Ali Özdemir Ersoy

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.

Therapeutic plasma exchange in patients with neurologic diseases: Retrospective multicenter study

Therapeutic plasma exchange (TPE) is commonly used in many neurological disorders where an immune etiology was known or suspected. We report our experience with TPE performed for neuroimmunologic disorders at four university hospitals. The study was a retrospective review of the medical records of neurological patients (n=57) consecutively treated with TPE between April 2006 and May 2007. TPE indications in neurological diseases included Guillain-Barrè Syndrome (GBS) (n=41), myasthenia gravis (MG) (n=11), acute disseminated encephalomyelitis (ADEM) (n=3), chronic inflammatory demyelinating polyneuropathy (CIDP) (n=1) and multiple sclerosis (MS) (n=1). Patient median age was 49; there was a predominance of males. Twenty-two patients had a history of other therapy including intravenous immunoglobulin (IVIG), steroid, azothioprin, and pridostigmine prior to TPE. Another 35 patients had not received any treatment prior to TPE. All patients were classified according to the Hughes functional grading scores pre- and first day post-TPE for early clinical evaluation of patients. The TPE was carried out 1-1.5 times at the predicted plasma volume every other day. Two hundred and ninety-four procedures were performed on 57 patients. The median number of TPE sessions per patient was five, and the median processed plasma volume was 3075mL for each cycle. Although the pre-TPE median Hughes score of all patients was 4, it had decreased to grade 1 after TPE. While the pre-TPE median Hughes score for GBS and MG patients was 4, post-TPE scores were decreased to grade 1. Additionally, there was a statistically significant difference between post-TPE Hughes score for GBS patients with TPE as front line therapy and patients receiving IVIG as front line therapy (1 vs. 3.5; p=0.034). Although there was no post-TPE improvement in Hughes scores in patients with ADEM and CIDP, patients with MS had an improved Hughes score from 4 to 1. Mild and manageable complications such as hypotension and hypocalcemia were also observed. TPE may be preferable for controlling symptoms of neuroimmunological disorders in early stage of the disease, especially with GBS.

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.

Factors that affect interictal cardiovascular autonomic dysfunction in temporal lobe epilepsy: Role of hippocampal sclerosis

The aim of this study was to evaluate possible factors affecting interictal cardiovascular autonomic function in temporal lobe epilepsy with complex partial seizures, paying special attention to hippocampal sclerosis. The study was carried out with 88 patients with epilepsy (22 with left hippocampal sclerosis, 22 with right hippocampal sclerosis, and 44 without hippocampal sclerosis) and 44 healthy subjects. All subjects underwent three tests of cardiac autonomic function: heart rate variation during resting activity, heart rate variation in response to deep breathing and blood pressure response to rising quickly from the supine position. Hippocampal sclerosis and disease duration were found to have significantly important effects on parasympathetic autonomic function, whereas seizure control and type of antiepileptic drug had significant effects on sympathetic autonomic function. This study shows that in addition to factors related to the chronic nature of epilepsy and antiepileptic drug use, hippocampal sclerosis may cause autonomic dysfunction during the interictal period in persons with temporal lobe epilepsy.

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.

Cornual Placenta Accreta Managed with Mini Modifified B-Lynch Suture Technique

7 lacenta accreta is much more common than placenta increta and percreta.1. The rate of placenta accreta increases in conjunction with cesarean deliveries.2 The overall incidence of placenta accreta is around 3 per 1000 deliveries, and there has been a considerable increase in the incidence of placenta accreta over the past few decades.3 About 75% of morbidly adherent placentas are placenta accretas; 18% are placenta incretas; and 7% of them are placenta percretas.4 The complications of placenta accreta are numerous and include damage to local organs, post-operative bleeding, infectious morbidities, multisystem organ failure, and maternal death.5