We present 2 p
atients with severe
and intr
act
able centr
al poststroke p
ain (CPSP)
after right posterol
ater
al th
al
amic inf
arcts who were successfully tre
ated with zonis
amide. The mech
anism of
action w
as presumed to be the suppression of over
acting th
al
amic rel
ay neurons by block
ade of low volt
age–
activ
ated c
alcium ch
annel or by incre
asing g
amm
a-
aminobutyric
acid (GABA) rele
ase. Zonis
amide c
an be one of the ther
apeutic options for severe CPSP
and might provide
an insight into the p
athogenesis of CPSP.<
a n
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a>
ass=""h3"">Perspective
The blockade of T-type VGCC or the increase in GABA release caused by zonisamide presumably suppresses abnormal activities of thalamic sensory neurons.