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Visual object agnosia (VOA) is a loss of the ability to recognize visible objects in patients with the intact primary visual functions and in the absence of dementia. The apperceptive and associative variants of VOA are marked out. The apperceptive VOA is thought to be due to «pre-semantic» impairment of visual information processing. The associative VOA is caused by the loss of access to knowledge about the objects, and its semantic subtype is due to the disintegration of this knowledge itself. It is important to diagnose VOA and its variants in time to provide individualized approaches to medical rehabilitation of patients. Case reports of apperceptive and associative VOA in acute ischemic stroke are presented in this paper. These case reports indicate the possibility of the development of apperceptive and associative VOA in unilateral acute ischemic brain lesion. The variants of VOA can be recognized only by a detailed neuropsychological examination.

The aim of the study was to assess the prognostic value of the plasma neuron-specific enolase (NSE) level as a predictor of functional outcome and motor function recovery in the acute period of ischemic stroke (IS)., Materials and Methods: Fifty patients with IS have been examined. On admission to the hospital and at 12-14 days after stroke onset, a clinical and neurological examination have been carried out with the supplementary quantitative assessment of neurological deficit severity according to the National Institutes of Health Stroke Scale (NIHSS), functional outcome according to the Modified Rankin Scale, and Rivermead Mobility Index. Enzyme immunoassay was used to determine NSE concentration in blood plasma in the acute period of the disease., Results: The NSE level in patients' blood plasma in the first 48 h after stroke onset positively correlates with the ischemic focus volume (r=0.49; p=0.003) and the severity of neurological symptoms (according to NIHSS) (r=0.33; p=0.02). NSE less than 2 ng/ml in the acute disease period is a predictor of good functional outcome 12-14 days after stroke onset (OR=12.4; р=0.006). The NSE level >2.6 ng/ml is associated with a high likelihood of lethal outcome.Neurological deficit below 15 according to NIHSS as well as the NSE level <2 ng/ml in the acute IS period are estimated as prognostic factors of significant recovery of motor function at 2 weeks after disease onset (OR=5.8; р=0.02)., Conclusion: Determination of NSE in blood plasma makes it possible to predict functional outcome of the disease development and the recovery of motor function in patients with IS., Competing Interests: Conflict of interest. There are no conflicts of interest related to this study.

Cerebral amyloid angiopathy (CAA) is caused by the deposition of β-amyloid in small vessels in the cerebral cortex and leptomeninges. Nowadays, CAA is recognized more often due to the development of neuroimaging technologies. The frequency of CAA increases in old age that explains its frequent association with cardiovascular diseases. Combination of CAA with atrial fibrillation (AF) causes particular difficulties in managing of the patients, since antithrombotic drugs prescribed to patients with AF mostly contraindicated in CAA because of increased risk of intracerebral hemorrhages. The article presents a case report of the patient with AF who was admitted to the stroke center with acute ischemic stroke. According to MRI, the focus of acute ischemia was small and localized in the cerebellum. This stroke was regarded as having an undetermined etiology according TOAST classification. Small-vessel occlusion subtype was not diagnosed because the TOAST criteria do not attribute an ischemic focus in the cerebellum to a lacunar stroke, while cardioembolic subtype was rejected due to a small (less than 1.5 cm in diameter) size of the focus. Probable CAA in the patient was diagnosed on the basis of the following MRI data: multiple cortical-subcortical micro-hemorrhages (T2*GRE); a single cortical focus with features of the hemorrhage at the stage of intracellular methemoglobin deposition (T1- weighted MR images); bilateral enlargement of perivascular spaces in semioval centers (FLAIR); a negative fronto-occipital gradient (T2-weighted MR images). A diagnosis of CAA was made in accordance with the 2010 Boston criteria and 2019 recommendations of the International CAA Association. The article discusses the hemorrhagic and non-hemorrhagic MRI features of CAA. Frequency of occurrence of cortical microinfarcts in CAA is discussed as well as their differences from small cardioembolic infarcts in AF. Algorithms for antithrombotic therapy for secondary prevention of ischemic stroke in patients with CAA and AF are considered.

Objective: The aim was to evaluate changes in cerebrovascular resistance (CVR) in combined traumatic brain injury (CTBI) in groups with and without intracranial hematomas (IH)., Materials and Methods: Treatment outcomes in 70 patients with CTBI (42 males and 28 females) were studied. Mean age was 35.5 ± 14.8 years (range, 15-73). The patients were divided into two groups: group 1 included 34 CTBI patients without hematomas; group 2 comprised 36 patients with CTBI and IH. The severity according to the Glasgow Coma Scale averaged 10.4 ± 2.6 in group 1, and 10.6 ± 2.8 in group 2. All patients underwent perfusion computed tomography (CT) and transcranial Doppler of both middle cerebral arteries. Cerebral perfusion pressure and CVR were calculated., Results: The mean CVR values in each group (both with and without hematomas) appeared to be statistically significantly higher than the mean normal value. Intergroup comparison of CVR values showed statistically significant increase in the CVR level in group 2 on the side of the removed hematoma (р = 0.037). CVR in the perifocal zone of the removed hematoma remained significantly higher compared with the symmetrical zone in the contralateral hemisphere (p = 0.0009)., Conclusion: CVR in patients with CTBI is significantly increased compared to the normal value and remains elevated after evacuation of hematoma in the perifocal zone compared to the symmetrical zone in the contralateral hemisphere. This is indicative of certain correlation between the mechanisms of cerebral blood flow autoregulation and maintaining CVR.

The cerebrovascular time constant (τ) theoretically estimates how fast the cerebral arterial bed is filled by blood volume after a sudden change in arterial blood pressure during one cardiac cycle. The aim of this study was to assess the time constant of the cerebral arterial bed in patients with traumatic brain injury (TBI) with and without intracranial hematomas (IH). We examined 116 patients with severe TBI (mean 35 ± 15 years, 61 men, 55 women). The first group included 58 patients without IH and the second group included 58 patients with epidural (7), subdural (48), and multiple (3) hematomas. Perfusion computed tomography (PCT) was performed 1-12 days after TBI in the first group and 2-8 days after surgical evacuation of the hematoma in the second group. Arteriovenous amplitude of regional cerebral blood volume oscillation was calculated as the difference between arterial and venous blood volume in the "region of interest" of 1 cm(2). Mean arterial pressure was measured and the flow rate of the middle cerebral artery was recorded with transcranial Doppler ultrasound after PCT. The time constant was calculated by the formula modified by Kasprowicz. The τ was shorter (p = 0.05) in both groups 1 and 2 in comparison with normal data. The time constant in group 2 was shorter than in group 1, both on the side of the former hematoma (р = 0.012) and on the contralateral side (р = 0.044). The results indicate failure of autoregulation of cerebral capillary blood flow in severe TBI, which increases in patients with polytrauma and traumatic IH.

The purpose of this study was to determine the relationship between cerebral tissue oxygen saturation and cerebral blood volume in patients with traumatic brain injury. Perfusion computed tomography of the brain was performed in 25 patients with traumatic brain injury together with simultaneous SctO2 level measurement using cerebral near-infrared oxymetry. The mean age of the injured persons was 34.5±15.6 years (range 15-65); 14 men, 11 women. The Injury Severity Score (ISS) values were 44.4±9.7 (range 25-81). The Glasgow Coma Score (GCS) mean value before the study was 10.6±2.1 (range 5-13). SctO2 ranged from 51 to 89%, mean 62±8.2%. Cerebral blood volume (CBV) values were 2.1±0.67 ml/100 g (min 1.1; max 4.3 ml/100 g). Cerebral blood flow (CBF) was 31.99±13.6 ml/100 g×min. Mean transit time (MTT) values were 5.7±4.5 s (min 2.8; max 34.3 s). The time to peak (TTP) was 22.2±3.1 s. A statistically significant correlation was found between SctO2 level and cerebral blood volume (CBV) level (R=0.9; p<0.000001). No other significant correlations were found between brain tissue oxygenation and other parameters of brain perfusion.

Aim: To assess the dynamic of intracranial pressure (ICP), cerebral perfusion pressure (CPP), and dynamic pressure reactivity index (PRx) during intrahospital transport., Materials and Methods: There were 33 comatose patients with severe traumatic brain injury (TBI). The mean age was 36.3 ± 4.8 years (range 19-45 years), and there were 17 men and 16 women. The median Glasgow Coma Scale score at admission was 6.2 ± 0.7. Computed tomography (CT) included native CT, perfusion CT, and CT angiography., Results: The mean CPPs before and after the CT scans were 95.9 ± 10.7 and 81.5 ± 12.5 mmHg respectively. The mean ICP before transport was 19.98 ± 5.3 mmHg (minimum 11.7; maximum 51.7). It was statistically significantly lower (p < 0.001) than during the transfer (26.1 ± 13.5 mmHg). During the period described all patients had increased ICP, especially during vertical movement in an elevator. During horizontal movement on the floor ICP remained higher (p < 0.05). The mean dynamic PRx before and after intrahospital transport was 0.23 ± 0.14 and 0.52 ± 0.04, respectively (p < 0.001). Average duration of the transfer and CT study was 15.3 ± 3.4 min., Conclusion: Intrahospital transport of patients with TBI may lead to a significant increase in ICP, dynamic PRx, and decreased CPP. The results suppose that the decision to perform brain CT in comatose patients with TBI should be carefully considered by clinicians.