Symptoms of a Thalamic Stroke - Oren Zarif - Thalamic Stroke

Patients can develop a variety of symptoms after a thalamic stroke. The symptoms can start with impaired sensation and progress to chronic pain and thermal dysregulation. Ultimately, the goal of treatment is to reestablish normal function and reduce the chance of future strokes. Rehabilitation focuses on increasing mobility, improving speech, and addressing occupational health issues. While the outlook for patients with a thalamic stroke varies significantly, recovery is possible for many.

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A recent study examined the impact of thalamic lesions on verbal memory and recollective recognition in patients with a unilateral ischemic thalamic stroke. The patients' symptoms were noted in three stages, involving identification of the lesion, projection of that lesion to axial sections in a Morel atlas, and the evaluation of the extent of the damage. The findings of the study are consistent with previous reports of similar brain lesions.

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A patient with a thalamic infarct presented with symptoms that included numbness, tingling, and pain on his right side. He presented with a right thalamic paramedian infarct and arterial hypertension. Symptoms of thalamic infarct can also be caused by other structural lesions, or metabolic disorders. Patients with a thalamic infarct also commonly have a central pontine myelinolysis and Wernicke encephalopathy.

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In the human literature, thalamic lesions in the left hemisphere affect recollection and familiarity. The researchers measured recollection using high-resolution structural MRI, and found that patients with left thalamic stroke had poor recollection but sparse familiarity. The lesion locations were quantified in order to evaluate the dual process thalamic models proposed by Aggleton. If the MD is damaged, this may impair recollection, and the same is true for the MTT.

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A thalamic lesion can also extend into the anterior pulvinar nucleus, resulting in CPSP. Montes et al. also described cases in which thalamic lesions extended into the anterior pulvinar nucleus after the hemiplegic lesion. Although the exact causes of CPSP are unknown, the most likely explanation is that the lesion in the anterior thalamic nucleus affects the brain's ability to detect pain.

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Anatomical and functional analyses were used to identify patients with an increased risk of developing thalamic pain after a thalamic stroke. The morphological and functional methods employed here are easy to reproduce. They are also not difficult to add to a routine patient workup. The findings have been replicated in other studies. A similar approach can be used to identify patients who are at a higher risk of developing thalamic pain.

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Infarcts in the thalamus were identified on computed tomography (CT) perfusion scans. These scans were useful in detecting acute ischemic stroke in the posterior circulation of the brain. A sagittal MRI with dynamic susceptibility contrast perfusion imaging can also detect cross cerebellar diaschisis. MRI can also identify thalamic infarcts.

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Several other studies have explored thalamic infarction and the prognosis after it. Others have studied vascular and functional changes in the thalamus. Powell R. Hughes and Duru AD have studied the anatomy of thalamic stroke and the thalamus. They concluded that there is no cure for thalamic stroke, but advances in stroke treatment have enabled many people to regain full function of their lives.

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The thalamus is the "micro-model" of the brain cortex and is crucial for language, memory, and language processing. Consequently, strokes in the thalamus are often asymmetric. This asymmetry explains why more people with a dominant-hemispheric stroke are admitted to hospital. In fact, the asymmetric nature of the thalamus' structure-function relationships is also responsible for the increased rates of recovery after a thalamic stroke.

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Aside from the thalamic infarction itself, some researchers have also noted the presence of other types of cognitive dysfunction in patients with a thalamic infarction. Although a thalamic infarction can result in a general amnesic syndrome, it can also be associated with severe memory disturbance or material-specific memory deficits. The latter can also involve frontal-thalamic functional systems.