By Louise M. Klebanoff, MD
Assistant Professor of Clinical Neurology, Weill Cornell Medical College
Dr. Klebanoff reports no financial relationships relevant to this field of study.
SYNOPSIS: In a careful anatomic and physiologic study of patients with thalamic stroke, the authors demonstrated that the combination of anterior pulvinar nucleus involvement with spinothalamic dysfunction predicts a “thalamic pain syndrome” with > 90% sensitivity.
SOURCE: Vartiainen N, et al. Thalamic pain: Anatomical and physiological indices of prediction. Brain 2016;139:708-722.
Approximately 25% of patients with a sensory stroke due to a thalamic lesion will develop central post-stroke pain. Thalamic pain is a severe, treatment-resistant pain syndrome. The pain is often described as burning or constrictive and is frequently accompanied by evoked pain (allodynia/hyperalgesia), paresthesias, or summation hyperpathia. The underlying mechanism that results in post-stroke thalamic pain is uncertain. It is currently impossible to predict which patients will develop this distressing syndrome.
There is agreement that thalamic pain develops following a stroke affecting the territory of the geniculo-thalamic artery, which includes the primary somatosensory thalamic nucleus (ventral posterior lateral [VPL]/ventral posterior medial thalamus [VPM]) and the anterior pulvinar, a major spinothalamic target. Although damage to the VPL initially was thought to be necessary for the development of thalamic pain, not all patients with strokes involving the VPL developed thalamic pain. Studies using atlas-based projection of MRI lesions in humans have suggested that lesions in the border between VPL and the anterior pulvinar were more likely to produce thalamic pain. Central pain is associated with abnormal thermonociception, with damage to the spino-thalamic-cortical system considered necessary for the development of thalamic pain; however, not all spinothalamic lesions lead to the development of thalamic pain.
To further define the localization and mechanism for the development of thalamic pain, the authors combined atlas-based localization of thalamic lesions with quantitative sensory examinations and physiological recordings of spinothalamic evoked potentials (laser-evoked potentials [LEPs]) in a group of 42 patients with thalamic stroke.
All 42 patients had MRI-documented unilateral thalamic stroke. Thirty-one patients had central post-stroke pain and 11 did not. Non-neuropathic causes of pain were specifically addressed and excluded. Sensory examination included testing of light touch, proprioception, graphesthesia, superficial pain, and heat sensation. Pain was considered thalamic central post-stroke pain when it was contralateral to the affected thalamic lesion with a plausible neuroanatomical correlate and an abnormal sensory examination. Spinothalamic function analysis included both negative and positive symptoms and was assessed clinically in 40 patients; pain thresholds were quantified using thermal laser pulses in 35 patients. The affected thalamic nuclei were defined by superimposing MRI data onto the human thalamic atlas.1
Abnormal sensory examinations were found in 45% of the thalamic pain patients and in 18% of the non-pain patients, but this was not a significant difference. Increased pain thresholds were seen exclusively in the thalamic pain group. In addition, in the thalamic pain patients, laser-evoked potentials were attenuated on the painful side compared with the normal side; this discrepancy was not seen in the non-pain patients. The development of thalamic pain was significantly associated with signs of abnormal spinothalamic function, either estimated by subjective heat thresholds, pain thresholds, or laser-evoked potentials.
In patients with thalamic pain, maximal lesion convergence was seen in the anterior pulvinar nucleus. In the pain-free patients, maximal lesion convergence was in the VPL. Both of these thalamic nuclei receive their blood supply via the geniculostriate artery. The only nucleus showing significantly higher incidence of involvement in pain patients than in pain-free patients (87% vs 36%) was the anterior pulvinar nucleus.
COMMENTARY
Combining anatomical and functional analyses helped predict which patients with thalamic stroke will develop central post-stroke pain syndrome. Anatomical and functional indexes of spinothalamic involvement were independently and significantly associated with the development of thalamic pain. Involvement of the VPL/VPM nuclei and the presence of lemniscal symptoms were common in all patients with thalamic stroke; however, their incidence was not significantly different in patients with or without thalamic pain. A logistic regression model combining spinothalamic dysfunction and anterior pulvinar nucleus involvement had a 93% sensitivity and 87% positive predictive value for the development of thalamic pain. Injury to the spinothalamic system within the posterior thalamus seems to be the main determinant of the development of thalamic pain syndrome.
This study provides a relatively simple way of predicting which patients with thalamic stroke are likely to develop a post-stroke thalamic pain syndrome. These measures can be used to plan controlled trials of medications and other interventions to reduce the development of this severe pain syndrome.
REFERENCES
- Morel A, et al. Multiarchitectonic and sterotactic atlas of the human thalmus. J Comp Neurol 1997;387:588-630.
In a careful anatomic and physiologic study of patients with thalamic stroke, the authors demonstrated that the combination of anterior pulvinar nucleus involvement with spinothalamic dysfunction predicts a “thalamic pain syndrome” with > 90% sensitivity.
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