As we mentioned in previous article, premenstrual syndrome effects over 70% to 90% of women before menopause in US and less for women in Southeast Asia because of their diet. Premenstrual syndrome (PMS) occurrence have more than double over past 50 years due to the acceptance of its as medical condition and caused by unhealthy diet with high in saturated food. Premenstrual syndrome is defined as faulty function of ovaries related to women menstrual cycle, it effects the women physical and emotional state and sometimes interference with daily activities as resulting of hormone fluctuation. The syndrome happens in one or two weeks before menstruation and then declining when the period starts. It is said the symptoms can be so severe that between 10-15% of women have to take time off work, costing businesses millions of dollars a year. In this article, we will discuss what exhibits insomnia to cause PMS.

1. Mineral deficiency
Calcium, magnesium and silicon are essential for women during menstrual cycle because they have a calming effects for the nervous system. Imbalance or deficiency of calcium, magnesium and silicon increase the tension of the brain’s cell resulting in insomnia.

2. Vitamin deficiency
Women with PMS are found to have low levels of vitamin B6 which is vital to convert trytophan to serotonin. Deficiency of vitamin B6 interferes the production of serotonin resulting in lessening the production of melatonin, a vital hormone in promoting a good nigh sleep.

3. Alcohol
Alcohol not only damages the liver in fat and protein metabolism, it also increases the tension of nervous system. Limit intake of less than one cup of wine everyday will helps to reduce the symptoms of insomnia.

4. Caffeine
Caffeine may helps to increase nervous system function but it may causes nervous tension and vitamin B6 deficiency as resulting of caffeine stimulating. It also causes unbalance of production of serotonin and melatonin hormone resulting in increasing the nervous tension leading to insomnia.

5. Low levels of melatonin
Melatonin is hormone which helps to regulate the sleep pattern of our body. some women with PMS found to have low levels of melatonin before period caused by low levels of serotonin and trytophan. Intake of food with high in serotonin and trytophan will help.

5. Insulin irregularity
Researchers exam the inter relationship between insomnia and insulin fluctuation found out that improving insulin balancing will helps to improve the sleep pattern and via versa.

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UroToday.com - The etiology of multiple sclerosis (MS)-emergent erectile dysfunction (ED) is still matter of debate, since both organic and psychological factors have been implicated. There is an association between sexual dysfunction (SD) and destructive lesions in the pons, in MS patients. Central and peripheral nerves systems play a key role in the erectile process. The innervation of the penis is both autonomic (sympathetic and parasympathetic) and somatic (sensory and motor). Pudendal nerves have a central role in erection. Tactile stimulation of the penile shaft activates parasympathetic fibers, which travel in the pudendal nerve and function through the spinal reflex arc from S2 to S4. Neural signals originating in the brain are transmitted to a thoracolumbar erection center and trigger the psychogenic erection associated with either fantasy or viewing erotic material. In addition, the ischiocavernosus and bulbospongiosus striated muscles, which located at the penile crus, are innervated by the motor pudendal nerve. Contraction of these muscles has a definite, contributory role in penile erection. Therefore, erection is a neurovascular event, and any disease or dysfunction affecting the brain, spinal cord, or cavernous and pudendal nerves can induce ED. With respect to placebo, sildenafil produced a 16% greater success rate for vaginal penetration, and a 15% greater rate for successful intercourse. For satisfaction with erection hardness, and satisfaction with the sexual experience, sildenafil did not produce two-fold greater rates. For all efficacy variables, sildenafil had similar or slightly greater scores compared with placebo.

Although some clinical trials have demonstrated an overall success rate of greater than 70%, certain patients will be refractory to treatment with sildenafil. Sildenafil acts a potentiator of local mediators to maintain smooth muscle relaxation and thus cannot act in the absence of intact penile innervation. In this study, most of the participants had abnormal pudendal nerve cortical somatosensory evoked potentials (PEPs). The incidence of ED after non-nerve sparing radical retropubic prostatectomy is up to 97%. This is due to cavernosal nerve damage. A poor response to sildenafil in postoperative patients with unilateral or non-nerve-sparing radical retropubic prostatectomy has been demonstrated. Direct-acting medications might be expected to be efficacious in nonresponders who have nerve injury or nerve damage. Fifty percent of the post prostatectomy patients who had failed with sildenafil, reported improved EF with intraurethral alprostadil.

Sexual dysfunction is a frequent disorder associated to MS, which contributes to the worsening of quality of life of these patients. During the course of MS, prevalence of SD becomes increasingly more common, affecting, after 10 years of disease duration, 40-70% of patients.

Interactions between neural structures are essential to all phases of human sexual response and functioning. Neurophysiological studies give invaluable information on the involvement of the parts of the nervous system that are essential in the control of sexual function. The pudendal nerve and its terminal branch (dorsal nerve of the penis) provide somatosensory innervation to the genitalia in men. Sensory pathways, which are important in reflexogenic erections, transmit information to the CNS via the dorsal penile nerve and the pudendal nerve. Therefore, a neurophysiological test that assesses the pudendal nerve function such as the PEPs, has great value in an objective evaluation of SD.

We did not recommend second or third type PDE-5 inhibitors for sildenafil non-responders. All three FDA approved PDE-5 inhibitors are targeting the same site of action. Studies from the industry tend to favor preference for their own drug, whereas independent studies tend to show no major difference in preference. Multiple well-designed studies have shown that, all three available PDE-5 inhibitors, have a very similar efficacy and safety profile. In our experiences, well-educated sildenafil non-responders, seldom respond to other type of PDE-5 inhibitors.

Written by M.R Safarinejad, MD as part of Beyond the Abstract on UroToday.com

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