No abstract

PPP is related to both patient and surgical factors. Patients with a high preoperative AAS score and high pain response to a standardized heat stimulus may preferably be treated using an operative technique with lowest risk for nerve damage.

Chronic pain after hernia repair is a significant problem and there is a need for a definitive assessment of its surgical treatment.

Inguinal herniotomy is one of the most frequent surgical procedures and chronic pain affecting everyday activities is reported in approximately 10% of patients. However, the neurophysiological changes and underlying pathophysiological mechanisms of postherniotomy pain are not known in detail, thereby precluding advances in treatment strategies and prophylaxis. Therefore, we examined forty-six patients reporting moderate to severe postherniotomy pain affecting daily activities for more than a year postoperatively, and compared them with a control group of patients without pain 1 yr postoperatively. A quantitative sensory testing protocol was used, assessing sensory dysfunction type, location and severity. We assessed the protocol test-retest variability using data from healthy control subjects. All patients (pain and pain-free) had signs of nerve damage, seen as sensory dysfunction. Detection thresholds for tactile and warmth stimulation were significantly increased while cold detection and pressure pain detection thresholds were significantly decreased in pain patients compared to controls. Repetitive punctuate and brush stimulation resulted in significantly more frequent and intense pain on the painful side than on the unaffected side in pain patients, and was not observed in controls. Our findings showed large and small fiber dysfunction in both pain and pain-free patients but more profound in pain patients and with signs of central sensitization (abnormal temporal summation). The specific finding of reduced pain detection threshold over the external inguinal annulus is consistent with damage to the cutaneous innervation territory of nervous structures in the inguinal region. The correspondence between pain location and sensory disturbance suggests that the pain is neuropathic in nature. Whether the underlying pathophysiological mechanisms are related to direct intraoperative nerve injury or nerve injury due to an inflammatory mesh response remains to be determined.

Cutaneous sensory block area of the TAP block is predominantly located lateral to a vertical line through the anterior superior iliac spine. The distribution is nondermatomal and does not cross the midline. The muscle-relaxing effect is significant and consistent. The block duration is approximately 10 hours with large variation.

Pre-operative widespread pressure pain hypersensitivity and pain catastrophizing are predictive of moderate severe post-TKA pain. If validated in a larger population, the clinically applicable tests should be considered in future interventions aiming to minimize post-operative pain in high-risk patients.

Chronic pain is a highly prevalent and poorly managed human health problem. We used microarray-based expression genomics in 25 inbred mouse strains to identify dorsal root ganglion (DRG)-expressed genetic contributors to mechanical allodynia, a prominent symptom of chronic pain. We identified expression levels of Chrna6, which encodes the α6 subunit of the nicotinic acetylcholine receptor (nAChR), as highly associated with allodynia. We confirmed the importance of α6* (i.e., α6-containing) nAChRs by analyzing both gain- and loss-of-function mutants. We find that mechanical allodynia associated with neuropathic and inflammatory injuries is significantly altered in α6* mutants, and that α6* but not α4* nicotinic receptors are absolutely required for peripheral and/or spinal nicotine analgesia. Furthermore, we show that Chrna6’s role in analgesia is at least partially due to direct interaction and cross-inhibition of α6* nAChRs with P2X2/3 receptors in DRG nociceptors. Finally, we establish relevance of our results to humans by the observation of genetic association in patients suffering from chronic postsurgical pain and temporomandibular pain.

To determine the incidence of pain related sexual dysfunction 1 year after inguinal herniorrhaphy and to assess the impact pain has on sexual function. In contrast to the well-described about 10% risk of chronic wound related pain after inguinal herniorrhaphy, chronic genital pain, dysejaculation, and sexual dysfunction have only been described sporadically. The aim was therefore to describe these symptoms in a questionnaire study. A nationwide detailed questionnaire study in September 2004 of pain related sexual dysfunction in all men aged 18-40 years undergoing inguinal herniorrhaphy between October 2002 and June 2003 (n=1015) based upon the nationwide Danish Hernia Database collaboration. The response rate was 68.4%. Combined frequent and moderate or severe pain from the previous hernia site during activity was reported by 187 patients (18.4%). Pain during sexual activity was reported by 224 patients (22.1%), of which 68 (6.7%) had moderate or severe pain occurring every third time or more. Genital or ejaculatory pain was found in 125 patients (12.3%), and 28 (2.8%) patients reported that the pain impaired their sexual activity to a moderate or severe degree. Pain during sexual activity and subsequent sexual dysfunction represent a clinically significant problem in about 3% of younger male patients with a previous inguinal herniorrhaphy. Intraoperative nerve damage and disposition to other chronic pain conditions are among the most likely pathogenic factors.