Ventroflexion of Neck
This is not really a specific disease but a clinical sign that has several different etiologies: myasthenia gravis, thiamine
deficiency, polymyositis, hypokalemia, organophosphate toxicity, hyperthyroidism, hereditary myopathies (Burmese, Devon Rex),
hypocalcemia, and portosystemic encephalopathy, polyneuropathy, hypernatremic polymyopathy, ammonium chloride toxicity. Overall,
cervical ventroflexion is a sign of generalized neuromuscular weakness in cats.
The chin usually rests near the thoracic inlet, with the eyes positioned dorsally to maintain a straight-ahead gaze. The cat
may have a slight protrusion of the dorsal aspects of the scapulae when weight is placed on thoracic limbs. The gait is often
stiff and a crouched, wide based stance is often seen in pelvic limbs.
Hereditary Myopathy of Devon Rex Cats
This is a congenital myopathy of Devon Rex cats that was initially described in 1993 by Malik et al. Physical abnormalities
can become evident anywhere from 3-23 weeks of age. Signs may include passive ventroflexion of the head and neck, dorsal protrusion
of the scapulae, megaesophagus and esophageal weakness, generalized appendicular weakness, and fatigability. Signs are slowly
progressive or static. Of the 6 cats originally described, 4 died suddenly of laryngospasm following obstruction of the larynx
or pharynx with food.
Serum creatine kinase concentrations are not elevated. Histopathological evaluation of muscle biopsy specimens varies depending
on the age of the animal at the time of collection. Dystrophic changes were evident in biopsies collected from older, more
severely affected cats. These signs all reflect dysfunction of striated muscle, while skeletal muscle pathology is suggestive
of a muscular dystrophy
Feline diabetic neuropathy
In poorly controlled diabetic cats, a distal symmetrical peripheral neuropathy may develop with progressive paraparesis and
a plantigrade gait (dropped hocks). Usually both hind limbs are affected, but some cases are unilateral. Clinical signs may
progress to also involve the thoracic limbs. The reported clinical incidence of neurologic signs is 8% although the true incidence
may be much higher.
Mizisin AP, Shelton GD, Burgers ML, et al. J Neuropathol Exp Neurol 2002;61:872-884: "Functional, structural, and biochemical
defects were detected in diabetic cat peripheral nerves compared to nondiabetic cats. A sensory and motor neuropathy was present
in diabetic cats' pelvic and thoracic limbs. Motor nerve conduction was more impaired than sensory nerve conduction and the
pelvic limb was more affected than the thoracic limb. Few electromyographic abnormalities were found. Histological changes
included Schwann cell injury and myelin defects. Nerve fructose increased with sorbitol accumulation."
Strict glycemic control reverses the clinical signs of neuropathy in some, but not all, cats. The reason that some cats don't
improve is not known. Experimental treatments: Acetyl-l-carnitine, 50 mg amino guanidine BID, methylcobalamin (? 3mg/cat/day
Spinal Muscular Atrophy in Maine Coon Cats
Spinal muscular atrophies are a group of inherited disorders characterized by degeneration of lower motor neurons, resulting
in progressive paresis to paralysis of voluntary skeletal muscles. Affected Maine coon kittens appear clinically normal until
15-17 weeks at which time pelvic limb weakness and fine generalized tremors are noted. Affected kittens may lose the ability
to jump by 5-12 months of age and walk with a pelvic limb sway. Stance is abnormal with hocks nearly touching and hind feet
pointing out at an angle from midline of 30-40(. Hyperesthesia may also be identified over the lumbar spine.
Affected cats also have elevation of serum CPK activity to 2-3 times normal. Neurogenic atrophy of muscle is found on biopsy.
The weakness and muscle wasting is slowly progressive; however, not incompatible with an acceptable quality of life for a
variable number of years as indoor pets.
The disorder is an autosomal recessive degeneration of motor neurons that results in weakness. Dr. John Fyfe at Michigan State
University has done most of the work in identifying this disease.
His lab has developed a DNA test (using cheek brushing cells) to identify carriers: Laboratory of Comparative Medical Genetics
at Michigan State University. http://mmg.msu.edu/faculty/fyfe/fyfeSMAtesting.pdf