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Urinary incontinence (UI) is a disease affecting quality of life of 200 million patients worldwide. It is characterized by involuntary loss of urine. The factors involved are cystitis, detrusor hyperreflexia, spinal injury, benign prostatic hyperplasia, etc. The surge in the number of reviews on this subject indicates the amount of research devoted to this field. The prevalence is increasing at an alarming rate but unfortunately, only a few medications are currently available for this condition. There are peripheral as well as central targets including cholinergic, vanilloid, prostaglandin, kinin, calcium channel, cannabinoid, serotonin, and GABA-receptors, which act by different mechanisms to treat different types of incontinence. Drugs acting on the central nervous system (CNS) increase urinary bladder capacity, volume, or pressure threshold for micturition reflex activation while peripherally acting drugs decrease the amplitude of micturition contraction and residual volume. Anticholinergic drugs specifically M3 receptor antagonists are the first choice but have frequent side effects such as dry mouth, CNS disturbances, etc. Therefore, there is a need to understand the biochemical pathways that control urinary dysfunction to determine the potential to which they can be exploited in the treatment of this condition. This article reviews the central and peripheral molecular targets and the potential therapeutic approaches to the treatment of UI.

The vast majority of patients with multiple sclerosis (MS) develop bladder control problems including urgency to urinate, urinary incontinence, frequency of urination, and retention of urine. Over 60% of MS patients show detrusor-sphincter dyssynergia, an abnormality characterized by obstruction of urinary outflow as a result of discoordinated contraction of the urethral sphincter muscle and the bladder detrusor muscle. In the current study we examined bladder function in female SWXJ mice with different defined levels of neurological impairment following induction of experimental autoimmune encephalomyelitis (EAE), an animal model of central nervous system inflammation widely used in MS research. We found that EAE mice develop profound bladder dysfunction characterized by significantly increased micturition frequencies and significantly decreased urine output per micturition. Moreover, we found that the severity of bladder abnormalities in EAE mice was directly related to the severity of clinical EAE and neurologic disability. Our study is the first to show and characterize micturition abnormalities in EAE mice thereby providing a most useful model system for understanding and treating neurogenic bladder.

This study represents the first paper of the effects of growth regulators on the physiochemical and phytochemical properties of the wax apple fruit, a widely cultivated fruit tree in southeast Asia. Net photosynthesis, sucrose phosphate synthase (SPS) activity, peel color, fruit firmness, juice content, pH value, total soluble solids (TSSs), and the sugar acid ratio were all significantly increased in growth regulators (PGRs) treated fruits. The application of gibberellin (GA3), naphthalene acetic acid (NAA), and 2,4-dichlorophenoxy acetic acid (2,4-D) significantly reduced titratable acidity and increased total sugar and carbohydrate content compared to the control. The 50 mg/L GA3, 10 mg/L NAA, and 5 mg/L 2,4-D treatments produced the greatest increases in phenol and flavonoid content; vitamin C content was also higher for these treatments. PGR treatment significantly affected chlorophyll, anthocyanin, and carotene content and produced higher phenylalanine ammonia lyase (PAL) and antioxidant activity levels. There was a positive correlation between peel color and TSS and antioxidant activity and both phenol and flavonoid content and PAL activity and anthocyanin formation. A taste panel assessment was also performed, and the highest scores were given to fruits that had been treated with GA3 or auxin. The study showed that application of 50 mg/L GA3, 10 mg/L NAA, and 5 mg/L 2,4-D once a week from bud development to fruit maturation increased the physiochemical and phytochemical properties of wax apple fruits.

Total renal ammonia production and ammonia precursor utilization were evaluated in patients under normal acid-base balance and in patients with 24-h NH4Cl acidosis by measuring (a) ammonia excreted with urine and that added to renal venous blood, and (b) amino acid exchange across the kidney. In 24-h acidosis not only urinary ammonia excretion is increased, but also total ammonia production is augmented (P less than 0.005) in comparison with controls. By evaluating the individual role of acid-base parameters, urine pH and urine flow in influencing renal ammonia production, it was shown that the degree of acidosis and urine flow are likely major factors stimulating ammoniagenesis. Both urine pH and urine flow are determinant in the preferential shift of ammonia into urine. In 1-d acidosis, renal extraction of glutamine was not increased and the total ammonia produced/glutamine N extracted ratio was higher than in controls (P less than 0.005) and was inversely correlated with the log of arterial bicarbonate concentration (P less than 0.001). In the same condition, renal glycine and ornithine uptake took place; the more severe the acidosis, the greater was the renal extraction of these amino acids (P less than 0.001). These data indicate that at the early stages of metabolic acidosis, in spite of a brisk increase in ammonia production, the mechanisms responsible for the increased glutamine use, which are operative in chronic acidosis, are not activated and other ammonia precursors, besides glutamine, are probably used for ammonia production.

Measurements of urinary flow rate were performed in 16 patients with established prostatitis before and after a course of antimicrobial therapy. Before treatment the maximum flow rates were poor with abnormal flow curves and significant improvement in voiding characteristics were observed with treatment (P less than 0.01). A preliminary electrophysiological (EMG) study of sphincter activity suggested that the obstruction to the flow of urine was at least in part due to failure of the external sphincter to relax during micturition. Although the total number of cases in this series was small the study showed that prostatitis was associated with a disorder of micturition which correlated with the other clinical features of the disease and could be objectively evaluated. Eradication of infection restored normal conditions in the lower urinary tract.

Purpose

Pituitary adenylate cyclase activating polypeptide (PACAP) and receptors are expressed in micturition pathways. Studies demonstrated roles for PACAP in detrusor smooth muscle contraction, facilitating ATP release from urothelium and PACAP antagonism reduced cyclophosphamide-induced bladder hyperreflexia.

Materials and Methods

PACAP contributions to micturition and somatic sensation were studied in PACAP knockout (PACAP−/−), littermate heterozygote (PACAP+/−) and wildtype (WT) mice using conscious cystometry with continuous intravesical saline or acetic acid (AA; 0.5%) instillation, urination patterns, somatic sensitivity testing of hindpaw and pelvic region with calibrated von Frey filaments and morphological assessments of urinary bladder.

Results

PACAP−/− mice exhibit increased bladder mass with fewer but larger urine spots. In PACAP−/− mice, the lamina propria and detrusor smooth muscle are significantly thicker whereas the urothelium is unchanged. PACAP−/− mice exhibit increased bladder capacity, void volume (VV) and longer intercontraction interval (ICI) with significantly increased detrusor contraction duration and large residual volume. WT mice respond to AA (0.5%) with a reduction in VV and a decreased ICI whereas PACAP+/− and PACAP−/− mice do not respond. PACAP−/− mice are less responsive to somatic stimulation. PACAP+/− also exhibit bladder dysfunction and somatic and visceral sensory abnormalities but to a lesser degree.

Conclusions

PACAP gene disruption contributes to changes in bladder morphology, bladder function and somatic and visceral hypoalgesia.

Trospium chloride is a quaternary ammonium compound, which is a competitive antagonist at muscarinic cholinergic receptors. Preclinical studies using porcine and human detrusor muscle strips demonstrated that trospium chloride was many-fold more potent than oxybutynin and tolterodine in inhibiting contractile responses to carbachol and electrical stimulation. The drug is poorly bioavailable orally (< 10%) and food reduces absorption by 70%– 80%. It is predominantly eliminated renally as unchanged compound. Trospium chloride, dosed 20 mg twice daily, is significantly superior to placebo in improving cystometric parameters, reducing urinary frequency, reducing incontinence episodes, and increasing urine volume per micturition. In active-controlled trials, trospium chloride was at least equivalent to immediate-release formulations of oxybutynin and tolterodine in efficacy and tolerability. The most problematic adverse effects of trospium chloride are the anticholinergic effects of dry mouth and constipation. Comparative efficacy/tolerability data with long-acting formulations of oxybutynin and tolterodine as well as other anticholinergics such as solifenacin and darifenacin are not available. On the basis of available data, trospium chloride does not appear to be a substantial advance upon existing anticholinergics in the management of urge urinary incontinence.

Ayurveda symbolises holistic approach towards treating diseases and better prevention than cure as its one of the main motto.1 In present paper, etiological based survey of 30 patients was carried out to assess dietary and habitual lifestyles of people suffering from hypertension, for this a detailed proforma based on classical etiological factors related to hypertension was used. After the detailed assessment it was found that, more percentage of etiological factors of Raktavaha Srotas (micro channels for the transportation of blood) (78.46%), Rasavaha Srotas (micro channels for the transport of chyme) (53.33%) were found influenced than that ofManovaha Srotas (micro channels for the conveyance of psyche) (27.67%)) and Medovaha Srotas (micro channels transporting of fats) (37.76%). Hence, it can be concluded that avoidance of these etiologies (Nidanaparivarjana) is a first step in the direction of control and management of hypertension.

OBJECTIVE

To investigate the effect of sensory neuron-specific receptors (SNSRs) activation on the micturition reflex in rats.

MATERIALS AND METHODS

Continuous cystometrograms (CMG, 0.04ml/min) were performed in female Sprague-Dawley rats under urethane anesthesia. After stable micturition cycles were established, a selective rat SNSR1 agonist, bovine adrenal medulla 8–22 (BAM8-22), was administered intravenously or intrathecally in normal rats or rats pretreated with capsaicin 4 days before the experiments. Micturition parameters were recorded and compared before and after drug administration.

RESULTS

Intravenous administration of BAM8-22 (3 to 100 μg/kg) significantly increased intercontraction intervals in dose dependent fashion, but did not affect residual urine or baseline pressure at any doses tested. Intrathecal administration of BAM8-22 (0.01 to 0.3 μg) also increased intercontraction intervals in dose dependent fashion, but did not affect residual urine or baseline pressure at any doses tested. These inhibitory effects of intravenous (30 μg/kg) or intrathecal (0.3 μg) administration of BAM8-22 were still observed after capsaicin pretreatment.

CONCLUSION

These results indicate that in urethane-anesthetized rats activation of SNSRs can inhibit the micturition reflex via the pathways independent of capsaicin sensitive C-fibers. Thus SNSRs could be a potential target for the treatment of bladder dysfunction such as overactive bladder.

OBJECTIVES—To examine the frequency and pathophysiology of micturitional disturbance in patients with Guillain-Barré syndrome.
METHODS—Micturitional symptoms were noted and neurological examinations made repeatedly during admission to hospital of patients with clinical and neurophysiologically definite Guillain-Barré syndrome. Urodynamic studies consisted of uroflowmetry, measurement of residual urine, urethral pressure profilometry, medium fill water cystometry, and external sphincter EMG.
RESULTS—Seven of 28 (25%) patients with Guillain-Barré syndrome showed micturitional disturbance. The symptoms included voiding difficulty in six, urinary retention in three, nocturnal urinary frequency in three, and urge incontinence in two. These micturitional symptoms appeared after weakness occurred, and improved gradually along with the neurological signs. All three patients who showed retention became able to urinate. Urodynamic studies were made on four symptomatic patients two of whom underwent repeated study. Disturbed bladder sensation was noted in one patient, bladder areflexia in one, and absence of the bulbocavernosus reflex in one. Cystometry showed decreased bladder volume in two and bladder overactivity in two, one of whom had urge urinary incontinence and the other urinary retention.
CONCLUSIONS—A quarter of the patients with Guillain-Barré syndrome tend to have micturitional disturbance. The patients studied had evacuation and storage disorders, as well as bladder areflexia and disturbed bladder sensation indicative of peripheral types of parasympathetic and somatic nerve dysfunction. Decreased bladder volume with bladder overactivity but no evidence of CNS involvement was also found, evidence that bladder overactivity also occurs in peripheral nerve lesions with probable pelvic nerve irritation.



Background

Xanthogranulomatous prostatitis is an unusual benign inflammatory process of prostate. Clinically it mimics prostatic carcinoma, requiring pathological examination for diagnosis.

Case presentation

A 60-year-old patient presented with 6 months history of increasing difficulty in micturition. On digital rectal examination prostate was hard and nodular and estimated weight was 50-gram. His serum prostate specific antigen (PSA) was 150 ng/ml. Clinically a locally advanced carcinoma of prostate was suspected. In view of severe obstructive urinary symptoms and significant post-micturition residual urine, transurethral resection of prostate was carried out. Histopathological examination of resected prostatic tissue revealed xanthogranulomatous prostatitis with no evidence of malignancy. Patient remains symptom free at 16 months follow-up and serum PSA has decreased to 6 ng/ml.

Conclusion

Xanthogranulomatous prostatitis is a benign inflammatory disorder of prostate that can clinically and even biochemically mimic prostatic carcinoma. A high degree of suspecion and close co-operation with pathologist is necessary for the diagnosis of xanthogranulomatous prostatitis.

In humans, the storage and voiding functions of the urinary bladder have a characteristic diurnal variation, with increased voiding during the day and urine storage during the night. However, in animal models, the daily functional differences in urodynamics have not been well-studied. The goal of this study was to identify key urodynamic parameters that vary between day and night. Rats were chronically instrumented with an intravesical catheter, and bladder pressure, voided volumes, and micturition frequency were measured by continuous filling cystometry during the light (inactive) or dark (active) phases of the circadian cycle. Cage activity was recorded by video during the experiment. We hypothesized that nocturnal rats entrained to a standard 12:12 light:dark cycle would show greater ambulatory activity and more frequent, smaller volume micturitions in the dark compared to the light. Rats studied during the light phase had a bladder capacity of 1.44±0.21 mL and voided every 8.2±1.2 min. Ambulatory activity was lower in the light phase, and rats slept during the recording period, awakening only to urinate. In contrast, rats studied during the dark were more active, had a lower bladder capacities (0.65±0.18 mL), and urinated more often (every 3.7±0.9 min). Average bladder pressures were not significantly different between the light and dark (13.40±2.49 and 12.19±2.85 mmHg, respectively). These results identify a day-night difference in bladder capacity and micturition frequency in chronically-instrumented nocturnal rodents that is phase-locked to the normal circadian locomotor activity rhythm of the animal. Furthermore, since it has generally been assumed that the daily hormonal regulation of renal function is a major driver of the circadian rhythm in urination, and few studies have addressed the involvement of the lower urinary tract, these results establish the bladder itself as a target for circadian regulation.

Coordination of the urinary bladder and the external urethral sphincter (EUS) is controlled by descending projections from the pons, and is also subject to modulation by segmental afferents. We quantified the effects on the micturition reflex of sensory inputs from genital afferents, traveling in the penile component of the somatic pudendal nerve, by electrical stimulation of the dorsal nerve of the penis (DNP) in α-chloralose anesthetized male cats. Depending on the frequency of stimulation (range 1–40 Hz), activation of penile afferents either inhibited contractions of the bladder and promoted urine storage or activated the bladder and produced micturition. Stimulation of the DNP at 5–10 Hz inhibited distension evoked contractions and increased the maximum bladder capacity before incontinence. Conversely, stimulation at 33 and 40 Hz augmented distension evoked contractions. When the bladder was filled above a threshold volume (70% of the volume necessary for distension evoked contractions), stimulation at 20–40 Hz activated de novo the micturition reflex and elicited detrusor contractions that increased voiding efficiency compared to distension evoked voiding. Electrical stimulation of the DNP with a cuff electrode or percutaneous wire electrode produced similar results. The ability to evoke detrusor contractions by activation of the DNP was preserved following acute spinal transection. These results demonstrate a clear role of genital afferents in modulating the micturition reflex and suggest the DNP as a potential target for functional restoration of bladder control using electrical stimulation.

The administration of vasodilating agents such as bradykinin and acetylcholine cause an increase in urinary sodium excretion. Yet the mechanisms involved in this natriuretic effect are not clear. Recent studies with another renal vasodilator, secretin have shown this drug also causes a profound increase in renal blood flow but without major changes in sodium excretion. To attempt to delineate the basis of this difference in sodium excretion with these drugs, the renal functional effects of secretin and bradykinin were compared at an equivalent vasodilating dose. Bradykinin increased renal blood flow from 222 to 342 ml/min, urine volume from 0.2 to 1.2 ml/min, and urine sodium excretion from 28 to 115 μeq/min. Urine osmolality fell from 1,230 to 401 mosmol/kg. Secretin caused a comparable increase in renal blood flow (216 to 325 ml/min) while changes in urine flow, sodium excretion, and urine osmolality were significantly less.

In further studies papillary plasma flow was estimated using the albumin accumulation technique. Control papillary plasma flow was 29 ml/min per 100 g. Bradykinin increased urinary sodium excretion 108 μeq/min and decreased urinary osmolality from 1,254 to 516 mosmol/kg in association with a rise in papillary plasma flow to 62 ml/min per 100 g. Urine sodium excretion, urinary osmolality, and urine flow rate, as well as papillary plasma flow rate (32 ml/min per 100 g) were unchanged from control when secretin was administered. Studies with acetylcholine were qualitatively similar to those of bradykinin. Renal blood flow increased from 150 to 248 ml/min, urinary sodium excretion increased from 20 to 243 μeq/min, urinary osmolality decreased from 1,237 to 411 mosmol/kg and papillary plasma flow increased from 39 to 52 ml/min per 100 g. It is suggested that the natriuretic effect of some vasodilators is due, at least in part, to alterations in medullary hemodynamics, as evidenced by the increase in papillary plasma flow seen with bradykinin and acetylcholine, but not secretin.

Purpose

The postmenopausal hypoestrogen condition is associated with various lower urinary tract dysfunctions, including frequency, urgency, stress urinary incontinence and recurrent urinary infection. We determined whether hypoestrogen induced lower urinary tract dysfunction after ovariectomy is also associated with an alteration in external urethral sphincter activity.

Materials and Methods

Bilateral ovariectomy was performed in female Sprague-Dawley® rats and sham operated rats served as controls. Transvesical cystometry and external urethral sphincter electromyogram activity were monitored 4, 6 and 12 weeks after sham operation or bilateral ovariectomy and at 6 weeks in bilaterally ovariectomized rats treated with estrogen.

Results

The micturition reflex was elicited in sham operated and bilaterally ovariectomized, urethane anesthetized animals. Post-void residual urine increased and voiding efficiency decreased in rats with 4 to 12 weeks of bilateral ovariectomy. The silent period of external urethral sphincter electromyogram activity was shortened significantly and progressively at increased times after bilateral ovariectomy. These effects were prevented by estradiol treatment.

Conclusions

As evidenced by shortening of the external urethral sphincter electromyogram silent period in ovariectomized rats, the disruption of coordination between the external urethral sphincter and the detrusor muscle could decrease urine outflow and in turn voiding efficiency. Estrogen replacement reverses these changes, suggesting that the central pathways responsible for detrusor-sphincter coordination are modulated by gonadal hormones.

Background/Objective:

A study on the response of the external anal sphincter (EAS) to the passage of urine through the urethra during micturition could not be found in the literature. We investigated the hypothesis that urine passage through the urethra effects EAS contraction to guard against possible flatus or stool leakage during micturition.

Methods:

The study was performed in 23 healthy volunteers (age, 38.6 ± 10.8 [SD] years; 14 men and 9 women). The EAS electromyogram (EMG) was performed during micturition by surface electrodes applied to the EAS. Also, the EAS EMG response to urethral stimulation by a catheter-mounted electrode was registered. The test was repeated after individual anesthetization of the EAS and urethra.

Results:

The EAS EMG recorded a significant increase (P < 0.01) during micturition and on urethral stimulation at the bladder neck. Stimulation of the prostatic, membranous, or penile urethra produced no significant change in the EAS EMG. Urethral stimulation after individual EAS and urethral anesthetization did not cause any changes in the EAS EMG.

Conclusions:

Urine passing through the urethra or urethral stimulation at the vesical neck produced an increase in the EAS EMG, which presumably denotes EAS contraction, which seems to guard against flatus or fecal leakage during micturition. EAS contraction on urethral stimulation is suggested to be mediated through a urethro–anal reflex. Further studies on this issue may potentially prove the diagnostic significance of this reflex in micturition and defecation disorders.

Acetazolamide, an inhibitor of the enzyme carbonic anhydrase, increased the urinary excretion of cyclic AMP in normal and parathyroidectomized rats. The increase was greater in rats with intact parathyroid glands than in parathyroidectomized rats. This rise in the urinary excretion of cyclic AMP was not due to an increase in urine flow or a change in urine pH. Furosemide caused an increase in urine flow, but did not affect the excretion of cyclic AMP or phosphate. Alkalinization of the urine with bicarbonate did not increase the urinary excretion of phosphate or cyclic AMP. Acetazolamide increased the productionof cyclic AMP by rat renal cortical slices in vitro. This effect was dose-dependent. Acetazolamide also stimulated the activity of renal cortical adenyl cyclase in a dose-dependent manner but had no effect on the activity of cyclic nucleotide phosphodiesterase. The pattern of urinary excretion of cyclic AMP and phosphate after administration of acetazolamide was similar to that observed in rats given parathyroid hormone. It is suggested that acetazolamide stimulates the renal production of cyclic AMP by activating adenyl cyclase and that this may be the mechanism by which this inhibitor of carbonic anhydrase produces phosphaturia.

Micturition, or urination, occurs involuntarily in infants and young children until the age of 3 to 5 years, after which it is regulated voluntarily. The neural circuitry that controls this process is complex and highly distributed: it involves pathways at many levels of the brain, the spinal cord and the peripheral nervous system and is mediated by multiple neurotransmitters. Diseases or injuries of the nervous system in adults can cause the re-emergence of involuntary or reflex micturition, leading to urinary incontinence. This is a major health problem, especially in those with neurological impairment. Here we review the neural control of micturition and how disruption of this control leads to abnormal storage and release of urine.

The lower urinary tract (LUT) comprises a storage unit, the urinary bladder, and an outlet, the urethra. The coordination between the two structures is tightly controlled by the nervous system and, therefore, LUT function is highly susceptible to injuries to the neuronal pathways involved in micturition control. These injuries may include lesions to the spinal cord or to nerve fibres and result in micturition dysfunction. A common trait of micturition pathologies, irrespective of its origin, is an upregulation in synthesis and secretion of neurotrophins, most notably Nerve Growth Factor (NGF) and Brain Derived Neurotrophic Factor (BDNF). These neurotrophins are produced by neuronal and non-neuronal cells and exert their effects upon binding to their high-affinity receptors abundantly expressed in the neuronal circuits regulating LUT function. In addition, NGF and BDNF are present in detectable amounts in the urine of patients suffering from various LUT pathologies, suggesting that analysis of urinary NGF and BDNF may serve as likely biomarkers to be studied in tandem with other factors when diagnosing patients. Studies with experimental models of bladder dysfunction using antagonists of NGF and BDNF receptors as well as scavenging agents suggest that those NTs may be key elements in the pathophysiology of bladder dysfunctions. In addition, available data indicates that NGF and BDNF might constitute future targets for designing new drugs for better treatment of bladder dysfunction.

Background

The reaction of the corpora cavernosa (CC), the corpus spongiosum (CS), the bulbocavernosus (BCM) and ischiocavernosus (ICM) muscles to passage of urine through the urethra during micturition is not known. We investigated the hypothesis that the passage of urine through the urethra stimulates the corporal tissue and cavernosus muscles.

Methods

In 30 healthy men (mean age 42.8 ± 11.7 years), the electromyographic activity (EMG) of the CC, CS, BCM, and ICM were recorded before and during micturition, and on interruption of and straining during micturition. These tests were repeated after individual anesthetization of urethra, corporal tissue, and cavernosus muscles.

Results

During micturition, the slow wave variables (frequency, amplitude, conduction velocity) of the CC and CS decreased while the motor unit action potentials of the BCM and ICM increased; these EMG changes were mild and returned to the basal values on interruption or termination of micturition. Micturition after individual anesthetization of urethra, corporal tissue and cavernosal muscles did not effect significant EMG changes in these structures, while saline administration produced changes similar to those occurring before saline administration.

Conclusion

The decrease of sinusoidal and increase of cavernosus muscles' EMG activity during micturition apparently denotes sinusoidal relaxation and cavernosus muscles contraction. Sinusoidal muscle relaxation and cavernosus muscles contraction upon micturition are suggested to be mediated through a 'urethro-corporocavernosal reflex'. These sinusoidal and cavernosus muscle changes appear to produce a mild degree of penile tumescence and stretch which might assist in urinary flow during micturition.

Objective: To define the nature of micturition disturbance in patients with acute idiopathic autonomic neuropathy (AIAN).

Methods: Micturitional symptoms were observed during hospital admissions and the in outpatient clinics in six patients with clinically definite AIAN (typical form in four, cholinergic variant in one, autonomic-sensory variant in one). Urodynamic studies included medium-fill water cystometry, external sphincter electromyography, and a bethanechol test.

Results: Four patients had urinary retention and two had voiding difficulty as the initial presentation. Patients with retention became able to urinate within a week (two to seven days). The major symptoms at the time of urodynamic studies (three weeks to four months after disease onset in most cases) were voiding difficulty and nocturnal frequency. None had urinary incontinence. Complete recovery from the micturition disturbance took from three months to >18 years. The recovery period was shorter in a patient with cholinergic variant, and it was longer in two patients who had a longer duration of initial urinary retention. Micturition disturbance tended to improve earlier than orthostatic hypotension. The major urodynamic abnormalities were detrusor areflexia on voiding (5), denervation supersensitivity to bethanechol (3); low compliance detrusor (1); and impaired bladder sensation (2). None had neurogenic motor unit potentials of the external sphincter muscles.

Conclusions: In patients with AIAN, urinary retention and voiding difficulty are common initial presentations. The underlying mechanisms seem to be pre- and postganglionic cholinergic dysfunction with preservation of somatic sphincter function. The bladder problems tend to improve earlier than orthostatic hypotension.

The dipstrip test for urinary nitrite is fairly unreliable in symptomatic urinary infections and only 104 (52%) of 200 symptomatic children with urinary infection attending an emergency department had a positive result. The test yielded positive results, however, in 83 of 100 outpatients with largely asymptomatic urinary infection attending a follow up clinic because of known predisposition to urinary infection. This difference was highly significant. The finding of urinary nitrite is highly specific for urinary infection and only 1% of 300 uninfected urine specimens gave a positive result. After addition of a broth culture of Escherichia coli to sterile urine incubation at 37 degrees C for four to six hours was required before the nitrite test yielded positive results. This suggests that frequency of micturition in urinary infection reduces the reliability of the nitrite test. On the other hand, the use of overnight, first morning urine specimens may further improve the sensitivity. If nitrite testing is used for screening for urinary infection at home, however, patients should be warned not to rely on a negative result in the presence of symptoms of urinary infection.

Ayurveda as well as Philosophy accepted the Guna as the basic entity of the Sristi. The Maha Gunas, i.e., Sattva, Raja, and Tama are the prime energy, from where the universe evolves, along with human beings. Dravya and Guna both have a Samavayi relationship in which Gunas reside in Dravya and have a secondary place to it. Guna has multifold meanings according to its use, in social, cultural, philosophical, and literary fields. The concepts of Ayurveda are expressed with Gunas. Samanya and Visesa are usually expressed in terms of Gunas; the classification, description, and function of Dravyas depends upon Guna; Karmas are manifested forms of Guna and Samavaya is the eternal, intimate relation of Dravya and Guna. The principles like Triskandha (Hetu, linga, ousadhi) of Ayurveda also narrated by Gunas, Hetus are narrated in the terms of Guna; the Laksanas are the reflections in the status of Gunas of bodily elements, and Cikitsa is in the form of administration of Viparita Gunas. The increased elements are treated by opposite Guna. So if Ruksa Guna is increased then it is to be managed by Snigdha Guna and vice-versa. So diseases can be treated by applying the Gunas, and drugs for the required patient can be selected by applying these Gunas. In support of the above concept, a study on the persons of Rasa-raktagata Sneha (hyperlipidemia) has been carried out assuming that the condition is an increased state of Snigdha Guna and treatment is done using Ruksa property drugs. Patients were divided into two groups, i.e., treatment group (Ruksa Guna drugs) and control group (placebo). The results were assessed after 45 days with the help of a specially prepared pro forma. All the important hematological, biochemical, and urine investigations were done. According to subjective and objective criteria, significant results were found for Group A as compared to Group B.

A double-blind cross-over trial of emepronium bromide (Cetiprin) in nocturnal frequency of micturition in a group of elderly women living in their homes showed that the drug was superior to placebo in diminishing urinary frequency, though not every person benefited. It is suggested that the drug may alter the established habit of rising at night to pass urine. Side-effects were negligible.

Measurements of intravesical pressure, urinary flow rate, retrograde cystographic residual urine, reflux of contrast medium into the prostatic ducts, and radiological prostate size were made in 45 men with benign prostatic hypertrophy. These factors were all found to be good clinical indices of the degree of urethral resistance to micturition; on the other hand, there was no relation between the latter and the severity of symptoms.

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