Effects of age, weight, hormones, and hibernation on breeding success in boreal toads (Bufo boreas boreas).

The goals of this study were to test the effects of exogenous hormones and hibernation on breeding behavior and gamete release by boreal toads (Bufo boreas boreas). Each year, a subset of 77 toads was hibernated and then paired with hibernated or nonhibernated mates and treated with luteinizing hormone releasing hormone analogue (LHRHa), human chorionic gonadotropin (hCG), or left untreated. Amplexus and egg and sperm production were recorded. At 1 yr of age, only 19% of pairs exhibited amplexus, and no sperm or eggs were produced. At 2 and 3 yr of age, most male toads treated with LHRHa exhibited amplexus (56.9% and 100%, respectively). Among 2-yr-old males, amplexus was more prevalent (P<0.05) in those that were hibernated than in those that were nonhibernated (54.0% and 33.3%, respectively), but most males in each group (93.3% and 75%, respectively) produced sperm in response to LHRHa treatment. Only one 2-yr-old and two 3-yr-old females produced eggs. At 4 yr of age, eight females produced eggs, but two died from egg retention. More nonhibernated than hibernated females developed eggs (7 of 10 vs. 1 of 10, P<0.05). Mean (+/-SD) weight of female toads producing eggs (58.9 +/- 11.9g) was greater (P<0.05) than that of nonproducing females (43.6 +/- 7.0g). Similarly, four of seven nonhibernated females (58.8+/-8.3g) produced eggs at 5 yr of age. All eggs were produced by females treated once with LHRHa. Number of eggs per female varied (141 to 3307), and development to tadpoles was low (0 to 36.5%), although tadpoles did become toadlets. In conclusion, male and female boreal toads matured at 2 and 4 yr of age, respectively, and heavier females were more likely to produce eggs. To enhance breeding success, males should be hibernated and treated with LHRHa. In contrast, female productivity was enhanced by improving their body condition instead of subjecting them to hibernation prior to LHRHa treatment.

Subdural hematomas of arterial origin.

Three cases of acute subdural hematoma related to bleeding aneurysm or arteriovenous malformation are presented. Various possible arterial sources of bleeding that may lead to subdural hematoma are reviewed. The complex cause and effect relationship between the presence of aneurysm or arteriovenous malformation and the occurrence of subdural hematoma in a head-injured patient is discussed. The pitfalls of reliance on the computed tomogram as a sole diagnostic test in the evaluation of head-injured patients or of unconscious patients with no available history are emphasized.