Prognostic values of optic nerve sheath diameter for comatose patients with acute stroke: An observational study.

BACKGROUND: Optic nerve sheath diameter (ONSD) measurement is one of the non-invasive methods recommended for increased intracranial pressure (ICP) monitoring. AIM: This study aimed to evaluate the roles of optic nerve sheath diameter (ONSD) and ONSD/eyeball transverse diameter (ETD) ratio in predicting prognosis of death in comatose patients with acute stroke during their hospitalization. METHODS: A total of 67 comatose patients with acute stroke were retrospectively recruited. The ONSD and ETD were measured by cranial computed tomography (CT) scan. All patients underwent cranial CT scan within 24 h after coma onset. Patients were divided into death group and survival group according to their survival status at discharge. The differences of the ONSD and ONSD/ETD ratio between the two groups and their prognostic values were compared. RESULTS: The ONSD and ONSD/ETD ratio were 6.07 ± 0.72 mm and 0.27 ± 0.03 in the comatose patients, respectively. The ONSD was significantly greater in the death group than that in the survival group (6.32 ± 0.67 mm vs 5.65 ± 0.62 mm, t = 4.078, P < 0.0001). The ONSD/ETD ratio was significantly higher in the death group than that in the survival group (0.28 ± 0.03 vs 0.25 ± 0.02, t = 4.625, P < 0.0001). The area under the receiver operating characteristic curve was 0.760 (95%CI: 0.637-0.882, P < 0.0001) for the ONSD and 0.808 (95%CI: 0.696-0.920, P < 0.0001) for the ONSD/ETD ratio. CONCLUSION: The mortality increased in comatose patients with acute stroke when the ONSD was > 5.7 mm or the ONSD/ETD ratio was > 0.25. Both indexes could be used as prognostic tools for comatose patients with acute stroke. The ONSD/ETD ratio was more stable than the ONSD alone, which would be preferred in clinical practice.

[Paroxysmal kinesigenic dyskinesia: 2 case reports].

Paroxysmal kinesigenic dyskinesia (PKD) is a rare neurological condition in which brief and frequent dyskinetic attacks are provoked by sudden movement. PKD is more common in men and can be idiopathic (commonly familial) or due to a variety of causes. The pathophysiology of PKD is uncertain but it could be an ion-channel disorder. Genetic linkage studies have isolated several loci on chromosome 16, and proline-rich transmembrane protein 2 (PRRT2) has been identified as a causative gene of PKD by using a combination of exome sequencing and linkage analysis. Antiepileptic drugs, particularly, carbamazepine are very helpful in a large proportion of cases. Sometimes it can be difficult to distinguish this syndrome from epilepsy. We reported 2 patients who presented abnormal involuntary attack. Evaluations included general physical examinations, endocrinologic and metabolic studies, video electroencephalograms and brain MRI imaging. All of these studies were normal. All of symptoms showed excellent response to carbamazepine.

TDAG51 in the anterior temporal neocortex of patients with intractable epilepsy.

TDAG51 (T cell death-associated gene 51) is an apoptosis-associated protein. Our aim was to investigate TDAG51 expression in the anterior temporal neocortex of patients with intractable epilepsy (IE), and then to discuss the possible role of TDAG51 in IE. Tissue samples from the anterior temporal neocortex of 33 patients who had surgery for IE were used to detect TDAG51 expression by immunohistochemistry, immunofluorescence, and Western blotting. We compared these tissues with nine histologically normal anterior temporal lobes from intracranial hypertension patients who had decompression procedures. TDAG51 was mainly expressed in the cytoplasm of neurons and glial cells. TDAG51 in IE was significantly higher than that in the controls. These findings were consistently observed using Western blotting, immunofluorescence, and immunohistochemistry techniques. TDAG51 in patients with IE was significantly higher when compared with levels in the controls. This finding suggests TDAG51 is consistent with a possible role of this gene in the evolution of the pathology in IE.

HSPBAP1 is found extensively in the anterior temporal neocortex of patients with intractable epilepsy.

Heat Shock Protein BAP1 (heat shock 27-kDa-associated protein 1, HSPBAP1) inhibits the function of heat shock protein 27, which has a neuroprotective effect during experimentally induced epileptic neuropathology. In our study, fluorescence quantitative polymerase chain reaction, immunohistochemistry, immunofluorescence, western blot were used to test the levels of HSPBAP1 mRNA and protein in surgical samples of the anterior temporal neocortex of patients with intractable epilepsy (IE) and normal controls samples. HSPBAP1 mRNA was abnormally expressed in the anterior temporal neocortex of patients with IE. Moreover, HSPBAP1 was found extensively in the cytoplasm of neurons and glial cells in all epilepsy specimens. Western blot showed a clear immunoreactive band of HSPBAP1 in IE specimens whereas it was absent in control specimens. The expression of HSPBAP1 mRNA and protein in the anterior temporal neocortex from patients with IE may play a role in the development of epileptic seizures in patients with cell loss in this brain region. Additional studies will be required to elucidate the mechanism by which HSPBAP1 affects brain function in IE.

Treatment of late lithium-pilocarpine-induced status epilepticus with diazepam.

PURPOSE: It is well known that status epilepticus (SE) becomes increasingly difficult to control over time. Previous studies have indicated that the electroencephalographic pattern at the time of intervention is predictive of the probability of successful treatment. However, these findings are based on studies limited to the first 2h of SE onset. Little data is available on the efficacy of treating SE at later time points. METHODS: The aim of the present study was to investigate the efficacy of diazepam (DZP) treatment given at two different phases of SE in a lithium-pilocarpine rat model: during continuous ictal discharges (CIDs, phase 3), and during late periodic epileptiform discharges (late PEDs, phase 5). Changes in cortical and hippocampal electroencephalographs (EEGs) were observed continuously during the phases of SE, as well as at 24, 36, 48, and 72h after SE onset. The effects of DZP treatment during CIDs or during late PEDs were compared to control DZP-untreated rats. RESULTS: In all three groups, hippocampal and cortical EEGs displayed five distinct phases of SE. There were no statistical differences in the duration of phases 1 and 2 among the three groups. Although DZP administration during CIDs did not terminate CIDs in most rats, it did significantly shorten the duration of phases 3 and 4 of SE. Importantly, DZP given during phase 5 successfully ended behavioral and electrographic seizures in most rats. CONCLUSIONS: Hippocampal and cortical EEGs displayed five distinct phases of SE that were similarly responsive to DZP treatment. Termination of electrographic seizures with DZP treatment was more effective in the last phase of SE (late PEDs) than in phase 3 (CIDs). These findings suggest that previous reports of DZPs decrease in efficacy over time may not be applicable to DZP treatment at 4h-post onset.

Gene polymorphism of platelet glycoprotein I balpha in Chinese patients with large- and small-artery subtypes of ischemic stroke.

The platelet surface glycoprotein (GP) I balpha, an important part of the GP I b-IX-V complex, participates in the formation of thrombosis by initially mediating platelet adhesion under high shear stress. The purpose of present study was to investigate the association between gene polymorphism of GP I balpha (human platelet antigen 2, HPA2) and ischemic stroke in a matched case-control study. One hundred patients and 100 matched controls were enrolled in the study. The cases were divided into large- and small-vessel subtypes of ischemic stroke according to Trial of Org10172 in Acute Stroke Treatment criteria. Genotyping for GP I balpha polymorphism was documented by polymerase chain reaction amplification and restriction enzyme analysis. There were no statistically significant differences in the GP I balpha HPA2 genotype distribution between ischemic stroke group, large-vessel subtype group, small-vessel subtype group and corresponding control groups. The heterozygote genotype of GP I balpha HPA2 was more frequent in the large-vessel subtype group (16.1%) than in the small-vessel subtype group (10.1%), but the difference was not statistically significant. Ourresults suggest that the polymorphism of the GP I balpha HPA2 genotype might not be a genetic risk factor of ischemic stroke.