Objective To investigate the changes of cognitive function of epileptic patients after antiepileptic drugs (AEDs) therapy. Methods Twenty eight cases of epileptic patients with new diagnosis and untreatment from March 2015 to February 2016 were collected. According to the seizure type, degree of attack and drug efficacy, patients were divided into three groups and treated with one of three AEDs, including Lamotrigine (LTG), Oxcarbazepine (OXC), and Sodium valproate (VPA). Among them, 11 were LTG group, 12 were OXC group and 5 were VPA group.Then the patients were followed up for 1 year. The clinical memory scale was used to analyze cognitive function of epileptic patients before and after therapy. Results Compared to 30 cases of healthy volunteers, the scores of memory quotient (P<0.01), directed memory (P<0.05), associative learning (P<0.05) and image free recall (P<0.01) of epileptic patients were obviously decreased before AEDs therapy.AEDs therapy reduced or controlled seizures in new diagnostic epileptic patients, and the total effective rate was 85.7%. In the clinical memory scale tests, the scores of memory quotient (P<0.01), directed memory (P<0.05), associative learning (P<0.05), portrait characteristics contact memory (P<0.05) were improved after therapy. The scores of image free recall and meaningless graphics recognition were also improved, but there was no statistical significance. Besides, there was a statistically significant improvement in the score of portrait characteristics contact memory after LTG treatment (P<0.05), and directed memory after VPA treatment (P<0.05). Conclusions Epileptic patients accompanied with cognitive deficits before drug intervention. Through standard AEDs treatment, seizures could be better controlled. The cognitive function of epileptic patients was not declined after short-term（within 1 year） intervention of LTG, OCX or VPA. Moreover some parts of the cognitive domain could be improved.
ObjectivesTo explore the characteristics of cognitive deficits of Benign epilepsy of childhood with centrotemporal spikes (BECTS).MethodsA total of 61 BECTS patients who visited Neurology Clinic of Xuanwu Hospital Capital Medical University between September 2010 to December 2019 and 60 healthy controls were enrolled in our study. All patients and healthy controls performed a series of neuropsychological tests to assess their cognitive function in the "Multi-dimensional psychology" of Beijing Normal University, including attention; memory; arithmetic calculation; language processing; executive function; visuospatial processing; visual perception; psychomotor speed. Lastly, independent sample t-test and friedman test were performed on the scores of BECTS group and controls using SPSS 20.0 and we conducted a multi-factor comprehensive analysis of correlation between clinical criteria and cognitive dysfunction in BECTS.ResultsCompared with 60 healthy controls, the as group got an average score of 19.56±2.91 in Paired Association Learning Test (P<0.001), (23.67±9.50) in Word Discrimination Test (P=0.017), (61.45±13.14) in Object Quantity Perception Task (P=0.040), (6.54±1.47) in Digit Span Test (P<0.001), (5.79±5.90) in Vocal Perception Test (P<0.001), (35.10±2.33) in Taylor Complex Figure Test (P<0.001) and (700.34±493.053) (P=0.008) in Choice Reaction Time Test. The results of these tests are inferior to the control group and the remaining 10 tests are of no statistical significance. There were 36 children with onset of seizure before 8 years of age. Compared with the patients experienced onset of illness at a later age, the 36 patients exhibited lower scores in most of the neuropsychological tests including Visual Tracking Task, Spatial Memory Task, Simple Subtraction Task, Number Comparison Test, Language Rhyme Test, Word Discrimination Testand Visual Perception Task (P<0.05). 34 patients received monotherapy, and 27 received a combination of 2 or 3 anti-epileptic drugs. The scores of attention, memory, visual perception and reaction tests in the multi drug treatment group were lower than those in the single drug treatment group (P<0.05).ConclusionsChildren with BECTS have impairment in attention, vocal perception, visual perception, memory and psychomotor speed. The younger the age of onset, the more severe the cognitive impairments. The degree of cognitive deficitsinchildren treated with multi drugs was more serious than that of children treated with single drugs.
Epilepsy is defined as a disorder of brain neural function, characterized by the persistent possibility of seizures, which are usually sudden, brief, and recurrent. Cognition is a process of receiving information from the external world and analyzing and processing it, such as memory, language, visual-spatial, executive, calculation, comprehension, and judgement. With the increasing awareness of health, more and more scholars have begun to pay attention to the relationship between cognitive dysfunction and epilepsy. Data shows that over 80% of epilepsy patients have lower cognitive abilities than healthy people, and over 50% of patients have significant cognitive problems, which have a negative impact on their quality of life even greater than the seizures themselves. Cognitive impairment in epilepsy patients not only hinders their own treatment progress, but also has a negative impact on their daily life, academic and job performance, which brings huge care and economic pressure to their families and a heavy economic burden to the whole society. This review aimed to assess cognitive modules and provide key information for early diagnosis and treatment of patients.
ObjectiveAnalyzing the seizure and cognitive outcome after different treatment by observation of a large group of intractable child epilepsy patients under 15 years old. MethodsCollecting data of children with Intractable epilepsy from Apirl 2008 to December 2013 in Sanbo Brain Hospital, Capital Medical University. Three historical cohorts of intractable child epilepsy defined by the final treatment including medication, curative operation and palliative operation depending on the surgical assessment and the families intension was retrospectively observed. 1 year and 3 years follow-up postoperatively were conducted including seizure outcome and cognitive outcome. ResultsThe curative operation group had significant better seizure free rate, and cognitive statement than medication group. And, the seizure free and cognitive outcome were better in palliative operation group than the medication group. ConclusionsEarly surgical intervention is highly recommended for intractable epilepsy chilelren in order to improve both the seizure and cognitive prognosis.
Objective This study aimed to observe the protective effects of 17β-estradiol (17β-E2) to the damage of phenobarbital (PB) upon the cognition of the newly-born rats. Methods Thirty healthy 3-day-old Sprague Dawley (SD) rats were randomly divided into 3 groups: control group (10 rats), PB group (10 rats) and PB+17β-E2 group (10 rats). The control group were injected saline water with a dose of 10 mL/(kg·d); the PB group were injected with PB of 10 mg/(kg·d); the PB+17β-E2 group were injected with PB 10 mg/(kg·d) and 17β-E2 300 ug/(kg·d). All the rats were intraperitoneal injected once a day after weighing, for three continuous days. They were normally raised to one month old and then 8 rats were selected out of each group respectively for water maze test. Results The PB group was reported to have increasing latent periods in finding the underwater stage compared with control group (P<0.05). In comparison with the PB group, the PB+17β-E2 group has a shorter latent period in finding the underwater stage, and furthermore statistically significantly fewer times in finding validation areas (P<0.05). During the 120s test, the stage quadrant journey to total journey ratio of PB+17β-E2 group was lower than the ratio of PB groups, but no statistics significance had been detected. The PB+17β-E2 group exhibits no significance difference from the control group in the above-mentioned indexes. Conclusions Even a short-term injection of PB with an usual clinical dose will bring a long-term damage to an immature brain in terms of the learning ability and memory, whereas the 17β-E2 may play a protective role in this course.
Objective To investigate the characteristics of cognitive function and its correlation to neuroendocrine status in patients with refractory depression. Methods A total of 41 patients diagnosed by ICD-10 as depression onset who have been treated with more than two antidepressants drugs, fulfilled the criteria of refractory depression. Another 40 patients diagnosed by ICD-10 as depression onset but who have not been treated, or have been treated with only one antidepressant drug were selected as controls. Patients in both groups were evaluated by WAIS-RC, STROOP, VF, TRAILS A, B, TOH and M-WCST, and the concentrations of CORT, ACTH, T3, FT3, T4, FT4, TSH were also determined. Results A significant difference was found in VF between the refractory depression group and the control group. This showed that the damage to short-term memory, attention and interference rejection capability was much more serious in the refractory depression group. The ACTH concentration in the refractory depression group was significantly different from that of the control group, which indicated that the damage to the Hypothalamic-pituitary-adrenal axis was more serious in the refractory depression group. In particular in relation to memory and attention defect. Conclusion Changes in the levels of CORT, ACTH, TSH, FT3 and T4 may be correlated to cognitive function damage in patients with refractory depression.
Nowadays, an increasing number of researches have shown that epilepsy, as a kind of neural network disease, not only affects the brain region of seizure onset, but also remote regions at which the brain network structures are damaged or dysfunctional. These changes are associated with abnormal network of epilepsy. Resting-state network is closely related to human cognitive function and plays an important role in cognitive process. Cognitive dysfunction, a common comorbidity of epilepsy, has adverse impacts on life quality of patients with epilepsy. The mechanism of cognitive dysfunction in epileptic patients is still incomprehensible, but the change of resting-state brain network may be associated with their cognitive impairment. In order to further understand the changes of resting-state network associated with the cognitive function and explore the brain network mechanism of the occurrence of cognitive dysfunction in patients with epilepsy, we review the related researches in recent years.
ObjectiveTo systematically review the influence of dexmedetomidine on early postoperative cognitive dysfunction in adult patients after receiving noncardiac surgery under general anesthesia. MethodsThe randomized controlled trials (RCTs) about the influence of dexmedetomidine on the early postoperative cognitive dysfunction of patients after receiving noncardiac surgery with general anesthesia was searched in PubMed, EBSCO, Springer, Ovid, The Cochrane Library (Issue 1, 2013), CNKI, VIP, WanFang Data and Google Scholar up to November 30th, 2013. The references of included literature were also retrieved manually. Two reviewers independently screened literature according to the inclusion and exclusion criteria, extracted data, and assessed the methodological quality of included studies. Then meta-analysis was performed using RevMan 5.2. ResultsA total of 22 RCTs involving 1 356 patients were enrolled. The results of meta-analysis indicated that:a) dexmedetomidine reduced the incidence of postoperative cognitive dysfunction on the first day (RR=0.38, 95%CI 0.29 to 0.49, P < 0.001), on the seventh day (RR=0.55, 95%CI 0.23 to 1.29, P=0.17); improved postoperative MMSE scores after surgery (on the first day:MD=2.38, 95%CI 1.42 to 3.34, P < 0.001; on the seventh day:MD=0.92, 95%CI 0.16 to 1.68, P=0.02), and decreased the expression of inflammatory factor IL-6 (instant:MD=-11.96, 95%CI-18.45 to-5.46, P=0.000 3; after 24 h:MD=-7.50, 95%CI-13.73 to-1.27, P=0.02); and TNF-α (instant:MD=-4.09, 95%CI-7.02 to-1.16, P=0.006)) in patients. b) No significant difference was found between two groups (MD=-0.97, 95%CI-2.37 to 0.43, P=0.17). ConclusionDexmedetomidine can effectively reduce the early-stage postoperative cognitive dysfunction, improve MMSE scores after the operation, and reduce inflammatory reaction. In addition, due to the limited quantity and quality of studies included, larger sample, high quality RCTs are needed to verify the abovementioned conclusion.
ObjectiveTo investigate the effects of hippocampal long-term potentiation (LTP) on cognitive dysfunction in immature epileptic rats. MethodsImmature epileptic rats were established by intraperitoneal injection of lithium chloride-pilocarpine (li-pilo). Racine classification standard modified by Becker was used to evaluate behavior of epileptic seizure, and the survival rats within RacineⅣmagnitude were selected in the experiment. The function of learning and memory of epileptic rats when they were adult was assessed using Morris water maze experiment, and their independent exploratory behavior was evaluated by the open-field test. Field potential was recorded by electrophysiological technology to detecte whether hippocampal LTP was essential of cognitive dysfunction. ResultsThe function of learning and memory was significantly impaired when compared with controls(n=8, t=10.86, P < 0.05;n=8, t=9.98, P < 0.05). In addition, independent exploratory behavior was significantly reduced when compared with controls(n=8, t=12.89, P < 0.05). Besides, CA1 hippocampal LTP induced by high-frequency stimulation presented the significant inhibition in epileptic rats with cognitive dysfunction when compared with controls(Slope:n=8, t=13.32, P < 0.05;Amplitude:n=8, t=20.02, P < 0.05). ConclusionInhibition of CA1 hippocampal LTP may be implicated in cognitive dysfunction of epileptic rats.
Lung cancer ranks first in the incidence of malignant tumors in China, which is seriously harmful to people’s life and health. Chemotherapy is an effective treatment for lung cancer, and it is also an important cause of cognitive dysfunction. Cognitive impairment is usually evaluated by subjective assessment, neuropsychological testing and neuroimaging research. The mechanism of cognitive impairment in patients with lung cancer caused by chemotherapy may include the accumulation of a large amount of endogenous tau protein in hippocampus, the induction of hippocampal neuroinflammation, and the direct killing effect of drugs on nerve cells. There is no effective treatment for chemotherapy-related cognitive impairment (CRCI), but current studies have found that cognitive education in the form of mind map, diet regulation, physical exercise and caring therapy may contribute to the improvement of cognitive function of lung cancer patients after chemotherapy. Based on the current research results, this article provides new ideas for the research and treatment of lung cancer patients with CRCI in terms of clinical characteristics, evaluation methods, influencing factors, mechanism and prevention strategies.