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Biomedical subjects

G J Parry

Publications and source records attributed to G J Parry.

70 records · Page 4Linked to original sources
PubMed1988

Relative utility of different electrophysiologic techniques in the evaluation of brachial plexopathies.

We report the results of detailed electrophysiologic studies in 23 patients with suspected brachial plexopathies. In five with neurogenic thoracic outlet syndrome, needle EMG and determination of size of ulnar sensory nerve action potentials (SNAPs) and thenar M waves were important in localizing the lesion; F-response and somatosensory evoked potential (SEP) studies were of more limited utility. All electrodiagnostic studies were normal in 10 patients with nonneurogenic thoracic outlet syndrome. In traumatic (three patients) or idiopathic brachial plexopathy (five patients), needle EMG was especially helpful but, in the former, SEP studies helped to guide management and, in the latter, to confirm the proximal site of the lesion when peripheral SNAPs were normal. The presence of preserved but small SNAPs but absent M waves in patients with traumatic plexopathies suggested a combined pre- and postganglionic lesion.

Action Potentials↗
PubMed1988

Mononeuritis multiplex: the yield of evaluations for occult rheumatic diseases.

We identified 35 patients who had electrodiagnostic evidence of mononeuritis multiplex and did not have diabetes or multiple nerve compressions. Their charts were reviewed to determine the etiologies of the mononeuritis multiplex and to determine how often the laboratory examination revealed a rheumatic disease in patients whose initial history and physical examination did not suggest that a rheumatic disease was present. In 11/35 (31%; CI = 17-49) a disorder capable of causing mononeuritis multiplex was diagnosed before the symptoms of mononeuritis multiplex began. Ten had a rheumatic disease; 1 had lymphoma. Nine of the other patients were suspected, on the basis of the history and physical examination, of having new onset of a rheumatic disease. Subsequent laboratory evaluation showed that 5/9 (56%; CI = 21-86) had a rheumatic disease, and 4/9 (44%; CI = 14-79) were unknowns. In 15/35 (43%; CI = 26-61) patients with mononeuritis multiplex, no rheumatic disease was suspected on the basis of the initial history and physical examination. The subsequent laboratory examination revealed an underlying rheumatic disease in 0/15 (0%; CI = 0-18). Mean clinical follow-up of 16 +/- 16 months in the patients with mononeuritis multiplex of unknown cause also failed to identify a rheumatic disease. Overall 19/35 (54%; CI = 37-71) did not have a rheumatic disease or any other known cause. Of the 14 patients with mononeuritis multiplex associated with a rheumatic disease, 5/14 (36%; CI = 13-15) had systemic lupus erythematosus; an additional patient had both lupus and the CREST syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)

Biopsy↗
PubMed1987

Somatosensory evoked potentials in chronic acquired demyelinating peripheral neuropathy.

We recorded somatosensory evoked potentials (SEPs) over the scalp in eight patients with chronic acquired demyelinating peripheral neuropathy. They were obtained from 15 nerves in which sensory nerve action potentials (SNAPs) were absent or not more than 1 microV, but from which motor responses could be elicited. Motor and sensory (SEP-derived) conduction velocity was determined from the difference in response latency with wrist and elbow stimulation. In 11 nerves, afferent conduction velocity was slowed. In 10, there was relatively equal slowing in sensory and motor axons, whereas in 1 there was disproportionate slowing in afferent fibers. In four nerves, afferent conduction velocity was within the normal range despite slowing of motor conduction. We conclude that SEPs may be useful in evaluating peripheral sensory conduction in the absence of SNAPs, but can provide misleadingly normal data, presumably because of central amplification of an attenuated response arising from a few axons that conduct normally.

Adult↗
PubMed1986

Transient focal conduction block following experimental occlusion of the vasa nervorum.

Injection of low-dose arachidonic acid into the rat femoral artery occludes the vasa nervorum of the tibial nerve and produces focal and generalized ischemia with transient effects on nerve conduction. Across a severely ischemic segment of the proximal tibial nerve there is a marked fall in amplitude of the compound muscle action potential (CMAP), indicating focal conduction block. There is also significant slowing of maximal motor conduction velocity (MCV) through this nerve segment, but no dispersion of the proximally elicited response. Distally, in a region of less severe ischemia, there is mild slowing of MCV, but no further decrement in the CMAP amplitude. The conduction block begins 5-15 minutes after injection, reaches a nadir at 30 minutes, and persists in more severe cases for at least 2 hours. Despite these prolonged electrophysiologic abnormalities, there is no evidence of axonal degeneration or segmental demyelination.

Action Potentials↗
PubMed1986

Gammopathy with proximal motor axonopathy simulating motor neuron disease.

We report a 38-year-old man with a pure motor syndrome and IgM gammopathy leading to flaccid quadriplegia. Improvement followed treatment with dexamethasone, cyclophosphamide, and plasmapheresis, but he died of pulmonary embolism. At autopsy, he had a proximal motor axonopathy with lymphocytic infiltration of ventral roots. Proximal motor neuropathy may masquerade as motor neuron disease. The association with gammopathy and response to treatment suggest that patients with motor neuron disease should be routinely screened for serum protein abnormalities.

Adult↗
PubMed1985

Transient conduction block following acute peripheral nerve ischemia.

We studied the effects of transient focal ischemia on the electrophysiologic function of rat sciatic nerves. Focal and generalized impairment of impulse conduction, measured by falling evoked muscle and nerve compound action potential amplitudes, occurred within 10 minutes of femoral artery occlusion. Conduction failure reached a nadir at 45-60 minutes and then improved to normal within 24 hours. Fastest motor and mixed nerve conduction velocities were reduced less than 15% of baseline values during the period of acute conduction block. There were no detectable morphological abnormalities at the site of conduction failure. Transient ischemia produces reversible conduction block without evident structural changes. The fall in amplitude without significant conduction slowing implies that slower conducting myelinated fibers are relatively more sensitive to the effect of acute ischemia.

Animals↗
PubMed1985

Sensory neuropathy with low-dose pyridoxine.

We describe 16 patients with neuropathy associated with pyridoxine abuse. The clinical picture of a pure sensory central-peripheral distal axonopathy was consistent. Pyridoxine dose was 0.2 to 5 g/d, and duration of consumption before symptoms was inversely proportional to the daily intake. In all patients with adequate follow-up, improvement followed discontinuation of pyridoxine. The ready availability of up to 1-gram tablets makes it likely that this neuropathy will continue to be seen.

Adult↗
PubMed1985

Electrophysiologic evaluation of lumbosacral radiculopathies: electromyography, late responses, and somatosensory evoked potentials.

We compared the diagnostic utility of EMG, F wave and H-reflex studies, and peroneal and dermatomal SEPs in evaluating 28 patients with clinically unequivocal L-5 or S-1 compressive root lesions. The single most useful electrophysiologic technique was EMG, which often provided evidence of denervation in a myotomal pattern when other electrophysiologic findings were normal. We found abnormal late responses in 14 patients, but always in association with EMG abnormalities. Peroneal-derived SEPs were always normal. Dermatomal SEPs confirmed the diagnosis in seven patients, including two in whom other electrophysiologic studies were normal.

Adolescent↗
PubMed1984

Azathioprine in the treatment of myasthenia gravis.

Twenty-four patients with myasthenia gravis were treated with azathioprine. Eighteen of the patients tolerated the drug. Six discontinued azathioprine therapy because of toxicity. Of the 18 patients, 15 (83%) improved while receiving azathioprine; in 8 (44%) improvement was felt to result solely from azathioprine. Initial response was seen after 4 to 10 months of treatment, with a mean of 6.4 months. Patients continued to improve for up to 24 months, with the mean time of peak improvement being 14 months. Relapse occurred within one year in all 6 patients in whom azathioprine administration was discontinued. Azathioprine is a reasonable alternative to corticosteroids in selected myasthenic patients requiring immunosuppression.

Adult↗
PubMed1982

Selective fiber vulnerability in acute ischemic neuropathy.

To study the relationship between fiber size and vulnerability to ischemia, we produced partial infarction of the proximal posterior tibial nerve of Wistar rats by injecting arachidonic acid into the ipsilateral femoral artery. In the resulting lesion degenerating fibers were concentrated in the center of the nerve. Distal to the infarct, surviving myelinated and unmyelinated fibers were evenly distributed throughout both fascicles. Smaller myelinated fibers (less than 6 micrometers in diameter) were more severely depleted than larger ones ( greater than 6 micrometer). Unmyelinated fibers were reduced in number in proportion to or to a greater extent than myelinated fibers. These findings demonstrate that large myelinated fibers are relatively less vulnerable to peripheral nerve ischemia than smaller fibers, and do not support the contention that unmyelinated fibers are inherently resistant to acute ischemia.

Acute Disease↗
PubMed1981

Arachidonate-induced experimental nerve infarction.

Despite the clinical importance of ischemia in the pathogenesis of many human neuropathies, little is known about the effect of circulatory compromise on the structure of peripheral nerves. This results in part from the lack of an entirely satisfactory model in which to study ischemic neuropathy. We therefore injected arachidonic acid, a potent stimulus to platelet aggregation and vasoconstriction, into the femoral artery of normal rats. This resulted in the rapid onset of focal infarction of the proximal posterior tibial nerve in all animals. Distally there was evidence of Wallerian degeneration but not of primary ischemic damage. The site and nature of the infarct and the temporal sequence of the pathological changes were highly consistent. This new method is a simple and highly reproducible means of producing experimental nerve infarction.

Animals↗
PubMed1977

Concentration of clonazepam in serum and cerebrospinal fluid of the sheep.

Following intravenous administration of clonazepam to sheep there was rapid equilibration of cerebrospinal fluid and unbound serum concentrations of the drug. The pharmacokinetics of clonazepam in sheep describe a 2-compartment model and the large volume of distribution suggests tissue binding of clonazepam. There was wide variation in serum concentration and at least 2 mg of clonazepam was necessary to attain the recommended therapeutic concentration.

Animals↗
PubMed1976

An animal model for the study of drugs in the central nervous system.

An animal model which allowed repetitive sampling of CSF is described. It had a wide potential application and was used to study the passage of clonazepam into the central nervous system. A highly sensitive clonazepam assay is described which allow measurement of CSF and free serum concentrations as low as 0.5 ng/ml. Clonazepam passed rapidly into the central nervous system and its CSF concentration closely approximated to the concentration of unbound clonazepam in serum. Protein binding of clonzaepam in the sheep was 90-95%.

Animals↗
PubMedDate not supplied

Mononeuropathy multiplex (AAEE case report #11).

Mononeuropathy multiplex is a syndrome of diverse causes, the most common of which is nerve ischemia due to microangiopathy associated with diabetes or the collagen-vascular diseases. The acquired inflammatory demyelinating neuropathies invariably are multifocal, although the clinical manifestations of these and other multifocal neuropathies may appear symmetrical. The identification of multifocal neuropathies is important because of the frequent therapeutic implications. A case of mononeuropathy multiplex associated with polyarteritis nodosa is described.

Action Potentials↗