Biomedical subjects

Y G Comair

Publications and source records attributed to Y G Comair.

34 records · Page 2Linked to original sources

PubMed1995

Childhood ganglioglioma and medically intractable epilepsy. A clinicopathological study of 15 patients and a review of the literature.

Gangliogliomas are an increasingly recognized cause of epilepsy in children. Several studies have shown that early surgical treatment is beneficial, but controversy exists regarding the type of surgical treatment required for optimal seizure control and to prevent tumor recurrence. To address this issue, we performed a retrospective review of 15 children operated on at the Cleveland Clinic during a 7-year period with medically intractable epilepsy who were found to harbor a ganglioglioma during the course of their work-up. Nine patients with mostly nondominant hemisphere tumors underwent tumor resection without the use of electrocorticography to guide additional resection of epileptogenic foci, while 6 other patients with dominant hemisphere tumors had subdural electrode grids placed to extraoperatively map zones of ictal onset and eloquent areas. The extent of tumor resection was then correlated to seizure outcome and tumor recurrence. Of the 11 patients who received a gross total resection, 9 are seizure-free while 2 have a greater than 90% reduction in their seizure frequency (100% 'good' outcome). There was no tumor recurrence in this group. Of the 4 patients who underwent a subtotal tumor resection, 1 is seizure-free while 3 have persistent seizures (25% 'good' outcome). All patients in this group have stable disease on follow-up magnetic resonance imaging. In those patients who received subdural electrode grids, the extent of resection of the zones of ictal onset did not correlate with seizure outcome. The mean follow-up was 42 months. We conclude that complete tumor resection is the most important factor for optimal seizure control and to prevent tumor recurrence.

Adolescent↗

PubMed1995

Cortical electrical stimulation in humans. The negative motor areas.

Summarizing, we have presented evidence in humans for two "negative motor areas" which we had speculated play a significant role in the planning of voluntary motor movements. A review of the more recent experimental literature shows that histological, physiological, and electrical stimulation studies in animals reveal the existence of two frontal regions that from the experimental data also seem to play an essential role in the preparation (as opposed to execution) of voluntary movements. Current available evidence suggests that these two areas (areas F5 and F6 of Rizzolatti et al.) correspond to the negative motor areas we have described in human studies. Also of interest is that Broca's area in the dominant hemisphere overlaps the corresponding negative motor area. This observation suggests that Broca's area has evolved from area F5 of monkeys specializing in the planning of fine movements necessary for speech production. We feel that current evidence suggests the existence of three mechanisms by which cortical stimulation (by electrical stimulation or by epileptic activation) can generate negative motor phenomena: 1. The "silent period," which is consistently contralateral, has a somatotopic distribution, and tends to affect predominantly muscles involved in fine movements. It is of relatively short duration and seems to be generated by the activation of cortical areas in the primary sensorimotor region. The H-reflex is not inhibited during the silent period, suggesting that the silent period is generated by a decrease in the excitatory input through direct corticospinal neurons on the spinal alpha motoneurons. It is possible that in normal individuals this system is used for fine tuning of fine distal movements. The negative myoclonus seen in some patients with focal cortical epilepsy is probably generated by this mechanism. The primary and supplementary "negative motor areas" described in this chapter. This effect also has a somatotopic distribution but can affect muscle bilaterally even if there is a clear predominance contralaterally. The negative motor effect does not influence postural tone and can be prolonged. The negative motor effect is probably produced by activation of agranular cortex immediately in front of the primary and supplementary face motor area. These cortical areas are probably used for organization and integration of fine motor movement. Activation of these areas would produce an apraxia of fine movements. Focal atonic seizures are probably generated by this mechanism. 3. The fast-conducting corticoreticulospinal pathways, which by activation of the brainstem inhibitory centers (NRPo, n.r. magnocellularis dorsal beta, and NRGc), tend to produce bilateral atonia of axial, postural muscles. This system probably does not depend on the presence of the direct corticospinal pathways. By analogy with cataplexy, which is probably produced by activation of similar brainstem inhibitory systems, we would expect the H-reflex to be markedly diminished or even to disappear during the atomic phase (64). This pathway would be used normally for postural adjustments and locomotion. The bilateral massive atonic seizures, seen most frequently in patients with severe and diffuse cortical lesions, are probably produced by this mechanism. However, the bilateral atonic seizures occasionally seen in patients with focal cortical lesions may also be produced by a similar mechanism.

Brain↗

PubMed1994

Temporal lobe epilepsy: presurgical localization with proton chemical shift imaging.

PURPOSE: To assess two-dimensional phase-encoded proton chemical shift imaging for potential clinical application in presurgical localization of temporal lobe epilepsy (TLE). MATERIALS AND METHODS: Interictal chemical shift imaging studies were performed in 25 patients (17 unilateral, eight bilateral epileptogenic abnormalities) and 12 healthy volunteers. Results were compared with those of electroencephalography. For each temporal lobe, the volume of interest (VOI) included mesial, lateral, anterior, and posterior areas. RESULTS: The epileptogenic zone was characterized by an abnormal pattern of decreased signal intensity in the N-acetylaspartate (NAA) peak, either increased or unchanged choline (Cho) level relative to creatine (Cr) signal intensity, and, occasionally, elevated lactate level. NAA/Cho was the most sensitive and reliable quantitative marker for abnormality. The sensitivity and specificity of this technique compared with EEG were 90% and 85%, respectively. The difference in NAA/Cho between epileptogenic and normal temporal lobes was highly significant (P < .001). No statistically significant difference was found between normal temporal lobes and patients' uninvolved temporal lobes. CONCLUSION: NAA/Cho is an excellent marker for localizing the epileptogenic zone in TLE.

Adolescent↗

PubMed1993

The prevention of oxyhemoglobin-induced endothelial and smooth muscle cytoskeletal injury by deferoxamine.

The oxidized breakdown products of hemoglobin are important in the pathogenesis of cerebral vasospasm because of their effects on the endothelium and the smooth muscle of the arterial wall. Cytoskeletal changes in cultured vascular cells are sensitive indicators of oxidative injury. Cultured endothelial cells and smooth muscle cells showed a dose-related disruption of the cytoskeleton, particularly the F-actin and vimentin filaments, when exposed to 10(-5) M oxyhemoglobin. The cytoskeletal injury was prevented by the addition of 10(-3) M deferoxamine or 1% albumin. These experiments support a role for deferoxamine in the pharmacological treatment of vasospasm. Furthermore, cytoskeletal studies of cultured arterial endothelial and smooth muscle cells provide a novel in vitro approach by which to study the cellular mechanisms of oxidant injury initiated by the breakdown products of hemoglobin.

Actins↗

PubMed1992

Neuropathologic findings in cortical resections (including hemispherectomies) performed for the treatment of intractable childhood epilepsy.

Despite the use of hemispherectomy in the treatment of medically refractory seizures since the early 1950's, few studies published have documented neuropathologic findings in the resected specimens. This report describes the neuropathologic findings in 38 children who underwent either hemispherectomy or multilobar cortical resection as treatment for medically intractable epilepsy between 1986 and 1990. Examination of the resected specimens revealed a variety of abnormalities which fell into four broad categories. Malformations or hamartomatous lesions were the dominant finding in 15 patients, whereas encephalomalacic lesions were the most prominent abnormality in 16; chronic pathogen-free encephalitits (Rasmussen's encephalitis) was present in 3 and an additional 3 children had Sturge-Weber-Dimitri syndrome. There were no gross or microscopic abnormalities in 1 patient. This report provides the first comprehensive description of the pathologic findings in a series of children with refractory epilepsy of varying types treated by hemispherectomy-multilobar resection.

Brain Ischemia↗

PubMed1992

Morphological substrates of infantile spasms: studies based on surgically resected cerebral tissue.

Extensive surgical resections of neocortical cerebral tissue (including hemispherectomies) from 13 infants and children with infantile spasms showed that 12 of 13 specimens contained either malformative and dysplastic lesions of the cortex and white matter (sometimes with associated hamartomatous proliferation of globular cells), or destructive lesions possibly acquired as a result of anoxic-ischemic injury, or a combination of the two. In brain tissue from 4 patients, coarse neuronal cytoplasmic fibrils resembling neurofibrillary tangles were seen in areas of dysplastic brain on silver-stained (Bielschowsky technique) sections. Immunohistochemical (immunoperoxidase) study of cortical lesions containing globular cells employing primary antibodies to glial fibrillary acidic protein and synaptophysin as markers of astrocytic and neuronal differentiation, respectively, revealed that many cells showed astrocytic and/or neuronal features, suggesting the local proliferation of primitive or multipotential neuroectodermal cells as one substrate for this seizure disorder. Morphological abnormalities of a severe degree and wide extent in the resected tissue (e.g., in one patient with hemimegalencephaly) often showed features to suggest that they may represent variants of tuberous sclerosis. These most likely result from abnormal movement and/or local proliferation of neuroectodermal precursors that have migrated from the germinal matrix to the cortical mantle. Cellular, molecular and neurophysiological study of these abnormalities is likely to yield information about basic molecular mechanisms of brain malformation and injury important in the pathogenesis of infantile spasms and other forms of focal or generalized epilepsy.

Cerebral Cortex↗

PubMed1992

Temporal and extended temporal resections for the treatment of intractable seizures in early childhood.

In our series of 33 children who underwent temporal and extended temporal lobe resections because of seizures, the average age at surgery was 7 years, 11 months. Sixteen cases (48%) were diagnosed as having tumors: low-grade astrocytoma (6), hamartoma (5), and ganglioglioma/neuroma (5). Other pathologic diagnoses included one or more cytoarchitectural abnormalities and/or reactive changes. Due to a more aggressive and early radiologic and electrophysiologic investigation of children with seizures, a resectable focus, e.g. neoplasm or structural abnormality, was found in a much younger age group of patients than previously reported. In children who had intractable seizures but normal radiologic studies, positron emission tomography was of great value in localizing the seizure focus. In a group of children with infantile spasms, seizures were controlled following the identification and resection of a focal lesion. Prompt detection and precise localization of lesions in the temporal lobe in the pediatric population may lead to surgical management and seizure control.

Adolescent↗

PubMed1985

Pharmacological action of FPL 55712 on canine cerebral arterial segments.

The pharmacological action of a leukotriene antagonist FPL 55712 was studied on canine cerebral arterial segments. FPL 55712 at concentrations of 10(-6)M and 10)-5)M showed dose-dependent inhibition of the constrictor responses of the artery to prostaglandin F2 alpha. The constrictor responses of the artery to either serotonin or haemoglobin were suppressed by 10(-5)M FPL 55712, while 10(-6)M FPL 55712 failed to alter the responses. The KCL-induced constriction was not affected by treatment with either 10(-6)M or 10(-5)M FPL 55712. The present results suggest that FPL 55712 has vasodilator properties other than those related to the inhibition of leukotrienes.

Animals↗

PubMed1984

Time-dependent changes in cerebral and cardiovascular parameters in isoflurane-nitrous oxide-anesthetized dogs.

The purpose of this study was to examine the time-dependent effects of isoflurane-nitrous oxide anesthesia on cerebral blood flow and metabolism and on cardiovascular parameters. Eleven 15-kg mongrel dogs were anesthetized with 0.8% isoflurane (approximately 1.3 MAC (minimal anesthetic concentration], 70% nitrous oxide, and 30% O2 and were paralyzed with pancuronium. Blood flow (using the radioactive microsphere technique) and cerebrovascular and cardiovascular parameters were measured 6 times at 30-minute intervals beginning 2 hours after the induction of anesthesia. In this experiment, cerebral blood flow was markedly elevated at 2 hours after the induction of anesthesia, but then declined progressively by 40 to 50% over the 2 1/2-hour time period investigated, approaching values for normal awake dogs. The decline was accompanied by a progressive decrease in the cerebral metabolic rate of oxygen and a constant rise in cerebrovascular resistance. Blood flow to organs outside the central nervous system declined progressively, but with more variability between tissues. The mean arterial pressure increased slightly, and the peripheral vascular resistance almost doubled, but cardiac index, cardiac work, and stroke volume all decreased gradually. We conclude that isoflurane-nitrous oxide anesthesia produces significant cerebral vasodilatation in dogs, but that this effect diminishes over time. These time-dependent circulatory changes merit further investigation in humans.

Anesthesia, General↗

PubMed1984

Cerebral and systemic vascular effects of naloxone in pentobarbital-anesthetized normal dogs.

In this study, 10 mongrel dogs were anesthetized with sodium pentobarbital and nitrous oxide. Blood flow was determined using the radioactive microsphere technique before and after the bolus intravenous injection of naloxone (10 mg/kg). Naloxone significantly increased cerebral blood flow to cerebral cortex and the total cerebral hemisphere without an associated change in the cerebral metabolic rate of oxygen. The increase in cerebral blood flow was proportional to the elevation in mean arterial pressure. There were no consistent changes in electrical activity as measured by electroencephalography (EEG) and Fourier analysis of EEG. Systemically, naloxone induced a proportional rise in mean arterial pressure and peripheral vascular resistance and also stimulated the myocardium, as evidenced by an improved cardiac index and stroke volume. These data suggest that naloxone may interfere with cerebral autoregulation or have direct vasodilatory effects on cerebral blood vessels that are not associated with opiate receptor blockade or changes in cerebral metabolism. In addition, naloxone did not appear to reverse the cerebral depressive effects of pentobarbital. Systemically, naloxone seemed to potentiate pentobarbital-induced vasoconstriction and reverse myocardial depression.

Anesthesia↗

PubMed1984

Effects of naloxone on cerebral blood flow and metabolism in isoflurane/nitrous oxide-anesthetized dogs.

The purpose of this study was to document the changes in the cerebral and systemic circulations that result from various doses of naloxone. Twenty-four dogs were anesthetized with 0.8% isoflurane and 70% nitrous oxide (1.3 minimal anesthetic concentration). Thirteen of the dogs received bolus injections of naloxone at logarithmically increasing doses 30 minutes apart. Blood flow to the brain and other organs was determined using the radioactive microsphere technique. Electrical activity was measured by electroencephalography (EEG). High dose naloxone increased both cerebral blood flow (CBF) and cerebral metabolism. The changes in CBF were most pronounced in structures containing a large amount of gray matter, particularly the cerebral cortex, brain stem, and cervical spinal cord. The increase in blood flow was proportionately greater than the increase in the cerebral metabolic rate of oxygen, and EEG activity was unchanged. Naloxone did not produce any significant cardiovascular changes or alterations in myocardial, renal, hepatic, stomach, jejunum, or temporalis and paraspinous muscle flow. Accordingly, it seems that naloxone may have direct cerebral vasodilator properties.

Anesthesia, General↗

PubMed1984

High dose naloxone produces cerebral vasodilation.

In this study, 12 dogs were anesthetized with sodium pentobarbital, and blood flows were determined using the radioactive microsphere technique. Ten dogs were first made acutely hypertensive by the infusion of norepinephrine and demonstrated preserved cerebral autoregulation. The administration of naloxone, 10 mg/kg i.v., in these animals produced a significant increase in cerebral blood flow and a proportional drop in cerebrovascular resistance with no change in the cerebral metabolic rate of oxygen or the electroencephalogram. Two additional spontaneously hypertensive dogs demonstrated a similar response to naloxone. These results suggest that high dose naloxone produces cerebrovasodilation either directly or through the inhibition of cerebral autoregulation.

Animals↗

PubMed1984

Effects of naloxone during high dose barbiturate anesthesia.

This experiment was performed to investigate the ability of naloxone to reverse high dose barbiturate anesthesia or produce cerebrovasodilation or changes in cerebral metabolism in dogs neuronally depressed by high doses of barbiturate. Six dogs were deeply anesthetized with sufficiently high doses of sodium pentobarbital to produce and then maintain isoelectric activity or cerebral silence on the electroencephalogram (EEG). Blood flows were determined using the radioactive microsphere technique both before and after the intravenous bolus injection of naloxone (10 mg/kg), which failed to produce any significant changes in cerebral blood flow, the cerebral metabolic rate of oxygen, cerebrovascular resistance, or EEG activity. Cardiovascular parameters were also essentially unchanged. Naloxone in a dose of 10 mg/kg i.v. produced no changes in the cerebral or systemic circulations or in brain metabolism during high dose sodium pentobarbital anesthesia.

Anesthesia, General↗

PubMed1984

Phenoxybenzamine in the treatment of causalgia. Report of 40 cases.

Forty consecutive cases of causalgia treated during a 7-year period are presented. The patients ranged in age between 17 and 55 years, and all patients were males who received their nerve injuries from missile or shrapnel wounds. The greater occipital nerve was involved in two cases, median nerve in 10, sciatic nerve in 12, brachial plexus in seven, cauda equina in five, and multiple nerves in four cases. Each patient was treated with phenoxybenzamine, a postsynaptic alpha 1-blocker and presynaptic alpha 2-blocking agent. The drug was given orally in gradually increasing increments until a maximum daily dose of 40 to 120 mg was reached. Duration of treatment was usually 6 to 8 weeks. Total resolution of pain was achieved in all cases. The follow-up period ranged between 6 months and 6 years. Side effects of phenoxybenzamine were minimal and transient, consisting primarily of mild orthostatic hypotension and ejaculatory problems. We conclude that oral phenoxybenzamine is a simple, safe, and effective treatment of causalgia.

Adolescent↗

PubMedDate not supplied

Neurosurgical treatment of refractory status epilepticus.

Refractory status epilepticus (RSE) is defined as status epilepticus that continues despite aggressive treatment. A 9.8-year-old boy with a past history of daily left focal motor seizures was transferred to University of California at Los Angeles (UCLA) Hospital in pentobarbital coma after 4 days in RSE. The RSE was treated with very high doses of all appropriate antiepileptic drugs (AEDs), alone and in combination. The pentobarbital was titrated to burst suppression on EEG, but whenever pentobarbital was decreased, the seizures recurred. An ictal positron tomography scan of glucose metabolism demonstrated a right frontal area of hypermetabolism corresponding to an epileptic focus on EEG and magnetic resonance lesion. Eight days after the boy was admitted to UCLA, the right frontal focus was surgically removed, with immediate control of the status epilepticus. Whereas before onset of RSE, he had daily focal seizures, the boy has been seizure-free postoperatively for greater than 1 year. Operative treatment should be considered in patients with RSE in whom a focus of seizure onset can be demonstrated and who are reasonably considered surgical candidates.

Child↗

PubMedDate not supplied

Dysembryoplastic neuroepithelial tumor: a clinicopathologic and immunohistochemical study of 11 tumors including MIB1 immunoreactivity.

The dysembryoplastic neuroepithelial tumor (DNT) is a rare, recently recognized neoplasm, characterized by a mixed glial-neuronal cell proliferation. We studied 11 cases of DNT including 6 males and 5 females (age range 2.1-39.4 years, mean 13.8 years). All patients presented with chronic epilepsy of 4.8 years mean duration. Nine tumors were located in the temporal lobe and 2 in the frontal lobe. Four tumors were located on the right side and 7 on the left. All tumors were characterized by a predominant oligodendrocyte-like cell component with intermixed normal appearing neurons and astrocytes. All were focally microcystic and 7 of 9 evaluable tumors were multinodular. Other observed histologic features included a focal arcuate vascular pattern in 7 tumors, calcification in 4 tumors, and a rare mitotic figure in 2 tumors. Necrosis and vascular hyperplasia were not observed in any of the tumors. Cortical architectural disorganization (cortical dysplasia) was observed in 9 of 10 evaluable cases. MIB1 (a marker of cellular proliferation) immunostaining was performed in all 11 tumors and MIB1 indices (number of positive tumor cells/100 tumor cells counted) ranged from 0-0.6 (mean 0.2). Four patients required at least 1 additional surgical procedure for tumor recurrence, related to an incomplete initial excision 2.1-4.4 years after their initial operation. All patients are seizure-free at their last follow-up. DNTs are low grade neoplasms which typically present with chronic epilepsy, are most frequently located in the temporal lobe, and occur most frequently in pediatric patients. Their appearance and association with cortical dysplasia suggest a maldevelopmental origin. The generally slow growth and relatively benign nature of DNT is reflected by their low MIB1 index.

Adolescent↗