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Mitral annular calcification (MAC) is a common finding especially among the elderly. Caseous calcification of the mitral annulus (CCMA) is a rare variant of MAC, which may be mistaken for an intracardiac tumor or abscess. The clinical significance of CCMA and its potential as a source for cerebral embolism is not known.A 76-year-old woman with an acute ischemic stroke was found to have CCMA on echocardiography apparent as a round mass with a central echolucent area and an echo-dense smooth border, in the periannular position of the mitral valve. She subsequently suffered a second embolic stroke. The central cavity of the CCMA seemed to communicate with the left atrium on echocardiography, suggesting the causal relationship between the second brain attack and the CCMA. She was anticoagulated and has not suffered any further strokes.Previous case reports have suggested that CCMA is a benign condition. This detailed report suggests that CCMA may be a potential source of embolic stroke. (T. Ohara). altered consciousness and quadriplegia. She had a history of controlled hypertension. On admission, her height, weight, and body temperature were 160 cm, 55 kg, and 36.1 • C, respectively. Her blood pressure was 192/96 mm Hg and heart rate 78 beats/min with regular rhythm. The electrocardiogram showed sinus rhythm, without any ST-T wave changes. Magnetic resonance imaging (MRI) of the brain showed new infarct lesions in the left thalamus and the cerebellum. Prompt treatment with intravenous recom-1878-5409/$ -see front matter

BackgroundPure dysarthria (PD) and dysarthria-facial paresis syndrome (DFP) mainly result from lenticulostriate artery territory infarction. PD and DFP are rare clinical entities, often grouped without distinction. The purpose of this study was to examine clinical and radiographic differences between PD and DFP due to unilateral internal capsule and/or corona radiata infarction.MethodsUsing a database that included consecutive patients with ischemic stroke admitted to the neurological stroke units of three hospitals within 7 days from onset between September 2011 and April 2014, we retrospectively extracted first-ever stroke patient data, who presented with PD or DFP with a single ischemic lesion localized in the internal capsule and/or corona radiata. Patients with weakness, ataxia, sensory deficit, or cortical symptoms were excluded. Ischemic lesion volume was calculated by the ABC/2 method on diffusion-weighted imaging (DWI). DWI images were normalized and superimposed to the template for PD and DFP. We compared patients' characteristics between PD and DFP.ResultsA total of 2126 patients, including 65 patients (3.1 %) with PD or DFP, were registered. Of these, 13 PD patients and 18 patients with DFP due to unilateral internal capsule and/or corona radiata infarction were included for analysis. Compared with DFP patients, PD patients had longer onset-to-door time (median 37.5 vs. 10.8 h, p = 0.031), shorter vertical length (C component) of ischemic lesions (median 12.0 vs. 18.8 mm, p = 0.007), and smaller ischemic lesion volume (median 285 vs. 828 mm3, p = 0.023). Ischemic lesions causing PD were located more frequently in the left hemisphere than DFP (92 % vs. 56 %, p = 0.045). The superimposed lesion pattern indicated that DFP had lesions more medial and involving posterior portions of the putamen and the caudate body, as well as more of the genu and posterior limb of the internal capsule, than PD. Ninety days after onset, symptoms disappeared in 21 (72 %) out of 29 patients.ConclusionsIn cerebral infarction limited to the internal capsule and/or corona radiata, PD is derived from smaller and left-sided lesions with delay in diagnosis compared with DFP. The clinical course of those with PD and DFP might be benign.

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Central pontine myelinolysis (CPM), which was originally considered to be the result of rapid correction of chronic hyponatremia, is not necessarily accompanied by hyponatremia or drastic changes in serum sodium level. Here, we report a case of an anorexic 55-year-old male with a history of pharyngo-laryngo-esophagogastrectomy, initially hospitalized with status epilepticus. Although his consciousness gradually recovered as we were controlling his convulsion, it deteriorated again with new onset of anisocoria, and magnetic resonance imaging (MRI) at this point revealed CPM. Rapid change of serum sodium or osmolarity, which is often associated with CPM, had not been apparent throughout his hospitalization. Instead, a review of the serum biochemistry test results showed that serum phosphate had drastically declined the day before the MRI first detected CPM. In this case, we suspect that hypophosphatemia induced by refeeding syndrome greatly contributed to the occurrence of CPM.

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