Classification and terminology
IBM stands for "inclusion body myositis:, not "inclusion body myopathy." The inclusion body refers to a histological finding of rimmed vacules in muscle tissue. However, IBM does not refer to the collection of diseases that feature these inclusion bodies. It refers to a specific disease entity.Multiple genetic diseases that feature inclusion bodies have been grouped into "hereditary inclusion body myopathies (hIBM)." Myopathy is used because inflammation is not a prominent finding. There is inconsistency in what individual disease entities fall under the category of hIBM. The term "sporadic inclusion body myositis" (sIBM) was introduced as a way to refer to IBM to avoid confusion with hIBM. However, one author discourages use of sIBM, as it implies that IBM and hIBM differ only in inheritance; they actually have unrelated mechanisms and manifestations of disease. Signs and symptoms
sIBM causes progressive muscle weakness. How sIBM affects individuals is variable, including the age of onset (which generally varies from the forties upwards) and rate of progression. Because of this variability, there is no "textbook case".Common early symptoms include frequent tripping and falling and difficulty going up stairs. Foot drop in one or both feet can occur. Part of the cause for this dysfunction is the early involvement of the quadriceps muscles. Weakness of the tibialis anterior muscle is responsible for foot drop. Another common early symptom is trouble manipulating the fingers, such as difficulty with tasks such as turning doorknobs or gripping keys. Weakness of finger flexion and ankle dorsiflexion occurs early.
Superior limbic keratoconjunctivitis (SLK, Théodores syndrome) is a disease of the eye characterized by episodes of recurrent inflammation of the superior cornea and limbus, as well as of the superior tarsal and bulbar conjunctiva. It was first described by F. H. Théodore in 1963. Symptoms and signs
Patients present with red eye, burning, tearing, foreign body sensation and mild photophobia. Upon examination, the conjunctiva appears inflamed and thickened, especially at the limbus. Pathophysiology
The development and pathophysiology of SLK is not well understood, but appears to involve microtrauma of keratoconjunctival surfaces. This mechanical hypothesis is supported by the increased lid apposition of exophthalmic thyroid patients, who are known to have an increased incidence of superior limbic keratoconjunctivitis. Diagnosis
Treatment
First-line treatments include topical corticosteroids and artificial tears. For non-responsive cases, potential treatments include topical ciclosporin A, vitamin A, autologous serum and injections of triamcinolone. Surgical treatment options include thermocauterization of the bulbar conjunctiva and conjunctival resection, typically under rose bengal (RB) staining to visualize affected areas. Epidemiology
Superior limbic keratoconjunctivitis tends to occur more often with dry eye syndrome (keratoconjunctivitis sicca), hyperthyroidism and hyperparathyroidism. It is also a rare complication associated with rheumatoid arthritis. Rarely, it may occur as a consequence of upper eyelid blepharoplasty surgery. References


== External links ==