Stroke after coronary bypass surgery is mainly related to diffuse atherosclerotic disease.

OBJECTIVE: This study aims to investigate the risk factors for postoperative stroke and analysis of outcome after coronary bypass surgery with cardiopulmonary bypass. METHODS: Between 1999 and 2008, 3248 consecutive patients who underwent isolated coronary surgery with cardiopulmonary bypass were prospectively enrolled in the study. Demographic and perioperative data were analyzed. Postoperative stroke was defined as severe adverse neurological events including permanent deficits or cerebral lesions with radiological demonstration of cerebral infarction within the first postoperative month. RESULTS: In total, 32 patients (0.9%) were determined with stroke. Univariate risk factors for postoperative stroke were determined as preoperative unstable angina (P = .006), Canadian Class of Angina (CCA) ≥ 3 (P = .001), preoperative creatinin level >1.2 mg/dL (P = .001), left main coronary artery disease (P = .04), chronic obstructive lung disease (P = .04), peripheral arterial disease (P < .001), New York Heart Association (NYHA) Class ≥ 3 (P = .004), preoperative renal insufficiency (P = .001), age > 65 years (P = .04), preoperative hypothyroidism (P = .02), postoperative low cardiac output state (P < .001), severe coronary artery disease requiring distal anastomosis ≥ 4 (P = .05), non-elective operation (P = .02), and body mass index ≥ 25 (P = .02). Multivariate analysis revealed peripheral arterial disease (odds ratio [OR], 5.2; 95% confidence interval [CI], 1.9-14.0; P = .001), severe coronary artery disease (OR, 3.1; 95% CI, 1.1-8.5; P = .02), and postoperative low cardiac output state (OR, 5.1; 95% CI, 1.4-18.2; P = .01) as the independent risk factors. CONCLUSIONS: Stroke after coronary bypass surgery with cardiopulmonary bypass is mainly related to diffuse atherosclerotic disease.

Tuberculous meningitis presenting with nonconvulsive status epilepticus.

Nonconvulsive status epilepticus (NCSE) is an enduring epileptic condition characterized by alteration in consciousness and continuous ictal discharges on the EEG. Various etiologies have been reported. We describe the case of a 66-year-old woman with altered mental status who was diagnosed with NCSE. A workup to explain the etiology revealed tuberculous meningitis (TBM) with increased cerebrospinal fluid protein and positive tuberculous DNA polymerase chain reaction and interferon-γ assay tests. She was treated according to the status epilepticus protocol with a four-drug anti-tuberculosis regimen to which she responded. TBM is a serious disease with insidious presentation and still constitutes a diagnostic challenge with its various presentations. Among the many presentations of tuberculosis, clinicians should consider NCSE.

Cortical excitability in juvenile myoclonic epileptic patients and their asymptomatic siblings: a transcranial magnetic stimulation study.

In this study, we aimed to evaluate motor cortical excitability changes in patients with juvenile myoclonic epilepsy (JME) and their asymptomatic siblings (AS) using single-pulse transcranial magnetic stimulation (spTMS). 21 patients with JME and their 21 AS were compared to 20 healthy controls. All of JME patients were receiving antiepileptic therapy and their seizures were well controlled. Firstly, standard EEG examinations and then TMS studies were performed. Resting motor threshold (RMT), motor evoked potential (MEP) amplitudes, the durations of central motor conduction time (CMCT) and cortical silent period (CSP) were measured. After TMS studies, EEG recordings were repeated in an hour to evaluate any effect of TMS study on EEG. There were no significant differences between the first and second EEG recordings. No seizures were recorded during and after the TMS study. RMT was found higher in JME patients than AS and normal controls. There were no significant differences between cortical MEP amplitudes and MEP amplitude/CMAP (compound muscle action potential) amplitude ratio in all three groups. CMCT duration was shorter in JME patients than AS. CSP durations of JME patients were found to be longer than controls. In AS, CSP durations were also found to be longer than controls but this difference was not found statistically significant. Our results suggested that although high MT may be related to antiepileptic therapy, the prolongation of CSP duration may reflect impairment of supraspinal and/or intracortical inhibitory mechanism in JME. To eliminate the drug effect, further studies are needed in newly diagnosed JME patients without medication and large series of their asymptomatic siblings.

Deep brain stimulation for Holmes' tremor related to a thalamic abscess.

BACKGROUND: Medical treatment is usually ineffective for Holmes' tremor, and surgery is the treatment of choice for many patients. Here we report the case of a 14-year-old girl who developed Holmes' tremor related to a thalamic abscess and was successfully treated with thalamic deep brain stimulation. CASE REPORT: The patient presented with left hemiparesis and headache and was hospitalized. Investigation revealed a thalamic abscess in the left cerebral hemisphere. The abscess was drained via stereotactic surgery and a course of antibiotic treatment was completed. Four months after treatment, the patient developed Holmes' tremor in her left upper extremity. When attempts at medical treatment with levodopa, clonazepam, and trihexyphenidyl all failed, an implant was placed and deep brain stimulation of the ventral intermediate nucleus of the thalamus was initiated. During 2.5 years of follow-up, her tremor diminished by 90%. CONCLUSION: This case demonstrates that medically resistant Holmes' tremor related to a thalamic lesion can be successfully treated with thalamic deep brain stimulation.