RESUMEN

Bilateral facial paralysis of diverse infectious aetiologies has been reported in HIV infected patients. We present a patient with bilateral facial palsy most likely due to herpes zoster meningoencephalitis in a patient with neutropenia and who subsequently tested HIV-positive.

Asunto(s)

RESUMEN

Besides sleep apnea, the main disorders of excessive daytime sleepiness include narcolepsy and hypersomnia. Narcolepsy is characterized by periods of irresistible sleepiness and sleep attacks of brief duration and, most often, by one or more of the auxiliary symptoms: cataplexy, sleep paralysis, and hypnogogic hallucinations. Generally, sleepiness and sleep attacks in hypersomnia are of longer duration and are more resistible than in narcolepsy; also, the auxiliary symptoms are absent. There are three types of hypersomnia: idiopathic, secondary, and periodic. Nocturnal sleep is typically disrupted in narcolepsy, whereas in idiopathic hypersomnia it is prolonged and in secondary hypersomnia it is variable. The exact causes of narcolepsy and idiopathic hypersomnia are unknown; however, there is evidence for genetic predisposition for either disorder. In secondary hypersomnia causative factors include: neurologic, such as head injuries, cerebrovascular insufficiency, and brain tumors; general medical, such as metabolic disorders, various intoxications, and conditions leading to brain hypoxia; and psychiatric, most notably depression. Although the cause of periodic hypersomnia is unclear, most research supports the notion of underlying organic disease. Often, the evaluation of patients with excessive daytime sleepiness can be completed in the office setting, based on the sleep history and a thorough neurologic, general medical, and psychiatric assessment. Whenever indicated, ancillary laboratory studies, such as computed tomography and magnetic resonance scans, should be performed. Sleep laboratory recordings generally are not necessary unless there is suspicion of sleep apnea or narcolepsy in the absence of auxiliary symptoms.(ABSTRACT TRUNCATED AT 250 WORDS)

Asunto(s)

RESUMEN

The effect of dimethylsulfoxide (DMSO) and iododeoxyuridine (IUdR) on the growth characteristics of two established human glioblastoma cell lines (FG and HMCN-1) was studied. The FG cell line has been characterized. The HMCN-1 cell line, established in our laboratory, consisted of fibroblastoid and polygonal cells that grew without contact inhibition. Subcutaneous injection of these cells into weanling athymic nude mice induced slowly growing, solid tumors that were histologically spindly with areas that were similar to the original tumor. Chromosomal analyses revealed a human heteroploid pattern with a modal number of 69. The cells of the original human glioma contained S-100 protein and glial fibrillary acidic protein (GFA protein), whereas the established cells failed to express markers. Prolonged treatment of glioma cells with DMSO generated a more adherent, normal human fibroblastoid phenotype that grew with contact inhibition. The new phenotype and proliferative restriction of these cells was evident as late as 50 days after discontinuation of treatment. The chemical induction of cell differentiation resulted in decreased tumorigenic potential in athymic nude mice.

Asunto(s)

RESUMEN

The presence of hyperglycemia prior to stroke or cardiac arrest can increase neuronal damage caused by brain ischemia. Acute hyperglycemia shows this effect in animal models of stroke. However, chronic hyperglycemia and chronic hyperglycemia with additional acute elevation of blood glucose are more common premorbid states for stroke patients. The effect of chronic hyperglycemia on regional cerebral blood flow (rCBF) is unclear but blood flow changes may play a role in this ischemic cell damage. We measured rCBF in awake restrained rats that had chronic hyperglycemia induced by treatment with streptozotocin. This was compared to that measured in rats made acutely hyperglycemic by injecting glucose into the peritoneal space. rCBF was measured in 17 brain regions using [14C]iodoantipyrine. During chronic hyperglycemia, when plasma glucose was 29 microns/ml, rCBF was decreased and a regional distribution of this effect was noted; 9 hindbrain regions showed a mean flow decrease of 14% while forebrain regions demonstrated less flow reduction. Acute elevation of plasma glucose during normoglycemia or superimposed on chronic hyperglycemia produced flow reductions of 7% for each 10 microns/ml increment in plasma glucose up to 60 microns/ml. Both chronic and acute hyperglycemia are associated with decreased rCBF and the mechanism for this effect does not appear to adapt to chronic hyperglycemia.

Asunto(s)

RESUMEN

Regional neurohypophyseal and cerebral blood flow were measured in 5 awake unstressed female sheep with radiolabelled microspheres before and after the intracarotid infusion of a 3% NaCl solution. Plasma arginine vasopressin (AVP) levels were concurrently measured by radioimmunoassay. Following intracarotid sodium chloride infusion, neural lobe (but not median eminence) blood flow significantly increased, as did plasma AVP levels. Directed thirst and water-seeking behavior was observed, accompanied by a global increase in cortical blood flow. We conclude that the neuroendocrine response and the behavioral display induced by intracarotid sodium chloride infusion are accompanied by increases in blood flow in selected brain regions.

Asunto(s)

RESUMEN

We analyzed four personal cases and 51 reported cases of dissecting aneurysms of the arteries of the head and neck. Subintimal dissection more commonly affects the intracranial vessels before age 40. In contrast, medial dissection tends to affect extracranial vessels after age 30. Vertebrobasilar dissection more variably affects either arterial plane. The reasons for these differing patterns of dissection are still not clear. In young subjects, the subintimal layer appears to be more susceptible; in contrast, the media becomes increasingly vulnerable with age, particularly in the presence of acquired medial disease.

Asunto(s)

RESUMEN

The presence of hyperglycemia before brain ischemia increases stroke-related morbidity and mortality in experimental animals and humans. However, little is known of the effect of hyperglycemia on regional cerebral blood flow (rCBF). Acute hyperglycemia was induced in awake but restrained rats by intraperitoneal injection of 50% D-glucose. Regional flow was determined using [14C]iodoantipyrine and quantitative autoradiography. Elevation of plasma glucose from 11 to 39 mM was associated with a 24% reduction in rCBF when compared with controls that received normal saline. Intraperitoneal D-mannitol produced an elevation of plasma osmolality equivalent to that observed with glucose. However, rCBF was only reduced by 10%. Hyperglycemia appears to produce a global decrease in rCBF in awake rats that cannot be completely explained by the attendant increase in plasma osmolality. If a similar influence is present during brain ischemia, hyperglycemia could extend areas of critical flow limitation.

Asunto(s)

RESUMEN

Choroid plexus blood flow was measured in adult female sheep using the radioactive microsphere technique. The response of choroid plexus, renal and cortical blood flow to the infusion of dopamine (11 sheep), haloperidol (7 sheep) and propranolol (6 sheep) were compared. Choroid plexus and renal blood flow significantly increased after dopamine infusion (55% and 49% respectively). Choroid plexus and renal blood flow decreased significantly following haloperidol infusion (-24% and 29% respectively). Cortical blood flow did not significantly change. Propranolol infusion did not significantly change blood flow in these regions. These observations suggest that dopaminergic mechanisms play a role in the regulation of choroid plexus as well as renal blood flow.

Asunto(s)

RESUMEN

An autoradiographic method (14C-iodoantipyrine autoradiography) was used to measure regional optic nerve blood flow (ONBF) under basal conditions in 11 adult female cats. Flow was measured in six regions of the optic nerve: (1) prelaminar, (2) laminar, (3) 1 mm post-laminar, (4) 4 mm post-laminar, (5) 6 mm post-laminar, and (6) intracranial optic nerve and chiasm. A gradient of flow rates was found with relatively high flow in the prelaminar, laminar, and 1-mm post-laminar optic nerve, and significantly lower flow in the 4- and 6-mm post-laminar nerve and in the intracranial optic nerve and chiasm. Blood flow in the 4- and 6-mm post-laminar nerve and in the intracranial nerve and chiasm was comparable to previously reported values for cerebral white matter in the cat. With alteration of mean arterial blood pressure (MABP), optic nerve blood flow demonstrated autoregulatory compensation in all areas.

Asunto(s)

RESUMEN

A 44-year-old woman with prolonged coma and hypotension following drug overdosage developed bilateral hemorrhagic infarcts in the dorsolateral brainstem. The regional distribution of these paired lesions corresponds to the area of confluence of penetrating arteries in the brainstem. It is suggested that under exceptional circumstances brainstem arterial end-zones may be vulnerable to anoxic-ischemic insult.

Asunto(s)

RESUMEN

Intracranial optic nerve blood flow was measured by the radiolabeled microsphere technique in 30 adult sheep under light barbiturate anesthesia. Regional blood-flow rates were determined under basal conditions. The responses of regional blood flow to alterations in PaCO2 and to changes in arterial blood pressure were also measured. Under basal conditions blood flow was comparable to that found in other cerebral white matter (14 +/- 1 ml/100 gm/min). Responses to hypercarbia and hypocarbia were also similar to reported measurements for other cerebral white matter. With alteration of arterial blood pressure, intracranial optic nerve blood flow remained constant within the limits of cerebral autoregulation.

Asunto(s)

RESUMEN

Regional neurohypophyseal and cerebral blood flows were measured by the radiolabeled microsphere technique in 30 adult sheep under light barbiturate anesthesia. Regional blood flows were determined under basal conditions. The responses of regional blood flow to alterations in arterial PCO2 and to changes in arterial blood pressure wee also determined. In addition, the relationship between regional neurohypophyseal blood flow and neurosecretory activity as judged by plasma arginine vasopressin levels was assessed. Under basal conditions median eminence blood flow averaged 461 ml.100 g-1.min-1 and did not significantly differ from neural lobe blood flow (436 ml.100 g-1.min-1). Blood flow in the neurohypophysis was about 8 times cortical and 16 times white matter blood flow in these animals. Median eminence and neural lobe blood flow proportionately increased far less than regional cortical or white matter blood flow under conditions of hypercarbia. With alteration of arterial blood pressure, regional neurohypophyseal blood flow remained constant beyond the limits of cerebral autoregulation. The neurohypophysis demonstrates a degree of blood flow homeostasis that exceeds that of any other brain area studied. Although the neurohypophysis is a diverticulum of the brain, its vascular system forms a unique functional as well as a unique anatomic unit.

Asunto(s)

RESUMEN

Cerebral blood flow (CBF) and cerebral metabolic rates (CMR) were studied in newborn dogs during insulin-induced hypoglycemia. Pups were anesthetized, paralyzed, and artificially ventilated with a mixture of 70% nitrous oxide and 30% oxygen to maintain normoxia and normocarbia. Experimental animals were given regular insulin (0.3 units/gm IV); controls received normal saline. CBF was determined using a modification of the Kety-Schmidt technical employing 133Xe as indicator. Arteriovenous differences for oxygen, glucose, lactate, and beta-hydroxybutyrate (beta-OHB) were also measured, and CMRO2 and CMRsubstrates calculated. Two groups of hypoglycemic dogs were identified; those in which blood glucose levels were greater than 0.5 mM (group 1), and those in which they were less than 0.5 mM (group 2). CBF did not change significantly from control values of 23 +/- 10 ml/min/100 g (mean +/- S.D.) at both levels of hypoglycemia. Similarly, hypoglycemia did not alter CMRO2 significantly from its initial level of 1.05 +/- 0.37 ml O2/min/100 g. Glucose consumption in brain during normoglycemia accounted for 95% of cerebral energy supply with minimal contributions from lactate (4%) and beta-OHB (0.5%). During hypoglycemia, CMRglucose declined by 29 and 52% in groups 1 and 2, respectively, while CMRlactate increased to the extent that this metabolite became the dominant fuel for oxidative metabolism in brain. The cerebral utilization of beta-OHB was unaltered by hypoglycemia. The findings indicate that insulin-induced hypoglycemia in the newborn dog is associated with an increase in cerebral lactate utilization, supplementing glucose as the primary energy fuel and thereby preserving a normal CMRO2. These metabolic responses may contribute to the tolerance of the immature nervous system to the known deleterious effects of hypoglycemia.

Asunto(s)

RESUMEN

Choroid plexus blood flow was measured in 29 adult female sheep using the radioactive microsphere technique. Basal blood flow, response to change in arterial carbon dioxide tension, and response to change in mean arterial blood pressure were determined. The results were compared to cerebral cortical blood flow values in the same sheep. Mean choroid plexus blood flow was 601 ml/100 g/min under basal conditions. Choroid plexus blood flow fell 31% with hypocarbia, a reduction comparable to that seen in cortex. With hypercarbia choroid plexus blood flow rose only 27% whereas cortical blood flow increased by 199%. Unlike cortical blood flow, choroid plexus blood flow fell significantly with pharmacogenic hypertension. The latter finding may reflect the absence of a blood-brain barrier in choroid plexus.

Asunto(s)

Asunto(s)

Asunto(s)

Asunto(s)

RESUMEN

Cerebral blood flow (CBF), CBF responses to changes in arterial CO2 tension, and cerebral metabolic rate for oxygen (CMRO2) were measured in newborn dogs, by means of a modification of the Kety and Schmidt technique employing 133Xe. Mongrel dogs of 1-7 days of age were paralyzed and passively ventilated with 70% N2O and 30% O2. CBF was derived by analysis of paired serial 20-microliter samples of arterial and of cerebral venous blood from the superior sagittal sinus. At an arterial PCO2 of 36.9 +/- 3.7 Torr and a mean arterial blood pressure of 62 +/- 10 Torr, CBF was 23 +/- 8 ml/min per 100 g. The arteriovenous oxygen content difference averaged 5.6 vol%, and CMRO2 was 1.13 +/- 0.30 ml O2/min per 100 g. CBF increased or decreased by 0.58 ml/min/100 g per Torr change in PCO2. Our results suggest that in the newborn, basal CBF and CBF responses to CO2 are considerably lower than in the adult and parallel the lower metabolic needs of the newborn brain.

Asunto(s)

RESUMEN

Cerebral blood flow autoregulation (CBFA) to changes in perfusion pressure has not been previously reported in the rat. A modification of the Kety and Schmidt technique employing 133Xenon was used to measure cerebral blood flow (CBF) in paralyzed adult Sprague Dawley rats passively ventilated with 70% nitrous oxide and 30% oxygen. At a mean arterial blood pressure (MABP) of 121 +/- 19 mm Hg, and a mean arterial PCO2 of 36.2 +/- 2.9 mm Hg, mean CBF was 103 +/- 22 ml/min/100 gm of brain. CBF responses to hypercarbia were 4.9 ml/min/100 gm per mm Hg change in arterial PCO2. CBF was measured during steady state levels of hypo- and hypertension induced by phlebotomy, or by intravenous metaraminol, over the MABP range of 48-205 mm Hg. From a MABP of 80 to 160 mm Hg. CBF remained nearly constant, indicating the presence of CBFA. However, when MABP exceeded 160 mm Hg, CBF became pressure dependent, indicating a "breakthrough" of autoregulation in acute severe hypertension.

Asunto(s)

RESUMEN

The incidence of Amanita mushroom poisoning seems to be increasing in the United States. Its neurological aspects contribute importantly to morbidity and mortality. In reported series, mortality has ranged from 50 to 90%, and survival following the appearance of coma was exceptional. The cause of nervous system involvement was uncertain. In the patient presented here, clinical and electroencephalographic observations were consistent with severe hepatic encephalopathy and correlated closely with liver function abnormalities. Despite the development of coma, full recovery followed the use of thioctic acid, an experimental therapeutic agent.

Asunto(s)