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Eur J Neurol. 1994 Nov;1(2):165-9. doi: 10.1111/j.1468-1331.1994.tb00066.x.

Bilateral thalamic damage, cortical hypometabolism and behavioural disturbances.

European journal of neurology

F A de Falco, A Soricelli, L Majello, A Modafferi, D Grossi

Affiliations

  1. Section of Neurology, S. Maria di Loreto Hospital, USL 44, Naples, ItalyDepartment of Nuclear Medicine, Naples, ItalyDepartment of Neurology, University "Federico II" of Naples, Naples, Italy.

PMID: 24283486 DOI: 10.1111/j.1468-1331.1994.tb00066.x

Abstract

Thalamic damage could be responsible for reduced metabolism in anterior cortical areas. In order to investigate an anatomical lesion and impairment of regional blood flow (rCBF) in distant cortical areas, we studied by magnetic resonance imaging (MRI) and single photon emission computed tomography (SPECT) a patient with bilateral thalamic infarction, who presented with sudden consciousness impairment, drowsiness, gaze paralysis, dysphagia and bilateral Babinski sign. Three weeks later the neurological symptoms disappeared, but a severe mental deterioration was evident MRI showed thalamic bilateral damage of posterior and medial areas, involving part of the pulvinar, more evident for the right thalamus. A (99m) Tc-HMPAO SPECT showed a decrease of rCBF over frontal and parietal regions, more evident for the right hemisphere. Six months later a severe memory impairment was still evident and MRI and SPECT picture were unchanged. The persistent memory defect could be related to a loss of cortical activation following the thalamic damage. The absence of primary lesions of cortical regions on CT scan and MRI and the neuroanatomical considerations on the diffuse projections running from medial nuclei and pulvinar to large parts of anterior neocortex supported this hypothesis.

1994 Lippincott Williams & Wilkins.

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