Deviation of the eye ball from its normal visual axis is called squint. It is of two types: (1) Paralytic, (2) Nonparalytic (concomitant). Paralytic squint: Supranuclear lesion—Produce the conjugate deviation or paresis affect both eyes simultaneously. Diplopia is not present. Nucleus, nerve or muscle—Lesion disturb the coordination of the eyes. So diplopia is present. Along with other signs/symptoms as limitation of ocular movements, False orientation, change the position of the head and vertigo. Varieties of ocular muscle palsy: (i) Lateral rectus muscle palsy, (ii) Superior oblique muscle palsy (iii) nerve palsy (iv) Total ophthalmoplegia are studied. The etiology of paralytic squint are due to central nervous system diseases, lesion of nerve trunk, trauma, tumors, degeneration of the 3rd nerve are discussed, e.g. Pseudo grafe’s lid sign, Argyl-Robertson pupil and Duane’s retraction syndrome. Muscle transplantation is discussed to overcome the existence diplopia. Concomitant strabismus: It is classified in to latent and manifest concmittant squint. Latent (hetrophoria) is further classified in to hyperphoria, hypophoria, esophoroa, exophoria and cyclophoria. Cover test, Maddox rod test are important to differentiate the different type of phorias. Manifest concomitant strabismus: The factors are as defective vision in one eye, opacity in the media and defective development one or more of the extrinsic muscles. It is of two types: i) Convergent, ii) Divergent. Primary deviation = Secondary deviation. It may be alternate squint and without diplopia with the normal ocular movements. Measurement of the angle of deviation is fixed by perimeter, synaptophore, position of corneal reflex. This type of squint is treated by orthoptic treatment and surgical treatment. This chapter contains 12 labeled diagrams and 2 charts.