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BACKGROUND: In brain death donors (BDDs), donor management is the key in the complex donation process. Donor management goals, which are standards of care or clinical parameters, have been considered an acceptable barometer of successful donor management. AIM: To test the hypothesis that aetiology of brain death could influence haemody namic management in BDDs. METHODS: Haemodynamic data (blood pressure, heart rate, central venous pressure, lactate, urine output, and vasoactive drugs) of BDDs were recorded on intensive care unit (ICU) admission and during the 6-h observation period (Time 1 at the beginning; Time 2 at the end). RESULTS: The study population was divided into three groups according to the aetiology of brain death: Stroke (n = 71), traumatic brain injury (n = 48), and postanoxic encephalopathy (n = 19). On ICU admission, BDDs with postanoxic encephalopathy showed the lowest values of systolic and diastolic blood pressure associated with higher values of heart rate and lactate and a higher need of norepinephrine and other vasoactive drugs. At the beginning of the 6-h period (Time 1), BDDs with postanoxic encephalopathy showed higher values of heart rate, lactate, and central venous pressure together with a higher need of other vasoactive drugs. CONCLUSION: According to our data, haemodynamic management of BDDs is affected by the aetiology of brain death. BDDs with postanoxic encephalopathy have higher requirements for norepinephrine and other vasoactive drugs.

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Impairments of memory, attention, and executive functioning are frequently reported after acute onset brain injury. MRI markers hold potential to contribute to identification of patients at risk for cognitive impairments and clarification of mechanisms. The aim of this systematic review was to summarize and value the evidence on MRI markers of memory, attention, and executive functioning after acute onset brain injury. We included ninety-eight studies, on six classes of MRI factors (location and severity of damage (n = 15), volume/atrophy (n = 36), signs of small vessel disease (n = 15), diffusion-weighted imaging measures (n = 36), resting-state functional MRI measures (n = 13), and arterial spin labeling measures (n = 1)). Three measures showed consistent results regarding their association with cognition. Smaller hippocampal volume was associated with worse memory in fourteen studies (pooled correlation 0.58 [95% CI: 0.46-0.68] for whole, 0.11 [95% CI: 0.04-0.19] for left, and 0.34 [95% CI: 0.17-0.49] for right hippocampus). Lower fractional anisotropy in cingulum and fornix was associated with worse memory in six and five studies (pooled correlation 0.20 [95% CI: 0.08-0.32] and 0.29 [95% CI: 0.20-0.37], respectively). Lower functional connectivity within the default-mode network was associated with worse cognition in four studies. In conclusion, hippocampal volume, fractional anisotropy in cingulum and fornix, and functional connectivity within the default-mode network showed consistent associations with cognitive performance in all types of acute onset brain injury. External validation and cut off values for predicting cognitive impairments are needed for clinical implementation.

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OBJECTIVES: To assess neurological outcome after targeted temperature management (TTM) at 33 °C vs. 36 °C, stratified by the severity of encephalopathy based on EEG-patterns at 12 and 24 h. DESIGN: Post hoc analysis of prospective cohort study. SETTING: Five Dutch Intensive Care units. PATIENTS: 479 adult comatose post-cardiac arrest patients. INTERVENTIONS: TTM at 33 °C (n = 270) or 36 °C (n = 209) and continuous EEG monitoring. MEASUREMENTS AND MAIN RESULTS: Outcome according to the cerebral performance category (CPC) score at 6 months post-cardiac arrest was similar after 33 °C and 36 °C. However, when stratified by the severity of encephalopathy based on EEG-patterns at 12 and 24 h after cardiac arrest, the proportion of good outcome (CPC 1-2) in patients with moderate encephalopathy was significantly larger after TTM at 33 °C (66% vs. 45%; Odds Ratios 2.38, 95% CI = 1.32-4.30; p = 0.004). In contrast, with mild encephalopathy, there was no statistically significant difference in the proportion of patients with good outcome between 33 °C and 36 °C (88% vs. 81%; OR 1.68, 95% CI = 0.65-4.38; p = 0.282). Ordinal regression analysis showed a shift towards higher CPC scores when treated with TTM 33 °C as compared with 36 °C in moderate encephalopathy (cOR 2.39; 95% CI = 1.40-4.08; p = 0.001), but not in mild encephalopathy (cOR 0.81 95% CI = 0.41-1.59; p = 0.537). Adjustment for initial cardiac rhythm and cause of arrest did not change this relationship. CONCLUSIONS: Effects of TTM probably depend on the severity of encephalopathy in comatose patients after cardiac arrest. These results support inclusion of predefined subgroup analyses based on EEG measures of the severity of encephalopathy in future clinical trials.

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OBJECTIVE: To study if comatose cardiac arrest patients can be assessed with a reduced number of EEG electrodes. METHODS: 110 routine EEGs from 67 consecutive patients, including both hypothermic and normothermic EEGs were retrospectively assessed by three blinded EEG-experts using two different electrode montages. A standard 19-electrode-montage was compared to the reduced version of the same EEGs, down-sampled to six electrodes (F3, T3, P3, F4, T4, P4). We used intra-rater and inter-observer statistics to assess the reliability of the reduced montage for background features and discharges. RESULTS: The reduced montage had almost perfect performance for background continuity (κ 0.80-0.88), including identification of highly malignant backgrounds (burst-suppression/suppression) (κ 0.85-0.94) and benign backgrounds (continuous/nearly continuous) (κ 0.85-0.91). We found substantial performance for identifying rhythmic/periodic discharges (κ 0.79-0.86). The reduced montage had high accuracy for assessment of both highly malignant (sensitivity 91-95%, specificity 94-99%) and benign (sensitivity 89-98%, specificity 91-96%) backgrounds, and periodic/rhythmic patterns (sensitivity 79-100%, specificity 89-99%), compared to the full montage. The inter-observer variability was not increased by the reduced montage. CONCLUSION: Reduced EEG had high performance for classifying important background and discharge patterns in this post cardiac arrest cohort. SIGNIFICANCE: Our results support the use of reduced EEG-montage for monitoring comatose cardiac arrest patients.

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BACKGROUND: Early consciousness recovery after cardiac arrest (CA) is one of the most explicit and self-evident prognostic factors for clinical outcomes. We aimed to evaluate the prognostic value of electroencephalography (EEG) phenotypes according to the American Clinical Neurophysiology Society's Critical Care EEG classification for predicting early recovery after CA. METHODS: Consecutive patients admitted to the ICU after CA were enrolled. We analyzed Glasgow Coma Scale (GCS) score within 10 days after CA and evaluated mortality within 28 days according to EEG pattern subtype. RESULTS: Among the total of 71 patients, 9 had periodic discharges (PDs) EEG pattern, 4 had rhythmic delta activity (RDA), 8 had spike-and-wave (SW), 22 had low voltage, 5 had burst suppression, and 23 had other EEG patterns. Initial GCS scores, GCS scores 3 days after CA (or 3 days after targeted temperature management [TTM]), and 10 days after CA (or 10 days after TTM) were significantly different among EEG subtypes (p < 0.001, respectively) (Table 2). GCS scores were significantly higher in RDA and the other EEG group compared to the PDs, SW, low voltage, and burst suppression groups (p < 0.001). Significant group × time interactions were observed for the follow-up period between EEG phenotypes (p < 0.001) demonstrating the most increase in the other EEG pattern group. CONCLUSIONS: Consciousness states were significantly worse in the PDs, SW, burst suppression, and low-voltage groups compared to the RDA and the other EEG pattern within 10 days after CA. The degree of consciousness recovery differed significantly by EEG pattern subtype within 10 days.

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AIM: To establish incidence, phenotype, long-term functional outcome, and early EEG predictors of delirium after cardiac arrest. METHODS: This is an ad hoc analysis of a prospective cohort study on outcome prediction of comatose patients after cardiac arrest. Patients with recovery of consciousness, who survived until hospital discharge, were subdivided in groups with and without delirium based on psychiatric consultation. Delirium phenotype and medical treatment were retrieved from patient files. All other data were prospectively collected. We used univariate analyses of baseline and early EEG characteristics for identification of possible delirium predictors. Association of delirium with neurological recovery at six months was analyzed with multinomial logistic regression analysis. RESULTS: Of 233 patients, 141 survived until hospital discharge, of whom 47 (33%) were diagnosed with delirium. There were no differences in baseline characteristics between patients with and without delirium. All delirious patients were treated with relatively high dosages of psychopharmaceuticals, mostly haloperidol and benzodiazepine agonists. Prevalent characteristics were disturbed cognition, perception and psychomotor functioning (98%). Half of the patients had language disorders or shouting. Delirium was associated with longer ICU and hospital admission, and more frequent discharge to rehabilitation centre or nursing home. There was a trend towards poorer neurological recovery. EEG measurements within 12 h after cardiac arrest could predict delirium with 91% specificity and 40% sensitivity. DISCUSSION: Delirium is common after cardiac arrest, and probably leads to longer hospitalization and poorer outcome. Optimal treatment is unclear. Early EEG holds potential to identify patients at risk.

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OBJECTIVE: To quantify the effects of propofol on the EEG after cardiac arrest and to assess their influence on predictions of outcome. METHODS: In a prospective multicenter cohort study, we analyzed EEG recordings within the first 72 h after cardiac arrest. At six time points, EEGs were classified as favorable (continuous background), unfavorable (generalized suppression or synchronous patterns with ≥50% suppression), or intermediate. Quantitative EEG included measures for amplitude, background continuity, dominant frequency, and burst-suppression amplitude ratio (BSAR). The effect of propofol on each measure was estimated using mixed effects regression. RESULTS: We included 496 patients. The EEG after propofol cessation had no additional value over EEG-based outcome predictions during propofol administration at 12 h after cardiac arrest. Propofol was associated with decreased EEG amplitude, background continuity and dominant frequency, and increased BSAR. However, propofol did neither increase the chance of unfavorable EEG patterns (adjusted odds ratio (aOR) 0.95 per increase of 2 mg/kg/h, 95%-CI: 0.81-1.11) nor decrease the chance of favorable EEG patterns (aOR 0.98, 95%-CI: 0.89-1.09). CONCLUSIONS: Propofol induces changes of the postanoxic EEG, but does not affect its value for the prediction of outcome. SIGNIFICANCE: We confirm the reliability of EEG-based outcome predictions in propofol-sedated patients after cardiac arrest.

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Sudden death in young people while performing intense physical activity has a very low prevalence but a significant burden in terms of loss of years of life in society and a strong social impact. We present the case of a 19-year-old man who had a cardiac arrest while playing a football match, with prolonged resuscitation, and multiple subsequent complications (acute renal failure, coagulopathy, digestive bleeding, ischaemic colitis, and need for implantable cardioverter-defibrillator placement and hemicolectomy). The onset of intensive early rehabilitation in a specialised centre minimised the sequels, improving the Rankin score from 4 to 2 and Barthel index from 0 to 95 points, allowing the patient to lead an almost autonomous life.

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OBJECTIVE: To assess the value of background continuity and amplitude fluctuations of the EEG for the prediction of outcome of comatose patients after cardiac arrest. METHODS: In a prospective cohort study, we analyzed EEGs recorded in the first 72 h after cardiac arrest. We defined the background continuity index (BCI) as the fraction of EEG not spent in suppressions (amplitudes < 10 µV for ≥ 0.5 s), and the burst-suppression amplitude ratio (BSAR) as the mean amplitude ratio between non-suppressed and suppressed segments. Outcome was assessed at 6 months and categorized as "good" (Cerebral Performance Category 1-2) or "poor" (CPC 3-5). RESULTS: Of the 559 patients included, 46% had a good outcome. Combinations of BCI and BSAR resulted in the highest prognostic accuracies. Good outcome could be predicted at 24 h with 57% sensitivity (95% confidence interval (CI): 48-67) at 90% specificity (95%-CI: 86-95). Poor outcome could be predicted at 12 h with 50% sensitivity (95%-CI: 42-56) at 100% specificity (95%-CI: 99-100). CONCLUSIONS: EEG background continuity and the amplitude ratio between bursts and suppressions reliably predict the outcome of postanoxic coma. SIGNIFICANCE: The presented features provide an objective, rapid, and reliable tool to assist in EEG interpretation in the Intensive Care Unit.

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OBJECTIVE: In postanoxic coma, EEG patterns indicate the severity of encephalopathy and typically evolve in time. We aim to improve the understanding of pathophysiological mechanisms underlying these EEG abnormalities. METHODS: We used a mean field model comprising excitatory and inhibitory neurons, local synaptic connections, and input from thalamic afferents. Anoxic damage is modeled as aggravated short-term synaptic depression, with gradual recovery over many hours. Additionally, excitatory neurotransmission is potentiated, scaling with the severity of anoxic encephalopathy. Simulations were compared with continuous EEG recordings of 155 comatose patients after cardiac arrest. RESULTS: The simulations agree well with six common categories of EEG rhythms in postanoxic encephalopathy, including typical transitions in time. Plausible results were only obtained if excitatory synapses were more severely affected by short-term synaptic depression than inhibitory synapses. CONCLUSIONS: In postanoxic encephalopathy, the evolution of EEG patterns presumably results from gradual improvement of complete synaptic failure, where excitatory synapses are more severely affected than inhibitory synapses. The range of EEG patterns depends on the excitation-inhibition imbalance, probably resulting from long-term potentiation of excitatory neurotransmission. SIGNIFICANCE: Our study is the first to relate microscopic synaptic dynamics in anoxic brain injury to both typical EEG observations and their evolution in time.

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OBJECTIVE: To report on a distinct effect of auditory and sensory stimuli on the EEG in comatose patients with severe postanoxic encephalopathy. METHODS: In two comatose patients admitted to the Intensive Care Unit (ICU) with severe postanoxic encephalopathy and burst-suppression EEG, we studied the effect of external stimuli (sound and touch) on the occurrence of bursts. RESULTS: In patient A bursts could be induced by either auditory or sensory stimuli. In patient B bursts could only be induced by touching different facial regions (forehead, nose and chin). When stimuli were presented with relatively long intervals, bursts persistently followed the stimuli, while stimuli with short intervals (<1s) did not induce bursts. In both patients bursts were not accompanied by myoclonia. Both patients deceased. CONCLUSIONS: Bursts in patients with a severe postanoxic encephalopathy can be induced by external stimuli, resulting in stimulus-dependent burst-suppression. SIGNIFICANCE: Stimulus induced bursts should not be interpreted as prognostic favourable EEG reactivity.

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Evolution of the EEG background pattern is a robust contributor to prediction of poor or good outcome of comatose patients after cardiac arrest. At 24h, persistent isoelectricity, low voltage activity, or burst-suppression with identical bursts predicts a poor outcome without false positives. Rapid recovery toward continuous patterns within 12h is strongly associated with a good neurological outcome. Predictive values are highest in the first 24h, despite the use of mild therapeutic hypothermia and sedative medication. Studies on reactivity or mismatch negativity have not included the EEG background pattern. Therefore, the additional predictive value of reactivity parameters remains unclear. Whether or not treatment of electrographic status epilepticus improves outcome is studied in the randomized multicenter Treatment of Electroencephalographic STatus epilepticus After cardiopulmonary Resuscitation (TELSTAR) trial (NCT02056236).

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Comatose patients after cardiac arrest have a poor prognosis. Approximately half never awakes as a result of severe diffuse postanoxic encephalopathy. Several neuroprotective agents have been tested, however without significant effect. In the present study, we used cultured neuronal networks as a model system to study the general synaptic damage caused by temporary severe hypoxia and the possibility to restrict it by ghrelin treatment. Briefly, we applied hypoxia (pO2 lowered from 150 to 20 mmHg) during 6 h in 55 cultures. Three hours after restoration of normoxia, half of the cultures were treated with ghrelin for 24 h, while the other, non-supplemented, were used as a control. All cultures were processed immunocytochemically for detection of the synaptic marker synaptophysin. We observed that hypoxia led to drastic decline of the number of synapses, followed by some recovery after return to normoxia, but still below the prehypoxic level. Additionally, synaptic vulnerability was selective: large- and small-sized neurons were more susceptible to synaptic damage than the medium-sized ones. Ghrelin treatment significantly increased the synapse density, as compared with the non-treated controls or with the prehypoxic period. The effect was detected in all neuronal subtypes. In conclusion, exogenous ghrelin has a robust impact on the recovery of cortical synapses after hypoxia. It raises the possibility that ghrelin or its analogs may have a therapeutic potential for treatment of postanoxic encephalopathy.

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The physical examination findings of early posthypoxic myoclonus (PHM) are associated with poor prognosis. Recent findings indicate that patients with multifocal PHM, assumed to have a cortical origin, have a comparable outcome to resuscitated patients without PHM. Generalized PHM, assumed to have a subcortical myoclonus origin, is still associated with a bad clinical outcome. It is not known whether the electroencephalographic (EEG) findings differ between the multifocal and generalized myoclonus groups nor is the clinical significance clearly defined. Forty-three patients with PHM were retrospectively derived from an EEG database. Patients were categorized as having multifocal (i), generalized (ii), or undetermined (iii) PHM. Outcome was expressed in cerebral performance category scores. The EEG background was categorized into isoelectric (I), low voltage (II), burst suppression (III), status epilepticus (SE; IV), diffuse slowing (V), and mild encephalopathic or normal (VI). 17 patients had generalized PHM and 23 had multifocal PHM (3 undetermined). The EEG showed more SE in generalized compared to multifocal PHM (64% vs 13%, P< .001). Diffuse slowing was more often present in multifocal PHM (52% vs 17%, P < .05). Early-onset myoclonus occurred significantly more often in generalized PHM, and early generalized PHM was invariantly associated with poor outcome. In conclusion, patients with generalized PHM showed more SE. These EEG findings might be either subcortical corollaries or primarily cortical phenomena. Our retrospective results conflict with currently used clinical criteria for myoclonus classification, and we suggest that more refined difference may be needed for accurate assessment of PHM. To better understand PHM, prospective research with standardized clinical assessment and quantitative EEG analysis is needed.

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Acute-onset alcohol-associated neuropathy is only occasionally reported, and delayed postanoxic encephalopathy is rare. Here, we report a male who developed acute multiple focal neuropathies and later delayed postanoxic encephalopathy after alcohol intoxication. He had hypoxia and rhabdomyolysis, presenting with acute renal failure initially, and cardiopulmonary support, including mechanical ventilation, led to improvement of the patient at the acute stage. He suffered from bilateral hand numbness and mild weakness of the right lower limb thereafter. Nerve-conduction study revealed no pickup of compound muscle action potential or sensory nerve action potential in the bilateral ulnar nerve, but showed attenuated amplitude of compound muscle action potential in the right femoral nerve. Multiple focal neuropathies were suspected, and he received outpatient rehabilitation after being discharged. However, the patient developed gradual onset of weakness in four limbs and cognitive impairment 23 days after the hypoxia event. Brain computed tomography showed low attenuation over bilateral globus pallidus, and brain magnetic resonance imaging disclosed diffuse increased signal intensity on T 2-weighted images and fluid-attenuated inversion recovery in bilateral white matter. He was admitted again under the impression of delayed postanoxic brain injury. Supportive treatment and active rehabilitation were given. He had gradual improvement in motor and functional status after rehabilitation. He could walk with festinating gait under supervision, and needed only minimal assistance in performing activities of daily living approximately 1 year later.

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One of the worst outcomes of acquired brain injury is the vegetative state, recently renamed 'unresponsive wakefulness syndrome' (VS/UWS). A patient in VS/UWS shows reflexive behaviour such as spontaneous eye opening and breathing, but no signs of awareness of the self or the environment. We performed a systematic review of VS/UWS prevalence studies and assessed their reliability. Medline, Embase, the Cochrane Library, CINAHL and PsycINFO were searched in April 2013 for cross-sectional point or period prevalence studies explicitly stating the prevalence of VS/UWS due to acute causes within the general population. We additionally checked bibliographies and consulted experts in the field to obtain 'grey data' like government reports. Relevant publications underwent quality assessment and data-extraction. We retrieved 1032 papers out of which 14 met the inclusion criteria. Prevalence figures varied from 0.2 to 6.1 VS/UWS patients per 100 000 members of the population. However, the publications' methodological quality differed substantially, in particular with regards to inclusion criteria and diagnosis verification. The reliability of VS/UWS prevalence figures is poor. Methodological flaws in available prevalence studies, the fact that 5/14 of the studies predate the identification of the minimally conscious state (MCS) as a distinct entity in 2002, and insufficient verification of included cases may lead to both overestimation and underestimation of the actual number of patients in VS/UWS.

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OBJECTIVE: To assess the incidence, quantified EEG characteristics, and prognostic significance of "burst-suppression with identical bursts" and to discuss potential pathophysiological mechanisms. METHODS: Burst-suppression EEGs were identified from a cohort of 101 comatose patients after cardiac arrest, and from our complete database of 9600 EEGs, since 2005. Patterns with and without identical bursts were classified visually by two observers. Of patients after cardiac arrest, outcomes were assessed at three and six months. Identical and non-identical burst-suppression patterns were compared for quantified EEG characteristics and clinical outcome. Cross correlation of burstshape was applied to the first 500 ms of each burst. RESULTS: Of 9701 EEGs, 240 showed burst-suppression, 22 with identical bursts. Identical bursts were observed in twenty (20%) of 101 comatose patients after cardiac arrest between a median of 12 and 36 h after the arrest, but not in the six patients with other pathology than cerebral ischemia, or the 183 with anesthesia induced burst suppression. Inter-observer agreement was 0.8 and disagreement always resulted from sampling error. Burst-suppression with identical bursts was always bilateral synchronous, amplitudes were higher (128 vs. 25 µV, p=0.0001) and correlation coefficients of burstshapes were higher (95% >0.75 vs. 0% >0.75, p<0.0001) than in burst-suppression without identical bursts. All twenty patients with identical bursts after cardiac arrest had a poor outcome versus 10 (36%) without identical bursts. CONCLUSION: "Burst-suppression with identical bursts" is a distinct pathological EEG pattern, which in this series only occurred after diffuse cerebral ischemia and was invariably associated with poor outcome. SIGNIFICANCE: In comatose patients after cardiac arrest, "burst-suppression with identical bursts" predicts a poor outcome with a high specificity.

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Delayed postanoxic encephalopathy causes relapse of cognitive impairment and movement deterioration in a few weeks after clinically complete recovery from initial anoxic or hypoxic insult. Delayed postanoxic encephalopathy is a rare condition, and its clinical symptoms are characterized by abulia, apathy, akinesia, confusion, agitation, parkinsonism, chorea, dystonia and/or progressive neurologic deficits. We reported two distinguished cases caused by carbon monoxide intoxication and mixed respiratory and metabolic lactic acidosis.

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BACKGROUND: Delayed postanoxic encephalopathy (DPE) is a demyelinating disorder in which cognitive, behavioral and movement deteriorations relapse in a few weeks after a complete recovery from initial hypoxic injury. To our knowledge, there have been no reports describing the temporal change of diffusion-weighted imaging (DWI) findings in DPE. METHODS: In a patient with DPE, serial brain MRI including DWI was performed at admission, 1, 3, 5 and 11 months after the onset of DPE. In order to obtain apparent diffusion coefficient (ADC) value of the lesion, we selected the same axial slices of the serial DWI and placed eight regions of interest (ROIs) in the periventricular white matter. Mean ADC values of ROIs and ADC map were serially compared. RESULTS: Compared to normal value, the ADC values of ROIs remained low at admission and one-month follow-up (0.68+/-0.08 and 0.67 +/- 0.08 X 10(-3)mm2/s) and then continued to increase on the 3, 5 and 11-month follow-up (0.78+/-0.05, 0.80+/-0.05 and 0.87 +/- 0.11 X 10(-3)mm2/s). Abnormal low signal density in both periventricular white matters on initial ADC map also disappeared slowly. Serial ADC maps revealed continuing diffuse cytotoxic edema over 1 month after the onset of DPE. CONCLUSIONS: Delayed cytotoxic edema associated with delayed clinical symptom of DPE might implicate that possible pathogenesis of DPE is apoptosis. DWI including ADC map might be useful to detect apoptotic brain lesion.

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To obtain the basic data of prognosis of acute carbon monoxide (CO) intoxication, one hundred and sixteen cases of CO intoxication defined by carboxyhemoglobin (COHb) and admitted via emergency room of Yeungnam University Hospital from Oct. '85 to April' 89 have been clinically analyzed and evaluated, including delayed postanoxic encephalopathy (DPE) and the following results were obtained. 1. The ratio of male to female was 1:1.5 and mental state was drowsy mostly (26.2% of 116 cases) 2. The more disturbed the mental state, the more decreased was the arterial pH and PaCO₂, which may be the result of metabolic acidosis. 3. The early laboratory findings in patients of CO intoxication were as follows: leukocytosis-65.5%, increase of hematocrit-23.3%, hyperglycemia-19.8%, increase of GPT-19.8% increase of creatinine-0.9% and glucosuria-12.1%. 4. The early findings of EKG were abnormal in 35.3%: change of rhythm-25.0%, abnormal ST segment 15.5% (change of rhythm and abnormal ST segment-5.2%) but the conduction disorder was not present. 5. The abnormal EEG above mild degree was 93.1%, of which moderate was most frequent (80.2%). 6. The incidence of DPE was 7.8% among all admitted CO patients. DPE cases had long duration of exposure time (8 hours), severe leukocytosis (20,000) and an abnormal EEG (MA).

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