Hyaline casts are cylindrical and clear, with a low refractive index, so they can easily be missed on cursory review under brightfield microscopy, or in an aged sample where dissolution has occurred whereas, on the other hand, phase contrast microscopy leads to easier identification. Given the ubiquitous presence of Tamm–Horsfall protein, other cast types are formed via the inclusion or adhesion of other elements to the hyaline base. Granular casts
The second-most common type of cast, granular casts can result either from the breakdown of cellular casts or the inclusion of aggregates of plasma proteins (e.g., albumin) or immunoglobulin light chains. Depending on the size of inclusions, they can be classified as fine or coarse, though the distinction has no diagnostic significance. Their appearance is generally more cigar-shaped and of a higher refractive index than hyaline casts. While most often indicative of chronic renal disease, these casts, as with hyaline casts, can also be seen for a short time following strenuous exercise. The "muddy brown cast" seen in acute tubular necrosis is a type of granular cast. Waxy casts
Thought to represent the end product of cast evolution, waxy casts suggest the very low urine flow associated with severe, longstanding kidney disease such as kidney failure. Additionally, due to urine stasis and their formation in diseased, dilated ducts, these casts are significantly larger than hyaline casts. They are cylindrical. They possess a higher refractive index.
If MG is confined to the ocular muscles for more than 3 years, there is a 94% likelihood that the symptoms will not worsen or generalize.Aside from asymmetric ptosis (which becomes worse with fatigue, sustained upgaze, and at the end of the day) and variable limitation of extraocular muscles/diplopia, other clinical signs of ocular MG include gaze-evoked nystagmus (rapid, involuntary, oscillatory motion of the eyeball) and Cogan’s lid twitch (upper lid twitch present when patient looks straight ahead after looking down for 10–15 seconds). Pathophysiology
Normally, muscle contraction is a result of electrical signals sent from the central nervous system to muscle fibers via nerve impulses. At the neuromuscular junction, this electrical message is converted into a chemical message as acetylcholine is released from nerve fibers and attaches to corresponding receptors on the muscle fiber. In MG, antibodies are produced that block acetylcholine receptors, preventing the molecule from binding to the receptor and leading to a breakdown in communication between the nervous system and the muscle, resulting in muscle fatigue, and sometimes paralysis. Autoantibodies against acetylcholine receptors are detectable in 70–90% of patients with generalized MG, but only 50% in ocular MG.

Predilection for eye muscles
The precise reasons for the preferential involvement of eye muscles in MG is not well understood, but there are several lines of thought. Functional hypotheses propose that although multiple muscles may be affected, a deficit may be more readily apparent in the eyes for several reasons.