Neuropathy is a major contributing factor to diabetic erectile dysfunction

Abstract

Erectile dysfunction (ED) in diabetes is multifactorial. So far, the impact of neuropathy has not been well determined. This study was performed to assess the frequency of abnormal neurophysiological tests in patients with ED due to diabetes compared to patients with ED due to nondiabetic neuropathies in order to estimate the contribution of neuropathy in diabetic ED. Forty-nine men with ED were studied. We classified ED as 'diabetic', 'neuropathic' or 'ED of other origin'. 26.6% of the men fulfilled the criteria of diabetic ED, 42.9% had neuropathic ED. In every patient history taking, a questionnaire focusing on autonomic symptoms other than ED, clinical examination, nerve conduction studies (NCS), sphincter ani electromyography (EMG), heart rate variability testing (HRV) and quantitative sensory testing (QST) was performed. Vascular function was assessed by the intracavernosal prostaglandin E1 (PGE1) injection test. The frequency of abnormal results in diabetic and neuropathic patients was compared. Vascular function was abnormal in only one patient with diabetic ED and three patients with neuropathic ED. Both groups had similar frequencies of autonomic symptoms other than ED (64% in diabetic vs. 64% in neuropathic patients), abnormal EMG (33% vs. 40%) and abnormal QST (vibratory perception 83% vs. 84%, cold perception 9% vs. 19%, warm perception 42% vs. 43%). Abnormal clinical findings (50% vs. 33%), NCS (75% vs. 50%) and HRV (39% vs. 25%) were slightly, but not significantly more frequent in men with diabetic ED than neuropathic ED. The tests indicating neuropathy showed abnormalities in men with diabetic ED as frequently as in men with neuropathic ED. Some tests even suggested neuropathy more often in diabetic than in neuropathic ED. The findings support the hypothesis that neuropathy contributes significantly to the pathophysiology of ED in diabetes mellitus. [Neurol Res 2001; 23: 651-654]     

Neuropathy is a major contributing factor to diabetic erectile dysfunction

Erectile dysfunction (ED) in diabetes is multifactorial. So far, the impact of neuropathy has not been well determined. This study was performed to assess the frequency of abnormal neurophysiological tests in patients with ED due to diabetes compared to patients with ED due to nondiabetic neuropathies in order to estimate the contribution of neuropathy in diabetic ED. Forty-nine men with ED were studied. We classified ED as 'diabetic', 'neuropathic' or 'ED of other origin'. 26.6% of the men fulfilled the criteria of diabetic ED, 42.9% had neuropathic ED. In every patient history taking, a questionnaire focusing on autonomic symptoms other than ED, clinical examination, nerve conduction studies (NCS), sphincter ani electromyography (EMG), heart rate variability testing (HRV) and quantitative sensory testing (QST) was performed. Vascular function was assessed by the intracavernosal prostaglandin E1 (PGE1) injection test. The frequency of abnormal results in diabetic and neuropathic patients was compared. Vascular function was abnormal in only one patient with diabetic ED and three patients with neuropathic ED. Both groups had similar frequencies of autonomic symptoms other than ED (64% in diabetic vs. 64% in neuropathic patients), abnormal EMG (33% vs. 40%) and abnormal QST (vibratory perception 83% vs. 84%, cold perception 9% vs. 19%, warm perception 42% vs. 43%). Abnormal clinical findings (50% vs. 33%), NCS (75% vs. 50%) and HRV (39% vs. 25%) were slightly, but not significantly more frequent in men with diabetic ED than neuropathic ED. The tests indicating neuropathy showed abnormalities in men with diabetic ED as frequently as in men with neuropathic ED. Some tests even suggested neuropathy more often in diabetic than in neuropathic ED. The findings support the hypothesis that neuropathy contributes significantly to the pathophysiology of ED in diabetes mellitus.     

Assessment of erectile function in diabetic and non-diabetic impotence by simultaneous recording of penile diameter and penile arterial pulse

Simultaneous monitoring of penile diameter and penile arterial pulse during laboratory-based erotic stimulation with film and fantasy, has been used to compare diabetic and non-diabetic impotent men with non-impotent controls. The degree of erection to erotic film distinguished between organic and psychogenic aetiologies. The diabetic group showed smaller penile pulse amplitude changes than the other two groups. Amongst the diabetics, severe autonomic neuropathy was associated with impaired erectile and penile pulse amplitude responses. Severe retinopathy was associated with smaller baseline penile pulse amplitude as well as smaller amplitude response. Blood pressure response to erotic stimuli did not differ between the three groups. An analysis of the temporal relationship between penile diameter change and pulse amplitude change revealed differences between the groups that may prove to have diagnostic as well as theoretical implications.     

Psychological theories and treatments of erectile impotence

The conceptual inaccuracies and the diagnostic difficulties encountered in the study of erectile impotence are underlined by the author. After a review and critique of the psychoanalytical and behavioral trends, of the "new sex therapy" and of cognitivism, the therapeutic methods which derive from these concepts are compared with each other. A particular attention is devoted to anxiety since its definition and prevalence varies considerably in the literature despite a misleading superficial similarity.     

Treatment of erectile impotence using a nocturnal penile tumescence conditioning procedure

Nocturnal penile episodes typically occur every 90–100 minutes during sleep in healthy male adults and last an average of 20–40 minutes. The treatment of a case of male erectile impotence using a conditioning procedure based on these nocturnal penile episodes is described. It is suggested that this procedure be used in those cases of erectile failure where the standard treatment components fail to generate an erectile response.     

Pharmacologically induced penile erection (PIPE) as a maintenance treatment for erectile impotence: A report of 41 cases

Forty-one patients with impotence, either organic in origin or unresponsive to psychosexual therapy, were treated by intracavernosal injections, in most cases using papaverine. Small test doses were given, progressing to higher doses if necessary, with instructions for self-injection. Older patients needed significantly higher doses than younger ones. Thirty-six of the 41 patients were able to achieve erections as a result of injections. Seventeen of these have continued self-injection at home; 14 achieved erections but had little or no further use of the injections at home; five achieved erections and used the treatment at home, but then discontinued it after the recovery of spontaneous erections. Five patients failed to achieve erections even with the maximum dose. Five patients early in the series experienced priapism, which was successfully treated. There were few other side effects.     

Effect of blood sampling on apomorphine-induced penile tumescence in erectile impotence: a case report.

Apomorphine HCl (Apo) (0.5 mg sc), but not placebo, induced an erectile response (monitored with a mercury strain gauge) lasting 40 min in an impotent hyperprolactinemic patient. Serial blood sampling modified the 40 min erectile response. Prompt detumescence followed by complete or partial restoration of tumescence occurred each time blood was drawn. This observation points to the sensitivity of the Apo-erectile response to experimental procedures subjectively perceived as anxiogenic.     

Severity of depression and hypothalamic-pituitary-adrenal axis dysregulation: identification of contributing factors

Severity of depression, as reflected by total scores on depression rating scales, has been established as one of several major sources of variance associated with hypothalamic-pituitary-adrenal axis dysregulation in patients with major depressive disorder. To determine which of the symptoms comprising clinically defined severity of illness contribute most to this relationship, we studied the associations between postdexamethasone plasma cortisol levels and components of the Hamilton Rating Scale for Depression (HRSD) in 114 patients with major depressive disorder. At pretreatment baseline, severity of depression was modestly but significantly correlated with postdexamethasone plasma cortisol; a large part of this relationship was associated with the anxiety components of the HRSD. When relationships between postdexamethasone plasma cortisol and severity measures were studied longitudinally during treatment, this contribution of the anxiety items persisted. The anxiety associated with depression appears to be a major clinical factor associated with the hypothalamic-pituitary-adrenal axis dysregulation in major depressive disorder.     

Postictal central apnea as a cause of SUDEP: evidence from near-SUDEP incident

While undergoing video-EEG monitoring, a 20-year-old woman had a 56-second convulsive seizure, after which she developed persistent apnea. The rhythm of the electrocardiogram complexes was unimpaired for approximately 10 seconds, after which it gradually and progressively slowed until it stopped 57 seconds later. Evaluation after successful cardio-respiratory resuscitation showed no evidence of airway obstruction or pulmonary edema. The patient had a previous cardio-respiratory arrest after a complex partial seizure without secondary generalization. Although epileptic seizures are known to be potentially arrhythmogenic to the heart, our observations strongly suggest that one probable mechanism of sudden unexplained death in epilepsy is the marked central suppression of respiratory activity after seizures.     

Schizophrenia as a GSK-3 dysregulation disorder

Converging evidence suggests that the regulation of glycogen synthase kinase 3 (GSK-3) might be important in schizophrenia. Atypical and typical antipsychotic drugs alter GSK-3 activity, as do drugs that induce psychosis. GSK-3 regulatory pathways are altered in schizophrenia, and many of the genes associated with schizophrenia directly or indirectly regulate GSK-3 activity. We propose a variant on the neurodevelopment and dopamine hypotheses of schizophrenia, whereby (i) an early dysfunction in GSK-3 regulation has neurodevelopmental consequences that predispose to disease and (ii) dysfunction in GSK-3 regulation in the adult brain alters dopamine signalling events, causing psychotic symptoms and cognitive dysfunction. If, as we suggest, GSK-3 regulation is crucial to schizophrenia, the Wnt and insulin signalling pathways become targets for therapy.     

Effect of bromocriptine in patients with apomorphine-responsive erectile impotence: an open study.

An open pilot study was undertaken to investigate the therapeutic effect of the dopaminergic agent, bromocriptine (BC), in impotent patients who developed an erectile response to the dopamine receptor agonist, apomorphine. Eight out of 17 patients reported improvement in ability to obtain an erection; five of these 8 subjects were able to achieve penetration. The optimum dose of BC was 2.5 - 11.25 mg/day. A double-blind placebo-controlled study is merited.     

Endorphins in male impotence: evidence for naltrexone stimulation of erectile activity in patient therapy

In the present study we evaluated whether naltrexone administration could stimulate sexual function in 30 male patients, ages 25 to 50 years, with idiopathic impotence of at least one year's duration and not of organic etiology. The patients received naltrexone (50 mg/day) or placebo, on a random basis for two weeks. Sexual performance, expressed as the number of full coitus/week, was assessed before (time 0) and during (on days 7 and 15) each treatment. The naltrexone therapy significantly increased the number of successful coitus compared to placebo after 7 and 15 days of treatment: improvement of sexual performance was evident in 11 out of the 15 treated patients. All the patients experienced a significant increase in morning and spontaneous full penile erections/week. No significant side effects were reported. Endocrine studies revealed no significant modification of plasma LH, FSH or testosterone by naltrexone, suggesting that the positive effect of the drug on sexual behavior was exerted at a central level. A two-month follow-up, at which time patients were off treatment, erectile capacity had returned to baseline in 10 patients, while five reported complete recovery of their sexual ability. We hypothesize that an alteration in central opioid tone is present in idiopathic impotence and is involved in the impairment of sexual behavior.     

Seizure as a cause of fracture

Of 2,800 patients admitted to hospital with a diagnosis of seizure, 1.1% (30/2,800) sustained fracture. Of these, 0.5% (15/2,800) had fracture due to direct trauma, 0.3% (7/2,800) had fracture as a consequence of seizure alone, and in 0.3% (8/2,800) the etiology was not determined. In the trauma group, 11 of 17 fractures involved the skull, nasal bones, and clavicle, while in the nontrauma group, the proximal humerus was the site in 6 of 9 fractures. These findings indicate that fracture is an uncommon complication of seizure and is extremely rare in the absence of trauma where, however, the fracture may be pathognomonic (bilateral posterior dislocation or fracture-dislocation of the shoulder) or highly suggestive (unilateral posterior dislocation, fracture-dislocation of the shoulder) of seizure.     

首发抑郁症患者甲状腺功能相关因素探讨

目的：探讨首发抑郁症患者甲状腺功能的特点及甲状腺功能与生活事件、抑郁焦虑情绪的关系。方法：对30例未用药的首发抑郁症患者（研究组）和30名健康志愿者（对照组）进行甲状腺激素（血清游离三碘甲状腺原氨酸（FT3）、游离甲状腺素（FT4）、血清三碘甲状腺原氨酸（T3）、甲状腺素（T4）、促甲状腺素（TSH）、抗甲状腺过氧化物酶抗体（Anti-TPO）、抗甲状腺球蛋白抗体（Anti-Tg）水平测定;并以汉密尔顿抑郁量表（HAMD）、汉密尔顿焦虑量表（HAMA）、生活事件量表（LES）及自动思维量表（ATQ）进行评定。结果：两组HAMD总分、HAMA总分、ATQ总分、LES负性分及LES总分比较,差异均有统计学意义（P均=0.000）;正性生活事件刺激量两组间差异无统计学意义（P=0.898）。两组FT3、FT4、T3、T4、TSH、Anti-TPO及Anti-Tg水平比较,差异无统计学意义（P均〉0.05）。研究组负性生活事件刺激量与Anti-TPO及Anti-Tg正相关（r=0.366、0.376;P〈0.05）,生活事件总刺激量与Anti-Tg正相关（r=0.370,P〈0.05）,正性生活事件刺激量与FT4正相关（r=0.391,P〈0.05）。结论：抑郁症患者可能存在免疫功能异常,免疫功能异常与负性生活事件的刺激强度有很大关系。     

Racism as a cause of depression

Racism is not just an added stress to individuals of minority ethnic groups (identified as racial groups) but is a pathogen which generates depression. In analysing this within a social model of depression indicating a few ways in which racism subtly - and not so subtly - affects self esteem, causes losses in a psychological sense, and promotes a sense of helplessness (Table 2) I have indicated ways in which this perspective should influence treatment. A more complex scheme summarising the matters raised in this paper are given in Table 3. It should be acknowledged that in depression (as in any other psychiatric illness), the patient is implicated in the genesis of the condition one way or another, but the emphasis given in this paper to a "victim" approach is deliberate and necessary. In dealing with depression among people who are victims of social condition be it racism or the unemployment it is all too easy to see the individual as the problem. We then see solutions merely in terms of changing or treating the individual and really get into quite a mess. For example the author was recently talking to a G.P. about a man who had become depressed because of unemployment. The G.P. wanted to give him an antidepressant. Yes X is "good for unemployment" he was told. He did not see the joke. The emphasis had already shifted. Even if we recognise the effects of racism in causing identity crises, low self esteem or a sense of helplessness, we must of course help the individual but we must keep reminding ourselves that the problem is not really the low self esteem or whatever, but the racism.(ABSTRACT TRUNCATED AT 250 WORDS)     

Emotion dysregulation as a maintenance factor of borderline personality disorder features

We examined within-individual changes in emotion dysregulation over the course of one year as a maintenance factor of borderline personality disorder (BPD) features. We evaluated the extent to which (1) BPD symptom severity at baseline predicted within-individual changes in emotion dysregulation and (2) within-individual changes in emotion dysregulation predicted four BPD features at 12-month follow-up: affective instability, identity disturbances, negative relationships, and impulsivity. The specificity of emotion dysregulation as a maintaining mechanism of BPD features was examined by controlling for a competing intervening variable, interpersonal conflict. BPD symptoms at baseline predicted overall level and increasing emotion dysregulation. Additionally, increasing emotion dysregulation predicted all four BPD features at 12-month follow-up after controlling for BPD symptoms at baseline. Further, overall level of emotion dysregulation mediated the association between BPD symptom severity at baseline and both affective instability and identity disturbance at 12-month follow-up, consistent with the notion of emotion dysregulation as a maintenance factor. Future research on the malleability of emotion dysregulation in laboratory paradigms and its effects on short-term changes in BPD features is needed to inform interventions.