Skew deviation is an unusual ocular deviation (strabismus), wherein the eyes move upward (hypertropia) in opposite directions. Skew deviation is caused by abnormal prenuclear vestibular input to the ocular motor nuclei, most commonly due to brainstem or cerebellar stroke. Other causes include multiple sclerosis and head trauma. Skew deviation is usually characterized by torticollis (head tilting) and binocular torsion. The exact pathophysiology of skew deviation remains incompletely understood. Skew deviation appears to be a perturbation of the ocular tilt reaction, which is itself is most likely a vestigial righting response used to keep fish and other lateral-eyed animals properly oriented.There are three types of skew deviations:Type 1: Upward deviation of both eyes; sound-induced vestibular symptoms; both eyes show counterclockwise rotary upward rotation
Type 2: Hypertropia in one eye; dorsolateral medullary infarctions; excyclotropia in the ipsilateral eye; hypertropia in the contralateral eye
Type 3: Simultaneous hypertropia one eye and hypotropia in the other eye; upper brainstem lesion

References
Further reading
Adams, Raymond D.; Victor, Maurice; Ropper, Allan H. (1997). Principles of Neurology (6 ed.). New York: McGraw Hill, Health Professions Division. ISBN 978-0-07-067439-4.
Brody myopathy, also called Brody disease, is a rare disorder that affects skeletal muscle function. BD was first characterized in 1969 by Dr. Irwin A. Brody at Duke University Medical Center. Individuals with BD have difficulty relaxing their muscles after exercise. This difficulty in relaxation leads to symptoms including cramps, stiffness, and discomfort in the muscles of the limbs and face. Symptoms are heightened by exercise and commonly progress in severity throughout adulthood. Signs and symptoms
Symptoms include stiffness and sometimes muscle cramping after exercise and especially when exposed to cold. The most commonly affected muscles are in the arms, legs, and eyelids. Individuals with Brody myopathy also sometimes experience weakness, myalgia, and rhabdomyolysis. Cause
Most cases of BD are inherited through autosomal recessive mutations in ATP2A1,  where each copy of the affected individuals gene contain a mutation. The gene involved in BD encodes the fast-twitch skeletal muscle ATPase, SERCA1. SERCA1 is a protein pump that uses ATP to pump Ca2+ ions from the cytosol to the sarcoplasmic reticulum in skeletal muscle. In those with BD, SERCA1 pumps are unable to effectively move Ca2+ across the membrane, leading to increased levels of cytoplasmic Ca2+. Increases in cytoplasmic Ca2+ levels interfere with muscle contraction, leading to the characteristic symptoms of BD.In some cases of BD, no mutations in ATP2A1 have been observed. Disease transmission in cases of non-ATP2A1 BD have been characterized as autosomal dominant pattern of inheritance.