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Objective The thalamus is the integrative hub of the brain with reciprocal connections throughout the cortex. This case report describes a right-handed 81-year-old male patient who experienced sudden onset cognitive impairment following a focal left anterior thalamic infarct. Methods With consent/assent, the patient was seen for a short neuropsychological assessment 6 weeks post stroke. Neuropsychological assessment included review of medical history, collateral intake, the Toronto Cognitive Assessment, Frontal Systems Behavior Scale-Family Rating Form, the Neuropsychiatric Inventory Questionnaire, and piano performance. Results The assessment revealed impaired performance on measures of orientation, memory, executive function, and language, as well as symptoms including hallucinations, apathy, and hypersomnolence, consistent with thalamic dementia. Remarkably, in this context, the patient maintained an ability to play piano and read music. Conclusions The case has implications for understanding the complex integrative functions of the thalamus, including how profound impairment can simultaneously present with cognitive strengths that may not be captured by performance on neuropsychological testing. This case also suggests that magnetic resonance imaging may be indicated in cases presenting with vascular risk factors and sudden onset cognitive impairment, given that computed tomography may not be sensitive to small subcortical infarcts. [ABSTRACT FROM AUTHOR]

Background and objective: Neuro‐ophthalmologic symptoms and retinal changes have been increasingly observed following thalamic stroke, and there is mounting evidence indicating distinct alterations occurring in the vision‐related functional network. However, the intrinsic correlations between these changes are not yet fully understood. Our objective was to explore the altered patterns of functional network connectivity and retina parameters, and their correlations with visual performance in patients with thalamic stroke. Methods: We utilized resting‐state functional MRI to obtain multi‐modular functional connectivity (FC), and optical coherence tomography‐angiography to measure various retina parameters, such as the retinal nerve fiber layer (RNFL), ganglion cell‐inner plexiform layer (GCIPL), superficial vascular complex (SVC), and deep vascular complex. Visual acuity (VA) was used as a metric for visual performance. Results: We included 46 patients with first‐ever unilateral thalamic stroke (mean age 59.74 ± 10.02 years, 33 males). Significant associations were found between FC of attention‐to‐default mode and SVC, RNFL, and GCIPL, as well as between FC of attention‐to‐visual and RNFL (p <.05). Both RNFL and GCIPL exhibited significant associations with FC of visual‐to‐visual (p <.05). Only GCIPL showed an association with VA (p =.038). Stratified analysis based on a disease duration of 6 months revealed distinct and significant linking patterns in multi‐modular FC and specific retina parameters, with varying correlations with VA in each subgroup. Conclusion: These findings provide valuable insight into the neural basis of the associations between brain network dysfunction and impaired visual performance in patients with thalamic stroke. Our novel findings have the potential to inform future targeted and individualized therapies. However, further comprehensive studies are necessary to validate our results. [ABSTRACT FROM AUTHOR]

The thalamus, and its projections to the cerebral cortex, are crucial for regulating sleep rhythms, such as sleep spindles, and for maintaining arousal and sleep homeostasis. Moreover, they play a significant role in memory, executive functioning, and attention. Altered thalamocortical circuitry caused by vascular lesions affects sleep–wake architecture and may contribute to cognitive deficits observed in thalamic stroke patients. This review summarizes the biology of the thalamus and current knowledge regarding the impact of thalamic circuitry on sleep regulation and cognition, drawing from clinical and pre-clinical studies. Furthermore, deep brain stimulation and transcranial magnetic stimulation are discussed as possible therapeutic approaches targeting thalamic circuits. Understanding the role of the thalamus in sleep and cognition opens new avenues for developing novel therapeutic strategies to improve sleep and cognitive functions in affected individuals. [ABSTRACT FROM AUTHOR]

Introduction: Since 2019, COVID-19 pneumonia caused by SARS-CoV-2 virus has led to a worldwide pandemic. Since then, various neurological manifestations of COVID-19 pneumonia have been reported. Neurological manifestations include headache, anosmia, seizures, and altered mental status. In some cases, it presents as stroke, encephalitis, and neuropathy. Artery of Percheron (AOP) is a variant in the posterior circulation. Here, a single artery arises from the posterior cerebral artery p1 segment. It supplies bilateral thalamus with or without midbrain. Thrombosis in this artery leads to clinical symptoms like reduced level of consciousness, altered mental status, and memory impairment. Case Report: Here, we present a case who presented with fever and altered sensorium without any focal neurological deficits and without known risk factors for stroke. His COVID-19 PCR was positive. He was initially diagnosed as COVID-19 pneumonia with encephalitis and was started on treatment for the same. His initial CT brain and lumbar puncture were normal. The next day, when MRI brain with and without contrast was done, the thalamic stroke due to AOP infarction was diagnosed and appropriate treatment for stroke was initiated. Discussion: Many patients miss the window for thrombolysis because of variable presentation in clinical symptoms with negative imaging. It is also difficult to assess the time of onset of stroke in this varied presentation. Our patient had fever and cough for 2 days and had altered mental status since the morning of admission. During hospital stay, he developed bilateral third nerve palsy. This case also highlights the importance of detailed evaluation in COVID-19 patients with neurological complaints. This helps to avoid delays in treatment and to improve clinical outcomes. As our knowledge of COVID-19 and its varied neurological manifestations evolve, we need to be prepared for more atypical presentation to facilitate timely interventions.

Purpose: Occlusion of artery of Percheron (AOP), a rare variant of paramedian branches of posterior cerebral artery, results in a characteristic pattern of ischemic lesions in bilateral paramedian thalami with or without midbrain and anterior thalami involvement. Aim: To evaluate the prevalence, the clinical, and the imaging features of AOP infarction in a single comprehensive stroke center experience. Methods: We retrospectively search in our stroke center database, patients with ischemic lesions in the AOP distribution. We collected clinical features and time between hospital admission and diagnosis. Imaging findings were categorized following a pre-selected classification. Results: Of 2830 ischemic stroke admitted in our center, we identified 15 patients with AOP infarction (0.53%). Clinical manifestations were variable, but oculomotor disturbances, particularly vertical gaze palsy, were the most observed, followed by consciousness impairment, varying from drowsiness to coma. The most frequent imaging pattern was bilateral paramedian thalamic infarction with midbrain infarction, and the V-sign was recognized in 6 cases from this group. In 8 patients a fetal origin of the PCA was observed. The average time from first hospital admission to diagnosis was 28.09 h. Conclusions: The prevalence of AOP infarction in our center was 0.53%. Diagnosis of AOP infarction can be challenging and should be suspected in case of sudden altered consciousness. [ABSTRACT FROM AUTHOR]

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 30min. 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. [ABSTRACT FROM AUTHOR]

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.

The artery of Percheron originates from the right or left posterior cerebral artery and is one of the options for normal blood supply to the paramedian portions of the thalamus. Stroke in this area has specific MRI changes, the most informative ones in diffusion-weighted imaging mode. With the involvement of the midbrain, its pial surface can display an additional pathognomonic V-shaped sign in 67%. The clinical manifestations are non-specific. In some cases, there is a triad of symptoms, which is distinguished into paramedian thalamic syndrome (vertical gaze palsy, neuropsychological disorders, and depressed level of consciousness up to coma). The symptoms of a midbrain lesion as oculomotor nerve group diseases, contralateral hemiparesis, hemiataxia or hemianesthesia, in combination with a triad, develop a thalamopeduncular or mesencephalon thalamic syndrome. The paper presents a clinical case of a 59-year-old man who was hospitalized with acute unconsciousness, a Glasgow coma scale of 13 scores, and disorientation. A neurological examination revealed vertical gaze palsy and upper limb ataxia. Brain MRI revealed characteristic bithalamic paramedian stroke. After completing the treatment, the patient was discharged showing incomplete clinical recovery.

This case report discusses a 51-year-old male who presented to the emergency department (ED) with left-sided hemiparesthesia and left leg incoordination. The initial brain computed tomography (CT) scan was negative, and the follow-up brain CT three days after the onset of symptoms was also negative. Although sensitivity and specificity are not 100%, CT remains the first-line diagnostic test for detecting a cerebrovascular accident (CVA). In this unique case, CT was not sufficient. Following two negative CT scans, magnetic resonance imaging (MRI) finally revealed the cause of this patient's symptoms, an ischemic incident in the right thalamus. Thalamic strokes typically present with contralateral hemiparesis and hemisensory loss, unreactive pupils, and gaze palsy with gaze deviation away from the side of the infarct. It is unusual to see a thalamic lesion present with pure hemiparesthesia without facial involvement. This patient's clinical presentation is discussed, as well as future investigations and ways to prevent this diagnostic delay. This case demonstrates the importance of follow-up imaging based on the clinical presentation of potentially subtle imaging findings., Competing Interests: Human subjects: Consent was obtained or waived by all participants in this study. Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work., (Copyright © 2024, Tadros et al.)

Post-stroke depression is the most common neuropsychiatric complication of stroke, and can occur early too late after stroke. However, having depression as an isolated clinical manifestation of stroke is extremely rare in the literature. We report the case of an ischemic vascular accident revealed by sudden onset depression in a 59-year-old female patient. On the basis of this report and a review of the literature we discuss the different hypotheses that may explain the underlying mechanisms. [ABSTRACT FROM AUTHOR]

Although rare, central post-stroke pain remains one of the most refractory forms of neuropathic pain. Repetitive transcranial magnetic stimulation (rTMS) has been reported to be effective in chronic cases. However, there are no data on the effects in the acute and subacute phases after stroke. In this study, we present a case of a patient with thalamic stroke with acute onset of pain and paresthesia who was responsive to rTMS. After a right thalamic stroke, a 32-year-old woman presented with drug-resistant pain and paresthesia on the left side of the body. There were no motor or sensory deficits, except for blunted thermal sensation and allodynia on light touch. Ten daily sessions were performed, where 10 Hz rTMS was applied to the hand area of the right primary motor cortex, 40 days after stroke. Before rTMS treatment (T0), immediately after treatment conclusion (T1), and 1 month after treatment (T2), three pain questionnaires were administered, and cortical responses to single and paired-pulse TMS were assessed. Eight healthy participants served as controls. At T0, when the patient was experiencing the worst pain, the excitability of the ipsilesional motor cortex was reduced. At T1 and T2, the pain scores and paresthesia' spread decreased. The clinical improvement was paralleled by the recovery in motor cortex excitability of the affected hemisphere, in terms of both intra- and inter-hemispheric connections. In this subacute central post-stroke pain case, rTMS treatment was associated with decreased pain and motor cortex excitability changes. [ABSTRACT FROM AUTHOR]

Although rare, central post-stroke pain remains one of the most refractory forms of neuropathic pain. Repetitive transcranial magnetic stimulation (rTMS) has been reported to be effective in chronic cases. However, there are no data on the effects in the acute and subacute phases after stroke. In this study, we present a case of a patient with thalamic stroke with acute onset of pain and paresthesia who was responsive to rTMS. After a right thalamic stroke, a 32-year-old woman presented with drug-resistant pain and paresthesia on the left side of the body. There were no motor or sensory deficits, except for blunted thermal sensation and allodynia on light touch. Ten daily sessions were performed, where 10 Hz rTMS was applied to the hand area of the right primary motor cortex, 40 days after stroke. Before rTMS treatment (T0), immediately after treatment conclusion (T1), and 1 month after treatment (T2), three pain questionnaires were administered, and cortical responses to single and paired-pulse TMS were assessed. Eight healthy participants served as controls. At T0, when the patient was experiencing the worst pain, the excitability of the ipsilesional motor cortex was reduced. At T1 and T2, the pain scores and paresthesia' spread decreased. The clinical improvement was paralleled by the recovery in motor cortex excitability of the affected hemisphere, in terms of both intra- and inter-hemispheric connections. In this subacute central post-stroke pain case, rTMS treatment was associated with decreased pain and motor cortex excitability changes.

Introduction: Impaired balance is one of the primary causes of functional limitations. Related to sensory deficits specifically, balance disorder in stroke may be caused by decreased central integration of sensory cues, including somatosensory, visual and vestibular input. Case Presentation: This case describes a 23-year-old male with bilateral thalamic stroke following surgical resection of a recurring optic nerve meningioma. He had a complex medical history and is legally blind. He presented to outpatient neurorehabilitation 5 months following his stroke. He demonstrated absent light touch sensation and absent proprioception and kinesthetic awareness in his upper extremities, lower extremities, and trunk. Secondary to absent proprioception and vision and significant impairments related to shunt malfunction, he required total assistance for all mobility at initial examination. Discussion: After 8 months of intensive rehabilitation, he demonstrated substantial improvements in all functional mobility and recovery of sensation. Rehabilitation included interventions such as electrical stimulation, fluidotherapy, repetitive task training, and most significantly, external augmented feedback. This feedback included sensory cues, auditory and tactile cues, and maximizing the use of vestibular input. This case demonstrates that neurorehabilitation can benefit patients with impaired use of sensory cues and central integration. [ABSTRACT FROM AUTHOR]

We present a case of sudden postischaemic onset of alien limb syndrome, with unintentional self-injury. Alien limb syndrome is an uncommon neurological disorder featured by uncontrolled and involuntary movements of a limb. Three variants of alien limb syndrome have been described: the anterior, featured by grasping of surrounding objects, the callosal, presenting with intermanual conflict, and the posterior, associated with involuntary levitation of the limb. Our patient suffered from an acute presentation of the posterior variant of the alien limb syndrome, resulting from an isolated thalamic stroke which was documented using 24-h computed tomography brain scan. Only one previous case of alien limb syndrome after thalamic infarct has been reported. Our case enhances the possibility that pure thalamic injury may represent a trigger for this condition.

Abstract Background Numb Chin Syndrome (NCS), which is also characterized as sensory neuropathy of the mental nerve, describes a mostly unilateral numbness of the chin and lower lip. Benign and malignant diseases are known to cause this circumscribed symptom, which can easily be overlooked or misdiagnosed. In this article we present the very rare case of a clinical NCS caused by thalamic lacunar infarction. As a pure sensory stroke it is a rare variant of the Cheiro-Oral Syndrome (COS). Case presentation A 63-year-old male patient received an emergency referral to our department after the patient had noticed a feeling of numbness of the left lower lip and chin on the previous day. The neurological examination revealed an approximately 2 × 3 cm area of hypoesthesia in the area of the chin and left lower lip and the cranial MRI an acute ischemia in the right thalamus. Conclusions In this case report we introduce a patient who clinically shows an NCS. Various diseases may be responsible for NCS, including malignancies or even central neurological disorders such as multiple sclerosis. A lacunar thalamic ischemia as a cause of NCS is very rare and to our knowledge described in the literature only in the contex of a COS in three cases. We wish to remind the reader, through this case, of the purely descriptive and syndromal character of the NCS and the importance for detecting underlying diseases. Furthermore we give a brief overview of the NCS and causative disorders.

Symptomatic cerebral infarcts with cryptogenic ischemic stroke pose diagnostic challenges due to unknown etiology. Notably, up to half of young individuals with cryptogenic stroke exhibit patent foramen ovale (PFO), while finasteride, which is used for male pattern baldness, elevates testosterone levels, potentially increasing the risk of thrombosis. Here, we present a case of thalamic infarction in a 21-year-old male devoid of cerebrovascular risk factors but with PFO and finasteride use. The patient presented with short-term memory issues, otherwise lacking medical history or substance use. Examination revealed neurological deficits, with imaging indicating a left thalamic infarct. Subsequent investigations identified PFO, prompting referral for closure, yielding symptomatic improvement. Furthermore, discontinuation of finasteride was advised due to its thrombotic association. Finasteride's inhibition of 5-alpha reductase 2 increases testosterone conversion to estrogen, potentially promoting thrombosis. Finasteride use can cause thrombotic events, emphasizing its risk. In conclusion, young embolic stroke patients warrant PFO evaluation alongside hypercoagulable workup, with closure benefiting those under the age of 55. Additionally, discontinuing finasteride may mitigate thrombosis risk., Competing Interests: The authors have declared that no competing interests exist., (Copyright © 2024, Gaddameedi et al.)

Supplemental digital content is available in the text. Thalamic dementia is an uncommon type of stroke that presents with disorientation, behavioral changes, and impairment of executive functions, with relative preservation of motor functions. It is typically caused by paramedian territory infarctions of the thalamus, most often due to ischemic insult at the tip of the basilar artery. In this report, we present a case of bilateral thalamic infarcts resulting in thalamic dementia with severe behavioral manifestations in a 64-yr-old man with no preexisting neuropsychiatric comorbidities. A trial of amantadine, a dopamine-promoting agent, in the acute rehabilitation unit in an attempt to manage his agitation led to multiple weeks of dramatic behavioral improvement and increased participation in therapies. Dopamine receptors are believed to be present at increased densities in thalamic nuclei with mesolimbic projections, suggesting that they are able to modulate limbic functions such as arousal, emotion, and memory. This case report, aimed both to increase the awareness of this uncommon stroke syndrome and describe the observed effect of amantadine, will ultimately help clinicians properly recognize thalamic dementia, minimize unnecessary investigations, and develop effective neurorehabilitation strategies in these patients. [ABSTRACT FROM AUTHOR]

Copyright of Mezdunarodnyj Nevrologiceskij Zurnal is the property of Zaslavsky O.Yu and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Mezdunarodnyj Nevrologiceskij Zurnal is the property of Zaslavsky O.Yu and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Mezdunarodnyj Nevrologiceskij Zurnal is the property of Zaslavsky O.Yu and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Mezdunarodnyj Nevrologiceskij Zurnal is the property of Zaslavsky O.Yu and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Paramedian thalamic strokes following occlusion of the posterior medial (paramedian) thalamic perforators have been previously described in great detail. However, the stroke syndrome associated with occlusion of posterior lateral (inferolateral) thalamic perforators is less commonly known. We present an illustrative case of an inferolateral thalamic perforator stroke mimicking a middle cerebral artery (MCA) syndrome and provide a review of the literature. A 62-year-old male presented with dysarthria, contralateral hemisensory loss, and contralateral weakness, concerning for possible MCA stroke. However, close examination revealed the hemiparesis to be ataxic in nature. Imaging revealed a left PCA P2 segment occlusion and lacunar infarction of the ventral lateral (VL) and ventral posterior (VP) thalamus, the main thalamic destination of cerebellar and sensory pathways. The case is unique because the P1 segment and posterior communicating artery (Pcom) remained patent, resulting in selective occlusion of only the posterior lateral (inferolateral) thalamic perforators at the P2 level. Acute loss of the posterior lateral (inferolateral) thalamic perforators at the proximal P2 segment results in a ventral lateral and ventral posterior thalamic stroke characterized by contralateral hemisensory loss, contralateral ataxic hemiparesis, and dysarthria. It is important to recognize the inferolateral thalamic stroke syndrome, as it may be mistaken clinically for an MCA occlusion. The benefit of mechanical thrombectomy for this type of stroke is not well established and should be considered carefully. [ABSTRACT FROM AUTHOR]

The abducens nerve (sixth cranial nerve) is essential for lateral eye movement, and its malfunction can cause a variety of issues with vision. Pseudo-abducens palsy is a rare neurological condition that causes a limitation in eye abduction, while the abducens nerve is still functioning. Thalamic pain syndrome, a severe complication of cerebrovascular events, presents as intense neuropathic pain provoked by temperature fluctuations. Although thalamic strokes are infrequently associated with ocular abnormalities, some studies suggest an association between isolated pseudo-abducens palsy and thalamic infarctions. The present study describes the case of a 38-year-old male patient with 1-day progressive diplopia and occipital headache who had abducens palsy on the left side as a result of a right thalamic infarction. The patient had a 10-year history of smoking and a 1-year history of hypertension, which was poorly controlled. The diagnosis was supported by a neurological examination, imaging and stroke etiology investigations. The patient recovered well within 5 days, highlighting the good prognosis of an acute thalamic presentation. In addition, a mini-review of the literature was performed and two similar reports were identified upon searching the literature using the Embase, Google Scholar, Lilacs, Medline, SciELO and ScienceDirect databases. On the whole, the present study demonstrates that understanding the complex neuronal connections inside the thalamus is critical for a proper diagnosis and appropriate intervention strategies in patients with thalamic stroke with oculomotor impairments. Further research is required to elucidate the underlying causes and develop treatment techniques for thalamic infarction consequences., Competing Interests: The authors declare that they have no competing interests., (Copyright: © 2024 Rissardo et al.)

We present a case of sudden postischaemic onset of alien limb syndrome, with unintentional self-injury. Alien limb syndrome is an uncommon neurological disorder featured by uncontrolled and involuntary movements of a limb. Three variants of alien limb syndrome have been described: the anterior, featured by grasping of surrounding objects, the callosal, presenting with intermanual conflict, and the posterior, associated with involuntary levitation of the limb. Our patient suffered from an acute presentation of the posterior variant of the alien limb syndrome, resulting from an isolated thalamic stroke which was documented using 24-h computed tomography brain scan. Only one previous case of alien limb syndrome after thalamic infarct has been reported. Our case enhances the possibility that pure thalamic injury may represent a trigger for this condition. [ABSTRACT FROM AUTHOR]

Background: A focal brain lesion influences the function and morphology in the connected intact regions remote from it. However, it is not well documented that thalamic stroke may induce secondary degeneration of the mammillary body (MB) or the fornix (Fx). Purpose: To investigate transneuronal degeneration (TND) in the MB and Fx following thalamic stroke on magnetic resonance imaging (MRI) and to assess the time course of these findings using serial MRI after stroke. Material and Methods: Conventional T2-weighted axial MR images were retrospectively evaluated in 24 cases of thalamic infarction or hemorrhage involving the anterior thalamic nucleus and/or mammillothalamic tract (MTT). We recorded any change in size and/or shape of the MB and Fx after the infarction and the days on which those structural changes occurred. Results: Ipsilateral atrophy of the MB was shown in 9/20 patients (45.0%). MRI revealed MB atrophy as a small round shape in almost half of the patients and was too small to visualize in one-third of them on axial planes. Ipsilateral atrophy of the Fx was found in 2/23 patients (8.7%) and was observed as a thin lined shape on MRI. The atrophy was observed on follow-up MRI scans dated 356–1779 days (mean = 910 ± 516 days) after onset. Conclusion: Damage to the anterior thalamic nucleus and/or MTT caused TND in the ipsilateral MB and/or Fx resulted in atrophy and asymmetry in less than half of patients studied, mostly within three years. [ABSTRACT FROM AUTHOR]

Copyright of Mezdunarodnyj Nevrologiceskij Zurnal is the property of Zaslavsky O.Yu and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Chronic pain conditions are associated with neuroplasticity within the central nervous system. In most patients the maladaptive consequence of neuroplasticity supports prolonged course of chronic pain, despite the absence of a commensurate etiology. From a pain neuromatrix perspective it can involve three different circuits within the central nervous system; the classical sensory pathway, the limbic system pathway, and the associative pathways involving the parietal cortical connections. Although this can be conceptualized as a fluid system composed of several interacting networks, it can be broadly separated into a nociceptive specific network of spino-thalamic neurons and second order neurons beyond thalamus that are not nociceptor specific. Thalamus acts as an important relay station that conveys nociceptive signaling to higher centres. Neuroplastic changes can potentially involve any parts within this neuromatrix. It is very uncommon to observe the sudden disappearance of such a chronic pain condition. Methods and results: In this case report, the author describes the clinical course of a patient with severe chronic low back pain (CLBP), whose pain suddenly disappeared after a stroke involving his left thalamus. Although extremely rare, existing case reports of such disappearance of pain with a secondary stroke in patients suffering from central post stroke pain (CPSP) are reviewed. The author further postulates hypotheses that could potentially explain this phenomenon based on the existing knowledge. Conclusions and implications: Although extremely rare and unpredictable, a thalamic stroke involving areas that are involved in chronic pain signaling can potentially lead to disappearence of an existing chronic pain condition. This is the first case report of such sudden disappearence of CLBP with well established nociceptive pathology supported by clinical and imaging findings. This unique case report could potentially generate ideas for future research and clinical treatment in the field of neuromodulation and brain stimulation. [ABSTRACT FROM AUTHOR]

Background: Physical, psychological, and/or social impairment can result after a stroke and can be exacerbated by pain. One type of pain after stroke, central poststroke pain, is believed to be due to primary central nervous system mechanisms. Estimated prevalence of central poststroke pain ranges widely from 8% to 55% of stroke patients, suggesting a difficulty in reliably, accurately, and consistently identifying central poststroke pain. This may be due to the absence of a generally accepted definition. Aim: We aimed to clarify the role of thalamic strokes and damage to the spinothalamic pathway in central poststroke pain patients. Also, we aimed to gain a current understanding of anatomic substrates, brain imaging, and treatment of central poststroke pain. Summary of review: Two independent reviewers identified 10,144 publications. Based on Preferred Reporting Items for Systematic Reviews and Meta-Analysis guidelines, we extracted data from 23 papers and categorized the articles' aims into four sections: somatosensory deficits, pathway stimulation, clinical trials, and brain imaging. Conclusions: Our systematic review suggests that damage to the spinothalamic pathway is associated with central poststroke pain and this link could provide insights into mechanisms and treatment. Moreover, historical connection of strokes in the thalamic region of the brain and central poststroke pain should be reevaluated as many studies noted that strokes in other regions of the brain have high occurrence of central poststroke pain as well. [ABSTRACT FROM AUTHOR]

Oculomotor abnormalities are rarely noted in thalamic strokes. We describe isolated right pseudoabducens palsy in a young patient with acute left thalamic infarction revealed by diffusion-weighted magnetic resonance imaging. The patient's horizontal diplopia and oculomotor palsy resolved within 3 days. This case supports the hypothesis that a lesion can cause isolated esotropia by interrupting descending inhibitory convergence pathways that traverse the paramedian thalamus and decussate in the subthalamic region to innervate the contralateral third oculomotor nucleus. Esotropia contralateral to the thalamic lesion results from tonic activation of the medial rectus, producing pseudoabducens palsy. [ABSTRACT FROM AUTHOR]

Abstract Transient Cerebral Arteriopathy (TCA) is one of the main causes of childhood stroke. Here we present an unusual case of Arterial Ischemic Stroke (AIS) caused by a TCA of posterior flow and originally located in the right thalamus. The detection of enterovirus in the cerebrospinal fluid allowed us to suppose a probable post infectious etiology. The course of symptoms was self-limited and the child had a complete clinical recovery after five days. A new ischemic lesion on the antero-inferior paravermian region of the left cerebellum was revealed by a following brain Magnetic Resonance Imaging (MRI) three months later and these findings were reported by further brain MRI control performed after 15 months. Comparing follow up Magnetic Resonance Angiography (MRA) with previous High Resolution Vessel Wall Magnetic Resonance Imaging (HRMI), we found a vessel narrowing at the level of the Posterior Inferior Cerebellar Artery that might explain the arteriopathy process. In conclusion, clinical and radiological course allow us to speculate that this multifocal cerebral arteriopathy might be a transient lesion due to enterovirus infection. To our knowledge, there are only three articles describing TCA enterovirus-related, and brain MRA was performed in only one case; in addition, no one with the involvement of the posterior circulation. [ABSTRACT FROM AUTHOR]

Diffusion tensor imaging (DTI) allows in vivo structural brain mapping and detection of microstructural disruption of white matter (WM). One of the commonly used parameters for grading the anisotropic diffusivity in WM is fractional anisotropy (FA). FA value helps to quantify the directionality of the local tract bundle. Therefore, FA images are being used in voxelwise statistical analyses (VSA). The present study used Tract-Based Spatial Statistics (TBSS) of FA images across subjects, and computes the mean skeleton map to detect voxelwise knowledge of the tracts yielding to groupwise comparison. The skeleton image illustrates WM structure and shows any changes caused by brain damage. The microstructure of WM in thalamic stroke is investigated, and the VSA results of healthy control and thalamic stroke patients are reported. It has been shown that several skeleton regions were affected subject to the presence of thalamic stroke (FWE, p < 0.05). Furthermore the correlation of quantitative EEG (qEEG) scores and neurophysiological tests with the FA skeleton for the entire test group is also investigated. We compared measurements that are related to the same fibers across subjects, and discussed implications for VSA of WM in thalamic stroke cases, for the relationship between behavioral tests and FA skeletons, and for the correlation between the FA maps and qEEG scores.Results obtained through the regression analyses did not exceed the corrected statistical threshold values for multiple comparisons (uncorrected, p < 0.05). However, in the regression analysis of FA values and the theta band activity of EEG, cingulum bundle and corpus callosum were found to be related. These areas are parts of the Default Mode Network (DMN) where DMN is known to be involved in resting state EEG theta activity. The relation between the EEG alpha band power values and FA values of the skeleton was found to support the cortico-thalamocortical cycles for both subject groups. Further, the neurophysiological tests including Benton Face Recognition (BFR), Digit Span test (DST), Warrington Topographic Memory test (WTMT), California Verbal Learning test (CVLT) has been regressed with the FA skeleton maps for both subject groups. Our results corresponding to DST task were found to be similar with previously reported findings for working memory and episodic memory tasks. For the WTMT, FA values of the cingulum (right) that plays a role in memory process was found to be related with the behavioral responses. Splenium of corpus callosum was found to be correlated for both subject groups for the BFR. [ABSTRACT FROM AUTHOR]

Altered sleep architecture and stroke share a reciprocal relationship. More than half of the stroke patients display sleep abnormalities including hypersomnia, insomnia, parasomnia, periodic limb movements, or sleep-disordered breathing. Conversely, one of the major causes of severe organic hypersomnia is acute brainstem strokes, involving thalamic infarctions, which may be reversible over 6–12 months. Here, we report a patient with increased lethargy and drowsiness who was diagnosed to have a right thalamic and hypothalamic ischemic stroke. [ABSTRACT FROM AUTHOR]

Apraxic agraphia (AA) is a so-called peripheral writing disorder following disruption of the skilled movement plans of writing while the central processes that subserve spelling are intact. It has been observed in a variety of etiologically heterogeneous neurological disorders typically associated with lesions located in the language dominant parietal and frontal region. The condition is characterized by a hesitant, incomplete, imprecise or even illegible graphomotor output. Letter formation cannot be attributed to sensorimotor, extrapyramidal or cerebellar dysfunction affecting the writing limb. Detailed clinical, neurocognitive, neurolinguistic and (functional) neuroimaging characteristics of three unique cases are reported that developed AA following a thalamic stroke. In marked contrast to impaired handwriting, non-handwriting skills, such as oral spelling, were hardly impaired. Quantified Tc-99m ECD SPECT consistently showed a decreased perfusion in the anatomoclinically suspected prefrontal regions. The findings suggest crucial involvement of the anterior (and medial) portion of the left thalamus within the neural network subserving the graphomotor system. Functional neuroimaging findings seem to indicate that AA after focal thalamic damage represents a diaschisis phenomenon. [ABSTRACT FROM AUTHOR]

Background: The essential role of the thalamus in neurocognitive processes has been well documented. In contrast, relatively little is known about its involvement in social cognitive processes such as recognition of emotion, mentalizing, or empathy. The aim of the study: This study was designed to compare the performance of eight patients (five males, three females, mean age ±SD: 63.7±7.9 years) at early stage of unilateral thalamic lesions and eleven healthy controls (six males, five females, 49.6±12.2 years) in neurocognitive tests (CogState Battery: Groton Maze Learning Test, GML; Groton Maze Learning Test- Delayed Recall, GML-DR; Detection Task, DT; Identification Task, IT; One Card Learning Task, OCLT; One Back Task, OBT; Two Back Task, TBT; Set-Shifting Task, S-ST) and other well-known tests (Benton Visual Retention Test, BVRT; California Verbal Learning Test, CVLT; The Rey-Osterrieth Complex Figure Test, ROCF; Trail Making Test, TMT part A and B; Color - Word Stroop Task, CWST; Verbal Fluency Test, VFT), and social cognitive tasks (The Penn Emotion Recognition Test, ER40; Penn Emotion Discrimination Task, EmoDiff40; The Penn Emotional Acuity Test, PEAT40; Reading the Mind in the Eyes Test, revised version II; Toronto Alexithymia Scale, TAS-20). Methods: Thalamic-damaged subjects were included if they experienced a single-episode ischemic stroke localized in right or left thalamus. The patients were examined at 3 weeks after the stroke onset. All were right handed. In addition, the following clinical scales were used: the Mini-Mental State Examination (MMSE), Spielberger State-Trait Anxiety Inventory (STAI), Beck Depression Inventory (BDI II). An inclusion criteria was a minimum score of 23/30 in MMSE. Results: Compared with the healthy controls, patients revealed significantly lower scores in CVLT, GML-DR, and VFT. Furthermore, compared to healthy controls, patients showed significantly delayed recognition of "happiness" in EmoDiff40 and significantly worse performance on Reading the Mind in the Eyes Test, revised version II. Neuropsychological assessment demonstrated some statistically significant deficits in learning and remembering both verbal and visual material, long-term information storing, problem solving, and executive functions such as verbal fluency. Conclusion: Patients at early stage of unilateral thalamic stroke showed both neurocognitive and social cognitive deficits. Further research is needed to increase understanding about diagnosis, early treatment, and prognosis of patients with thalamic lesions. [ABSTRACT FROM AUTHOR]