Biomedical subjects

Bruce V Taylor

Publications and source records attributed to Bruce V Taylor.

5 recordsLinked to original sources

PubMed2006

Utility of serum Campylobacter specific antibodies in determining prior Campylobacter infection in neurological disease.

Campylobacter jejuni has been implicated in the pathogenesis of Guillain-Barre syndrome (GBS); however, little information exists on the utility of Campylobacter serology in determining recent infection in the patient population. C. jejuni specific antibodies (CAs) were measured in 420 blood donors (controls), 99 patients with recent C. jejuni infection, 34 patients with central nervous system disorders (neurology controls), and 44 patients with peripheral nervous system (PNS) disorders: 18 with GBS, 12 with MND and 14 with chronic inflammatory neuropathies. Elevated CA titres consistent with recent C. jejuni infection were found in six of the 44 patients with PNS disorders (three with GBS, two with neuropathy, and one with MND, only one of whom had a history of recent C. jejuni infection), compared with two of 454 controls (p = 0.00001). Therefore, we conclude that CAs are often raised in patients with PNS disorders who do not have a history of recent C. jejuni gastroenteritis, so Campylobacter serology may be an unreliable marker of recent infection in this patient group.

Acute Disease↗

PubMed2005

Diabetic neuropathies. Classification, clinical features, and pathophysiological basis.

Diabetes mellitus is associated with a wide spectrum of neuropathy syndromes, ranging from a mild asymptomatic distal sensory neuropathy to a severe disabling radiculoplexus neuropathy. As the pathophysiology of these separate conditions is better understood, classification of the various phenotypes becomes important because of treatment implications. Here we provide a short summary of the history of the classification of diabetic neuropathies and try to describe the most common forms classified according to their presumed pathophysiology. We have tried to include epidemiological data where available, as well as histopathology of nerve in several diabetic neuropathies.

Diabetic Neuropathies↗

PubMed2004

Diabetic amyotrophy progressing to severe quadriparesis.

Diabetic amyotrophy is a distinctive form of diabetic neuropathy usually characterized by the abrupt onset of pain and asymmetric proximal leg weakness and wasting. Involvement of the upper limbs is unusual, and prognosis is said to be good. We describe two patients, each with type II diabetes mellitus, who presented with diabetic amyotrophy progressing to severe quadriparesis. One patient remains severely disabled. The clinical spectrum of diabetic amyotrophy includes progression to severe quadriparesis.

Diabetes Mellitus, Type 2↗

PubMed2004

Multifocal motor neuropathy: pathologic alterations at the site of conduction block.

The pathologic changes of nerves in multifocal motor neuropathy (MMN), a rare neuropathy with selective focal conduction block of motor fibers in mixed nerves, remain essentially unstudied. Fascicular nerve biopsy of 8 forearm or arm nerves in 7 patients with typical MMN was undertaken for diagnostic reasons at the site of the conduction block. Abnormalities were seen in 7 of 8 nerves, including a varying degree of multifocal fiber degeneration and loss, an altered fiber size distribution with fewer large fibers, an increased frequency of remyelinated fiber profiles, and frequent and prominent regenerating fiber clusters. Small epineurial perivascular inflammatory infiltrates were observed in 2 nerves. We did not observe overt segmental demyelination or onion bulb formation. We hypothesize that an antibody-mediated attack directed against components of axolemma at nodes of Ranvier could cause conduction block, transitory paranodal demyelination and remyelination, and axonal degeneration and regeneration. Alternatively, the antibody attack could be directed at components of paranodal myelin. We favor the first hypothesis because in nerves studied by us, axonal pathological alteration predominated over myelin pathology. Irrespective of which mechanism is involved, we conclude that the unequivocal multifocal fiber degeneration and loss and regenerative clusters at sites of conduction block explains the observed clinical muscle weakness and atrophy and alterations of motor unit potentials. The occurrence of conduction block and multifocal fiber degeneration and regeneration at the same sites suggests that the processes of conduction block and fiber degeneration and regeneration are linked. Finding discrete multifocal fiber degeneration may also provide an explanation for why the functional abnormalities remain unchanged over long periods of time at discrete proximal to distal levels of nerve and may emphasize a need for early intervention (assuming that efficacious treatment is available).

Adult↗

PubMed2004

Neuroglial responses to CNS injury: prospects for novel therapeutics.

Immune-mediated therapies can reduce the relapse rate in multiple sclerosis. However, there is no clear-cut evidence that any of these therapies substantially alter the long-term outcome for patients with progressive multiple sclerosis. The neurological disability that all too frequently accompanies multiple sclerosis is ultimately due to injury to target cells, principally oligodendroglia, within the nervous system. Recent data suggest that activation of leukemia inhibitory factor-receptor signaling is an important component of a neurobiological response that serves to limit the extent of immune-mediated injury. Therefore, inactivation of this pathway could provide a novel approach to the treatment of demyelinating disease.

Animals↗