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Biomedical subjects

D A Chad

Publications and source records attributed to D A Chad.

15 recordsLinked to original sources
PubMed1991

Coexistence of Lambert-Eaton myasthenic syndrome and subacute cerebellar degeneration: differential effects of treatment.

A 61-year-old woman presented with two paraneoplastic neurologic disorders--Lambert-Eaton myasthenic syndrome (LEMS) and subacute cerebellar degeneration (SCD)--that antedated the diagnosis of small-cell carcinoma of the lung by 15 months. Plasmapheresis initiated before the identification of the tumor had a beneficial effect on LEMS but did not affect the SCD. Chemotherapy administered for treatment of the primary tumor was also associated with improvement of LEMS but, like plasmapheresis, had no effect on SCD. While the pathogenesis of both LEMS and SCD is thought to be mediated predominantly by humoral immune factors, a differential therapeutic response indicates that mechanisms of tissue damage or susceptibility to tissue injury, or both, differ in these two disorders.

Female↗
PubMed1991

Neuromuscular complications of systemic cancer.

In patients with cancer, neuromuscular dysfunction often develops as a result of some combination of direct effects of the cancer, from complications of therapy, or from paraneoplastic syndromes. Direct effects include leptomeningeal involvement by tumors (most frequently of the breast and lung) causing polyradiculopathy and compressive brachial and lumbar plexopathies that produce distinctive and typically painful syndromes. The differentiation between radiation and tumor-associated brachial plexopathies may be difficult, however. Peripheral neuropathy is an important dose-limiting toxic side effect of two commonly utilized agents, vincristine and cisplatin. Recent studies have suggested that this complication may be ameliorated or even prevented by prophylactic administration of protective agents. Finally, cancer can cause neuromuscular dysfunction through more remote effects and can produce a variety of paraneoplastic syndromes that include subacute sensory neuropathy. Lambert-Eaton myasthenic syndrome, and the neuropathy associated with paraproteinemia. In some syndromes, the presence of specific antibodies that cross-react with both neuromuscular tissues and primary tumors strongly suggests an immune-mediated pathogenesis. In some patients, immunosuppressive therapies and plasmapheresis may relieve symptoms.

Humans↗
PubMed1990

Human immunodeficiency virus (HIV)-associated myopathy: immunocytochemical identification of an HIV antigen (gp 41) in muscle macrophages.

In a patient with acquired immunodeficiency disease syndrome (AIDS) and muscle weakness, a muscle biopsy specimen disclosed degeneration of muscle fibers, regeneration, and focal endomysial mononuclear inflammation. A conspicuous feature was the presence of perivascular macrophages within the endomysium that showed positive immunostaining for human immunodeficiency virus (HIV) (gp 41) antigen. HIV was not detected within myofibers. Our findings suggest an important role for the HIV-infected macrophage in the pathogenesis of this myopathy.

Acquired Immunodeficiency Syndrome↗
PubMed1989

AAEE case report #20: hereditary motor and sensory neuropathy, type I.

A case study is reported regarding a 32-year-old man with classic clinical and electrophysiologic features of hereditary motor and sensory neuropathy, type I (HMSN I), a slowly progressive autosomal dominant condition marked by slow motor and sensory velocities and generalized segmental demyelination. Another clinically similar autosomal dominant neuropathy (HMSN II) is distinguished from HMSN I by nearly normal nerve conduction velocity. Acquired demyelinating neuropathy may occasionally resemble HMSN I clinically, but the former demonstrates electrophysiologic features not seen in the latter such as conduction block, dispersed compound muscle action potentials, and differential slowing of conduction velocity. Neuropathologic studies of HMSN I suggest that both neuronal and Schwann cell distrubances play a role in pathogenesis.

Adult↗
PubMed1989

Chronic cough as the presenting symptom of oculopharyngeal muscular dystrophy.

A patient had chronic, persistent cough as the presenting symptom of the neuromuscular disorder oculopharyngeal dystrophy (OPD). The presence of a significant smoking history initially resulted in the cough incorrectly being attributed to COPD. By using a systematic diagnostic approach, the correct etiology was determined.

Aged↗
PubMed1988

Amyotrophic lateral sclerosis. Recent advances in pathogenesis and therapeutic trials.

We reviewed the current status of pathogenesis and therapeutic trials in amyotrophic lateral sclerosis (ALS). Clinical studies have identified several rare but definable causes for apparent ALS. Certain clinical features previously considered unlikely to occur in ALS are found on careful examination. Epidemiologic surveillance and recent studies of neurotoxic plant seeds used in Guam have shed light on the pathogenesis of endemic ALS. Extensive analyses of biochemical, metabolic, immunologic, viral, and toxic factors have provided provocative results requiring further studies. Reflecting on some of these hypotheses, therapeutic trials have been performed more vigorously than ever. Amyotrophic lateral sclerosis is now investigated at the molecular genetic level. Human autopsy and experimental animal studies have expanded our understanding of basic mechanisms involving motoneuronal degeneration. In the future, we must continue a relentless search for the pathogenesis of ALS, prospective clinical studies to define the limits of ALS, and well-designed, controlled therapeutic trials.

Amyotrophic Lateral Sclerosis↗
PubMed1987

Motor neuron disease and paraproteinemia.

We studied two patients with motor neuron disease and paraproteinemia. One had amyotrophic lateral sclerosis (ALS) and IgG lambda monoclonal gammopathy. The second had slowly progressive muscular atrophy and an IgM kappa paraprotein, followed by a biclonal gammopathy when an IgA kappa paraprotein appeared. Treatment with immunosuppressive agents and plasmapheresis lowered the serum concentration of the paraproteins. The ALS syndrome progressed despite therapy. The other patient improved, was stable for several years, but then deteriorated despite continued therapy.

Aged↗
PubMed1987

Sciatica: an early manifestation of thoracic vertebral osteochondroma.

We describe a 36-year-old woman with a thoracic vertebral osteochondroma who presented with radicular leg pain. This benign tumor is uncommon in the vertebral column, and radicular pain is an unusual manifestation of a thoracic spinal lesion. Myelography and computed tomography aided in diagnosis; surgical resection resulted in an excellent clinical response.

Adult↗
PubMed1986

Neuropathy associated with cryoglobulinemia.

A patient with severe subacute sensory ataxia was found to have an IgM (kappa) cryoglobulin. Clinical, electrophysiologic, and sural nerve biopsy studies indicated that axonal degeneration and segmental demyelination both played a role in the pathogenesis of this neuropathy. Corticosteroid therapy was associated with notable clinical improvement and a 50% decrease in cryoglobulin concentration.

Adenocarcinoma↗
PubMed1986

Motor fibers in the sural nerve.

In an ischemia-induced model of an acute motor neuron disorder, there is anterior horn cell damage with Wallerian degeneration in ventral roots; dorsal root ganglia and dorsal roots are unaffected. In a mixed nerve there is axonal degeneration reflecting loss of motor fibers. The sural nerve is normal showing that it does not contain motor fibers. This observation is relevant to the neuropathology of motor neuron disease where axonal degeneration found in the sural nerve suggests involvement of sensory fibers.

Animals↗
PubMed1986

Perineuritis and ulcerative colitis.

We describe the association of chronic polyneuropathy with ulcerative colitis. Electrophysiologic studies disclosed a severe neuropathy with both axonal and demyelinating features. The CSF protein content was 875 mg/dl. Sural nerve biopsy revealed perineuritis. Peripheral neuropathy with perineuritis may be an immunologically mediated extraintestinal manifestation of ulcerative colitis.

Colitis, Ulcerative↗
PubMed1986

Slow resolution of multifocal weakness and fasciculation: a reversible motor neuron syndrome.

A 25-year-old man with multifocal weakness and fasciculation was thought to have motor neuron disease. Signs progressed for 1 year, plateaued, and 3 years later resolved almost completely. There was no evidence of paraproteinemia, lymphoproliferative disorder, or vasculitis, and myelography was normal. Electrodiagnostic study disclosed multifocal, acute and chronic denervation that evolved into a picture consistent with residuals of old multifocal radiculopathy without active denervation. Prolongation of F response, absence of H-reflex, and conduction block in a proximal nerve segment suggested multifocal demyelination. A proximal motor neuropathy, perhaps demyelinating, may cause some of the benign motor neuron syndromes that simulate motor neuron disease.

Adult↗