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Biomedical subjects

Martin Quinn

Publications and source records attributed to Martin Quinn.

12 recordsLinked to original sources
PubMed2005

Uterine innervation after hysterectomy for chronic pelvic pain with, and without, endometriosis.

OBJECTIVE: Chronic pelvic pain is associated with a wide range of clinical conditions that include endometriosis. The precise cause, mechanisms of pain, and natural history are imprecise. Patterns of uterine innervation have been studied after hysterectomy for chronic pelvic pain with and without endometriosis. STUDY DESIGN: Tissue blocks were taken from the lower one half of the uterus after hysterectomy for advanced endometriosis (n = 16 specimens; group 1) and for chronic pelvic pain without endometriosis (n = 15 specimens; group 2). The control group consisted of uteri that were removed for painless gynecologic conditions (n = 25 specimens; group 3). Tissue sections from the lower one half of the uterus were stained with anti-S100 to demonstrate patterns of innervation, and nerve fiber profiles were counted by standardized techniques; qualitative differences were also recorded. RESULTS: In uteri from women with advanced endometriosis, there were increased numbers of nerve fiber profiles compared with control specimens (group 1 vs group 3; P = .0013, Mann Whitney U test). There were also increased numbers of nerve fiber profiles in uteri that were associated with chronic pelvic pain without endometriosis (group 2 vs group 3; P = .04, Mann Whitney U test). There were no differences in nerve fiber count in uteri from groups 1 and 2 (P = .35, Mann Whitney U test). Comparing both groups of uteri with controls (groups 1 and 2 vs 3) demonstrated marked differences in nerve fiber counts (P = .002, Mann Whitney U test). Two distinctive patterns of reinnervation that were observed: disruption of nerve bundles (collateral sprouting with microneuroma formation) and ingrowth around blood vessels (perivascular nerve fiber proliferation). There were increased numbers of microneuromas (groups 1 and 2 vs 3; P = .001, chi-squared test with Yates correction) and perivascular nerve fiber proliferation (groups 1 and 2 vs 3; P = .008, chi-squared test with Yates correction) in the myometrium in chronic pelvic pain with, and without, endometriosis compared with the control group. CONCLUSION: Nerve fiber proliferation and other features of reinnervation have been observed in the isthmic regions of uteri that were removed at hysterectomy for chronic pelvic pain with and without endometriosis. There were no quantitative differences between the groups with chronic pelvic pain and endometriosis. These observations provide an alternative explanation for the source of pain and other clinical symptoms in these clinical settings.

Adult↗
PubMed2005

Pre-eclampsia and partial uterine denervation.

Pre-eclampsia is characterised by a maternal syndrome of hypertension and proteinuria, that is frequently associated with reduced fetal growth. The characteristic histopathological observation in the placental bed is narrowing and atherosis of the distal branches of the uterine arteries at, and around, the deciduo-myometrial interface. In the maternal kidneys there is swelling of the glomerular capillaries and mesangium with some inclusions in the basement membrane ("glomeruloendotheliosis") and evidence of vasoconstriction in many other organs. Untreated maternal hypertension leads to convulsions (eclampsia) which may result in maternal and fetal death. The nerve plexus at the endometrial(decidual)--myometrial interface was first reported in 1959 though has received little attention in the intervening years. It appears to play an important role in maintaining the separation of two tissues with intrinsic proliferative potential (endometrium and myometrium). The present hypothesis proposes that damage to the nerve plexus at the endometrial-myometrial interface causes impaired control of a third proliferative tissue (invading trophoblast) resulting in the characteristic histological changes. Growth factors produced by nerves and blood vessels may contribute to the process of normal placentation e.g. nerve growth factor, vascular endothelial growth factor, etc. and these processes may be compromised in areas of denervation. Neural connections between the uterine and renal innervations (L1, 2) result in renal vasoconstriction and widespread systemic maternal vasoconstriction in an attempt to provide increased blood flow for the uteroplacental circulation (maternal hypertension, small-for-gestational age fetus). Loss of these neural connections through the same process of partial uterine denervation may cause reduced fetal growth without the maternal circulatory changes of pre-eclampsia (maternal normotension, small-for-gestational age, fetus). Variations in maternal circulatory compliance alter the "phenotype" of the condition such that prior maternal hypertension may cause pre-eclampsia through intrarenal mechanisms without significant fetal growth restriction. Increases in circulatory compliance in multiparity prevent the typical features of the condition, or, if they are expressed then they present in a different sequence with haematological and hepatic consequences presenting before the renal manifestations (HELLP syndrome, haemolysis, elevated liver enzymes, low platelets).

Denervation↗
PubMed2004

Obstetric denervation-gynaecological reinnervation: disruption of the inferior hypogastric plexus in childbirth as a source of gynaecological symptoms.

Difficult vaginal deliveries damage branches of the inferior hypogastric plexus as they are distributed to the pelvic viscera. The initial denervatory injury is often asymptomatic. Nerve fibre proliferation along the course of damaged nerve trunks results in chaotic reinnervation of the visceral stroma and subsequent sensory pelvic symptoms including chronic pelvic pain, painful heavy periods, painful intercourse, urinary frequency and urgency, irritable bowel symptoms and vulval pain. Each symptom may be described as pain, or discomfort, in response to light touch (allodynia). In other visceral sites allodynic syndromes are frequently associated with aberrant neural repair. Nerve fibre proliferation has now been reported in every viscus in the female pelvis though its antecedents have not been established. It is proposed that clinical presentations with one, or more, sensory pelvic symptoms occur some years after a difficult intrapartum episode; the initial denervatory injury is succeeded by nerve fibre proliferation in the affected organs. The precise pathoanatomy, mechanisms of intrapartum injury and clinical presentation remote from the intrapartum episode, may have obscured the common aetiology of many sensory pelvic syndromes.

Denervation↗
PubMed2004

Endometriosis: the consequence of neurological dysfunction?

Endometriosis describes endometrium found outside the uterine cavity and is frequently associated with clinical presentations of chronic pelvic pain, dysmenorrhoea, dyspareunia and subfertility. It was originally attributed to retrograde menstruation with endometrium passing in a reverse direction along the Fallopian tubes into the peritoneal cavity though this theory does not account for the spectrum of intrapelvic findings. Denervation followed by reinnervation in the uterine isthmus is proposed as the primary source of clinical symptoms, and, retrograde menstruation with adhesion of endometrium to injured tissue surfaces the variable laparoscopic findings. Primary sources of denervation are difficult intrapartum episodes (parous women) and persistent straining to achieve defaecation (nulliparous women). Progressive reinnervation including stromal nerve fibre proliferation, microneuroma formation and periarterial nerve fibre proliferation, takes place over five to ten years. Damage to uterine innervation interrupts normal patterns of uterine contractility, causing loss of fundocervical polarity which promotes retrograde menstruation. Ectopic endometrium may be a marker for prior tissue damage and does not contribute to the clinical symptoms--the disease may have been largely defined by an epiphenomenon.

Clinical Trials as Topic↗