Delayed post-hypoxic leukoencephalopathy is a clinical syndrome caused by a lesion of the white matter of the brain with an acute onset developing several days after emerging from coma. The reason of delayed post-hypoxic leukoencephalopathy is prolonged cerebral hypooxygenation, it often results from carbon monoxide poisoning, less often it is associated with acute brain hypoxia caused by respiratory failure, an overdose of opiates. The leading role in the clinical picture of delayed post-hypoxic leukoencephalopathy is played by the duration and severity of cerebral anoxia in the acute period of the disease. The period of temporary well-being of a patient with an episode of acute hypoxia lasts 2 to 40days. Pathogenesis and pathophysiology have not been well studied. Its development after carbon monoxide poisoning is considered to be caused by direct myelinotoxic effect. Itis essential to collect a detailed history for diagnosing a case, neurovisualization is an informative method for investigation. Magnetic resonance imaging may detect the signs that are pathognomonic for delayed post-hypoxic leukoencephalopathy, that is diffuse hyperintensity of the white matter of the cerebral hemispheres in T2-mode, symmetry of the damage of both cerebral hemispheres, damage of the subcortical gray matter globus pallidus. The standards for the treatment of delayed post-hypoxic leukoencephalopathy have not been developed. The use of glucocorticoids has been described, perspective use of amantadine were shown in case of frontal-subcortical syndrome. There are recommendations on prescribing the following therapy for the patients with delayed post-hypoxic leukoencephalopathy: hyperbaric oxygenation, coenzymeQ10, vitaminE and groupB. We present a clinical observation that demonstrates the complexity of the clinical picture of delayed post-hypoxic leukoencephalopathy, the difficulty of its diagnosis without taking into account information about previous carbon monoxide poisoning. The results of magnetic resonance imaging at the onset of the disease are considered to be of utmost interest. The clinical observation of the patient presented in the article allows us to make an assumption about pathogenesis and contributes to search for means aimed at preventing the development of delayed post-hypoxic leukoencephalopathy in people with acute carbon monoxide poisoning.
The authors present a case-report of genetically tested dopa-responsive dystonia, also known as Segawa’s syndrome, in a 32-year-old woman. The genetic forms and their clinical presentation are described. Symptoms began in early childhood with running disability. The patient’s first complaint was twisting of her toes during walking when she was 12 years old. The condition remained stable up to 20 y. o., when some improvement was noticed. Symptoms progressed with involvement of upper limbs at the age of 25. By the age of 32 the patient was directed to Movement Disorders Clinic, where Dopa-responsive dystonia was suspected. The manifestations were dramatically responsive to low doses of levodopa-carbidopa, confirming the diagnosis of dopa-responsive dystonia. The genetic test identified a GCH1 (chr14:55369161G>A) pathogenic mutation.
Area postrema syndrome (APS) develops in patients with lesions found in the floor of the fourth ventricle and manifests with nausea, intractable vomiting, and hiccup. APS is most commonly associated with neuromyelitis optica spectrum disorders although it may develop in some other conditions as well.
We have presented a case study of APS with positional vertigo developed in a 41-year-old woman caused by acute disseminated encephalomyelitis after COVID-19 vaccination. Quasi benign paroxysmal positional vertigo acutely manifested with nausea, vomiting, and vertigo that dramatically worsened with head movement. Physical examination revealed patchy hypesthesia on the left side of the face and decreased convergence of the left eye. MRI scan showed a lesion adjacent to the floor of the fourth ventricle (area postrema). The manifestations totally regressed on glucocorticoids without any relapse during 1-year follow-up.
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