Unilateral Thalamic Infarction Research Articles

An atypical stroke manifestation: Sleep disturbance in unilateral thalamic lesion

Thalamic strokes may present with a wide variety of symptoms depending on their location, volume and lateralization. Hypersomnia is a less frequent manifestation, that has been associated with unilateral paramedian thalamic ischemic lesions. We report a case of a patient who presented to the emergency department (ED) with sudden onset of hypersomnolence. Initial head computed tomography (CT) showed no signs of acute ischemia. Follow-up head CT 24 h after thrombolysis exposed a hypodense lesion on the left ventromedial thalamic and mesencephalic regions, with corresponding T2/FLAIR hyperintensity and diffusion restriction on brain magnetic resonance imaging, confirming a recent ischemic stroke. Clinicians should be aware of the association between acute hypersomnia and strategic unilateral thalamic infarcts, particularly when the initial CT scan has no signs of acute ischemia.

Unilateral thalamic infarction onset with lethargy: A case report and literature review

Infarct-induced lethargy is a common disabling symptom that lacks a consensual definition and a standardized method of care. Identifying the causes of the infarct in the thalamic reticular nucleus (TRN) induced lethargy is crucial in stroke patients. A 68-year-old female patient was admitted to the hospital with lethargy and weakness in the right limb. A computed tomography (CT) scan performed at the presentation showed no bleeding. She was given intravenous thrombolysis. A head computed tomography (CT) scan clearly showed that the infarct was located in the TRN. After 1 hour of treatment, the weakness in the patient's limb was relieved. However, she was still lethargic, but her lethargy symptoms improved after 3 days. Our case highlights that despite the small size of the infarct, the patient was unconscious, which makes it difficult for physicians to understand and treat the condition, resulting in trouble managing the case. We performed a literature review and proposed that the infarction located in the TRN causes lethargy. However, further clinical and pathophysiological research is still needed to improve patient care.

Characterization of Macular Structural and Microvascular Changes in Thalamic Infarction Patients: A Swept-Source Optical Coherence Tomography-Angiography Study.

Background: The retina and brain share similar neuronal and microvascular features. We aimed to investigate the retinal thickness and microvasculature in patients with thalamic infarcts compared with control participants. Material and methods: Swept-source optical coherence tomography (SS-OCT) was used to image the macular thickness (retinal nerve fiber layer, RNFL; ganglion cell-inner plexiform layer, GCIP), while OCT angiography was used to image the microvasculature (superficial vascular plexus, SVP; intermediate capillary plexus, ICP; deep capillary plexus, DCP). Inbuilt software was used to measure the macular thickness (µm) and microvascular density (%). Lesion volumes were quantitively assessed based on structural magnetic resonance images. Results: A total of 35 patients with unilateral thalamic infarction and 31 age–sex-matched controls were enrolled. Compared with control participants, thalamic infarction patients showed a significantly thinner thickness of RNFL (p < 0.01) and GCIP (p = 0.02), and a lower density of SVP (p = 0.001) and ICP (p = 0.022). In the group of patients, ipsilateral eyes showed significant reductions in SVP (p = 0.033), RNFL (p = 0.01) and GCIP (p = 0.043). When divided into three groups based on disease duration (<1 month, 1–6 months, and >6 months), no significant differences were found among these groups. After adjusting for confounders, SVP, ICP, DCP, RNFL, and GCIP were significantly correlated with lesion volume in patients. Conclusions: Thalamic infarction patients showed significant macular structure and microvasculature changes. Lesion size was significantly correlated with these alterations. These findings may be useful for further research into the clinical utility of retinal imaging in stroke patients, especially those with damage to the visual pathway.

Intracranial Neurenteric Cyst in a Patient with Acute Unilateral Thalamic Infarction.

Neurenteric cysts are a rare type of foregut duplication cyst that are classified as intracranial or spinal and are associated with central nervous system abnormalities.Neurenteric cysts are usually benign and slow-growing, so conservative treatment can be provided if there are no symptoms.Thalamic stroke may be caused by arterial or venous infarction.Cardioembolism is the most common cause of thalamus infarction; variations in blood supply to the thalamus should be investigated in affected patients.

Modeling Vestibular Compensation: Neural Plasticity Upon Thalamic Lesion.

The present study in rats was conducted to identify brain regions affected by the interruption of vestibular transmission and to explore selected aspects of their functional connections. We analyzed, by positron emission tomography (PET), the regional cerebral glucose metabolism (rCGM) of cortical, and subcortical cerebral regions processing vestibular signals after an experimental lesion of the left laterodorsal thalamic nucleus, a relay station for vestibular input en route to the cortical circuitry. PET scans upon galvanic vestibular stimulation (GVS) were conducted in each animal prior to lesion and at post-lesion days (PLD) 1, 3, 7, and 20, and voxel-wise statistical analysis of rCGM at each PLD compared to pre-lesion status were performed. After lesion, augmented metabolic activation by GVS was detected in cerebellum, mainly contralateral, and in contralateral subcortical structures such as superior colliculus, while diminished activation was observed in ipsilateral visual, entorhinal, and somatosensory cortices, indicating compensatory processes in the non-affected sensory systems of the unlesioned side. The changes in rCGM observed after lesion resembled alterations observed in patients suffering from unilateral thalamic infarction and may be interpreted as brain plasticity mechanisms associated with vestibular compensation and substitution. The second set of experiments aimed at the connections between cortical and subcortical vestibular regions and their neurotransmitter systems. Neuronal tracers were injected in regions processing vestibular and somatosensory information. Injections into the anterior cingulate cortex (ACC) or the primary somatosensory cortex (S1) retrogradely labeled neuronal somata in ventral posteromedial (VPM), posterolateral (VPL), ventrolateral (VL), posterior (Po), and laterodorsal nucleus, dorsomedial part (LDDM), locus coeruleus, and contralateral S1 area. Injections into the parafascicular nucleus (PaF), VPM/VPL, or LDDM anterogradely labeled terminal fields in S1, ACC, insular cortex, hippocampal CA1 region, and amygdala. Immunohistochemistry showed tracer-labeled terminal fields contacting cortical neurons expressing the μ-opioid receptor. Antibodies to tyrosine hydroxylase, serotonin, substance P, or neuronal nitric oxide-synthase did not label any of the traced structures. These findings provide evidence for opioidergic transmission in thalamo-cortical transduction.

Dystonia and asterixis in acute thalamic infarct

Movement disorders following stroke is a well known phenomena both during acute stage as well as in later phases. The type of movement depends on the site of involvement, it is however not uncommon to have more than one type of movement disorder following a stroke. We present a patient with combined dystonia and asterixis following a unilateral thalamic infarct, whose dystonia persisted on follow up while the asterixis faded away with time.

Investigation of risk factors, topographic location and stroke mechanisms of unilateral isolated and posterior cerebral ARTERY thalamic infarcts.

In this study, we aimed to examine the risk factors, topographic features and stroke mechanisms of acute ischemic unilateral infarcts of thalamus. Patient with isolated thalamic infarct and those with posterior cerebral artery (PCA) infarction who were admitted to our hospital between January 2014 and January 2017 with acute unilateral thalamic infarction (TI) were included in this study (isolated thalamic infarction/ isolated TI; thalamic and posterior cerebral artery infarction/PCA+TI). Demographic characteristics and vascular risk factors of the patients were determined. Thalamic infarct areas were recorded topographically as anterior, posteromedial, ventrolateral, posterolateral, more than one area, and variant areas. Stroke mechanism was determined according to the criteria of "Trial of Org 10172 in Acute Stroke Treatment" (TOAST). Patients with isolated TI and PCA TI were compared according to risk factors, stroke mechanism and infarct topography. Forty-three patients with a mean age of 63.3 ± 14.5 years were included in the study. Twenty-eight patients (60.1%) were found to have isolated TI and the remaining 15 patients (34.9%) had PCA+TI. 32.1% of patients with isolated TI had sensory symptoms on presentation, and 60% of patients with PCA-TI had sensorimotor symptoms. The mean age, the mean score on National Institutes of Health Stroke Scale (NIHSS) and the mean frequency of atrial fibrillation were higher in PCA+TI patients than in isolated-TI patients (p: 0.04, p: 0.004, p: 0.02 respectively). 32.6% of the patients had ventrolateral, 30.2% had posteromedial involvement. Ventrolateral topography was seen in 46.7% of the PCA+TI patients, while posteromedial topography was seen in 39.3% of the isolated-TI patients. 53.6% of the isolated-TI had small vessel disease etiology, while 40% of the PCA+TI had cardioembolic etiology, and the other 40% had large artery atherosclerosis. Our study showed that the most ommon stroke mechanism in patients with thalamic infarction is the small vessel disease. Isolated TI and PCA+TI patients differ in terms of etiologic mechanism and infarct topography. Variant territorial involvement and multiple area involvements can be quite common in thalamic infarcts.

单侧丘脑梗死致双侧共济失调1例 A Case of Bilateral Ataxia after Unilateral Thalamic Infarction

单侧丘脑梗死致双侧共济失调1例 A Case of Bilateral Ataxia after Unilateral Thalamic Infarction

Proliferation of Bilateral Nerve Fibers Following Thalamic Infarction Contributes to Neurological Function Recovery: A Diffusion Tensor Imaging (DTI) Study.

BackgroundThe aim of this study was to investigate the reorganization in ipsilesional and contralesional thalamic radiation fibers after unilateral focal thalamic stroke in sensory disturbance patients.Material/MethodsWe recruited 12 patients with acute unilateral thalamic infarction and sensory disturbance and 12 healthy age- and sex-matched controls. All patients underwent diffusion tensor imaging (DTI) and were assessed with National Institutes of Health stroke scale (NIHSS), Barthel index (BI), and paragraph 8 of NIHSS (NIHSS8) at 1 week (W1), 4 weeks (W4), 3 months (M3), and 6 months (M6) after thalamic infraction. The relationship between FA changes and the clinical scores changes were then examined.ResultsNIHSS and NIHSS8 scores decreased while BI scores increased gradually from W1 to M6 in patients, but not in controls. FA values of the patients gradually increased in ipsilesional and contralesional thalamic radiation fibers from W1 to M6. In addition, the FA values in patients were significantly higher at M3 and M6 compared to W1. No significant changes were observed in the controls. Regarding the relationship between FA changes and the clinical scores changes, the FA increases were negatively correlated with NIHSS and NIHSS8 decrease while FA increases were positively correlated with BI increases.ConclusionsOur results indicate that reorganization occurred after unilateral focal thalamic infarct not only in ipsilesional, but also in contralesional thalamic radiation fibers in patients with sensory disturbance. In addition, the results suggested that the reorganization can support and promote stroke restoration.

A Case of Unilateral Thalamic Venous Infarct with Unilateral Choroid Plexus Haemorrhage in Deep Venous System Thrombosis

A Case of Unilateral Thalamic Venous Infarct with Unilateral Choroid Plexus Haemorrhage in Deep Venous System Thrombosis

Complete recovery of restless legs syndrome after unilateral thalamic and tegmental infarction: A case report

Complete recovery of restless legs syndrome after unilateral thalamic and tegmental infarction: A case report

Anatomical Variations in the Posterior Circle of Willis and Vascular Pathologies in Isolated Unilateral Thalamic Infarction.

To characterize relations between configurations of the posterior part of the Circle of Willis (CoW) and the occurrence of unilateral thalamic infarction. From a magnetic resonance imaging report database, we identified and analyzed 111 patients with acute isolated unilateral thalamic infarction on diffusion-weighted imaging (DWI). Vascular pathologies were noted on magnetic resonance angiography (MRA) and the diameter of the posterior communicating artery (PComA) and the P1 and P2 segments of the posterior cerebral artery determined. Most infarctions were observed in the territory of the inferolateral arteries (70.2%), followed by the paramedian (16.3%), tuberothalamic (8.7%), and posterior choroidal arteries (4.8%). Relevant vascular pathologies included stenosis of the basilar artery (4.5%), P1 segment stenosis (4.5%)/occlusion (.9%), and P2 segment stenosis (14.4%)/occlusion (4.5%). Paramedian thalamic infarction was associated with ipsilateral P1 segment hypoplasia/absence (P < .001); tuberothalamic infarction with ipsilateral PComA hypoplasia/absence (P = .08). Furthermore, the diameter of the relevant CoW segment was smaller in patients with ipsilateral thalamic infarction. Assessment of CoW configuration on MRA may be helpful to understand the appearance of unilateral thalamic stroke independent from stroke etiology. A smaller diameter of the relevant CoW segment might be a risk factor for ipsilateral thalamic stroke in the corresponding thalamic vascular territory.

A case of unilateral thalamic venous hemorrhagic infarct in deep venous system thrombosis

Cortical venous thrombosis (CVT) is a common and frequently unrecognized type of stroke that affects approximately five people per million annually and accounts for 0.5-1% of all strokes. Exact incidence in India is yet to be documented. Puerperal CVT may account for the majority of CVT cases in India. Cerebral venous sinus thrombosis (CVST) usually affects young to middle aged groups. Outcome of CVST patients may vary from complete recovery to permanent neurological deficits, with varying presentation of the natural course of the disease. Factors related to poor outcome were papilledema, altered consciousness, coma, age older than 33 years, diagnostic delay >10 days, intracerebral hemorrhage, and involvement of the straight sinus. This case report is of thrombosis in the deep venous system of brain causing venous infarction of unilateral thalamus. There are very few cases reported all over the world with unilateral thalamic venous infarct. Prognosis of unilateral deep cerebral vein thrombosis is said to be better than that of bilateral thrombosis, if detected early and timely treated. Patient with a unilateral thrombosis may show complete recovery from his neurologic symptoms. Reports of reversible edema of the thalamus are well documented. In this case, patient is overall well preserved except that he continues to have recent memory impairment even after 4 weeks of discharge from hospital.

Unilateral thalamic infarction presenting as vertical gaze palsy: a case report

IntroductionVertical gaze palsy is a recognized manifestation of midbrain lesions. It rarely is a consequence of unilateral thalamic infarction.Case presentationWe report the case of a 48-year-old African-American woman who presented to our facility with vertical gaze palsy and evidence of left medial thalamic infarct on diffusion-weighted imaging without coexisting midbrain ischemia. The etiology of infarct was determined to be small vessel disease after extensive investigation.ConclusionsThis report suggests a possible role of the thalamus as a vertical gaze control center. Clinicoradiological studies are needed to further define the role of the thalamus in vertical gaze control.

Unilateral Thalamic Infarction in Vein of Galen and Straight Sinus Thrombosis

Deep cerebral venous thrombosis is an uncommon event. It usually involves the halami and adjacent areas on both sides. Unilateral thalamic infarction is extremely rare subsequent to deep cerebral venous thrombosis. Imaging findings of a female in the postpartum period with unilateral thalamic infarction and basal ganglia edema are presented.

Thalamic infarct presenting as apparent life‐threatening event in infants

Thalamic infarction with distinct manifestations is well-described in adults but less well-delineated in children. We report two infants who presented with an apparent life-threatening event (ALTE) with very early magnetic resonance imaging (MRI) demonstrating a unilateral thalamic infarction. Subsequent MRI demonstrated bilateral changes in the brain stem and basal ganglia, which were in keeping with profound hypoxic ischaemic injury. We propose the thalamic infarction to be the primary event precipitating a profound hypoxic ischaemic injury as an alternative explanation to the neuroimaging observation. Thalamic infraction may have a causal role in ALTE. Early and appropriate neuroimaging is required to detect these changes.

Unilateral Venous Thalamic Infarction in a Child Mimicking a Thalamic Tumor

Unilateral thalamic infarction is a rare condition in adults. This is a case report of a young child presenting with left-sided hemiparesis of sudden onset due to an unilateral venous thalamic infarction. This was attributed to an asymmetric thrombosis of the cerebral internal veins, a partial thrombosis of the vein of Galen and straight sinus. Magnetic resonance imaging resulted primarily in the differential diagnosis of a cerebral tumor or an intracerebral abscess, leading to stereotactic puncture. Subsequent magnetic resonance venography facilitated the correct diagnosis. Heparin-induced thrombocytopenia necessitated anticoagulation treatment with hirudin and later, warfarin. The patient made a complete recovery. We conclude that unclear unilateral thalamic lesions might be symptomatic of a cerebral deep venous thrombosis and might mimic a thalamic tumor. In uncertain cases, we suggest rapid performance of magnetic resonance angiography.

A Case of Unilateral Thalamic Hemorrhagic Infarction as a Result of the Vein of Galen and Straight Sinus Thrombosis

Straight sinus vein thrombosis represents 15% of all diagnosed sinus vein thrombosis. Thrombotic occlusion of the deep cerebral venous system, the straight sinus, and the vein of Galen causes centrally located and usually bilateral thalamic infarcts. Unilateral thalamic venous infarction is extremely rare. The clinical and radiologic findings can be nonspecific and diagnostically challenging. We report a patient with this unusual condition and review the available literature.

Bilateral Ageusia in a Patient with a Left Ventroposteromedial Thalamic Infarct: Cortical Localization of Taste Sensation by Statistical Parametric Mapping Analysis of PET Images

Unilateral taste loss is usually observed on the side contralateral to a thalamic infarction, despite gustatory function being represented bilaterally. We report a rare case of bilateral taste loss in a patient with an acute left unilateral thalamic infarction, with unilateral left insular hypometabolism demonstrated by statistical parametric map analysis of PET images. Our observations suggest that the left insular cortex and left ventroposteromedial thalamic nuclei are critical to bilateral gustatory sensation.

Thalamic infarct presenting with thalamic astasia

Astasia, inability to stand unsupported despite good strength, resembles the marked balance impairment of patients with vestibulocerebellar disease. We describe a patient with unilateral thalamic infarct that presented with astasia. A 76-year-old hypertensive woman was admitted to our hospital because of marked unsteadiness. On neurological examination, she could not stand unsupported and the woman's body swayed back and forth markedly. The swaying was not compensated for by her taking a step forward or backward, and she frequently collapsed when support was withdrawn. Diffusion-weighted magnetic resonance image revealed a discrete infarct within the right posterolateral thalamus. Brain single photon emission computerized tomography revealed markedly decreased regional cerebral blood flow within in the right thalamus with concomitant left superior cerebellar region. We discuss the possible pathomechanisms of thalamic astasia.