Electrographic Seizures in Pediatric Systemic Cancer Patients with acute Unexplained Encephalopathy Diagnostic role of Bedside Emergent Ã¢â€°Â¥ 30min EEG
Muhammad Akbar Malik was trained in General Pediatrics in Pakistan and then was trained in Pediatric Neurology in Frenchay Hospital Bristol, UK. He established Pediatric Neurology department and worked for five years in Lahore Children Hospital. Now he heading a charity project: Top-Down-Bottom-Up project, aiming to provide pediatric neurology services at door-steps of out-reached poor communities in Pakistan.
Systemic pediatric cancer patients are prone to become critically ill and may develop seizures and encephalopathy, which can result in permanent neurologic disability. There are few techniques for monitoring brain functions in these patients, especially in resource-poor settings. The emergent bed-side electroencephalogram (EEG) can be useful. Purpose: to determine, usefulness of emergent bedside EEG features among these patients with unexplained coma (GCS≤8) of ≤6 hrs duration. Methodology & Theoretical Orientation: Prospective EEG assessment of 40 systemic cancer patients consecutively diagnosed and admitted in neurointensive care units. Patients with brain tumor, brain metastasis, seizures or those with known cause of coma were excluded. Findings: Over a period of 2 year, 40 children; boys 65% and girls 35%, with systemic cancer patients with a median age of 9.8 years were studied. This cohort underwent bed-side EEG of ≥ 30 minutes, which was abnormal in 100% of the records. The most common EEG abnormalities were invariant mixed theta-delta slowing (27.5%), followed by low-amplitude delta pattern plus epileptiform discharges (20%) and there was electrographic evidence of EEG seizures in 17(42.5%) of the cohort. These electrographic seizures were present in 55.5% of 18 patients with subtle convulsions, whereas were documented only in 20% of the 22 patients without such movements. Electrographic seizures among patients with subtle convulsions responded to anticonvulsant drugs in 75% cases as compared 50% such response among patients without such convulsions. Conclusion& Significance: seizures are common among critically ill children with systemic cancer. Bed-side EEG record of ≥30 minutes is useful in such patients. Recommendations are made for emergent ≥ 30min EEG among systemic cancer patients with unexplained acute coma.
Diagnoses and treatments of chronic alcoholic toxic cerebral encephalopathy: an expert consensus Specialized Committee Professional Board of Brain and Spinal Cord Injury, Neurology Branch of Chinese Medical Doctor Association
Ying Peng, M.D. & Ph.D. From 1997 to 2001, he got his post-doctor training in National Institutes of Health, USA. Now He is working in Sun Yaat-Sen Memorial Hospital, Sun Yat-Sen University as a full-professor. His current research fields include: 1. Addiction & Toxic Encephalopathy; 2. Gene therapy of Neurological Disease; 3. Cerebral ischemic stroke; 4.Brain injure and neural regeneration. He got 7 funds during the period of working in the University of Hong Kong and 16 grants after working in the Sun Yat-Sen Memorial Hospital. He published 105 papers in SCI journals. Additionally, he got the “Fellows Award for Research Excellence 2001”, sponsored by National Institutes of Health of USA., and the “Second Prize for Scientific Technique Progress Award of Guangdong Province” in China.
Chronic alcoholism encephalopathy is a common disease existing all over the world, which is an important symptom of alcohol abuse and alcoholism. In order to promote neurologists’ understanding, popularize the standardized diagnosis and treatment of chronic alcoholism encephalopathy, we have made extensive discussion to reach the following consensus on the principles related to the clinical diagnosis and treatment on chronic alcoholism encephalopathy.
I. Definition of chronic alcoholic encephalopathy
Chronic alcoholism encephalopathy is a chronic and recrudescent brain disease caused by alcohol acting on the brain tissue due to long-term drinking, that is to say, a seriously poisoning condition on the central nervous system caused by excessive drinking for a long time, and almost all patients have dependently chronic pathogenesis of alcohol syndrome.
II. Clinical manifestations and characteristics of chronically alcoholic encephalopathy
We divide chronic alcoholism encephalopathy into 6 kinds of syndrome according to the patient’s clinical manifestation and the condition of onset and the duration of the disease, including Wernicke encephalopathy, Coxsackoff syndrome, chronic alcoholism dementia, alcoholic tremor-delirium, alcoholic epilepsy, alcoholically mental and behavioral disorders.
III. Clinical diagnosis of chronic alcoholic encephalopathy
The coring symptoms/diagnostic criteria for alcohol dependence are described in DSM-4/ICD-10 as followings (3 Or more of the following within 12 months): (1)Alcoholic tolerance;(2)interrupting symptoms/reactions after stopping drinking; (3)Excessive intake; (4)Beyond control and abstinence; (5)Spending a lot of time seeking, acquiring and ingesting alcohol; (6)The intention of social communication is decreased; (7)Regardless of any adverse consequences. The clinicians should be based on the above-mentioned diagnostic criteria, combined with the clinical manifestations and imaging characteristicsfor comprehensive judgment.
IV. Treatment of chronically alcoholic encephalopathy
Abstinence from alcohol: Currently first-line medicine: Nalmefen, naloxone, dithiolam, aconic acid; The second-line medicine: Baclofen, topiramate, benzodiazepines, tricyclic antidepressants, high-dose antioxidants. Others include etiological treatment, correction on nutritional disorders, brain-protecting therapy, rehabilitation therapy and others.
Dr. Xiaoni Zhang has her expertise in clinical and mechanism studies of substance dependence. Dr. Zhang has completed her M.D. and M.S. at Sun Yat-Sen University. She is currently a resident at Department of Neurology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University. Her research field is focused on substance dependence and morphine-induced immunosuppressive effects.
Objectives: Studies have shown that opiate and heroin dependence causes alterations in serum lipids. In this study, we investigated the relationship between different types of substance dependence and serum lipid levels.
Methods: Serum lipid levels were measured in 97 patients with different types of substance dependence (heroin, methamphetamine, ketamine, and codeine phosphate dependence), and in 99 healthy subjects. The clinical characteristics of substance-dependent patients were also investigated.
Results: Serum total cholesterol (TC; 3.74±1.02 mmol/L, P=0.017) and high-density lipoprotein cholesterol (HDL-C; 1.12±0.19, P=0.007) levels were lower, and triglyceride levels (TG; 1.73±0.89 mmol/L, P=0.008) were higher in the heroin dependence group compared to the control group. Serum TG (1.74±1.11 mmol/L, P=0.000), HDL-C (1.44±0.30 mmol/L, P=0.011), apolipoprotein A-1 (ApoA-1; 1.55±0.28 g/L, P=0.000), and apolipoprotein B (ApoB; 1.55±0.28 g/L, P=0.000) levels were higher in the methamphetamine dependence group, while serum TG (2.49±1.56 mmol/L, P=0.000) and ApoB (0.93±0.25 g/L, P=0.000) levels were higher in the ketamine dependence group compared to the control group. Additionally, the codeine dependence group exhibited higher serum TG (1.94±1.34 mmol/L, P=0.000) and ApoB (0.82±0.28 g/L, P=0.003) levels. We also found that patients with psychotic symptoms had significantly higher TG levels in the heroin, methamphetamine, and ketamine dependence groups, and lower TC and HDL-C levels in the heroin dependence group.
Conclusions: Our data suggested that different types of substance dependence caused varying degrees of change in serum lipid levels, and that hypertriglyceridemia was consistent with psychotic symptoms in substance abuse patients.
King Faisal Specialist Hospital and Research Centre Saudi Arabia
Faida El Bitar is the professor in the Department of Genetics at King Faisal Specialist Hospital and Research Centre, Saudi Arabia. She is currently working in the Alzheimers project.
Alzheimer’s disease (AD) is the most common cause of dementia in the elderly. The toxicity of b-amyloid (Ab) peptides is thought to be involved in neuronal damage in this pathology. Multiple studies focused on role of neuroprotective molecules to attenuate the toxic consequences of Ab peptides in the development of AD.
In the present work, our objective is to investigate in vitro if PAC which is the synthetic analogue of curcumin displays neuroprotective activity against Ab peptide-induced neurotoxicity, using rat neuroblastoma B104 as cell culture model. Our results showed that PAC is not neurotoxic per se. In addition, PAC showed a striking neurotrophic activity in cells cultured at low density. This neuronal outgrowth increases importantly with increasing days of culture starting from 2 folds increase at day 2 to 3 folds increase at day 5. The number of neurites per cell rises also in presence of PAC.
Most importantly, we demonstrate the capacity of PAC to correct sAb25-35 neurotoxicity. The percentage of cell viability increases significantly by PAC at 0.5µM in presence of sAb 25-35 compared to that in presence of the peptide alone .Interestingly, our neurotrophic and neuroprotection studies showed the PAC was 20 times more efficient than curcumin. Both PAC and curcumin displayed an effect on cell-cell interaction.
Thus, our results revealed neuroprotective properties of PAC against Ab peptide. The continuity in examining the mechanism(s) underlying PAC activity is promising towards identifying efficient therapy for AD.
To study the heteroplasmy and phenotype correlations of mtDNA 3243A>G mutation in 7 Han Chinese families using restrict fragment length polymorphism (RFLP) and pyrosequencing (Pyro). Methods Seven probands were pathologically and genetically diagnosed as mitochondrial diseases with 3243A>G mutation. The clinical phenotypes were studied in 39 maternal family members. 5 were diagnosed as mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS), 2 with pure mitochondrial myopathy (MM), 1 with early neuropathy, ataxia, and retinitis pigmentosa (NARP) syndrome. Six with diabetes, 3 with hearing loss, and 20 family members are normal. Blood DNA from 37 members were detected with RFLP and pyrosequencing. mtDNA 3243A>G heterogeneity were analyzed. Results Mutation load in blood of 5 MELAS patients were 15.7% by RFLP (29% by Pyro), 12.8% (19% by Pyro), 40.1% (53% by Pyro), 25.8% (30% by Pyro), 28.3% (59% by Pyro). Mutation load in 2 MM patients were 13.7% (29% by Pyro) and 76.8% (79% by Pyro), and that in the NARP patient was 20.0% (57% by Pyro). Six family members with diabetes were range from 3.7%-7.6% (0%-14% by Pyro). Three family members with hearing loss were range from 4%-18.2% (6%-18%). The mutation load of 14 normal family members range from 2% to 12.5% (0%-5% by Pyro). Detection by Pyro is more accurate than RFLP when mutation load is lower than 10%. The mutation load is higher in those earlier age of onset.
Conclusion Pyrosequencing is more reliable when mutation load is lower than 10%. The mutation load is negatively correlate to the age of onset in this research.