Seizures in an Arabian foal due to suspected prolonged transient neonatal hypoparathyroidism

Abstract

Summary This Case Report describes a 5‐week‐old male Arabian foal of Egyptian bloodline with generalised seizures due to hypocalcaemia. The laboratory changes in this foal were consistent with an abnormal regulation of calcium as occurs with hypoparathyroidism. Prolonged transient neonatal hypoparathyroidism as reported in man was suspected. The foal received oral calcium and vitamin D3 supplementation combined with the calcium sparing diuretic carbonic anhydrase inhibitor acetazolamide. Calcium concentrations increased gradually over 6 months. In Arabian foals, especially those of Egyptian bloodline suffering suspected juvenile epilepsy, hypocalcaemia should be ruled out as a cause of seizures.

The applicability of ambulatory electroencephalography (AEEG) in healthy horses and horses with abnormal behaviour or clinical signs of epilepsy

“…The fact that in 6 out of 10 equine patients pathological activity was still detected is promising. Since 1985, reports have been published on the use of EEG in horses (De Lahunta 2001;Lacombe et al 2001;Robinson et al 2003;Schwarz & Van den Hoven 2011). Although Lewin and T€ onhardt (1998), amongst others, described the materials and methods of EEG in detail, a precise description of the characteristics of the abnormal waves encountered (Lacombe et al 2011;Schwarz & Van den Hoven 2011) is sometimes less clear.…”

Metabolic encephalopathies in foals – pay attention to the serum biochemistry panel!

“…1997). For the foal described by Schwarz and van den Hoven (2012) in this issue, generalised seizures were attributed to hypocalcaemia due to suspected hypoparathyroidism. The syndrome described in the foal can be compared to late onset neonatal hypocalcaemia in human infants, which has several possible causes, including increased phosphate load, hypomagnesaemia, vitamin D deficiency, PTH resistance and hypoparathyroidism (Jain et al .…”

“…The preceding case report by Schwarz and van den Hoven (2012) serves as a good reminder of the need to identify quickly any biochemical abnormalities that may be responsible for (or contributing to) the seizure activity. Although metabolic encephalopathies are not the most common cause of seizures, they may be more treatable than other causes, particularly if treatment is initiated early in the disease process.…”