Successful use of zonisamide for central poststroke pain.
We present 2 patients with severe and intractable central poststroke pain (CPSP) after right posterolateral thalamic infarcts who were successfully treated with zonisamide. The mechanism of action was presumed to be the suppression of overacting thalamic relay neurons by blockade of low voltage-activated calcium channel or by increasing gamma-aminobutyric acid (GABA) release. Zonisamide can be one of the therapeutic options for severe CPSP and might provide an insight into the pathogenesis of CPSP.


CONCLUSIONS
The blockade of T-type VGCC or the increase in GABA release caused by zonisamide presumably suppresses abnormal activities of thalamic sensory neurons.
Takahashi
Yuji
Y
Department of Neurology, Toshiba Hospital, Tokyo, Japan. TAKAHASHIY-INT@h.u-tokyo.ac.jp
Hashimoto
Kouichi
K
Tsuji
Shoji
S
D000927:Anticonvulsants / Q000627:therapeutic use*; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D020747:Calcium Channels, T-Type / Q000187:drug effects; D002544:Cerebral Infarction / Q000503:physiopathology; D048909:Diabetes Complications; D006801:Humans; D007555:Isoxazoles / Q000627:therapeutic use*; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D010146:Pain / Q000188:drug therapy* / Q000209:etiology*; D020521:Stroke / Q000150:complications*; D000078305:Zonisamide; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D000927:Anticonvulsants; D002121:Calcium Channel Blockers; D020747:Calcium Channels, T-Type; D007555:Isoxazoles; D000078305:Zonisamide; D005680:gamma-Aminobutyric Acid