Oculomotor nerve palsy or oculomotor neuropathy is an eye condition resulting from damage to the third cranial nerve or a branch thereof. As the name suggests, the oculomotor nerve supplies the majority of the muscles controlling eye movements (four of the six extraocular muscles, excluding only the lateral rectus and superior oblique). Damage to this nerve will result in an inability to move the eye normally. The nerve also supplies the upper eyelid muscle (levator palpebrae superioris) and is accompanied by parasympathetic fibers innervating the muscles responsible for pupil constriction (sphincter pupillae). The limitations of eye movement resulting from the condition are generally so severe that patients are often unable to maintain normal eye alignment when gazing straight ahead, leading to strabismus and, as a consequence, double vision (diplopia). Presentation
A complete oculomotor nerve palsy will result in a characteristic displacement outward (exotropia) and downward (hypotropia). The outward displacement occurs because the lateral rectus muscle (innervated by the sixth cranial nerve) maintains muscle tone in comparison to the paralyzed medial rectus. The downward displacement occurs because the superior oblique muscle (innervated by the fourth cranial or trochlear nerve) is unantagonized by the paralyzed superior rectus, inferior rectus and inferior oblique. The affected individual will also have a ptosis, or drooping of the eyelid, and mydriasis (pupil dilation). Causes
Oculomotor palsy can arise as a result of a number of different conditions. Non traumatic pupil-sparing oculomotor nerve palsies are often referred to as a "medical third," with those affecting the pupil being known as a "surgical third."
History
Unlike rejection and infection, CAV in the transplanted heart was not initially a predicted outcome. Early survivors of heart transplants soon developed this form of vasculopathy of their coronary arteries, initially identified at post-mortems. There were early suggestions that preventing cytomegalovirus (CMV) infection could decrease the prevalence of CAV. The impact of CAV has changed over time, with early recipients being younger, having more rejection and cardiovascular risk factors and less use of statins. Later recipients used statins routinely and were introduced to the immunosuppressive agent mycophenolate mofetil (MMF) and CMV prophylaxis. In addition, the later recipients were monitored for antibody-mediated cardiac allograft rejection (AMR).Before 2010 there was no uniform international standards for the nomenclature of CAV. A consensus statement on a standard language for CAV was first published in 2010 by the ISHLT. This was devised in a similar way to the earlier acute rejection grading system by endomyocardial biopsy. Research directions
Antibody-mediated cardiac allograft rejection (AMR) is a significant factor leading to the rapid progression of CAV. Future research directions in this area may include prospective databases that correlate clinical factors with surveillance of the incidence and severity of AMR, the frequency of CMV infection, and the use of immunosuppressants. The role of inducing immune tolerance has yet to be established. == References ==