Vascular dementia by thalamic strategic infarct

Lanna, Maria Elisa de Oliveira; Madeira, D.; Alves, Gilberto Sousa; Alves, Carlos Eduardo; Valente, Letice; Laks, Jérson; Engelhardt, Eliasz

doi:10.1590/s0004-282x2008000300027

Cited by 10 publications

(9 citation statements)

References 19 publications

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“…In the clinical composition of the AM nuclei stroke, associated to hippocampal and frontal dysexecutive syndromes with impairment of abstraction and working memory (Tables 2 and 3), a Korsakoff syndrome of mild intensity was present which was characterized by confabulation, adding diencephalic dementia features to the syndrome [22], where the memory deficits were more expressive than the dysexecutive, associated with moderate to severe apathy and depression, reported in Lanna et al [49].…”

Section: Discussionmentioning

confidence: 82%

“…The manifestation of clinical amnesia is, inseparably, related to damage of the nuclei and intrathalamic bundles specific of connection with hippocampal region, of variable intensity, [19,22,25,26,39,44,[46][47][48][49] and differs from dysexecutive symptoms with deficits of abstraction, planning, organization and sequencing of tasks, which may be present due to interruption of any level of direct thalamus-frontal connections [4,18,22,23], including lesions of the anterior nuclei territory, it is believed, which save the MTT, a rare condition without amnesia, found by Línek et al [46] in the stroke in this territory.…”

Section: Discussionmentioning

confidence: 99%

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Cognitive disconnective syndrome by single strategic strokes in vascular dementia

Lanna¹,

Alves

Sudo

et al. 2012

Journal of the Neurological Sciences

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Section: Discussionmentioning

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Cognitive disconnective syndrome by single strategic strokes in vascular dementia

Lanna¹,

Alves

Sudo

et al. 2012

Journal of the Neurological Sciences

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“…Cerebral infarction is typically caused by occlusion of arterioles and consequent acute ischemia. If the lesion is located in regions responsible for cognitive function, such as the frontal lobe and thalamus, it will induce a “strategic” infarct, leading to cognitive dysfunction (Lanna et al, 2008). …”

Section: Vascular Pathophysiology Underlying Vcid—how Does Vasculamentioning

confidence: 99%

The impact of cerebrovascular aging on vascular cognitive impairment and dementia

Yang

Sun

et al. 2017

Ageing Research Reviews

153

128

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As human life expectancy rises, the aged population will increase. Aging is accompanied by changes in tissue structure, often resulting in functional decline. For example, aging within blood vessels contributes to a decrease in blood flow to important organs, potentially leading to organ atrophy and loss of function. In the central nervous system, cerebral vascular aging can lead to loss of the integrity of the blood-brain barrier, eventually resulting in cognitive and sensorimotor decline. One of the major of types of cognitive dysfunction due to chronic cerebral hypoperfusion is vascular cognitive impairment and dementia (VCID). In spite of recent progress in clinical and experimental VCID research, our understanding of vascular contributions to the pathogenesis of VCID is still very limited. In this review, we summarize recent findings on VCID, with a focus on vascular age-related pathologies and their contribution to the development of this condition.

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“…In the context of dAVFs, the hallmarks of the symptom complex-deficits in executive function, memory, learning, attention, disinhibition, and confabulation-correspond best to the anteromedial and central thalamic regions. 12,20,21,38,43,51,56,59,62,65,74,85 Sensory and motor symptoms typically ascribed to posterolateral and inferior thalamic distributions tend to be uncommon or absent in patients with dAVFs. The term thalamic dementia syndrome has also been applied to patients having similar symptoms related to other pathological conditions affecting the thalami, including deep venous system thrombosis, bilateral diencephalic tumors, viral and prion diseases, osmotic myelinolysis, and toxic insults (see Table 4).…”

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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Vascular dementia by thalamic strategic infarct

Cited by 10 publications

References 19 publications

Cognitive disconnective syndrome by single strategic strokes in vascular dementia

Cognitive disconnective syndrome by single strategic strokes in vascular dementia

The impact of cerebrovascular aging on vascular cognitive impairment and dementia

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

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