Transient splenial lesion after recovery of cerebral vasoconstriction and posterior reversible encephalopathy syndrome: a case report of eclampsia.

We describe a 34-year-old eclamptic woman with transient splenial lesion (TSL) after reversible cerebral vasoconstriction (RCV) and posterior reversible encephalopathy syndrome (PRES). She developed a headache, generalized convulsion and severe hypertension at an uncomplicated virginal delivery. Brain MRI disclosed T2-hyperintensity lesions in the posterior circulation territories. Two weeks later, T2-hyperintensity lesions had vanished. MR angiography (MRA) revealed segmental vasoconstriction in the right posterior, left internal and middle cerebral arteries. At one month after onset, MRA was normalized. T2-weighted imaging depicted asymptomatic isolated TSL. These radiological changes of the present patient highlighted the serial relationship between PRES, RCV and TSL in eclampsia.

Repeated non-enhancing tumefactive lesions in a patient with a neuromyelitis optica spectrum disorder.

A 51-year-old woman had developed fever and consciousness disturbance at 47 years of age. Brain magnetic resonance imaging (MRI) revealed acute disseminating encephalomyelitis (ADEM)-like lesions without gadolinium enhancement (GDE). One year later, she had an episode of bilateral optic neuritis and cerebellar ataxia. Speech deficit and right hand weakness occurred at the age of 51 years. Neurological examination showed motor aphasia, finger agnosia, right-left disorientation, and right hand paresis. Neuromyelitis optica (NMO)-IgG was seropositive. Cerebrospinal fluid examination showed negative results for myelin basic protein and oligoclonal IgG band. The IgG index was normal. Brain MRI revealed a tumefactive lesion in the left temporo-parietal region and conglomerate ovoid lesions in the pericallosal regions. No GDE was found in the brain lesions. Visual evoked potential test showed bilateral prolongation of P100 latencies. She was treated twice with methylprednisolone pulse therapy followed by oral prednisolone, but the motor aphasia did not respond to steroid treatment. She had no prior history of myelitis and was diagnosed as NMO spectrum disorder (NMOSD). Similar to previous studies of NMO-IgG seropositive extensive brain lesions, this patient with NMOSD indicated no GDE in tumefactive lesions at two episodes of encephalopathy. Compared to multiple sclerosis (MS), a high frequency of non-enhancing tumefactive lesions is reported in patients with NMO or NMOSD. The absence of GDE in tumefactive lesions could help to differentiate between NMO and MS.

Cheiro-oral syndrome associated with lateral medullary infarction.

A 62-year-old man was admitted to our department because of the sudden onset of dysaesthesia in the right perioral region of the face and right hand. Neurological examination demonstrated a loss of pain and temperature sensation in both the right perioral region and in the fingers of the right hand. These findings suggested damage to parts of the ipsilateral spinothalamic and trigeminothalamic ascending tracts, producing restricted sensory impairment of the perioral region and ipsilateral hand. This is the first reported case of a medullary lesion causing cheiro-oral syndrome.

Cardiovascular risk and neuroradiological profiles in asymptomatic vertebrobasilar dolichoectasia.

BACKGROUND: Clinicoradiological variability of vertebrobasilar dolichoectasia (VBD) is known. Little is known about cardiovascular disease (CVD) risk and neuroradiological profiles of asymptomatic VBD. METHODS: A total of 7,345 adults (5,534 men and 1,811 women) underwent physical checkup (PC) and brain magnetic resonance (MR) studies between 2004 and 2007. Asymptomatic VBD was diagnosed by neurological examination and MR angiography. Neuroradiological features were analyzed in VBD subjects. CVD risk factors were compared between VBD subjects and 5,000 controls matched by sex and age. RESULTS: Ninety-six subjects (85 men and 11 women) had asymptomatic VBD. The detection rate was 1.3% and the male/female ratio 2.5. The mean age +/- SD was 60.4 +/- 10.6 years (60.0 +/- 10.2 in men and 64.0 +/- 13.1 in women). As compared to controls, the frequency of hypertension, obesity, smoking, dyslipidemia, diabetes mellitus and a family history of stroke or CVD was increased significantly in VBD subjects. The mean diameter +/- SD of the basilar artery (BA) was 4.7 +/- 0.2 mm. Only 4 subjects (4%) had a severe degree of elongation and lateral displacement of the BA. Contact of the vertebral artery with the rostral ventrolateral medulla (AMC) was found in 81 subjects: right AMC in 22 subjects and left AMC in 59 subjects. Frequency of hypertension was significantly higher in the left-AMC subjects (57%) than in subjects with right AMC (9%) and no AMC (5%). Other neuroradiological findings revealed small infarcts in 42 subjects, brainstem compression in 4, hydrocephalus in 4 and brain saccular aneurysm in 3. CONCLUSIONS: Asymptomatic VBD was detected in 1.3% of the Japanese PC group. Our data indicated male predominance, multiple CVD risk factors, neurovascular hypertension and small infarcts in asymptomatic VBD.

Scopolamine-induced migraine like headache.

OBJECTIVE: Scopolamine butylbromide (SB), a muscarinic receptor antagonist, is used commonly in gastric X-ray examination in the physical check-up in Japan. This study describes clinical features of SB-induced headache. PATIENTS AND METHODS: SB-induced headache was defined as headache that started within 20 minutes after intramuscular administration of SB (20 mg/body). The Primary and the secondary headaches were diagnosed according to the ICHD-II criteria. SB-induced headache was classified as headache induced by acute substance use or that due to exposure (ICHD-II code 8.1). Clinical features and background of subjects with SB-induced headache were analyzed. We also estimated the frequency of SB-related headache between migraineurs and non-migraineurs. RESULTS: A total of 54 subjects (39 women and 15 men) experienced SB-induced headache. All subjects had the present history of migraine. Nine subjects had > or =2 times of the headache. Mean age (SD) was 46.2 (9.7) years [46.2 (9.7) for women and 46.3 (10.0) for men]. Clinical hallmarks of headache showed that pulsating / throbbing pain occurred in diffuse or bilateral head sites. Headache worsened at 20-30 minutes from the onset and persisted for 6-18 hours, and ameliorated gradually 8 hours later. All subjects had repeated nausea and vomiting. Severity of headache revealed severe degree requiring complete bed rest in 50 subjects (92.6%). SB-induced headache had similar characteristics as migraine without aura (MO) attacks. Liver and renal functions were normal in all SB-related migraineurs. They had no allergic history of medication and food. In 1,865 non-migraine controls, one healthy subject had a mild degree of migraine like headache triggered by SB injection. CONCLUSION: SB triggers a severe degree MO like headache or worsens pre-existing migraine in some migraineurs. SB-induced headache could contribute to disequilibrium between acetylcholine and other neuropeptides. We should use SB more carefully as it can be an aggravating drug of migraine.

A case of Vernet syndrome with varicella zoster virus infection.

A 40-year-old man was admitted to our department, because of sudden onset of dysphagia, hoarseness, left neck pain and headache. There were no skin lesions. On neurological examination, there were paralysis of the left soft palate and constrictor muscles of the pharynx, weakness of the left sternocleidomastoid and left upper trapezius. In cerebrospinal fluid (CSF) examination, cell count and protein concentration were elevated. Antibody titer to varicella zoster virus (VZV) was elevated in both the serum and CSF. And VZV-DNA was detected by PCR from CSF. Gd enhanced MRI showed the nodular lesion at the left jugular foramen. The diagnosis of Vernet's syndrome (VS) associated with VZV infection was made. The patient's symptoms were immediately improved with 30 mg of prednisone and 3 g of varaciclovir daily for 14 days. Only a few cases of VS due to VZV have been reported previously. Our case is the first case that detected VZV-DNA in CSF by PCR.