The term "Navicular Disease" has been a concern of horse owners for many years. In fact, navicular disease has been determined as a cause of lameness in horses as early as 1752 when the syndrome was originally described. The term "Navicular Disease" itself is misleading. A "disease" implies a specific cause and therefore specific therapy (e.g., Lyme Disease caused by Borrelia buradorferi and treated with tetracyclines). Therefore, the term "Navicular Disease" has been replaced by the more accurate term, "Navicular Syndrome" which implies multiple causes and therapeutic approaches based on the individual patient.

Navicular syndrome is one of several conditions leading to heel soreness or lameness. In order to understand this syndrome as well as these other conditions, a diagrammatical representation of the equine foot is shown below. Pertinent anatomical features are labeled and the ticked lines/arrows represent the "heel" region for this discussion.

• the navicular bone,

• the navicular bursa,

• the deep digital flexor tendon below the pastern joint (PI-PII),

• the back of the coffin joint,

• the back of the pastern joint,

• the corium of bars,

• the frog ñ sole,

• the digital cushion,

• and skin on back of pastern and heel bulbs.

Specific conditions causing heel lameness that can be alleviated by this nerve block include - puncture wounds (nails, wire sticks) to the back 1/3 of the foot; fractures of the navicular bone, back of coffin bone or side bones; corns; stone bruises; sheared heels; very low injuries to the deep digital flexor tendon; navicular syndrome; and less often laminitis or pedal osteitis. Most of the above conditions are acute causes of heel lameness with the exception of navicular syndrome.

Navicular syndrome is usually a chronic bilateral foreleg lameness in horses of all ages. It is most often seen in Quarter horses, Thoroughbreds, and Warmblood breeds. Horses with this syndrome have a choppy, shuffling type gait and tend to wear the toes of their feet leaving the heels to grow longer. This leads to a smaller, upright, contracted appearing foot. Lameness associated is most evident in the inside leg on harder concussive surfaces with the horse lunged in a tight circle. The exact cause for this syndrome is yet to be discovered although several theories have been put forth. Horses with an upright conformation, small feet, or that are improperly shod may be at higher risk since they transmit more of the concussive forces through the navicular region as the navicular bone bears much of the weight between pastern and coffin bone during weight bearing. In doing this, the navicular bone is forced back against the deep digital flexor tendon which is taut during this phase. This repetitive pressure may result in damage and inflammation to the navicular bone precipitating chronic lameness. Radiographs (x-rays) are useful to evaluate the structural changes within the navicular bone but do not always correlate with navicular syndrome associated lameness. Some horses may be sound with large structural navicular changes whereas others may be extremely lame with minimal radiographic changes. The most commonly seen changes are enlarged blood vessel channels, "lollipop lesions", spurring, tiny fractures off the navicular edge, cystic or lytic areas within the bone, and erosion of the contact area between the navicular bone and deep digital flexor tendon.

Since horses bear between 60 and 65% of their weight on their forelimbs, foreleg lameness is a common source of unsoundness. Heel lameness can be caused by several conditions most of which are acute with the exception of navicular syndrome. Navicular syndrome is a multifactorial condition, not a specific disease, and as such therapy must individualized to each patient. Diagnosis is based on clinical findings (characteristic gait, hoof tester response, specific nerve blocks, and palpation) and radiographic evaluation supportive of navicular remodeling. Treatment is fourfold. The mainstay is shoeing which is discussed by Kirk Adkins. Medical therapy such as anti inflammatory/analgesics (bute) and vasodilators (isoxuprine) may be used. Management plays a role, these horses need to be exercised daily as prolonged rest tends to increase lameness. Lastly, surgical intervention is used for refractory cases (palmar digital neurectomy) which may allow use of the horse for approximately 1 to 3 years.

At the time this article was published (1994), Edward Voss was a Large Animal Medicine Resident II at the Veterinary Medicine Teaching Hospital, University of California, Davis.