Anteromedian, Central, and Posterolateral Infarcts of the Thalamus

Carrera, Emmanuel; Michel, Patrik; Bogousslavsky, Julien

doi:10.1161/01.str.0000147039.49252.2f

Cited by 167 publications

(146 citation statements)

References 42 publications

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“…Arterial strokes will follow arterial distributions, while neoplasms are more inclined to circumscribe tissue planes. 2,4,11,15,27,45,58,70 Deep AVFs and deep venous thromboses produce T2/FLAIR hyperintensities centered within the bilateral anteromedial thalamic regions, though extensions beyond the thalami are reported in a significant number of cases. 5,18,21,22,76,77 In many instances, a definitive diagnosis for the thalamic dementia syndrome cannot be reached after history, physical examination, and MRI.…”

Section: Thalamic Dementia Syndrome: Differential Diagnosis and Workupmentioning

confidence: 99%

Dural arteriovenous fistula-induced thalamic dementia: report of 4 cases

Holekamp

Mollman

Murphy

et al. 2016

JNS

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Nonhemorrhagic neurological deficits are underrecognized symptoms of intracranial dural arteriovenous fistulas (dAVFs) having cortical venous drainage. These symptoms are the consequence of cortical venous hypertension and portend a clinical course with increased risk of neurological morbidity and mortality. One rarely documented and easily misinterpreted type of nonhemorrhagic neurological deficit is progressive dementia, which can result from venous hypertension in the cortex or in bilateral thalami. The latter, which is due to dAVF drainage into the deep venous system, is the less common of these 2 dementia syndromes. Herein, the authors report 4 cases of dAVF with venous drainage into the vein of Galen causing bithalamic edema and rapidly progressive dementia. Two patients were treated successfully with endovascular embolization, and the other 2 patients were treated successfully with endovascular embolization followed by surgery. The radiographic abnormalities and presenting symptoms rapidly resolved after dAVF obliteration in all 4 cases. Detailed descriptions of these 4 cases are presented along with a critical review of 15 previously reported cases. In our analysis of these 19 published cases, the following were emphasized: 1) the clinical and radiographic differences between dAVF-induced thalamic versus cortical dementia syndromes; 2) the differential diagnosis and necessary radiographic workup for patients presenting with a rapidly progressive thalamic dementia syndrome; 3) the frequency at which delays in diagnosis occurred and potentially dangerous and avoidable diagnostic procedures were used; and 4) the rapidity and completeness of symptom resolution following dAVF treatment.http://thejns.org/doi/abs/10.3171/2015.5.JNS15473Key words dural arteriovenous fistula; cortical venous hypertension; thalamic edema; nonhemorrhagic neurological deficit; thalamic dementia; vascular disorders ©AANS, 2016 davF-induced thalamic dementiaBorden-Shucart classification system-based not only on angiographic appearance but also mode of presentationto permit more accurate risk stratification and assist with clinical decision making for the type and timing of dAVF treatment (Table 1). 68,91One relatively underappreciated type of NHND is progressive dementia resulting from dAVF-induced cortical venous hypertension, though correct diagnosis and treatment is increasing, thanks to improved imaging techniques.18,79 Dural AVF-induced progressive dementia can be differentiated as either cortical or thalamic in origin-2 categories that have relatively distinct patterns of clinical symptomatology 18,54,62,80,85 and highly specific venous outflow patterns.18,80 Of the two, dAVFinduced thalamic dementia is less frequent, with only 15 published cases reported in the literature to date. All were individual case reports, and several lacked adequate clinical, radiographic, and/or treatment specifics to permit detailed assessment as to manner of presentation, underlying hemodynamic pathophysiology, and long-term outcome. 18,[21][22][23]...

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Section: Thalamic Dementia Syndrome: Differential Diagnosis and Workupmentioning

confidence: 99%

Dural arteriovenous fistula-induced thalamic dementia: report of 4 cases

Holekamp

Mollman

Murphy

et al. 2016

JNS

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“…Comparisons of when thalamic strokes do and do not induce amnesia have consistently found that damage to this tract is the best predictor of memory loss (Von Cramon et al 1985;Ghika-Schmid and Bogousslavsky 2000;Van der Werf et al 2000, 2003bCarrera et al 2004). One of these studies also linked recognition deficits to mammillothalamic tract damage ( Van der Werf et al 2003b).…”

Section: The Anterior Thalamic Nucleimentioning

confidence: 99%

“…A second patient was described with memory problems associated with pathology in the caudal intralaminar nuclei (e.g., including the center median nucleus and the parafascicular nucleus), but these problems appeared to be due to a loss of attention and increased distractibility (Mennemeier et al 1992). Problems with arousal and levels of awareness have since been further linked with damage to the intralaminar nuclei (Van der Werf et al 2002;Carrera et al 2004) but again could reflect disconnections due to white matter damage.…”

Section: Intralaminar and Midline Thalamic Nucleimentioning

confidence: 99%

Unraveling the contributions of the diencephalon to recognition memory: A review

Aggleton¹,

Dumont²,

Warburton³

2011

Learn. Mem.

137

111

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Both clinical investigations and studies with animals reveal nuclei within the diencephalon that are vital for recognition memory (the judgment of prior occurrence). This review seeks to identify these nuclei and to consider why they might be important for recognition memory. Despite the lack of clinical cases with circumscribed pathology within the diencephalon and apparent species differences, convergent evidence from a variety of sources implicates a subgroup of medial diencephalic nuclei. It is supposed that the key functional interactions of this subgroup of diencephalic nuclei are with the medial temporal lobe, the prefrontal cortex, and with cingulate regions. In addition, some of the clinical evidence most readily supports dual-process models of recognition, which assume two independent cognitive processes (recollective-based and familiarity-based) that combine to direct recognition judgments. From this array of information a "multi-effect multinuclei" model is proposed, in which the mammillary bodies and the anterior thalamic nuclei are of preeminent importance for recollective-based recognition. The medial dorsal thalamic nucleus is thought to contribute to familiarity-based recognition, but this nucleus, along with various midline and intralaminar thalamic nuclei, is also assumed to have broader, indirect effects upon both recollective-based and familiarity-based recognition.Clinical studies repeatedly show that diencephalic pathology can impair recognition memory. Even so, there is no agreed locus within the diencephalon responsible for this memory loss and, hence, no agreed mechanism to explain the impairment. The present review examines both clinical and animal findings, and from this information a multi-effect multi-nuclei (MEMN) model emerges to explain the contributions of the diencephalon to recognition memory.At the outset, it is necessary to refine the focus of this review and to define some of its principal terms. The diencephalon comprises the thalamus and hypothalamus but, as will be explained, only the more medial parts of the diencephalon will be considered in detail. Recognition memory refers to the ability to detect whether a stimulus (e.g., a word, face, picture, object, or sound) has previously been encountered. As a consequence, this review is not about item identification (sometimes also confusingly referred to as recognition). Likewise, conditions that have broad disruptive effects on cognition, e.g., dementia, will not be considered even though recognition is typically impaired. Distinctions will be made between "item recognition," where the task is to determine if an individual item is novel or familiar, and "associative recognition," where all the individual items being experienced are familiar, but their particular combination is novel. A further, distinct ability is "recency" discrimination-the ability to determine which of two familiar stimuli has been experienced more recently. Both studies of amnesia and electrophysiological recordings show how recency memory and recogniti...

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“…The vascular territory of the lesion suggests a cardiac source of embolism. [2][3][4] Lipomas are benign nonmyxomatous neoplasms of the heart that normally cause no symptoms and their diagnosis is often accidental. [5][6][7] They represent 10% of the overall cardiac tumor masses arising from cardiac tissue and they are most frequently located in the right atrium.…”

Section: Brief Communicationsmentioning

confidence: 99%

“…2,3 Its etiological relationship with stroke is not well established. We describe the case of a thalamic stroke probably caused by paradoxical embolism from a right atrial lipoma through a patent foramen ovale.…”

mentioning

confidence: 99%

Anterior Thalamic Infarction as Initial Manifestation of a Right Atrial Lipoma

Erro

Ajuria

Olaz

et al. 2009

Can. J. Neurol. Sci

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Cardiac tumors are an infrequent source of embolism to the brain in young adults. Myxomas are the most common among them and they are mainly located in the left atrium.1 Cardiac lipomas are a very rare benign neoplasm of the heart usually located in the right atrium.2,3 Its etiological relationship with stroke is not well established. We describe the case of a thalamic stroke probably caused by paradoxical embolism from a right atrial lipoma through a patent foramen ovale. CASE REPORTA 46-year-old male with mild hypertension, presented with speech and behavioral alterations first noticed on awakening without a previous Valsalva manoeuvre. On admission his blood pressure was 150/90 mm Hg, with a pulse of 70 beats/min and O 2 saturation of 97%. He was apyretic and cardiac and cervical auscultation was unremarkable. On neurologic examination, a non-fluent dysphasia with word finding difficulties, right facial paresis and a left Horner's syndrome was observed. He also presented mild right hemiparesis and myoclonic-dystonic movements in lower limbs (NIHSS 7). Cervical and Transcranial Doppler (TCD) were normal. Cranial computerized tomography was normal. A cranial magnetic resonance (MR) demonstrated on diffusion sequences the presence of an acute non-hemorrhagic infarction involving the anterior area of the left thalamus ( Figure 1A). Perfusion MR sequences and cerebral magnetic angioresonance were normal. The patient was admitted to the stroke unit. Conservative treatment was initiated. No arrhythmia was registered during hospitalization. Duplex sonography excluded atherosclerotic lesions in the carotid arteries. The next day, a right to left massive shunt was found on TCD bubble study ( Figure 1B). This test was performed using agitated saline as a contrast agent. Thrombophilic screening, neoplastic markers and autoimmune assays were negative. Transthoracic and transesophageal echocardiograms (TEE) were performed showing a mobile mass of homogeneous density attached to the free wall of the right atrium ( Figure 1C). No other cardioembolic lesions such as aortic plaques or dysfunctional left ventricle were found. The mass could be optimally assessed by cardiac MR as a well defined, slightly lobulated and homogeneous lesion, strongly hyperintense on T1 sequences, with low signal intensity on Fat-suppressed sequences (T2 STIR) and without contrast enhancement after gadolinium administration ( Figure 1D), highly suggestive of a lipoma. A patent foramen ovale (PFO) without associated aneurysmal septum could also be seen on TEE. The mass and the foramen ovale were surgically removed THE CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES 379

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Anteromedian, Central, and Posterolateral Infarcts of the Thalamus

Cited by 167 publications

References 42 publications

Dural arteriovenous fistula-induced thalamic dementia: report of 4 cases

Dural arteriovenous fistula-induced thalamic dementia: report of 4 cases

Unraveling the contributions of the diencephalon to recognition memory: A review

Anterior Thalamic Infarction as Initial Manifestation of a Right Atrial Lipoma

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