Thalamic Pain Syndrome

PAIN CHARACTERISTICS

The patient typically reports a burning, stinging, stabbing, or shooting pain; hyperalgesia to temperature and touch are often noted. Pain may travel unilaterally from the extremities to sometimes being accompanied by facial paresthesias; anesthesia may also occur in regions affected by the stroke. CPSP is more common in right-sided strokes. Primarily, this is a very persistent syndrome with daily intermittent pain lasting seconds to minutes. The occasional relief is limited to a few hours; however; the hypersensitivity, hyperpathia, or allodynia continue in response to various stimuli.

PATHOPHYSIOLOGY

The thalamus plays a central role in modulation of sensory information between the periphery and cerebral cortex. There are various hypothesized mechanisms underlying the pathophysiology of CPSP, including central imbalance, central disinhibition, and central sensitization. Central imbalance is associated with the clinical finding of dissociated sensory loss characterized by hypersensitivity to thermal and noxious stimuli, with preserved sensory perception to touch and vibration. It is speculated that this symptom pattern is attributable to an imbalance of inputs among spinothalamic tracts and spared dorsal column/medial lemniscus activity. Central disinhibition may account for abnormal thermal sensation with burning pain and cold allodynia related to the medial thalamus and anterior cingulate cortex. The concept of central sensitization postulates that changes in electrophysiologic properties of nociceptive neurons lead to hyperexcitability through multiple mechanisms. There is still no acceptable precise clinical correlation with a specific underlying pathophysiologic mechanism.

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