Some veterinarians and hoof care practitioners recommend exercising the horse on varied terrain to stimulate and strengthen the caudal hoof structures. Medication
Vasodilators improve the blood flow into the vessels of the hoof. Examples include isoxsuprine (currently unavailable in the UK) and pentoxifylline. Anticoagulants can also improve blood flow. The use of warfarin has been proposed, but the extensive monitoring required makes it unsuitable in most cases. Anti-inflammatory drugs are used to treat the pain, and can help the lameness resolve sometimes if shoeing and training changes are made. Include Nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and other joint medications. The use of intramuscular glycosaminoglycans has been shown to decrease pain in horses with navicular disease, but this effect wanes after discontinuation of therapy. Oral glycosaminoglycans may have a similar effect.Bisphosphonates can be useful in cases where bone remodeling is causing pain.Gallium nitrate (GaN) has been hypothesized as a possible treatment for navicular disease, but its benefits have not been confirmed by formal clinical studies. One pilot study examined horses given gallium nitrate in their feed rations. While it was absorbed slowly, it did stay in the animals system, providing a baseline dosage for future studies. Surgery
Palmar digital neurectomy (or "nerving" or "denerving") is not without adverse side effects and should therefore be used as a last resort. In this procedure, the palmar digital nerves are severed, so the horse loses sensation in the back of the foot.
The symptoms may start appearing as early as a few hours after birth and up to three months of age. Around three-fourths of affected children present with neonatal seizure. Other seizure types such as focal or generalized tonic seizures, epileptic  spasms or other epileptic manifestations may occur at the course of the disease. The distinctive feature of the phenotype is severe progressive encephalopathy with delay in development and abnormal neurological examination delay (hypotonia, lethargy, poor eye contact, difficulties in feeding) usually being present even before the onset of other symptoms. Head circumference is usually normal at onset but microcephaly may develop over time. Family history is usually normal. Causes
There are varied etiologies related to EME that are mainly genetic abnormalities (mutations), brain structure abnormalities, or inborn metabolic defects. Another common reason rather than structural brain abnormality is inborn metabolic defects. Sometimes a metabolic disorder that affects how the brain works may lead to EME. While most of these metabolic disorders cannot be reversed, sometimes treating the underlying disorder can help. Vitamin-responsive epileptic encephalopathies are rare but significant reasons. Genetics
A growing number of genetic aetiologies have been linked to the phenotype of EME and Otahara syndrome and diagnosis by genetic testing can nowadays be achieved in around 50 percent of cases. Some examples of well described genetic aetiologies include: KCNQ2- DEE. • SCN2A-DEE • STXBP1-DEE. • CDKL5-DEE• KCNT1-DEE and UBA5-DEE. Acquired
No acquired aetiologies are known for EME although etiology remains unknown for a small percentage of patients after genetic, metabolic, and imaging workup.