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.

Deep cerebral venous thrombosis is a rare pathology and hard to diagnose cause of the acute cerebrovascular diseases. Commonly, the veins of Galen and Rosenthal affected by the non-isolated deep cerebral venous thrombosis are described in most of the publications. The article presents a clinical case of an extremely rare isolated deep cerebral venous thrombosis in a female patient aged 31 years with a burdened obstetric history and thrombophilia. The disease onset started with increasing hypertension headache, congestive changes in the fundus, cerebellar and pyramidal signs. Magnetic resonance imaging (MRI) of the brain revealed a pattern of a multi-focal brain lesion. Thus, the primary diagnosis of «multiple sclerosis» was established, so the patient received pulse therapy. Differential diagnosis was conducted with systemic connective tissue diseases. Regression of headaches, of changes in the fundus, dynamic neuroimaging data, and the results of hematology test made it possible to diagnose «deep cerebral venous thrombosis». During the anticoagulant therapy, there was a positive dynamics: the foci significantly regressed according to MRI data, the patient became pregnant and delivered a healthy child. The article describes the characteristics of MRI images on deep cerebral venous thrombosis, which can be used to diagnose this patholo gy. KEYWORDS: deep cerebral venous thrombosis, сerebral venous sinus thrombosis, thrombophilia, coagulopathy, infertility, headache, multiple sclerosis. FOR CITATION: Matveeva T.V., Ibatullin M.M., Gaifutdinov R.T. et al. Isolated deep cerebral venous thrombosis. Russian Medical Inquiry. 2020;4(9):595–600. DOI: 10.32364/2587-6821-2020-4-9-595-600.

Aim. To study clinical and paraclinical features in patients with cerebral vascular diseases and their response to treatment. Methods. 121 patients with cerebral vascular diseases (32 males, 89 females, mean age 63.6±8.8 years) were studied before and after the treatment. Patients were divided into groups according to the disease severity. Neurological status, emotional sphere were assessed, other study methods were also used. Results. Neurological symptoms characterizing pyramidal, vestibulo-cerebellar and extrapyramidal syndromes were the most frequent in patients with various cerebral vascular diseases. Symptoms characterizing vestibulo-cerebellar syndrome improved after treatment: dynamic ataxia was present in 66.7% of patients with hypoxic ischemic encephalopathy stage I before treatment compared to 29.2% after treatment, in 44.0% of patients with hypoxic ischemic encephalopathy stage II before treatment compared to 32.0% after treatment, truncal cerebellar ataxia was present in 86.7% of patients before and in 64.0% of patients after treatment and was associated with cognitive potential increase revealed at emotional sphere estimation. The effectiveness of the treatment was confirmed by other study methods. Conclusion. Neurological symptoms including lateral nystagmus, truncal and appendicular ataxia, characterizing vestibulocerebellar syndrome, may be improved after treatment in patients with all groups of cerebral vascular disorders, with the decrease of emotional factor influence and further improvement of the cognitive potential.

No abstract