Pretreatment Blood Pressure is a Simple Predictor of Hemorrhagic Infarction after Intravenous Recombinant Tissue Plasminogen Activator (rt-PA) Therapy.

BACKGROUND: Hemorrhagic infarction (HI) is among the most severe complications that can occur following the administration of intravenous recombinant tissue plasminogen activator (rt-PA). In the present study, we aimed to determine the optimal cut-off points of blood pressure (BP) for HI after rt-PA treatment, and to compare our findings with those for other prediction models. METHODS: We analyzed data from 109 consecutive patients with stroke treated at our hospital between 2009 and 2016. HI was confirmed via computed tomography or magnetic resonance imaging. Patients were classified into a symptomatic HI group, an asymptomatic HI group, and a non-HI group. BP was measured on admission and before rt-PA treatment. Glucose Race Age Sex Pressure Stroke Severity (GRASPS) and Totaled Health Risks in Vascular Events (THRIVE) scores were also calculated. Receiver operating characteristic (ROC) analysis was used to determine factors associated with symptomatic and asymptomatic HI. RESULTS: Among the 109 total patients, 25 patients developed symptomatic HI, while 22 patients developed asymptomatic HI. ROC analysis for predicting symptomatic and asymptomatic HI revealed that the area under the curve for pretreatment systolic BP (SBP) was .88 (95% confidence interval[CI]: .83-.94), while those for GRASPS and THRIVE scores were .75 (95% CI: .66-.85) and .69 (95% CI: .59-.79), respectively. We identified an optimal cut-off point of 160 mm Hg (sensitivity: 82.3%; specificity: 76.6%; diagnostic accuracy: 80.0%; positive predictive value: 76.6%; negative predictive value: 82.5%). CONCLUSIONS: Pre-treatment SBP may be a simple predictor of symptomatic and asymptomatic HI in patients with stroke undergoing rt-PA treatment.

[A case of neuromyelitis optica spectrum disorders, with slowly progressive bulbar palsy, mimicking a motor neuron disease].

A 52-year old woman first noted dysphagia four months before admission followed by dysarthria two months later. She then developed weakness of all limbs and became unable to walk. All these symptoms, associated with tongue atrophy, slowly progressed, leading to the initial clinical impression of a motor neuron disease, although her nerve conduction study and electromyography showed no abnormalities. Her brain MRI with T2 weighted/diffusion weighted image (DWI)/fluid attenuated inversion recovery (FLAIR) revealed a high signal lesion located at dorsal medulla oblongata. She proved positive for anti-aquaporin 4 antibody, which confirmed the diagnosis of neuromyelitis optica spectrum disorders (NMOSD). We conclude that NMOSD may initially present with progressive bulbar palsy and pyramidal tract disorder over a few months, mimicking a motor neuron disease. Awareness of this atypical presentation helps establish an early diagnosis of this treatable entity.

[A case of hyperkalemic periodic paralysis presenting progressive myopathy with tubular aggregates].

A 33-year-old man admitted to our hospital for the evaluation of progressive muscular atrophy of his left lower leg. From his childhood, he had suffered from transient attacks of limb paralysis and myalgia lasting about 1 hour. At age 30, the muscle weakness and atrophy of his left lower leg emerged and progressed gradually. Muscle MR images showed atrophy and fat replacement in left lower leg, and muscle biopsy revealed tubular aggregates (TA). Genetic analysis showed heterozygous c.2111C>T/p.T704M missense mutation of SCN4A gene, which causes hyperkalemic periodic paralysis (HyperPP). Although HyperPP is rare, it is quite critical for clinicians to recognize that the patients of HyperPP often present progressive myopathy. We emphasize the importance of paying attention to progressive myopathy and discuss the pathological mechanism of myopathy through this case report.