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Biomedical subjects

N Pillay

Publications and source records attributed to N Pillay.

29 records · Page 2Linked to original sources
PubMed1986

Delayed evoked potentials in patients with ankylosing spondylitis.

Visual, brainstem auditory and somatosensory evoked potentials were studied in 30 patients with ankylosing spondylitis (AS). Twenty-four patients were male and 6 were female. The mean age was 44 years and the mean duration of AS was 16 years (range 1-34 years). Evoked potential abnormalities affecting the visual pathways were recorded in 18 (60%) patients. Somatosensory evoked potentials were abnormal in 19 (63%) patients, and 9 patients had impaired function on brainstem auditory evoked potentials. The pathophysiology of these abnormalities is unknown. We recommend that caution be exercised in interpreting delayed evoked potentials if multiple sclerosis is suspected in a patient with AS.

Adult↗
PubMed1984

Clinical application of evoked potentials.

Visual, brainstem and somatosensory evoked potentials have added new dimensions to electrophysiological studies. Signal averaging has made it possible to record low-amplitude electrical potentials in the nervous system in response to external stimuli. Clinical abnormalities are indicated by latency prolongations, furnishing objective evidence for suspected or subclinical disease. The tests are most extensively used for the diagnosis of multiple sclerosis. Other indications include hearing and visual evaluation, especially in neonates, diagnosis of brainstem and cerebellopontine angle tumours, monitoring the integrity of sensory function during surgery for scoliosis or neurosurgical procedures and differentiating toxic or metabolic causes of coma from irreversible structural lesions. The tests are non-invasive and considered in conjunction with the clinical data provide useful electrodiagnostic tools.

Adult↗
PubMed1984

Internuclear ophthalmoplegia and "optic neuritis": paraneoplastic effects of bronchial carcinoma.

A 56-year-old man developed bilateral internuclear ophthalmoplegia and "optic neuritis" as remote effects of a bronchial carcinoma. These clinical findings correlated pathologically with secondary demyelination of the medial longitudinal fasciculus and with round cell infiltration and adhesive arachnoiditis of the optic nerve. There was no evidence of CNS metastasis. "Optic neuritis" and internuclear ophthalmoplegia may be paraneoplastic effects of systemic cancer.

Carcinoma, Bronchogenic↗
PubMed1976

Cryptococcal meningitis: our experience in 24 black patients.

The records of 24 patients with cryptococcal meningitis, admitted to King Edward VIII Hospital in Durban, were reviewed. There were 21 adults and 3 children over periods of 10 and 18 years, respectively. Slightly more males were affected. The age distribution was fairly even. The common clinical presentations were headache, neck stiffness, mental changes, cranial nerve palsies and papilloedema. The diagnosis was proved by the presense of Cryptococcus neoformans in the cerebrospinal fluid (CSF) in 21 of the patients, and in pathological tissue in the remaining 3 patients. A significant percentage of patients presented with an initial polymorphonuclear leucocyte predominance in the CSF. The other CSF findings were elevated protein and low sugar levels. Tuberculosis was the common coexisting disease. We found the mortality rate of 58% to be very high and a significant number of patients died even after adequate treatment with amphotericin B either singly or in combination with 5-fluorocytosine.

Adolescent↗
PubMedDate not supplied

Electrographic and clinical correlates of secondary bilateral synchrony.

Reverting to the more strict definition of secondary bilateral synchrony (SBS) of Tukel and Jasper (1952), we reexamined clinical and EEG correlates of this phenomenon. SBS occurred in 57 of 10,410 consecutive patients (0.5%) recorded in our laboratory. SBS originated in the frontal lobe in 51% of patients, significantly more often than the incidence of frontal spikes among controls. The best indicator of SBS origin was the most active spike focus which localized the onset in 52 of the 57 patients (91%) and falsely identified the origin in only one. Other focal or lateralizing clinical and EEG features appeared each in a minority of patients and lateralized and/or localized SBS origin with the following incidences when present: seizure manifestations (86%), neurological examination (95%), focal delta (100%), focal or unilateral theta (100%), and offset of bisynchronous paroxysms (96%). However, the most active spike focus triggered SBS in all but two instances when these other features appeared. Reliability of such indicators of SBS origin may obviate the need for depth electroencephalography in such patients. The presence of more than one spike focus in 96% of patients and three or more foci in 77% suggests that SBS results from a complex interaction of multiple potentially epileptogenic regions, instead of spread from a single focus as previously thought.

Adolescent↗
PubMedDate not supplied

Phosphate energy metabolism during domoic acid-induced seizures.

The effect of domoic acid-induced seizure activity on energy metabolism and on brain pH in mice was studied by continuous EEG recording and in vivo 31P nuclear magnetic resonance (NMR) spectroscopy. Mice were divided into ventilated (n = 6) and nonventilated (n = 7) groups. Baseline EEG was 0.1-mV amplitude with frequence of > 30-Hz and of 4-5 Hz. After intraperitoneal (i.p.) administration of domoic acid (6 mg/kg), electrographic spikes appeared at increasing frequency, progressing to high-amplitude (0.1-0.8 mV) continuous seizure activity (status epilepticus). In ventilated mice, the [31P]NMR spectra showed that high-energy phosphate levels and tissue pH did not change after domoic acid administration or during the intervals of spiking or status epilepticus. Nonventilated mice showed periods of EEG suppression accompanied by decreases in the levels of high-energy phosphate metabolites and in pH, corresponding to episodic respiratory suppression during the spiking interval. In all animals, status epilepticus was followed by a marked decrease in EEG amplitude that progressed rapidly to isoelectric silence. [31P]NMR spectra obtained after this were indicative of total energy failure and tissue acidosis. In a separate group of ventilated mice (n = 4), domoic acid-induced status epilepticus was accompanied initially by an increase in mean arterial blood pressure (MAP) that slowly returned to baseline level. Isoelectric silence was accompanied by a decrease in MAP to 75 +/- 8 mm Hg. These experiments suggest that domoic acid-induced seizures are not accompanied by an increase in substrate demand that exceeds supply.

Adenosine Triphosphate↗
PubMedDate not supplied

Effect of sustained pyridoxine treatment on seizure susceptibility and regional brain amino acid levels in genetically epilepsy-prone BALB/c mice.

Epilepsy-prone and epilepsy-resistant substrains were selectively bred from a strain of BALB/c mice; audiogenic-sensitive epilepsy-prone animals showed enhanced sensitivity to chemical convulsants. Treatment with pyridoxine (100 mg/L in drinking water) initiated at mating and continued throughout pregnancy and the life of the offspring abolished the enhanced sensitivity to chemical convulsants and reduced the severity of audiogenic seizures. Withdrawal of pyridoxine restored the enhanced seizure sensitivity. [1H] Nuclear magnetic resonance (NMR) spectroscopy of perchloric acid extracts of tissue was used to determine the concentrations of several compounds [N-acetylaspartate (NAA), GABA, glutamate, aspartate, alanine, taurine, creatine, cholines, inositol] in the hippocampus, neocortex, brainstem, and cerebellum of untreated and pyridoxine-treated 6-week-old female animals. The ratios of the concentrations of excitatory to inhibitory putative neurotransmitter amino acids tended to be higher in epilepsy-prone animals, with the most pronounced difference being a significantly elevated glutamate/GABA ratio in every brain region examined. Pyridoxine treatment abolished this imbalance in the hippocampus, brainstem, and cerebellum, but not in the neocortex. Treatment of epilepsy-resistant animals with pyridoxine using the same protocol decreased the glutamate/GABA concentration ratio in the hippocampus, brainstem, and neocortex and resulted in impaired development of the animals. The amino acid imbalance and the accompanying seizure susceptibility in these genetically epilepsy prone mice may originate from an inborn error in pyridoxine metabolism or in a pyridoxine-dependent enzyme system.

Acoustic Stimulation↗