A focal ischemic stroke of the somatosensory thalamus produces persistent spontaneous pain-like behavior.

Ischemic injury to the somatosensory ventrobasal (VB) thalamus is strongly associated with central post-stroke pain (CPSP), yet preclinical models of selective focal ischemic VB injury remain limited. Here, we developed a mouse model of ischemic VB stroke using photothrombotic occlusion. Stroke-affected mice exhibited persistent spontaneous facial grimace throughout the four-week observation period, consistent with a sustained affective behavioral state. Hindpaw mechanical hyposensitivity and postural abnormalities were transient, emerging early after stroke and resolving within two weeks. These evoked and postural measures were not correlated with facial grimace behavior across time points, indicating dissociation between persistent grimace behavior and transient sensory or motor phenotypes. Immunohistochemistry showed increased thalamic glial activation, and VPL microgliosis was positively associated with four-week facial grimace severity. Together, these findings establish a reproducible model of focal ischemic somatosensory thalamic stroke characterized by persistent spontaneous facial grimace behavior alongside dissociated transient evoked and postural changes. This model provides a framework for investigating mechanisms associated with CPSP following ischemic thalamic injury.