This includes the development of (1) a mottled appearance of the retina and retinal pigment epithelium (RPE) that gives the same visual appearance of Bone Spicule patterns (but are not Bone Spicules), (2) a waxy yellow appearance of the optic disk, and (3) the attenuation of blood vessels in size and Arterial/Venous ratio as they enter and exit the Optic Disk of the retina and transverse it.Non-syndromic RP (RP appears alone without other co-morbidities) usually presents a variety of the following symptoms:
Night blindness
Tunnel vision (due to loss of peripheral vision)
Latticework vision(due to patchy loss of peripheral vision)

loss of depth perception
Photopsia (Spontaneously occurring flashes/blinking/swirling/shimmering lights)
Photophobia (aversion to bright lights)
Development of the appearance of melanin pigment in a bone spicule pattern in the fundus (not bone tissue)
Slow adjustment from dark to light environments and vice versa
Blurring of vision
Poor color separation
Loss of central vision is the last to go, because this is a disease of the rods and not the cones which are the highest in number in the Central Vision (Macula and Fovea)
Eventual blindness (legally defined as 20 degrees or less in the best seeing eye or visual acuity of 20/200 or worse. Majority of patients do not go totally Blind, they quite often retain limited non-functional vision. Causes
RP may be:
(1) non-syndromic, that is, it occurs alone, without any other clinical findings,
(2) syndromic, with other neurosensory disorders, developmental abnormalities, or complex clinical findings, or
(3) secondary to other systemic diseases. RP combined with deafness (congenital or progressive) is called Usher syndrome.
Retinitis pigmentosa (RP) is a genetic disorder of the eyes that causes loss of vision. Symptoms include trouble seeing at night and decreasing peripheral vision (side and upper or lower visual field). As peripheral vision worsens, people may experience "tunnel vision". Complete blindness is uncommon. Onset of symptoms is generally gradual and often begins in childhood.Retinitis pigmentosa is generally inherited from one or both parents or rarely it can be newly evolved from a miscoding during DNA division. It is caused by genetic miscoding of proteins in one of more than 300 genes involved. The underlying mechanism involves the progressive loss of rod photoreceptor cells that line the retina of the eyeball. The rod cells secrete a neuroprotective substance (Rod-derived cone viability factor, RdCVF) that protects the cone cells from apoptosis (cell death). However, when the rod cells die, this substance is no longer provided. This is generally followed by the loss of cone photoreceptor cells. Diagnosis is by eye examination of the retina finding dark pigment deposits caused by the rupture of the underlying retinal pigmented epithelial cells, given that these cells contain a pigment known as melanin. Other supportive testing may include the electroretinogram (ERG), visual field testing (VFT), ocular coherence tomography (OCT) and DNA testing to determine the gene responsible for a persons particular type of RP (now called Inherited Retinal Dystrophy (IRD).There is currently no cure for retinitis pigmentosa. Efforts to manage the problem may include the use of low vision aids, portable lighting, or orientation and mobility training.