Paramedian Thalamic Stroke Research Articles

Depression and anxiety in acute ischemic stroke involving the anterior but not paramedian or inferolateral thalamus.

Emotional and cognitive deficits are prevalent in strokes involving the thalamus. In contrast to cognitive deficits, emotional deficits have not been studied prospectively in isolated thalamic stroke. In 37 ischemic thalamic stroke patients (57.0 [50.0; 69.5] years [median (Q1; Q3)], 21 males, 5 anterior, 12 paramedian, 20 inferolateral vascular territory), and 37 non-stroke control patients matched for age and sex, we prospectively examined depression, anxiety, activities of daily living, and quality of life at 1, 6, 12, and 24 months post-stroke using the Hospital-Anxiety-and-Depression Scale (HADS), Nürnberger-Alters-Alltagsaktivitäten scale (NAA), and Short Form-36 (SF36) questionnaire. Voxel-based lesion-symptom mapping (VLSM) and lesion-subtraction analyzes were performed to determine associations between questionnaire scores and thalamic stroke topography. At 1 month post-stroke, anterior thalamic stroke patients had higher depression scores [8.0 (7.5; 10.5)] than paramedian [4.5 (1.0; 5.8)] and inferolateral [4.0 (1.0; 7.0)] thalamic stroke patients. Furthermore, anterior thalamic stroke patients had higher anxiety scores [11.0 (8.0; 14.5)] than their matched controls [2.5 (2.0; 2.5)], paramedian [4.5 (1.0; 5.8)] and inferior [4.0 (1.0; 7.0)] thalamic stroke patients. Depression and anxiety scores in anterior thalamic stroke patients remained high across the follow-up [depression: 9.0 (3.5; 13,8); anxiety:10.05 (2.8, 14.5)].Physical health assessed by SF36 was intact in anterior [1 month post-stroke: T-score = 55.9 (37.0; 57.6)] but reduced in inferolateral [44.5(32.4; 53.1)] thalamic stroke, whereas mental health was reduced in anterior thalamic stroke [32.0 (29.8; 47.3)].VLSM confirmed that voxels in the anterior thalamus around Montreal Neurological Institute (MNI) coordinates X = -8, Y = -12, Z = 2 were more often affected by the stroke in depressed (HADS-score ≥ 8) than non-depressed (HADS-score < 8) patients and voxels around coordinates X = -10, Y = -12, Z = 2 were more often affected in anxious (HADS-score ≥ 8) than non-anxious (HADS-score < 8) patients. Anterior, but not paramedian or inferolateral thalamic stroke was associated with depression and anxiety. Even though our results are mostly significant in the left thalamus, this observation on stroke laterality might be confounded by the fact that the right hemisphere was underrepresented in our study.

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.

Frequency, clinical presentation and outcome of vigilance impairment in patients with uni- and bilateral ischemic infarction of the paramedian thalamus

Ischemic stroke of the paramedian thalamus is a rare differential diagnosis in sudden altered vigilance states. While efforts to describe clinical symptomatology exist, data on the frequency of paramedian thalamic stroke as a cause of sudden impaired vigilance and on accompanying clinical signs and outcome are scarce. We retrospectively analyzed consecutive patients admitted to a tertiary stroke center between 2010 and 2019 diagnosed with paramedian thalamic stroke. We evaluated frequency of vigilance impairment (VI) due to paramedian thalamic stroke, accompanying clinical signs and short-term outcome in uni- versus bilateral paramedian lesion location. Of 3896 ischemic stroke patients, 53 showed a paramedian thalamic stroke location (1.4%). VI was seen in 29/53 patients with paramedian thalamic stroke and in 414/3896 with any stroke (10.6%). Paramedian thalamic stroke was identified as causal to VI in 3.4% of all patients with initial VI in the emergency department and in 0.7% of all ischemic stroke patients treated in our center. Accompanying clinical signs were detected in 21 of these 29 patients (72.4%) and facilitated a timely diagnosis. VI was significantly more common after bilateral than unilateral lesions (92.0% vs. 21.4%; p < 0.001). Patients with bilateral paramedian lesions were more severely affected, had longer hospital stays and more frequently required in-patient rehabilitation. Paramedian thalamic lesions account for about 1 in 15 stroke patients presenting with impaired vigilance. Bilateral paramedian lesion location is associated with worse stroke severity and short-term outcome. Paying attention to accompanying clinical signs is of importance as they may facilitate a timely diagnosis.

Individual spindle detection and analysis in high-density recordings across the night and in thalamic stroke

Sleep spindles are thalamocortical oscillations associated with several behavioural and clinical phenomena. In clinical populations, spindle activity has been shown to be reduced in schizophrenia, as well as after thalamic stroke. Automatic spindle detection algorithms present the only feasible way to systematically examine individual spindle characteristics. We took an established algorithm for spindle detection, and adapted it to high-density EEG sleep recordings. To illustrate the detection and analysis procedure, we examined how spindle characteristics changed across the night and introduced a linear mixed model approach applied to individual spindles in adults (n = 9). Next we examined spindle characteristics between a group of paramedian thalamic stroke patients (n = 9) and matched controls. We found a high spindle incidence rate and that, from early to late in the night, individual spindle power increased with the duration and globality of spindles; despite decreases in spindle incidence and peak-to-peak amplitude. In stroke patients, we found that only left-sided damage reduced individual spindle power. Furthermore, reduction was specific to posterior/fast spindles. Altogether, we demonstrate how state-of-the-art spindle detection techniques, applied to high-density recordings, and analysed using advanced statistical approaches can yield novel insights into how both normal and pathological circumstances affect sleep.

Bilateral paramedian thalamic infarct: A report of five cases

Aim: The aim of this study is to analyze the incidence, etiology, symptoms, diagnostic process and treatment of bilateral thalamic infarct on the basis of our own experience. Case series: Five cases of bilateral paramedian thalamic stroke with different clinical manifestations are presented. In two patients the presence of artery of Percheron was detected. Comment: The bilateral thalamic infarct is an unusual and rare type of ischemic stroke. Due to the variety of symptoms, it may be difficult to diagnose without MR imaging. Symptoms may be transient, but frequently a persistent neurological deficit is observed. The thalamus is the “centre” for all impulses reaching the brain. It is involved in cognitive functions, emotional and motor responses. Therefore, impaired consciousness and behavioral changes are the main symptoms of thalamic stroke.

Memory Profiles after Unilateral Paramedian Thalamic Stroke Infarction: A Comparative Study.

We performed extensive neuropsychological assessment of two male patients (matched for age and educational level) with similar (localization and size) unilateral paramedian ischemic thalamic lesions (AB on the left and SD on the right). Both patients showed severe memory impairments as well as other cognitive deficits. In comparison to SD, AB showed severe impairment of executive functions and a more severe deficit of episodic/anterograde memory, especially in the verbal modality. The findings of this single case study suggest the possibility that the profile and severity of the executive dysfunction are determinant for the memory deficits and depend on from the side of the lesion. In addition to a material-side-specific (verbal versus visual) deficit hypothesis, the differential diencephalo-prefrontal contributions in mnestic-processing, in case of paramedian thalamic stroke, might also be explained in terms of their stage-specificity (encoding versus retrieval).

Artery of Percheron Infarction as an Unusual Cause of Coma: Three Cases and Literature Review

Stroke due to occlusion of the artery of Percheron (AOP), an uncommon anatomic variant supplying the bilateral medial thalami, may raise diagnostic challenges and cause life-threatening symptoms. Our objective here was to detail the features and outcomes in three patients who required intensive care unit (ICU) admission and to review the relevant literature. Description of three cases and literature review based on a 1973-2013 PubMed search. Three patients were admitted to our ICU with sudden-onset coma and respiratory and cardiovascular dysfunctions requiring endotracheal mechanical ventilation. Focal neurological deficits, ophthalmological signs (abnormal light reflexes and/or ocular motility and/or ptosis), and neuropsychological abnormalities were variably combined. Initial CT scan was normal. Cerebral MRI demonstrated bilateral paramedian thalamic infarction, with extension to the cerebral peduncles in two patients. Consciousness improved rapidly and time to extubation was 1-4 days. All three patients were discharged alive from the hospital and two had good 1-year functional outcomes. Similar clinical features and outcomes were recorded in the 117 patients identified in the literature, of whom ten required ICU admission. Bilateral paramedian thalamic stroke due to AOP occlusion can be life threatening. The early diagnosis relies on MRI with magnetic resonance angiography. Recovery of consciousness is usually rapid and mortality is low, warranting full-code ICU management.

Bilateral Thalamic Infarction and DSA Demonstrated AOP after Thrombosis

Bilateral paramedian thalamic stroke is a special ischemic pattern that results from occlusion of the artery of Percheron (AOP), a rare anatomic variant of the paramedian arteries. We report a case of bilateral thalamic infarctions, with a dramatic improvement after thrombolysis. DSA demonstrated recanalization of AOP with possible unreported variation.

A Case of Transient Hypersomnia with Increased Slow Wave Sleep after Unilateral Paramedian Thalamic Infarction

Received June 7, 2011 Revised June 10, 2011 Accepted June 20, 2011 Address for correspondence Jee Hyun Kim, MD, PhD Department of Neurology, Dankook University College of Medicine, 359 Manghyang-ro, Dongnam-gu, Cheonan 330-715, Korea Tel: +82-41-550-3292 Fax: +82-41-550-6245 E-mail: fever26@paran.com Paramedian thalamic stroke is known to be associated with hypersomnia, usually with bilateral lesions. We report a case of one patient who developed transient hypersomnia after unilateral paramedian thalamic infarction. A 79-year-old female patient with right paramedian thalamic infarction presented with left hemiparesis and hypersomnia. A night polysomnogram, 10 days after symptom onset, showed increased slow wave sleep and the presence of slow wave sleep throughout the entire night. Hypersomnia improved 7 weeks after the onset of symptom. J Korean Sleep Res Soc 2011;8:20-23

Improvement of sleep architecture in the follow up of a patient with bilateral paramedian thalamic stroke

Normal sleep architecture and arousal require an intact thalamus. Thalamic vascular lesions, particularly in the paramedian region may cause arousal disturbances and hypersomnolence. Although hypersomnolence is one of the main characteristics of acute bilateral paramedian thalamic infarcts, there are only scarce reports in literature concerning polysomnographic follow-up of these patients. The few reported cases in literature show that sleep stages do not significantly change from the acute to chronic phase. We present a case report of a patient with a bilateral paramedian thalamic infarct in which a polysomnographic evaluation of sleep was performed four days and five months after stroke. In the acute phase, polysomnography showed an impairment of phase 2 NREM and absence of phase 3 and 4 NREM with absent sleep spindles. After the acute stroke phase, hypersomnolence improved and sleep spindles reappeared as well as phase 3 and 4 of NREM sleep. Our patient clear clinical and polysomnographic improvement makes us suppose that in this case the initial impairment could have been essentially due to a functional transitory impairment of the thalamocortical and corticothalamic connections. This case report is peculiar because it discloses a marked improvement of sleep architecture which to the best of our knowledge has not been clearly described before.

Síndrome de la arteria de Percheron: variabilidad clínica y diagnóstico diferencial

Synchronous bilateral paramedian thalamic stroke (SBPTS), usually equated to Percheron artery infarction, is considered to be uncommon and difficult to diagnose clinically. Its characterization is based on the original description plus a few small series.To characterize SBPTS clinically by collecting cases and identifying the key difficulties for an early diagnosis.Six cases at our centre plus another 115 located by systematic literature search and critical reading of articles fulfilled the criteria for SBPTS. An analysis was made of the variables age, gender, vascular risk factors, aetiology, alterations and fluctuations of consciousness, need for intubation, cognitive-behavioural disorders, pupillary changes, other neurological focal disorders and brainstem involvement on imaging studies.Of note in our series were disorders of consciousness (n=5), their fluctuations (n=3) and the diagnostic delay (seven days, with MRI in four patients). In only one case was a bilateral thalamic lesion seen on the initial CT. Joint analysis of all the cases showed a mean age of 61 years, a predominance of men (58%), the presence of vascular risk factors in 77%, a mainly cardioembolic aetiology (34% among those that were specified), sensory involvement in 75% (intubation in 7% and fluctuations in 16.5%), cognitive-behavioural disorders in 43%, oculomotor in 73%, pupillary in 31%, other in 67% and specified brainstem lesion in 37%.The SBPTS syndrome has a variable presentation with a low sensitivity on the initial CT, requiring brain MRI for typification. This explains the diagnostic difficulty and the fact that its frequency is probably underestimated.

Development of hypersomnia after bilateral paramedian thalamic stroke: case report

Development of hypersomnia after bilateral paramedian thalamic stroke: case report

Evolution of Neurological, Neuropsychological and Sleep-Wake Disturbances After Paramedian Thalamic Stroke

The clinical features and natural course of paramedian thalamic stroke is poorly known. The aim of this study was to characterize the evolution of neurological, neuropsychological, and sleep-wake deficits after paramedian thalamic stroke. Forty-six consecutive patients, aged 48.4+/-16.6 years, were studied. Fourteen had bilateral, 16 left-sided, and 16 right-sided lesions. Assessment included neurological examinations, estimation of sleep needs, formal neuropsychological tests (n=27), and polysomnographies (n=31). Functional outcome was followed up over 1 year in 31 patients with the modified Rankin Scale and Barthel index. Oculomotor palsy (76% of patients), mild gait ataxia (67%), deficits of attention (63%), fluency and error control (59%), learning and memory (67%), and behavior (67%) were common in the acute stroke phase. Outcome was excellent with right-sided infarcts but mostly incomplete with bilateral and left-sided lesions. This was mainly related to persistent frontal lobe-related and cognitive deficits found in 100% bilateral and 90% left-sided, but only 33% right-sided strokes. Initially, hypersomnia was present in all patients associated with increased stage 1 sleep, reduced stage 2 sleep, and reduced sleep spindles. Sleep needs improved in patients with bilateral and almost disappeared with unilateral lesions after 1 year. Sleep architecture remained abnormal with the exception of sleep spindles that increased. Whereas neurological deficits and hypersomnia recover to large extent in patients with paramedian thalamic stroke, the frontal lobe-related and cognitive deficits, which are mainly linked with bilateral and left-sided lesions, often persist. As such, stroke outcome is better in right-sided than bilateral or left-sided infarcts.

Paramedian thalamic stroke syndrome

The SA Journal of Radiology is the official journal of the Radiological Society of South Africa and the Professional Association of Radiologists in South Africa and Namibia. The SA Journal of Radiology is a general diagnostic radiological journal which carries original research and review articles, pictorial essays, case reports, letters, editorials, radiological practice and other radiological articles.

Evolution of neurological, neuropsychological and sleep-wake disturbances in paramedian thalamic stroke

Evolution of neurological, neuropsychological and sleep-wake disturbances in paramedian thalamic stroke

Reduced sensorimotor inhibition in the ipsilesional motor cortex in a patient with chronic stroke of the paramedian thalamus

Objective Unilateral or bilateral paramedian infarction in the region of the thalamus and upper midbrain may lead to hypersomnia. To determine whether unilateral infarction of the paramedian thalamus leads to changes in excitability of ipsilesional primary motor hand area (M1). Methods We describe a patient with chronic stroke of the right dorsomedian and intralaminar thalamic nuclei, who suffered from mild persistent hypersomnia. We studied the excitability of the right and left M1 with transcranial magnetic stimulation (TMS) in the patient, and in 10 healthy controls. Results In contrast to healthy controls, contralateral electrical stimulation of the median nerve failed to induce short-latency afferent inhibition (SAI) in the ipsilesional M1. Other measures of corticomotor excitability and somatosensory evoked potentials were normal. Conclusions The selective loss of ipsilateral SAI in a patient with paramedian thalamic stroke suggests that during wakefulness, the intact paramedian thalamus facilitates the excitability of intracortical inhibitory circuits, which process thalamocortical sensory inputs in the ipsilateral M1. This preliminary finding suggests that measurements of SAI may provide a means of probing the integrity of some neural pathways, which are involved in the control of wakefulness and arousal. Significance In addition to the established role of the paramedian thalamus in arousal and memory, our observation suggests that thalamocortical projections from the paramedian thalamus contribute to the integration of sensory input at the cortical level during wakefulness.

MRI of paramedian thalamic stroke with sleep disturbance.

The paramedian thalamus is believed to play an important role in the regulation of sleep, and disturbances of sleep regulation are known to occur in paramedian thalamic stroke (PTS). We examined 12 consecutive patients with PTS and sleep disturbance by MRI. Two distinct groups of patients could be defined: six presenting with severe hypersomnia (group 1) and six with slight sleepiness (group 2). On MRI, all patients had ischaemic lesions involving the paramedian thalamic nuclei, the centre of the lesions being the dorsomedial and centromedial thalamic nuclei. In group 1 the lesions were bilateral, butterfly-shaped infarcts involving the paramedian nuclei (three cases); or unilateral with an extension into the subthalamic nuclei. In group 2 the lesions were unilateral and limited to the paramedian nuclei, mainly the dorsomedial nucleus. Bilateral lesions can be attributed to a common origin in some cases for both paramedian thalamic arteries and the mesencephalic arteries.

Hypersomnia following paramedian thalamic stroke: MRI findings with electroclinical correlation

Hypersomnia following paramedian thalamic stroke: MRI findings with electroclinical correlation

Hypersomnia following paramedian thalamic stroke: a report of 12 patients.

Paramedian thalamic stroke (PTS) is a cause of organic hypersomnia, which in the absence of systematic sleep-wake studies has been attributed to disruption of ascending activating impulses and considered a "dearoused" state. However, an increasing mount of data suggests a role of the thalamus in sleep regulation and raises the possibility that a sleep disturbance contributes to hypersomnia in PTS. We evaluated 12 patients with magnetic resonance imaging-proven isolated PTS and hypersomnia with 10 to >20 hours of sleep behavior per day. Nocturnal polysomnographic findings paralleled the severity of hypersomnia. All subjects had increased stage 1 NREM sleep, reduced stage 2 NREM sleep, and reduced numbers of sleep spindles. In patients with severe hypersomnia, slow-wave (stages 3-4) NREM sleep was often reduced, but there were no major REM sleep alterations. Daytime sleep behavior was associated mostly with stage 1 sleep by electroencephalogram; there was no correlation between hypersomnia and results of nap tests. We conclude that hypersomnia following PTS is accompanied by deficient arousal during the day and insufficient spindling and slow-wave sleep production at night. These observations support the hypothesis of a dual role of the paramedian thalamus as "final common pathway' for both maintenance of wakefulness and promotion of NREM sleep.