Ischemic strokes and hemorrhagic strokes can cause lesioning in the thalamus. The lesions, usually present in one hemisphere of the brain, most often cause an initial lack of sensation and tingling in the opposite side of the body. Weeks to months later, numbness can develop into severe and chronic pain that is not proportional to an environmental stimulus, called dysaesthesia or allodynia.
As initial stroke symptoms, numbness and tingling, dissipate, an imbalance in sensation causes these later syndromes, characterizing Dejerine–Roussy syndrome. Although some treatments exist, they are often expensive, chemically based, invasive, and only treat patients for some time before they need more treatment, called “refractory treatment.”
Research into its underlying mechanisms and treatment options could benefit from a valid animal model. Nine different animal models have been published, but there are relatively few reports on successful reproductions of these models and so far only little advances in the understanding or the management have been made relying on these models. In general, the construct validity (similarity in underlying mechanisms) of these animal models is relatively high, although this cannot be evaluated into depth because of lack of understanding the mechanisms through which thalamic stroke can lead to thalamic pain syndrome. The face validity (symptom similarity) is relatively low, mainly because pain in these models is tested almost exclusively through evoked mechanical/thermal hypersensitivity assessed by reflexive measures and given the conflicting results with similar tests in patients with thalamic pain syndrome. The predictive validity (similarity in treatment efficacy) has not been evaluated in most models and incorporates difficulties that are specific to thalamic pain syndrome.
De Vloo et al., compare the different models regarding these types of validity and discuss the robustness, reproducibility, and problems regarding the design and reporting of the articles establishing these models. They conclude with various proposals on how to improve the validity and reproducibility of thalamic pain syndrome animal models. Until further improvements are achieved, prudence is called for in interpreting results obtained through these models 1).