Summary The records of 74 horses that recovered from anaesthesia after surgery for a small intestinal lesion from 1994 to 1999 were reviewed. Sixty‐three horses (85%) had a strangulating lesion and 43 of these (68%) had a resection and anastomosis. Four of 11 horses (36%) without a strangulating lesion had a resection and anastomosis. Sixty‐three horses (85%) survived to discharge, with a survival rate of 53/63 in horses with a strangulating lesion (84%) and 10/11 (91%) in others. For all lesions, short‐term survival for all end‐to‐end anastomoses (91%; 21/23) and for no resection (92%; 23/25) were superior (P<0.05) to survival for jejunocaecal anastomosis (76%; 19/25). Fourteen horses (19%) had a repeat abdominal surgery during hospitalisation; 9 of these (64%) survived short‐term. Postoperative ileus developed in 7/70 horses (10%) after surgery for a problem other than proximal enteritis, and all had a strangulating lesion. Postoperative ileus (POI) was more likely after a jejunocaecostomy than after other procedures, and did not develop after a jejunojejunostomy. Survival >7 months was 52/69 (75%) and for >12 months was 39/57 (68%). The estimated prevalence of adhesions was 13%. Short‐term survival was poorest in horses that had a jejunocaecostomy, but long‐term survival was less affected by the anastomosis used. The sharpest decline in survival was during the first postoperative week and postoperative mortality then declined over time after surgery. A postoperative protocol that allowed early postoperative feeding was well tolerated. The results confirm that the overall prognosis after small intestinal surgery in horses is improved over earlier findings.

Thyroid hormones play a critical role in the metabolic activity of the adult brain, and neuropsychiatric manifestations of thyroid disease have long been recognised. However, it is only recently that methodology such as functional neuroimaging has been available to facilitate investigation of thyroid hormone metabolism. Although the role of thyroid hormones in the adult brain is not yet specified, it is clear that without optimal thyroid function, mood disturbance, cognitive impairment and other psychiatric symptoms can emerge. Additionally, laboratory measurements of peripheral thyroid function may not adequately characterise central thyroid metabolism. Here, we review the relationship between thyroid hormone and neuropsychiatric symptoms in patients with primary thyroid disease and primary mood disorders.

Adult neurogenesis in the hippocampus is impaired in schizophrenic patients and in an animal model of schizophrenia. Amongst a plethora of regulators, the immune system has been shown repeatedly to strongly modulate neurogenesis under physiological and pathological conditions. It is well accepted, that schizophrenic patients have an aberrant peripheral immune status, which is also reflected in the animal model. The microglia as the intrinsic immune competent cells of the brain have recently come into focus as possible therapeutic targets in schizophrenia.We here used a maternal immune stimulation rodent model of schizophrenia in which polyinosinic-polycytidilic acid (Poly I:C) was injected into pregnant rats to mimic an anti-viral immune response. We identified microglia IL-1β and TNF-α increase constituting the factors correlating best with decreases in net-neurogenesis and impairment in pre-pulse inhibition of a startle response in the Poly I:C model. Treatment with the antibiotic minocycline (3mg/kg/day) normalized microglial cytokine production in the hippocampus and rescued neurogenesis and behavior. We could also show that enhanced microglial TNF-α and IL-1β production in the hippocampus was accompanied by a decrease in the pro-proliferative TNFR2 receptor expression on neuronal progenitor cells, which could be attenuated by minocycline. These findings strongly support the idea to use anti-inflammatory drugs to target microglia activation as an adjunctive therapy in schizophrenic patients.3