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At least 667 records · Page 37Linked to original sources
PubMed2001

Percutaneous afferent neuromodulation for the refractory overactive bladder: results of a multicenter study.

PURPOSE: More than 20 million Americans have an overactive bladder, the predominant symptoms being frequency, urgency, urge incontinence and pelvic pain. While the etiology is not completely understood, most investigators believe the causes to be many and the pelvic floor to be intimately related. Whatever the etiology, traditional therapies, including dietary manipulation, bladder drill, medications and physical therapy, are often poorly tolerated and/or ineffective. We report a prospective, multicenter clinical trial that was undertaken to determine the safety and efficacy of percutaneous peripheral afferent nerve stimulation for treatment of refractive overactive bladder and/or pelvic floor dysfunction. MATERIALS AND METHODS: A total of 53 patients with overactive bladders, in whom all traditional therapy failed, were enrolled in 1 of 5 sites within the United States. Patients received weekly percutaneous electrical stimulations via a 34 gauge needle placed near the tibial nerve 3 finger breadths above the ankle. Urodynamic studies, detailed voiding diaries, quality of life surveys, and incontinence impact questionnaires were completed before, during and after the study. RESULTS: Of the patients with a mean age of 57.4 years 89% (47 of 53) completed the 12-week study. A total of 71% of patients were classified as treatment successes by the investigators and were started on long-term treatment. On average patients noticed a 25% reduction in mean daytime and 21% reduction in mean nighttime voiding frequencies (p <0.05). Urge incontinence was reduced by an average of 35% (p <0.05). Statistically significant improvements were noted in selective pain and quality of life indexes. No significant adverse events related to treatment were noted in any patients. CONCLUSIONS: Percutaneous peripheral afferent nerve stimulation offers a safe, minimally invasive and effective treatment for managing refractive overactive bladder and/or pelvic floor dysfunction.

Adult↗
PubMedDate not supplied

[Biological factors of PTSD: neurotransmitters and neuromodulators].

Subjects with posttraumatic stress disorder exhibit abnormalities in many psychobiological systems. Studies of the effects of stress on learning and memory processes suggest that fear conditioning, behavioural sensitisation, and a failure of extinction may be important in the persistence and reexperiencing of traumatic memories and stress sensitivity. All these symptoms are supported by specific biological mechanisms including NMDA receptors, noradrenergic system, etc. Recent findings show that amino acid transmitters, glutamate and GABA, are intimately involved in the process of factual memory registration, and suggest that amine neurotransmitters, norepinephrine and serotonin, are involved in encoding emotional memory. In addition, research suggests that 5-HT neurones have directs effects on both adrenergic and HPA function. Such findings provide important information that should guide current pharmacological practice and the development of innovative biological therapeutics.

Adaptation, Psychological↗
PubMedDate not supplied

[Dopamine antibodies as neuromodulators of behavioral reactions in mice of different genotypes].

A possibility of the long-term modification of inborn behavioral features of different mice genotypes (C57B1/6 and BALB/c) by active immunization with dopamine-bovine serum albumin conjugate was investigated. Significant interstrain differences were found in the effects of dopamine antibodies on the open-field behavior and the content of neurotransmitters in the brain cortex and striatum. It was shown that the active immunization of mice to dopamine produces an increase in the functional activity of brain dopamine receptors. The extent, to which this increase is pronounced, is genotype-dependent.

Animals↗
PubMed2002

Neuromodulative treatment of overactive bladder--noninvasive tibial nerve stimulation.

BACKGROUND: Conservative treatment of overactive bladder employes behavioral or invasive neuromodulatory inhibition of miction reflex and administration of anticholinergic drugs. MAIN PURPOSE: The aim of this study was to use non-invasive stimulation of the tibial nerve with the intention to achieve desired therapeutic effects without iatrogenic nerve damage using a superficial electrostimulation. METHODS: All patients suffered from overactive bladder (OAB) without bladder outlet obstruction. OAB was examined by the Behavioral urge score BUS (0.0--the best and 1.0--the worst score), the International prostate symptom score IPSS (0--the best and 35--the worst score) and the Incontinence quality of life questionnaire IQOL (0.0--the worst and 1.0--the best index). The patients were divided into 3 groups: Group I--patients with electrode attached behind the medial ankle of the left lower extremity. The intensity of stimulation corresponded to 70% of the maximum amplitude of response from musculus abductor hallucis. Frequency of stimulation was 1 Hz and duration of the square impulse was 0.1 ms. Surface stimulation lasted 30 minutes and was repeated once a week. Group II--patients were treated by oral oxybutynin 5 mg t.i.d. Group III--patients without treatment. The BUS, IPSS, and IQOL were repeated after the treatment. RESULTS: The study included 28 females of average age 54 year (range 45 to 63). Mean IPSS was 17 (range 12 to 21), mean index of quality of life IQOL was 30 (range 12 to 78) and mean BUS score was 0.68 (range 0.50 to 0.86). Group I with stimulation did achieve statistically significant changes following the treatment: decrease of mean IPSS from 17 +/- 3 points to 6 +/- 4 points after the treatment, increase in mean IQOL from 36 +/- 10 to 68 +/- 20 and decrease of mean BUS from 0.65 +/- 0.12 to 0.43 +/- 0.16. Group II had similar statistically significant differences after the treatment of OAB. Group III noted no changes in the complaints. CONCLUSION: Noninvasive stimulation had improved subjective symptom related to overactive bladder, had no adverse events and was well tolerated. (Fig. 1, Tab. 1, Ref. 18.).

Female↗
PubMed1992

[Changes in impulse activity of neurons of the CA3 area of the hippocampus under the effects of neuromodulator neurotropin].

Neurotropin (Nippon Zoki Co, Ltd) effects on firing patterns of the CA 3 hippocampus neurons in rabbits under a 24-h food deprivation was studied. Neuronal firing was recorded in a state of hunger (40 neurons) and under neurotropin (27 neurons) injected through a catheter implanted into the lateral brain ventricles. Initially, in 20% of neurons histograms had a bimodal interspike interval distribution: 1.5-25 ms and 100-400 ms. Neurotropin (50 microliters) increased the baseline spike rate regularity of hippocampus neurons. Histograms had a monomodal interspike interval distribution. Neurotropin (70 microliters) inhibited firing patterns and histograms, had trimodal interspike interval distribution: 1.5-5 ms; 250-400 ms and 1000 ms. Thus, these data suggested the involvement of neuro-immuno-modulator mechanisms in organization of firing patterns in rabbits.

Adjuvants, Immunologic↗
PubMedDate not supplied

[The role of neuromodulators (substance P and calcitonin gene-related peptide) in the development of neurogenic inflammation in the oral mucosa].

Vatous observations carried out in the course of the years have shown that certain neuropeptides have a possible role to play as inflammation mediators. The substances on which attention has been principally focused are: substance P, calcitonin gene-related peptide, capsaicin an histamine. Knowledge acquired in this field, however, does not yet permit us to sufficiently clarify the role, not to speak of the possible action mechanism, on the basis of which these neuropeptides act, although it is confirmed that these substances have been found first in laboratory animals and later also in human tissues in the course of experimentally induced neurogenic inflammation. The need to know more and more about inflammatory mechanisms and the increasingly complex possibilities offered by the application of technology in the field of medical research have led to many small advance in our knowledge of what is involved in inflammation. In fact it has been understood that behind the typical signs of inflammation (the famous four cardinal signs of Celsus: pain, redness, swelling, heat) no abstract entities or strange alchemies are concealed, but a series of well-known, classified substance, the so-called "inflammation mediators", namely a variety of substances of cellular or plasmatic origin united by the fact that exist, in stationary state conditions, in the form of inactive precursors, or sequestered in intracellular sites where they are unable to carry out their action. Following an inflammatory stimulus, they are activated, or their synthesis can be induced, or their release from intracellular sequestration sites in favoured; in any case they are stored in the disturbance district in concentrations that are such as to act on their respective targets, triggering event s that characterise the various stages of the inflammatory process.

Calcitonin Gene-Related Peptide↗
PubMed2004

[Nociceptin/orphanin FQ (N/OFQ)--the opioid, antiopioid or neuromodulator?].

Nociceptin/orphanin FQ (N/OFQ) is a neuropeptide discovered in the middle of the 1990. It possesses an amino acid sequence very similar to those of endogenous opioid peptides (particularly dynorphin A). However, N/OFQ lacks the N-terminal tyrosine necessary for activation of mu-, kappa- and delta- opioid receptors and therefore does not bind to opioid receptors but to its own nociceptin receptor (NOP). Opioid peptides also do not bind to the NOP receptor. In spite of structural similarities, the pharmacological profile of N/OFQ is different from and, in many cases, opposite to that of the opioids. Intracerebroventricular injection of N/OFQ induces hyperalgesia and decreases the analgesic actions of opioids, but induces analgesia when given intrathecally. N/OFQ blocks the rewarding effects of morphine, ethanol, and psychostimulants such as cocaine and amphetamine, but given alone it does not have rewarding effect. N/OFQ is metabolized to shorter fragments, such as N/OFQ(1-13), N/OFQ(1-11), N/OFQ(1-7) and N/OFQ(1-6). These fragments show biological activity. The effects of N/OFQ include regulation of the release of numerous neurotransmitters and hormones, as NOP receptors are located presynaptically in different brain structures. The aim of this review was to present current opinion on the role of N/OFQ in nociception, reward and drug dependence.

Animals↗