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Biomedical subjects

G J Parry

Publications and source records attributed to G J Parry.

At least 55 records · Page 3Linked to original sources
PubMed1992

Multifocal motor neuropathy.

We believe that our present understanding of these syndromes is insufficient to separate CIDP from MMN clearly and consider MMN to be a remarkably multifocal, predominantly motor variant of CIDP with the very unusual electrophysiologic feature of conduction block confined to motor axons. Further studies are clearly needed to clarify fully the relationship between CIDP and MMN and the relationship of MMN and other motor syndromes to various ganglioside antibodies.

Autoimmune Diseases↗
PubMed1991

Effect of piroxicam on the blood-retina barrier in experimentally induced diabetes in rats.

The effect of piroxicam on the blood-retina barrier was evaluated in rats with experimentally induced diabetes. Diabetes was induced in rats by intraperitoneal injection of streptozocin (STZ). Diabetic rats were divided into two equal groups: those treated with piroxicam, a long-acting platelet inhibitor, and an untreated control group. Vitreous fluorophotometry (VFP) was performed both before and two weeks after induction of diabetes and piroxicam intake. Streptozocin-induced diabetes caused an alteration in the blood-retinal barrier evidenced by an increase in vitreous fluorescein concentration in diabetic rats compared with normal rats. Piroxicam intake did not lead to significant change in vitreous fluorescein concentrations. However, the examination had to be terminated at two weeks because of cataract formation. The piroxicam treated group showed less incidence of lens opacity formation (59.1% compared to 81.8% in the untreated group, p = 0.0006). Piroxicam administration appears to protect the diabetic rat eye against lens opacification.

Animals↗
PubMed1991

Clinical and electrophysiological assessments in ALS patients.

Since the relationships between traditional assessments in ALS patients have not been defined, three clinical and four electrophysiological assessments were performed in a cross-sectional study of 87 ALS patients. The clinical assessments produced Norris ALS scores, muscle strength scores and illness durations (DUR). The electrophysiological assessments produced scores for motor unit interference pattern, denervation potentials, compound muscle action potential, and fasciculations. The individual muscle scores were averaged to produce mean scores, and Spearman rank correlations were performed on the mean scores. The association between Norris ALS and mean muscle strength (MMS) scores is significant (p less than .001, rs = 0.84), and these scores are significantly correlated with mean interference pattern (0.77, 0.82), mean denervation potential (-0.63, -0.70), and mean compound muscle action potential scores (0.55, 0.60), respectively. Correlations between IP and DP scores (-0.71), IP and CMAP scores (0.62), and DP and CMAP (-0.56) scores are also significant. Scatterplots of the data and regression lines suggest linear relationships between each of these assessments. Illness duration and fasciculation scores are not strongly correlated (rs less than 0.55) with any of the other clinical or electrophysiological assessments.

Amyotrophic Lateral Sclerosis↗
PubMed1991

The effect of aminoguanidine on the blood-retinal barrier in streptozocin-induced diabetic rats.

The effect of aminoguanidine hydrochloride (AG) on the blood-retinal barrier was studied in rats with streptozocin-induced diabetes. Half of the rats were given AG (100 mg/kg/day) while the remainder received no treatment. Vitreous fluorophotometry was performed on all rats before STZ injection and 2 weeks after induction of diabetes mellitus. Two weeks after STZ injection the mean 60-minute vitreous fluorescein concentration following dye injection had increased more in the nontreated group than in the AG-treated group, suggesting that AG may have some beneficial effect on the breakdown of the blood-retinal barrier.

Animals↗
PubMed1991

Effect of pyridoxine on the blood-retina barrier in experimentally induced hyperglycemia in rats.

We studied the effects on the blood-retina barrier of pyridoxal S phosphate, the biologically active form of vitamin B6 (pyridoxine), in 23 male Long-Evans rats in which hyperglycemia had been induced by means of intraperitoneal injection of streptozocin. Twelve rats were treated with pyridoxine, and 11 rats served as the control group. Vitreous fluorophotometry was used to quantitatively evaluate the effect of pyridoxine. The procedure was done before and 2 weeks after the induction of hyperglycemia, readings being taken 5 and 60 minutes after injection of the dye. In both groups the mean vitreous fluorescein levels after hyperglycemia was induced were significantly higher than those before hyperglycemia was induced (p less than 0.05). The mean levels before hyperglycemia was induced were not significantly different between the two groups. The mean level 60 minutes after injection of the dye after hyperglycemia was induced was lower in the treated group than in the untreated group, although not significantly so. The incidence of lens opacities at 5 weeks was higher in the untreated group than in the treated group (p less than 0.01). We conclude that administration of pyridoxine to hyperglycemic rats for 5 weeks has no significant effect on the permeability of the blood-retina barrier.

Animals↗
PubMed1990

Normocalcemic tetany abolished by calcium infusion.

Tetany is a disorder of increased neuronal excitability usually associated with hypocalcemia. We studied a patient with typical tetanic cramps that responded to intravenous infusion of calcium despite normal serum concentrations of total and ionized calcium. Three generations were affected by similar symptoms, suggesting that this is a dominantly inherited disorder of neuronal hyperirritability.

Action Potentials↗
PubMed1990

Peripheral neuropathy associated with eosinophilia-myalgia syndrome.

In 1989, the Centers for Disease Control recognized the existence of an epidemic illness characterized by myalgia and eosinophilia in individuals taking preparations containing L-tryptophan. We evaluated 3 patients with eosinophilia-myalgia syndrome who presented with subacute progressive neuropathies. The neuropathies were predominantly motor and maximal in the lower extremities. Two patients were confined to a wheelchair and one was ventilator-dependent and bedridden. Sensory loss predominantly involved small fiber modalities. Electrophysiological studies showed multifocal marked conduction slowing and conduction block indicating segmental demyelination, with associated axonal degeneration that was accentuated distally. Examination of sural nerve biopsy specimens demonstrated axonal degeneration in all 3 patients and perivascular infiltrates in 2. Levels of quinolinic acid, a neurotoxic metabolite of L-tryptophan, were elevated in the cerebrospinal fluid in the 2 patients in whom it was measured. The cause of the neuropathy is unknown but may include immune mechanisms or toxicity of eosinophils, L-tryptophan, its metabolic products, or contaminants within L-tryptophan preparations.

Adult↗
PubMed1990

Acute changes in blood glucose affect resistance to ischemic nerve conduction failure.

We studied resistance to ischemic nerve conduction failure (RINCF) following rapid alterations of blood glucose in normal and diabetic rats. We measured RINCF hourly for 4 hours in normal and diabetic rats. We then made normal rats hyperglycemic and diabetics euglycemic. In normal rats, we measured RINCF sequentially for 4 hours immediately after glucose injection and once after 1, 2, 3, or 4 hours of hyperglycemia. In diabetics, we measured RINCF sequentially for 4 hours after insulin injection. In normal rats, in sequential measurements, RINCF progressively fell but glucose injection prevented this fall. Hyperglycemia without preceding ischemia increased RINCF. In diabetic rats, sequential measurements also produced a decline in RINCF, accentuated with insulin injection. The results suggest that both glucose and insulin are important in determining the response of peripheral nerve to ischemia. They also underscore the importance of knowing the blood glucose and time of most recent insulin injection when measuring RINCF.

Animals↗
PubMed1990

Lower motor neuron disease in a patient with autoantibodies against Gal(beta 1-3)GalNAc in gangliosides GM1 and GD1b: improvement following immunotherapy.

We followed a patient with a lower motor neuron form of motor neuron disease whose neurologic disorder improved following immunotherapy. The patient did not have an M protein but did have IgM antibodies to ganglioside GM1 detectable at serum titers of 1:2,000 by ELISA. These antibodies were found only in the IgM fraction with lambda light chains and immunoreacted with GD1b and Gal (beta 1-3) GalNAc.

Adult↗
PubMed1990

Piroxicam may reduce the rate of progression of experimental diabetic neuropathy.

We studied the effect of piroxicam, a long acting inhibitor of platelet aggregation, on the evolution of neuropathy in diabetic rats. We treated half of the rats with piroxicam and serially studied sensory and motor nerve conduction during 20 weeks of diabetes. The sensory nerve action potential amplitude was the same in treated and untreated rats before diabetes, and declined steadily as duration of diabetes increased. In treated rats, the amplitude fell more slowly and by 16 weeks and thereafter was significantly higher than in untreated rats. Sensory conduction velocity and motor nerve conduction studies were not affected by piroxicam treatment. The results suggest that piroxicam may slow the rate of progression of neuropathy in diabetic rats, probably by inhibiting platelet aggregation.

Action Potentials↗
PubMed1989

Studies of resistance to ischemic nerve conduction failure in normal and diabetic rats.

Increased resistance to ischemic nerve conduction failure (RINCF) has been demonstrated in the spontaneously diabetic BB Wistar rat as well as in non-insulin dependent but hyperglycemic litter-mates. There is marked variability in the severity of the ischemic resistance in insulin dependent rats but not in the non-insulin dependent litter-mates suggesting that the administration of insulin could acutely alter RINCF. We therefore studied the effects of rapid normalization of the blood glucose on RINCF in diabetic rats. Injection of insulin produced a rapid fall in blood glucose to normal levels by 2 h. This was closely followed by a significant fall in RINCF which reached normal levels by the time that the blood glucose had been normal for 2 h. These results suggest that increased RINCF in diabetes is a function of the availability of substrate for energy metabolism which is directly related to the blood glucose concentration and underscores the importance of measuring the blood glucose level whenever measurements of nerve function are made.

Animals↗
PubMed1989

Diabetic truncal neuropathy presenting as abdominal hernia.

Two patients with longstanding type II diabetes mellitus presented with focal, unilateral protrusion of the abdominal wall, thought to be due to abdominal hernia. They were evaluated extensively for intra-abdominal pathology but none was found. In one patient, the protrusion was associated with spontaneous burning pain and hyperpathia, but in the other it was painless. In the patient seen during the acute phase there was denervation in paraspinal and abdominal muscles on EMG examination. In both patients, the protrusion subsided without specific treatment in 2 to 4 months. This seldom-described manifestation of diabetic truncal neuropathy masquerading as abdominal hernia needs a higher profile to avoid misdiagnosis and unnecessary investigation. Diagnosis may be quickly established by EMG examination of the paraspinal and abdominal muscles.

Abdomen↗
PubMed1988

Peripheral neuropathies associated with human immunodeficiency virus infection.

Peripheral neuropathies may complicate all stages of infection with human immunodeficiency virus (HIV). Acute inflammatory demyelinating polyneuropathy, sensory ganglioneuritis, and acute cranial nerve palsy all may occur 2 to 3 weeks after acute HIV infection. Acute inflammatory demyelinating polyneuropathy, chronic inflammatory demyelinating polyneuropathy, and polyradiculopathy may occur with otherwise asymptomatic HIV virus infection. Neuropathy is one of the most common neurological manifestations of the acquired immunodeficiency syndrome (AIDS)-related complex, occurring in as many as 20% of these patients. Acute or chronic inflammatory demyelinating polyneuropathy (38%) and mononeuropathy multiplex (29%) are most frequently seen, and usually there is a good prognosis, with the neuropathy resolving spontaneously or with steroids or plasmapheresis. Neuropathy occurring with AIDS is reportedly uncommon but probably is underreported, especially in seriously ill patients. By contrast with AIDS-related complex, the neuropathy associated with AIDS is usually a distal symmetrical polyneuropathy (72%), with inflammatory neuropathy, mononeuropathy multiplex, and polyradiculopathy occurring rarely. The pathogenesis of acute or chronic inflammatory demyelinating polyneuropathy and possibly of mononeuropathy multiplex is probably autoimmune. The pathogenesis of distal symmetrical polyneuropathy is less clearly established and may be infectious, toxic, or nutritional. Polyradiculopathy most likely is infectious; cytomegalovirus is a leading contender for infectious agent, but herpes simplex virus and HIV are other possibilities.

AIDS-Related Complex↗
PubMed1988

Multifocal acquired demyelinating neuropathy masquerading as motor neuron disease.

We report five patients with pure motor neuropathy characterized by multifocal weakness, muscle atrophy that was sometimes profound, cramps, and fasciculations with relatively preserved reflexes. The clinical picture led to an initial diagnosis of motor neuron disease in all cases, but nerve conduction studies revealed multifocal conduction block confined to motor axons and predominantly involving proximal nerve segments. Routine sensory nerve conduction studies, ascending compound nerve action potentials, and somatosensory evoked potentials were all normal even through nerve segments in which motor conduction was severely blocked. Onset of symptoms was insidious, and progression was indolent. In two cases, after many years of neuropathy, sensory abnormalities developed but remained clinically trivial. These unusual cases probably have the same pathogenesis as previously described patients with persistent multifocal conduction block. Distinction from motor neuron disease is critical, since chronic demyelinating neuropathy may respond to treatment.

Action Potentials↗
PubMed1988

The spectrum of peripheral neuropathy associated with ARC and AIDS.

Peripheral neuropathy is increasingly recognized as a complication of the Acquired Immune Deficiency Syndrome (AIDS) and AIDS-related complex (ARC), but the varied clinical features have been incompletely described. Thirty homosexual men with peripheral neuropathy were evaluated in this study. Twenty-one had ARC and nine had AIDS. Four distinct clinical syndromes were recognized: distal sensorimotor polyneuropathy, chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), mononeuropathy multiplex, and progressive polyradiculopathy. Four patients with clinical, electrophysiologic, and histologic evidence of CIDP and severe progressive weakness improved with plasma exchange, three regaining normal function.

AIDS-Related Complex↗
PubMed1988

Conduction block without demyelination following acute nerve infarction.

Incomplete infarction of the tibial nerve was produced in 37 rats by injecting arachidonic acid into the femoral artery. Sciatic-tibial motor nerve conduction studies were performed 1, 2, 3 and 7 days later. In all animals the evoked motor responses were of low amplitude and morphological examination showed axonal degeneration. In 20 rats the response elicited by proximal stimulation was of lower amplitude than the distal response indicating focal conduction block in a proportion of those axons which had survived the ischemia and were not degenerating distally. The conduction block resolved over several days and in all but one rat had disappeared by 7 days. Morphological examination of semithin sections and single teased myelinated axons revealed no evidence of segmental demyelination. The rapid resolution of conduction block and the lack of significant segmental demyelination suggest that it has a metabolic basis. We suggest that hypoperfusion of the subperineurial region of the proximal tibial nerve, the region surrounding the infarct through which surviving axons pass, may be sufficient to temporarily block impulse transmission in these surviving axons without producing morphological changes.

Action Potentials↗