PubMed Health⌕ Search

Biomedical subjects

Ted M Burns

Publications and source records attributed to Ted M Burns.

17 recordsLinked to original sources
PubMed2007

Fatal encephalitis in a patient with refractory celiac disease presenting with myorhythmia and carpal spasm.

We report the case of a woman with refractory celiac disease who developed abnormal spontaneous movements of the extremities and face consistent with myorhythmia. Investigation led to a diagnosis of encephalitis, confirmed by postmortem examination. The movements were likely caused by nonparaneoplastic encephalitis associated with refractory celiac disease. Etiologic and diagnostic considerations and treatment options are discussed.

Aged↗
PubMed2006

Novel myelin protein zero mutation (Arg36Trp) in a patient with acute onset painful neuropathy.

We present a patient with acute onset painful polyneuropathy found to have a novel MPZ mutation (Arg36Trp). The Arg36Trp mutation described in this report occurs at a putative adhesion interface. An alternative explanation for his polyneuropathy was not found and his mother was identified to have polyneuropathy and carry the same mutation. Two hundred normal controls were without this base alteration. The temporal profile of the index case may provide further indirect evidence suggesting an immune mechanism contributing to the pathogenesis of some cases of MPZ mutations. We predict that other rapid symptom onset polyneuropathies will be found to have direct genetic susceptibility.

Acute Disease↗
PubMed2005

Myotonic dystrophy.

Explore the source record for details and available documents.

Anticipation, Genetic↗
PubMed2005

Management of common neurologic conditions in sports.

Neurological conditions are common in athletes. Trauma can cause direct central (eg, concussion or hemorrhage) or peripheral (eg, stinger) injury. Also, as neurological conditions in athletes become better understood, more people who have pre-existing conditions are becoming involved in organized sports. This article reviews assessment and initial management of head injury, stingers, seizures, and headaches. Return-to-play criteria are also discussed.

Athletic Injuries↗
PubMed2005

An update on the classification and treatment of vasculitic neuropathy.

Vasculitic neuropathy usually presents with painful mononeuropathies or an asymmetric polyneuropathy of acute or subacute onset. The disorder should be classified as being systemic or non-systemic. Systemic vasculitis should be further classified into one of the primary and secondary forms. Although specific treatment regimens vary among neurologists, basic principles can be applied. Corticosteroids and cytotoxic drugs have been the mainstay of treatment for most forms of vasculitic neuropathy. Here we discuss dosing, potential side-effects, and management recommendations of conventional treatments. New treatments showing promise include intravenous immunoglobulin and biological agents and trials of the newest treatments are being reviewed. Future trials should compare commonly used treatment regimens and better establish the efficacy of newer, potentially safer, treatments.

Humans↗
PubMed2004

Chronic inflammatory demyelinating polyradiculoneuropathy.

For much of the 20th century, our understanding of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) was limited because the condition went by several different names; clinical and histopathologic descriptions were often combined with those of similar neuropathic disorders including Guillain-Barré syndrome, the hereditary hypertrophic polyneuropathies, and other chronic polyneuropathies; and the means to sufficiently study and treat the condition had not been developed. Major advances in the understanding of CIDP occurred mid century and included the development of the experimental allergic neuritis (EAN) model, the elaboration of nerve conduction studies, and the discovery of corticosteroids. In the 1970s, CIDP finally emerged as a distinct entity with well-defined clinical, histopathologic, and electrodiagnostic features. Diagnostic criteria were developed, and subsequent treatment trials proved the efficacy of corticosteroids, plasma exchange, and intravenous immunoglobulin.

Adrenal Cortex Hormones↗
PubMed2004

Multifocal slowing of nerve conduction in metachromatic leukodystrophy.

Polyneuropathy is invariably associated with the late-infantile form of metachromatic leukodystrophy (MLD), and occurs frequently in the early juvenile, juvenile, and adult variants. Uniform slowing of nerve conduction velocity is the neurophysiologic hallmark of metachromatic leukodystrophy and other inherited demyelinating polyneuropathies. To evaluate the consistency of this principle, we reviewed nerve conduction studies in 9 children with late-infantile or early-juvenile metachromatic leukodystrophy. Each child had significant slowing of motor nerve conduction velocity (NCV). The compound muscle action potentials showed abnormal temporal dispersion in 3 of the 9 children, which is usually regarded as the hallmark of acquired demyelinating polyneuropathies. There are reports of multifocal slowing in other hereditary processes including X-linked Charcot-Marie-Tooth disease, hereditary neuropathy with liability to pressure palsies, and adrenomyeloneuropathy. Although multifocal NCV slowing in a child with polyneuropathy is seen most commonly in acquired conditions, a hereditary process, including MLD, cannot always be excluded in this setting.

Action Potentials↗
PubMed2003

Neurosarcoidosis.

Sarcoidosis is a multisystem granulomatous disorder of unknown etiology first named and described in the 19th century. The diagnosis usually requires the finding of noncaseating epithelioid cell granulomas in more than one organ and exclusion of other disorders known to cause granulomatous disease. The incidence of nervous system involvement in sarcoidosis is about 5%. Sarcoidosis may involve any part of the nervous system. Corticosteroids remain the mainstay of treatment of neurosarcoidosis.

Adrenal Cortex Hormones↗
PubMed2003

Oculobulbar involvement is typical with Lambert-Eaton myasthenic syndrome.

Oculobulbar symptoms and/or signs were present in 18 of 23 (78%) of Lambert-Eaton myasthenic syndrome (LEMS) patients evaluated at the Lahey Clinic (Table). Sixty-five percent (15 of 23) of our patients had ptosis and/or diplopia, each present in 11 individuals. Bulbar signs and symptoms, including dysarthria in 10 and dysphagia in 8 patients, also were observed among our LEMS population. More than one prereferral oculobulbar feature occurred in 13 of our LEMS patients. Prereferral diagnostic considerations included myasthenia gravis, myopathies, and psychiatric disorders. These findings suggest that these atypical characteristics served to dissuade some colleagues from a diagnosis of LEMS. Thus, the presence of oculobulbar symptoms and signs cannot be used to exclude LEMS from the differential diagnosis.

Adult↗
PubMed2003

Current therapeutic strategies for patients with polyneuropathies secondary to inherited metabolic disorders.

Supportive care, symptomatic treatment, and patient education should be provided for patients with inherited or acquired polyneuropathies. In addition, specific treatment is available for many of the acquired polyneuropathies. Genetic counseling is valuable for many patients with inherited polyneuropathies, but only rarely is specific treatment an option for these patients. However, specific treatments are available for many of the rare and devastating systemic disorders associated with polyneuropathies. Thus, clinicians must promptly diagnose these inherited disorders so that specific treatment may be initiated. The clinical features of these rare inherited disorders are emphasized.

Adult↗
PubMed2002

Clinical versus quantitative vibration assessment: improving clinical performance.

In 3 large cohorts (total of 787 patients), clinical vibration impairment (CVI) of the great toe using a tuning fork was compared with quantitative vibration threshold (QVT). Using a stepwise multivariate analysis, we assessed demographic and anthropomorphic patient characteristics associated with the difference between CVI and QVT for the various cohorts and the chosen QVT ranges of percentile abnormality. We also compared CVI or QVT abnormality with a composite score of nerve conduction abnormality to confirm that QVT is a valid measure of severity of neuropathy. Highly significant associations between CVI and QVT were found in all 3 cohorts studied, regardless of the chosen QVT percentile level of abnormality. However, in the 2 cohorts evaluated by many different physicians, CVI overestimated QVT much more often than underestimated it. The discordance between CVI and QVT in all QVT abnormality percentile levels was associated with age, height and body surface area (BSA) in 1 cohort, with age and BSA in another cohort, and with age in the third cohort. In the third cohort, the correlation between QVT and the composite score of nerve conduction abnormality was significantly higher than the correlation between CVI and the composite score. Using a tuning fork, neuromuscular physicians overestimate vibration sensation loss more often than when QVT testing is done, which employs quantitative stimuli, a broad range of stimulus magnitudes, null stimuli, validated algorithms of testing and validated reference values. To improve assessment of vibration sensation, physicians should take into account age, height and weight (or body surface area) when judging vibration abnormalities. Applying some useful approaches to quantitative sensory testing might improve the accuracy of clinical sensory testing.

Adult↗
PubMedDate not supplied

Neuromuscular complications of cancer diagnosis and treatment.

Neuromuscular disorders are a common cause of morbidity in patients with cancer. They can be a direct effect of the primary malignancy, a paraneoplastic effect, or a treatment complication. Malignant neoplasms may infiltrate or compress nerve roots, plexi, and peripheral nerves, causing various sensory and motor symptoms. Electrodiagnostic testing, cerebrospinal fluid analysis, and neuroimaging are helpful in confirming the diagnosis. Treatment for neuropathies of neoplastic origin involves irradiation and chemotherapy, which may improve pain, but usually does not improve neurologic function. Paraneoplastic syndromes are rare and sometimes result from production of autoantibodies directed against neural antigens present in tumor tissues. They commonly precede any symptoms related to the cancer itself, and discovery of such syndromes necessitates a thorough investigation to look for an occult neoplasm. Treatment of the underlying cancer occasionally improves neurologic function. Both brachial and lumbosacral plexopathies may represent a complication of radiotherapy. Electrodiagnostic tests particularly are helpful; these diagnostics demonstrate the presence of myokymic discharges, which are suggestive of radiation injury. Many chemotherapeutic agents may cause peripheral neurotoxicity and associated acute and chronic peripheral neuropathies, particularly if given to patients with preexisting hereditary or acquired neuropathies. These side effects are a limiting factor in cancer treatment. Other potential neuromuscular problems related to cancer include side effects of steroids and other immunosuppressants, effects secondary to bone marrow transplantation, and infections. Early recognition and management of these disorders will improve patient outcome and quality of life.

Antineoplastic Agents↗