Cases reported "Hypoxia, Brain"

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1/45. Pseudo-subarachnoid hemorrhage: a rare neuroimaging pitfall.

    OBJECTIVE: We report an unusual case of the CT appearance of diffuse subarachnoid hemorrhage in a patient with anoxic encephalopathy, a situation which neurosurgeons, neurologists, and neuroradiologists should be aware of. CLINICAL PRESENTATION: A young man collapsed unconscious in jail after abusing an unknown quantity and variety of drugs. CT scan showed a picture compatible with diffuse subarachnoid hemorrhage. INTERVENTION: As the patient had a Glasgow Coma Score of 3 no heroic intervention was undertaken. An autopsy performed 40 hours after the initial ictus and 24 hours after death revealed no evidence of subarachnoid hemorrhage but gross and microscopic evidence of anoxic encephalopathy. CONCLUSION: Anoxic encephalopathy can mimic diffuse subarachnoid hemorrhage on CT.
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2/45. Anaesthetic management of a pregnant patient in a persistent vegetative state.

    pregnancy in a patient in a persistent vegetative state presents challenging therapeutic questions about the level of supportive management required, the assessment of fetal well-being, the timing and mode of delivery and the anaesthetic management of labour and delivery. We report the case of a 29-yr-old woman who had a favourable fetal outcome despite suffering hypoxic brain damage after a suicide attempt by a drug overdose. She was managed until the onset of labour on an intensive care unit and had a spontaneous vaginal delivery assisted by epidural anaesthesia.
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3/45. Prognostic value of evoked potentials and sleep recordings in the prolonged comatose state of children. Preliminary data.

    OBJECTIVES: sleep recordings and evoked potentials (EPs) were used in five comatose children to evaluate their predictive value for outcome following a severe comatose state. methods AND SUBJECTS: The protocol included EEG, Brainstem Evoked Responses (BERs), Somatosensory evoked potentials (SEPs) and polysomnography. From 10 to 15 days post-coma (D10 to D15), EEG and clinical examinations were carried out every second day, then one day in four from 15 to 30 days post-coma (D15 to D30), and one day in seven from D30 to six months (M6). evoked potentials and polysomnography were recorded on D10-D15 or D30 in the second month (M2) and in M6. Of the five children, three were in anoxic coma and two in traumatic coma. All had extensive lesions and a glasgow coma scale (GCS) score of less than five. The results of the EEG, polysomnographic and EP recordings were compared to the clinical outcome. RESULTS AND CONCLUSION: In the three anoxic comas we observed BER abnormalities and the absence of SEP N20 associated with wide cortical lesions with brainstem extension. sleep recordings showed major alterations of the wake-sleep cycle without any improvement in M6. Abnormalities included loss of the normal REM-sleep pattern associated with alteration of NREM sleep and periods of increase in motor activity without EEG arousal. This sleep pattern appeared to be associated with involvement of the brainstem. In the two traumatic comas, alterations of the early cortical SEP responses were less severe and the BERs were normal. Some sleep spindles were observed as well as the persistence of sleep cycles in the first weeks post-coma. The combined use of EEG, EPs and polysomnography improved the outcome prediction in comparison with the use of just one modality. EPs and sleep recordings were far superior to clinical evaluation and to GCS in the appreciation of the functional status of comatose children. The reappearance of sleep patterns is considered to be of favorable prognosis for outcome of the coma state, as is the presence of sleep spindles in post-trauma coma. This study showed that EPs and sleep recordings help to further distinguish between patients with good or bad outcomes.
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4/45. The minimally conscious state in children.

    The minimally conscious state (MCS) is a condition of severely altered consciousness in which minimal but definite behavioral evidence of self- or environmental awareness is shown. Diagnostic criteria recently have been proposed for entry into and emergence from the MCS. We present clinical and neuroimaging data on 5 children diagnosed with MCS and discuss the limited information available concerning its epidemiology, etiology, pathology, and prognosis. Issues related to the evaluation and care of children suspected of having MCS are also reviewed as well as current ethical and legal controversies.
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5/45. Neurological outcome prediction in a cardiorespiratory arrest survivor.

    Outcome prediction of neurological recovery in an unconscious survivor of cardiorespiratory arrest is difficult and uncertain. We describe the case of a 25-yr-old post-arrest survivor who made a remarkable neurological improvement despite a seemingly hopeless prognosis. Conventional clinical and neurophysiological assessments need to be interpreted with care in the presence of uncontrolled seizure activity and sedative medications. The measurement of biochemical markers in the serum and cerebrospinal fluid may be useful in helping the clinician to arrive at a more accurate neurological outcome prediction.
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6/45. Delayed encephalopathy after strangling.

    An 11-year-old boy who had been the victim of a strangling attempt was asymptomatic for one week whereupon involuntary movements involving the trunk and limbs developed, along with repetitive episodes of opisthotonos and autonomic dysfunction. Meanwhile, he remained alert and appeared to be mentally intact. An electroencephalogram was normal. He died 13 weeks after the onset of the neurological disorder. The neuropathological examination showed cavitating lesions in the caudate nucleus, putamen, and globus pallidus bilaterally, with sparing of the white matter. The delayed onset of a progressively evolving neurological disorder has been noted in various forms of hypoxicischemic insult, including previously reported cases of strangling, but its occurrence cannot be predicted from the preceding clinical state or course. In the cases in which abnormal movements have been predominant, the pathological findings have been similar despite diversity in the preceding circumstances. We suggest the underlying metabolic disorder common to these cases may be lactic acidosis, and that they should be studied for evidence of a biochemical defect.
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7/45. Acquired heterotopic ossification in the settings of cerebral anoxia and alternative therapy: two cases.

    Acquired Heterotopic Ossification (HO) has been well described in the literature as a recognized complication following spinal cord injury, traumatic brain injury and joint arthroplasty. Commonly, large proximal limb joints are affected. The underlying mechanisms for ectopic bone formation remain poorly elucidated. Post-stroke hemiplegia as a cause of neurogenic HO is rare, and no published reports of HO occurring after anoxic brain injury in adults have been documented. This study reports two unusual cases of acquired HO: (1) Polyarticular HO involving the ankle joint in a 24-year-old Chinese female who suffered severe anoxic encephalopathy following near drowning which resulted in persistent vegetative state; and (2) elbow HO in chronic post-stroke hemiplegia occurring as a complication of alternative therapy following repeated forceful manipulation by a traditional practitioner in a 46 year-old male.
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8/45. Misdiagnosing the vegetative state after severe brain injury: the influence of medication.

    patients who suffer severe brain damage may be left unaware of self and of the environment and in a permanent vegetative state (PVS). The difficulties in correctly ascertaining unawareness after brain injury have been emphasized by a number of authors. It is well recognized that toxic-metabolic and drug-induced cerebral depression occurs acutely after brain injury. However, less attention has been drawn to the effects of medication months after brain injury and the way in which medication may confound assessment of awareness and, thus, the reliable assessment of long-term prognosis. This paper describes two patients who sustained a severe and well-documented structural brain injury, one hypoxic and one traumatic. Both were unaware when first seen at 3 months post-injury, but both have made useful functional recovery. The paper discusses their progress and how the early prescription of large doses of anti-epileptic drugs, sedatives and anti-spastic agents in these circumstances may result in an initial misdiagnosis of the vegetative state.
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9/45. Recovery from near death following cerebral anoxia: A case report demonstrating superiority of median somatosensory evoked potentials over EEG in predicting a favorable outcome after cardiopulmonary resuscitation.

    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.
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10/45. Post-interval syndrome after carbon monoxide poisoning.

    Carbon monoxide (CO) exposure and toxicity is a potentially lethal disorder with immediate and delayed side effects. A 24-y-old driver was admitted to the University-based emergency department with altered mental status. He was found unconscious in the driver's seat of his vehicle in an indoor garage the morning before. An estimated 7 h later, he was comatose and taken to a nearby village clinic. oxygen was administered immediately. Later, he was transferred to the university hospital. At the 12th h after exposure, the glasgow coma scale score was 12/15 (E3, M5, V4). Co-oximetry disclosed a carboxyhemoglobin concentration of 10.5%. Normobaric oxygen was administered. He recovered completely the 3rd d after exposure; however, on the 7th d disorientation and agitation was noted, and the interval form of CO poisoning and leukoencephelopaty were suspected, for which he was readmitted the 10th d after exposure. Analysis of cerebrospinal fluid and blood revealed no abnormalities. magnetic resonance imaging on the 11th d after exposure demonstrated an ischemic area in the posterior temporoparietal area. The patient continued improvement to discharge at 7th d of the second admission. Close follow-up should be scheduled for CO-poisoned patients to rule out the post-interval syndrome for at least 1 mo. This should also include those with apparent clinical and laboratory recovery.
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