Cases reported "Hypoxia, Brain"

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1/32. 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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2/32. levodopa and bromocriptine in hypoxic brain injury.

    BACKGROUND: Postanoxic encephalopathy is frequent in patients presenting with abrupt cardiac arrest or respiratory failure. Little is known about the effectiveness of oral medications on the cognitive and motor consequences. OBJECTIVE: To present data suggesting partial improvement after administration of levodopa/benserazide. methods: After observing partial benefit in one case, each patient admitted to rehabilitation following brain anoxia was systematically treated with levodopa/benserazide (200/50 to 400/100 mg/day), then bromocriptine (15 mg/day). RESULTS: In the first patient, brain anoxia was severe, with secondary agitation, quadriparesis, involuntary movements, inattention and communication disorders. Introduction of levodopa/benserazide resulted in reduction of agitation and involuntary movements and improvement of communication, thus facilitating care and rehabilitation efforts. A weaning test resulted in rapid worsening. The four following patients also presented with anoxia of variable severity. Marked improvement was observed in case 2, presenting with agitation, loss of orientation, amnesia, postural disorders, involuntary movements and dysphagia, with a withdrawal test resulting in immediate re-enhancement of symptoms. Modest improvement was observed in patient 3, who had hypokinesia, rigidity, adynamia, impaired attention, and reduced verbal fluency. Patient 4 presented with memory disorders without motor difficulties: mild improvement was observed in daily life and memory tests. In patient 5 who also presented with severe memory disorders, the benefit was absent. In each case, bromocriptine was introduced 3-4 weeks following levodopa, but without additive effect. Both treatments could be interrupted after a few months, without worsening. CONCLUSIONS: levodopa and benserazide can be of benefit in the few months following brain anoxia, especially on some of the motor disorders and apathy, but the benefit is inconstant and modest on memory disorders. anoxia could alter dopaminergic mesencephalic systems, which activate the striatal and mediobasal frontal cortex, and these disorders could be partially reversible by medical treatment.
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3/32. Computed tomography and magnetic resonance imaging findings of brain damage by hanging.

    We reported computed tomography (CT) and magnetic resonance imaging (MRI) findings of brain damage of a 61-year-old man who attempted suicide by hanging. Unenhanced CT demonstrated multiple hyperdense areas indicating subcortical and subarachnoid hemorrhages and brain swelling. MRI demonstrated not only hemorrhagic findings, but also ischemic findings in the middle brain and cerebral cortex. Multifocal cerebral hemorrhages might be caused by venous hypertension due to compression of the jugular veins.
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4/32. Neonatal citrullinemia: comparison of conventional MR, diffusion-weighted, and diffusion tensor findings.

    Conventional MR, diffusion-weighted, and diffusion tensor imaging were performed in an 8-day-old girl with citrullinemia. She had severe hyperammonemia for several days. On conventional T2-weighted MR images, symmetric, confluent high signal intensity was found in the bilateral thalami, basal ganglia, cortex, and subcortical white matter. Diffusion-weighted imaging demonstrated decreased apparent diffusion coefficient in these areas, reflecting cytotoxic edema. Follow-up MR imaging at the age of 4 months revealed subcortical cysts, ulegyric changes, and atrophy, which were most prominent in the occipital lobes. diffusion tensor imaging revealed decreased anisotropy throughout the brain, consistent with diffuse injury to the oligodendro-axonal unit. Diffusion-weighted and diffusion tensor imaging are valuable techniques for the detection of irreversible brain damage and for the characterization of hyperintense lesions on T2-weighted MR images in patients with the neonatal form of citrullinemia.
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5/32. Delayed postanoxic encephalopathy: a case report and literature review.

    Delayed postanoxic encephalopathy is a rare condition in which patients appear to make a complete clinical recovery after an episode of anoxia or hypoxia but then develop a relapse characterized by apathy, confusion, agitation, and/or progressive neurologic deficits. The incidence of delayed postanoxic encephalopathy is unclear but has been reported to range from less than 1 to 28 per 1000 in patients who have suffered hypoxic or anoxic events. The exact pathogenesis remains unknown. We describe a case of an independently living 51-year-old woman admitted to an inpatient rehabilitation unit 11 days after a respiratory arrest. At admission, she exhibited cognitive and visual deficits that were relatively mild but prevented a safe return to independent living. Two days later, she developed the sudden onset and rapid worsening of parkinsonian symptoms and excruciating bilateral lower-extremity pain. The pain was intractable, and over the next 2 days she progressed to being unable to walk or perform her activities of daily living without maximum assistance. A diagnosis of delayed postanoxic encephalopathy was made, and the patient responded to a trial of carbidopa and levodopa as well as redirection of her physical and occupational therapy programs. This case illustrates the unusual presentation of delayed postanoxic encephalopathy during inpatient rehabilitation and suggests that this condition should be considered if patients who have suffered an anoxic or hypoxic event show a sudden neurologic deterioration.
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keywords = visual
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6/32. A cognitive neuropsychological and psychophysiological investigation of a patient who exhibited an acute exacerbated behavioural response during innocuous somatosensory stimulation and movement.

    We report findings from a cognitive neuropsychological and psychophysiological investigation of a patient who displayed an exacerbated acute emotional expression during movement, innocuous, and aversive somatosensory stimulation. The condition developed in the context of non-specific white matter ischaemia along with abnormalities in the cortical white matter of the left anterior parietal lobe, and subcortical white matter of the left Sylvian cortex. Cognitive neuropsychological assessment revealed a pronounced deficiency in executive function, relative to IQ, memory, attention, language and visual processing. Compared to a normal control group, the patient [EQ] displayed a significantly elevated skin conductance level during both innocuous and aversive somatosensory stimulation. His pain tolerance was also significantly reduced. Despite this, EQ remained able to accurately describe the form of stimulation taking place, and to rate the levels of pain intensity and pain affect. These results suggest that EQ's exaggerated behavioural response and reduced pain tolerance to somatosensory stimulation may be linked to cognitive changes, possibly related to increased apprehension and fear, rather than altered pain intensity or pain affect per se.
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keywords = cortex, visual
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7/32. MRI demonstration of cortical laminar necrosis and delayed white matter injury in anoxic encephalopathy.

    We performed serial radiological examinations on a patient with anoxic encephalopathy. In the early term after the anoxic insult, T1-weighted MRI revealed high signal intensity areas distributed laminarly in the cerebral cortex and diffusely in the putamen, which were thought to reflect the cortical necrosis and necrosis in the putamen. Single photon emission computed tomography using I-123 isopropylamphetamine showed persistent hypoperfusion in the arterial watershed zones. T2-weighted MRI performed several months after the anoxic episode revealed diffuse high-intensity lesions in the arterial water-shed zones. These delayed-onset white matter lesions continued to extend over several months.
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8/32. Selective sparing of Betz cells in primary motor area in hypoxic-ischemic encephalopathy.

    Two cases of postoperative hypoxic-ischemic encephalopathy are described in which Betz cells of the primary motor area were selectively spared. In one patient the hypoxic-ischemic encephalopathy led to a vegetative state and in the other patient to a spastic quadriparesis and cortical blindness. In contrast to the relative sparing of Betz cells, purkinje cells of the cerebellar cortex were totally destroyed. These two cases suggest that Betz cells are relatively resistant to hypoxic-ischemic insult under certain conditions.
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9/32. The complete apallic syndrome--a case report.

    In six patients with apallic syndrome the EEG was isoelectric, although the patients were breathing spontaneously and vegetative functions remained stable for a long period of time. No cortical somatosensory evoked potentials could be recorded in four of the patients examined. Cranial CT performed in three patients revealed extensive hypodensity of the cortex, whereas the brain stem showed no major damage. This syndrome is labelled a "complete apallic syndrome". None of our patients, and none of the 23 patients described in the literature, recovered.
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10/32. Obsessive-compulsive and other behavioural changes with bilateral basal ganglia lesions. A neuropsychological, magnetic resonance imaging and positron tomography study.

    Eight patients are reported who shared the combination of bilateral basal ganglia lesions and a frontal lobe-like syndrome. The main features were inertia and loss of drive, with preservation of intellectual function. Some patients showed stereotyped activities with compulsive and obsessive behaviour which were sometimes highly elaborate in pattern. Extrapyramidal clinical signs were absent or mild. Brain damage, related to anoxic or toxic encephalopathy, was demonstrated by CT scans and MRI. The lesions appeared to be confined to the lentiform nuclei, particularly affecting the pallidum, although there was generalized brain atrophy in 2 cases. Positron emission tomography (PET) in 7 patients revealed hypometabolism of the prefrontal cortex relative to other parts of the brain. The PET studies suggest dysfunction of the prefrontal cortex as a result of damage to the lentiform nuclei. These clinical, anatomical and functional observations emphasize the role of the circuits linking the prefrontal associative cortex and some specific areas of the neostriatum, including the pallidum. The existence of distinct nonoverlapping circuits in the motor field or in the associative field can explain the fact that basal ganglia lesions may give rise to a clinical picture that is either purely motor, purely behavioural (as in some of our patients), or both. Similarities existed between some symptoms found in our patients and certain features of major psychiatric illnesses such as severe depression, catatonic schizophrenia, and obsessive-compulsive disorder. This raises the hypothesis that some aspects of these psychiatric disorders could be related to structural and physiological disturbances in the systems linking the frontal associative cortex and the basal ganglia.
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