Lateral Thalamic Infarcts

773

589

Background-This article reviews the anatomy, connections, and functions of the thalamic nuclei, their vascular supply, and the clinical syndromes that result from thalamic infarction. Summary of Review-Thalamic nuclei are composed of 5 major functional classes: reticular and intralaminar nuclei that subserve arousal and nociception; sensory nuclei in all major domains; effector nuclei concerned with motor function and aspects of language; associative nuclei that participate in high-level cognitive functions; and limbic nuclei concerned with mood and motivation. Vascular lesions destroy these nuclei in different combinations and produce sensorimotor and behavioral syndromes depending on which nuclei are involved. Tuberothalamic territory strokes produce impairments of arousal and orientation, learning and memory, personality, and executive function; superimposition of temporally unrelated information; and emotional facial paresis. Paramedian infarcts cause decreased arousal, particularly if the lesion is bilateral, and impaired learning and memory. Autobiographical memory impairment and executive failure result from lesions in either of these vascular territories. Language deficits result from left paramedian lesions and from left tuberothalamic lesions that include the ventrolateral nucleus. Right thalamic lesions in both these vascular territories produce visual-spatial deficits, including hemispatial neglect. Inferolateral territory strokes produce contralateral hemisensory loss, hemiparesis and hemiataxia, and pain syndromes that are more common after right thalamic lesions. Posterior choroidal lesions result in visual field deficits, variable sensory loss, weakness, dystonia, tremors, and occasionally amnesia and language impairment. Conclusions-These vascular syndromes reflect the reciprocal cerebral cortical-thalamic connections that have been interrupted and provide insights into the functional properties of the thalamus.

Section: Inferolateral Artery Infarctionmentioning

confidence: 62%

Section: Inferolateral Artery Infarctionmentioning

confidence: 99%

Section: Thalamic Blood Supply and Vascular Syndromesmentioning

confidence: 99%

See 1 more Smart Citation

Vascular Syndromes of the Thalamus

Schmahmann

2003

773

589

“…29 Later clinicians clarified the clinical findings in patients with pontine infarction related to basilar artery occlusion 30 ; patients with cerebellar infarction at various loci in the cerebellum [31][32][33][34][35] ; midbrain, thalamic, and occipital and temporal lobe infarction in patients with embolism to the "top-of-the-basilar" artery 35,36 ; and patients with small localized infarcts in the pons, medulla, and thalamus caused by disease of the penetrating artery supply. 35,[37][38][39][40][41][42][43][44][45][46] …”

Section: Clinicoanatomic Correlationsmentioning

confidence: 99%

Posterior Circulation Ischemia: Then, Now, and Tomorrow

Caplan

2000

173

103

know and appreciate where we are now and where we are going in the future, it is essential to know where we have been. We cannot afford to relive and repeat the history of stroke every several decades. Posterior circulation stroke represents a microcosm of stroke in general. In this presentation I first review the development of ideas regarding brain and posterior circulation ischemia and its recognition and treatment. I then share some recent data from a large prospective registry of patients with posterior circulation ischemia. Finally, I look ahead to reflect on what I believe should be the future directions for research and for the care of patients with posterior circulation disease.Patients who present to physicians and hospitals with symptoms that suggest posterior circulation ischemia are handled differently from patients who have symptoms that suggest anterior circulation disease in the great majority of medical facilities in the United States and in the world. A patient who has an attack of dizziness with diplopia and ataxic gait usually has a brain image but seldom has vascular or cardiac investigations. A diagnosis of "vertebrobasilar insufficiency" (VBI) is often made, and physicians then debate whether or not to treat with warfarin-type anticoagulants, and, if so, for how long and at what intensity. In contrast, a patient who has right-hand weakness and aphasia is usually evaluated and treated quite differently at the very same facilities. Brain imaging, cardiac investigations, noninvasive vascular tests of the carotid and intracranial anterior circulation with the use of extracranial and transcranial ultrasound and/or MR angiography (MRA) and CT angiography, and catheter angiography are often pursued, depending on the local technological capabilities and experience of the treating physicians. An effort is made to identify the etiology and mechanism of the ischemia. Treatment is then chosen among a variety of possibilities (including carotid artery surgery, angioplasty, anticoagulants, and antiplatelet aggregants) depending on the nature, location, and severity of the occlusive disease and the mechanism of ischemia.Why should anterior and posterior circulation ischemia be handled so differently? Does this schizophrenic approach make sense? After all, the internal carotid artery and its branches and the vertebral (VA) and basilar arteries (BA) and their branches are just a few inches apart; they are made of the same coats and look the same under the microscope except for size. These vessels carry the same blood under the same blood pressure. The diseases that affect the blood vessels in the 2 circulations are the same. Do stroke mechanisms really differ between the 2 circulations? How did this differing approach originate, and does it continue to make sense today? These are some questions that I will attempt to answer as I review the development of ideas about posterior circulation ischemia and as I report recent data. Development of IdeasHerein I review how knowledge about the posterior circulation ...

“…10 - 15 We describe 23 cases of hypesthetic ataxic hemiparesis with CT-or MRI-documented infarct in the posterior limb of the internal capsule. Special attention is superiorly to the level of the body of the lateral ventricle constituted the most common pattern, present in nine patients (8)(9)(10)(11)(12)(13)(14)16, and 18) ( Figure 1, Table 1). Eight patients (5-7, 15, 17, 19, 21, and 23) had abnormalities confined to the posterior two thirds of the posterior limb of the internal capsule without visible superior extension.…”

mentioning

confidence: 99%

Capsular hypesthetic ataxic hemiparesis.

Helgason

Wilbur

1990

Twenty-three patients with hypesthetic ataxic hemiparesis underwent computed tomography or magnetic resonance imaging. Twenty-two patients had infarcts of lacunar or slightly larger size in the contralateral posterior limb of the internal capsule. In 15 patients the infarct extended superiorly into the adjacent paraventricular region, and in seven it extended into the lateral thalmus. In eight patients the infarct was limited to the posterior limb of the internal capsule, and in only two patients was an ipsilateral to capsular pontine lacune found. Despite a location similar to that of pure motor and pure sensory lacunar stroke, hypesthetic ataxic hemiparesis correlates with larger infarcts, most often located in the posterior medial superior territory of the antierior choroidal artery. Some infarcts appeared to be localized immediately posterolateral to this region, in the posterior cerebral artery territory. The presence and extent of infarction is better detected by the addition of magnetic resonance imaging to computed tomography. (Stroke 1990;21:24-33)