Evaluation of a selective neurectomy model for low urethral pressure incontinence in female dogs.

OBJECTIVE: To develop a model of low urethral pressure incontinence and compare the relative contributions of the pudendal and hypogastric nerves with urethral function by performing selective neurectomy and ovariohysterectomy in dogs. ANIMALS: 19 healthy Foxhounds. PROCEDURE: Dogs were allocated into 2 groups. The first group (10 dogs) underwent bilateral hypogastric neurectomy and ovariohysterectomy and subsequent bilateral pudendal neurectomy. The second group (9 dogs) underwent bilateral pudendal neurectomy and subsequent hypogastric neurectomy and ovariohysterectomy. Urethral pressure profilometry and leak point pressure (LPP) tests were performed before and after each neurectomy. RESULTS: Before surgery, mean +/- SD LPP and maximal urethral closure pressure (MUCP) in all dogs were 169.3 +/- 24.9 cm H2O and 108.3 +/- 19.3 cm H2O, respectively; these values decreased to 92.3 +/- 27 cm H2O and 60.7 +/- 20.0 cm H2O, respectively, after both selective neurectomy surgeries. There was a progressive decline of LPP after each neurectomy; however, MUCP decreased only after pudendal neurectomy. Fifteen dogs had mild clinical signs of urinary incontinence. All dogs appeared to have normal bladder function as indicated by posturing to void and consciously voiding a full stream of urine. Urinary tract infection did not develop in any dog. CONCLUSIONS AND CLINICAL RELEVANCE: Hypogastric and pudendal neurectomy and ovariohysterectomy caused a maximum decrease in LPP whereas pudendal neurectomy caused a maximum decrease in MUCP. IMPACT ON HUMAN MEDICINE: This model may be useful for evaluation of treatments for improving urinary control in postmenopausal women.

Lobar holoprosencephaly in a Miniature Schnauzer with hypodipsic hypernatremia.

A 9-month-old male Miniature Schnauzer was examined because of a lifelong history of behavioral abnormalities, including hypodipsia. Diagnostic evaluation revealed marked hypernatremia and a single forebrain ventricle. The behavioral abnormalities did not resolve with correction of the hypernatremia, and the dog was euthanatized. At necropsy, midline forebrain structures were absent or reduced in size, and normally paired forebrain structures were incompletely separated. Findings were diagnostic for holoprosencephaly, a potentially genetic disorder and the likely cause of the hypodipsia. Similar evaluation of affected Miniature Schnauzer dogs may reveal whether holoprosencephaly routinely underlies the thirst deficiency that may be seen in dogs of this breed.