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Delayed post-hypoxic leukoencephalopathy is a clinical syndrome caused by a lesion of the white matter of the brain with an acute onset developing several days after emerging from coma. The reason of delayed post-hypoxic leukoencephalopathy is prolonged cerebral hypooxygenation, it often results from carbon monoxide poisoning, less often it is associated with acute brain hypoxia caused by respiratory failure, an overdose of opiates. The leading role in the clinical picture of delayed post-hypoxic leukoencephalopathy is played by the duration and severity of cerebral anoxia in the acute period of the disease. The period of temporary well-being of a patient with an episode of acute hypoxia lasts 2 to 40days. Pathogenesis and pathophysiology have not been well studied. Its development after carbon monoxide poisoning is considered to be caused by direct myelinotoxic effect. Itis essential to collect a detailed history for diagnosing a case, neurovisualization is an informative method for investigation. Magnetic resonance imaging may detect the signs that are pathognomonic for delayed post-hypoxic leukoencephalopathy, that is diffuse hyperintensity of the white matter of the cerebral hemispheres in T2-mode, symmetry of the damage of both cerebral hemispheres, damage of the subcortical gray matter globus pallidus. The standards for the treatment of delayed post-hypoxic leukoencephalopathy have not been developed. The use of glucocorticoids has been described, perspective use of amantadine were shown in case of frontal-subcortical syndrome. There are recommendations on prescribing the following therapy for the patients with delayed post-hypoxic leukoencephalopathy: hyperbaric oxygenation, coenzymeQ10, vitaminE and groupB. We present a clinical observation that demonstrates the complexity of the clinical picture of delayed post-hypoxic leukoencephalopathy, the difficulty of its diagnosis without taking into account information about previous carbon monoxide poisoning. The results of magnetic resonance imaging at the onset of the disease are considered to be of utmost interest. The clinical observation of the patient presented in the article allows us to make an assumption about pathogenesis and contributes to search for means aimed at preventing the development of delayed post-hypoxic leukoencephalopathy in people with acute carbon monoxide poisoning.

Long QT syndrome (LQTS) encompasses one or more gene mutations of cardiac ion channels predisposing patients to ventricular dysrhythmias and sudden cardiac death. Due to seizures from dysrhythmia-induced cerebral anoxia, LQTS is often misdiagnosed as epilepsy. We discuss the decision to place an ICD

Current EEG criteria for the diagnosis of non-convulsive status epilepticus in critically ill patients with repetitive generalised or focal epileptiform discharges primarily rely on a widely accepted low cut-off frequency limit of 2.5-3 Hz for non-evolving patterns, or on discharge evolution of frequency, location or mophology. The secondary criterion is a significant clinical or EEG improvement following acute administration of a rapidly acting antiepileptic drug, such as lorazepam. We describe a comatose patient after out-of-hospital cardiac arrest, in whom very slow (1-Hz), non-evolving generalised periodic epileptiform discharges against an almost completely depressed background would suggest substantial anoxic damage and poor neurological outcome. Yet, reloading with propofol for diagnostic purposes completely dispersed generalised periodic epileptiform discharges and revealed previously absent biological activity, raising the possibility of non-convulsive status epilepticus that was subsequently confirmed. Brain MRI showed no significant anoxic brain damage and EEG improved, but the patient died from severe cardiopulmonary complications. These observations suggest that in rare cases, slow, non-evolving generalised periodic epileptiform discharges may reflect non-convulsive status epilepticus rather than diffuse irreversible cerebral anoxia, while reloading with propofol can be used as an additional secondary diagnostic criterion.

Hyperbaric oxygen (HBO) therapy has been used in a number of conditions characterized by global ischemia (as opposed to focal ischemia of stroke), and anoxia, and leading to impairment of consciousness. Conditions such as coma due to brain injury and anoxia associated with drowning and hanging are discussed under the following headings: (1) pathophysiology, (2) rational basis of HBO therapy, (3) review of animal experimental studies, and (4) review of human clinical studies. Finally case studies are given.

Resumen El signo del cerebelo blanco o signo reverso es un hallazgo imagenologico poco frecuente en la tomografia de craneo; se presenta especialmente en ninos con lesiones cerebrales difusas despues de un insulto anoxico. Se manifiesta como una disminucion difusa de la densidad de los hemisferios cerebrales, con perdida de la diferenciacion de sustancia gris-blanca y un aumento relativo en la densidad del talamo, el tallo cerebral y el cerebelo bilateral, pero puede no ser simetrico. A continuacion, presentamos el caso de un paciente masculino de 15 anos, quien presenta un episodio de intoxicacion exogena por sustancias desconocidas y episodios convulsivos y en quien la tomografia de craneo simple mostro este infrecuente signo.

Summary Background Cervical hematoma with airway compromise is a severe complication that may be rapidly lethal or result in irreversible cerebral anoxia if the hematoma is not urgently decompressed. It is therefore indispensable to know the essential relevant elements as well as predictive criteria for this complication before envisioning ambulatory thyroidectomy. Methods The Association francophone de chirurgie endocrinienne (AFCE) sought to answer several questions raised by the proposal of ambulatory thyroidectomy and to propose recommendations based on a review of the literature, an inquiry sent out to members of the AFCE, and an in-depth research of the medicolegal risks involved, based essentially on jurisprudence. The details scrutinized included preoperative selection criteria, the characteristics of the operation and the basic elements of postoperative surveillance. Conclusions The standard today is at least an overnight hospital stay. In fact, hospital stay can be less than 24 h because the risk of cervical compressive hematoma is very unusual beyond this interval. Ambulatory (outpatient) thyroidectomy (0 nights) is possible under certain conditions for highly selected patients according to criteria described in the literature that also define relative contra-indications. In case of life-threatening or functional complications, the surgeon stands first in the line of responsibility. The surgeon must therefore ensure that the patient and family were fully informed of the contra-indications, the normal course of postoperative events, of pertinent elements of postoperative surveillance and of the conditions under which the patient can be safely discharged. The surgeon must also realize that this type of management is time-consuming.

Tracheal agenesis is an extremely rare, typically fatal congenital tracheal malformation. Lack of prenatal symptoms and emergent presentation usually lead to a failure to arrive at the correct diagnosis and manage the airway properly before the onset of irreversible cerebral anoxia. We report the case history of an infant born with immediate respiratory failure who was diagnosed with tracheal agenesis. The clinical presentation, embryology, classification, and surgical management are discussed.

SUMMARY Breath-Holding spells are a dramatic and commonly observed clinical phenomenon in childhood. The underl- ying pathophysiologic mechanisms in breath-holding spells are result from autonomic nervous system dysregu- lation. Cerebral anoxia is the ultimate factor responsible for the loss of consciousness observed in the severe forms of breath-holding spells.It's known that, there is relation between breath-holding spells and iron-deficiency ane- mia, and the spells resolve after oral iron supplemantati- on.In children with breath-holding spells, even though without anemia, there might be different degrees of iron- deficiency.In early diagnosis of iron- deficiency, sTfR le- vel was very important. At the same time, in children with iron-deficiency ,zinc deficiency also migt be found. That's why, plasma zinc levels should be controlled in those children.

Summary A 16-year-old girl working in a paint and dye-casting factory of aniline dyes presented to the emergency with cyanosis, fever and altered sensorium. She had been diagnosed as a case of malaria and treated with chloroquine elsewhere. At admission, her saturation was 79%, which did not improve despite mechanical ventilation with 100% oxygen. Her PaO2 levels, however, remained high-140 mmHg. The observed difference in PaO2 and SpO2 prompted us to investigate her for methemoglobinemia, which was confirmatory. Despite symptomatic and specific treatment, she succumbed to her illness possibly due to late presentation and prolonged cerebral anoxia. Though the girl’s raised methemoglobin levels may be explained by her history of exposure to aniline dyes, the temporal association of her methemoglobinemia related symptoms with chloroquine administration cannot be ignored. We believe that this rare complication of chloroquine therapy should be kept in mind before prescribing it to any child with malaria.

Background Transcranial magnetic stimulation combined with electroencephalography (TMS/EEG) represents a valuable tool to probe cortical excitability and connectivity. Although several procedures have been devised to abolish TMS-related artifacts, direct evidence that it is possible to record TMS-evoked potentials (TEPs) that purely reflect cortical responses to TMS are still lacking. Objective To demonstrate that when TMS is delivered on a human head with intact nerves, scalp and ocular muscles, TEPs are present only if a functional portion of cortex is targeted and is absent otherwise. Methods We performed extensive navigated TMS/EEG mappings in three vegetative state patients and in eight healthy controls. Patients were selected based on the extension of their cortical lesions as revealed by structural/functional imaging: the cerebral cortex was globally damaged in Patient 1 due to cerebral anoxia, Patient 2 showed a traumatic damage affecting one cerebral hemisphere, while Patient 3 was characterized by one left sided and one right-sided focal ischemic lesion. Results In Patient 1, TMS performed at any targeted cortical site did not elicit statistically significant TEPs. In Patient 2, TEPs were absent when the damaged hemisphere was targeted, while were present over the healthy side. In Patient 3, significant TEPs were absent when cortical lesions were targeted and present otherwise. Significant TEPs were always present in healthy controls. Conclusions These findings suggest that, provided that appropriate experimental procedures are employed, TEPs are genuine cortical responses detectable only when preserved cortical tissue is stimulated. Hence, a dependable assessment of cortical excitability and connectivity in brain-injured patients requires the use of neuronavigated TMS.

Some people report a near-death experience (NDE) after a life-threatening crisis. We aimed to establish the cause of this experience and assess factors that affected its frequency, depth, and content.In a prospective study, we included 344 consecutive cardiac patients who were successfully resuscitated after cardiac arrest in ten Dutch hospitals. We compared demographic, medical, pharmacological, and psychological data between patients who reported NDE and patients who did not (controls) after resuscitation. In a longitudinal study of life changes after NDE, we compared the groups 2 and 8 years later.62 patients (18%) reported NDE, of whom 41 (12%) described a core experience. Occurrence of the experience was not associated with duration of cardiac arrest or unconsciousness, medication, or fear of death before cardiac arrest. Frequency of NDE was affected by how we defined NDE, the prospective nature of the research in older cardiac patients, age, surviving cardiac arrest in first myocardial infarction, more than one cardiopulmonary resuscitation (CPR) during stay in hospital, previous NDE, and memory problems after prolonged CPR. Depth of the experience was affected by sex, surviving CPR outside hospital, and fear before cardiac arrest. Significantly more patients who had an NDE, especially a deep experience, died within 30 days of CPR (p0.0001). The process of transformation after NDE took several years, and differed from those of patients who survived cardiac arrest without NDE.We do not know why so few cardiac patients report NDE after CPR, although age plays a part. With a purely physiological explanation such as cerebral anoxia for the experience, most patients who have been clinically dead should report one.

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OBJETIVO: Apresentar um estudo de caso de reabilitação com procedimentos de estruturação de rotina para realização das atividades de vida diária (AVDs). PACIENTE: Quadro de anóxia cerebral, com déficit de memória verbal e visual, desorientação temporal, abulia e bradipsiquismo. MÉTODO: Estruturação de horários fixos na rotina diária; exposição a um calendário 3 vezes ao dia; caminhadas diárias; monitorização do familiar na execução de tarefas de auto cuidado, fornecendo auxílio mediante comandos verbais curtos e pistas específicas. RESULTADOS: Foram observados aumento da iniciativa, maior autonomia nas AVDs, diminuição do período de latência para qualquer resposta, melhora da atenção, orientação temporal e bradipsiquismo. CONCLUSÕES: Estratégias de controle do comportamento trazem ganhos e limitações para pacientes e familiares. Embora obriguem a adaptação a uma rotina pouco flexível, promovem o aprendizado através da automatização de procedimentos que se valem de mecanismos de memória implícita preservados. Estes recursos podem elevar o grau de autonomia do paciente em casa.

Delayed postanoxic encephalopathy (DPE) is a rare condition that presents after apparent recovery from acute cerebral anoxia. DPE, which consists of cognitive and neuropsychiatric deficits, appears between one and three weeks after cerebral anoxia. We present a patient with DPE secondary to acute cocaine and heroin intoxication with typical cranial MRI changes. The clinical improvement of the patient could be related to the improvement in white matter lesions despite the characteristics of the ADC map.

A fifty year-old woman died after drowning in a swimming-pool. Rescue and ambulance paramedic teams started resuscitation attempts followed by a medical care helicopter team. Acute haematemesis, mucosal tears and gastric micro perforations occurred, due to the cardiorespiratory resuscitation manoeuvres. Death occurred seven days later due to the cerebral anoxia and multiorgan failure. Forensic investigations excluded possible malpractice during external cardiac massage as responsible for the woman’s death, while Judicial Authority considered the death as the consequence of the delayed intervention of the swimming-pool rescue team.

The burst-suppression (BS) pattern of the EEG occurs in a rather limited number of conditions. It has been observed in deep stages of general anesthesia and in conjunction with sedative overdoses. It is also known to occur in the wake of cardiorespiratory arrest. Undercutting of the cortex has been found to result in BS activity. Rare neonatal epileptic encephalopathies also give rise to BS. Our personal interest was prompted by the consistent finding of BS activity in rats following cerebral anoxia (nitrogen inhalation, airway obstruction): after periods of EEG flatness, BS activity developed, followed by periodic bursts and diffuse slowing. On the other hand, earlier literature (before 1960) showed virtually no observation of BS, neither in anoxic patients, nor in animal experiments. It is likely that the introduction of modern intensive care treatment has engineered episodes of BS activity, probably due to modifications of the anoxic cerebral pathology.

Historical background and past knowledge: The earliest reference to BHS, then referred to as infantile form of temper tantrums or infantile syncope, were made by Rillet and Barthezin in 1843, and by Meigsin in 1848. Subsequently in the 20th century, various authors published their clinical viewpoints on its pathophysiology and prognostic significance. Based on the color change demonstrated by the child during the spell, BHS were classified as cyanotic, pallid and mixed. Till the 1960’s, despite several hypotheses, the pathophysiology and etiology remained largely nebulous and uncertainities existed regarding the outcome. Multiple factors like disturbed parent-child relationship, hereditary autonomic instability, self asphyxiation, decreased cerebral blood flow secondary to increased intrathoracic pressure due to spontaneous valsalva manoeuvre and altered cerebral mechanism secondary to various stimuli were implicated for cyanotic BHS [1]. For the pallid form, circulatory failure secondary to asystole leading to cerebral anoxia was considered the most probable hypothesis [2].

Objectives To evaluate the results of covered Cheatham-Platinum stent implantation in the management of native coarctation of the aorta and report intermediate and long-term follow-up. Background Covered stents are being used increasingly in severe and complex coarctation of the aorta mainly to reduce risk of aortic wall complications. There is, however, limited data on the intermediate and long-term outcome. Patients and Methods Fifty-six patients received 59 covered Cheatham-Platinum stents (January 2002–December 2011) at a single center—in 54 patients as primary treatment and in 2 as a rescue. Mean age was 22.25 ± 1.2 (11–56) years and mean weight 58.6 ± 2.1 (32–99) kg. Primary end points were reduction in systolic pressure gradient and an increase in coarctation segment diameter. Changes in antihypertensive medicines and complications were recorded on follow-up. Results Mean coarctation segment diameter increased from 4.69 ± 0.20 to 15.1 ± 3.2 mm (P

Although standard EEG is performed routinely in patients with disorders of consciousness after coma, its prognostic value is still debated. The aim of the present study was to evaluate the role of standard EEG in predicting the recovery of cognitive functioning in patients affected by severe disturbances of consciousness after coma caused by cerebral anoxia. A standard EEG was recorded at admission to our Rehabilitation Department in 15 patients experiencing impaired consciousness because of cerebral anoxia. We quantified EEG abnormalities using the Synek scale (1988). Cognitive functioning was measured with the levels of cognitive functioning scale at the time of admission and after 3 months of recovery. EEG scores were significantly correlated with both levels of cognitive functioning scores at admission (P = 0.004) and change in levels of cognitive functioning score after 3 months (P < 0.001). The first correlation confirms the relationship between EEG and cognitive functioning, while the second correlation indicates the prognostic value of EEG in cognitive outcome. In conclusion, standard EEG is a simple and readily available tool with significant prognostic value in patients with disorders of consciousness after coma caused by cerebral anoxia.

The protective effects of BMY-21502 (1-[[1-[2-(trifluoromethyl)-4-pyrimidinyl]-4-piperidinyl]methyl]-2- pyrrolidinone) against cerebral anoxia were investigated using various models in mice, in comparison with those of other cerebroactive drugs. Oral administration of BMY-21502 (10-100 mg/kg) significantly prolonged the survival time in KCN (2.4 mg/kg, i.v.)-induced anoxia. Oxiracetam and idebenone exerted similar but weak protection at doses above 100 mg/kg, p.o. and only at a dose of 100 mg/kg, p.o., respectively. Significant protection by BMY-21502 against moderate hypobaric hypoxia was observed at doses of 30 and 100 mg/kg, p.o. Idebenone (100 and 300 mg/kg, p.o.) significantly prolonged the survival time of mice in this model, but oxiracetam (30-300 mg/kg, p.o.) did not. Oral administration of all of these drugs (BMY-21502, 3-300 mg/kg; Oxiracetam, 100-1000 mg/kg; Idebenone, 100-1000 mg/kg) failed to increase the number of gasps and the duration of gasping in the decapitated head of mice as a complete ischemic model. The anti-anoxic effect of BMY-21502 in the KCN-anoxia model was blocked by pretreatment with scopolamine. These findings suggest that BMY-21502 has an anti-anoxic action superior to those of the other cerebroactive drugs used, and activation of the CNS cholinergic system is involved as one of the causative mechanisms for the anti-anoxic effect of BMY-21502.

Summary 1. The effects of anoxia on the electrocardiogram can be prevented by theinjection of cytochrome C. 2. Subjects seem to tolerate anoxia more easily when they have been previously injected with cytochrome C. 3. The effects of anoxia in impairing visual discrimination can be overcomeby the intravenous injection of cytochrome C. 4. The effects of anoxia in slowing the cerebral functions required for code transliteration can be overcome by the injection of cytochrome C.

To investigate mechanisms of cerebral anoxia tolerance, cerebrocortical intracellular calcium ([Ca2+]i) and pH (pHi) regulation were compared in turtles (Trachemys scripta) and laboratory rats. [Ca2+]i and pHi in living 200 to 300-microns-thick cortical brain slices were measured with the fluorescent indicators fura-2/acetoxymethyl ester (AM) and 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein during exposure to anoxia. Within 5 min, [Ca2+]i increased to > 1,000 nM in rat brain slices exposed to anoxia but [Ca2+]i was normal even after 5 h of anoxia in turtles. ATP levels remained normal in anoxic turtle brain but fell rapidly in rats. During anoxia, pHi fell by 0.25 +/- 0.08 pH units in rats but only 0.10 +/- 0.04 in turtles (P < 0.05). Inhibition of glycolysis in anoxic turtle brain with iodoacetate resulted in large increases in [Ca2+]i but prior exposure of slices to anoxia resulted in greatly attenuated calcium entry. The reduction in calcium flux was greater with increasing exposure to anoxia, suggesting progressive arrest of calcium channel activity. Tolerance of cerebral anoxia in turtles may be related to anaerobic ATP production, arrest of calcium channels, and attenuation of changes in pHi.

Autoerotic asphyxia is the practice of self-inducing cerebral anoxia, usually by hanging, strangulation, or suffocation, during masturbation. This study investigated the relationships between: asphyxiators' ages; two paraphilias commonly accompanying autoerotic asphyxia, bondage and transvestism; and various other types of simultaneous sexual behaviour. Subjects were two concurrent series totalling 117 males aged 10–56 who died accidentally during autoerotic asphyxial activities. Data concerning sexual paraphernalia at the scene of death or among the deceased's effects were extracted from coronors' files using standardised protocols. Anal self-stimulation with dildos, etc., and self-observation with mirrors or cameras were correlated with transvestism. Older asphyxiators were more likely to have been simultaneously engaged in bondage or transvestism, suggesting elaboration of the masturbatory ritual over time. The greatest degree of transvestism was associated with intermediate rather than high levels of bondage, suggesting that response competition from bondage may limit asphyxiators' involvement in a third paraphilia like transvestism.

For the most part, the clinical picture is the expression of autogenic pathology and, unless the anatomical insult represents a major structural compromise, it contributes little to the clinical picture. Autogenic pathology created by the processing of peripheral neurological impulses altered by the presence of anatomical insults is created independently of the gravity of the anatomical insults. Even in the presence of a survivable insult, autogenic pathology is often fatal. Each successful resuscitation effort identifies a patient with a survivable insult who almost died before autogenic pathology was removed by cerebral anoxia, and/or electric shock. Similar patients who suffer terminal brain damage cannot be identified. Cardinal receptors furnish the embryo with its first neural contact with its environment. On completion of embryological migration, they occupy a position in the skin overlying the root of their spinal nerve. Cardinal receptors are functionally segmented to the specific distribution of their spinal nerve and use the stable neurological impulses from the skin to furnish the cadence by which peripheral impulses are processed and valued. Selected cardinal receptors may be specifically stimulated by saline infiltration that produces intradermal blebs in the skin overlying their spinal nerve's root. An augmented burst of infiltration pain immediately followed by symptomatic relief identifies monitoring cardinal receptors. The identification of monitoring receptors confirms the presence of pathology found within the specific distribution of their spinal nerve. Peripheral impulses processed within the cadence of highly stimulated cardinal receptors are assigned an insignificant value. Assigning an insignificant value to peripheral impulses altered by the presence of an anatomical insult removes autogenic pathology from the clinical picture. The immediate onset of profound symptomatic relief heralds the removal of autogenic pathology. Visceral pathology is monitored by bilateral pairs of cardinal receptors so it produces discomfort perceived without specific location information. Therefore, the specific visceral distribution has been discounted and is virtually unknown. However, when visceral pathology is correlated with bilateral pairs of monitoring cardinal receptors there are no patient variations.

Prognostication of comatose patients after cardiac arrest presents many challenges. Most clinicians rely upon clinical neurological examination findings to predict outcome. The outcome is usually considered unfavorable when a patient experiences persistent brainstem dysfunction. However, prognostic scales, which rely upon brainstem dysfunction alone, are flawed. Some patients with brainstem dysfunction recover while patients with preserved brainstem function often die without awakening as a result of irreversible destruction of the cerebral cortex.

An electroencephalogram disclosing electrocerebral silence (ECS) after cardiopulmonary resuscitation (CPR) is usually considered an unfavorable prognostic indicator associated with brain death or persistent vegetative state. I report a case of a comatose patient following cardiac arrest, whose initial electroencphalography (EEG) was isoelectric taken 5 h after onset. Median somatosensory evoked potentials (SSEP) obtained immediately after the initial EEG were normal. He then underwent gradual recovery of neurologic function with incremental improvement on serial EEG study, and eventually achieved full neurological recovery. SSEP proved to be a more reliable predictor of a neurological outcome that was ultimately favorable.

A 57-year-old, previously healthy tourist sustained closedhead trauma during a high-speed motor vehicle collision. She was found unconscious at the scene with a Glasgow coma scale score of 3. She suffered a multitude of injuries including frontal scalp lacerations and cervical cord injury. Upon arrival at the hospital, she suffered cardiopulmonary arrest of up to 12 minutes without a perfusing rhythm and was intubated.

Hanging is one of the most common methods of suicide in India in which death of the individual occurs instantaneously. However, a few cases have been reported in literature in which death has occurred after a certain period of time or the patient has survived after prolonged resuscitative measures. A case of a 20-year-old female is described who survived for nine days after hanging, remaining unconscious throughout in the hospital. She died due to cerebral damage caused by cerebral anoxia.

Most victims of non-lethal (suicidal) hanging are young men and survivors are uncommon. Laryngo tracheal injuries and spinal injuries, although reported in 20-50% of post mortem examinations, are infrequent in survivors. Pulmonary complications are implicated in most in hospital deaths. Initial neurological presentation is of limited prognostic value; a poor initial presentation does not exclude a good recovery if managed in time [1]. We present a case of a suicidal hanging that presented with features of cerebral anoxia and developed non cardiogenic pulmonary edema. Early resuscitation and aggressive management led to complete recovery without any residual neurological deficit.

We report a 36-year-old woman with ventricular fibrillation, subsequent sudden clinical cardiac death, and a prolonged brain anoxia. After a successful resuscitation coronary angiography revealed congenital ostial left main coronary artery (LMCA) stenosis. Surgical anastomosis of the left internal mammary artery (LIMA) to LAD led to a complete recovery. Postoperative electrophysiological examination, mainly programmed ventricular stimulation, failed to excite any rhythm disturbances. Cathet. Cardiovasc. Intervent. 48:67-70, 1999.

Although cerebral anoxia is not thought to be responsible for triggering near-death experiences (NDEs), the issue is not so clear in the case of hypercapnia. Detection of normal blood gases in Michael Sabom's (1982) case study seems to be the major reply to suggestions that hypercapnia may have a causal role in NDEs. We argue, however, that routine arterial measures of blood gases are not a reliable indicator of cerebral levels.

Background: Cerebral metabolic monitoring in critical neurological patients allows the assessment of neuronal tissue response to injury and to plan the best therapy to correct each critical brain situation. Aim: To evaluate the usefulness of cerebral metabolic monitoring in patients with acute cerebral injury. Patients and methods: A retrospective analysis of 29 patients with acute brain injury, in whom a catheter was located in the bulb of the jugular vein to perform a cerebral metabolic monitoring. These patients were compared with others that were not subjected to this monitoring. The evolution at six months of follow up was assessed using the Glasgow outcome score, considering a favorable evolution when this score was 4 or greater. Results: Patients with an hyperemic state on admission or after optimization of therapy did not have hospital mortality, and 73% had Glasgow outcome score of 4 or greater at six months of follow up. On the other hand, 50% of those with hypoperfusion or global ischemia died during hospitalization and 72% had a Glasgow outcome score of 3 or less at six months. Patients not subjected to cerebral metabolic monitoring behave as those with hypoperfusion or global ischemia. Conclusions: Cerebral metabolic monitoring is an useful tool to optimize the management of patients with acute cerebral injury, and those patients with an hyperemic cerebral state have the best prognosis.

Hanging leads to post-anoxic encephalopathy and cerebral death by gradual or acute, partial or complete failure of brain oxygen supply, in relation with a circulatory arrest at the cephalic level. Attempted suicide is the most common situation, but accidental hanging may also occur.

While it has been reported that ischemic stroke significantly increases the risk of delayed dementia,1,2 the underlying mechanisms are not well understood. Hypoxic and ischemic (HI) injury resulting from cerebral hypoperfusion due to systemic illness has been proposed as a pathogenic mechanism in certain subgroups of patients.1,3 Thus, the aim of this study was to investigate whether cerebral HI injury resulting from certain systemic illnesses (e.g., cardiac arrhythmias, cardiac failure, pneumonia, seizures, sepsis) would be an independent risk factor for the development of incident dementia after ischemic stroke.

The aims were to study excitatory amino acid dependent mechanisms that contribute to evolution of brain damage after hypoxia-ischemia (HI) and to evaluate the neurotoxicity of N-methyl-D-aspartate receptor (NMDAR) antagonists in the immature brain.HI was induced in 7-day-old rats by unilateral carotid occlusion and 1-2 h of hypoxia. Posttreatment with the NMDAR antagonist MK-801 and the AMPA receptor antagonist NBQX, and pre- or posttreatment with the voltage dependent Na+ channel blocker BW1003C87 was evaluated by morphology and hemispheric weight 3 and 14 days after HI. Cerebral energy metabolites, energy utilization, glucose utilization (RCGU), mitochondrial respiration, morphology and blood flow (CBF) were studied after HI in controls and in MK-801 posttreated rats.The possible neurotoxicity of NMDAR antagonists was evaluated by RCGU and heat shock protein 72 (HSP72) expression.MK-801 (0.3-0.5 mg/kg) and NBQX (40 mg/kg) reduced brain injury by 38-61% and 27%, respectively. MK-801 neuroprotection was not related to hypothermia. Pretreatment with BW1003C87 (10 mg/kg) reduced brain injury by 45% whereas posttreatment was ineffective. Between 2-6 h after HI, the energy utilization and CBF were unaltered, the high energy phosphate levels recovered to 75% of control and mitochondrial respiration decreased by 46%. The RCGU and tissue lactate levels were increased. Posttreatment with MK-801 reduced energy utilization by 43% and RCGU by 30 % and improved mitochondrial function by 42% but did not affect the tissue levels of ATP and phosphocreatine at 3 h. Between 8-24 h, regions with low RCGU and loss of the neuronal marker microtubule associated protein 2 replaced regions with high RCGU. A secondary deterioration of high energy phosphates was prevented by MK-801. CBF declined by 80% between 24 and 48 h after HI. MK-801 or MgSO4 did not increase RCGU or induce HSP72 expression. In conclusion, evolution of brain damage is related to NMDAR and AMPA receptor dependent processes during reperfusion. Activation of NMDARs sustains the energy demand and impairs the energy production which may be critical for the survival of the tissue.

Ischemia and reperfusion afterward provoke a characteristic series of events which is common among tissues. Many of the changes produced by ischemia are easily measurable with non-invasive optical or electrode probes in intact or isolated tissues. Among these changes are shifts toward reduction of the electron carriers of the mitochodrial respiratory chain, depletion of tissue oxygen, suppression of the tissue’s functional activities and loss of ion homeostasis. Figure 1 is a composite drawing which illustrates some of these typical events in the cerebral cortex of an anesthetized rat.

Mild ischemic insults may limit damage from subsequent ischemic insults in heart and brain (Murry et al., 1986; Kato et al., 1992; Li et al., 1992; Liu et al., 1992; Walker et al., 1993). This phenomenon was defined as ischemie preconditioning (IPC). In brain, for example, 3 min of sublethal ischemia followed by 3 days of reperfusion protected against hippocampal CA1 neuronal damage after 8 min of ischemia (Liu et al., 1992). Preconditioning also improved evoked potential recovery in hippocampal slices (Schurr et al., 1986; Schurr and Rigor, 1987). Studies reported here seek to further characterize IPC in intact brain and to derive insights into its mechanism through studies in hippocampal slices. The rationale for these studies is derived from the belief that understanding the mechanisms of IPC could offer unique insights into basic mechanisms of ischemie injury and into potential therapies to ameliorate the consequences of anoxia or ischemia.

A six-year old girl wrote to God: ‘Granny is very sick. Mommy says she will die, What is death? I don’t want her to die and I don’t want to die. But I would like to know what death is.’ We don’t know whether God replied to her question but we do know that, young or old, the question raised by the little girl is the oldest and most persistent and absorbing of all in its interest. What is death: extinction? or is there some sort of afterlife?

It is a fact, that there is no definite criterion for dengue encephalitis. Initially, dengue encephalopathy should be discarded for a correct diagnosis of encephalitis. Cerebral anoxia, edema and/or toxicity secondary to liver failure and electrolyte dysfunction are determinants of dengue encephalopathy and should be excluded [1]. In response to Dr. Varatharaj, the need of a validation and adoption of a dengue encephalitis case definition is fundamental. Especially for clinicians who are unfamiliar with this disease. We suggest that for the definition of dengue encephalitis some points should be followed