Findings suggested that computed tomographic-guided brain biopsy is feasible in horses and can be used to establish a diagnosis in horses with intracranial masses.

No abstract

Two ponies presented with mild abdominal pain and mild diarrhoea one hour after ingestion of roots of a black locust tree. On admission, symptoms had progressed to depression, weakness and the passing of dark, firm faeces. Treatment was symptomatic and supportive, aiming at the evacuation of the toxin from the gastrointestinal tract. One pony developed severe, reversible neurological signs associated with transient hyperammonaemia in the absence of liver disease. After 24 h the ammonia level returned to normal and central nervous signs disappeared. Both ponies recovered completely. This report describes the ingestion of black locust closely followed by the development of central nervous signs and hyperammonaemia. Increased ammonia absorption due to the intestinal wall inflammation caused by the toxins of the black locust tree, as well as increased ammonia production by enteric bacteria is therefore considered a plausible pathophysiological mechanism of the neurological signs displayed in black locust intoxicatio

Five equine herpesvirus 1 (EHV-1) genome sequences with links to an EHV-1 outbreak with neurological disorders after a horse gathering in Valencia, Spain, in February 2021, were determined. All strains showed the closest relationships to strains from Belgium and the United Kingdom, indicating a common source of infection.

Transcranial magnetic stimulation and measurement of the magnetic motor-evoked potentials (MMEPs) in the thoracic and pelvic limbs of four recumbent horses and one recumbent donkey were used to assess the integrity of the descending motor pathways, in order to confirm or exclude a descending motor tract lesion as the cause of the recumbency. In two of the animals abnormal MMEPs were recorded; in one of the horses a lesion along the cervical spinal cord due to a fracture of the fifth cervical vertebra was diagnosed and confirmed by radiography and postmortem examination; in another horse, damage to the peripheral nerves of the left forelimb was diagnosed and confirmed postmortem when a large abscess was found to have been compressing the peripheral nerves at the level of the last cervical vertebra. In the three other animals, normal MMEPs were recorded, and laminitis, rhabdomyolysis and physitis were diagnosed as the causes of the recumbency.

No abstract

Little information is available on medical imaging of the adrenal glands in horses. We investigated the feasibility of transrectal ultrasonography to characterize the normal equine adrenal gland. Transrectal ultrasonography was performed in 25 healthy horses using a 7.5 MHz linear array probe at a displayed depth of 8 cm. Transrectal ultrasonography of the right adrenal gland was not feasible. For the left adrenal gland, the left kidney, the abdominal aorta, the left renal artery, the left renal vein, and the cranial mesenteric artery were used as landmarks. The size of the left adrenal gland was variable, but it generally appeared as a long, flat structure with a hyperechoic medulla surrounded by a hypoechoic cortex. The most cranial part of the gland could not be delineated appropriately in 11 horses (44%). The mean (+/-SD) thickness of the gland and medulla was 0.66 +/- 0.15cm (n = 25) and 0.28 +/- 0.09 cm (n = 25) near the caudal pole, 0.87 +/- 0.25 cm (n = 14) and 0.40 +/- 0.18 cm (n = 12) near the cranial pole, and 0.89 +/- 0.18 cm (n = 25) and 0.36 +/- 0.13 cm (n = 25) in the middle of the gland, respectively. The mean (+/-SD) length of the entire adrenal gland and of the medulla was 6.22 +/- 0.77 cm (n = 14) and 5.45 +/- 0.71 cm (n = 6), respectively. Transrectal ultrasonography allowed adequate visualization of the left adrenal gland in horses.

The case of a horse with acute symptoms of excitement, exaggerated fright reactions and trembling is presented. In addition to these cerebral symptoms, mild cerebellar ataxia and a renal tubular lesion were diagnosed. Suspected swainsonine poisoning was confirmed by the presence of the toxin (154 ng/ml) in the serum sample taken immediately after admission. A good recovery was seen after fluid therapy with supplementation of potassium, a dopamine drip and administration of diazepam. The effects of the toxin, by inhibiting the lysosomal enzyme α-mannosidase and mimicking the genetic mannosidosis, are discussed