Self-Reported Sexual Function and Sexual Arousability in Women with Epilepsy

Summary: Purpose: Women with epilepsy are at risk for sexual dysfunction but the frequency and types of dysfunction have not been well characterized.
Methods: Self-reported sexual function was evaluated in 116 women aged 18-65 years with epilepsy and no concomitant medical or psychiatric illness, including 99 with localization-related epilepsy (LRE) and 17 with primary generalized epilepsy (PGE). Variables evaluated included seizure frequency, age of seizure onset, and antiepileptic drug (AED) exposure. Standardized inventories assessed sexual functioning, sexual arousability and anxiety, sexual behavior, and depression.
Results: Although sexual experience was not reduced, women with PGE and LRE reported significantly less sexual arousability and women with LRE reported significantly more sexual anxiety. Women with LRE experienced significantly more dyspareunia, vaginismus, arousal insufficiency, and sexual dissatisfaction, whereas women with PGE experienced an-orgasmia and sexual dissatisfaction. Sexual symptoms were not associated with seizure frequency, AED exposure, sexual experience, depression, or prepubertal seizure onset.
Conclusions: In contrast to subjects of previous research, the women in our study did not have a disorder of sexual desire, but more than one third experienced disorders of sexual arousal, implying a physiological deficit. Although the etiology for these arousal phase dysfunctions has not been defined, such conditions are treatable and warrant referral to a gynecologist versed in the treatment of sexual disorders.     

Neurocognitive and Symptom Correlates of Self-Reported Childhood Sexual Abuse in Schizophrenia Spectrum Disorders

This study examined whether self-reported childhood sexual abuse in schizophrenia spectrum disorders is linked with severity of neurocognitive deficits. The Wisconsin Card Sorting Test, California Verbal Learning Test, and select WAIS III subtests were administered to 15 participants with schizophrenia or schizoaffective disorder who had been sexually abused and to 28 participants with no abuse history. Controlling for age and premorbid IQ, a MANCOVA indicated there were group differences (f(9, 31) = 5.53, p < .001). Subsequent ANCOVA indicated that the sexual abuse group performed more poorly on tests of working memory and information processing speed. Childhood sexual abuse is associated with more severe working memory deficits in adults with schizophrenia spectrum disorders.     

Organizational Actions of Sex Hormones on Sexual Partner Preference

EB—for the first 2 weeks posthatch) and unisex housing during juvenile development independently resulted in a preference for females over males in two-choice tests, and only females that experienced both EB treatment and unisex living were more likely than controls to pair with other females in colony tests. In a second experiment, females injected with an estrogen synthesis inhibitor for the first week posthatch preferred to spend time near females instead of males in two-choice tests, unlike control females. These experiments suggest that sexual partner preference may result from organizational hormone actions in this pair-bonding species. Possible neural mechanisms or sites that could underly hormonal organization of sexual partner preference in birds and mammals include the anterior hypothalamic/preoptic area, the corticomedial amygdala, and its avian homologue nucleus taeniae of the archistriatum, the septum, and peripheral sensory processes.     

Olfaction and neurodegeneration in HD

Olfactory deficits are present in many neurodegenerative diseases. It is not known, however, whether the olfactory deterioration is caused by a common neural deficit, or whether it is unique to each disease. We report here the effect of degeneration of different brain structures on olfactory impairment in Huntington's disease as determined by voxel-based morphometric analysis. The structures with the greatest effect on the olfactory deficit were the entorhinal cortex, the thalamus, the parahippocampal gyrus, and the caudate nucleus. Although various neuroimaging studies have shown previously that the caudate nucleus is involved in olfaction, this is the first demonstration that it is related to an olfactory dysfunction in a neurodegenerative disease. The results are discussed in relation to other neurodegenerative diseases.     

Flavor and the Formation of Category-Specific Processing in Olfaction

The perception of flavor occurs when objects, such as food and drink, are placed in the mouth. Although the sensation that ensues depends upon inputs from multiple sensory modalities, due to a combination of oral referral and common sensory qualities (e.g., odors and tastes can both be sweet), it is experienced as a unitary flavor perception. In this paper, it is proposed that neural processing within the somatomotor mouth area of the Rolandic operculum mediates oral referral and causes the neural binding of multimodal inputs to create a flavor percept. It is further proposed that unimodal taste and unimodal smell neurons alter the selectivity of bimodal taste/smell cells only if the binding mechanism in the somatomotor mouth area is active. The encoded flavor object is thus represented by a bounded pattern of response that includes the sculpted bimodal cells as well as the unimodal responses distributed across the insula, operculum, anterior cingulate cortex, and orbitofrontal cortex. Once an odor is encoded in this way, the odor acquires the ability to reactivate this encoded percept, whether experienced orthonasally or retronasally. Finally, it is proposed that one manifestation of this process is the existence of category-specific processing in olfaction.     

Olfaction and apathy in Parkinson's disease

BackgroundOlfactory deficits are frequent among patients with idiopathic Parkinson's disease (PD). Additionally, apathy (as quantified by the Apathy Evaluation Scale), is more prevalent in PD patients compared to the general population. Olfactory impairment and apathy are associated with dysfunction in overlapping brain regions. Neuroimaging studies indicate that the anterior cingulate gyrus and medial orbitofrontal cortex are hypoactive in apathetic patients and are also involved in secondary olfactory processing. However, no study until this point has been published investigating whether there is any association between olfactory dysfunction and apathy in PD patients.MethodsIn our study seventy consecutive patients with PD took the Brief Smell Identification Test (B-SIT), completed the Apathy Evaluation Scale (AES) and were administered the Folstein Mini-Mental Status exam (MMSE).ResultsApathetic PD patients performed poorly on the B-SIT compared with non-apathetic PD patients and olfactory impairment correlated with apathy. The simultaneous disruption of olfaction and emotion in Parkinson's could be the result of disease pathology in brain regions involved in both olfactory and emotional processing and reinforces the idea that this link between olfaction and emotions may have clinical consequences.     

Olfaction and social drive in schizophrenia

BACKGROUND: The neurobiology of social dysfunction in schizophrenia is unknown, but smell identification deficits (SIDs) exist in schizophrenia, and olfaction is related to social affiliation in other mammals. The SIDs have been linked with negative symptoms and the deficit syndrome, but any specificity of SIDs for social dysfunction is unstudied. Low intelligence might explain this relationship, if it is associated with both negative symptoms and SIDs. We examined whether SIDs in schizophrenia were related broadly to negative symptoms, as are a number of other neuropsychological measures, or whether they might show a more specific relationship with social drive. METHODS: Smell Identification Test scores, Wechsler Adult Intelligence Scale-Revised IQ, symptomatology assessed with the Positive and Negative Syndrome Scale, and the deficit syndrome were determined in 70 patients with DSM-IV schizophrenia. RESULTS: The SIDs were related to negative symptoms and the deficit syndrome, but the association of SIDs with diminished social drive explained both relationships. Smell identification was also related to Wechsler Adult Intelligence Scale-Revised IQ, but intelligence was independent of the relationship of SID and social drive. The worse Smell Identification Test scores in male patients were attributable to a greater preponderance of men with the deficit syndrome. CONCLUSIONS: These analyses demonstrated independent relationships of Smell Identification Test scores to social drive and intelligence that together accounted for almost 50% of the variance in Smell Identification Test scores. There may be common neural substrates for the low social drive and SIDs in schizophrenia.     

The Role of HINT1 in Methamphetamine-Induced Conditioned Place Preference

Drug addiction is a chronically relapsing disorder in humans; yet, the underlying mechanism remained unclear. Recent studies suggested that the histidine triad nucleotide binding protein 1 (HINT1) may play significant roles in diverse neuropsychiatric diseases including drug addiction. In our present study, we used different batches of mice to establish the different stages of methamphetamine (METH)-induced conditioned place preference (CPP) to explore the dynamic changes throughout the process of addiction in different brain regions, including prefrontal cortex (PFC), nucleus accumbens (NAc), corpus striatum (CPu), and hippocampus (Hip). We found that in NAc of the METH group mice, the HINT1 expression level initially increased after acquisition phases, and then dropped to the normal level after extinction phase, and again increased after reinstatement phase. However, there was no statistical difference in the HINT1 expression level in other three encephalic regions (PFC, CPu, and Hip). Therefore, the HINT1 protein, particularly in the NAc, plays a vital role in the METH-induced CPP. However, the precise mechanisms will require further investigation.     

Olfaction and taste processing in autism.

BACKGROUND: Autism is often associated with sensory symptoms, but few studies have examined chemosensory functions in this population. We examined olfactory and taste functioning in individuals with autism to characterize chemosensory processing and test competing hypotheses about underlying brainstem versus cortical abnormalities. METHODS: Twenty-one participants (10-18 years) with autism were compared with 27 well-matched control participants with typical development. Taste identification was tested via sucrose, NaCl, citric acid, and quinine solutions applied to standard locations on the anterior tongue. Taste detection thresholds were established in the same regions with electrogustometry, and olfactory identification was evaluated with "Sniffin' Sticks." RESULTS: Participants with autism were significantly less accurate than control participants in identifying sour tastes and marginally less accurate for bitter tastes, but they were not different in identifying sweet and salty stimuli. Taste detection thresholds via electrogustometry were equivalent. Olfactory identification was significantly worse among participants with autism. CONCLUSIONS: True differences exist in taste and olfactory identification in autism. Impairment in taste identification with normal detection thresholds suggests cortical, rather than brainstem dysfunction. Further research is needed to determine the neurologic bases of olfactory and taste impairments, as well as the relationship of chemosensory dysfunction to other characteristics of autism.     

Olfaction directs skilled forelimb reaching in the rat

Rats were trained to reach for food pellets, which varied in size from 20 to 300 mg, from one of 21 locations on a shelf located just outside a test cage. After a barrier was lifted, giving access to a food pellet, latency to contact the food was timed, number of reaches to contact the food were counted, the distance of each misplaced reach from the food was measured and the success or failure of each attempt was noted. Control rats walked along the front of the cage sniffing to locate the food. Once they located a food pellet, they inserted their nose between the bars of the cage, sniffed the food for one to three respiratory cycles, raised their snout slightly, and then inserted a forepaw to grasp the food. They seldom required more than three reaches to contact the food and on about half of all trials they were successful in grasping the food. They were more successful in grasping medium-sized food pellets. Performance was unchanged on all measures after vision was occluded with eye patches. Following olfactory bulb removal, however, the rats no longer sniffed to locate the food or sniffed the food prior to initiating a reach. Rather they systematically moved along the length of the cage inserting their snout between the bars at each possible food location and without sniffing reached for the food 'as if blind'. Latency, number of reaches to contact the food and the distance of misplaced reaches increased whereas success rate remained unchanged. Substantial additional impairments were not produced when the bulbectomized rats were given visual occlusion. The study demonstrates that rats locate food and direct reaching using olfaction. The results are discussed in terms of the sensory control of skilled limb use and their relevance to the evolution of the sensory guidance of limb use.     

Olfaction in Parkinson's disease and related disorders

Olfactory dysfunction is an early 'pre-clinical' sign of Parkinson's disease (PD). The present review is a comprehensive and up-to-date assessment of such dysfunction in PD and related disorders. The olfactory bulb is implicated in the dysfunction, since only those syndromes with olfactory bulb pathology exhibit significant smell loss. The role of dopamine in the production of olfactory system pathology is enigmatic, as overexpression of dopaminergic cells within the bulb's glomerular layer is a common feature of PD and most animal models of PD. Damage to cholinergic, serotonergic, and noradrenergic systems is likely involved, since such damage is most marked in those diseases with the most smell loss. When compromised, these systems, which regulate microglial activity, can influence the induction of localized brain inflammation, oxidative damage, and cytosolic disruption of cellular processes. In monogenetic forms of PD, olfactory dysfunction is rarely observed in asymptomatic gene carriers, but is present in many of those that exhibit the motor phenotype. This suggests that such gene-related influences on olfaction, when present, take time to develop and depend upon additional factors, such as those from aging, other genes, formation of α-synuclein- and tau-related pathology, or lowered thresholds to oxidative stress from toxic insults. The limited data available suggest that the physiological determinants of the early changes in PD-related olfactory function are likely multifactorial and may include the same determinants as those responsible for a number of other non-motor symptoms of PD, such as dysautonomia and sleep disturbances.     

Olfaction in child and adolescent anorexia nervosa

Previous studies indicate disturbed olfactory functions in anorexia nervosa with presumable relationship to the clinical symptom of food aversion and weight loss. However, these studies are in part limited due to inadequately matched control samples, insufficient exclusion criteria, complex interactions of the olfactory and trigeminal system, and the lack of regard to co-morbidity and medication. Thus, we investigated olfactory function in 26 female adolescent patients with anorexia nervosa and 23 healthy controls matched for age, gender, handedness, and intelligence. No significant group differences were identified. Controlling for co-morbid disorders, psychopharmacological treatment, and depressivity revealed superior olfactory identification performance in the "pure" anorexia nervosa group (n = 15) in contrast to the controls. Superior identification may be mediated by increased attentional processes towards food stimuli in patients with anorexia nervosa. Effects of co-morbidity and medication highlight the role of neurobiological factors in the etiology of anorexia nervosa. Furthermore, as other neuropsychiatric disorders such as Parkinson's disease or attention deficit hyperactivity disorder show distinct olfactory function patterns, olfaction may be suitable as phenotypic marker with potential relevance for (differential) diagnosis in neuropsychiatric disorders.     

Triangular Fuzzy Neutrosophic Preference Relations and Their Application in Enterprise Resource Planning Software Selection

Cognitive Computation - Enterprise resource planning (ERP) system selection is one of the most important topics in an ERP implementation program that ensures the success of the system. Because of...