Introduction: The thalamic syndrome, first described by Dejerine and Roussy, is a central neuropathic pain syndrome occurring after thalamic stroke, often associated with a mild paresis. It is a form of central post-stroke pain. Treatment is challenging and often not satisfying.
Methods: 30 rats were tested for thermal and mechanical pain and motor performance, and were then randomly allocated into a lesion group (L; electrolytic thalamic lesioning; n=22) and a sham group (S; sham surgery; n=8). Pain and motor tests were repeated weekly over the next 4 weeks. Next, after CT and MR imaging, 3 bipolar electrodes were implanted. L was randomly divided into a cavity wall electrode group (E; electrodes aiming for the ventral cavity wall; n=11) and a random electrode group (C; electrodes aiming for a random brain target not related to motor or pain behaviour; n=11). In S, electrodes were implanted at the same coordinates as in W. Motor tests were then repeated during deep brain stimulation (DBS; biphasic, 130Hz, 200µs at 0%-50%-75%-100% of the highest tolerated amplitude (HTA; amplitude above which side effects are observed)). Afterwards, local field potentials (LFPs) were recorded in resting state.
Results: After but not before lesioning, motor scores were significantly (P<.05) worse in L vs. S, while pain scores did not differ.
In C, DBS at 50%, 75% or 100% HTA did not improve motor scores significantly as compared to 0% HTA in W or to DBS in C or S. LFPs obtained from identical anatomical locations in C and S rats differed significantly.
Conclusions: In a thalamic syndrome rat model with motor deficits but no mechanical or thermal hyperalgesia, the tested DBS parameters did not alleviate symptoms.
Patient Care: Despite the fact that a few medications have shown level 1 evidence of efficacy, treating CPSP remains challenging and satisfactory pain relief is achieved only in a minority of patients. Second-line treatments include various neuromodulation techniques, such as motor cortex stimulation (MCS) and deep brain stimulation (DBS) mostly targeting either the sensory thalamus (ST; terminatio lemniscorum/ventral posterolateral (VPL)/ventral posteromedial (VPM)), or the periaqueductal gray (PAG)/periventricular gray (PVG). However, even with these neuromodulation techniques, >50% reduction in pain scores is achieved in only one third of patients in the long term.
Therefore, developing new neuromodulation techniques for treating CPSP is of utmost importance.
This is a first proof that abnormal brain cavity wall stimulation and recording is feasible, can induce effects (categorized as side effects) and could be used as a generic technique for treating symptoms associated with abnormal brain cavities.
Learning Objectives: After studying this poster, participants should be aware of the fact that the wall of an abnormal brain cavity could be used as a potential target for deep brain stimulation, and that this generic approach could be applied for treating central post-stroke pain caused by a thalamic infarctions.