Is cholesterol a culprit in Alzheimer's disease?

A pivotal role for cholesterol influence on production of the putative AD toxin, amyloid beta (Abeta), has been amply demonstrated. More importantly, this relationship has consistently been identified in both in vivo and in vitro studies. Lowering cholesterol levels has been shown to cause a beneficial effect on Abeta levels in animal models, and epidemiological data indicate a beneficial effect on the risk of AD with prior statin use. Blinded, placebo-controlled clinical investigations assessing the benefit of statins on cognitive indices in mild to moderate AD are ongoing and one will be reported on soon. A prospective study assessing the effect of statin use on the risk of AD is under way as an observational component of a placebo-controlled primary prevention trial testing anti-inflammatory agents. Nevertheless, the foregoing suggests that routine monitoring and intervention for elevated cholesterol levels among the elderly could promote more than a healthy heart.     

Is a first acute symptomatic seizure epilepsy? Mortality and risk for recurrent seizure

Purpose:   To compare mortality and subsequent unprovoked seizure risk in a population-based study of acute symptomatic seizure and first unprovoked seizure due to static brain lesions.
Methods:   We ascertained all first episodes of acute symptomatic seizure and unprovoked seizure due to central nervous system (CNS) infection, stroke, and traumatic brain injury (TBI). Subjects were residents of Rochester, Minnesota, identified through the Rochester Epidemiology Project's records-linkage system between 1/1/55 and 12/31/84. Information was collected on age, gender, seizure type, etiology, status epilepticus (SE), 30-day and 10-year mortality, and subsequent episodes of unprovoked seizure.
Results:   Two hundred sixty-two individuals experienced a first acute symptomatic seizure and 148 individuals experienced a first unprovoked seizure, all due to static brain lesions. Individuals with a first acute symptomatic seizure were 8.9 times more likely to die within 30 days compared to those with a first unprovoked seizure [95% confidence intervals (CI) = 3.5–22.5] after adjustment for age, gender, and SE. Among 30-day survivors, the risk of 10-year mortality did not differ. Over the 10-year period, individuals with a first acute symptomatic seizure were 80% less likely to experience a subsequent unprovoked seizure compared with individuals with a first unprovoked seizure [adjusted rate ratio (RR) = 0.2, 95% CI = 0.2–0.4].
Discussion:   The prognosis of first acute symptomatic seizures differs from that of first unprovoked seizure when the etiology is stroke, TBI, and CNS infection. Acute symptomatic seizures have a higher early mortality and a lower risk for subsequent unprovoked seizure. These differences argue against the inclusion of acute symptomatic seizures as epilepsy.     

Is seizure detection based on EKG clinically relevant?

Objective

Real-time EKG-based automated seizure detection is emerging as a complement or supplement to that based on cortical signals, but its value is unproven. This study assesses the clinically relevance of EKG-based seizure detection by comparing the information content in EKG and ECoG.

Methods

ECoGs (6935 h; 241 clinical and 4311 sub-clinical seizures) with simultaneous EKG from 81 subjects undergoing surgical evaluation were used in these analyses. Differences, if any, between clinical and sub-clinical seizures in variables such as intensity, duration and their product severity, were investigated with a multi-variate regression model.

Results

Highly statistically significant differences in severity between clinical and sub-clinical seizures were discerned with EKG and ECoG. Furthermore, EKG-based seizure severity was linearly correlated with that estimated using ECoG.

Conclusions

These findings support the notion that EKG-based seizure detection is clinically relevant in certain localization-related epilepsies, providing similar information to that yielded by neuronal electrical signals.

Significance

The information content equivalence between EKG and ECoG would enable automated seizure detection, quantification and therapy delivery, without resorting to cortical monitoring. The considerably higher S/N and ease of acquisition and processing of EKG compared to ECoG/EEG may foster widespread clinical applications of this novel detection approach.     

Fatal brain edema in a child after ingestion of amitriptyline: Is the culprit amitriptyline?

Tricyclic antidepressants are among the drugs most frequently involved in pediatric exposures. We report here a case of a fatality in a 2.5-year-old boy after he ingested an overdose of amitriptyline . He developed seizure, hypotension, and his pupils became dilated which were interpreted as signs of TCA overdosages at first. However, his serum Na level was low (110 mEq L⁻¹) and his clinical and laboratory data were consistent with SIADH. Hypotonic fluid administration with SIADH contributed to fatal outcome and hyponatremia and cerebral edema appeared to be the main pathological processes.     

Television‐induced electronegative photoparoxysmal response: an extratemporal seizure mimic?

Video‐EEG monitoring is an established gold‐standard procedure for diagnosis and differentiation of epileptic and non‐epileptic seizures. Epilepsy misdiagnosis, to which factors such as EEG artifact misinterpretation contribute to, is common, and can have long‐lasting iatrogenic repercussions to the clinical management of affected patients. Among the many types of responses to photic stimulation, artifacts and physiologic and epileptic responses are possible. All of these can interfere with EEG interpretation when provoked by a source of illumination. Photic‐induced responses are of increasing relevance given the ubiquity of screens and other light‐emitting electronics in our modern world. One of these, the photoparoxysmal response, is a frequent finding in photosensitive patients with genetic generalized epilepsies. Various responses beyond abnormal occurrence of cortical spikes or spike‐and‐wave discharges are known to occur on EEG in response to intermittent photic stimulation (IPS), with different clinical implications. To our knowledge, we report a unique electronegative photoparoxysmal response during video‐EEG monitoring induced by fluctuating illumination caused by a distant television screen. This response mimicked an extratemporal seizure in a young woman with frontal lobe epilepsy, admitted for presurgical evaluation. Novel electronegative responses to electronic devices during video‐EEG monitoring merit consideration by EEG interpreters to help avoid misdiagnosis.     

Concussive convulsions: seizure or no seizure?

Convulsions following traumatic brain injury (TBI) represent a diagnostic and therapeutic challenge. They can be differentiated into late (> 7 days after TBI), early (1 - 7 days after TBI), immediate (within the first 24 h after TBI), and impact seizures (within seconds after TBI). Some authors suggest that most impact seizures are non-epileptic in origin and hence coined the term "concussive convulsions" for benign impact seizures. Early and late post-traumatic seizures frequently indicate structural brain damage and transition to chronic, post-traumatic epilepsy. The data for impact seizures or concussive convulsions is less clear: only a small percentage of impact seizures is associated with structural brain damage and the development of post-traumatic epilepsy, rather the majority of cases are benign and associated with an excellent prognosis. Here, we present a case report as a starting point for pathophysiological and clinical considerations regarding convulsions that start within seconds after TBI.     

Is the integrate-and-fire model good enough?--a review.

We review some recent results on the behaviour of the integrate-and-fire (IF) model, the FitzHugh-Nagumo (FHN) model, a simplified version of the FHN (IF-FHN) model and the Hodgkin-Huxley (HH) model with correlated inputs. The effect of inhibitory inputs on the model behaviour is also taken into account. Here, inputs exclusively take the form of diffusion approximation and correlated inputs mean correlated synaptic inputs (Sections 2 and 3). It is found that the IF and HH models respond to correlated inputs in totally opposite ways, but the IF-FHN model shows similar behaviour to the HH model. Increasing inhibitory input to single neuronal models, such as the FHN model and the HH model can sometimes increase their firing rates, which we termed inhibition-boosted firing (IBF). Using the IF model and the IF-FHN model, we theoretically explore how and when IBF can happen. The computational complexity of the IF-FHN model is very similar to the conventional IF model, but the former captures some interesting and essential features of biophysical models and could serve as a better model for spiking neuron computation.     

Is monoamine oxidase inhibitor induced myoclonus serotoninergically mediated?

Summary In the present study a single case observation of myoclonus during sleep-wave transition was monitored in a depressed patient treated with the monoamine oxidase inhibitor, phenelzine. The myoclonus had a rhythm of 1 c/second and lasted for two years, the duration of phenelzine treatment. Myoclonus appeared neither during wakefulness nor during sleep, but at wake-sleep-wake transitions. This switch myoclonus was associated with phasic muscle hyperactivity during REM sleep.Methysergide a 5-HT suppressor, decreased the switch myoclonus frequency and the REM muscle hyperactivity, indicating serotoninergic involvement in the mechanism of phenelzine induced myoclonus.