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The purpose and indications for continuous electroencephalography monitoring (CEEG) in intensive care unit (ICU) patients include seizure detection, monitoring the effects of treatment (including depth of sedation), grading and classification of EEG abnormalities, ischemia detection and prognostication. Practical considerations of ICU CEEG include: choice of montages (patterns of electrode placement and connections), EEG electrodes, recognition of artifacts, and the use of automated or computerized analysis. These aspects are reviewed, along with an identifcation of current advances and challenges for the future of CEEG in the ICU.

Continuous EEG Monitoring is becoming a commonly used tool in assessing brain function in critically ill patients. However, there is no uniformly accepted nomenclature for EEG patterns frequently encountered in these patients such as periodic discharges, fluctuating rhythmic patterns, and combinatio

Objective: To evaluate the possible role of the default mode network (DMN) in consciousness and assess the diagnostic or prognostic potential of DMN connectivity measures in the assessment of a patient group lacking cognitive awareness. Methods: DMN connectivity was established using independent component analysis of resting-state fMRI data in patients with reversible (n = 2) and irreversible (n = 11) coma following cardiac arrest and compared to healthy controls (n = 12). Results: A present and intact DMN was observed in controls and those patients who subsequently regained consciousness, but was disrupted in all patients who failed to regain consciousness. Conclusions: The results suggest that the DMN is necessary but not sufficient to support consciousness. Clinically, DMN connectivity may serve as an indicator of the extent of cortical disruption and predict reversible impairments in consciousness.

The syndrome of involuntary craniofacial lingual movements in the setting of acute intensive care-acquired quadriplegia (critical illness neuromyopathy) following sepsis-associated encephalopathy has not been previously described. We suggest a localization and treatment for this disabling condition.Three patients (2 female) from our center were quadriplegic from critical illness neuromyopathy when they developed involuntary craniofacial lingual movements following sepsis-associated encephalopathy.Extensive investigations failed to identify an etiology for the abnormal movements. Movements were of large amplitude, of moderate speed, and semi-rhythmic in the jaw, tongue, and palate, persistent and extremely bothersome to all patients. Injection with Botulinum toxin type A was very beneficial.Involuntary craniofacial lingual movements in the setting of flaccid quadriplegia following sepsis-associated encephalopathy are consistent with focal craniofacial brainstem myoclonus and constitutes a new syndrome. Botulinum toxin type A treatment maybe helpful in treatment.

Hyperacute hepatic failure (HHF) has a high mortality rate that is most commonly due to severe cerebral edema. However, brain swelling and marked clinical and EEG suppression are potentially reversible, even though the same findings are associated with a very poor neurological outcome in anoxic-ischemic encephalopathy. We present three cases that illustrate neurological recovery despite severe brain swelling and loss of EEG activity. All patients recovered conscious awareness, including one who transiently lost cranial nerve reflexes. Despite deep coma, markedly suppressed EEG and brain edema, aggressive control of ICP may lead to good recovery in acute hepatic failure.

Respiratory electrophysiological studies are of essential value in diagnosing and managing patients with respiratory failure, but assessment of the sensory phrenic nerve fibres has been neglected. We recorded phrenic nerve somatosensory evoked potentials (SSEPs) by combining neurophysiological and neuroimaging techniques in three healthy subjects. Evoked potentials of the phrenic nerve showed the highest amplitude at CP3, determined by the modified 10–20 EEG system, and occurred at a constant latency, PI at 12.0 ± 0.6 ms, and NI at 17.3 ± 0.8 ms. Single photon emission computer tomography (SPECT) performed during phrenic nerve stimulation revealed focal neuronal activation in the somatosensory pathways. Intravenously administered Tc-99m Ethyl Cysteinnate Dimmer (ECD) was used as a blood flow tracer to obtain baseline and activated images. After image registration, baseline images were compared voxel-by-voxel with the activation images. The mean inter-subject summation image of the activated state was compared with that of the baseline state using ten normal subjects. The extent of the total voxel volume increase on the mean images of the 3 activated SPECT images was 0.7%, and a mean signal increase of 22%. For further anatomic localization of regional increases in signal, the magnetic resonance image (MRI) scan of each subject was registered and superimposed on the activated stage SPECT image. This method may be used clinically to study the pathophysiology of impaired central respiratory drive.

The authors report a case of a 71-year-old man who developed myoclonic status epilepticus and coma after daily ingestion of colloidal silver for 4 months resulting in high levels of silver in plasma, erythrocytes, and CSF. Despite plasmapheresis, he remained in a persistent vegetative state until his death 5.5 months later. Silver products can cause irreversible neurologic toxicity associated with poor outcome.

There has recently been interest in neuroleptic malignant syndrome (NMS) as the disorder has been better characterized. Nms is still poorly recognized, however, by most physicians. Hyperpyrexia, rigidity, altered consciousness, autonomic instability, and enzymatic evidence of muscle breakdown after drug intake are the cardinal features. The authors of this article review the proposed pathogenesis, complications, and treatment of NMS.

Encephalopathy and polyneuropathy occur in 70% of septic patients. The encephalopathy is diffuse, appears early, is often severe, but reverses quickly with successful treatment of the sepsis. The electroencephalogram is a sensitive indicator of the incidence and severity of the encephalopathy, but computed tomograms of the brain and cerebrospinal fluid findings are unremarkable. Critical-illness polyneuropathy develops later and in association with multiple-organ failure. Recovery is more gradual. Difficulty in weaning from the ventilator is an important early manifestation. Electromyography should be routinely performed to establish the diagnosis. The polyneuropathy is a primary axonal degeneration, predominantly of distal motor fibers. A persistent deficit may eventuate in severe cases. Whether muscle is affected as consistently as brain and peripheral nerve, and by the same process, has not been determined. Medications used in critical care units, notably sedatives and neuromuscular blocking agents, often confuse the clinical picture. The neurological pathophysiology is unknown but current evidence suggests that nervous system dysfunction arises through the same mechanisms as for systemic organs in the septic syndrome.

Forty-three patients who had sepsis and multiple organ failure (critical illness) were studied prospectively to determine the incidence and severity of peripheral nerve function and to correlate such function with a number of variables. Electrophysiologic studies indicated a primary axonal degeneration of motor and sensory fibers in 30 (70 percent). Fifteen (30 percent) had the clinical signs of difficulty in weaning from assisted ventilation, weakness of limb muscles, and reduced or absent deep tendon reflexes. Full recovery from the polyneuropathy occurred among the 23 (53 percent) who survived, except three who had a very severe polyneuropathy. A peripheral nerve function index, computed from electrophysiologic measurements, showed statistically significant (p less than 0.01) negative correlations with the time in the critical care unit, and the serum glucose value; the serum albumin level showed a positive correlation. Multiple regression analyses indicated all three factors accounted for 47 percent (r2 = 0.4678) of all potential variables. In a separate analysis, the nerve function index correlated with the amplitude of the diaphragm compound muscle action potential (p less than 0.01). The results were consistent with the polyneuropathy being due to the same mechanisms that are currently postulated to cause dysfunction in this syndrome of other organ systems (including the neuromuscular respiratory system).

Objective: To systematically review outcomes in comatose survivors after cardiac arrest and cardiopulmonary resuscitation (CPR). Methods: The authors analyzed studies (1966 to 2006) that explored predictors of death or unconsciousness after 1 month or unconsciousness or severe disability after 6 months. Results: The authors identified four class I studies, three class II studies, and five class III studies on clinical findings and circumstances. The indicators of poor outcome after CPR are absent pupillary light response or corneal reflexes, and extensor or no motor response to pain after 3 days of observation (level A), and myoclonus status epilepticus (level B). Prognosis cannot be based on circumstances of CPR (level B) or elevated body temperature (level C). The authors identified one class I, one class II, and nine class III studies on electrophysiology. Bilateral absent cortical responses on somatosensory evoked potential studies recorded 3 days after CPR predicted poor outcome (level B). Burst suppression or generalized epileptiform discharges on EEG predicted poor outcomes but with insufficient prognostic accuracy (level C). The authors identified one class I, 11 class III, and three class IV studies on biochemical markers. Serum neuron-specific enolase higher than 33 μg/L predicted poor outcome (level B). Ten class IV studies on brain monitoring and neuroimaging did not provide data to support or refute usefulness in prognostication (level U). Conclusion: Pupillary light response, corneal reflexes, motor responses to pain, myoclonus status epilepticus, serum neuron-specific enolase, and somatosensory evoked potential studies can reliably assist in accurately predicting poor outcome in comatose patients after cardiopulmonary resuscitation for cardiac arrest.

Editors' Note: The 1994 guidelines for the diagnosis of the vegetative state (VS) should be revised, Young and Owen suggest. Estraneo et al. agree, pointing to the development of new, advanced tools that improve recognition of discernible intentional responses in patients with prolonged anoxic VS. Some corrections and interesting additions to the historical article on cerebral PET scanning are made by Singhal. Okun et al. agree and explain the challenge of word count limit. Chafic Karam, MD, and Robert C. Griggs, MD # {#article-title-2} Estraneo et al.1 prospectively …

About 40% of patients with cardiac arrest can be resuscitated with restoration of spontaneous circulation and respiration. The overall 1 year survival rate of initially unconscious survivors resuscitated from cardiac arrest has been variably quoted to be between 10 and 25% [1, 2]. Anoxic-ischemic encephalopathy is the principal cause of mortality in at least 30–40% of those who die; only 3–10% return to their previous lifestyle, including employment [3]. Under 1% survive in a persistent vegetative state (PVS) [4]. Since primary cardiac arrest is so common, the problems of assessment and management of anoxic-ischemic encephalopathy are of great importance to the intensivist and emergency physician.

Amino acids and their derivatives are transported into and out of cells by a variety of permease types which comprise several distinct protein families. We here present a systematic analysis of a group of homologous transport proteins which together comprise the eukaryotic-specific amino acid/auxin permease (AAAP) family (TC #2. 18). In characterizing this family, we have (1) identified all sequenced members of the family, (2) aligned their sequences, (3) identified regions of striking conservation, (4) derived a family-specific signature sequence, and (5) proposed a topological model that appears to be applicable to all members of the family. We have also constructed AAAP family phylogenetic trees and dendrograms using six different programs that allow us to trace the evolutionary history of the family, estimate the relatedness of proteins from dissimilar organismal phyla, and evaluate the reliability of the different programs available for phylogenetic studies. The TREE and neighbor-joining programs gave fully consistent results while CLUSTAL W gave similar but non-identical results. Other programs gave less consistent results. The phylogenetic analyses reveal (1) that many plant AAAP family proteins arose recently by multiple gene duplication events that occurred within a single organism, (2) that some plant members of the family with strikingly different specificities diverged early in evolutionary history, and (3) that AAAP family proteins from fungi and animals diverged from the plant proteins long ago, possibly when animals, plants and fungi diverged from each other. The Neurospora protein nevertheless exhibits overlapping specificity with those found in plants. Preliminary evidence is presented suggesting that proteins of the AAAP family are distantly related to proteins of the large ubiquitous amino acid/polyamine/choline family (TC #2.3) as well as to those of two small bacterial amino acid transporter families, the ArAAP family (TC #2.42) and the STP family (TC #2.43).

Septic encephalopathy resembles many metabolic encephalopathies and is largely reversible, although some survivors of severe septic illness may have residual cognitive problems. These deficits may relate to microscopic abnormalities in the brain that we have found at autopsy. Biochemical abnormalities are directly related to the severity of the encephalopathy. It is unlikely that organ failure accounts for the early encephalopathy, but multi-organ failure probably contributes to brain dysfunction in advanced sepsis.

Metabolic encephalopathies are common among patients in the critical care unit. Septic, hypoxic-ischaemic, hepatic and uraemic encephalopathies are most frequently seen. They produce global neurological dysfunctions ranging from lethargy or mild confusion to coma. Metabolic encephalopathies must be distinguished from other conditions such as structural brain lesions, infections of the central nervous system or drug reactions. Neurological manifestations are often present in the early stages of systemic illness and may be the first symptom. The severity of encephalopathy generally correlates with that of the systemic illness. Appropriate investigations often include drug and metabolic screens, cultures of blood and cerebrospinal fluids and neuro-imaging studies. Electroencephalogram is useful to grade the severity of encephalopathy. With some exceptions such as hypoxic-ischaemic encephalopathy, most metabolic encephalopathies are reversible unless secondary complications such as brain herniation occurred. Treatment is generally that of the underlying systemic illness and supportive measures.

The four principles of ethical behaviour are autonomy of the patient, beneficence, non-maleficence and justice. The physician must strive to do what is best for the patient while respecting that person's wishes. This allows for decision-making, including withdrawal of care, using the patient's advance directives. Brain death is equivalent to death and should not pose decision-making problems. Making decisions for the patient who was never competent requires close co-operation among physicians, other care-givers and substitute decision-makers, while respecting ethical principles and the risk-to-benefit ratio. In most countries euthanasia, while controversial, is illegal. Safeguards and ethical principles for the enrollment of patients in clinical trials, the importance of informed consent and conduct as an expert witness all involve the above ethical principles and responsibility.

Respiratory electrophysiological studies are of essential value in diagnosing and managing patients with respiratory failure, but assessment of the sensory phrenic nerve fibres has been neglected. We recorded phrenic nerve somatosensory evoked potentials (SSEPs) by combining neurophysiological and neuroimaging techniques in three healthy subjects. Evoked potentials of the phrenic nerve showed the highest amplitude at CP3, determined by the modified 10-20 EEG system, and occurred at a constant latency, PI at 12.0 +/- 0.6 ms, and NI at 17.3 +/- 0.8 ms. Single photon emission computer tomography (SPECT) performed during phrenic nerve stimulation revealed focal neuronal activation in the somatosensory pathways. Intravenously administered Tc-99m Ethyl Cysteinate Dimer (ECD) was used as a blood flow tracer to obtain baseline and activated images. After image registration, baseline images were compared voxel-by-voxel with the activation images. The mean inter-subject summation image of the activated state was compared with that of the baseline state using ten normal subjects. The extent of the total voxel volume increase on the mean images of the 3 activated SPECT images was 0.7%, and a mean signal increase of 22%. For further anatomic localization of regional increases in signal, the magnetic resonance image (MRI) scan of each subject was registered and superimposed on the activated stage SPECT image. This method may be used clinically to study the pathophysiology of impaired central respiratory drive.

Of 49 patients with nonconvulsive seizures studied with continuous EEG monitoring, the overall mortality was 33% (16/49).Of the 23 patients with nonconvulsive status epilepticus (NCSE), 13 died (mortality 57%). Individual variables significantly associated with mortality were age, presence of NCSE, seizure duration, hospital and NICU length of stay, and delay to diagnosis and etiology (acute illness versus remote symptomatic). With multivariate logistic regression, only seizure duration (p = 0.0057, OR = 1.131/hour) and delay to diagnosis (p = 0.0351, OR = 1.039/hour) were associated with increased mortality. Acute symptomatic cases could not be adequately classified as either absence, simple, or complex partial status epilepticus when the impairment of consciousness arose from the initial illness. Current classifications of status epilepticus are inadequate for such cases.NEUROLOGY 1996;47: 83-89

In the study of Crepeau et al.,1 there are several findings of interest. These include both novel and confirmatory results: 1) the EEG classification had prognostic value for favorable and unfavorable outcomes; 2) patients with electrographic reactivity were much more likely to recover consciousness than those who did not; 3) the EEG can vary and this can yield prognostic information; 4) all 5 patients with seizures died; 5) episodic low-amplitude events, essentially a burst-suppression pattern, did not have the sinister prognosis that had been found in earlier studies where hypothermia was not used.

OBJECTIVE: To document the criteria used to declare brain death in a pediatric critical care unit (PCCU). DESIGN: Retrospective chart review. SETTING: Regional PCCU in southwestern Ontario. PATIENTS: Sixty patients 16 years of age or less declared brain dead from January 1987 through December 1992. OUTCOME MEASURES: Presence or absence of documentation of irreversible deep coma, nonresponsive cranial nerves, absent brain-stem reflexes, persistent apnea after removal from ventilator, presence or absence of blood flow detected by radioisotope scanning, presence or absence of electroencephalographic evidence of electrocerebral activity. RESULTS: The 60 patients accounted for 1.5% of all PCCU admissions; 17 were under 1 year of age. In 39 cases brain death was diagnosed using clinical criteria ("certified brain death"), which could not be fully applied in the remaining 21 cases ("uncertifiable but suspected brain death"). Electroencephalography and cerebral blood-flow studies with technetium-99m hexamethyl-propyleneamine oxime were used as ancillary tests in 16 patients with certified brain death and in 17 with uncertifiable but suspected brain death who survived long enough to be tested. Electrocerebral silence was demonstrated in all nine patients who underwent electroencephalography. Cerebral blood flow was undetectable in 26 of the 30 patients tested, and an abnormal pattern of blood flow was seen in the remaining 4, all of whom received a diagnosis of certified brain death. CONCLUSIONS: Pediatricians in this large tertiary care referral centre are using clinical criteria based on the 1987 guidelines of the CMA to diagnose brain death in pediatric patients, including neonates. When clinical criteria cannot be fully applied, ancillary methods of investigation are consistently used. Although the soundness of this pattern of practice is established for adults and older children, its applicability to neonates and infants still needs to be validated.

Neurologic complications of systemic illnesses may affect any part of the nervous system in various conditions. In many systemic disorders, however, an acute confusional state is the first manifestation. It is urgent to make a definitive diagnosis and begin specific and supportive therapy to lessen mortality and morbidity. A case of severe septic illness with central and peripheral nervous system complications is reviewed. Septic encephalopathy and critical illness polyneuropathy are common conditions in the general ICU. The neuropathy often is the underlying cause for failure to wean from the ventilator.

Objective: To develop a method for automatically detecting non-convulsive seizures in ICU. Background Seizures are found in at least 8% of ICU patients; of these, 50-100% have only non-convulsive seizures detectable only by continuous EEG monitoring. Non-convulsive seizure duration and delay to treatment have been shown to be associated with increased mortality [1]. Seizure detection and management is problematic: a skilled electroencephalographer is not always available, generating a need for an automated seizure detection system. Design/Methods: Using a database of 179 ICU patients undergoing continuous EEG (148d) monitoring, we have developed a method that quantifies seizure-related evolution in a two-dimensional feature space consisting of EEG frequency and power. The method was evaluated in an independent data set of 53 ICU and epilepsy monitoring unit (EMU) patients (50d) [2]. All data were analyzed by an experienced electroencephalographer (BY), who marked the onsets and offsets of ten first seizures in each recording using commonly accepted seizure criteria [1]. Seizure detection was classified successful, if it took place within 15 minutes of the first marked seizure. Results: 10/19 seizure patients of the development data set were detected (false positive rates (FPR): median 0.00/hour, mean 0.34/hour). In the evaluation data set 6/8 seizure patients were detected (FPRs: 0.06/hour, 0.52/hour). Undetected patients were either in status epilepticus (SE) or had no seizures with evolutionary characteristics. Most false detections were caused by EMG. Conclusions: The method demonstrates good potential in detecting seizures with evolution, which further can be visualized in 2-D plane, facilitating seizure recognition at the bedside. To cover the full range of seizure disorders, the method needs to be integrated with methods suitable for spike detection and SE monitoring, such as WSE [3]. Further work will focus also on reducing FPR. Supported by: GE Healthcare, Finland OY. Disclosure: Dr. Tanner has received research support from GE Healthcare. Dr. Sarkela has received research support from GE Healthcare. Dr. Tolonen has received personal compensation for activities with GE Healthcare as an employee. Dr. Norton has nothing to disclose. Dr. Davies-Schinkel has nothing to disclose. Dr. Sharpe has nothing to disclose. Dr. Young has nothing to disclose.

Ipsilateral third nerve palsy with early pupillary enlargement is an important sign of transtentorial herniation from a supratentorial mass lesion. A case of frontal, intraparenchymal haemorrhage is reported in which the first ocular manifestation of transtentorial herniation was enlargement of the contralateral pupil. The ipsilateral pupil dilated only after complete oculomotor palsy of the contralateral eye. After partial frontal lobectomy and removal of blood clot, the ipsilateral third nerve recovered before the contralateral third nerve. Clinical findings localised the contralateral third nerve lesion to an extra-axial site. The possible mechanisms of contralateral third nerve compression are discussed. This seems to be the first example of pupillary enlargement as a false localising sign from a contralateral, supratentorial, intraparenchymal mass lesion.

Physicians and surgeons have long recognized that septic illness may be accompanied by abnormal brain functions; however, no systematic, comprehensive study has been done to define the clinical and laboratory features of the syndrome of sepsis-associated encephalopathy. We undertook such a prospective study in a tertiary care hospital and found that of 69 patients with fever and microbial cultures, 32 had marked brain dysfunction, 17 showed mild encephalopathy, and 20 were clinically nonencephalopathic. Severe cases showed obtundation and paratonic rigidity while milder cases showed confusion, inappropriate behavior, inattention, disorientation, and writing errors. There were no focal neurological deficits. The following factors correlated with the severity of brain dysfunction: adult respiratory distress syndrome; fatal outcome; certain types of EEG abnormality; axonal peripheral neuropathy; elevated peripheral white blood cell count; elevated serum levels of alkaline phosphatase, bilirubin, creatinine, phosphate, potassium, and urea; reduced blood pressure and reduced serum albumin level. Our data suggest that brain functions fail with dysfunction of other organs in septic illness. Pathogenetic mechanisms are discussed. The brain dysfunction should be regarded as potentially reversible, even in severely encephalopathic cases. Prompt control of the infection is the most important measure in controlling the encephalopathy and in preventing the increased mortality found with severely encephalopathic patients.

The clinical and pathological features, including electron microscopy of a sporadic case of neuroaxonal dystrophy with findings of both Hallervorden-Spatz syndrome (HS) and Seitelberger's disease (SD) are presented. The patient presented with a slowly progressive illness with seizures, extrapyramidal symptoms, cerebellar ataxia, dementia, spasticity, myoclonic movements and a severe demyelinating peripheral neuropathy with secondary muscular atrophy. Neuropathological examination disclosed cerebral and cerebellar atrophy and excessive pigmentation of the globus pallidus and substantia nigra. Spheroids were widely distributed within the central and peripheral nervous system. Numerous neurofibrillary tangles (NFTs) were found within the hippocampal cortex, neocortex and brain stem. Extensive granulovacuolar degeneration (GVD), Hirano bodies and Lewy bodies were also demonstrated. Severe loss of myelin from the peripheral nerves and muscular denervation were striking features. We wish to report this case which shares findings of both entities, HSS and SD.

Effect of Continuous Infusion of Morphine on the Electroencephalogram of Infants, Admitted to a Neonatal Intensive Care Unit

We report 11 adults who exhibited myoclonic status epilepticus (MSE) after cardiac arrest. Based on pathologic, electroencephalographic, and clinical evidence, we conclude that our patients died from the initial anoxic-ischemic insult rather than as a result of MSE. We suggest that the seizures in these nonsurvivors were self-limited events arising from lethal damage to neurons. Thus, in patients with bilaterally synchronous facial myoclonus, bilateral loss of pupillary or oculovestibular reflexes, and suppression and burst-suppression on EEG, it is not warranted to use anesthetic barbiturates to treat MSE.

A computer program is presented which calculates Zoeppritz's displacement amplitude coefficients, displacement potential coefficients, and Knott's energy coefficients for plane harmonic elastic waves of P or SV type incident on a plane interface between two isotropic, homogeneous elastic solids. A discussion of these three basic types of coefficients is included. Results of applying the program to a sample case are presented in the form of a graph of the energy coefficients computed for all possible wave types and over a range of angle of incidence of 0° to 90°.

The Edinburgh Breast Screening Clinic in its first year completed the initial screening examination of 3005 invited women, who were apparently in good health, aged between 40 and 60 years; 141 were referred for a surgical opinion; 70 women ultimately underwent biopsy and 9 proved to have carcinoma. The indications for biopsy are described together with methods of management of the various lesions.

Myo-inositol was given orally to nine multiple sclerosis patients and nine healthy control subjects. Pattern reversal evoked potential testing was used to assess its effect. The principal positive wave increased in amplitude, duration and area in a dose-dependent manner in the multiple sclerosis group compared with controls. Cerebrospinal fluid concentrations of myo-inositol in multiple sclerosis and controls were similar. The significance of these observations is discussed in relation to recent discoveries in inositol phospholipid function.

The principal ultrasonic signs of death of the fetus in the first 12 weeks of pregnancy are reviewed and illustrated. Several new signs, one probably due to CO2 in the conceptus, are recorded. The use of two-dimensional B scanning and multiplanar stereoscopic sonar is made.