Thalamic Stroke Research Articles

Secondary damage and neuroinflammation in the spinal dorsal horn mediate post-thalamic hemorrhagic stroke pain hypersensitivity: SDF1-CXCR4 signaling mediation.

Central post-stroke pain (CPSP) is an intractable neuropathic pain, which can be caused by primary lesion of central somatosensory system. It is also a common sequelae of the thalamic hemorrhagic stroke (THS). So far, the underlying mechanisms of CPSP remain largely unknown. Our previous studies have demonstrated that SDF1-CXCR4 signaling in the hemorrhagic region contributes to the maintenance of the THS pain hypersensitivity via mediation of the thalamic neuroinflammation. But whether the spinal dorsal horn, an initial point of spinothalamic tract (STT), suffers from retrograde axonal degeneration from the THS region is still unknown. In this study, neuronal degeneration and loss in the spinal dorsal horn were detected 7 days after the THS caused by intra-thalamic collagenase (ITC) injection by immunohistochemistry, TUNEL staining, electron microscopy, and extracellular multi-electrode array (MEA) recordings, suggesting the occurrence of secondary apoptosis and death of the STT projecting neuronal cell bodies following primary THS via retrograde axonal degeneration. This retrograde degeneration was accompanied by secondary neuroinflammation characterized by an activation of microglial and astrocytic cells and upregulation of SDF1-CXCR4 signaling in the spinal dorsal horn. As a consequence, central sensitization was detected by extracellular MEA recordings of the spinal dorsal horn neurons, characterized by hyperexcitability of both wide dynamic range and nociceptive specific neurons to suprathreshold mechanical stimuli. Finally, it was shown that suppression of spinal neuroinflammation by intrathecal administration of inhibitors of microglia (minocycline) and astrocytes (fluorocitrate) and antagonist of CXCR4 (AMD3100) could block the increase in expression levels of Iba-1, GFAP, SDF1, and CXCR4 proteins in the dorsal spinal cord and ameliorate the THS-induced bilateral mechanical pain hypersensitivity, implicating that, besides the primary damage at the thalamus, spinal secondary damage and neuroinflammation also play the important roles in maintaining the central post-THS pain hypersensitivity. In conclusion, secondary neuronal death and neuroinflammation in the spinal dorsal horn can be induced by primary thalamic neural damage via retrograde axonal degeneration process. SDF1-CXCR4 signaling is involved in the mediation of secondary spinal neuroinflammation and THS pain hypersensitivity. This finding would provide a new therapeutic target for treatment of CPSP at the spinal level.

Alterations of optic tract and retinal structure in patients after thalamic stroke.

ObjectivesTo investigate the association between degeneration of retinal structure and shrinkage of the optic tract in patients after thalamic stroke.Materials and methodsPatients with unilateral thalamic stroke were included. Structural magnetic resonance imaging (MRI) and optical coherence tomography (OCT) were performed to obtain parameters of optic tract shrinkage (lateral index) and retina structural thickness (retinal nerve fiber layer, RNFL; peripapillary retinal nerve fiber layer, pRNFL; ganglion cell-inner plexiform layer, GCIP), respectively. Visual acuity (VA) examination under illumination was conducted using Snellen charts and then converted to the logarithm of the minimum angle of resolution (LogMAR). We investigated the association between LI and OCT parameters and their relationships with VA.ResultsA total of 33 patients and 23 age-sex matched stroke-free healthy controls were enrolled. Patients with thalamic stroke showed altered LI compared with control participants (P = 0.011) and a significantly increased value of LI in the subgroup of disease duration more than 6 months (P = 0.004). In these patients, LI were significantly associated with pRNFL thickness (β = 0.349, 95% confidence interval [CI]: 0.134–0.564, P = 0.002) after adjusting for confounders (age, sex, hypertension, diabetes, dyslipidemia, and lesion volume). LI and pRNFL were both significantly associated with VA in all patients (LI: β = −0.275, 95% CI: −0.539 to −0.011, P = 0.041; pRNFL: β = −0.023, 95% CI: −0.046 to −0.001, P = 0.040) and in subgroup of disease duration more than 6 months (LI: β = −0.290, 95% CI: −0.469 to −0.111, P = 0.002; pRNFL: β = −0.041, 95% CI: −0.065 to −0.017, P = 0.003).ConclusionShrinkage of the optic tract can be detected in patients with thalamic stroke, especially after 6 months of stroke onset. In these patients, the extent of optic tract atrophy is associated with pRNFL thickness, and they are both related to visual acuity changes.

Case report: Improved behavioral and psychiatric symptoms with repetitive transcranial magnetic stimulation at the bilateral DLPFC combined with cognitive and behavioral therapy in a patient with unilateral thalamic hemorrhage

Behavioral and psychological symptoms are not uncommon after thalamic stroke, and are often intractable despite medication and behavioral interventions. Repetitive transcranial magnetic stimulation (rTMS) is as an adjunctive therapeutic tool for neuropsychiatric diseases, and bilateral rTMS has been recently introduced to maximize the therapeutic effect. Herein, we report the case details of a patient with unilateral left thalamic hemorrhage without cortical lesions who had treatment-resistant neuropsychiatric symptoms. We hypothesized that bilateral rTMS targeting the bilateral dorsolateral prefrontal cortices (DLPFCs) would positively affect thalamocortical neural connections and result in neuropsychiatric symptom improvement. The patient received a total of 10 sessions of bilateral rTMS over 2 weeks, applied at the DLPFCs, with high frequency in the left hemisphere and low frequency in the right hemisphere. After each rTMS treatment, computer-based cognitive-behavioral therapy was administered for 30 min. Behavioral and psychological symptoms, including hallucinations, aggressiveness, aberrant motor activity, disinhibition, and abrupt emotional changes, were significantly improved as assessed by the Neuropsychiatric Inventory Questionnaire. These effects persisted for up to 1 month. This case demonstrates the clinical potential of bilateral rTMS treatment in patients with intractable neurocognitive impairment after thalamic stroke.

The topography of thalamic stroke has an impact on associated slow wave sleep and cognitive changes

The topography of thalamic stroke has an impact on associated slow wave sleep and cognitive changes

The Clinical Relevance of the Thalamogeniculate Arteries in Endoscopic Endonasal Surgery for Giant Pituitary Adenomas in the Interpeduncular Fossa.

Bilateral thalamic stroke is usually due to compromised artery of Percheron, an anatomical variation of the vascular supply of the thalamus. The stroke in this area is very uncommon, and is mainly due to top of the basilar syndrome. Other causes are extremely rare. We describe the case of a patient with a pituitary adenoma who underwent surgery and later presented with a bilateral thalamic infarct, suggesting compromise of the artery of Percheron. This would be the third case published in the literature about this complication. We present a literature review about the vascular supply of the thalamus, the artery of Percheron, and its involvement in pituitary surgery.

Long-term follow-up of motor cortex stimulation on central poststroke pain in thalamic and extrathalamic stroke.

To investigate the long-term effects of motor cortex stimulation (MCS) on central poststroke pain (CPSP) in patients with thalamic and extrathalamic stroke. We retrospectively analyzed 21 cases of CPSP patients who were treated with MCS. Pain intensity was evaluated using the visual analog scale (VAS) and Neuropathic Pain Symptom Inventory (NPSI) before the operation and at follow-up assessments. Sleep quality was evaluated using the Pittsburgh Sleep Quality Index (PSQI). The average follow-up time was 65.43 ± 26.12 months. In the thalamus stroke group (n=11), the mean preoperative VAS score was 8.18 ± 0.75 and the final mean follow-up VAS score was 4.0 ± 2.14. The mean total NPSI score at the last follow-up (20.45 ± 12.7) was significantly reduced relative to the pre-MCS score (30.27 ± 8.97, p < 0.001). Similarly, the mean PSQI value at the last follow-up (12.63 ± 1.91) was significantly reduced compared with the pre-MCS value (16.55 ± 1.97, p < 0.001). In the extrathalamic stroke group (n=11), the mean preoperative VAS score was 8.2 ± 0.79 and the final mean follow-up VAS score was 6.6 ± 2.12. The mean total NPSI score before MCS was not statistically different from that at the last follow-up. There were no statistical differences in sleep quality before versus after surgery. Motor cortex stimulation has higher long-term efficacy in CPSP patients with stroke confined to the thalamus than in CPSP patients with stroke involving extrathalamic structures.

Posterior circulation ischemic stroke not involving the brainstem is associated with cardiovascular autonomic dysfunction.

Ischemic stroke may induce cardiovascular autonomic dysfunction, but most previous studies have included patients with anterior circulation ischemic stroke or brainstem stroke. It remains unclear whether posterior circulation ischemic stroke (PCIS) without brainstem involvement also compromises cardiovascular autonomic modulation (CAM). Therefore, we aimed to assess CAM in PCIS patients with and without brainstem involvement. In four subgroups of 61 PCIS patients (14 occipital lobe, 16 thalamic, 12 cerebellar, and 19 brainstem strokes) and 30 healthy controls, we recorded RR intervals (RRIs), systolic (SBP) and diastolic blood pressure (DBP), and respiration at supine rest during the first week after stroke onset. We calculated parameters reflecting total CAM (RRI-standard deviation [RRI-SD], RRI-total powers), predominantly sympathetic CAM (RRI-low-frequency [LF] powers and SBP-LF powers] and parasympathetic CAM (root mean square of successive RRI differences [RMSSD], RRI-high-frequency [HF] powers), sympathetic-parasympathetic balance (RRI-LF/HF ratios), and baroreflex sensitivity (BRS). Values were compared among the four PCIS groups and controls using one-way ANOVA Kruskal-Wallis tests, with post-hoc analyses. Significance was assumed for p &lt; 0.05. In each PCIS subgroup, values for RRI, RRI-SD, RMSSD, RRI-HF powers, and BRS were significantly lower, while SBP-LF powers were higher than in the controls. Only in patients with occipital lobe stroke were RRI-LF/HF ratios significantly higher than in controls. Otherwise, autonomic variables did not differ among the four PCIS subgroups. During the first week after stroke onset, our PCIS patients with occipital lobe, thalamic, cerebellar, or brainstem strokes all had reduced cardiovagal modulation, compromised baroreflex, and increased peripheral sympathetic modulation. The RRI-LF/HF ratios suggest that sympathetic predominance is slightly more prominent after occipital lobe stroke. PCIS may trigger cardiovascular autonomic dysfunction even without brainstem involvement.

Quantitative and Fiber-Selective Evaluation for Central Poststroke Pain.

The electrophysiological recording can be used to quantify the clinical features of central poststroke pain (CPSP) caused by different lesion locations. We aimed to explore the relationship between clinical features and lesion location in patients with CPSP using the current perception threshold (CPT) approach. Here, patients underwent the standardized CPT measure at five detection sites on both the contralesional and ipsilesional sides, using a constant alternating-current sinusoid waveform stimulus at three frequencies: 2000 Hz, 250 Hz, and 5 Hz. 57 CPSP patients were recruited in this cross-sectional study, including 13 patients with thalamic lesions and 44 patients with internal capsule lesions. Patients with a thalamic lesion had more frequent abnormal Aδ and C fibers than those with an internal capsule lesion (69.2% versus 36.4%, p value = 0.038; 53.8% versus 63.6%, p value = 0.038). The patients with internal capsule lesions had more frequent abnormal Aβ fibers than those with thalamic lesions (53.8% versus 63.6%, p value < 0.001). The sensory dysfunction in the patients with thalamic lesions was more likely to occur in the upper limbs (i.e., the shoulder (p value = 0.027) and the finger (p value = 0.040)). The lower limbs (i.e., the knee (p value = 0.040) and the toe (p value = 0.005)) were more likely to experience sensory dysfunction in the patients with internal capsule lesions. Hyperesthesia was more likely to occur in the thalamic patients, and hypoesthesia was more likely to occur in the patients with internal capsule lesions (p value < 0.001). In patients with thalamic lesions, Visual Analogue Scale (VAS) had a positive correlation with 5 Hz CPT on the shoulder (r = 0.010, p value = 0.005), 250 Hz CPT on the finger (r = 0.690, p value = 0.009) from the contralesional side, and 2000 Hz CPT on the knee (r = 0.690, p value = 0.009). In patients with internal capsule lesions, VAS had a positive correlation with 2000 Hz CPT on the knee (r = 0.312, p value = 0.039) and foot (r = 0.538, p value < 0.001). In conclusion, the abnormal fiber types, sensory dysfunction territory, and clinical signs of CPSP in thalamic stroke differ from those in internal capsule stroke. Implementation of the portable and convenient CPT protocol may help clarify the locations of different stroke lesions in various clinical settings.

P.071 Case report: cheiro-oral syndrome secondary to thalamic ischemic stroke

Background: Patient with small thalamic infarct may present with a variety of subtle and seemingly disconnected sensory deficits which can be easily missed. Methods: Here we report a case of an 80 years ‘old Chinese female presenting sudden onset persistent sensory symptoms over perioral area and right hand. The patient underwent further investigation with Brain MRI. The patient underwent further investigation with Brain MRI. A literature review was conducted and the patient’s clinical finding was compared with the literature. Results: The patient’s presentation was consistent with clinical manifestation of type 1 Cheiro-Oral syndrome. Brain MRI performed the day after admission revealed small non-hemorrhagic infarction involving the left thalamus. The diagnosis was type 1 cheiro-oral syndrome secondary to left thalamic ischemic stroke. Conclusions: This report highlights both clinical presentations of cheiro-oral syndrome and correlating clinical symptomatology with anatomic localization. It is important for physicians to recognize this rare condition with subtle presentations for complete work-up and definitive treatment.

Acute confusional state in a patient with bilateral thalamic ischemic stroke

The acute confusional state is one of the most common reasons for neurologic consultation in the hospital setting and the plethora of causes can truly be daunting. The etiology can vary from structural, metabolic, toxic to systemic infections. Our purpose is to present a rare case of acute confusional state in a patient with bilateral thalamic ischemic stroke due to occlusion of the artery of Percheron (AOP). A 79-year-old woman with a history of hypertension and surgery for lumbar disc herniation, managed on antiplatelet therapy, angiotensin receptor blocker and diuretics, was admitted for acute confusion and paresthesia of all four limbs. She had disorientation in time and space, abnormal behavior, decreased muscle strength in both lower limbs (paraparesis 2/5 MRC since the surgery), paresthesia in all four limbs and was unable to walk due to generalized weakness. Laboratory analysis showed high blood levels of cholesterol and glucose. Both head CT and cerebral MRI showed bilateral ischemic changes in the thalami, suggesting an infarct along the artery of Percheron territory. However, no clear cause for the stroke could be identified. Screening for coagulation abnormalities and autoimmune disorders (lupus anticoagulant, anti-beta-2 glycoprotein, anti-cardiolipin, anti-nuclear and anti-ds DNA antibodies) came back negative. There were no pathological finds on the echocardiogram and electrocardiogram, while cervical Doppler ultrasound showed atherosclerosis without stenosis.

Gli esiti dello stroke ischemico del bambino: afasia e talamo

Left thalamic stroke in adults commonly results in thalamic aphasia, which is characterized by defects in lexical and semantic abilities associated with fluency and comprehension disabilities and intact word repetition. Although few cases have been reported, aphasia with similar features can also be present as a consequence of left-brain hemisphere stroke in children, which has usually a poorer prognosis if compared with that of the adult population. The paper reports the case of a 20-month-old female child that developed aphasia after an ischemic stroke that involved the left anteromedial thalamus. In these cases it is necessary to initiate an early rehabilitation treatment, possibly supported by augmentative and alternative communication techniques.

MiR-223 ameliorates thalamus hemorrhage-induced central poststroke pain via targeting NLRP3 in a mouse model.

Central poststroke pain (CPSP) is a central neuropathic pain syndrome that occurs following a stroke and mainly manifests as pain and paresthesia in the body region corresponding to the brain injury area. At present, due to the lack of clinical attention given to CPSP, patients suffer from long-term pain that seriously affects their quality of life. Current literature indicates that microRNA (miR)-223 can impede inflammation and prevent collateral damage. The NLR family pyrin domain containing 3 (NLRP3) inflammasome induces IL-18 and IL-1β secretion and maturation and participates in the inflammatory response. Previous evidence has confirmed that miR-223 can negatively regulate NLRP3 in the development of inflammatory responses. However, whether the miR-223 targeting of NLRP3 is involved in CPSP remains unclear. In the present study, the expression of miR-223 was detected by reverse transcription-quantitative PCR analysis. The expression levels of NLRP3, caspase-1, ASC, IL-18, IL-1β, ERK1/2, p-ERK1/2 and GFAP were detected by western blot analysis. The results demonstrated that thalamic hemorrhagic stroke triggered by microinjection of collagenase Ⅳ (Coll IV) into the ventral posterior lateral (VPL) nucleus results in pain hypersensitivity. miR-223 expression level were significantly reduced in the CPSP model. The expression levels of NLRP3, caspase-1, ASC, IL-18 and IL-1β were significantly increased in the CPSP model. The expression level of GFAP was detected to determine astrocyte activation. The results demonstrated that astrocyte activation induced by Coll IV produced a CPSP model. The p-ERK1/2 expression level was demonstrated to be significantly increased in the CPSP model. The introduction of an miR-223 agomir significantly attenuated thalamic pain and significantly decreased the levels of NLRP3, caspase-1, ASC and proinflammatory cytokines (IL-18 and IL-1β). Furthermore, introducing a miR-223 antagomir into the VPL nucleus of naïve mice mimicked thalamic pain and significantly increased the levels of NLRP3, caspase-1, ASC and proinflammatory cytokine levels (IL-18 and IL-1β). These results indicated that miR-223 inhibited NLRP3 inflammasome activity (caspase-1, NLRP3 and ASC), which ameliorated thalamus hemorrhage-induced CPSP in mice via NLRP3 downregulation. In conclusion, these results may determine the mechanisms underlying CPSP and facilitate development of targeted therapy for CPSP.

Evolution of Neuropsychological Deficits in First-Ever Isolated Ischemic Thalamic Stroke and Their Association With Stroke Topography: A Case-Control Study.

Background:The thalamus plays an essential role in cognition. Cognitive deficits have to date mostly been studied retrospectively in chronic thalamic stroke in small cohorts. Studies prospectively evaluating the evolution of cognitive deficits and their association with thalamic stroke topography are lacking. This knowledge is relevant for targeted patient diagnostics and rehabilitation.Methods:Thirty-seven patients (57.5±17.5 [mean±SD] years, 57% men) with first-ever acute isolated ischemic stroke covering the anterior (n=5), paramedian (n=12), or inferolateral (n=20) thalamus and 37 in-patient controls without stroke with similar vascular risk factors matched for age and sex were prospectively studied. Cognition was evaluated using predefined tests at 1, 6, 12, and 24 months. Voxel-based lesion-symptom mapping was used to determine associations between neuropsychological deficits and stroke topography.Results:Patients with anterior thalamic stroke revealed severe deficits in verbal memory (median T score [Q1–Q3]: 39.1 [36.1–44.1]), language (31.8 [31.0–43.8]), and executive functions (43.8 [35.5–48.1]) at 1 month compared with controls (verbal memory: 48.5 [43.6–61.0], language: 55.7 [42.3–61.1], executive functions: 51.3 [50.1–56.8]). Patients with paramedian thalamic stroke showed moderate language (44.7 [42.8–55.9]) and executive (49.5 [44.3–55.1]) deficits and no verbal memory deficits (48.1 [42.5–54.7]) at 1 month compared with controls (59.0 [47.0–64.5]; 59.6 [51.1–61.3]; 52.5 [44.2–55.3]). The language and executive deficits in paramedian thalamic stroke patients almost completely recovered during follow-up. Intriguingly, significant deficits in verbal memory (44.7 [41.5–51.9]), language (47.5 [41.8–54.1]), and executive functions (48.2 [46.2–59.7]) were found in inferolateral thalamic stroke patients at 1 month compared with controls (50.5 [46.7–59.9]; 57.0 [51.2–62.9]; 57.4 [51.2–60.7]). Language, but not executive deficits persisted during follow-up. Voxel-based lesion-symptom mapping revealed an association of verbal memory deficits with anterior thalamus lesions and an association of non-verbal memory, language, and executive deficits with lesions at the anterior/paramedian/inferolateral border.Conclusions:All 3 stroke topographies exhibited significant deficits in diverse cognitive domains, which recovered to a different degree depending on the stroke localization. Our study emphasizes the need for comprehensive neuropsychological diagnostics to secure adequate patient rehabilitation.

A Newborn with an Incidental Finding on Cranial Ultrasonography.

A Newborn with an Incidental Finding on Cranial Ultrasonography.

The thalamic hand: an enigmatic sequela of thalamic stroke.

The thalamic hand: an enigmatic sequela of thalamic stroke.

Abstract WMP31: Thrombotic Microangiopathy -? A Missed Diagnosis Of Cryptogenic Stroke

Background: Thrombotic microangiopathy (TMA) is a potentially life-threatening condition caused by small-vessel platelet microthrombi. The estimated incidence of clopidrogel-associated TMA is 1 per 1600 to 5000. The principal treatment is to withdraw clopidrogel. However, the diagnosis of clopidrogel induced TMA may be challenging because of the subtle presentation and co-morbidities confounding the diagnosis of TMA. Case: A 57 y.o. female presented with h/o hypertension, dyslipidemia with suspected cryptogenic strokes since 2018 (left thalamic stroke in 6/2020, left parietal stroke in 4/2020, chronic infarcts in frontal lobes from MRI brain on 9/17/2020 with normal CT angiogram of neck and brain and echocardiography ). She was on clopidrogel since April 2020. Patient was admitted on 6/14/2020 with racing thoughts for four weeks. The psychiatrist confirmed delirium. The EEG showed no focal lesion. Hematological workup revealed thrombocytopenia, elevated LDH and red cell fragments. The ADAMTS13 (a disintegrin and metalloproteinase, with a thrombospondin type 1 motif, member 13) level was &lt;3%. Thrombotic microangiopathy was diagnosed. Steroids and plasma exchange were initiated and clopidrogel discontinued. Patient was discharged on prednisone. However, ADAMTS13 on 7/17/2020 was still &lt;3%. As initial ANA and anti-ds-DNA were reported positive, patient was started on rituximab 375mg/m 2 weekly infusions with which ADAMTS13 increased to 75%. The repeat ANA and anti-ds-DNA were negative. When patient was reviewed on 5/20/2021 she was off steroids and independant of her ADLs. Discussion: Thrombotic microangiopathy is a medical emergency, with a mortality of 90% if untreated. Treatment with plasma exchange and corticosteroids significantly reduces the mortality to ∼10% to 15%. Early diagnosis of TMA is prudent, as recovery from TMA may appear to be complete, but patients may have persistent cognitive abnormalities if the diagnosis is not made early.

Bilateral fornix infarction presented with acute amnesia: case report

ABSTRACT Acute episodes of amnestic syndrome can be a challenging diagnostic problem. Except for nonvascular etiology, thalamic strokes or infarction involving several temporal lobe structures has been reported in earlier cases. The authors report a patient who suddenly developed memory loss without any other focal neurologic deficits. Brain magnetic resonance imaging (MRI) with diffusion-weighted imaging (DWI) performed 1 day after onset revealed acute infarction involving the bilateral fornix column and the genu of corpus callosum. Because simple fornix infarcts often have no obvious positive neurological signs, most of the related manifestations were provided by family members, are easy to be diagnosed falsely, and missed in clinical areas, we suggest that bilateral fornix infarction should be considered in the diagnosis of an acute onset amnestic syndrome.

Influence of sensory integration training on sensory motor functions in patients with thalamic syndrome

IntroductionThalamic stroke causes impairment in sensory motor functions; these changes in perception lead to pain and deteriorate postural stability. The goal of this study was to investigate the influence of sensory integration training on pain and posture stability in patients with thalamic syndrome.MethodsOverall, 30 patients of both sexes, aged 45–65 years, diagnosed with a thalamic stroke were randomly allocated into 2 groups. The control group received selected sensory training of the conventional physical therapy program and the study group received sensory integration training with the Biodex Balance System beside the conventional physical therapy program.ResultsThe intra-group comparisons with MANOVA revealed statistically insignificant differences in pain, as well as overall, anteroposterior (forward and backward), and mediolateral (right and left) limits of stability after the treatment in the control group (&lt;i&gt;p&lt;/i&gt;-value of 0.180, 0.301, 0.792, 0.247, 0.381, and 0.847, respectively). In the study group, there was a statistically significant decrease in pain and improvement in overall, anteroposterior (forward and backward), and mediolateral (right and left) limits of stability after the treatment (&lt;i&gt;p&lt;/i&gt;-value of 0.01 for pain and 0.000 for each of the 5 limit of stability variables, respectively). The inter-group comparisons showed statistically significant differences in favour of the study group (&lt;i&gt;p&lt;/i&gt; = 0.000).ConclusionsAdding the sensory integration training program was effective to decrease pain and improve posture stability in patients with thalamic syndrome.

Bilateral thalamus stroke due to percheron artery

Bilateral thalamus ischemic stroke is a rare condition that carries significant morbidity and mortality in comparison to other forms of stroke. It is usually associated with an anatomical variant with the thalamic paramedian arteries arising from a common trunk from the posterior cerebellar artery, known as Percheron artery. This infarct is difficult to be recognized and early recognition of this syndrome improves survival and functional recovery. We report a case of bilateral thalamic stroke after cardiac surgery.

Наслідки таламічних інсультів: проспективне клінічне когортне дослідження

Актуальність. Інсульт є другою за частотою причиною смертності у світі, поступаючись лише смертності від серцево-судинних захворювань. Проте на сьогоднi опубліковано недостатньо прoспективних клінічних досліджень, у яких описані й проаналізовані клінічні характеристики та наслідки таламічних інсультів. Мета дослідження: визначити особливості наслідків гострого таламічного інсульту в проспективному клінічному когортному дослідженні, забезпечивши всебічний клінічний і нейровізуалізаційний аналіз результатів лікування та наслідків гострого таламічного інсульту. Матеріали та методи. Ми провели проспективне клінічне когортне дослідження 319 пацієнтів iз гострим ішемічним інсультом, які надійшли до неврологічного центру Олександрівської клінічної лікарні (м. Київ, Україна) протягом перших 24 годин з моменту розвитку хвороби. Усі пацієнти пройшли комплексне клініко-неврологічне, лабораторне, ультразвукове та ней-ровізуалізаційне обстеження. Результати. Серед 319 хворих iз гострим ішемічним інсультом нейровізуалізаційно підтверджений таламічний інсульт діагностовано в 34 (10,6 %) ocіб: у 22 (середній вік 61,9 ± 10,2 року) виявлено гострий ізольований інфаркт таламусу, а в 12 пацієнтів (середній вік 59,0 ± 9,6 року) — гострий таламічний крововилив. Описані, проаналізовані та порівняні клінічні наслідки інфарктів різних таламічних територій.