The pathomechanisms and treatment strategy for rare presentations of reversible cerebral vasoconstriction syndrome (RCVS) with anti-phospholipid syndrome (APS) remain to be determined. We report a 67-year-old woman with APS who presented with ischemic stroke due to RCVS. She was treated with low-dose cilostazol and lomerizine hydrochloride, which resulted in functional improvement and recovery of vasoconstriction within 12 weeks. Her plasma endothelin-1 level was decreased after relief of vasoconstriction, compared with the pre-treatment condition. Increased plasma endothelin-1 may be related to the underlying pathomechanism of RCVS with APS, against which cilostazol and lomerizine hydrochloride could be effective.

A 9-year-old female reported left-sided, excruciatingly severe, stabbing orbital pain with cranial autonomic symptoms. The attacks continued for 1 year with a remission period of 2 months. Each attack duration was approximately 120 minutes with a frequency of two to three times a day. The patient was diagnosed with chronic cluster headache (CCH) according to the third edition of the International Classification of Headache Disorders. A combination of low-dose verapamil and lomerizine once a week decreased the frequency of the attacks, and oral sumatriptan became an effective abortive therapy. No case reports of pediatric CCH have been previously published in Japan.

A 55-year-old man with no history of stroke or migraine presented to the clinic with cognitive impairment and depression that had been experiencing for two years. Neurological examination showed bilateral pyramidal signs, and impairments in cognition and attention. Brain MRI revealed multiple lacunar lesions and microbleeds in the deep cerebral white matter, subcortical regions, and brainstem, as well as diffuse white matter hyperintensities without anterior temporal pole involvement. Cerebral single-photon emission computed tomography (SPECT) revealed bilateral hypoperfusion in the basal ganglia. Gene analysis revealed an arginine-to-proline missense mutation in the NOTCH3 gene at codon 75. The patient was administered lomerizine (10 mg/day), but the patient\'s cognitive impairment and cerebral atrophy continued to worsen. Follow-up testing with MRI three years after his initial diagnosis revealed similar lacunar infarctions, cerebral microbleeds, and diffuse white matter hyperintensities to those observed three years earlier. However, MRI scans revealed signs of increased cerebral blood flow. Together, these findings suggest that the patient\'s cognitive impairments may have been caused by pathogenesis in the cerebral cortex.

We report a rare case of benign paroxysmal vertigo (BPV) of childhood transitioning into basilar migraine (BM) that was effectively treated with lomerizine. A 6-year-old male visited our hospital complaining of repeated attacks of vertigo for 3 months. The patient\'s vertigo attacks lasted for several hours and were accompanied by nausea, vomiting, intense fear and loss of consciousness. No nystagmus was observed during the vertigo attacks. Blood tests and imaging examinations revealed no abnormal findings. The results of electronystagmography and the caloric test were unremarkable. Pure-tone audiometry revealed profound right-side sensorineural hearing loss. Among the differential diagnoses, delayed endolymphatic hydrops, epilepsy and BM were considered. Delayed endolymphatic hydrops was considered unlikely since no nystagmus occurred during the vertigo attacks and there was no change in hearing; electroencephalography revealed no epileptic seizure waves. The attacks of vertigo were well-controlled with lomerizine. The patient was diagnosed with BM since the use of lomerizine, an agent for the treatment for migraine, was effective. Since it was reported that BPV is closely related to migraine and the onset of the vertigo attacks was accompanied by a loss of consciousness, we concluded that this patient had BM transitioning from BPV.