Bilateria
The remaining animals, the great majority—comprising some 29 phyla and over a million species—form a clade, the Bilateria, which have a bilaterally symmetric body plan. The Bilateria are triploblastic, with three well-developed germ layers, and their tissues form distinct organs. The digestive chamber has two openings, a mouth and an anus, and there is an internal body cavity, a coelom or pseudocoelom. These animals have a head end (anterior) and a tail end (posterior),  a back (dorsal) surface and a belly (ventral) surface, and a left and a right side.Having a front end means that this part of the body encounters stimuli, such as food, favouring cephalisation, the development of a head with sense organs and a mouth. Many bilaterians have a combination of circular muscles that constrict the body, making it longer, and an opposing set of longitudinal muscles, that shorten the body; these enable soft-bodied animals with a hydrostatic skeleton to move by peristalsis. They also have a gut that extends through the basically cylindrical body from mouth to anus. Many bilaterian phyla have primary larvae which swim with cilia and have an apical organ containing sensory cells. However, over evolutionary time, descendant spaces have evolved which have lost  one or more of each of these characteristics. For example, adult echinoderms are radially symmetric (unlike their larvae), while some parasitic worms have extremely simplified body structures.Genetic studies have considerably changed zoologists understanding of the relationships within the Bilateria. Most appear to belong to two major lineages, the protostomes and the deuterostomes.
Symptoms
The most common symptoms of acquired and transient cortical blindness include:

A complete loss of visual sensation and of vision
Preservation/sparing of the abilities to perceive light and/or moving, but not static objects (Riddoch syndrome)
A lack of visual fixation and tracking 
Denial of visual loss (Anton–Babinski syndrome)
Visual hallucinations 
Macular sparing, in which vision in the fovea is spared from the blindness. Causes
The most common cause of cortical blindness is ischemia (oxygen deprivation) to the occipital lobes caused by blockage to one or both of the posterior cerebral arteries. However, other conditions have also been known to cause acquired and transient cortical blindness, including:

Congenital abnormalities of the occipital lobe
Head trauma to the occipital lobe of the brain
Bilateral lesions of the primary visual cortex
Infection
Creutzfeldt–Jakob disease (CJD), in association with a rapid onset of dementia
rarely Dissociative identity disorder (DID)
Side effect of some anti-epilepsy drugs (AEDs)
Hyperammonemia
Eclampsia and, rarely, pre-eclampsiaThe most common causes of congenital cortical blindness are:

Traumatic brain injury (TBI) to the occipital lobe of the brain
Congenital abnormalities of the occipital lobe
Perinatal ischemia
Encephalitis
Meningitis

Diagnosis
A patient with cortical blindness has no vision but the response of his/her pupil to light is intact (as the reflex does not involve the cortex). Therefore, one diagnostic test for cortical blindness is to first objectively verify the optic nerves and the non-cortical functions of the eyes are functioning normally. This involves confirming that patient can distinguish light/dark, and that his/her pupils dilate and contract with light exposure. Then, the patient is asked to describe something he/she would be able to recognize with normal vision.