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

Atypical panic attacks include features such as focal paresthesias or sensory distortions, but attempts to demonstrate a relationship to partial seizures have been unsuccessful. Two patients with atypical panic attacks had attacks during EEG monitoring: one during a routine EEG in the EEG laboratory, the other at home during ambulatory monitoring. Focal paroxysms of sharp wave activity appeared on both patients' EEGs coincident with the spontaneous onset of panic attack symptoms. Both patients remained conscious. The correlation of focal paroxysmal EEG changes with panic attack symptoms suggests that these attacks were produced by partial seizure activity. Further study of the relationship between panic attacks and seizures is indicated.
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PMID:Focal paroxysmal EEG changes during atypical panic attacks. 842 35

While temporal lobe epilepsy is often considered in the differential diagnosis of patients with anxiety or panic disorders, other types of epilepsy can confound the presentation or treatment of adults with panic disorders. The cases of two patients are presented who were initially thought to have temporal lobe epilepsy producing panic attacks, but who were subsequently found to have primary generalized seizures. The clinical implications are discussed.
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PMID:Absence seizures associated with panic attacks initially misdiagnosed as temporal lobe epilepsy: the importance of prolonged EEG monitoring in diagnosis. 846 Dec 81

The goal of this paper is to draw conclusions about the usefulness of the standard EEG in psychiatry. In general, two thirds of psychiatric referrals for an EEG are expected to provide useful information. The emphasis in schizophrenia is placed on left-sided abnormalities, especially on the left temporal area. In mood disorders the emphasis is on right-sided foci, in addition to the controversial 6/sec spike and wave complexes, small sharp spikes and positive spikes. In the acute stage of alcoholism, a relationship is seen between the degree of intoxication and the amount of slow activity, while in the chronic stage an increase in slow activity is seen, but another change is fast activity on the temporal areas. During withdrawal a low seizure threshold can be seen as irregular bilateral spike and wave complexes. During abstinence 2-4 yr may be required before slow wave sleep is normal in all regards. Among the organic mental syndromes, delirium shows slow activity, except in delirium tremens, which often is associated with a normal record with fast activity. In dementia the prevalence of EEG abnormalities is related to the degree of impairment. After five sessions of ECT diffuse slow waves are often seen. In other conditions, among developmental disorders about one half of autistic children show abnormalities and epileptiform activity is not uncommon. Mild nonspecific abnormalities are seen in about 40% of dyslexics and also in behavior disorders. Anxiety disorders include anorexia nervosa, showing abnormal background activity related to the effect of starvation on cerebral metabolism. In panic attacks paroxysmal activity can be seen. In borderline personality positive spikes have been (again) associated with impulsivity and 6/sec spike and wave complexes with interpersonal problems. Of the drugs of abuse psilocybin and phencyclidine are often associated with generalized epileptiform patterns and with marijuana the alpha shows a decreased frequency with increased amplitude. Typically, an increase in slow activity is seen with psychotropic drugs if there is a change in the level of awareness. Finally, distinctive personality traits are, at times, seen in temporal lobe epilepsy and the phenomenon of "forced normalization" may appear when seizures stop and psychotic symptoms appear.
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PMID:A review of the usefulness of the standard EEG in psychiatry. 871

Studies of psychiatric out-patients from India have found that diagnosis of some of the subcategories of the dissociative and conversion disorders of the ICD and DSM classificatory systems are rarely made in this setting. Moreover, it was found that a significant percentage of patients seen in psychiatric practice may not fit into the defined subcategories of dissociative (conversion) disorders of these systems of classification. We studied the prevalence of various ICD-10 and DSM-IV categories of dissociative (conversion) disorders and our own proposed category of 'brief dissociative stupor' (BDS), among all the in-patients of a psychiatric unit in a general teaching hospital, over a 2-year period. There were 18 patients who fulfilled our criteria for BDS and 18 patients in the second group which included all of the remaining subjects with a diagnosis of any other subcategory of dissociative disorder according to ICD-10. Our analysis revealed that there were no patients with a diagnosis of dissociative amnesia, fugue, stupor, trance and possession disorders or identity disorders. There were significantly more female patients in the BDS group, and they also had significantly more comorbid Axis-I diagnoses and panic attacks. Since 50% of our patients fulfilled the criteria for BDS, there is clearly a need for further studies to establish the prevalence of this subcategory in patients from other centres. The classification of these patients with this phenomenology is problematic. Inclusion of a subcategory of dissociative non-epileptic seizures, instead of dissociative convulsions, should improve the classification of dissociative (conversion) disorders.
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PMID:Limited utility of ICD-10 and DSM-IV classification of dissociative and conversion disorders in India. 911 49

Cocaine stimulates the secretion of corticosterone and ACTH, probably through a CRF-related mechanism, indicating that the drug activates the HPA axis. Indeed, cocaine has been reported to produce anxiety and to precipitate episodes of panic attack during chronic use and withdrawal in humans and to induce anxiogenic behavior in animals. Cocaine also alters benzodiazepine receptor binding in discrete regions of the rat brain. Some of these changes in binding are obviously related to the convulsions and seizures which are often observed in an acute cocaine overdose. However, data from behavioral studies have suggested that some of these effects may be related directly to cocaine reinforcement since receptor changes also were observed when binding in the brains of rats that self-administered cocaine was compared with that from animals that had received identical yoked, but non-contingent infusions of the drug. In this regard, pretreatment with the benzodiazepine receptor agonists chlordiazepoxide and alprazolam decreased cocaine self-administration without decreasing food-reinforced responding, suggesting that these effects were specific for cocaine. Since this attenuation of self-administration was reversed by increasing the unit dose of cocaine, it is likely that these drugs were decreasing cocaine reinforcement. In contrast, exposure to stress increases vulnerability to self-administer psychostimulants. In these experiments, low-dose cocaine self-administration was related directly to stress-induced increases in plasma corticosterone, such that plasma corticosterone was always greater than 150 ng/ml for rats which subsequently self-administered cocaine at doses of 0.125 mg/kg/infusion or lower, suggesting a threshold for the hormone in cocaine reinforcement. In other experiments, bilateral adrenalectomy completely abolished the acquisition of intravenous cocaine self-administration in naive rats, while metyrapone decreased ongoing self-administration. In addition, ketoconazole pretreatment resulted in patterns of self-administration that were virtually indistinguishable from that observed during saline extinction, suggesting that plasma corticosterone is not only important, but may even be necessary for cocaine reinforcement. The mechanisms through which adrenocorticosteroids alter cocaine reinforcement remain to be determined, but there is increasing evidence that the mesocorticolimbic dopaminergic system is involved. In particular, the medial prefrontal cortex appears to be at least one brain region where dopamine and adrenocorticosteroids may interact to affect cocaine reinforcement.
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PMID:A neuroendocrine role in cocaine reinforcement. 922 28

This paper attempts to elucidate whether common (nonspecific) brain mechanisms are responsible for seizures of epileptic and nonepileptic origin. A comparative study of the following 4 paroxysmal disorders--partial epileptic seizures, paroxysmal dystonia, pseudoseizures and panic attacks was performed. Spontaneous (EEG-mapping) and evoked (contingent negative variation-CNV) bioelectrical activity was measures in all patients several times during interictal periods and after 24-hour sleep deprivation. The main common neurophysiological features of these types of paroxysmal disorders were the increased total power of spontaneous electrical activity, an asymmetric increase of theta-EEC power in the right hemisphere, an increase in total amplitude of CNV. Readiness of the brain for the development of the paroxysms was characterized by dynamic increases of the above parameters of spontaneous and evoked bioelectrical activity.
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PMID:[A neurophysiological model of the "paroxysmal brain" (cerebral mechanisms in the genesis of paroxysmal states)]. 977 Nov 28

Episodes of anxiety have been reported to be the most common psychological symptoms in patients with partial seizures. They may occur before, during and after seizures and can also appear in isolation without any convulsive symptoms. The epileptic anxiety syndrome is strikingly similar to panic attacks, and panic disorder is an important differential diagnosis. The close relationship between epileptic seizures and panic attacks is of special interest for a better pathophysiological understanding of panic attacks. In the literature an epileptiform neuronal activity is discussed as a possible underlying mechanism for panic disorder. The finding that anxiety was the most common experiential phenomenon produced by electrical stimulation of amygdala and hippocampus with depth electrodes points in this direction. PET has demonstrated abnormalities of hippocampal structures during the nonpanic state of patients with panic disorder. In addition, some EEG studies have demonstrated a high incidence of epileptiform EEG patterns in patients with panic disorder with or without agoraphobia. This was the reason why several investigators proposed that a subset of panic attacks may be related to abnormal epileptiform neuronal activity in the limbic system. The size of this subset is difficult to determine because discharges in the depth of the limbic system often cannot be seen in the scalp EEG. Concerning the hypothetical pathophysiological mechanism of panic disorder therapeutic measures were taken with antiepileptic agents. The best results were obtained for valproic acid. It seems to be reasonable to make a therapeutic trial with antiepileptic medication after nonresponse to standard pharmacotherapy.
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PMID:[Limbic ictus as a condition for anxiety attacks]. 1023 7

To further elucidate the inheritance pattern and range of phenotypic manifestations of benign familial temporal lobe epilepsy (FTLE), we report a large family recently identified in southern Italy. There were 8 patients (4 men), ranging in age from 31 to 68 years in three generations. One affected patient was deceased at the time of the study. Genealogical study strongly supported autosomal dominant inheritance with incomplete penetrance, as three unaffected individuals transmitted the disease. Clinical anticipation could not be assessed because of the ascertainment method. Male to male transmission occurred. Identifiable antecedents for seizures were present in only two patients, who had a simple febrile convulsion and a closed head trauma, respectively. Migraine was overrepresented in this family. Onset of seizures ranged from 17 to 52 years (mean: 27 years). All patients had weekly simple partial seizures suggestive of temporal origin with vegetative or experiential phenomena. Very rare partial complex seizures occurred in 6/7 patients. One had two generalized nocturnal seizures as well. Two had previously been misdiagnosed as having gastritis or panic attacks, and one had not been diagnosed. Interictal anteromesiotemporal spiking was seen in 5/7 patients, and occurred mostly during NREM sleep. Neurological examination, brain CT or MR scans were normal. Antiepileptic medication always controlled the seizures.
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PMID:Familial temporal lobe epilepsy autosomal dominant inheritance in a large pedigree from southern Italy. 1064 40

This paper describes a patient suffering from agoraphobia with panic disorder and with a history of self-induced epileptic seizures. The anxiety syndrome causing the admission to hospital could be diagnosed as non epileptic. He was treated successfully with a behaviour therapy. We discuss the possible interactions between anxiety disorders and epileptic seizures and some diagnostic demarcations. We conclude that even people with mild forms of epilepsy may develop an anxiety disorder arising from the fear of again getting epileptic seizures. To work out the different syndromes of epileptic seizures and of panic attacks should be part of the therapy.
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PMID:[Agoraphobia with panic disorder or epilepsy? Differential diagnostic considerations in a case]. 1094 77

The relationship between epilepsy and behavioral disturbances has been a subject of controversy since the 19th century. Affective changes may occur prior, during, or after the ictal discharge. Depression is the most prevalent comorbidity. Anxiety, panic attacks, and pseudoseizures may resemble complex partial seizures, and their diagnosis and treatment may be confusing, even to experienced clinicians. Epilepsy-related psychosis is less common, manifesting occasionally with symptoms that are indistinguishable from schizophrenia. There is no clear evidence of a distinct "epileptoid" personality, and interictal violence is extremely rare. Pharmacologic treatment with anticonvulsants remains the cornerstone of treatment. In case of psychiatric comorbidities or refractory seizures, the diagnosis should be re-examined.
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PMID:The relationship of psychiatric illnesses and seizures. 1135 88


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