Accommodative spasm

The adverse effects of pilocarpine are caused by the induction of miosis. The contraction of the ciliary muscle causes the lens to displace forward, which can lead to accommodation spasm, myopia, and brow ache. Pupillary constriction can also affect night vision. Pilocarpine should be avoided in patients with severe myopia, as it increases the risk of developing retinal detachment. Systemic effects may occur at higher concentrations and include, nausea, vomiting, diarrhea, and bradycardia. 

Carbachol stimulates the same muscarinic receptor as pilocarpine and also inhibits acetylcholinesterase, the enzyme that metabolizes acetylcholine. Carbachol is more potent than pilocarpine, but it causes more accommodation spasm and brow ache and may also cause anterior uveitis. Carbachol is rarely used today because of the side-effect profile. 

Because of its activity at muscarinic receptor sites on the iris sphincter and ciliary muscles, pilocarpine causes pupillary constriction and varying degrees of accommodative spasm, depending on the patient s age. Longterm therapy with pilocarpine or other miotics alters iris muscle activity and may cause permanent miosis resulting from loss of iris radial muscle tone and from fibrosis of the sphincter muscle. 

Pilocarpine therapy should be avoided in certain patients (Box 10-10).This drug is contraindicated in patients with cataract, especially nuclear sclerotic and posterior subcapsular cataract, because the drug can affect vision and may accelerate the formation of lens opacities. Pilocarpine is generally contraindicated in patients younger than 40 years of age because of the intolerable accommodative spasm and refractive changes. Because breakdown of the blood-aqueous barrier occurs with the use of pilocarpine and other miotics, particularly in the presence of neovascular and uveitic glaucoma, pilocarpine should be avoided in these patients. 

In general, transient myopia results from edema of the ciliary body, lenticular edema, or accommodative spasm. Topically administered cholinergic agonists are well... 

Parasympathomimetics (direct acting) Pilocarpine Carbachol Increase aqueous outflow Miosis, accommodative spasm, constriction of visual field, retinal tears, cataracts, periorbital pain, precipitation of angle[Pg.76]

The changes associated with OPC effects on the M-cholinoreactive system are of no small importance in the development of poisoning. OPC induce contraction of the orbicular muscle of eye, which results in pupil narrowing (miosis) and accommodation spasm, bronchial musculature (bronchospasm), musculature of the gastro-intestinal tract, bladder, uterine as well as amplify secretory function of the stomach and intestine. All these effects are determined by the anti-cholinesterase action of OPC on the peripheral M-cholinoreactive systems. 

Ciliary muscle spasm due to contraction of the ciliary sphincter muscle, with accommodative. spasm, myopia, and reduced visual acuity. 

Systemic effects which may occur from cholinergic eye-drops include nausea, diarrhoea, abdominal pain, muscle spasm and weakness, sweating, lacrimation, salivation, hypotension, bradycardia, bronchial constriction, respiratory failure and nightmares. Ocular effects, contributing to the decrease in lOP, are pupillary constriction, ciliary muscle contraction, dilatation of the conjunctival and iris blood vessels and increased aqeous outflow. The visual complications include accommodative spasm, myopia and reduced visual acuity changes in vision sensitivity, dark adaptation and visual fields may occur (20 ). 

The pharmacological actions of physostigmine are similar to those of cholinergic drugs. Topical instillation into the eye produces miosis, spasm of accommodation and decrease in intraocular pressure. Physostigmine is well absorbed after oral as well as parenteral administration and also produces central cholinergic actions because of penetration into blood brain barrier. 

Physostigmine (eserine sulfate) causes miosis and spasm of accommodation it also lowers intraocular pressure and hence can be used in the treatment of wide-angle glaucoma. As it is lipid soluble, it penetrates into the brain rapidly, raises the acetylcholine concentration and, in toxic amounts, may cause cholinergic CNS toxicity, which is characterized by restlessness, insomnia, tremors, confusion, ataxia, convulsions, respiratory depression, and circulatory collapse. These effects are reversed by atropine. 

Actions Applied topically to the cornea, pilocarpine produces a rapid miosis and contraction of the ciliary muscle. The eye undergoes a spasm of accommodation, and vision is fixed at some particular distance, making it impossible to focus (Figure 4.7). [Note the opposing effects of atropine, a muscarinic blocker, on the eye (see p. 45).] Pilocarpine is one of the most potent stimulators of secretions such as sweat, tears, and saliva, but it is not used for this purpose. 

An alkaloid of natural plant origin, pilocarpine is a direct-acting cholinergic agonist with a dominant action at both peripheral and central muscarinic sites. The cholinomimetic action of pilocarpine on smooth muscle muscarinic receptors generally results in contraction.The response of intraocular smooth muscle to pilocarpine is pupillary constriction, spasm of accommodation, and reduction of lOP. 

Eye miosis and spasm of the ciliary muscle occur so that the eye is accommodated for near vision. Intraocular pressure falls due, perhaps, to dilation of vessels at the point where intraocular fluids pass into the blood. 

Pilocarpine (ophthalmic) Muscarinic receptors Pupillary constriction and spasm of accommodation... 

Spasm of the ciliary muscle may impair accommodation and is associated with severe headache. Long-lasting miosis, associated with eye pain, was a notable clinical sign in the Tokyo Subway (underground railway) terrorist attack with sarin and the same was true of the sarin attack at Matsumoto (Nohara and Segawa, 1996). 

FIGURE 77 Physostigmine causes miosis and spasm of accommodations it also lowers intraocular pressure and hence can be used in the treatment of wide-angle glaucoma. 

Carbaminoylcholine chloride, a synthetic derivative of choline, is not destroyed by cholinesterase. Carbachol is a rather long-acting and powerful miotic, which can cause various ocular side effects, i.e. headaches, ocular and periorbital pain, twitching of the eyelids, ciliary congestion and spasm of accommodation. Rapid formation of cataracts was observed in 3 patients. Carbachol must be formulated with a wetting agent to increase penetration. 

---