The thin overgrowth of transparent cells over the eyes aperture, originally formed to prevent damage to the eyespot, allowed the segregated contents of the eye chamber to specialise into a transparent humour that optimised colour filtering, blocked harmful radiation, improved the eyes refractive index, and allowed functionality outside of water. The transparent protective cells eventually split into two layers, with circulatory fluid in between that allowed wider viewing angles and greater imaging resolution, and the thickness of the transparent layer gradually increased, in most species with the transparent crystallin protein.The gap between tissue layers naturally formed a biconvex shape, an optimally ideal structure for a normal refractive index. Independently, a transparent layer and a nontransparent layer split forward from the lens: the cornea and iris. Separation of the forward layer again formed a humour, the aqueous humour. This increased refractive power and again eased circulatory problems. Formation of a nontransparent ring allowed more blood vessels, more circulation, and larger eye sizes. Relationship to life requirements
Eyes are generally adapted to the environment and life requirements of the organism which bears them. For instance, the distribution of photoreceptors tends to match the area in which the highest acuity is required, with horizon-scanning organisms, such as those that live on the African plains, having a horizontal line of high-density ganglia, while tree-dwelling creatures which require good all-round vision tend to have a symmetrical distribution of ganglia, with acuity decreasing outwards from the centre.
Adverse effects
These are principally anticholinergic:

Dry mouth
Blurred vision
Cognitive changes
Drowsiness
Constipation
Urinary retention
Tachycardia
Anorexia
Severe delirium and hallucinations (in overdose)While some studies suggest that use of anticholinergics increases the risk of tardive dyskinesia (a long-term side effect of antipsychotics), other studies have found no association between anticholinergic exposure and risk of developing tardive dyskinesia, although symptoms may be worsened.Drugs that decrease cholinergic transmission may impair storage of new information into long-term memory. Anticholinergic agents can also impair time perception. Pharmacology
Benzatropine is a centrally acting anticholinergic/antihistamine agent. It is a selective M1 muscarinic acetylcholine receptor antagonist. Benzatropine partially blocks cholinergic activity in the basal ganglia and has also been shown to increase the availability of dopamine by blocking its reuptake and storage in central sites, and as a result, increasing dopaminergic activity. Animal studies have indicated that anticholinergic activity of benzatropine is approximately one-half that of atropine, while its antihistamine activity approaches that of mepyramine. Its anticholinergic effects have been established as therapeutically significant in the management of Parkinsonism. Benzatropine antagonizes the effect of acetylcholine, decreasing the imbalance between the neurotransmitters acetylcholine and dopamine, which may improve the symptoms of early Parkinsons disease.Benzatropine analogues are atypical dopamine reuptake inhibitors, which might make them useful for people with akathisia secondary to antipsychotic therapy.Benzatropine also acts as a functional inhibitor of acid sphingomyelinase (FIASMA).Benzatropine has been also identified, by a high throughput screening approach, as a potent differentiating agent for oligodendrocytes, possibly working through M1 and M3 muscarinic receptors. In preclinical models for multiple sclerosis, benzatropine decreased clinical symptoms and enhanced re-myelination.