Brain, Vol. 115, No. 3, 795-807, 1992
© 1992 Guarantors of Brain
research-article |
BRAIN ENERGY METABOLISM IN BILATERAL PARAMEDIAN THALAMIC INFARCTS: A POSITRON EMISSION TOMOGRAPHY STUDY
1Service Hospitalier Frédéric Joliot Orsay 2INSERM U334 Orsay 3INSERM U320 Caen 4Hôspital Neurologique Lyon 5Clinique des Maladies du système Nerveux Paris 6CIERM, Hôspital Bicêtre Le Kremlin-Bicêtre 7Service de Neurologie, Hôpital Henri Mondor Creteil, France
Correspondence to:
Correspondence to: Dr J. C. Baron, INSERM U320, Boulevard H. Becquerel, BP 5027, 14021 Caen Cedex, France
Positron emission tomography (PET) studies of the cerebral metabolic rate of oxygen (CMRO2) were performed in seven consecutive patients with bilateral paramedian thalamic infarcts (BPTI), selected on neuroradiological and clinical criteria. The latter consisted of sudden onset of coma or confusion followed by a persistent amnesia of varying severity, with or without language impairment and frontal lobe signs. There was a highly significant decrease of CMRO2 for the whole cortex as well as for all the regions analysed: medial-frontal, latero-frontal, temporal, sensorimotor and posterior associative cortex. The mean regional metabolic ratios (region/whole cortex CMRO2) were not significantly different from controls, indicating an essentially uniform effect in the cortex, except the sensorimotor ratio which was significantly increased. Diffuse cortical hypometabolism most likely reflects thalamo-cortical deafferentation secondary to damage to the non-specific thalamic nuclei, while sparing of the latero-ventral thalamus presumably explains the relative preservation of the sensorimotor cortex metabolism. Although no clear-cut individual relationship was found between magnitude of cortical hypometabolism and the severity and pattern of neuropsychological impairment, the data suggest that the former underlies and/or reflects the latter. Further studies with higher resolution PET devices might shed more light on the relationships between distinct cognitive patterns and specific topography of cortical hypometabolism in BPTI patients.
.
Received July 15, 1991. Revised January 3, 1992. Accepted March 10, 1992.
*Present address: Dipartimento di Scienze Neurologiche dell'Universita degli studi La Sapienza di Roma, 00184 Roma, Italy
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
R. van Reekum, D. T. Stuss, and L. Ostrander Apathy: Why Care? J Neuropsychiatry Clin Neurosci, February 1, 2005; 17(1): 7 - 19. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. H. Taber, C. Wen, A. Khan, and R. A. Hurley The Limbic Thalamus J Neuropsychiatry Clin Neurosci, May 1, 2004; 16(2): 127 - 132. [Full Text] [PDF] |
||||
![]() |
P. Remy, M. Zilbovicius, P. Cesaro, P. Amarenco, J.-D. Degos, and Y. Samson Primary Somatosensory Cortex Activation Is Not Altered in Patients With Ventroposterior Thalamic Lesions : A PET Study Stroke, December 1, 1999; 30 (12): 2651 - 2658. [Abstract] [Full Text] [PDF] |
||||
![]() |
O. Sabri, E.-B. Ringelstein, D. Hellwig, R. Schneider, M. Schreckenberger, H.-J. Kaiser, M. Mull, and U. Buell Neuropsychological Impairment Correlates With Hypoperfusion and Hypometabolism but Not With Severity of White Matter Lesions on MRI in Patients With Cerebral Microangiopathy Stroke, March 1, 1999; 30(3): 556 - 566. [Abstract] [Full Text] [PDF] |
||||
![]() |
Y D V. D. Werf, J G E Weerts, J Jolles, M P Witter, J Lindeboom, and P. Scheltens Neuropsychological correlates of a right unilateral lacunar thalamic infarction J. Neurol. Neurosurg. Psychiatry, January 1, 1999; 66(1): 36 - 42. [Abstract] [Full Text] |
||||


