Abstract Details

Title Biphasic Neurovascular Changes in Prolonged Migraine Aura in Familial Hemiplegic Migraine Type 2 (FHM2)

Topic Headache

Presentation(s) S55 - (-)

Poster/Presentation
Number 005

Objective

Background We recently reported neurovascular changes in prolonged migraine aura in FHM2, in which hyperperfusion was frequently shown in the predominantly affected cerebral hemisphere, but hypoperfusion was seen in a few attacks of HMPA. The cause of the reversed blood flow pattern despite similar attack was not elucidated (Iizuka, et al. JNNP.2012;83:205-212).

Design/Methods We retrospectively evaluated CBF SPECT data obtained for 11 years from 3 members of this family with a heterozygous p.H916L mutation in the ATP1A2 gene. We plotted SPECT data according to the interval between CBF study and the onset of HMPA. In one attack we assessed both CBF and cerebral glucose metabolism during acute stage of HMPA and interictal state.

Results Ten attacks of HMPA were evaluated. 1) In a single attack, CBF studies showed biphasic CBF pattern beginning with early hypoperfusion followed by sustained hyperperfusion lasting 8 days, and FDG-PET also showed increased cerebral glucose metabolism associated with ipsilateral hyperperfusion on day 4. 2) 3D-SSP Z-score maps disclosed multifocal hypoperfusion in the affected hemisphere during early stage of 3 attacks. 3) Hypoperfusion in the affected hemisphere was seen only within 19 hours of the onset of HMPA in 4 attacks, while hyperperfusion was seen 18 hours or later in 7 attacks.

Conclusions This is the first report showing biphasic CBF changes in the attack of HMPA. Our study suggests that hemiplegic migraine aura could be initiated by functional alteration similar to cortical spreading depression but probably of multifocal origin in the affected cerebral hemisphere. Subsequently developing persistent hyperperfusion is probably associated with sustained activation of the trigeminovascular system and parasympathetic nerves, and increased cerebral glucose metabolism during hyperperfusion phase is likely caused by synaptic activation.

Authors/Disclosures
Takahiro Iizuka, MD (Department of Neurology, Kitasato University School of Medicine) PRESENTER	The institution of Dr. Iizuka has received research support from EUROIMMUN Japan Co., Ltd.
	No disclosure on file
	No disclosure on file
Juntaro Kaneko	Juntaro Kaneko has nothing to disclose.
	No disclosure on file
Junichi Hamada, MD, PhD (Dpet of Neurology, Kitasato University Kitasato Institute Hospital)	No disclosure on file
Kazutoshi Nishiyama, MD, PhD	Kazutoshi Nishiyama, MD, PhD has nothing to disclose.
	No disclosure on file

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