Acute cerebral microbleeds at the edge of lacunar strokes: cause or result.

We investigated the pathogenic relationship between cerebral microbleeds and lacunar strokes. Two cases of lacunar strokes in the region of the basal ganglia, a 72-year-old man and a 67-year-old man, were studied; both cases showed cerebral microbleeds in the stroke areas. The cerebral microbleeds were surrounded by oedema, and the oedema faded out over time, suggesting the cerebral microbleeds had developed acutely. The cerebral microbleeds were located at the ventrolateral edge of the lacunar infarctions, and the locations appeared to be at or near the sites of occlusion of the lenticulostriatal branches. Although a cerebral microbleed and a lacunar infarction may be two unrelated events on juxtapositioned vessels, or a cerebral microbleed may be haemorrhagic conversion of an infarction, a cerebral microbleed could cause an occlusion of the arterial branch, leading to lacunar infarction of its supplying territories.

Upward gaze palsy and convergence insufficiency as a rare presentation of primary intraventricular haemorrhage.

A primary intraventricular haemorrhage (PIVH) usually presents with non-localised neurological symptoms since the haematoma is limited to the ventricles. However, it is sometimes associated with focal neurological signs, whose pathophysiologies are not confirmed. Here, we report on a case of PIVH who showed rare manifestations in the acute stage: upward gaze palsy and convergence insufficiency. The CT and MRI showed intraventricular haematoma without evidence of parenchymal haemorrhage, local mass effect around midbrain or hydrocephalus. There had been bilateral papilloedema, and it resolved along with improvement of the ophthalmic symptoms, suggesting a possible causal relation to increased intracranial pressure. The ophthalmic abnormalities suggested injury of the rostral part of the midbrain, especially the region around the dorsal midbrain tectum. It should be known that PIVH is one of the causes of acutely developing upward gaze palsy and convergence insufficiency.

[A case of recurrent cerebral infarction during treatment with oral tyrosine kinase inhibitors for chronic myelogenous leukemia].

A 76-year-old man, diagnosed with chronic myeloid leukemia in 2010, had been on nilotinib for 7 years. He presented with right hemiparesis in September 2017. He had no history of hypertension, diabetes, hyperlipidemia, heart disease, or smoking. Brain MRI revealed a border-zone infarction of the left cerebral hemisphere and a rapidly progressing severe left internal carotid artery (ICA) stenosis. He was initiated on clopidogrel and bosutinib instead of nilotinib. He presented with right hemiparesis once again in December 2017. Brain MRI revealed the border-zone infarction of the left cerebral hemisphere and a more progressed, severe bilateral ICA stenosis. A carotid ultrasound demonstrated iso-intense and concentrically narrowed ICA on both sides. Carotid artery stenting of the left ICA was performed in February 2018, and clopidogrel was replaced by cilostazol to provide a drug-induced rush. Carotid artery stenting of the right ICA was performed in June 2018 and cervical angiogram demonstrated that there were no residual artery stenoses in the bilateral stent. In recent years, several case reports suggest that tyrosine kinase inhibitors (TKIs) are associated with progressive artery stenosis and cause cerebral infarction. Brain imaging tests should be conducted to evaluate arterial stenosis progression for patients with a history of taking TKI when an arterial vascular event occurs.

[Infliximab treatment trial in a patient with neuro-Behçet's disease unresponsive to other treatments].

A 22-year-old man with a previous uveitis episode was admitted to our hospital because of persistent hiccup. On admission, he presented right-upper quadrantanopia, mydriasis and lack of the light reflex in the left eye, left-sided hemiplegia, and bilateral pathologic hyperreflexia. The MR fluid attenuated inversion recovery images showed left side dominant, high intensity lesions on the brainstem and the diencephalon. The HLA-B51 was positive. The CSF IL-6 was extremely elevated (998 pg/ml: reference value < = 6.0 pg/ml). Based on these, we concluded he had the neuro-Behçet's disease and treated him by high dose intravenous corticosteroids. This treatment improved his symptoms and MRI lesions, and decreased the CSF IL-6 levels initially. On 13th day after the first his discharge, however, dysarthria appeared and the CSF IL-6 levels elevated again. In addition to the high dose intravenous corticosteroids therapy for acute attack, 15 mg/week of methotrexate was started to prevent the recurrence. Even with this prevention, meningitis related to neuro-Behçet's disease occurred within six weeks. We administered 5 mg/kg of infliximab intravenously at 0, 2, 6, and 14 weeks. After the infliximab treatment, his symptoms improved and the IL-6 levels decreased, and no recurrence has occurred. This case supports that infliximab, anti-TNF-alpha agent, is a good candidate for neuro-Behçet's disease treatment when it is resistant to conventional immunosuppressive agents such as corticosteroids or methotrexate.

Micturitional disturbance due to bilateral medial frontal lobe lesions in a patient with multiple sclerosis.

A 41-year-old man with multiple sclerosis (MS) complained of nocturnal enuresis at the third exacerbation. Neurological examination revealed echopraxia, forced grasp reflexes and palmo-mental reflexes. The urodynamic studies showed neither spinal cord nor peripheral nerve involvements. His brain magnetic resonance images (MRIs) revealed new lesions at the bilateral medial frontal lobes. The intravenous methylprednisolone therapy improved nocturnal enuresis and made brain MRI lesions smaller and gone. In addition to frequently observed spinal cord lesions, we should consider some medial frontal lesions to be responsible for micturitional disturbance in patients with MS.