In ophthalmology, accommodative excess (also known as excessive accommodation or accommodation excess) occurs when an individual uses more than normal accommodation (focusing on close objects) for performing certain near work. Accommodative excess has traditionally been defined as accommodation that is persistently higher than expected for the patients age. Modern definitions simply regard it as an inability to relax accommodation readily. Excessive accommodation is seen in association with excessive convergence also. Symptoms and signs
Blurring of vision due to pseudomyopia
Headache
Eye strain
Asthenopia
Trouble concentrating when reading

Causes
Causes related to refractive errors
Accommodative excess may be seen in the following conditions:
Hypermetropia: Young hypermetropes use excessive accommodation as a physiological adaptation in the interest of clear vision. Myopia: Young myopes performing excessive near work may also use excessive accommodation in association with excessive convergence. Astigmatism: Astigmatic eye may also be associated with accommodative excess. Presbyopia: Early presbyopic eye may also induce excessive accommodation. Improper or ill fitting spectacles: Use of improper or ill fitting spectacles may also cause use of excessive accommodation. Causes related to systemic drugs
Use of systemic drugs like Morphine, Digitalis, Sulfonamides, Carbonic anhydrase inhibitors may cause accommodative excess. Causes related to diseases
Unilateral excessive accommodation-Trigeminal neuralgia, and head trauma may cause ciliary spasm and may cause accommodative excess. Bilateral excessive accommodation-Diseases like Encephalitis, Syphilis, Head trauma, Influenza, Meningitis may cause ciliary spasm and bilateral excessive accommodation. Secondary to Convergence insufficiency
Accommodative excess may occur secondary to convergence insufficiency also. In convergence insufficiency near point of convergence will recede, and positive fusional vergence (PFV) will reduce.
Penciclovir is a guanosine analogue antiviral drug used for the treatment of various herpesvirus infections. It is a nucleoside analogue which exhibits low toxicity and good selectivity. Because penciclovir is absorbed poorly when given orally (by mouth) it is more often used as a topical treatment. It is the active ingredient in the cold sore medications Denavir (NDC 0135-0315-52), Vectavir and Fenivir. Famciclovir is a prodrug of penciclovir with improved oral bioavailability. Penciclovir was approved for medical use in 1996. Medical use
In herpes labialis, the duration of healing, pain and detectable virus is reduced by up to one day, compared with the total duration of 2–3 weeks of disease presentation. Mechanism of action
Penciclovir is inactive in its initial form. Within a virally infected cell a viral thymidine kinase adds a phosphate group to the penciclovir molecule; this is the rate-limiting step in the activation of penciclovir. Cellular (human) kinases then add two more phosphate groups, producing the active penciclovir triphosphate. This activated form inhibits viral DNA polymerase, thus impairing the ability of the virus to replicate within the cell. The selectivity of penciclovir may be attributed to two factors. First, cellular thymidine kinases phosphorylate the parent form significantly less rapidly than does the viral thymidine kinase, so the active triphosphate is present at much higher concentrations in virally infected cells than in uninfected cells. Second, the activated drug binds to viral DNA polymerase with a much higher affinity than to human DNA polymerases. As a result, penciclovir exhibits negligible cytotoxicity to healthy cells.