RESUMO
Background: Bilateral symmetrical simultaneous thalamic hemorrhages are extremely rare. Case presentation: A 52-year-old female patient with a history of untreated hypertension, ischemic heart disease and type 2 diabetes mellitus was admitted with somnolence, disorientation, 3/5 right-sided hemiparesis and blood pressure of 200/110 mmHg. Cranial CT scan showed bilateral thalamic hemorrhages, with bilateral intraventricular propagation and subarachnoid component along the frontal, parietal and occipital lobes. CT angiography did not show any source of bleeding or cerebral vein or sinus thrombosis. Coagulation laboratory parameters were in normal range.The patient was treated with a combination of intravenous and oral antihypertensive medication; five days later she become normotensive with improving motor function but was still somnolent.Six weeks later she was fully alert, motor functions continued to improve, but had severe cognitive deficit. Repeated neuropsychological assessment showed a slow and moderate improvement of a major neurocognitive impairment. At discharge her Mini Mental State Examination score was 13/30 and Addenbrooke's Cognitive Examination III score was 42/100.Cranial MRI scan eight weeks later depicted subacute-chronic stages of the bilateral hemorrhages, regression of perifocal edema, cerebral microbleeds in the left external capsule and the pons.At discharge after 2 months, she was alert, had no focal neurological signs, but was unable to care for herself due to lack of motivation, spatial and temporal disorientation and severe cognitive deficit. Conclusion: Simultaneous bilateral thalamic hemorrhages are extremely rare, the most commonly observed symptom is cognitive impairment. Our case was caused by hypertensive crisis, but in the differential diagnosis, sinus thrombosis, hemorrhagic transformation of ischemic stroke and various hemophilias should be considered.
RESUMO
OBJECTIVE: Bradykinesia has been associated with beta and gamma band interactions in the basal ganglia-thalamo-cortical circuit in Parkinson's disease. In this present cross-sectional study, we aimed to search for neural networks with electroencephalography whose frequency-specific actions may predict bradykinesia. METHODS: Twenty Parkinsonian patients treated with bilateral subthalamic stimulation were first prescreened while we selected four levels of contralateral stimulation (0: OFF, 1-3: decreasing symptoms to ON state) individually, based on kinematics. In the screening period, we performed 64-channel electroencephalography measurements simultaneously with electromyography and motion detection during a resting state, finger tapping, hand grasping tasks, and pronation-supination of the arm, with the four levels of contralateral stimulation. We analyzed spectral power at the low (13-20 Hz) and high (21-30 Hz) beta frequency bands and low (31-60 Hz) and high (61-100 Hz) gamma frequency bands using the dynamic imaging of coherent sources. Structural equation modelling estimated causal relationships between the slope of changes in network beta and gamma activities and the slope of changes in bradykinesia measures. RESULTS: Activity in different subnetworks, including predominantly the primary motor and premotor cortex, the subthalamic nucleus predicted the slopes in amplitude and speed while switching between stimulation levels. These subnetwork dynamics on their preferred frequencies predicted distinct types and parameters of the movement only on the contralateral side. DISCUSSION: Concurrent subnetworks affected in bradykinesia and their activity changes in the different frequency bands are specific to the type and parameters of the movement; and the primary motor and premotor cortex are common nodes.
