Limbic stimulation-induced hypersexuality

Postictal sexual drive levels induced by limbic discharges were studied in eight adult male cats. Although sexual drive was exclusively dependent upon the presence or absence of testosterone, the level or degree of drive was dependent on the relative amounts of circulating testosterone and catecholamines in addition to the bioelectric state of the testosterone-binding cells. The limbic discharge was thought to induce postictal hypersexuality by its propagated discharge, suppressing the association neocortex and simultaneously activating the sexual hormone-binding cells of the diencephalon. The dissociation of the neocortex from the diencephalon was considered as a functional postictal diaschisis. These postictal physiologic changes were thought to account for the irrational automatic behavior and memory loss characteristic of patients with psychomotor seizures.     

A neurophysiologic model for aggressive behavior in the cat

A neurophysiologic model for aggessive behavior in the cat is proposed. Stimulus-bound and seizure-bound aggression was evaluated in relation to limbic and basal ganglia induced seizures (after-discharges). Electrically induced limbic and basal ganglia afterdischarges were used because they are known to implicate septohypothalamic sites from which aggression can be elicited by direct stimulation. The occurrence of behavioral aggression is correlated with the discharge characteristics of a single discharging system and with two interacting discharging systems. Aggression is composed of autonomic and somato-motor components which poses relatively low and high thresholds, respectively, for their activation. Aggression occurring during a combined septum and amygdala discharge was more intense and prolonged than with a septum discharge alone. Participation of a slow frequency discharging basal ganglia system activated seizurebound aggression in an otherwise nonaggressive limbic seizure. The limbic and basal ganglia stimulations and after-discharges lowered the excitability threshold of the aggression system and made it more vulnerable to being activated by external stimuli, such as visual and auditory stimuli. These observations are reminiscent of patients with aggressive behavior associated with psychomotor seizures.     

Effects of naloxone on hippocampal seizure activity

Although the presence of several types of opiate receptors and ligands has been demonstrated within the hippocampus, little is known about the circumstances in which endogenous opiates may be released. Previous studies have suggested that opiates may be involved in producing seizure activity within the hippocampus, or alternatively, that they may be released by seizure activity within the limbic system to prolong the period of postictal depression and thereby prevent the recurrence of seizures during this period. In this experiment we examined the effect of opiate receptor blockade produced by 20 mg/kg ip naloxone on the duration of afterdischarge produced by high-frequency hippocampal stimulation and on inhibition of subsequent seizure activity in male Sprague-Dawley rats. Contrary to the stated hypotheses, naloxone had no effect on either measure.     

Sleep and arousal mechanisms in experimental epilepsy: epileptic components of NREM and antiepileptic components of REM sleep

Neural generators related to different sleep components have different effects on seizure discharge. These sleep-related systems can provoke seizure discharge propagation during nonrapid eye movement (NREM) sleep and can suppress propagation during REM sleep. Experimental manipulations of discrete physiological components were conducted in feline epilepsy models, mostly in the systemic penicillin epilepsy model of primary generalized epilepsy and the amygdala kindling model of the localization-related seizure disorder, temporal lobe epilepsy. The sleep-wake state distribution of seizures was quantified before and after discrete lesions, systemic and localized drug administration, and/or photic stimulation, as well as in relation to microdialysis of norepinephrine. We found that (1) neural generators of synchronous EEG oscillations--including tonic background slow waves and phasic "arousal" events (sleep EEG transients such as sleep spindles and k-complexes)--combine to promote electrographic seizure propagation during NREM and drowsiness, and antigravity muscle tone permits seizure-related movement; (2) neural generators of asynchronous neuronal discharge patterns reduce electrographic seizures during alert waking and REM sleep, and skeletal motor paralysis blocks seizure-related movement during REM; (3) there are a number of similarities between amygdala-kindled kittens and children with Landau-Kleffner Syndrome (LKS) that suggest a link among seizures, sleep disorders, and behavioral abnormalities/regression.     

Diagnosing a male hysteric: Don Juan-type

The aim of this paper is to provide a clinical account of a male hysteric, Don Juan-type, taken from the early stages of treatment. The patient presented with a relationship problem but there soon emerged a form of compulsive sexuality or hypersexuality in his love relations that became a central feature of the clinical picture. This hypersexuality expressed itself in a compulsive need to stage, or to stage-manage, interpersonal scenaria of a sexual or sexualised nature. These scenaria, which were repeated in different variations and with different personnel, are seen by the author as a dramatisation of the primal scene with the patient taking up the position of the oedipal father. Explanations for the disappearance of male hysteria are given, including a new theory which claims that an imbalance in psychoanalytic theory itself led to the feminisation of hysteria. This critique allows certain forms of hypersexuality in men to be promoted as a form of hysteria, the most common example being Don Juanism-a form of compulsive sexuality that encompasses normative, conversion and character features. The paper also examines the male hysteric's developmental agenda. What the patient's compulsive sexual tableaux exposed was that he had never faced a separation that was not a triangular experience. This meant that his separations were experienced as two developmental agonies telescoped into one-separation (pre-oedipal) and exclusion (early oedipal). This combination, the author suggests, is so frightening in a particular group of men as to explain the choice of hysteria as opposed to some other choice of neurosis.     

Aggression in temporal lobe epilepsy and limbic psychotic trigger reaction implicating vagus kindling of hippocampus/amygdala (in sinus abnormalites on MRIs)

Five aspects associated with potentially aggressive partial limbic seizures are interrelated: (1) Five out of six unselected (consecutively referred) White, male out-of-character aggressive felons (mean age 33) had histories of recurrent nasopharyngeal infections, four with congruent MRIs, two of these MRIs also showed cortical atrophy, three men had histories of various seizures, and one scalp EEG was “congruent with seizures in the temporal regions.” All men had histories of head injuries. The diagnoses of their bizarre acts during a brief psychosis were partial limbic seizures in an “exhibitionist” with temporal lobe epilepsy (TLE) and proposed limbic psychotic trigger reaction (LPTR) in four “murderers”, based on 13 specific symptoms and signs. (2) The men's nasopharyngeal (medical) conditions are hypothesized to be associated with intermittent mild stimulation of the vagus nerve. Supportive evidence shows that (3) experimental vagus stimulation has the most excitatory impact on hippocampus and amygdala, which are also (4) the most susceptible to limbic seizure kindling (by intermittent subthreshold stimuli). (5) even by contrast, high-voltage energy level and frequently applied vagus nerve stimulation (VNS), which is used as an antiepileptic treatment; however, VNS has elicited seizures in some patients.     

Changes of Cingulothalamic Topographic Excitation Patterns and Avoidance Response Incubation over Time Following Initial Discriminative Conditioning in Rabbits

Neurons in particular layers of cingulate cortex and in limbic thalamic nuclei exhibit peak firing rates in response to a positive conditional stimulus (CS+) in particular stages of discriminative learning. A given area is maximally activated by the CS+ in the initial, an intermediate, or a late stage of behavioral acquisition, and activation in all of the areas diminishes as training continues after the peak of activation occurs. Thus, the topographic distribution of activation in these areas depends on the stage of behavioral acquisition. The present study determined whether the acquisition-related changes of the topographic distributions of peak firing rates in CS-elicited activity are driven exclusively by the repetition of conditioning trials (i.e., practice) or may occur as well with the passage of time, similar to putative processes of memory consolidation. Multiunit activity was recorded in cingulate cortex and in the anterior dorsal (AD), anterior ventral (AV), and medial dorsal (MD) thalamic nuclei as rabbits learned to step in response to a warning tone (CS+) to prevent a scheduled foot-shock, and to ignore a different tone (CS-) not predictive of foot-shock. The rabbits received two training sessions, S1 and S2. S2 followed S1 immediately in one group of rabbits and after 48 h in a different group. Significant neuronal discharge increments occurred from S1 to S2 in the 48-h group but not in the 0-h group, for the areas (posterior cingulate cortex, AV thalamic nucleus) that previously showed only late-stage activation. Significant discharge increments occurred from S1 to S2 in the 0-h group but not in the 48-h group in areas (anterior cingulate cortex, the AD, and MD thalamic nuclei) that previously exhibited early stage activation. These results indicate that the trial-driven topographic distribution changes also occur with the passage of time after limited initial training. It is suggested that the trial-driven and time-related changes may have a common functional relevance concerning memory consolidation.     

Limbic system seizures and aggressive behavior (superkindling effects)

Integrative Psychological and Behavioral Science - This study was done to further analyze the neural mechanisms underlying aggressive behavior associated with psychomotor or temporal lobe seizures....     

The impact of age at seizure onset on the likelihood of atypical language representation in children with intractable epilepsy

Studies have suggested that early postnatal lesions are associated with a greater likelihood of atypical speech representation than lesions acquired later in life. Comparison groups have been defined differently across studies, with age typically being treated as a dichotomous (i.e., early versus late lesion onset) rather than continuous variable. Thus, little is known about the age at which children become less likely to exhibit atypical representation following a brain insult. This study examined the likelihood of typical versus atypical speech representation in children with intractable epilepsy (n = 75). Age of seizure onset was treated as a continuous variable to examine whether there was a naturally occurring cut-off point after which the rate of atypical speech representation decreased. A much higher proportion of children with seizure onset prior to the fifth year showed atypical speech representation as compared to children whose seizures began after 5 years of age.     

Neonatal seizures: early-onset seizure syndromes and their consequences for development

The determination of the developmental consequences of seizure syndromes in the neonate is based upon a number of factors which include: understanding of the clinical and electroencephalographic (EEG) features of neonatal seizures; current theories of the mechanisms by which neonatal seizures are generated; a current classification of neonatal seizures; potential etiologic and risk factors for seizures; and therapies. In addition, different seizure types, mechanisms of generation and etiologies of cerebral dysfunction may vary with conceptional age of the infant. There are a few distinct neonatal epileptic syndromes, which are rare, have been well described: benign neonatal convulsions; benign neonatal familial convulsions; early myoclonic encephalopathy and early infantile epileptic encephalopathy. The prognosis for the first two is relatively good while the outcome for the other two with encephalopathy is catastrophic. However, the majority of neonatal seizures occur as acute, reactive events in association with a wide range of etiologic factors. These etiologic factors, as well as those of the more traditionally defined syndromes, are the main determinants of eventual developmental outcome of neonates who experience seizures. Although experimental data suggests that some epileptic seizures eventually may have physiological, histological, metabolic, or behavioral consequences, there is yet direct evidence in humans to suggest that the occurrence of seizures themselves in the neonate is the main determinant of long-term outcome.     

Roles of anoxia and noise-induced hearing loss in the postictal refractory period for audiogenic seizures in mice.

The present series of experiments demonstrated a postictal refractory period for audiogenic seizures in DBA/2J mice, which was not related to hearing loss but apparently was related to anoxia. Unlike many previous studies, Experiment 1 controlled for the effects of noise exposure upon hearing sensitivity and demonstrated reduced susceptibility to subsequent audiogenic seizures for at least 1 hr after initial clonic-tonic convulsions. The postictal refractory period was shown to result from the occurrence of seizures per se, not from noise exposure alone. Experiment 2 demonstrated deficiencies of sensorimotor functions that accompanied reduced postictal seizure susceptibility. The two phenomena had similar time courses of recovery, which suggested a common mechanism, probably anoxia, associated with the initial convulsions. In support of this view, Experiment 3 showed that recovery from both phenomena was expedited by allowing subjects to breathe increased O2. The role of anoxia in fatal convulsions was suggested by the finding that subjects experiencing clonic-tonic convulsions in a high-O2 environment survived without exception. In contrast, seizures of air-breathing controls were almost always fatal. Taken together, the data indicate that the postictal reduced susceptibility to audiogenic seizures was closely related to metabolic depletion (in particular, anoxia). The pattern of recovery of susceptibility further suggests that the effects of anoxia impair the spread of seizure activity through the central nervous system, although the initiation of seizures is also affected for a short time.     

Speech abnormalities in seizures: a comparison of absence and partial complex seizures

In order to determine whether speech changes are useful in differentiating seizure types, a study was done in which speech abnormalities during two distinct seizure types, partial complex and absence seizures, were compared. Speech changes noted during prolonged electroencephalographic and video monitoring were compared in 16 patients with 47 partial complex seizures and 19 patients with 95 absence seizures. Speech changes were common during both seizure types. Although some significant differences in speech patterns were noted in the two seizure types, the degree of overlap was such to preclude using speech changes alone as the sole clinical criteria in differentiating the seizures.     

Epileptic tendencies in relation to behavioral responses to a novel environment in the Mongolian gerbil

The severity of epileptic-like seizures in gerbils (Meriones unguiculatus), placed in an open field, is directly related to their ambulatory activity on subsequent trials. An inverse relationship, however, occurs between seizure severity and oriented, bipedal rearing behavior on subsequent trials. Principal components and multiple linear regression analyses support the hypothesis that ambulation and rearing have different underlying neuronal mechanisms. If these two activities are considered as measures of arousal and attention, respectively, then epileptic-like seizures may be caused by hyperactivity of mechanisms which induce arousal.     

The default mode network and altered consciousness in epilepsy

The default mode network has been hypothesized based on the observation that specific regions of the brain are consistently activated during the resting state and deactivated during engagement with task. The primary nodes of this network, which typically include the precuneus/posterior cingulate, the medial frontal and lateral parietal cortices, are thought to be involved in introspective and social cognitive functions. Interestingly, this same network has been shown to be selectively impaired during epileptic seizures associated with loss of consciousness. Using a wide range of neuroimaging and electrophysiological modalities, decreased activity in the default mode network has been confirmed during complex partial, generalized tonic-clonic, and absence seizures. In this review we will discuss these three seizure types and will focus on possible mechanisms by which decreased default mode network activity occurs. Although the specific mechanisms of onset and propagation differ considerably across these seizure types, we propose that the resulting loss of consciousness in all three types of seizures is due to active inhibition of subcortical arousal systems that normally maintain default mode network activity in the awake state. Further, we suggest that these findings support a general "network inhibition hypothesis", by which active inhibition of arousal systems by seizures in certain cortical regions leads to cortical deactivation in other cortical areas. This may represent a push-pull mechanism similar to that seen operating between cortical networks under normal conditions.     

Peri-ictal and ictal cognitive dysfunction in epilepsy

Disturbances in cognitive function, particularly memory, are a common complaint of patients with epilepsy. Factors contributing to cognitive dysfunction are the type of epilepsy, type and frequency of seizures, anti-epileptic drugs and the location of underlying brain lesions. Whilst a great deal of attention has been paid to permanent cognitive impairment, the nature and underlying mechanisms of ictal and peri-ictal cognitive changes are poorly understood. In-depth investigation of seizure related cognitive dysfunction is of great clinical relevance, as these changes are potentially reversible and treatable, thus reducing the cumulative effect of frequent seizures. Greater knowledge of peri-ictal and ictal cognitive dysfunction would improve seizure prediction, localization of seizure focus and assessment of treatment effectiveness, greatly reducing distress and disability. This paper will review current understanding of peri-ictal and ictal cognitive dysfunction and discuss future directions for research.     

Effects of early seizures on later behavior and epileptogenicity

Both clinical and laboratory studies demonstrate that seizures early in life can result in permanent behavioral abnormalities and enhance epileptogenicity. Understanding the critical periods of vulnerability of the developing nervous system to seizure-induced changes may provide insights into parallel or divergent processes in the development of autism. In experimental rodent models, the consequences of seizures are dependent on age, etiology, seizure duration, and frequency. Recurring seizures in immature rats result in long-term adverse effects on learning and memory. These behavioral changes are paralleled by changes in brain connectivity, changes in excitatory neurotransmitter receptor distribution, and decreased neurogenesis. These changes occur in the absence of cell loss. Although impaired cognitive function and brain changes have been well-documented following early-onset seizures, the mechanisms of seizure-induced dysfunction remain unclear.     

The consequences of uncontrolled epilepsy

The consequences of epilepsy can be quite severe and include shortened lifespan, excessive bodily injury, neuropsychological and psychiatric impairment, and social disability. There is evidence that seizures cause brain injury, including neuronal death and physiological dysfunction. Mortality rates are 4-7 times higher in people with medically refractory seizures, and injury rates are substantial, ranging from one per 20 person-years to as much as one per 3 person-years. Quality of life is impaired in epilepsy, and relates to seizure control. Psychosocial disabilities, including lower social interaction with reduced marriage rates and reduced employment levels, are more common in people with refractory seizures. Complete seizure control is desirable, since seizures potentially constitute a serious threat to health and well-being. Therefore, satisfactory seizure control should be defined as having no seizures. Treatment should be directed to preventing seizures whenever possible and achieving control early in the course of illness. The risks of uncontrolled seizures outweigh the risks of aggressive medical or surgical therapy.     

Cellular abnormalities and synaptic plasticity in seizure disorders of the immature nervous system

The nervous system has an enhanced capacity to generate seizures during a restricted phase of postnatal development. Studies in animals and particularly in in vitro brain slices from hippocampus and neocortex have been instrumental in furthering an understanding of the underlying processes. Developmental alterations in glutaminergic excitatory synaptic transmission appear to play a key role in the enhanced seizure susceptible of rodents during the second and third week of life. Prior to this period, the number of excitatory synapses is relatively low. The scarcity of connections and the inability of the existing synapses to release glutamate when activated at high frequencies likely contribute importantly to the resistance of neonates to seizures. However, at the beginning of week 2, a dramatic outgrowth of excitatory synapses occurs, and these synapses are able to faithfully follow activation at high frequencies. These changes, coupled with the prolonged nature of synaptic potentials in early life, likely contribute to the ease of seizure generation. After this time, seizure susceptibility declines, patterns of local synaptic connectivity remodel, and some synapses are pruned. Concurrently, the duration of excitatory postsynaptic potentials shortens due at least in part to a switch in the subunit composition of postsynaptic receptors. Other studies have examined the mechanisms underlying chronic epilepsy initiated in early life. Models of both cortical dysplasia and recurrent early-life seizures suggest that alterations in the normal development of excitatory synaptic transmission can contribute importantly to chronic epileptic conditions. In the recurrent early-life seizure model, abnormal use-dependent selection of subpopulations of excitatory synapses may play a role. In experimental cortical dysplasia, alterations in the molecular composition of postsynaptic receptor are observed that favor subunit combinations characteristic of infancy.     

Massively multiplayer online role-playing game-induced seizures: a neglected health problem in Internet addiction.

As the Internet has become rapidly and widely integrated into society, Internet addiction has become a growing psychosocial problem. However, epileptic seizure, another out-of-the-ordinary health problem, is often neglected in this regard. Ten patients who experienced epileptic seizures while playing the newest genre of electronic games -- Massively Multiplayer Online Role-Playing Games (MMORPGs) -- were investigated. Patients were predominantly male young adults, and most of the events were generalized tonic-clonic seizures, myoclonic seizures, and absences. These patients should be categorized into idiopathic generalized epilepsies. Even though photosensitivity was an important factor, behavioral and higher mental activities also seemed to be significant seizure precipitants. Results demonstrated that MMORPG-induced seizures were not analogous to the ordinary video game-induced seizures. Significantly, an epileptic seizure warning did not always appear on the websites of MMORPGs and instructions for the software. While the prevalence of MMORPG-induced seizures remains unknown, it may exceed our expectations and impact our society. Not only for clinical neurologists but also for the primary physicians, educators, sociologists, and global online game publishers, there should be an awareness of this special form of reflex seizures in order to provide an appropriate health warning to MMORPG players.     

Types of sexual transference and countertransference in psychotherapeutic work with children and adolescents

The question of normal sexuality begins to arise in the treatment of severely sexually abused or sexually offending patients. The author suggests that it is an interesting and delicate moment during the process of recovery when less perverse, more normal sexuality appears mixed with, or even disguised by, the more habitual perverse fantasies. Writers in the adult field have drawn distinctions between perverse, eroticized and normal erotic transferences, and between Oedipal and post-Oedipal sexuality. Some have also distinguished between countertransferences in the analyst of an erotised versus a normal erotic nature. The paper discusses whether these distinctions could have any relevance for child patients. Freud and Klein have taught us much about the child's sexuality in relation to his interest in and attraction to his parents as sexual beings. But can we also detect some origins in earlier experiences in infancy of the child's later capacity to feel himself a sexual being capable of being wanted by an other? How might such a feeling of sexual self-worth differ from narcissism and from sexualised exhibitionism? The paper asks how therapists might deal with such problems and such possibly healthy developments.