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Biomedical subjects

I Osorio

Publications and source records attributed to I Osorio.

35 records · Page 2Linked to original sources
PubMed1990

The characteristics and mechanisms of visual disturbance associated with anticonvulsant therapy.

Eight epileptic patients receiving anticonvulsants had recurrent visual disturbances in the form of diplopia and oscillopsia in the horizontal or vertical planes. The symptoms could be ascribed to impaired vergence mechanisms, vertical nystagmus, or abnormalities of the vestibulo-ocular reflex. Other eye movements, such as pursuit and gaze-holding, were also affected, but did not lead to complaints. Episodes of visual disturbance were often preceded by prodromes of ocular or systemic discomfort, after which oscillopsia or diplopia evolve rapidly. The symptomatology was stereotyped but unique for each patient and may reflect idiosyncratic susceptibility to the ocular motor side effects of anticonvulsants. Six of the 8 patients were taking carbamazepine and phenytoin in combination, which have similar effects on the ocular motor system.

Adult↗
PubMed1985

Activity of respiratory neurons during NREM sleep.

The purpose of this study was to analyze differences in the activity of medullary respiratory neurons in the unanesthetized, intact cat during wakefulness and non-rapid-eye-movement (NREM) sleep. We studied single respiratory neurons located within a 1-2 mm deep, 8-10 mm long zone that followed, and included in its dorsal aspect, the retrofacial and ambiguus nuclei. The analysis of variance was used to detect respiratory activity, and cycle-triggered histograms were plotted. The respiratory signal strength and consistency of the respiratory activity were quantified with the eta 2 statistic. We determined for each breath in wakefulness and NREM sleep the average discharge rate during the active phase of the cell, the number of action potentials during the active phase of the cell, and durations of both the cycle and inspiration. Differences in discharge rates and in the number of discharges between wakefulness and NREM sleep were tested with the t test. A bimodal distribution of eta 2 values for the population of neurons indicated there were two groups of respiratory cells: those with eta 2 values less than 0.3 and those with values greater than 0.3. The former we call weak respiratory cells; the latter, strong respiratory cells. Strong and weak cells were classified further as inspiratory or noninspiratory on the basis of the shape of their cycle-triggered histograms. Within the class of strong inspiratory cells, those with the highest eta 2 values 1) reached their peak discharge rate early, 2) discharged at high rates throughout inspiration, and 3) were inactive during expiration. The values of these variables diminished progressively in inspiratory cell groups with lower eta 2 values. Most cells were less active in NREM sleep than in wakefulness. Similar proportions of weak and strong cells and inspiratory and noninspiratory cells were affected by sleep. The reduction in sleep of the activity of strong inspiratory cells was consistent with a general relationship between this activity and the duration of inspiration. Lower discharge rates were associated with longer breaths; higher rates with shorter breaths. This relationship existed within both NREM sleep and wakefulness, and the plot of the relationship across these states formed a continuous function. The reduction in discharge rate in sleep was greater for weak than for strong inspiratory cells: the correlation coefficient between percent change in rate and eta 2 values was -0.636 for inspiratory cells, but it was not significant (-0.265) for noninspiratory cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1985

Epileptic gaze deviation and nystagmus.

We studied a patient with stereotyped focal seizures characterized by leftward conjugate eye- and head-turning followed by nystagmus. Eye deviation was associated with the appearance of seizure activity, recorded over the right temporo-occipital scalp, that did not spread frontally. The initial eye deviation consisted of a staircase of small saccades. The subsequent nystagmus showed rightward decreasing-velocity exponential slow phases and normal leftward quick phases. Saccadic eye movements due to seizures may occur via projections from posterior cortical areas as well as from the frontal eye fields.

Aged↗
PubMed1980

Absence of REM and altered NREM sleep in patients with spinocerebellar degeneration and slow saccades.

The pontine tegmentum contains the neurons responsible for generation of saccadic eye movements and certain phases of sleep. We studied two genetically unrelated patients with spinocerebellar degeneration and slow saccadic eye movements. Multiple all-night sleep studies in both patients disclosed absence of REM and stage 4 sleep with an extremely short stage 3 and long stage 2. Both patients had a sleep stage (X) not previously reported. These are the first awake and ambulatory humans in whom consistent absence of REM sleep has been demonstrated. Both behaved appropriately during wakefulness and showed no overt psychological abnormalities.

Adult↗
PubMed1979

gamma-Hydroxybutyric acid is not a GABA-mimetic agent in the spinal cord.

gamma-Hydroxybutyric acid (GHB), a pharmacologically active central nervous system constituent, has been postulated to function as a gamma-aminobutyric acid (GABA) agonist. This hypothesis was tested directly on GABAergic synapses in isolated, superfused frog spinal cord. Addition of GHB to the superfusate produced effects on primary afferent terminals that were distinctly different from the effects of GABA. Thus, although both compounds depressed dorsal root potentials, GHB hyperpolarized terminals while GABA depolarized the same structures. The GABA responses were antagonized by bicuculline and picrotoxin, but these alkaloids did not change GHB's actions. In addition, GHB altered neither high-affinity uptake by cord slices, nor potassium-evoked release of tritiated GABA from them. GHB did not directly release GABA from spinal slices preloaded with [3H]GABA. These observations suggest that the central nervous system actions of GHB are not dependent upon its ability to activate GABAergic synapses or to modify GABAergic mechanisms.

Animals↗
PubMedDate not supplied

Treatment of refractory generalized tonic-clonic status epilepticus with pentobarbital anesthesia after high-dose phenytoin.

We report the results of treatment of refractory generalized tonic-clonic status epilepticus in 17 adults. Of 13 patients who received high-dose phenytoin (PHT, mean dose 23.8 mg/kg), seizure control was sustained in five patients. In 12 cases, anesthetic doses of pentobarbital rapidly suppressed convulsions, but sustained control required prolonged treatment. Break-through seizures were, in most cases, explained by inadequate serum pentobarbital concentrations, although we could not establish a therapeutic range of serum concentrations. EEG monitoring is necessary to assess the therapeutic response but is not a reliable index of depth of anesthesia. Some cases developed pharmacodynamic tolerance to pentobarbital. The most serious treatment complications were cardiorespiratory, but the most common and disabling side effects, although reversible, were neurologic. Fifteen patients were discharged from the hospital in stable condition; two patients died, but not as a direct consequence of treatment. Our results suggest a very good outcome of pentobarbital anesthesia for patients in refractory status epilepticus who are a reasonable medical risk and who receive optimal medical management.

Adolescent↗
PubMedDate not supplied

Phenytoin-induced seizures: a paradoxical effect at toxic concentrations in epileptic patients.

We examined the incompletely defined convulsant action of phenytoin (PHT) at toxic concentrations in humans. A retrospective chart review (1979-1985) yielded 96 cases (90 patients), meeting both clinical and laboratory criteria for PHT intoxication. Seven patients, all with epilepsy, had one or more seizures while toxic. However, in only two patients (2.1%) with serum concentrations of 93.2 and 69.7 micrograms/ml was a causal relationship deemed highly probable. Seizures did not occur in most toxic epileptic patients with total serum PHT concentrations as high as 85.1 micrograms/ml or in any of the nonepileptic patients with concentrations as high as 64.2 micrograms/ml. The lack of convulsant action of PHT in these patients suggests that seizure risk may be multifactorial and also that PHT is a weak convulsant. We conclude that PHT at very high concentrations can rarely exacerbate seizures or even precipitate generalized status in some epileptic patients, a paradoxical effect.

Adolescent↗
PubMedDate not supplied

Aggravation of penicillin-induced epilepsy in rats with locus ceruleus lesions.

The rate and pattern of development of seizures induced by penicillin injected intraperitoneally were determined in rats that had been depleted of brain norepinephrine (NE) by bilateral injections of the neurotoxin 6-OH dopamine into the locus ceruleus. Behavioral observations and scalp electrographic recordings were made after injection and the efficacy of NE depletion was determined by high performance liquid chromatography measurement of cortical levels of NE and its metabolites. We found that in comparison to sham-operated control rats, NE-depleted rats had a significantly shorter latency to first observable myoclonic jerk, the first epileptic discharge, the first convulsion with sustained epileptic discharges, and a longer duration of convulsions. We observed a similar electrographic pattern of multifocal spikes with bilateral synchrony in both groups. However, more of the control rats (six of 12) had convulsions as compared to the lesioned rats (four of 12). These findings are consistent with previous evidence that depletion of neocortical NE facilitates the development of epileptiform activity in the CNS; however, a convulsive state was not induced by NE depletion.

Animals↗
PubMedDate not supplied

Antiepileptic drug intoxication: factors and their significance.

A retrospective chart review (1979-1985) was performed to identify probable causes of intoxication with antiepileptic drugs (AEDs). We identified 141 patients meeting clinical and laboratory criteria for intoxication and 17 with clinical signs but with serum concentrations within the therapeutic range. The majority were epileptic patients; almost half were treated with monotherapy, most with phenytoin (PHT). The causes of intoxication in the epileptic patients were iatrogenic (41%), inappropriate dose self-adjustment (34%), suicide attempt (18%), inappropriate caretaker dose adjustment (9%), accidental ingestion (8%), unrecognized drug interaction (6%), and association with intercurrent illness (2%). Twenty-two patients had more than one probable cause of intoxication. In nonepileptic patients the causes were suicide attempt (50%), accidental ingestion (27%), and iatrogenic (23%). Most patients had signs of ocularmotor and vestibulocerebellar dysfunction. Rarely described manifestations of intoxication, such as seizures or choreoathethosis, were observed in a few patients. The average hospital stay was 6.9 days; there was no mortality, and all patients recovered fully. We conclude that AED intoxication is a major but preventable cause of morbidity and that suicide attempts are an important and underrecognized contributor in both epileptic and non-epileptic patients.

Accidents↗