Cases reported "Carbon Monoxide Poisoning"

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1/8. Four deaths due to carbon monoxide poisoning in car washes.

    In a period of 13 months, three separate incidents of lethal carbon monoxide (CO) poisoning in closed car wash bays resulted in the deaths of 4 white men aged 20 to 36 years. Each man appears to have been intoxicated with mind-altering substances, which may impair judgment, perception of outside conditions, and self-awareness. All four died in winter months. For three men, the deaths were ruled accidental, and for the remaining man, the previous deaths appear to have provided a model for suicide. Warning signs may not be effective to prevent future CO deaths in car washes because of the possible role of intoxication. Mechanical or electronic methods to prevent a bay door from closing completely may be preferable.
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2/8. Visual loss as a late complication of carbon monoxide poisoning and its successful treatment with hyperbaric oxygen therapy.

    PURPOSE: To present recovery from vision loss due to CO poisoning with Hyperbaric oxygen (HBO) therapy in two patients. methods: Two female patients developed visual deterioration after carbon monoxide (CO) poisoning and were treated with hyperbaric oxygen therapy (HBO). Clinical examination, including visual acuity assessment, visual field examination and visual evoked potentials (VEPs) before and after the HBO therapy were performed. RESULTS: In Case 1 the visual loss started on the third day with visual acuity at the level of perception of hand movements at 10 cm in the right eye and finger count at 10 cm in the left eye. The visual evoked potentials (VEPs) had low amplitudes and prolonged (128 msec bilaterally) latencies (implicit times). After 48 sessions and 52 days of HBO therapy, the visual acuity became 0.2 in the right eye and 0.15 in the left eye. Visual field examination revealed homonymous right lower quadrant anopsia. The VEPs also improved. In Case 2 the visual acuity was 0.2 in the right eye and 0.1 in the left eye on the 6th day following the accident when the patient was admitted for treatment. The VEP latencies were within normal limits. After 36 days and 35 sessions of HBO therapy, the visual acuity became 0.7 on both eyes. The visual fields completely normalised. The VEP latencies in this case also became shorter. CONCLUSION: It appears that the adverse effects of CO poisoning continue to progress during the late period and we believe that HBO treatment in this period may still be effective and will prevent some of the neurological sequelae such as visual loss from becoming permanent. Clinical, neurological, neuropsychological, visual outcome seems to be favourable even if HBO treatment started as late as 6 or 8 days after the exposure to CO.
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3/8. 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.
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4/8. Apperceptive agnosia due to carbon monoxide poisoning. An interpretation based on critical band masking from disseminated lesions.

    Apperceptive visual agnosia is normally held to be a specific deficit in 'apperception' - a hypothetical postsensory stage in visual processing. This paper describes the investigation of a patient diagnosed as suffering from a classical apperceptive agnosia resulting from carbon monoxide poisoning. Controlled behavioural testing confirmed the apparent agnosia but revealed that he could be trained to make a number of visual discriminations which had not been apparent from routine clinical examination and that he suffered a number of subtle sensory impairments which likewise had not hitherto been apparent. Evoked potential recording to grating patterns showed a complex pattern of brain responses involving interactions between spatial frequency, orientation and hemisphere recorded from. The data suggested that the agnosia was caused by sensory impairments rather than a deficit in apperception. We proposed that the impairments were caused by loss of certain spatial frequency and orientation information but rejected an interpretation based on the concept of processing channels in favour of one based on object contour masking by a peppery field defect caused by disseminated lesions. This interpretation received some support from fine grain static perimetry, contrast sensitivity function measurement and orientation discrimination in the two hemifields. Qualitatively similar results were obtained in normal subjects whose field was artificially masked. The results have implications for theories of visual agnosia and for theories of vision based on the concept of processing channels.
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5/8. Preserved visual imagery in visual form agnosia.

    We investigated the ability of a patient (D.F.) with profound visual form agnosia to perform a variety of tasks requiring visual imagery. Despite her inability to discriminate between objects and patterns of different shapes, sizes, and orientations, D.F. showed quite normal visual imagery involving these same 'visual' properties when the images were drawn from long-term memory. Thus, she was able both to scan mental images in search of particular features and to form new images by combining several known images. While there is growing evidence that perception and imagery share common neural substrates, the fact that D.F. shows intact visual imagery in the face of a massive perceptual deficit in form vision challenges recent suggestions that these two psychological processes share common input pathways in early vision. It is suggested that regions in the occipitotemporal pathway may be important for the generation of visual images while regions in the posterior parietal system might be involved in the manipulation of these images.
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6/8. Copying without perceiving: motor imagery in visual form agnosia.

    Patient DF has severely impaired visual contour perception, despite being able to use that same visual information to guide her motor actions. We report that DF has developed a strategy to overcome some of her perceptual deficits. DF was first asked to copy single lines set at different orientations. She performed surprisingly accurately, although her responses were slow. When questioned, DF reported imagining tracing the line with her finger before copying the line on paper, although she was still unable to discriminate perceptually between different line orientations. We found that time restraints, or the requirement to perform secondary concurrent tasks, severely disrupted DF's orientation copying ability. We conclude that DF can use pure motor imagery to compensate for some of her perceptual difficulties.
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7/8. Disturbance of central vision after carbon monoxide poisoning.

    BACKGROUND: Cerebral achromatopsia is a disturbance of colour perception which may be complete or partial. CLINICAL RECORD: A 28-year-old male patient presented five months after carbon monoxide poisoning with achromatopsia. The achromatopsia was unaccompanied by an inability to recognise faces (prosopagnosia) nor was there any disorder of form or depth perception. RESULTS: magnetic resonance imaging showed bilateral sharply defied areas of haemorrhagic infarction in the globus pallidus with extensive infarction involving temporal and occipital lobes and with apparent partial sparing of the visual cortex, presumably due to arterial insufficiency. The disturbance of central colour vision resolved spontaneously after a further period of 6 months. CONCLUSION: The symptom of achromatopsia is analysed with particular reference to the recent work of Professor Zeki on disturbance of central colour vision following CO poisoning and the unusual MRI findings.
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8/8. Vision without knowledge.

    A brain-damaged patient (D.F.) with visual form agnosia is described and discussed. D.F. has a profound inability to recognize objects, places and people, in large part because of her inability to make perceptual discriminations of size, shape or orientation, despite having good visual acuity. Yet she is able to perform skilled actions that depend on that very same size, shape and orientation information that is missing from her perceptual awareness. It is suggested that her intact vision can best be understood within the framework of a dual processing model, according to which there are two cortical processing streams operating on different coding principles, for perception and for action, respectively. These may be expected to have different degrees of dependence on top-down information. One possibility is that D.F.'s lack of explicit awareness of the visual cues that guide her behaviour may result from her having to rely on a processing system which is not knowledge-based in a broad sense. Conversely, it may be that the perceptual system can provide conscious awareness of its products in normal individuals by virtue of the fact that it does interact with a stored base of visual knowledge.
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