A case of carbon monoxide intoxication presenting subacute dementia as the initial symptom]

We reported a 67-year-old woman who had developed abnormal behavior and dementia from January 21, 2001 and deteriorated to akinetic mutism on February 15. T2-weighted magnetic resonance imaging showed high intensity in bilateral globus pallidus and a rapid spreading of diffuse high intensity in bilateral deep white matter. Later on, we got an important information that she had used a little coal stove three times about three weeks before presenting the initial symptom. She was diagnosed as carbon monoxide intoxication and treated with hyperbaric oxygen from March 1. A remarkable improvement on dementia and motor disability was observed. We conclude that this case is the first reported example of a case of intermittent carbon monoxide intoxication presenting subacute dementia as an initial symptom.     

Secondary mania in a patient with delayed anoxic encephalopathy after carbon monoxide intoxication caused by a suicide attempt

We report herein a female patient presenting with delayed anoxic encephalopathy after carbon monoxide (CO) intoxication. Five months after she attempted suicide in her car using burning charcoal, she showed manic symptoms including aggressive behaviors, irritability, decreased total sleep time, increased energy and sexual interest, and hyperactivity, as well as illusions and visual hallucinations related to bugs, certain animals, monsters and her ex-husband. Fluid-attenuated inversion recovery and T2-weighted images in brain magnetic resonance imaging showed white-matter hyperintensity in the frontal lobe and periventricular area. Her manic symptoms and psychotic features improved following daily administration of valproate (600 mg) and olanzapine (10 mg). These observations indicate that clinicians should monitor for delayed neuropsychiatric symptoms in patients with CO intoxication.     

Clinical outcome and brain MRI four years after carbon monoxide intoxication

Brain damage from carbon monoxide intoxication has not been extensively studied with magnetic resonance imaging. We report the clinical outcome and brain magnetic resonance imaging in three individuals simultaneously exposed to toxic levels of carbon monoxide four years previously. Lesions are seen in multiple locations and do not correlate well with the clinical condition.     

Generalized chorea due to delayed encephalopathy after acute carbon monoxide intoxication

Movement disorder due to delayed encephalopathy after carbon monoxide (CO) intoxication is uncommon. Generalized chorea, presenting as an initial symptom of delayed encephalopathy, is extremely rare. We describe a 60-year-old woman, who had completely recovered from acute CO poisoning, developed mental and behavioral changes, urinary incontinence and generalized chorea 2 weeks thereafter. T2-weighted brain magnetic resonance imaging showed extensive hyperintensity of the bilateral periventricular and subcortical white matter and the globus pallidus. Brain single-photon emission computed tomography (SPECT) with technetium-99 ethylene cysteine dimer showed inhomogeneous perfusion in the cerebral cortex, with decreased uptake in bilateral frontal regions. Delayed encephalopathy after acute CO intoxication was diagnosed, and the symptoms gradually improved after hyperbaric oxygen therapy (HBOT). This case report demonstrates that generalized chorea may be one of the initial presenting symptoms of delayed encephalopathy after acute CO intoxication. We hypothesize that the generalized chorea in our patient may have been caused by the subcortical white matter lesions, which most likely interrupted the basal ganglia-thalamocortical circuits and that HBOT may be the treatment of choice for such patients.     

Neurologic and psychiatric sequelae of carbon monoxide poisoning

Carbon monoxide intoxication may result in neuropsychiatric abnormalities that can be overlooked or not fully appreciated. The authors describe two female patients who developed troublesome cognitive and emotional problems following carbon monoxide poisoning and stress the value of the precise neuropsychological testing and prolonged clinical observation in such cases.     

精神病院中所见的胰岛素瘤

对精神科少见的胰岛素瘤１３例进行临床分析。发现这些病人起病均有诱因，而且负性精神因素较多见，均伴有意识障碍，这些病例均被误诊为功能性精神病、癫痫及脑炎等。作者对误诊原因进行了分析     

A case of delayed post-anoxic encephalopathy after acute carbon monoxide poisoning

The authors report the case of a young 18 year-old man presenting delayed encephalopathy after severe intoxication with carbon monoxide, and transient cerebral swelling. This condition is characterized by diffuse demyelinating lesions of both cerebral hemispheres, the mechanism of which is unknown.     

A case suspected of acute gas poisoning by carbon monoxide (CO), presenting with progressive diffuse leukoencephalopathy associated with marked brain edema]

A 51-year-old man was found comatose in a decerebrate posture in a cottage. Brain MRI showed diffuse high-signal-intensity areas in the white matter on T 2-weighted and FLAIR images, and diffusion-weighted images showed marked diffuse high intensity areas in the white matter. Initially inflammatory demyelinating diseases were suspected and methylprednisolone pulse therapy was administered. However, no improvement was noted. On close inspection of the cottage, a gas generator was discovered in the poorly ventilated room. He was therefore suspected to have suffered from gas intoxication, including carbon monoxide (CO). Hyperbaric oxygen therapy was administered, but without any improvement. The diffuse white matter lesions and brain edema progressed with time and the patient died of cerebral herniation. Autopsy revealed no inflammatory processes. Most cases with CO intoxication show hyperintense lesions in the globus pallidus on both sides in T 2-weighted images, and some cases show lesions only in the white matter without any involvement of the globus pallidus. The progressive clinical course, diffuse leukoencephalopathy and brain edema may be due to apoptosis of oligodendrocytes. CO intoxication is thus important in the differential diagnosis of diffuse white matter lesions of the cerebrum.     

Partial Recovery from Cortical Blindness Following Monoxide Intoxication

Patients with carbon monoxide (CO) intoxication may show neurological signs such as headache, seizures, extrapyramidal findings, and coma. However, cortical blindness is rare in these cases. This study describes a woman exhibiting confusion and axial rigidity after CO intoxication. Ten days after intoxication, her pupils were isonormocoric and reactive to light. A fundoscopic examination was normal, but visual acuity was light-perception in both eyes. There were diffuse EEG slow waves. Magnetic resonance imaging (MRI) demonstrated bilateral hyperintensity in the basal ganglia. The P100 latencies of visual evoked potentials (VEP) were increased and dispersed. One year later, the patient's visual acuity was almost normal and VEPs showed mild dispersion in P100 latencies. The authors found this case of interest because cortical blindness due to CO intoxication is only rarely seen with a relatively good outcome.     

Partial recovery from cortical blindness following carbon monoxide intoxication

Patients with carbon monoxide (CO) intoxication may show neurological signs such as headache, seizures, extrapyramidal findings, and coma. However, cortical blindness is rare in these cases. This study describes a woman exhibiting confusion and axial rigidity after CO intoxication. Ten days after intoxication, her pupils were isonormocoric and reactive to light. A fundoscopic examination was normal, but visual acuity was light-perception in both eyes. There were diffuse EEG slow waves. Magnetic resonance imaging (MRI) demonstrated bilateral hyperintensity in the basal ganglia. The P100 latencies of visual evoked potentials (VEP) were increased and dispersed. One year later, the patient's visual acuity was almost normal and VEPs showed mild dispersion in P100 latencies. The authors found this case of interest because cortical blindness due to CO intoxication is only rarely seen with a relatively good outcome.     

Regional cerebral blood flow after marijuana smoking.

Regional CBF was measured with the 133Xe inhalation technique before and thrice after smoking marijuana of two strengths and placebo in 20 physically and mentally healthy male volunteers with a previous history of exposure to marijuana. They were drug-free at the time of the study. Blood pressure, pulse rate, end-tidal carbon dioxide, end-tidal carbon monoxide, and forehead skin perfusion were quantified during the CBF measurements. Blood samples were drawn for quantification of plasma levels of delta 9-tetrahydrocannabinol (THC) before and during the 2 h after smoking marijuana or placebo. Drug-induced intoxication and changes in mood were quantified with rating scales. Marijuana smoking was associated with bilateral CBF increase, which was maximal 30 min later. Greater CBF increases were seen in the frontal region and right hemisphere. No significant CBF changes were seen after placebo. Pulse rate and respiration increased significantly after marijuana but not placebo. Both marijuana and placebo smoking were associated with increased end-tidal carbon monoxide. CBF increase in both hemispheres correlated significantly with degree of intoxication, plasma levels of THC, and pulse rate.     

Evidence of vascular disease from CT scanning in late onset epilepsy.

The CT scans of 74 patients presenting with late-onset epilepsy not due to cerebral tumour were compared with those of an age and sex-matched control group for evidence of cerebral vascular disease. Changes in the scan indicative of cerebral atrophy (enlarged ventricles and cortical sulci) were seen in similar numbers in both patients and controls. However, the scans revealed a highly significant excess of ischaemic lesions in the epileptic patients, in the form of discrete areas of infarction and low attenuation of the periventricular white matter. These changes, which were only seen in two of the controls, were present in 13 of the epileptic patients. The median age at the onset of epilepsy in the 13 patients with ischaemic lesions was 62 years, and they showed an increased incidence of systemic vascular disease and of abnormal neurological signs. In six of the 13 cases, however, clinical examination was normal and CT scanning provided the only evidence of underlying vascular disease.     

A positron emission tomography study of patients with acute carbon monoxide poisoning treated by hyperbaric oxygen

Seven patients with an acute and severe carbon monoxide intoxication were treated with hyperbaric oxygen and underwent a positron emission tomographic examination 2–5 days after the acute event. Although the final clinical outcome was good in all patients, ischaemic changes were observed. Three patients with temporary sequelae after hyperbaric oxygen treatment showed the most severe changes, mainly in striatum and thalamus. Although positron emission tomographic examination cannot predict the final outcome, it can show the regions at risk for development of late complications following carbon monoxide poisoning.     

15例急性CO中毒伴发急性脑梗死的临床及MRI、MRA研究

目的评价MRI、MRA对急性CO中毒伴发急性脑梗死的诊断价值。方法回顾分析15例经临床确诊的急性CO中毒伴发急性脑梗死患者的头颅MRI、MRA资料。结果15例患者急性脑梗死病变部位:MRI为点状、片状异常信号;DWI表现为高信号;ADC为低信号;ADC值为(0.55±0.14)×10~(-3) mm~2/s;病灶直径(8.62±9.27)mm。病灶部位:10例脑叶,7例基底节及侧脑室旁,2例小脑,2例苍白球,1例脑干。12例侧脑室前后角白质周围片状、云雾状长T_1、长T_2异常信号病灶;11例双侧基底节及侧脑室旁点状长T_1、长T_2异常信号为陈旧性腔隙性梗死;7例脑萎缩。13例MRA表现:8例(61.53%)动脉狭窄,5例(38.46%)动脉管腔僵硬。结论应用头颅MRI、MRA对急性CO中毒伴发急性脑梗死的早期临床诊断、病情程度及预后的评估有一定的实用价值。     

A brain syndrome associated with delayed neuropsychiatric sequelae following acute carbon monoxide intoxication

A summary of clinical data is presented on 34 men and 52 women patients with brain syndrome associated with delayed neuropsychiatric sequelae following acute carbon monoxide intoxication. Their ages ranged from 34 to 82 years, with peak incidence in the sixth and seventh decade. Possible etiological factors were age, duration of unconsciousness on acute intoxication, and previous physical illness. The onset was relatively sudden after the apparent clear period which ranged from 2 to 40 days (mean 22.5 days). The most frequent symptoms were apathy, dull facial expressions, dementia, such as amnesia and disorientation, hypokinesia, mutism, irritable distractibility, urinary and/or fecal incontinence, gait disturbance and abnormal neurological signs and reflexes. EEG was abnormal in 33 of the 57 cases (58%). Of 27 patients who were given a computed tomographic brain scan, 15 patients were abnormal. The prognosis was relatively good in the follow-up study of 56 patients. Only age was related to a better prognosis.     

Unexplained neurological events during bathing in young people: Possible association with the use of gas geysers

Here, we report sudden, unexplained neurological collapse in 14 young people while bathing with hot water associated with the use of liquefied petroleum gas (LPG)-based water heaters (gas geysers) in ill-ventilated bathrooms. None of the patients reported any circumstantial evidence of seizures or prior epilepsy. One patient developed cortical blindness and demonstrated posterior leucoencephalopathy on imaging studies. The remaining patients made rapid and excellent recovery without any residual neurological sequelae. In these cases, the results of all routine investigations, i.e., serum chemistry, brain imaging (computed tomography in 2 and magnetic resonance imaging in 10) and electroencephalography were normal. The clinical clustering of these cases in winter months with similar presentations of reversible encephalopathy probably indicates an inhalational toxin exposure. Therefore, we postulate a hypothesis that harmful emissions consisting of carbon monoxide (CO), hydrocarbon gases (HC) and nitrogen oxides (NOx), produced by incomplete combustion of LPG might be responsible for the cellular injury and subsequent transient neurological deficits. Physicians should be aware of this entity in order to avoid misdiagnosis of this condition as seizures, and a public awareness should also be created regarding the proper use of these devices.     

The benign spectrum of hypothalamic hamartomas: Infrequent epilepsy and normal cognition in patients presenting with central precocious puberty

PurposeHypothalamic hamartoma (HH) is the main structural cause of central precocious puberty (CPP). HH is frequently associated with cognitive impairment and epileptic encephalopathies. Disease severity in case series from neurology services may be biased towards more neurologically impaired patients.AimTo perform a prospective cognitive evaluation in patients with HH presenting with CPP in an endocrinology outpatient clinic setting.MethodsWe evaluated fifteen consecutive patients with CPP due to HH presenting to an endocrinology outpatient clinic. CPP was diagnosed at a median age of 0.7 yr (0.4–7 yr). Mean age at neurologic evaluation was 13.9 yrs. Eight patients (53.3%) were male. Epileptic seizures occurred in 5/15 (33%) patients. Two patients presented a single unprovoked seizure (SUS). Three patients were diagnosed with epilepsy. Cognitive evaluation, using age-appropriate Wechsler Intelligence Scale, was performed in 11 patients.ResultsAll patients without epilepsy, including two patients with a history of a SUS, had normal neurologic and cognitive evaluation. Epilepsy and SUS were only seen in patients with sessile HH. Three patients with epilepsy presented cognitive or behavioral findings. Reduced intelligence quotients (IQ), in the borderline range, were noted in both patients with epilepsy who underwent full cognitive evaluation. We found no significant correlation between HH diameter or shape and mean full-scale IQ.ConclusionsPatients who presented with isolated CPP without epilepsy displayed normal cognition when evaluated after a mean period of 13 years. Occurrence of epilepsy, seen in a minority of patients, but not of a single seizure, was associated with mild cognitive deficit and behavioral disturbances in this case series.     

Parkinsonian syndrome caused by carbon monoxide poisoning. Preliminary results of the treatment with bromocriptine]

Parkinsonism is the most frequent neurological complication of carbon monoxide intoxication. Its prognosis is severe and Dopa is ineffective. We treated 9 patients (mean age 60.89 +/- 6.10 years) with bromocriptine (5 à 30 mg daily). Webster's scores were improved under treatment. Our study suggests that early administration of bromocriptine might be an effective therapy of carbon monoxide induced parkinsonism.     

Neurologic and radiologic manifestations of three girls surviving acute carbon monoxide poisoning

We report the neurologic and radiologic manifestations of three adolescent girls with acute carbon monoxide poisoning. The girls were found collapsed and unconscious in a bathroom where liquid petroleum gas was being used as heating fuel. As hyperbaric oxygen therapy was not available locally, they only received oxygen supplementation via nasal cannula (4 L/minute) as treatment in the first 2 days. On transfer to a tertiary center in Hong Kong, evolving neurologic manifestations of visual acuity and field deficits, confusion, and focal motor weaknesses were observed. Focal infarctions were evident in cerebral computed tomography in one patient and cortical lesions on magnetic resonance imaging in all three patients. [18F]Fluorodeoxyglucose (FDG) positron emission tomography (PET) revealed additional decreased metabolism in the basal ganglia in two patients, which was typical of carbon monoxide poisoning. The neurologic deficits resolved completely at 3 weeks after the exposure, but psychologic symptoms succeeded. This report serves to alert clinicians to the varied neuro-ophthalmologic manifestations and psychologic impairment even with the same duration of carbon monoxide poisoning. PET might be more sensitive in detecting cerebral injuries specific for carbon monoxide poisoning.     

Magnetic Resonance Imaging Findings on Carbon Monoxide Intoxication

Four patients who had carbon monoxide intoxication were examined by brain magnetic resonance imaging (MRI) and computed tomography (CT). Three were unconscious in the acute stage of intoxication. On regaining consciousness. neuropsychological symptoms and signs remained. In these patients, T2-weighted MRI demonstrated hyperintensity lesions in the cerebral cortex, most prominent in the watershed zone. The fourth patient had only memory disturbance and was not unconscious during the acute intoxication. The T1-weighted MRI showed hyperintensity in the bilateral pallidal regions. MRI demonstrated lesions more clearly than did CT.