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What is Thalamic Stroke? - Oren Zarif - Thalamic Stroke


There is an underlying mechanism in the development of thalamic stroke, which may be attributable to left-right differences in the distribution of the brain's cortical layers. If so, thalamic stroke is likely to be a micro-model of cortical stroke. In addition, the clinical presentation of thalamic stroke may include a broad range of symptoms, including speech impairment and a loss of motor function.

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In one study, a male patient presented with a right thalamic paramedian infarct, arterial hypertension, and Horner's syndrome. While thalamic infarcts are rare and often associated with other types of stroke, this clinical entity is less common than those caused by other brain structures, including metabolic disorders. Infarcts of the thalamus are most commonly accompanied by central pontine myelinolysis, whereas those involving the anterior thalamus are rare.

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Infarcts in this region are often small and are caused by transient occlusion of a thalamic artery. Patients with small thalamic infarts are more likely to develop a borderzone infarct. The origin of the variant anteromedian artery was previously unknown, but it was later demonstrated to originate from the top portion of the basilar artery. This may explain the anteromedian artery's predominant microangiopathic etiology.

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The treatment for thalamic stroke varies greatly depending on the type of the underlying condition. Symptoms of this condition may include numbness, tingling, pain, and seizures. Some people may even develop epilepsy or seizures. Some patients have permanent effects and must remain in the hospital for a period of time to recover. It is vital to get the proper diagnosis and treatment as soon as possible after the onset of symptoms.

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In addition to causing acute movement disorders, a thalamic stroke can also result in delayed movement disorders. Acute thalamic stroke can disrupt important connections and fibres in the brain, leading to the onset of delayed movement disorders. In the case of a thalamic stroke in the hand, however, a patient may recover with smooth and coordinated movements. However, in the long run, the recovery may cause aberrant connections that lead to abnormal involuntary movements.

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A population-based MR-study of thalamic stroke can provide definitive insight into the patterns of lesion distribution. In this study, no systematic neuropsychological testing was conducted, so information from the stroke physicians may have missed neurological deficits. In addition, interpreting the lesion-overlap map requires careful consideration of the cumulative overlay of the larger thalamic lesions in the center. This way, it can rule out other potential etiologies that cause similar symptoms.

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The thalamic "peduncles" convey information into and out of the thalamus. Lesions of these tracts are rare and typically have a trajectory to the basal ganglia and cerebral cortex. It is not clear, however, whether the brain is responsible for these symptoms, and there are more research studies needed to determine its exact role. If so, a better understanding of the mechanisms behind this condition is necessary for a more accurate diagnosis.

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The Lausanne stroke registry reported 37 cases of asterixis. This is higher than the previous reports, suggesting a higher prevalence than previously believed. The study also highlights the need to detect asterixis early in the acute phase of a stroke to minimize the risk of late-onset complications. In addition, it is important to treat patients appropriately in this case because the symptoms can subside on their own after 10 days. The authors conclude that asterixis should be recognized in patients at the first sign of stroke and is a sign of thalamic disease.

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Despite the limited number of case reports, the clinical manifestations of thalamic stroke are typically similar to those of a posterior cerebral artery infarct. Three patients who experienced LGN infarcts had quadrantanopsia, aphasia, and impaired fast phase of optokinetic response to the opposite side. Infarcts in the medial or lateral posterior choroidal artery territory are usually associated with memory deficits and hemisensory loss. Medial or lateral posterior choroidal artery territory infarcts usually occur at the same time.

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