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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Toxigenic mold activities produce metabolites that are either broad-spectrum antibiotics or mycotoxins that are cytotoxic. Indoor environmental exposure to these toxigenic molds leads to adverse health conditions with the main outcome measure of frequent neuroimmunologic and behavioral consequences. One of the immune system disorders found in patients presenting with toxigenic mold exposure is an abnormal natural killer cell activity. This paper presents an overview of the neurological significance of abnormal natural killer cell (NKC) activity in chronic toxigenic mold exposure. A comprehensive review of the literature was carried out to evaluate and assess the conditions under which the immune system could be dysfunctionally interfered with leading to abnormal NKC activity and the involvement of mycotoxins in these processes. The functions, mechanism, the factors that influence NKC activities, and the roles of mycotoxins in NKCs were cited wherever necessary. The major presentations are headache, general debilitating pains, nose bleeding, fevers with body temperatures up to 40 degrees C (104 degrees F), cough, memory loss, depression, mood swings, sleep disturbances, anxiety, chronic fatigue, vertigo/dizziness, and in some cases, seizures. Although sleep is commonly considered a restorative process that is important for the proper functioning of the immune system, it could be disturbed by mycotoxins. Most likely, mycotoxins exert some rigorous effects on the circadian rhythmic processes resulting in sleep deprivation to which an acute and transient increase in NKC activity is observed. Depression, psychological stress, tissue injuries, malignancies, carcinogenesis, chronic fatigue syndrome, and experimental allergic encephalomyelitis could be induced at very low physiological concentrations by mycotoxin-induced NKC activity. In the light of this review, it is concluded that chronic exposures to toxigenic mold could lead to abnormal NKC activity with a wide range of neurological consequences, some of which were headache, general debilitating pains, fever, cough, memory loss, depression, mood swings, sleep disturbances, anxiety, chronic fatigue, and seizures.
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PMID:The neurological significance of abnormal natural killer cell activity in chronic toxigenic mold exposures. 1462 99

Patients with low-grade gliomas may live without disease progression for many years after initial diagnosis and treatment, but long-term cognitive deficits, which affect up to 90% of patients, can have a sustained negative effect on their daily functioning and quality of life. Cognitive deficits in patients with low-grade gliomas may be caused by the tumor itself or by various other factors including tumor-related epilepsy, tumor treatment (surgery, radiotherapy [RT], medical therapy [including chemotherapy]), psychological stress, or a combination of these. Although some studies suggest a strong link between RT and neurocognitive sequelae, other studies have found little evidence that RT is a major risk factor for cognitive deficits and suggest that other factors may play a major role. The results of a recent cross-sectional study involving 195 patients with low-grade gliomas (104 of whom received RT) strongly suggest that standard focal RT with fractional doses less than 2 Gy is not generally associated with an increased risk of cognitive deficits, but that higher fractional doses are likely to result in cognitive disability. Notably, the presence and severity of epileptic seizures and/or the use of antiepileptic drugs were more strongly associated with cognitive deficits than was RT. This and other studies suggest that disease and treatment factors other than standard focal RT may be more important with respect to increasing the risk of neurocognitive sequelae in patients with low-grade gliomas.
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PMID:Neurocognitive sequelae in the treatment of low-grade gliomas. 1476 85

Ictal heart rate was investigated in otherwise subclinical epileptic seizures to test the hypothesis as to whether ictal tachycardia is physiological and not a physical or psychological stress response. In addition, we aimed to evaluate the localizing significance of pure ictal tachycardia. We included 21 epilepsy patients, who showed an ictal EEG seizure pattern during 22, otherwise subclinical seizures. All patients underwent ictal video-EEG recordings to evaluate the possibility of resective epilepsy surgery. The changes in heart rate in these patients were investigated in order to determine their relationship to localization and duration of EEG seizure patterns. Ictal tachycardia was observed in 41% of the otherwise subclinical seizures (nine out of 22), and significantly more often in seizures arising from the temporal lobe than from extratemporal regions (62% versus 11%, p < 0.0018). The seizure duration as defined by EEG was significantly positively correlated with an increase of heart rate (p = 0.043). Ictal heart rate can increase as a result of epileptic activation of autonomic cortex, reflecting a temporal lobe autonomic influence. Thus, measurement of heart rate should be included in the evaluation of otherwise subclinical epileptic seizures, because of its localizing value.
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PMID:Heart rate increase in otherwise subclinical seizures is different in temporal versus extratemporal seizure onset: support for temporal lobe autonomic influence. 1616 28

The influence of psychological states on physiological responses during exercise is of considerable importance to individuals for which the efficiency of energy production is critical to occupational performance. Numerous studies have shown that aerobic fitness is associated with enhanced cardiovascular efficiency at rest and that responses to mental stress demonstrate evidence of increased sensitivity (relative increase in HR response) and enhanced efficiency (a decrease in absolute HR). However, the effect of aerobic fitness and its impact on cardiorespiratory (CR) responses to psychological stress during exercise has not been investigated. Therefore, the purpose of this study was three-fold; (1) to examine during exercise, anxiety, effort sense, and CR responses to a mental challenge, (2) to examine anxiety and heart rate (HR) responses from rest to exercise with mental challenge between below average fitness (Low Fit) and well-above average fitness (Hi Fit) individuals (exercising at similar relative intensities), and (3) to examine anxiety, effort sense, and CR responses of Low Fit and Hi Fit individuals to a mental challenge during exercise at a similar relative intensity. Twelve Low Fit and eleven Hi Fit subjects participated in two, 32-minute cycle ergometer rides at 65 % of VO2max. In the mental challenge condition (MCC), subjects rode while participating in mentally challenging tasks (Stroop Color-Word task and mental arithmetic) from min 6 to min 14 of the protocol. In the no mental challenge condition (NMCC), subjects exercised at the same intensity and duration without a stressor. Subjects were counter-balanced between fitness levels and condition. HR, VE, VE/VO2, RR, VO2, RER, effort sense (RPE), and state anxiety (SAI) were assessed at 5, 14, 24, and 30 min. SAI was also assessed at - 5 min before exercise and after 15 min of recovery. In addition, the NASA task load index (NTLX) was used to assess perceived overall workload. SAI increased significantly at 14 min in the MCC. NTLX scores indicated that the MCC was perceived as a greater overall workload. Furthermore, HR, VE, VE/VO2, and RR were significantly elevated during the mental challenge condition at 14 min. The Hi Fit subjects tended to respond to the dual stress of exercise and mental challenge with a relative increase in HR, while absolute HR was similar in both groups. An examination of fitness group differences revealed that SAI and NTLX were similar for Low Fit and Hi Fit subjects when exercising in the MCC, although, Hi Fit subjects demonstrated lower HR responses from 6 min to 14 min. VE, VE/VO2, and RR were similar for Low Fit and Hi Fit subjects. These results suggest that psychological stress during physical activity can exacerbate cardiorespiratory responses and suggests that factors that impact CR adjustment to mental challenge from resting baseline may differ from the factors that impact CR adjustment to mental challenge during exercise. Finally, fitness level attenuates HR and may attenuate additional cardiorespiratory responses while participating in a dual stress condition, of exercise and mental challenge.
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PMID:Cardiorespiratory responses of Hi Fit and Low Fit subjects to mental challenge during exercise. 1661 43

People with epilepsy (PWE), particularly those with more severe seizures, are at risk of premature death. The contribution of deaths unrelated to epilepsy to this risk is likely to be significant. Recent studies indicate that comorbid conditions are similarly increased in PWE. The reason for these increases in unrelated deaths and comorbid conditions is unclear. In this article, we argue that having seizures is psychologically stressful, and that this stress can lead to a whole range of pathophysiological changes that may trigger various physical illnesses. Hence, psychological stress may be a significant factor contributing to the increase in mortality and comorbidity rates in PWE. This speculation is unlikely to be proven at this stage because of the complexity of the trials required. In PWE who continue to have seizures, more needs to be done to help them cope with the stress. Additionally, attention needs to be paid to improve nutritional status and physical fitness. These steps are likely to enhance the overall health of PWE and may reduce premature mortality and comorbidity rates.
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PMID:Mortality and morbidity rates are increased in people with epilepsy: is stress part of the equation? 1707 Jan 12

Temporal lobe epilepsy (TLE) is the most common cause of intractable adult epilepsy. It is proposed that different kinds of epilepsy be classified into one of two categories, which correspond to the two basic kinds of neurons in the brain, that is, as diseases of oscillators or as diseases of resonators. Oscillator (or pacemacker) neurons are endowed with intrinsic conductances that permit periodic spontaneous generation of action potentials; in contrast, resonators are neurons which process information coming from sensory stimuli or from other neurons. A literature review supports the idea that TLE is a disease of faulty resonators. This means that seizures do not arise de novo in the seizure focus. The seizure focus responds to normal input with an abnormally large discharge that causes seizures. The most frequent trigger for TLE is psychological stress. A previously published theory of stress is reviewed. The stress circuit runs from the hippocampus to the amygdala to the dorsal raphe nucleus to the entorhinal cortex and back to the hippocampus. Cell loss in the dentate is central to the pathophysiology of both chronic stress and TLE, which establish a "vicious circle" relationship with one another. Once it is grasped that TLE is a disease of resonators and that all seizures in TLE are triggered, then it makes sense to address the major recognized trigger, which is stress. New therapeutic ideas for decreasing seizure frequency in TLE include the use of anti-depressants, ethosuximide (which blocks firing in the dorsal raphe nucleus), and mood-stabilizers (which block firing in the entorhinal cortex). The latter category includes several recognized anti-epileptic drugs. Drugs from all three categories should be used simultaneously and on an empirical basis in each patient.
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PMID:Temporal lobe epilepsy is a disease of faulty neuronal resonators rather than oscillators, and all seizures are provoked, usually by stress. 1751 76

A 77-years-old woman was admitted to our hospital due to uncontrolled myoclonus and generalized seizure. Since the age of 17, she has been suffering from myoclonic jerks and partial convulsions in her right arm. Administration of several unknown anticonvulsants had not alleviated her condition. She was able to spend her life without a handicap, except for the symptoms described above. She has been experiencing psychological stress since the age of 50, which has resulted in worsening of her symptoms, and she was prescribed phenytoin, carbamazepine, and phenobarbital, which were also ineffective. When a generalized convulsive attack occurs, she shows rapid muscle twitches in her right arm and her consciousness is clear. She also has cerebellar ataxia in her extremities. Brain magnetic resonance imaging (MRI) showed obvious cerebellar atrophy, and an electroencephalogram revealed a diffuse spike and wave complexes. A surface electromyogram (EMG) confirmed myoclonus in both arms. We diagnosed her as having juvenile myoclonus epilepsy and initiated sodium valproate monotherapy, which relieved the symptoms. The observed cerebellar ataxia might be due to long-term administration of phenytoin. When a neurologist encounters an intractable seizure without loss of consciousness, surface EMG is useful for diagnosing this treatable disease.
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PMID:[Case of juvenile myoclonic epilepsy misdiagnosed as simple partial seizure for more than 60 years]. 1917 10

Stress has been considered the most frequently self-reported precipitant of seizures in people with epilepsy. The literature documents that physical stress, that is, physical exercise, can have beneficial effects in people with epilepsy. In view of evidence indicating that sensitivity to stress is reduced after a physical exercise program, physical activity could be a potential candidate for stress reduction in people with epilepsy. This review considers how physical exercise could contribute to reduce seizure susceptibility and, hence, seizure frequency. Possible mechanisms by which exercise can be beneficial for people with epilepsy are highlighted. Hypothalamic-pituitary-adrenal axis adaptation, neurotransmitter system modulation, and metabolic and neuroendocrine changes may interfere with seizure susceptibility. The psychological stress of different sports activities is an important concern that must also be taken into account. Overall, among stress reduction therapies for the treatment of seizures, exercise might be a potential candidate.
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PMID:Physical exercise in epilepsy: what kind of stressor is it? 1983 11

It is well established that the neurotransmitter norepinephrine (NE) has anticonvulsant properties. However, NE may also have proconvulsant properties under some conditions, both in animal epilepsy models and in humans. This paper examines the hypothesis that this neurotransmitter has proconvulsant properties, where much of the pharmaceutical evidence comes from rodent models. In assessing the elevated NE epilepsy hypothesis, the following seven lines of evidence are examined that include studies of: (1) antidepressants that raise the level of NE; (2) clonidine and other alpha 2 adrenergic agonist drugs that lower the level of NE; (3) prazosin and other drugs that affect alpha adrenoceptors; (4) propranolol and other drugs that affect beta adrenoceptors; (5) pheochromocytoma, which is a rare cancer of the adrenal glands that can boost NE levels; (6) comorbidity of epilepsy with bipolar disorder, hypertension, and obesity, where all four conditions may involve elevated NE; and (7) psychological stress, which is associated with increased release of NE. The body of evidence supporting the NE proconvulsant hypothesis is consistent with the notion that elevated, endogenous noradrenergic transmission is an etiological factor in some cases of epilepsy.
Seizure 2010 Jul
PMID:Is elevated norepinephrine an etiological factor in some cases of epilepsy? 2049 25

Psychogenic nonepileptic seizures (PNES) resemble epileptic seizures and are often misdiagnosed and mistreated as the latter. Occasionally, epileptic seizures are misdiagnosed and mistreated as PNES. 70% of PNES cases develop between the second and fourth decades of life, but this disease can also affect children and the elderly. At least 10% of patients with PNES have concurrent epileptic seizures or have had epileptic seizures before being diagnosed with PNES. Psychological stress exceeding an individual's coping capacity often precedes PNES. Clinicians can find differentiating between PNES and epileptic seizures challenging. Some clinical features can help distinguish PNES from epileptic seizures, but other features associated with PNES are nonspecific and occur during both types of seizures. Diagnostic errors often result from an overreliance on specific clinical features. Note that no single feature is pathognomonic for PNES. When typical seizures can be recorded, video-EEG is the diagnostic gold standard for PNES, and in such cases a diagnosis can be made with high accuracy. When video-EEG reveals no epileptiform activity before, during or after the ictus, thorough neurological and psychiatric histories can be used to confirm the diagnosis of PNES. In this article, we review the clinical features that can help clinicians differentiate between PNES and epileptic seizures.
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PMID:Differentiating between nonepileptic and epileptic seizures. 2138 14


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