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  • Writer's pictureOren Zarif

Thalamic Infarction - Oren Zarif - Thalamic Stroke

A recent study investigated the effects of medial thalamic lesions on recollection and familiarity in the ischemic brain. Twenty-five healthy individuals were matched to twelve patients who had suffered a left hemisphere stroke. Three experiments measured familiarity and recollection in each group. The lesion locations were quantified in order to evaluate the dual process thalamic models proposed by Aggleton. The dual process model predicts that lesions in the MTT would result in impairment in familiarity.

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The distribution pattern of thalamic stroke is difficult to categorize. However, there are several topographic patterns. Each symptom has a unique etiology and manifestation. In the case of thalamic stroke, each of these two patterns is indicative of a distinct etiology. The corresponding lesion map should be interpreted accordingly. For instance, a lesion overlapping map should consider the cumulative overlap of all large lesions in the center of the thalamus.

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The right tuberothalamic artery may be involved in the right thalamic infarction. In a similar study, the ventral amygdalofugal pathway links the amygdala with the medial thalamic nucleus. Despite the lack of direct evidence to suggest a thalamic artery involvement, a patient with symptoms of thalamic stroke may have been affected by the artery of Percheron.

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Treatment after thalamic stroke is focused on regaining ability as quickly as possible and reducing the risk of another stroke. Rehabilitation includes physical therapy, occupational therapy, and speech therapy. Recovery time varies, but recovery is possible for many patients. It may take weeks or months to fully recover from a thalamic stroke. Survivors may have some permanent symptoms. If you or someone you know has suffered from thalamic stroke, make sure you seek medical attention immediately.

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While thalamic vascular supplies have been described in previous studies, little information has been published on the long-term outcome of thalamic infarcts. To address this problem, researchers in China evaluated thamic infarcts using cerebral CTA and MRA. The authors concluded that the arteries that supply the thalamus were mostly derived from the PCA. The patients with thalamic infarcts had shorter OTD compared to patients without this arterial artery. The majority of patients recovered with only mild sensory impairment, while some died.

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Neuropsychological deficits after thalamic infarction of the posterior choroidal artery were also limited. One study from the Lausanne group reported quadrantanopsia in three patients with LGN infarcts. The patients also had a poor fast phase of optokinetic response in the opposite hemibody. Patients with medial thalamic infarcts showed impaired memory and anosognosia.

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This patient presented with altered mental status, but MRI results were negative. He had improved by the time a lumbar puncture was scheduled. A thalamic MRI revealed infarcts in both thalami. Moreover, his MRI revealed that he had bilateral thalamic infarcts, despite a previous negative diagnosis of a left thalamic stroke. This case demonstrates that a CT scan is a sensitive tool for detecting a thalamic variant.

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A thalamic infarction may occur when a thalamic lesion is a significant cause of vascular syndromes. However, other types of lesions affect different areas of the brain, and a thalamic lesion may have unintended consequences on these systems. These lesions can result in ataxia, sensory loss, or a disorder of the inferolateral artery. The symptoms may vary from person to person.

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While the occurrence of left hemispheric thalamic stroke is on the rise, more patients than right hemispheric thalamus lesions are admitted to hospitals. In fact, the frequency of left hemispheric infarcts is 1.9 times higher than in right hemispheric lesions. The lesion map of the thalamic infarcts shows asymmetric relationships in anteromedian thalamic vascular territories. Left-sided thalamic lesions also occur frequently with neuropsychological symptoms. However, lacunar syndromes were not associated with left-sided ITS lesions.

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Intralaminar nuclei of the thalamus are involved in motivation and arousal. Their connectivity patterns are similar in both the MD and the fronto-orbital cortex. An interruption of these circuits may cause disconnection between the posterior orbital cortex and the anterior cingulated gyrus. The ventral amygdalofugal pathway is also connected to the MD. Its loss may cause amnesia and emotional dysregulation.

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