In right-handed individuals, aphasia resulting from right hemisphere damage is termed crossed aphasia and has a very low occurrence rate. Additionally, aphasia due to thalamic lesions often involves hemorrhage, with infarction cases less frequently reported. We present the case of an 81-year-old right-handed female who developed aphasia due to a right thalamic infarction. She exhibited characteristics typical of thalamic aphasia observed in left thalamic lesions. Furthermore, jargon agraphia manifested during writing tasks. This may suggest disinhibition of the left hemisphere writing motor memory by the right hemisphere language function.

BACKGROUND: Patients with thalamic infarction experience abnormal blockages of multinucleated vessels, affecting the body and thereby the thalamus. Most patients with thalamic infarction have an adverse prognosis, which seriously affects their safety. Therefore, it is essential to analyze the independent risk factors that influence the prognosis of patients with thalamic infarction and develop corresponding preventive measures.
OBJECTIVE: To explore the effect of non-high-density lipoprotein cholesterol (non-HDL-C) and Homocysteine (Hcy) levels in cognitive impairment in thalamic infarction.
METHODS: From March 2019 to March 2022, 80 patients with thalamic infarction were divided into a group with cognitive impairment [Montreal Cognitive Assessment (MoCA) score < 26; 35 patients] and a group with normal cognitive function (MoCA score of 26-30; 45 patients) according to the MoCA score. In addition, 50 healthy people in the same period were selected as the control group. A correlation between the non-HDL-C and Hcy levels and the MoCA score and receiver operating characteristic curve was observed, and the serum non-HDL-C and Hcy levels were analyzed for the diagnosis of cognitive impairment in patients with thalamic infarction. According to the Modified Rankin Scale (MRS) score, 80 patients with thalamic infarction were divided into a good prognosis group (MRS score ≤ 2) and a poor prognosis group (MRS score >2).
RESULTS: The non-HDL-C and Hcy levels were significantly higher in the group with cognitive impairment than in the group with normal cognitive function (P < 0.05). There was no significant difference in the non-HDL-C level between the control group and the group with normal cognitive function (P > 0.05). The MoCA scores of the group with cognitive impairment were significantly lower than those of the group with normal cognitive function and the control group (P < 0.05). There was a significant difference between the control group and the group with normal cognitive function (P < 0.05). The non-HDL-C and Hcy levels were correlated with the MoCA score (P < 0.05), cognitive impairment [areas under the curve (AUC) = 0.709, 95% confidence interval (95%CI): 0.599-0.816], the non-HDL-C level, and could predict cognitive impairment in patients with thalamic infarction (AUC = 0.738, 95%CI: 0.618-0.859). Hcy combined with non-HDL-C levels can predict cognitive impairment in patients with thalamic infarction (AUC = 0.769, 95%CI: 0.721-0.895).There were 50 patients in the good prognosis group and 30 patients in the poor prognosis group. Compared with the good prognosis group, in the poor prognosis group, the National Institutes of Health Stroke Scale (NIHSS) score, non-HDL-C level, Hcy level, large-area cerebral infarction, atrial fibrillation, and activated partial prothrombin time were statistically significant (P < 0.05). The non-HDL-C level, the Hcy level, the NIHSS score, extensive cerebral serum, and atrial fibrillation may all be independent risk factors for poor prognosis in patients with thalamic infarction (P < 0.05).
CONCLUSIONS: Non-HDL-C and Hcy levels are positively correlated with cognitive impairment in patients with thalamic infarction. Non-HDL-C and Hcy levels can be used in the diagnosis of cognitive impairment in patients with thalamic infarction, and the combined detection effect is better. The main factors affecting the prognosis of patients with thalamic infarction are the non-HDL-C level, the Hcy level, the NIHSS score, large-area cerebral infarction, and atrial fibrillation. Clinically, corresponding preventive measures can be formulated based on the above factors to prevent poor prognosis and reduce mortality.

A 62-year-old Japanese man with a history of smoking, hypertension and paroxysmal atrial fibrillation presented sudden-onset disturbance of consciousness. He had a fluctuating consciousness, transient apnea, and vertical gaze palsy. Brain diffusion-weighted MRI showed hyperintense signals in the rostral midbrain and bilateral paramedian thalami, and the diagnosis of midbrain and bilateral thalamic infarction was made. The midbrain lesion corresponded with midbrain V sign, a characteristic finding of this infarction. Although there are several other deseases causing bilateral thalamic lesion, this sign is very helpful in distinguishing the disease from others. On the other hand, CT angiography visualized another variant of thalamoperforating arteries instead of Artery of Percheron (AOP), the common variant in bilateral thalamic infarction. This case indicates that other anatomical variants of thalamoperforating arteris besides AOP could cause this infarction.

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.

Transient global amnesia (TGA) can be caused by medications, ischemia, metabolic abnormalities, and seizures. We describe two cases of TGA following coil embolization for a basilar-tip aneurysm. A 73-year-old woman developed transient acute anterograde amnesia after coil embolization for a basilar-tip aneurysm. Diffusion-weighted imaging (DWI) revealed an ischemic lesion in the anterior nucleus of the thalamus. A 67-year-old woman developed transient acute amnesia after a stent-assisted coil embolization of a basilar-tip aneurysm. A DWI showed ischemic lesions in the anterior nucleus of the thalamus. Any ischemic changes to areas of the anterior nucleus that are fed by the thalamoperforating and premammillary arteries should be considered in a differential diagnosis for TGA in patients who have undergone coil embolization for a posterior circulation cerebral aneurysm.

BACKGROUND: Hemichorea usually results from vascular lesions of the basal ganglia. Most often, the lesion is contralateral to the affected limb but rarely, it may be ipsilateral. The pathophysiology of ipsilateral hemichorea is still poorly understood. We review the literature on hemichorea due to ipsilateral cerebral infarction and explore possible mechanisms for its occurrence.
METHODS: A 72-year-old woman presented with complaints of involuntary movements of the muscles of the left side of the face and mild weakness of the right limbs. Her symptoms had started suddenly 1 d earlier. After admission to the hospital, the involuntary movements spread to involve the left limbs also. Magnetic resonance imaging revealed a left thalamic infarction. The patient\'s hemichorea subsided after treatment with haloperidol (2 mg per time, 3 times/d) for 3 d; the hemiparesis resolved with rehabilitation physiotherapy. She is presently symptom free and on treatment for prevention of secondary stroke. We review the literature on the occurrence of ipsilateral hemichorea following thalamic infarction and discuss the possible pathomechanisms of this unusual presentation.
CONCLUSIONS: Ipsilateral hemichorea following a thalamic stroke is rare but it can be explained by structure of the extrapyramidal system. The thalamus is a relay station that exerts a bilateral control of motor function.

Occlusion of the artery of Percheron (AoP) causes bithalamic paramedian infarct (BTPI). Although it can be diagnosed easily in its pure form, it can be underdiagnosed in cases with concomitant extrathalamic acute infarcts (plus-BTPI) as it may be difficult to determine whether BTPI is due to occlusion of AoP or two different paramedian arteries even with conventional angiography. This study was performed to highlight plus-BTPI that could result from occlusion of AoP rather than of two distinct paramedian arteries using topographic evaluation of bithalamic infarcts. We retrospectively reviewed imaging and clinical databases for patients admitted to radiology department between 2013 and 2019. Two radiologists independently evaluated the results of imaging studies, and findings reached by consensus were used in the analysis. This retrospective review yielded 34 patients with bithalamic infarct. Each affected thalamic vascular region was investigated separately. Any patient could have more than 2 different vascular zone infarct. The affected thalamic vascular territories were paramedian (n = 24), inferolateral (n = 13), anterior (n = 10), and posterior (n = 7). When we evaluated bithalamic infarcts in terms of symmetrically affected territories, the distribution of symmetric affected territories was as: paramedian (n = 18), inferolateral (n = 2), anterior (n = 1), and posterior (n = 1). BTPI had a 4.5-fold higher frequency than the sum of symmetric involvement of other territories (p = 0.0552, OR = 4.5,95%CI 0.93-21.5). In addition, mesencephalic involvement was only observed in BTPI, and not in other patterns (p < 0.001). The fact that in bilateral thalamic infarcts the symmetric involvement of paramedic territory is significantly higher and mesencephalic involvement is seen only in BTPI can suggest that plus-BPTI may develop due to AoP occlusion rather than occlusion of two distinct paramedian arteries.

BACKGROUND: Thalamic blood supply consists of four major vascular territories. Out of them paramedian arteries supply ipsilateral paramedian thalami and occasionally rostral mid brain. Rarely both paramedian arteries arise from a common trunk that arise from P1 segment of one sided posterior cerebral artery (PCA). This is usually due to hypoplastic or absent other P1 and this common trunk is termed Artery of Percheron (AOP). Its prevalence is in the range of 7-11% among the general population and AOP infarcts account in an average of 0.4-0.5% of ischemic strokes. Clinical presentation of AOP infarction is characterized by impaired arousal and memory, language impairment and vertical gaze palsy. It also can present with cerebellar signs, hemi paresis and hemi sensory loss. We herein present a case of AOP infarction presenting as transient loss of consciousness and nuclear third nerve palsy.
METHODS: A 51 year old previously healthy male, was brought to us, with a Glasgow coma scale (GCS) of 7/15. GCS improved to 11/15 by the next day, however he had a persisting expressive aphasia. Right sided nuclear third nerve palsy was apparent with the improvement of GCS. He did not have pyramidal or cerebellar signs. Thrombolysis was not offered as the therapeutic window was exceeded by the time of diagnosis. Diagnosis was made using magnetic resonance imaging (MRI) that was done after the initial normal non-contrast computer tomography (NCCT) brain. He was enrolled in stroke rehabilitation. Aspirin and atorvastatin was started for the secondary prevention of stroke. He achieved independency of advanced daily living by 1 month, however could not achieve full recovery to be employed as a taxi driver.
CONCLUSIONS: Because of the rarity and varied clinical presentation with altered levels of consciousness, AOP infarcts are easily overlooked as a stroke leading to delayed diagnosis. Timely diagnosis can prevent unnecessary investigations and the patient will be benefitted by early revascularization. As it is seldom reported, case reports remain a valuable source of improving awareness among physicians about this clinical entity.

UNASSIGNED: Some complications associated with cisternal drainage have been reported; however, there are few reports on direct vascular injury caused by cisternal drain. We experienced two rare cases of thalamic infarction caused by cisternal drain placement during open clipping for a ruptured anterior communicating artery (AcomA) aneurysm through an anterior interhemispheric approach.
UNASSIGNED: Two cases of ruptured AcomA aneurysm were treated by surgical clipping through an anterior interhemispheric approach, and then a cisternal drain was inserted from opticocarotid space toward prepontine cistern. Postoperatively, the magnetic resonance imaging showed unilateral anterior-medial thalamic infarction in both two cases. By reviewing the postoperative computed tomography and digital subtraction angiography, it was suspected that the cisternal drain, which was inserted slightly deep, obstructed the P1 perforator because of an anatomical variation involving a lowered basilar bifurcation and caused postoperative unilateral paramedian thalamic infarction.
UNASSIGNED: To avoid these complications, neurosurgeons should consider the potential for P1 perforator injury related to cisternal drain placement.

One uncommon type of ischemic stroke is occlusion of the artery of Percheron (AOP) leading to infarction of the paramedian thalami and mesencephalon. There are several variants of thalamic blood supply, and identifying the potential presence and infarction of an AOP is important in diagnosis and treatment of ischemic strokes affecting the thalami and mesencephalon, especially because of the unusual and variable presentation of these forms of ischemic strokes. This short review includes and discusses the case of a 58-year-old woman with an AOP infarct and indicates the importance of recognizing an AOP infarct early despite its clinical variations in order to treat the stroke in a timely fashion. This short review also includes a discussion of imaging modalities in such cases and clinical differential diagnoses to consider with management strategies.