The thalamus and behavior

Carrera, Emmanuel; Bogousslavsky, Julien

doi:10.1212/01.wnl.0000219679.95223.4c

Cited by 268 publications

(198 citation statements)

References 45 publications

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“…All patients had ischemia in the paramedian (n ϭ 10, 2 bilateral) or tuberothalamic (n ϭ 9, 2 bilateral) artery, leading to a partially different lesion localization and symptomatic profiles. 5,6 We focused on chronic lesions (the lesion-test interval varied between 1 and 12 years; Table 1). The experimental procedure was approved by the ethics committee of the local Faculty of Medicine.…”

Section: Techniquementioning

confidence: 99%

“…1,2 In the postacute phase of ischemic disease, the surviving tissue may shrink 3,4 and a ventricular enlargement may take place secondary to the ischemic episode. 5,6 These local changes have not been addressed in previous lesion-symptom mapping studies. 7 The present method serves to quantitatively assess the damage to thalamic substructures, taking these issues into account.…”

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confidence: 98%

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Quantitative Assessment of Chronic Thalamic Stroke

Pergola

Suchan

Koch

et al. 2012

AJNR Am J Neuroradiol

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SUMMARY:The procedure presented quantitatively assesses thalamic lesions in the chronic phase of an ischemic episode. The structural MR images of 19 patients with ischemia in the thalamus were assessed by radiologic inspection. An independent rater allocated the damage to the thalamic nuclei. The assessments showed 89% accordance with the radiologic inspection (P Ͻ .001). This procedure ranks the extent of the damage to thalamic nuclei and accounts for postacute rearrangement of the neural tissue.ABBREVIATIONS ILN ϭ intralaminar nuclei of the thalamus; MD ϭ mediodorsal nucleus of the thalamus; MID ϭ midline nuclei of the thalamus; PU ϭ pulvinar; VA ϭ

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Section: Techniquementioning

confidence: 99%

mentioning

confidence: 98%

Quantitative Assessment of Chronic Thalamic Stroke

Pergola

Suchan

Koch

et al. 2012

AJNR Am J Neuroradiol

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“…However, vascular lesions affecting subcortical structures, mainly the caudate nucleus and thalamus, may result in a clinical syndrome resembling bvFTD [2,3].…”

Section: Dear Editormentioning

confidence: 99%

“…Frontal-like syndromes secondary to paramedian strokes are probably due to thalamo-frontal disconnection and behavioral changes consisting of personality abnormalities with disinhibited behavior associated with apathy and amnesia were reported [3]. Amnesia is also a frequent sign after paramedian infarcts, but the role of the intralaminar and dorsomedial nuclei is still controversial [5,6].…”

Section: Dear Editormentioning

confidence: 99%

“…However, vascular lesions affecting subcortical structures, mainly the caudate nucleus and thalamus, may result in a clinical syndrome resembling bvFTD [2,3].We report a case of paramedian thalamic stroke mimicking frontotemporal dementia. A 58-year-old righthanded man was referred to our hospital because of behavioral and cognitive changes formerly diagnosed as bvFTD.…”

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confidence: 92%

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Frontal dementia related to thalamic stroke: a case report

et al. 2012

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The behavioral variant of frontotemporal dementia (bvFTD) is characterized by modifications of personality, social behavior and cognition and relies on a neurodegenerative process [1]. However, vascular lesions affecting subcortical structures, mainly the caudate nucleus and thalamus, may result in a clinical syndrome resembling bvFTD [2,3].We report a case of paramedian thalamic stroke mimicking frontotemporal dementia. A 58-year-old righthanded man was referred to our hospital because of behavioral and cognitive changes formerly diagnosed as bvFTD. His medical history was negative for previous illness and the patient neither smoked nor drank alcohol. In July 2010, the patient suddenly presented with loss of consciousness and was admitted to a nearby hospital. After a few days the decreased level of consciousness resolved and he developed amnesia and personality changes such as disinhibition, apathy and loss of selfactivation. Toxicological exams, routine CSF analysis including total proteins, count cell, glucose and CSF culture were normal at admission. CT scan performed within twelve hours the onset of disturbances was also normal. The patient was diagnosed as affected by a conversion disorder. Because of the disturbances, the patient left his job and moved to live with his sister since he was not able to care for himself. After 6 months, the patient was submitted to a neuropsychological screening, showing an impairment of executive functions and amnesia. A diagnosis of frontotemporal dementia was supposed. The patient was referred to our Center in January 2011. The neurological examination was normal. Neuropsychological tests confirmed an alteration of executive functions as well as verbal and visual memory deficits. This was coupled with behavioral disturbances of apathy and depression. Brain MRI showed a mild frontotemporal atrophy with ventricular dilatation but also a left thalamic infarct in the paramedian territory (Fig. 1). The patient started therapy with paroxetine (20 mg/day) and memantine (10 mg/day). At 6-month and 1-year, follow-up neuropsychological test showed a further recovery of cognitive functions and behavioral disturbances (Table 1). The caregivers also reported a gradual improvement of disturbances since the onset. Brain CT confirmed thalamic infarction. We made a diagnosis of a thalamic stroke as the cause of dementia, because of the sudden onset and the gradual improvement of the clinical syndrome and the correspondent finding of an ischemic lesion. Routine blood tests, hemocoagulative screening and autoantibody pattern were normal. Electrocardiogram and carotid ultrasonography did not show any alterations. The transthoracic echocardiogram, the transcranial Doppler sonography and the transoesophageal echocardiography detected the patent foramen ovale (PFO) and the patient was started anticoagulant therapy. After 2 years, the

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Association of Neocortical Volume Changes With Cognitive Deterioration in Relapsing-Remitting Multiple Sclerosis

Amato¹,

Portaccio²,

Goretti³

et al. 2007

Arch Neurol

207

151

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Background : We previously reported selective decreases of neocortical volumes in patients with early relapsing-remitting (RR) multiple sclerosis (MS) with mild cognitive impairment, with a good correlation between cortical volumes and cognitive measures.Objective: To assess the relevance of gray matter changes over time to changes in cognition in RRMS.Design: A longitudinal survey after 2.5 years. Each patient underwent a magnetic resonance imaging (MRI) protocol identical to that performed at baseline; cognitive performance was reassessed with the Rao Brief Repeatable Battery of Neuropsychological Tests in Multiple Sclerosis. Setting: Two university MS clinics.Patients: Of 41 patients with RRMS who participated in the original cross-sectional study, 28 were available for the follow-up evaluation (18 women; mean±SD age, 37.1±8.9 years; mean±SD MS duration, 7.3±2.9 years; mean±SD Expanded Disability Status Scale score, 1.8±1.5). Main Outcome Measures:We measured the percentage of brain volume changes, normalized cortical volume (NCV) changes, and normalized deep gray matter volume changes on conventional T1-weighted MRIs and changes in lesion load on T2-weighted MRIs. The number of tests failed on the Rao Brief Repeatable Battery were used to classify the patients as cognitively deteriorating or stable or improving.Results: We identified 12 of 28 cognitively deteriorating and 16 of 28 stable or improving patients. These subgroups did not differ in the mean±SD percentage of brain volume changes (−2.1%±1.2% vs −1.3%±1.3%; P=.11), normalized deep gray matter volume changes (−2.1±2.8 mL vs −0.6±3.1 mL; P=.60), and changes in lesion load on T2-weighted MRIs (1.9±2.6 mL vs 1.6±2.3 mL; P=.73). However, NCV changes were significantly higher in deteriorating than in stable or improving patients (−43.0±18.9 mL vs −17.8 ± 26.6 mL; P = .007). In deteriorating patients, NCV changes were correlated with performance in a verbal fluency test (r=0.73; PϽ.001). In a regression model, only NCV changes were significantly associated with deteriorating cognitive performance (odds ratio, 0.8; 95% confidence interval, 0.7-0.9). Conclusion:Progressive neocortical gray matter loss is relevant to MS-associated cognitive impairment and may represent a sensitive marker of deteriorating cognitive performance in RRMS.

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The thalamus and behavior

Cited by 268 publications

References 45 publications

Quantitative Assessment of Chronic Thalamic Stroke

Quantitative Assessment of Chronic Thalamic Stroke

Frontal dementia related to thalamic stroke: a case report

Association of Neocortical Volume Changes With Cognitive Deterioration in Relapsing-Remitting Multiple Sclerosis

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