Robert W. Brennan

Regional cerebral blood flow decreases during chronic and acute hyperglycemia.

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.

Cerebral blood flow and metabolism during hypoglycemia in newborn dogs.

: 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 technique employing 133Xe as indicator. Arteriovenous differences for oxygen, glucose, lactate, and β‐hydroxybutyrate (β‐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 β‐OHB (0.5%). During hypoglycemia, CMRglucose. declined by 29 and 52% in groups 1 and 2, respectively, while CMR,lactate increased to the extent that this metabolite became the dominant fuel for oxidative metabolism in brain. The cerebral utilization of β‐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.

Acute cerebellar hemorrhage Analysis of clinical findings and outcome in 12 cases

Although a majority of reported cases of cerebellar hemorrhage are subacute or chronic, an acute form of cerebellar hemorrhage occurs that results in coma within 48 hours of onset and is probably always fatal without surgical intervention. Our experience with 12 consecutive patients with proved acute cerebellar hemorrhage is summarized. Of three patients treated with aggressive medical therapy alone, none survived more than 48 hours. In seven of nine operated cases, emergency surgery was undertaken solely on the strength of clinical diagnosis without radiologic confirmation. Three died postoperatively. Of six survivors, two recovered fully, and two show mild and two moderate residua. The major factors influencing survival were the rate of evolution of signs and the level of consciousness at the moment of surgery.

Diphenylhydantoin intoxication attendant to slow inactivation of isoniazid.

1 N T 0 X I C A T I 0 N WITH DIPHENYLHYDANTOIN (DPH) is seen occasionally among patients receiving this drug concurrently with antitubercular drugs. The signs and symptoms of DPH intoxication-generally a triad of nystagmus, ataxia, and drowsiness-are reliable indications that the blood level of unmetabolized DPH is above 20 p g per milliliter.1 Such toxic reactions are rare in the absence of factors known to interfere with DPH metabolism when patients receive the ordinary dosage (4 to 5 mg. per kilogram daily). Kutt et a1.2 described a condition of low tolerance to DPH endemic among inhabitants of a tuberculosis ward. Some epileptic patients, who had taken 300 mg. of DPH daily for years without incident, developed florid symptoms of DPH intoxication soon after antitubercular chemotherapy was begun. Isoniazid (INH) in these individuals caused a reversible depression of DPH metabolism; as unmetabolized DPH accumulated, intoxication ensued. In studies in vitro, DPH metabolism was inhibited by isoniazid in concentrations of the same order of magnitude as those attained in clinical usage.3 However DPH intolerance in this clinical setting was sporadic and unpredictable, affecting only a minority of patients receiving both drugs. Individual variations of isoniazid metabolism on a genetic basis were reported by Evans and associates.4 Slow inactivation of isoniazid is a common genetic trait leading to sustained high levels of free drug and predisposing to doserelated complications of isoniazid therapy, for example, peripheral neuropathy.5 We thought that slow inactivation of isoniazid might be the basic factor in determining which patients would develop DPH intoxication when given the drugs concurrently. This study was undertaken [l] to determine whether an individual’s inborn pattern of isoniazid metabolism might correlate with risk of DPH intoxication and [Z] to test, in experimental animals, the effects of graded plasma concentrations of isoniazid on plasma levels of DPH.

Choroid plexus blood flow: evidence for dopaminergic influence

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.

Migraine secondary to head trauma in wrestling: A case report

Head trauma has been reported to cause significant but temporary focal neurologic signs in children and adolescents.’ The findings described include transient hemiparesis, somnolence, irritability, vomiting, blindness, and brainstem signs. These episodes of reversible neurologic dysfunction may resemble classical migraine, and may have a similar underlying mechanism. Matthews2 reported &dquo;classical migraine&dquo; attacks after &dquo;heading&dquo; the ball among British football players. The authors have observed a similar phenomenon in a college wrestler. Treatment with the 8-adrenergic blocker, propranolol, provided control of symptoms and permitted him to participate in intercollegiate wrestling.

Neurologic complications of acute myelomonoblastic leukemia of four years' duration

An adult with acute nonlymphoblastic leukemia involving the central nervous system is presented. Unusual features included: (1) Focal signs and radiographic evidence of sagittal sinus occlusion early in the course of disease; (2) progressive meningeal, cranial nerve, and spinal nerve involvement despite a 4-year bone marrow remission; (3) intracerebral tumor formation, and (4) retrobulbar optic neuritis associated with microscopic findings of herpeslike viral particles. The incidence of clinically overt neurologic disease in adults with acute nonlymphoblastic leukemia seems to have increased in tandem with improved chemotherapy. The prophylactic treatment of the central nervous system during prolonged remission of adult acute nonlymphoblastic leukemia may prove of benefit to these patients.

Choroid plexus blood flow in the sheep.

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.

A Comparison of Alternative Distributed Dynamic Cluster Formation Techniques for Industrial Wireless Sensor Networks

In this paper, we investigate alternative distributed clustering techniques for wireless sensor node tracking in an industrial environment. The research builds on extant work on wireless sensor node clustering by reporting on: (1) the development of a novel distributed management approach for tracking mobile nodes in an industrial wireless sensor network; and (2) an objective comparison of alternative cluster management approaches for wireless sensor networks. To perform this comparison, we focus on two main clustering approaches proposed in the literature: pre-defined clusters and ad hoc clusters. These approaches are compared in the context of their reconfigurability: more specifically, we investigate the trade-off between the cost and the effectiveness of competing strategies aimed at adapting to changes in the sensing environment. To support this work, we introduce three new metrics: a cost/efficiency measure, a performance measure, and a resource consumption measure. The results of our experiments show that ad hoc clusters adapt more readily to changes in the sensing environment, but this higher level of adaptability is at the cost of overall efficiency.

Bilateral facial palsy secondary to herpes zoster meningoencephalitis in a HIV-positive woman

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.