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Some New Finding In Neurological Fields

Absence seizures: A review of recent reports with new concepts


Absence seizures with bilateral spike-wave (SW) complexes at 3Hz are divided into the childhood form, with onset at around 6years of age, and the juvenile form, with onset usually at 12years of age. These seizures typically last 9-12s and, at times, are activated by hyperventilation and occasionally by photic stimulation. Generalized tonic-clonic (GTC) seizures may also occur, especially in the juvenile form. There may be cognitive changes, in addition to linguistic and behavioral problems. Possible mechanisms for epileptogenesis may involve GABAergic systems, but especially T-calcium channels. The thalamus, especially the reticular nucleus, plays a major role, as does the frontal cortex, mainly the dorsolateral and orbital frontal areas, to the extent that some investigators have concluded that absence seizures are not truly generalized, but rather have selective cortical networks, mainly ventromesial frontal areas and the somatosensory cortex. The latter network is a departure from the more popular concept of a generalized epilepsy. Between the “centrencephalic” and “corticoreticular” theories, a “unified” theory is presented. Proposed genes include T-calcium channel gene CACNA1H, likely a susceptible gene in the Chinese Han population and a contributory gene in Caucasians. Electroencephalography has revealed an interictal increase in prefrontal activity, essential for the buildup of the ictal SW complexes maximal in that region. Infraslow activity can also be seen during ictal SW complexes. For treatment, counter to common belief, ethosuximide may not increase GTC seizures, as it reduces low-threshold T-calcium currents in thalamic neurons. Valproic acid and lamotrigine are also first-line medications. In addition, zonisamide and levetiracetam can be very helpful in absence epilepsy.

Acetylcholinesterase inhibition and insulin resistance in late onset Alzheimer’s disease

Background: Insulin resistance (IR) may play a role in most pathogenic processes that promote the development of late onset Alzheimer’s disease (LOAD). This study was designed to evaluate whether galantamine influenced peripheral IR in LOAD.Methods: Ninety-five consecutive elderly patients, 40 LOAD and 55 non-demented patients were evaluated. IR was calculated with HOMA and modified-HOMA. All the patients were evaluated through comprehensive geriatric assessments at baseline and at 6, 12 and 18 months.Results: Over three 6-month periods of galantamine treatment, compared to the baseline values, there was a significant increase at 6 and 12 months in the MMSE and at 6 months in the IADL scores (t = 3.25, p = 0.002 and t = 2.69, p = 0.011 for MMSE; t = 2.03, p = 0.049; for IADL, respectively). Although, there was an improvement in MMSE and IADL scores of galantamine-treated patients, there was no significant change in IR indexes and correlation between IR indexes and cognitive status in both groups during the treatment period.Conclusions: This study showed no relation between cognitive improvement and IR by galantamine therapy in AD. In conclusion, peripheral IR and central nervous system IR may be different, and galantamine itself may show its effects without affecting the insulin-signaling pathway.

Frequency, prognosis and surgical treatment of structural abnormalities seen with magnetic resonance imaging in childhood epilepsy

The epidemiology of lesions identified by magnetic resonance imaging (MRI), along with the use of pre-surgical evaluations and surgery in childhood-onset epilepsy patients has not previously been described. In a prospectively identified community-based cohort of children enrolled from 1993 to 1997, we examined (i) the frequency of lesions identified by MRI; (ii) clinical factors associated with ‘positive’ MRI scans; and (iii) the utilization of comprehensive epilepsy evaluations and neurosurgery. Of the original cohort of 613 children, 518 (85%) had usable MRI scans. Eighty-two (16%) had MRI abnormalities potentially relevant to epilepsy (‘positive’ scans). Idiopathic epilepsy syndromes were identified in 162 (31%) of whom 3% had positive scans. The remainder had non-idiopathic epilepsy syndromes of which 22% had positive MRI findings. Multiple logistic regression analysis identified non-idiopathic epilepsy and abnormal motor-sensory (neurological) examinations as predictors of a positive MRI scan. Of the non-idiopathic patients with normal neurological exams and who were not pharmacoresistant, 10% had positive MRI scans, including four patients with gliomas. Evaluations at comprehensive epilepsy centres occurred in 54 pharmacoresistant cases. To date 5% of the imaged cohort or 8% of non-idiopathic epilepsy patients have undergone surgical procedures (including vagal nerve stimulator implantation) to treat their epilepsy (n = 22) or for tumours (n = 6) without being drug resistant. Applying our findings to the general population of children in the USA, we estimate that there will be 127/1 000 000 new cases per year of pharmacoresistant epilepsy, and 52/1 000 000 childhood-onset epilepsy patients undergoing epilepsy evaluations. In addition, approximately 27/1 000 000 will have an epilepsy-related surgical procedure. These findings support recommendations for the use of MRI in evaluating newly diagnosed paediatric epilepsy patients, especially with non-idiopathic syndromes, and provide estimates on the utilization of comprehensive evaluations and surgery.

?Cognitive versus behavioral ADHD phenotype: what is it all about

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The A DHD PASS assessment is discussed. 100 combined and 50 inattentive ADHD patients with DSM IV – TR criteria, no comorbidity, and no previous treatment were enrolled. Those with SNAP-IV>or =2.5/1.8 (teacher/parents) [n=96] were randomly assigned to 1 of 3 treatment groups: Concerta, humanistic psychology, and Concerta+psychology. Those with SNAP-IV<2.5/1.8 [n=54] to 1 of 2 groups: Concerta and Concerta+psychology. All of them [n=150]we administered the SNAP-IV and cognitive DN:CAS battery at baseline and 6 and 12 months later. Cluster analysis and paired Student t-test were applied. The cluster analysis produced three cognitive profiles: one [n=96] with planning dysfunction and SNAP-IV>or =2.5/1.8, the majority [n=76] combined ADHD; another [n=38]with successive processing dysfunction and SNAP-IV<2.5/1.8, the majority [n=28] inattentive ADHD; and another [n=16]without cognitive dysfunction and with SNAP-IV<2.5/1.8, [n=8] combined and [n=8]inattentive. Only planning ameliorated at 12 months assessment. It was better in group 3 (p<0.1) than in group 1 (p<0.5), than in group 2 (p<0.4/0.3). Remission was parallel to planning improvement, group 3>group 1>group 2. PASS assessment in ADHD may be relevant.


August 12, 2009 - Posted by | 1

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