Cases reported "Hypoxia, Brain"

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1/21. Voxel-based mapping of brain hypometabolism in permanent amnesia with PET.

    In this study, we used voxel-based mapping methods to compare the resting cerebral metabolic rate of glucose (CMRglc) measured with PET in five patients with permanent amnesia (three with chronic Wernicke-Korsakoff and two with postanoxia syndrome) to that of nine healthy age-matched subjects. We assessed (i) a group pattern of relative hypometabolism; and (ii) the consistency of this group pattern, if any, in individual subjects, according to etiology. The results from the group analysis documented that permanent amnesia is associated with hypometabolism in the thalamus, posterior cingulate cortex, and mesial prefrontal cortex (near the anterior cingulate gyrus), bilaterally, as well as in the left supramarginal and middle temporal gyri. The individual analysis showed that this group pattern was found in essentially each patient, regardless of the cause of amnesia. Thus, permanent amnesia is subtended by dysfunction in structures belonging to Papez/limbic circuits as well as in left-hemisphere areas typically concerned with verbal functions, probably through a mechanism of thalamo-cortical disconnection and possibly involved in retrograde amnesia. The use of a voxel-based method allowed us to map a common network of synaptic dysfunction in a neuropsychological syndrome regardless of etiology. Our results indicate that this should be a powerful method in functional neuropsychology.
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2/21. Use of cerebral oximetry to detect and manage cerebral desaturation with a rapidly expanding neck hematoma.

    BACKGROUND: We report a case in which cerebral oximetry was used to successfully demonstrate when cerebral oxygen saturation is dangerously low. methods: In a 60-year-old-man with end-stage multiple myeloma and hyperviscosity syndrome, a rapidly expanding hematoma developed after insertion of an internal jugular central venous catheter. As the hematoma expanded, the patient became lethargic and disoriented (Glasgow Coma Score of E2/M4-5/V2-ETT). His platelet count was 17,000.mm(-3), hemoglobin was 4.5 g/dl, partial thromboplastin time was 51 s, and his international ratio was 1.7. Although carotid pulses became unpalpable, blood pressure and heart rate remained stable. Cerebral oximeter probes positioned on the patient's forehead showed that cerebral oxygen saturation was 22-26% bilaterally. The surgery team was advised to surgically evacuate the hematoma. RESULTS: The hematoma was evacuated and a small needle hole in the right internal jugular vein adjacent to the central-venous catheter was found and repaired. Cerebral oxygen saturation increased to 56-58% within 1 h and stabilized near 60%. The patient awoke with normal cognitive function. CONCLUSION: This case demonstrates how cerebral oximetry can be used to give quantitative evidence of cerebral hypoxia, thus showing that immediate surgical intervention is necessary.
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3/21. Monitoring of cerebral oxygen saturation with a jugular bulb catheter after near-drowning and respiratory failure.

    We report on monitoring oxygen saturation with a jugular bulb fiber-optical catheter in an 18-month-old girl after fresh water near-drowning followed by acute respiratory failure. The first measured cerebral oxygen saturation was 22% despite normal values for arterial and central venous oxygen saturation. After conventional therapy had failed to improve cerebral oxygen saturation, we started veno-venous extracorporeal membrane oxygenation. Normal levels of cerebral oxygen saturation were achieved after six hours. The girl was extubated after seven days and discharged after twenty-five days in good general condition and without obvious evidence of neurological damage. We believe that in this case of near-drowning, monitoring cerebral oxygen saturation with a jugular bulb catheter was important for surveillance of cerebral hypoxia.
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4/21. 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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5/21. Anoxic encephalopathy: a case study of an eight-year-old male with no residual cognitive deficits.

    anoxia is generally associated with impaired learning, memory, attention, and planning. We present a case of near-drowning (5-15 minute anoxia) with subsequent 15 hour coma that is extremely unique because of (1) the absence of neuropsychological and neurological deficits 3 1/2 months post-injury, and (2) the availability of pre-injury intelligence testing for comparison. Findings are important as previous research has suggested residual deficits will be evident after much briefer coma. The present findings suggest anoxic encephalopathy does not automatically result in neurological or cognitive impairment.
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6/21. 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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7/21. 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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8/21. Identification of hypometabolic areas in the brain using brain imaging and hyperbaric oxygen.

    Current neurologic assessments consider idling neurons and ischemic penumbras to be metabolically lethargic and electrically nonfunctional or nonviable. diagnosis, prognosis, and therapeutics of central nervous system dysfunctions require differentiation between viable and nonviable neurons. It is necessary to develop and document efficacious and safe techniques for reactivating idling neurons. The authors present a case study of a near drowning 12 years earlier. Areas of cortical hypometabolism were identified by using SPECT imaging in conjunction with hyperbaric oxygen therapy (HBOT). Delayed imaging after HBOT (1 hour, 1.5 atm abs) suggested viable but metabolically lethargic neurons. After HBOT (80 1-hour treatments, monoplace chamber, 1.5 atm abs), marked improvements in cognitive and motor functioning were demonstrated. The data support the hypothesis that idling neurons and ischemic penumbras, when given sufficient oxygen, are capable of reactivation. Thus, changes in tracer distribution after a single exposure to HBOT may be a good prognostic indicator of viable neurons. HBOT may be valuable not only in recovery from anoxic encephalopathy but also from other traumatic and nontraumatic dysfunctions of the central nervous system, including stroke. HBOT in conjunction with physical and rehabilitative therapy may help reactivated idling neurons to remain permanently active.
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9/21. Anoxic brain injury following near-drowning in children. rehabilitation outcome: three case reports.

    PRIMARY OBJECTIVE: To describe the outcome of near-drowning and rehabilitation contexts for recovery. methods AND PROCEDURES: Standardized measures were used to emphasize the functional impact of deficits over the first year post-injury in three children <2 years. Multimodal contexts for meaningful interplay were early adapted to the three cases. MAIN OUTCOMES AND RESULTS: The clinical pathways of recovery are identified. Initially all three cases manifested a generalized dystonia. Case 1 exhibited a good outcome with transient dyskinetic-dystonic syndrome; subsequently Balint's syndrome emerged. In this case, the rehabilitation approach was organized on the pickup of direct perception of task-specific affordances. Cases 2 and 3 had poor outcomes presenting the worsening of torsion dystonia (status dystonicus) that hindered rehabilitation intervention. CONCLUSIONS: The dynamic reaggregation of spatial organization through meaningful interaction in specific ecological contexts is the principal goal of rehabilitation intervention. Status dystonicus represents the worst feature for recovery.
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10/21. Use of a polyethylene body jacket to prevent feeding tube removal in an agitated patient with anoxic encephalopathy.

    Maintaining a feeding tube in place in the agitated patient following a traumatic brain injury or anoxic encephalopathy is a familiar problem. However, a survey of the literature employing the medline system provided no solutions. This case study of a 36-yr-old patient with anoxic encephalopathy illustrates a new method of preventing feeding tube removal using a modified polyethylene body jacket. The patient had repeatedly pulled out his gastrostomy tube despite the use of four-way restraints, a posey, behavior modification and anti-psychotic medications at levels near sedation. A polyethylene jacket with an S-shaped tunnel for feeding tube exit was constructed to cover the abdomen. Findings: 1) The patient was unable to disturb the feeding tube. 2) The recessed design of the jacket's tunnel did not traumatize the feeding tube or obstruct fluid flow. 3) nursing staff encountered no problems in placing or removing the orthosis. 4) skin integrity was maintained. 5) The orthosis did not interfere with therapies.
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