Bilateral thalamic glioma: case report

Hirano, Hirofumi; Yokoyama, Shunichi; Nakayama, Masaki; Nagata, Seiki; Kuratsu, Jun Ichi

doi:10.1007/s002340000380

Cited by 27 publications

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“…We believe that the rapid progressive dementia in our patient was secondary to the involvement of the dorsomedial thalamic nuclei and their connections with the temporal and frontal lobes, as described by Hirano and Kouyialis (8,10).…”

Section: █ Discussionsupporting

confidence: 61%

“…By performing an extensive review of the literature and updating the already presented series (2,8,21), we can state that a total of 59 cases have been published to the best of our knowledge (excluding the present case).…”

Section: █ Discussionmentioning

confidence: 78%

“…Symptoms mainly comprise mental deterioration, personality changes, and apathy, rather than focal neurological signs (17,21). This is not the case of pediatric patients who rarely present with personality disorders even in the case of large tumors (4,8).…”

Section: █ Discussionmentioning

confidence: 99%

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Bilateral thalamic glioma - case report and review

Bălaşa¹,

Balasa²,

Egyed-Zsigmond³

et al. 2014

Turkish Neurosurgery

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diagnosis reported as 3 years in patients with grade II BLTG (2,10).We present the case of a BLTG manifesting with fast progressive cognitive dysfunction leading to dementia in an elderly patient. █ CASE REpORTA 72-year-old right handed male, treated only for essential arterial hypertension stage I, presented 3 months prior to admittance, with gradual deterioration of the cognitive functions and intermittently aggressive behavior towards close relatives. The symptoms progressed gradually, with the patient not being able to perform basic everyday tasks and presenting periods of extreme agitation. █ INTRODUCTIONPrimary thalamic gliomas are rare and have been presented in recent reports with an incidence of 0.84-5.2% among all intracranial tumors (2,4,15,18).Bilateral thalamic gliomas (BLTG) constitute a unique intracranial tumoral pathology typically manifested by varying degrees of personality disorder. The rate of BLTG is much lower than that of unilateral thalamic glioma and cannot be objectively expressed in any way at present (4-7,13).Imaging in BLTG is typical and reveals large tumors with symmetrical and strictly limited involvement of bilateral thalami, without any apparent connecting tumoral tissue (2).The prognosis of BLTG is poor and a rapid fatal evolution has been observed (14) with the longest period of survival after the Bilateral thalamic glioma is extremely rare and the incidence cannot be adequately expressed. We present the case of a 72 years old male suffering from the rapid deterioration of cognitive function to moderately severe dementia in a short period of time. Magnetic resonance studies demonstrated a bilateral thalamic glioma with a minimal focal gadolinium uptake in the left thalamus. Biopsy was performed and pathology report was of anaplastic astrocytoma, WHO grade III. Radiotherapy was proposed but was rejected by the patient's relatives. The patient deceased 57 days later. We performed an extensive review of the literature and by updating the previous described series we can state that to the best of our knowledge this is the 60th case described in the literature and the second eldest patient presented. Patients suffering from this disease present a poor prognosis, the longest survival described being of 3 years in patients diagnosed with grade II bilateral thalamic glioma. Adjuvant therapy in form of radiotherapy to the thalami is most commonly used but the benefits are unclear. The natural progression of WHO grade III bilateral thalamic glioma left untreated, as can be seen from our case, has an even poorer outcome.

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Section: █ Discussionsupporting

confidence: 61%

Section: █ Discussionmentioning

confidence: 78%

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Bilateral thalamic glioma - case report and review

Bălaşa¹,

Balasa²,

Egyed-Zsigmond³

et al. 2014

Turkish Neurosurgery

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“…The presence of diffusion restriction most strongly suggests arterial stroke, toxicity, infection, or, to a lesser degree, lymphoma or deep venous thrombosis. 1,2,4, [25][26][27]35,39,42,45,50,57,60,70,90 Conversely, diffusion restriction has not been found in patients with dAVF-induced thalamic dementia. Strong gadolinium enhancement is most consistent with a high-grade neoplasm; 26,27,58 however, other conditions including dAVFs can also have some degree of gadolinium enhancement.…”

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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“…[4][5][6]10,11,15) The patients were nine men and seven women aged from 8 to 70 years (mean 39 years). Principal symptoms included personality change, confusion, memory loss, apathy, emotional lability, and dementia.…”

Section: Discussionmentioning

confidence: 99%

Bilateral Thalamic Glioma. Case Report.

Uchino

Kitajima

Miyazaki

et al. 2002

Neurol. Med. Chir.(Tokyo)

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A 35-year-old woman presented with a bilateral thalamic glioma manifesting as dysesthesia over the left side of the body and mental deterioration. T 1 -weighted magnetic resonance imaging revealed enlarged bilateral thalami with homogeneous isointensity and no enhancement after gadolinium administration. Histological examination of a stereotactic biopsy specimen identified anaplastic astrocytoma. Radiotherapy and chemotherapy failed to arrest tumor growth. She subsequently died. Magnetic resonance imaging and clinical findings support the view that bilateral thalamic gliomas represent a distinct clinicopathologic entity among thalamic tumors.

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Bilateral thalamic glioma: case report

Cited by 27 publications

References 0 publications

Bilateral thalamic glioma - case report and review

Bilateral thalamic glioma - case report and review

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

Bilateral Thalamic Glioma. Case Report.

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