with CTS.

Carpal Tunnel Syndrome↗
PubMed2003

Surface electromyographic recording of volitional activity: a technique to detect partial motor conduction block.

Partial motor conduction block, an electrophysiological hallmark of demyelination, helps to identify acquired demyelinating neuropathies but its electrophysiological detection can be difficult. We report a technique that may be helpful in this regard. Twenty-five patients with partial motor conduction block secondary to acquired demyelinating polyneuropathy (ADP), 7 with amyotrophic lateral sclerosis (ALS), 7 with stroke, and 11 control subjects, were studied. Amplitude of compound muscle action potentials was recorded after distal electrical (E) stimulation and for volitionally (V) induced responses in 82 muscles. Mean +/- SD V/E ratio was 12.3 +/- 6.6 for ADP patients, 58.1 +/- 17 for ALS patients, 11.4 +/- 9 for stroke patients, and 55.4 +/- 12.3 for controls. The V/E ratios for patients with partial motor conduction block and stroke were significantly reduced compared with ALS patients and healthy controls (P < 0.05). Surface electromyographic (EMG) recording for determination of the V/E ratio may be a useful technique for detection of a proximal conduction block if a central lesion or poor effort can be excluded. Further study of this novel technique is necessary.

Action Potentials↗
PubMed2002

Worsening of multifocal motor neuropathy during pregnancy.

Three women with multifocal motor neuropathy (MMN) were treated during pregnancy. Compared with their pregestation strength, the women became weaker in previously involved muscles and showed new weakness in previously unaffected muscles. All were treated with IV immunoglobulin during pregnancy and improved in strength. After pregnancy, strength in all patients returned to the prepregnancy state. The authors conclude that pregnancy may worsen MMN.

Adult↗
PubMed2002

Neuromuscular diseases and disorders of the alimentary system.

This review outlines the relationship and interaction between neuromuscular diseases and disorders of the alimentary system. Neuromuscular manifestations of gastrointestinal and hepatobiliary diseases are first considered. Such diseases may cause neuromuscular disorders by leading to nutritional deficiency or by more direct mechanisms. The pathogenesis, clinical features, and treatment of these various neuromuscular manifestations are discussed. The impact of disorders of nerve, neuromuscular transmission, and muscle on the alimentary system is then reviewed. The main sequelae are impaired deglutition and gastrointestinal dysmotility. The management of these complications is considered.

Avitaminosis↗