Central poststroke pain and Wallenberg's lateral medullary infarction

Frequency, character, and determinants in 63 patients

D. J L MacGowan, M. N. Janal, W. C. Clark, R. N. Wharton, R. M. Lazar, Ralph L Sacco, J. P. Mohr

Research output: Contribution to journalArticle

115 Citations (Scopus)

Abstract

Central poststroke pain (CPSP) is an infrequently recognized complication of lateral medullary infarction (LMI). We determined the frequency, nature, and predictors of this complication in 63 patients with LMI. The hypothesis tested was that the degree of clinical sensory loss and extent of infarction seen on MRI, both graded by a predetermined scoring scale, would be predictive of CPSP. We also performed quantitative sensory testing (QST) of thermal and pressure sensation thresholds in a subgroup of 19 patients (nine with CPSP and 10 without) to analyze in detail the spinothalamic and trigeminothalamic systems mediating these modalities from both sides of the face and body. We analyzed these results for specific markers of C PSP. Results: CPSP developed in 25% (16/63) of the patients, all within 6 months. This was constant and severe with frequent allodynia, but responded in all cases to amitriptyline and recurred promptly on attempted weaning. CPSP affected the ipsilateral peri-orbital region most commonly, either alone or in combination with the contralateral limbs. Ipsilateral neurotrophic facial ulceration developed in two cases. CPSP correlated significantly (Fisher's exact test, p < 0.0002) with the degree of clinical sensory loss but not with the size of infarction seen on MRI (Fisher's exact test, p = 0.7). QST revealed a highly specific (100%) and sensitive (89%) finding for CPSP-thresholds from the cheek contralateral to the LMI were normal in eight of nine cases with CPSP and abnormal in all of the 10 cases without CPSP. Abnormalities in the face contralateral to the infarct are referable to the crossed trigeminothalamic tract in the medullary reticular formation medial to the infarcted lateral medulla. We conclude that this argues for the theory that central pain is caused by denervation sensitivity of the 'paleo'-reticulothalamic connections due to a selective 'neo'- spinothalamic lesion.

Original languageEnglish
Pages (from-to)120-125
Number of pages6
JournalNeurology
Volume49
Issue number1
StatePublished - Jul 1 1997
Externally publishedYes

Fingerprint

Infarction
Pain
Amitriptyline
Pain Threshold
Reticular Formation
Cheek
Hyperalgesia
Denervation
Weaning
Extremities
Hot Temperature
Pressure

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

MacGowan, D. J. L., Janal, M. N., Clark, W. C., Wharton, R. N., Lazar, R. M., Sacco, R. L., & Mohr, J. P. (1997). Central poststroke pain and Wallenberg's lateral medullary infarction: Frequency, character, and determinants in 63 patients. Neurology, 49(1), 120-125.

Central poststroke pain and Wallenberg's lateral medullary infarction : Frequency, character, and determinants in 63 patients. / MacGowan, D. J L; Janal, M. N.; Clark, W. C.; Wharton, R. N.; Lazar, R. M.; Sacco, Ralph L; Mohr, J. P.

In: Neurology, Vol. 49, No. 1, 01.07.1997, p. 120-125.

Research output: Contribution to journalArticle

MacGowan, DJL, Janal, MN, Clark, WC, Wharton, RN, Lazar, RM, Sacco, RL & Mohr, JP 1997, 'Central poststroke pain and Wallenberg's lateral medullary infarction: Frequency, character, and determinants in 63 patients', Neurology, vol. 49, no. 1, pp. 120-125.
MacGowan, D. J L ; Janal, M. N. ; Clark, W. C. ; Wharton, R. N. ; Lazar, R. M. ; Sacco, Ralph L ; Mohr, J. P. / Central poststroke pain and Wallenberg's lateral medullary infarction : Frequency, character, and determinants in 63 patients. In: Neurology. 1997 ; Vol. 49, No. 1. pp. 120-125.
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