Signs and symptoms
Excessive blinking and spasming of one or both eyes – characterized by uncontrollable eyelid closure of durations longer than the typical blink reflex. The spells of spasming may last for minutes or even hours
Uncontrollable contractions or twitches of the eye muscles and surrounding facial area. Some sufferers have twitching symptoms that radiate into the nose, face, cheeks, and sometimes, the neck area
Dryness of the eyes
Sensitivity to the sun and bright light

Causes
Some causes of blepharospasm have been identified; however, the causes of many cases of blepharospasm remain unknown. Some people with blepharospasm have a history of dry eyes, light sensitivity, and even fatigue. Others report no eye problems before onset of symptoms. Some drugs can induce blepharospasm, such as those used to treat Parkinsons disease, as well as hormone treatments, including estrogen-replacement therapy for women going through menopause. Blepharospasm can also be a symptom of acute withdrawal from benzodiazepines. Prolonged use of benzodiazepines can induce blepharospasm and is a known risk factor for the development of blepharospasm.Blepharospasm may also come from abnormal functioning of the brains basal ganglia. Simultaneous dry eye and dystonias such as Meiges syndrome have been observed. Blepharospasms can be caused by concussions in some rare cases, when a blow to the back of the head damages the basal ganglia.Multiple sclerosis can cause blepharospasm. Treatment
Drug therapy for blepharospasm has proved generally unpredictable and short-termed. Anticholinergics, tranquillizing drugs and botulinum toxin are the mostly used therapeutic options. However serious side effects can be observed as well as failure of therapy.
: 553  Type 2 MPGN is a subgroup of C3 glomerulopathy, a newly proposed diagnosis which also encompasses C3 Glomerulonephritis (C3GN). Type 3 MPGN, which is caused by immune complex deposition in the subepithelial space. Rapidly progressive glomerulonephritis
Rapidly progressive glomerulonephritis, also known as crescentic GN, is characterised by a rapid, progressive deterioration in kidney function. People with rapidly progressive glomerulonephritis may present with a nephritic syndrome. In management, steroid therapy is sometimes used, although the prognosis remains poor. Three main subtypes are recognised:: 557–558 
Type 1 is Goodpasture syndrome, an autoimmune disease also affecting the lung. In Goodpasture syndrome, IgG antibodies directed against the glomerular basement membrane  trigger an inflammatory reaction, causing a nephritic syndrome and the coughing up of blood. : 557  High dose immunosuppression is required (intravenous methylprednisolone) and cyclophosphamide, plus plasmapheresis. Immunohistochemistry staining of tissue specimens shows linear IgG deposits. Type 2 is characterised by immune-complex-mediated damage, and may be associated with systemic lupus erythematosus, post-infective glomerulonephritis, IgA nephropathy, and IgA vasculitis. : 558 
Type 3 rapidly progressive glomerulonephritis, also called pauciimmune type, is associated with causes of vascular inflammation including granulomatosis with polyangiitis (GPA) and microscopic polyangiitis. No immune deposits can be seen on staining, however blood tests may be positive for the ANCA antibody. : 558–559 Histopathologically, the majority of glomeruli present "crescents". Formation of crescents is initiated by passage of fibrin into the Bowman space as a result of increased permeability of glomerular basement membrane. Fibrin stimulates the proliferation of endothelial cells of Bowman capsule, and an influx of monocytes.