Appraisal of the burden of genital warts from a healthcare and individual patient perspective.

OBJECTIVE: Worldwide, genital warts, caused by human papillomavirus (HPV) is a common, sexually transmitted disease. The overall disease management strategy for genital warts should be determined not only by the prevalence, but also by the impact of the disease on individuals and society. The purpose of this study was therefore to investigate the epidemiological, economic and quality of life (QoL) burden of genital warts. METHODS: A systematic literature review was conducted on the epidemiology, QoL and management cost of genital warts in the USA, UK and France, based on studies published between 1998 and 2008. Due to scarcity of data, all studies reporting standardized QoL assessments among patients with genital warts were utilized, regardless of country of origin. Original studies were preferred over information cited in review articles. RESULTS: Data from three countries suggest that genital warts occur in 0.06-0.23% of the population each year. Despite the fact that spontaneous remissions occur frequently (up to 40%), patients often prefer immediate treatment. While treatment can be costly in absolute terms (€163-510 per treatment episode), these costs are lower compared with other sexually transmitted infections (STIs). Modest reductions in QoL have been noted, which may be mitigated through adequate patient education and support. CONCLUSIONS: While genital warts are an inconvenience for many patients, the occurrence may be lower than often quoted in the literature, and the economic burden on society is less than for other prominent STIs. However, concerted efforts to establish improved data collection and surveillance systems are needed in order to accurately define the burden of genital warts on individuals and society.

Knockdown of spinal metabotropic glutamate receptor 1 (mGluR(1)) alleviates pain and restores opioid efficacy after nerve injury in rats.

1. Nerve injury often produces long-lasting spontaneous pain, hyperalgesia and allodynia that are refractory to treatment, being only partially relieved by clinical analgesics, and often insensitive to morphine. With the aim of assessing its therapeutic potential, we examined the effect of antisense oligonucleotide knockdown of spinal metabotropic glutamate receptor 1 (mGluR(1)) in neuropathic rats. 2. We chronically infused rats intrathecally with either vehicle, or 50 microg day(-1) antisense or missense oligonucleotides beginning either 3 days prior to or 5 days after nerve injury. Cold, heat and mechanical sensitivity was assessed prior to any treatment and again every few days after nerve injury. 3. Here we show that knockdown of mGluR(1) significantly reduces cold hyperalgesia, heat hyperalgesia and mechanical allodynia in the ipsilateral (injured) hindpaw of neuropathic rats. 4. Moreover, we show that morphine analgesia is reduced in neuropathic rats, but not in sham-operated rats, and that knockdown of mGluR(1) restores the analgesic efficacy of morphine. 5. We also show that neuropathic rats are more sensitive to the excitatory effects of intrathecally injected N-methyl-D-aspartate (NMDA), and have elevated protein kinase C (PKC) activity in the spinal cord dorsal horn, two effects that are reversed by knockdown of mGluR(1). 6. These results suggest that activity at mGluR(1) contributes to neuropathic pain through interactions with spinal NMDA receptors and PKC, and that knockdown of mGluR(1) may be a useful therapy for neuropathic pain in humans, both to alleviate pain directly, and as an adjunct to opioid analgesic treatment.

Use of event-related brain potentials (ERPs) to assess eyewitness accuracy and deception.

This study investigated eyewitness identification using ERPs. Twenty participants completed two eyewitness lineup tasks (standard and deception conditions). For the standard condition, participants tried to accurately identify the culprit, whereas in the deception condition, they were asked to deceptively conceal their recognition of the culprit. Identification rates based on P300 patterns were calculated using two different individual analysis procedures (A and B) that varied in stringency. Correct identification rates for the standard condition were 100% for both procedures A and B. For the deception condition, correct identification rates of the concealed culprit were 90%, and 70% respectively for procedures A and B. Data from a prior study [the culprit-absent condition from Lefebvre, C.D., Marchand, Y., Smith, S.M. & Connolly, J.F., 2007. Determining eyewitness identification accuracy using event-related brain potentials (ERPs). Psychophysiology, 44, 894-904.] was reanalysed to investigate differences in false identification rates based on procedures A and B. False identifications were substantially higher when using procedure A (29%) versus procedure B (0%). Overall, superiority was found for procedure B compared to procedure A based on Grier's A'.

Determining eyewitness identification accuracy using event-related brain potentials (ERPs).

This study investigated the use of event-related brain potentials (ERPs) as a neurophysiological measure of eyewitness identification accuracy during a lineup task (ERP-lineup). Time delay between viewing the crime and completing the ERP-lineup (no-delay, 1-h delay and 1-week delay conditions) and culprit presence or absence were also manipulated. Results demonstrated that a P300 provided a reliable index of recognition of the culprit relative to the other lineup members across all time delay conditions. Although participants' accuracy decreased at the 1-week time delay compared to no delay and the 1-h time delay, the P300 effect remained strong for participants that made correct identifications irrespective of the time delay. In addition, the P300 was attenuated or was not elicited when the culprit was absent from the lineup.

A comparison of the glutamate release inhibition and anti-allodynic effects of gabapentin, lamotrigine, and riluzole in a model of neuropathic pain.

The effects of treatment with the anti-convulsant agents, lamotrigine and riluzole were compared with gabapentin in a rat experimental model of neuropathic pain. Rats were treated intraperitoneally, with gabapentin (30, 100 and 300 mg/kg), lamotrigine (2, 10 and 50 mg/kg) or riluzole (6 and 12 mg/kg) prior to, and every 12 h for 4 days following chronic constriction injury (CCI) of the sciatic nerve. Mechanical and cold sensitivity were assessed prior to surgery (baseline) and then at 4, 8 and 12 days following CCI. The four-day treatment with each of the agents was effective at producing reductions in the development of mechanical and cold hypersensitivity for periods ranging from the fourth to 12th day. The highest doses of each of the agents were also assessed on formalin-induced nociceptive behaviors and on formalin-induced increases in extracellular glutamate (Glu) and aspartate (Asp) in the spinal cord dorsal horn (SCDH) of awake behaving rats using in vivo microdialysis. Nociceptive scores in formalin test were significantly decreased by gabapentin (300 mg/kg i.p.) and riluzole (12 mg/kg i.p.), but not by lamotrigine (50 mg/kg i.p.). Formalin-induced increases in glutamate levels in SCDH were lowered significantly, as compared with the controls, with all drugs both in the first phase and second phases, with the greatest effects for riluzole and gabapentin. Similar suppressive effects of the drugs were observed on formalin-induced increases in spinal aspartate, except that gabapentin and lamotrigine produced effects only during the second phase. Riluzole produced profound and prolonged reductions in the spinal levels of glutamate and aspartate both for basal and formalin-stimulated release. In conclusion, the results suggest that the anti-convulsant agents gabapentin, lamotrigine and riluzole may reduce the development of hyperalgesia in a rat model of neuropathic pain by reducing the spinal release of glutamate. Riluzole's pronounced suppressive effects on spinal EAA levels is attributed to its established role as a glutamate release inhibitor and an enhancer of glutamate transporter activity.