Dear Editor,
In the United States, an acute stroke occurs every 40 seconds, with stroke accounting for one in six deaths in 2021. Worldwide, strokes are the third leading cause of disability and the second leading cause of death [
1,
2].
Lacunar infarcts are one of the most common subtypes of ischemic stroke and may symbolize future risks of progressive disease in small perforating arteries, venules of the brain, and capillaries, categorized as small-vessel disease [
3]. These types of strokes are small, 15 mm in diameter, and primarily occur in noncortical regions [
4]. However, lacunar strokes can differ by the size of the underlying brain infarct: small lacunar strokes commonly result from hypertensive small-artery disease, while larger ones originate from atheroma or an occlusion [
5]. Twenty-five percent of ischemic strokes are categorized as lacunar [
6]. This condition also contributes to 40% of dementia cases [
7]. Considering demographics, men are at a greater risk of cognitive impairment from acute lacunar stroke [
8]. These findings demonstrate that severe motor complications are common contributors to life-long disabilities in stroke patients.
Although lacunar strokes occur in small vessels, thrombolysis has been shown to confer a significant reduction in stroke severity (as measured by post–tissue plasminogen activator [post-tPA] US National Institutes of Health Stroke Scale [NIHSS]) as well as functional outcomes (as measured by the modified Rankin score). A secondary analysis of the WAKE-UP trial included 108 patients with lacunar stroke, of which 51% received alteplase [
9]. Fifty-nine percent in this group had a favorable outcome compared to those receiving the placebo. Similarly, a secondary analysis of the Alteplase Compared with Tenecteplase trial found that patients with lacunar infarcts did better after thrombolysis, including fewer (zero) cases of intracranial hemorrhage [
10].
The patient described in this study suffered a right-sided thalamic stroke. The thalamus is part of the limbic system and is comprised of different subgroups of nuclei that serve unique roles, from relaying sensory and motor skills to regulating alertness and consciousness [
11]. Thalamic strokes can manifest in many forms depending on which artery is compromised [
12]. The posterior choroidal artery supplies the posterior portion of the thalamus, including the lateral and geniculate bodies, and damage to this area can impact visual processing. Separately, the paramedian artery supplies the medial aspects of the thalamus, where damage can result in memory issues and sleep disturbances [
13]. Meanwhile, the tuberothalamic artery supplies the anterior and anterolateral parts of the thalamus, and infarcts in these areas can lead to impairments in arousal, orientation, memory, and personality. However, perhaps the most vulnerable territory is the inferolateral area; here, the inferolateral thalamic artery supplies the lateral aspects of the thalamus, and damage to it can cause contralateral sensory loss, hemiparesis, and pain syndromes [
14].
A 75-year-old man presented to the emergency department with left arm and leg weakness that occurred as he was sitting at his desk. Symptoms also included numbness in his left lip, leg, and arm. He was also drowsy, requiring active stimulation (verbal, tactile) to stay awake. Upon presentation to the emergency department, the patient’s vital signs were: temperature at 36.5 °C, pulse at 82 beats per minute, respiratory rate at 16 breaths per minute, blood pressure at 156/83 mmHg, and pulse oximetry at 94% on room air. His past medical history was significant for hypertension, dyslipidemia, and peripheral arterial disease, and he was a nonsmoker. His NIHSS score was 6 points, with 1 point for questions 1a and 1b (level of consciousness and getting the month wrong), 1 point each for questions 5a and 6a (left-sided motor weakness), 1 point for question 8 (sensory), and 1 point awarded for left-sided neglect (question 11). Computed tomography imaging did not demonstrate intracerebral hemorrhage.
Since the patient was within the 4.5-hour timeframe for tissue plasminogen activator, he was administered 10% of the alteplase dose as a bolus and the remainder as an infusion (
Fig. 1). Subsequent to this, the patient’s weakness improved, and his post-thrombolysis NIHSS score was 4 points. Magnetic resonance imaging revealed an acute lacunar infarct in the right thalamus (
Fig. 2), and the patient was admitted to the intensive care unit. By the next morning, his neglect had resolved, and his NIHSS score was 1 point, for residual numbness. A transesophageal echocardiogram was unremarkable. Electrocardiography did not reveal any evidence of atrial fibrillation. He was discharged home on day 3 after optimization of his medications and provision of modifiable stroke risk factor education.
DISCUSSION
Thalamic strokes, while less common than strokes in other parts of the brain, present unique diagnostic and therapeutic challenges due to the complex role the thalamus plays in sensory, motor, and cognitive processing. The thalamus is crucial for relaying information between various regions of the brain, and lesions here can result in diverse and often profound clinical manifestations. Thalamic strokes can affect both sides of the brain, with right- and left-sided strokes producing different symptomatology based on the functional specialization of the thalamus.
The thalamus is a vital relay center located in the diencephalon, consisting of several distinct nuclei that process sensory, motor, emotional, and cognitive information [
15]. The thalamus can be divided into various functional regions, with each responsible for processing specific types of information; for example, the ventral posterior nucleus processes somatosensory input, while the anterior and medial thalamic nuclei are involved in emotional and cognitive functions. The thalamus communicates with both cortical and subcortical structures, which is why lesions here can exert widespread effects.
Thalamic strokes typically result from ischemia due to occlusion of the perforating arteries, which arise from the posterior cerebral artery and the posterior communicating artery. These strokes can be either ischemic or hemorrhagic in nature, although the former type is far more common. The clinical presentation varies depending on the involved part of the thalamus and hemisphere. The right thalamus is thought to be more highly involved in spatial processing and attention, while the left thalamus plays a larger role in language, verbal memory, and logical thinking [
16].
Right-sided thalamic strokes typically affect functions related to spatial awareness, attention, and emotional regulation. Right-sided lesions result in sensory deficits on the left side of the body, affecting touch, temperature, and pain perception [
16]. One of the hallmark features of right-sided thalamic infarcts is hemispatial neglect, particularly when the lesion involves the pulvinar nucleus. This condition is characterized by a lack of awareness of the left side of space, which may extend to neglecting objects, people, or even parts of the body [
16].
Damage to the right thalamus can result in emotional blunting, apathy, or even disinhibited behaviors, which are linked to the thalamus’ role in processing emotional stimuli [
15]. This often appears as a lack of emotional responsiveness or inappropriate affect, which can complicate social interactions [
17]. Since we primarily dealt with this patient in the emergency department, we were not able to assess the full extent of his emotional repertoire.
Thalamic strokes, whether involving the right or left thalamus, result in a wide range of symptoms that reflect the diverse functions of the organ. The clinical manifestations of these strokes depend on the precise location of the lesion within the thalamus and the affected hemisphere. Right-sided thalamic strokes are often associated with spatial neglect and emotional disturbances, while left-sided strokes tend to involve language deficits and cognitive impairments. Accurate diagnosis using neuroimaging and early thrombolysis is essential for improving patient outcomes.
NOTES
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Ethics statement
Written informed consent for publication of the research details and clinical images was obtained from the patient.
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Author contributions
Conceptualization: all authors; Investigation: all authors; Supervision: LG; Writing–original draft: all authors; Writing–review & editing: all authors. All authors read and approved the final manuscript.
All authors read and approved the final manuscript.
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Conflicts of interest
The authors have no conflicts of interest to declare.
-
Funding
The authors received no financial support for this study.
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Data availability
Data sharing is not applicable as no new data were created or analyzed in this study.
Fig. 1.Timeline of case presentation. ER, emergency room; NIHSS, US National Institutes of Health Stroke Scale; tPA, tissue plasminogen activator; CT, computed tomography; MRI, magnetic resonance imaging.
Fig. 2.Magnetic resonance imaging coronal slice image demonstrating an acute lacunar infarct in the right thalamus.
REFERENCES
- 1. Bhasin G, Ganti L. Bibliometric analysis of the usage of tenecteplase for stroke. Int J Emerg Med 2024;17:167.
- 2. Ganti L. Management of acute ischemic stroke in the emergency department: optimizing the brain. Int J Emerg Med 2025;18:7.
- 3. Niles J, Bhasin G, Ganti L. Large right middle cerebral artery stroke with hemorrhagic transformation. Int J Emerg Med 2024;17:138.
- 4. Markus HS, de Leeuw FE. Cerebral small vessel disease: recent advances and future directions. Int J Stroke 2023;18:4-14.
- 5. Bailey EL, Smith C, Sudlow CL, Wardlaw JM. Pathology of lacunar ischemic stroke in humans: a systematic review. Brain Pathol 2012;22:583-91.
- 6. Wiseman S, Marlborough F, Doubal F, Webb DJ, Wardlaw J. Blood markers of coagulation, fibrinolysis, endothelial dysfunction and inflammation in lacunar stroke versus non-lacunar stroke and non-stroke: systematic review and meta-analysis. Cerebrovasc Dis 2014;37:64-75.
- 7. Fure B, Bruun Wyller T, Engedal K, Thommessen B. Cognitive impairments in acute lacunar stroke. Acta Neurol Scand 2006;114:17-22.
- 8. Steinke W, Ley SC. Lacunar stroke is the major cause of progressive motor deficits. Stroke 2002;33:1510-6.
- 9. Barow E, Boutitie F, Cheng B, et al. Functional outcome of intravenous thrombolysis in patients with lacunar infarcts in the WAKE-UP trial. JAMA Neurol 2019;76:641-9.
- 10. Siddiqi AZ, Ignacio K, Kaveeta C, et al. Safety and efficacy of intravenous thrombolysis by infarct type in patients with no visible occlusion: a secondary analysis of the AcT trial. J Am Heart Assoc 2025;14:e037577.
- 11. Torrico TJ, Munakomi S. Neuroanatomy, thalamus [updated 2023 Jul 24]. In: StatPearls [Internet]. StatPearls Publishing; [cited 2025 Jan 22]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK542184/
- 12. Karussis D, Leker RR, Abramsky O. Cognitive dysfunction following thalamic stroke: a study of 16 cases and review of the literature. J Neurol Sci 2000;172:25-9.
- 13. Obayashi S. Cognitive and linguistic dysfunction after thalamic stroke and recovery process: possible mechanism. AIMS Neurosci 2021;9:1-11.
- 14. Jones EG. The thalamus. 2nd ed. Cambridge University Press; 2007.
- 15. Henriksen O, Petersen SI, Sorensen L. Right hemispatial neglect after thalamic stroke: a neuropsychological study. Brain Cognit 2015;93:34-40.
- 16. Chen XY, Wang Q, Wang X, Wong KS. Clinical features of thalamic stroke. Curr Treat Options Neurol 2017;19:5.
- 17. Schmahmann JD. Vascular syndromes of the thalamus. Stroke 2003;34:2264-78.
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