Füsun Erdoğan

A 12-month study of the efficacy of rivastigmine in patients with advanced moderate Alzheimer's disease

The efficacy of a centrally active cholinesterase inhibitor, rivastigmine tartrate (ENA 713), in patients with advanced moderate Alzheimer’s disease (AD) was evaluated in a 12-month placebo-controlled study. We aimed to investigate whether there was any evidence for the benefits of rivastigmine in patients with severe disease. These patients were compared with matched controls. In this study, 24 patients with advanced moderate AD received rivastigmine for 12 months. Another 20 patients received placebo. Mean daily doses of rivastigmine in the higher-dose group at 3, 6, 9, and 12 months were 6.1 ± 1.0, 8.3 ± 1.2, 8.9 ± 1.3, and 10.7 ± 1.6 mg/day, respectively. Cognitive abilities were assessed using the 11-item cognitive subscale of the Alzheimer Disease Assessment Scale (ADAS-cog). Forty-five percent of placebo-treated patients declined by at least 4 points on the ADAS-cog. Conversely, only 18.3% of patients treated with rivastigmine declined by 4 or more points. Functional disabilities, as assessed using the Disability Assessment for Dementia Scale, remained significantly superior in rivastigmine-treated patients compared with placebo-treated patients. Patients benefited from high-dose rivastigmine treatment on all outcome measures, including the Mini-Mental State Examination, Progressive Deterioration Scale, as well as the Global Deterioration Scale. Patients receiving rivastigmine for 12 months significantly improved compared with placebo-treated patients (p < 0.001). By 52 weeks, patients originally treated with 6–12 mg/day rivastigmine had a significantly better cognitive function than patients originally treated with placebo. Long-term rivastigmine treatment appeared to be well tolerated in patients with advanced moderate AD and significantly benefits the cognitive and functional symptoms of AD.

The effects of pentylenetetrazole-induced status epilepticus on behavior, emotional memory, and learning in rats

Status epilepticus (SE) can cause spatial learning, memory, and behavioral deficits; however, little information is available, especially regarding the effects of such seizures on emotional memory and learning functions. We investigated the effects of SE on emotional memory, learning, and behavior in mature rats over short and long periods. SE was induced in 50- to 60-day-old rats (P50-P60) using intraperitoneal injections of pentylenetetrazole (PTZ, n = 20); control rats received saline (n = 10). All animals were tested with elevated T-maze and open-field tests on the 1st, 7th, 14th, and 180th days after SE to evaluate emotional memory, learning, and behavior. The number of fecal boli increased, and one-way escape latency was long in a short period after SE. PTZ-induced SE causes transient memory deficits, which is related to unconditioned fear, but it did not cause any persistent abnormalities of behavior, emotional memory, and learning in mature rats.

A comparison of the circadian rhythms and the levels of melatonin in patients with diurnal and nocturnal complex partial seizures

The aim of the present work was to assess serum melatonin levels and melatonin circadian rhythm in patients with diurnal and nocturnal complex partial epilepsy. Daily rhythms of melatonin were studied in patients with diurnal complex partial epilepsy (n=10), patients with nocturnal complex partial epilepsy (n=10), and a control group (n=10). All patients were under carbamazepine treatment. Serum melatonin samples were taken at 1000, 2200, 0100, and 0500 hours. We found that melatonin circadian rhythm was normal in all patients when compared with controls. Melatonin levels were low in both patients with nocturnal and patients with diurnal complex partial epilepsy compared with the control group at 1000, 2200, 0100, and 0500 hours; a statistically significant decrease in melatonin levels was observed in the patients with epilepsy at 1000 hours only. These findings suggest that melatonin levels and circadian rhythm of melatonin do not differ between patients with nocturnal and patients with diurnal complex partial epilepsy. Further detailed research is necessary to determine the factors that govern the nocturnal or diurnal occurrence of complex partial seizures.

The relationship between fatigue and depression, and event-related potentials in epileptics.

The aim of the present study was to establish the rate of fatigue and the relationship between fatigue, depression, and P300 in people with epilepsy. We compared Fatigue Severity Scale (FSS) and Beck Depression Inventory (BDI) scores and event-related potentials (ERPs) of people with epilepsy (n=73) with those of controls (n=31). The rate of fatigue was found to be 42.4%, and fatigue and depression were positively correlated. There was an interaction between fatigue and ERPs, but the effect of ERPs on fatigue was greater. While polytherapy was a major factor affecting ERPs, depression had no effect on ERPs in people with epilepsy. The data suggest that fatigue is an important finding and is strongly correlated with cognitive processes and depression. Polytherapy contributed to cognitive disturbances and, hence, fatigue, whereas depression had no effect on cognitive processes in people with epilepsy.

Different seizure types and skin lesions in oculocerebrorenal syndrome of lowe

Oculocerebrorenal syndrome of Lowe is an X-linked recessive disorder localized to Xq24-26.1. The phenotypic features of this disorder are Fanconi-type renal failure, mental retardation, and various eye abnormalities. Seizures may accompany the disease, and the skin-related findings are poorly defined. This case of a 9-year-old patient, diagnosed as having and followed for oculocerebrorenal syndrome of Lowe, has been presented for his seizures, which were initially myoclonic but subsequently atonic, and for his skin findings, understood to be trichoepithelioma, cystic in nature, and stemming from mature hair follicles. In monitoring the disease, the manifestation of the seizures as atonic seizures accompanied by focally initiated secondary generalized epileptic discharges is a finding previously undefined in oculocerebrorenal syndrome of Lowe. Moreover, the presence of dermal findings of a cystic nature is reported in few cases of this syndrome. In this rare syndrome, it is necessary to be aware of the presence of atonic seizures, which have an association with the progression of the disease that has not been previously reported in the literature, and of the cystic dermal lesions as part of the syndrome.

Ketamine reduces lidocaine-induced seizures in mice.

Systemic toxic reactions to local anesthetics are brought about by absolute overdosage, and, most commonly, inadvertent intravascular injections. The anti-convulsant action of ketamine has been studied. However, the effect of ketamine on lidocaine-induced convulsions has not been reported. This study investigated the effect of ketamine on lidocaine-induced seizures in mice. Mice (32–41 g) were divided into 2 groups, 15 in each group, and were pretreated with intraperitoneal normal saline solution or intraperitenoeal (ip) ketamine before lidocaine. Group 1 (N = 15) received 75 mg kg ip lidocaine; Group 2 (N = 15) received 20 mg kg ketamin ip; 5 min later 75 mg kg lidokaine ip were applied. Clinical features, incidences, latencies, durations, and mortality rate of convulsions were recorded. After 75 mg kg lidocaine injection, ataxia, loss of righting reflex, and generalized tonic-clonic convulsions were seen within 2–5 min in Group 1. Generalized tonic-clonic convulsions were seen in 8 mice and deep sedation was seen in 7 mice in Group 2 (p < .05). Generalized status epilepticus occurred in one mouse in both groups. Three mice from Group l and one mouse from Group 2 died during convulsions. There were no differences between the two groups with regard to the onset and duration of seizures (p > .05). It was concluded that ketamine significantly prevented lidocaine-induced generalized tonic-clonic seizures; on the other hand, the lethality of lidocaine was least reduced by ketamine.

EMX2-independent familial schizencephaly: clinical and genetic analyses.

Schizencephaly is a human brain malformation distinguished by full‐thickness unilateral or bilateral clefts through the neocortex. Heterozygous mutations in the EMX2 locus are reported to give rise to schizencephaly. However, the comprehensive identification of causative genetic loci is precluded by a lack of large pedigrees and genome‐wide linkage analyses. We present here a large Turkish pedigree with three individuals with schizencephaly. The similarity of clinical signs in affected individuals strongly suggests an underlying genetic cause; however, genome‐wide linkage analysis rules out EMX2 linkage and instead suggests additional candidate loci. These results indicate that genetic forms of schizencephaly are likely to be heterogeneous.

Effects of pentylenetetrazole-induced status epilepticus on behavior, emotional memory and learning in immature rats

Status epilepticus (SE) can be harmful to the developing brain. Our knowledge of the emotional and behavioral consequences of generalized SE in developing animals remains limited. Therefore, we investigated the short- and long-term effects of pentylenetetrazole (PTZ)-induced SE on emotional memory and learning and behavioral parameters in immature rats. SE was induced in 16- to 20-day-old rats (P16-P20) using intraperitoneal injections of PTZ (n=21); control rats received saline (n=10). All animals were tested using an elevated T-maze and open-field test 2, 14, 30, and 180 days after SE, to evaluate emotional memory and learning and behavior. Anxiety levels decreased 2 and 14 days after SE, and conditioned learning of PTZ-treated immature rats was better than that of the control rats. These results indicate that a decreased anxiety level facilitates conditioned learning. Behavioral changes are transient, and no emotional memory or learning deficits occur following PTZ-induced SE in immature rats.

Pseudoephedrine-induced nonconvulsive status epilepticus.

Nonconvulsive status epilepticus (NCSE) is defined as a change in behavior and/ormental processes from baseline in the absence ofmajor motor signs associated with continuous epileptiform discharges on the EEG [1]. Diverse pharmacological agents such as psychotropics, cephalosporins, and antineoplastic drugs have been mentioned as a frequent cause of drug-induced generalized NCSE [2]. Pseudoephedrine is a stereoisomer of ephedrine and is commonly found in over-thecounter cold medications. An analysis of 140 adverse events reported by physicians to the U.S. Food and Drug Administration between 1997 and 1999 revealed seven cases of seizures temporally associated with ephedra ingestion [3]. To our knowledge, NCSE induced by the use of pseudoephedrine has not been reported before. Here, we describe a case of generalized NCSE precipitated by the use of pseudoephedrine. An apparently healthy 31-year-old woman who had been taking combinations of 30 mg pseudoephedrine HCl, 500 mg paracetamol, 20 mg dextromethorphan HBr (Benical Cold) and 20 mg/5 mL pseudoephedrine HCl, 10 mg/5 mL dextromethorphan HBr, 2 mg/5 mL chlorpheniramine maleate (Vicks VapoDry) twice daily during the last 10 days was referred to the emergency department of our hospital because of a generalized convulsion. According to her history she hadhad only one complex partial seizure at age 8. Since then she had had no seizures andwas not receiving any antiepileptic treatment. On arrival she was confused. Systolic blood pressure was 130 mm Hg, diastolic blood pressurewas 80 mmHg, heart rate was 76 beats/minute, respiration rate was 20/minute, and temperaturewas 36.0 °C. Laboratory tests revealed a normal complete blood cell count (white cell count 8120/μL, hemoglobin 13.5 g/dL, platelet count 148×10/μL) and blood sugar level of 83 mg/dL. The results of liver function testswere normal. Creatine kinasewas 63 IU/ L, bloodureanitrogen12 mg/dL, creatinine0.80 mg/dL, sodium137mEq/ L, potassium 3.7 mEq/L, and chloride 107 mEq/L. Fifteen minutes after arrival, she had another generalized convulsion. Shewas given diazepam and then loaded with valproate 20 mg/kg. The convulsion was relieved; however, during the following 2 hours, her level of consciousness and mental state progressively worsened. On neurological examination she was lethargic with impaired orientation. MRI findings were normal. An urgent EEG showed intermittent generalized bursts of polyspike–wave and spike–wave complexes at 1–2 Hz with frontal maximum suggestive of NCSE (Fig. 1A). Immediately after this EEG, the patient was placed on continuous EEG monitoring. Treatment with 10 mg diazepam and 20 mg/kg phenytoin was initiated. The recording then showed continuous irregular polyspike–wave and spike–wave complexes interrupted by short runs (2–3 seconds) of regular basic rhythm(Fig. 1B). Onehour later, the patient recovered consciousness and the EEG showed alpha waves without epileptiformdischarges (Fig. 1C). Cerebrospinalfluidvalueswere also normal. Over the following days she experienced gradual clinical improvement. Several EEGs revealed an excess of theta waves but no epileptiform activity. Finally, the patient was discharged with a normal baseline mental status and EEG.

Prevalence of and influencing factors for chronic headaches among pregnant women.

To determine the prevalence of headaches and their influencing factors among pregnant women.