In cases like this record we describe an instance of isolated oculomotor nerve palsy connected with antibodies to mitotic spindle apparatus (anti-MSA). of isolated third nerve palsy are due to disease areas that influence the a5IA vascular program including diabetes mellitus and hypertension.1 However we should consider other notable causes in young individuals without vasculopathic risk elements carefully. Multiple sclerosis Sjogren’s symptoms antiphospholipid symptoms and a5IA leukemia relating to the central anxious system are hardly ever reported as factors behind isolated oculomotor nerve palsy 2 3 but oculomotor nerve palsy connected with antibodies to mitotic spindle equipment (anti-MSA an auto-antinuclear antibody) is not reported to day. An individual is described by us with isolated oculomotor nerve palsy connected with anti-MSA. Case record A 28-year-old female developed painful vertical diplopia. She have been experiencing a cold for just one week. She got no significant contributory past background no systemic illnesses such as for example diabetes mellitus hypertension or coagulopathy. A full ophthalmologic examination was performed. Her best corrected visual acuities were 20/25 in the right eye and 20/30 in the left eye. Alternate cover prism test revealed 10 prism diopters of hypertropia in the right eye. She had limited depression and adduction in the right a5IA eye as well (Figure 1). The forced duction test was negative. There was no relative afferent pupillary defect. Figure 1 Nine cardinal directions of gaze showing exodeviation limitation of adduction and infraduction in the right eye at initial visit. We performed laboratory tests including a complete blood cell count erythrocyte sedimentation rate C-reactive protein rheumatoid factor antinuclear antibodies antineutrophil cytoplasm antibodies and serologic tests for viral markers. We also performed a chest x-ray and brain magnetic resonance imaging. The laboratory findings were unremarkable with the exception of positive rheumatoid factor (titer 1:320) and antinuclear antibody (mitotic spindle fiber type titer 1:620). Brain magnetic resonance imaging with gadolinium enhancement revealed no abnormal findings. We believed that the patient had pupil-sparing incomplete third nerve palsy (mainly involving the inferior division) related to autoimmune disease so admitted her and treated her with intravenous methylprednisolone 250 mg four times daily for three days and tapered the steroid thereafter. Her extraocular movements resolved completely at two weeks after steroid pulse therapy. The last follow-up visit was performed six weeks after the initiation of steroid pulse therapy. During the follow-up period she manifested no significant neurological sequelae. Discussion Anti-MSA antibodies are not associated with a defined autoimmune pathology but some studies have reported anti-MSA in the sera of patients with connective tissue diseases infections autoimmune hepatitis vasculitis primary antiphospholipid syndrome malignancy and fever of unknown origin.4 5 The aforementioned autoimmune diseases are well associated with oculomotor nerve palsy. However the present report is the first reported case of a patient with isolated oculomotor nerve palsy associated with anti-MSA. The mitotic spindle apparatus is a5IA a unique structure of microtubules and associated proteins involved in the segregation and reorganization of chromosomes during cell division. Anti-MSA a5IA is identified during the immunofluorescent detection of antinuclear antibodies which are associated with autoimmune diseases.6 7 There are two possible mechanisms related to this cranial neuropathy with autoimmune diseases namely “vascular” (due to damage of the vasa nervorum) or an “immunologic cause” (due to lymphocytic infiltration of the nerve).8 The patient had an excellent and rapid response to intravenous methylprednisolone treatment and completely recovered two weeks after the start of steroid pulse therapy. Therefore lymphocytic infiltration or autoantibodies to Rabbit Polyclonal to ACAD10. components of the cranial nerves might play an important role. Lui et al2 also reported on a patient with unilateral oculomotor nerve palsy and Sjogren’s syndrome who experienced an almost complete recovery of both ptosis and diplopia after two weeks of treatment and an immunologic neuropathic process was thought to be the cause. In conclusion although oculomotor nerve paralysis is usually believed to be.