Can a seizure help? The public's attitude toward electroconvulsive therapy

Despite controversial discussions in the general population, little is known about the public's attitude toward electroconvulsive therapy (ECT). We examined in a representative opinion survey (N=1737) (1) whether the lay public views ECT as an appropriate treatment for schizophrenia and depression, and (2) how demographic, psychological, sociological, and cultural variables influence attitudes. Most respondents (57%) considered ECT as a harmful treatment, and only a small number (1.2%) were in favor of ECT. A large number of respondents did not consider ECT as a treatment. We identified three predictors of negative attitude toward ECT (younger age, cultural area, greater degree of contact with the mentally ill; R2=0.042). The finding was not affected by the type of illness. Thus, having a prejudice toward ECT is a 'uniform attitude' that does not significantly vary between individual, demographic, or cultural contexts.     

Can patients perform volitional motor acts at the start of a seizure?

A seizure warning device might allow some individuals with partial seizures to protect themselves against consequences of seizures, but a prerequisite is the ability to take volitional action in response to a warning. The authors reviewed consecutive seizures in their epilepsy monitoring unit to determine whether patients could squeeze an event bulb, as instructed, at the start of their seizure. Only complex partial seizures with EEG changes and with the patient on camera were analyzed. Data were obtained from 77 patients, 42 with scalp monitoring and 35 with depth electrodes. Forty-seven percent had a left-hemisphere focus, 42% a right-hemisphere focus, and 11% multifocal seizures. The seizure focus was temporal in 68%. A magnetic resonance imaging consistent with mesial temporal sclerosis was seen in 29% of patients. Overall, 44% of the patients made at least one attempt to reach for the event bulb at the start of their seizures. Among the 72% of patients who gave a history of auras, 53% were able to press the event bulb compared to 20% with no history of auras (P = 0.016). EEG changes occurred a mean of 2.9+/-30.5 seconds after reaching for the bulb for scalp-recorded seizures (n = 20), and 16.2+/-13.7 seconds before behavior for depth-recorded seizures (n = 14, difference significant at P = 0.02). Neither seizure focus nor seizure laterality influenced the ability to press the event bulb. The authors conclude that nearly half of individuals with complex partial seizures can take volitional motor action at the start of their seizure. A method to enhance the intensity and timeliness of a seizure warning would not be wasted.     

What makes a simple partial seizure complex?

The assessment of ictal consciousness has been the landmark criterion for the differentiation between simple and complex partial seizures over the last three decades. After review of the historical development of the concept of “complex partial seizure,” the difficulties surrounding the simple versus complex dichotomy are addressed from theoretical, phenomenological, and neurophysiological standpoints. With respect to consciousness, careful analysis of ictal semiology shows that both the general level of vigilance and the specific contents of the conscious state can be selectively involved during partial seizures. Moreover, recent neuroimaging findings, coupled with classic electrophysiological studies, suggest that the neural substrate of ictal alterations of consciousness is twofold: focal hyperactivity in the limbic structures generates the complex psychic phenomena responsible for the altered contents of consciousness, and secondary disruption of the network involving the thalamus and the frontoparietal association cortices affects the level of awareness. These data, along with the localization information they provide, should be taken into account in the formulation of new criteria for the classification of seizures with focal onset.     

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.     

Can mutation‐mediated effects occurring early in development cause long‐term seizure susceptibility in genetic generalized epilepsies?

Epilepsy has a strong genetic component, with an ever‐increasing number of disease‐causing genes being discovered. Most epilepsy‐causing mutations are germ line and thus present from conception. These mutations are therefore well positioned to have a deleterious impact during early development. Here we review studies that investigate the role of genetic lesions within the early developmental window, specifically focusing on genetic generalized epilepsy (GGE). Literature on the potential pathogenic role of sub‐mesoscopic structural changes in GGE is also reviewed. Evidence from rodent models of genetic epilepsy support the idea that functional and structural changes can occur in early development, leading to altered seizure susceptibility into adulthood. Both animal and human studies suggest that sub‐mesoscopic structural changes occur in GGE. The existence of sub‐mesoscopic structural changes prior to seizure onset may act as biomarkers of excitability in genetic epilepsies. We also propose that presymptomatic treatment may be essential for limiting the long‐term consequences of disease‐causing mutations in genetic epilepsies.     

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.     

Can natural ways to stimulate the vagus nerve improve seizure control?

The vagus nerve (VN) is the longest cranial nerve, innervating the neck, thorax and abdomen, with afferent fibers transmitting a range of interoceptive stimuli and efferent fibres to somatic structures and autonomic preganglions. Over the last few decades, electrical stimulation of the VN using implanted devices (VNS) has been developed leading to its approval for the treatment of epilepsy and depression. More recently, non-invasive devices to stimulation the VN have been developed. The VN has many functions and the activity that is most amenable to assessment is its effect in controlling the cardiac rhythm. This can be easily assessed by measuring heart rate variability (HRV). Decreased HRV is a result of poorer vagal parasympathetic tone and is associated with a wide range of ill health conditions including a higher risk of early mortality. People with epilepsy, particularly those with poorly controlled seizures, have been shown to have impaired parasympathetic tone. So, might natural ways to stimulate the VN, shown to improve parasympathetic tone as indicated by increased HRV, improve seizure control? There are numerous natural ways that have been shown to stimulate the VN, improving HRV and hence parasympathetic tone. These natural ways fall mainly into 3 categories – stress reduction, exercise, and nutrition. Though the natural ways to stimulate the VN have been shown to increase HRV, they have not been shown to reduce seizures. The exception is listening to Mozart's music, which has been shown to increase parasympathetic tone and decrease seizures. Clearly much more work is required to examine the effect of the various ways to increase HRV on seizure occurrence.     

Can lesions to the motor cortex induce amyotrophic lateral sclerosis?

A recent staging effort for amyotrophic lateral sclerosis (ALS) has demonstrated that the TDP-43 neuropathology may initiate focally in the motor cortex in the majority of patients. We searched our data bank for patients with lesions of the motor cortex which preceded disease onset. We performed a search of our patient- and MRI-data bank and screened 1,835 patients with amyotrophic lateral sclerosis for frontal lobe/motor cortex lesions. We found 18 patients with definite ALS who had documented and defined lesions of the motor cortex, which preceded the initial ALS symptoms by 8–42 years. In the vast majority (15/18) of the patients, the onset of ALS was closely related to the focal lesion since it started in a body region reflecting the damaged cortical area. The findings suggest that initial lesions to the motor cortex may be a contributing initiating factor in some patients with ALS or determine the site of onset in individuals pre-disposed to ALS.     

Do dreams reflect a biological state?

The purpose of this study was to prospectively evaluate the hypothesis that dreams reflect biological states. Inpatients on a nonacute cardiology service were studied. Dream material was gathered by an independent interviewer using the Staged Interview Technique, a newly developed interview technique that limited bias. The outcome measures used were obtained at the time of cardiac catheterization. Different levels of severity of cardiac disease with these measures were interpreted as representing different biological states. The patients' dreams were evaluated for the predicted correlations of the number of dream references to death (men) and separation (women) with different levels of severity of heart disease. The severity of heart disease was evaluated with anatomical (coronary angiography) and physiological (ejection fraction) measures obtained at cardiac catheterization, each represented by a 6-point scale of increasing severity. There was no correlation of the number of dream references with the severity of abnormalities on coronary angiography. However, the number of dream references to death and separation correlated with the severity of cardiac dysfunction, as measured by the ejection fraction, which is a more sensitive parameter of disease severity. The data provided prospective support for the hypothesis by showing that dreams reflected a biological state, the ejection fraction. This suggested a possible biological "meaning" of dreams.