|
|
||||||||
From the Neurobehavior Program (Drs. Nasreddine and Saver), the UCLA Stroke Center (Dr. Saver), and the Department of Neurology (Drs. Nasreddine and Saver), UCLA School of Medicine, Los Angeles, CA.
Objective To assess whether the thalamic pain syndrome of Dejerine-Roussy is produced preferentially by right diencephalic lesions and to elucidate its clinical features.
Background Several experimental paradigms suggest that the right hemisphere is specialized for monitoring somatic states, including mediating pain. However, clinical studies of pain laterality have been inconclusive, possibly due to pathophysiologic diversity among analyzed patients. We collected reports of central pain laterality in a single, well-demarcated disorder, the Dejerine-Roussy syndrome.
Design/Methods Reports from English, French, and German literature were identified through Medline search and bibliography-guided retrieval. Inclusion criteria were (1) thalamic lesion documented by CT, MRI, or postmortem examination and (2) contralateral pain. Exclusion criteria were (1) tumoral/nonvascular etiology (to optimize anatomic localization), (2) symptoms consisting solely of evoked dysesthesia without spontaneous pain, or (3) sidedness of lesion not clearly indicated. Cases were analyzed for laterality as well as secondary anatomic and clinical variables.
Results Literature search identified 274 cases. After exclusions, 180 remained. A total of 114 had a right-sided thalamic lesion, 66 left-sided (p < 0.001). Laterality predominance was greater among men than women. The frequency of other components of the Dejerine-Roussy syndrome—sensory impairment, hemiparesis, ataxia, and choreoathetosis—did not significantly differ between right and left groups. Pain onset was within the first week poststroke in 36%. Frequency of spontaneous pain was 14% after any thalamic stroke and 24% after geniculothalamic artery territory stroke.
Conclusion Right-sided lesions predominate among reported cases of the thalamic pain syndrome. This preferential involvement of the nondominant thalamus in pain processing is supportive evidence of a nondominant hemisphere specialization in monitoring somatic states.
This article has been cited by other articles:
![]() |
B. Kumar, J. Kalita, G. Kumar, and U. K. Misra Central Poststroke Pain: A Review of Pathophysiology and Treatment Anesth. Analg., May 1, 2009; 108(5): 1645 - 1657. [Abstract] [Full Text] [PDF] |
||||
![]() |
G. Wang and S. M. Thompson Maladaptive Homeostatic Plasticity in a Rodent Model of Central Pain Syndrome: Thalamic Hyperexcitability after Spinothalamic Tract Lesions J. Neurosci., November 12, 2008; 28(46): 11959 - 11969. [Abstract] [Full Text] [PDF] |
||||
![]() |
P D McGeoch, L E Williams, R R Lee, and V S Ramachandran Behavioural evidence for vestibular stimulation as a treatment for central post-stroke pain J. Neurol. Neurosurg. Psychiatry, November 1, 2008; 79(11): 1298 - 1301. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. D. Schmahmann Vascular Syndromes of the Thalamus Stroke, September 1, 2003; 34(9): 2264 - 2278. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. H. Taber, A. Rashid, and R. A. Hurley Functional Anatomy of Central Pain J Neuropsychiatry Clin Neurosci, November 1, 2001; 13(4): 437 - 440. [Full Text] [PDF] |
||||
![]() |
K. L. Casey Forebrain mechanisms of nociception and pain: Analysis through imaging PNAS, July 6, 1999; 96(14): 7668 - 7674. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Ruggieri, A. Polizzi, L. Pavone, and S. Musumeci Thalamic Syndrome in Children With Measles Infection and Selective, Reversible Thalamic Involvement Pediatrics, January 1, 1998; 101(1): 112 - 112. [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |