Spasms visual

Toxicity Toxicity is characterized by an exaggeration of parasympathomimetic effects which may include the following Headache visual disturbance lacrimation sweating respiratory distress Gl spasm nausea vomiting diarrhea AV block tachycardia bradycardia hypotension hypertension shock mental confusion cardiac arrhythmia tremors. 

Ophthalmic-Transient stinging and burning corneal clouding persistent bullous keratopathy retinal detachment transient ciliary and conjunctival injection ciliary spasm with resultant temporary decrease of visual acuity. 

Ophthalmic - Transient stinging and burning tearing ciliary spasm conjunctival vascular congestion temporal, peri-, or supra-orbital headache superficial keratitis-induced myopia blurred vision poor dark adaptation reduced visual acuity in poor illumination in older individuals and in individuals with lens opacity. 

Of particular importance in the geriatric patient Due to systemic absorption bradycardia, hypotension, dizziness, fatigue, depression, anxiety, hallucinations, broncho-spasm, impotence due to topical administration stinging, tearing, blurred vision, light sensitivity/photophobia, dryness, decreased visual acuity... 

Vigabatrin Irreversibly inhibits GABA-transaminase 70% bioavailable not bound to plasma proteins not metabolized, ti/2 5-7 h (not relevant because of mechanism of action) Partial seizures, infantile spasms Toxicity Drowsiness, dizziness, psychosis, visual field loss Interactions Minimal... 

Vigabatrin is used as an adjunctive antiepileptic in patients with resistant partial epilepsy with or without secondary generalization, unresponsive to other therapy [2]. Nowadays, vigabatrin is rarely used in the treatment of partial seizures due to several irreversible visual field constrictions associated with its chronic use [57-62], It is regarded by many authorities as a drug of choice in infants with west syndrome (infantile spasms), particularly in cases associated with tuberous sclerosis [62],... 

Use and exposure Selenium is an essential trace element for human health. However, acute and prolonged periods of exposure to high concentrations of selenium compounds cause adverse health effects in humans. The symptoms include garlicky breath irritation of eyes, skin, nose, and throat visual disturbances headache nausea vomiting chills fever weakness violent cough bitter metallic taste in the mouth nose bleeds dyspnea bronchial spasms bronchitis pulmonary edema gastrointestinal tract disturbance ... 

Recurrent retinal arteriolar spasm with associated visual loss has been described in a 68-year-old man with hypertension treated with atenolol (SEDA-17, 236). 

Vigabatrin is used mainly in the treatment of refractory partial seizures and infantile spasms. Weight gain and mostly transient sedation are its most common adverse effects, but visual field defects are the main cause for concern and severely restrict its use. 

The efficacy and adverse effects of steroids and vigabatrin in children with infantile spasms have been reviewed (38). The authors found a high rate of visual field defects and concluded that although vigabatrin is efficacious it does not seem to be more effective than steroids or corticotrophin, and that the benefits of vigabatrin do not justify the associated risks of possible irreversible visual changes. 

The long-term retinal effects of vigabatrin in children are unknown, and visual field testing is usually impossible. Recent evidence has suggested that a short course of vigabatrin (6 months) in children with infantile spasms may be sufficient (54) and minimizes the potential for visual adverse effects. 

Of 30 children with epilepsy (14 boys and 16 girls, aged 4-20 years) taking vigabatrin for infantile spasms and simple and complex partial epilepsy, who had never complained of ophthalmologic disturbances, 4 had visual field... 

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]

Chronic use of chloroquine may produce cinchon-ism, a syndrome characterized by headache, visual changes, and gastrointestinal disturbances. Visual disturbances are associated with retinal artery spasm. Ototoxicity may also occur. Dermatologic reactions, particularly a lichenoid skin eruption, may result from chronic chloroquine use. 

Quinine The antimalarial agent quinine is derived from the bark of the cinchona tree along with several other alkaloids and salicylate (aspirin). Many of these agents produce similar toxic features (cinchon-ism) in patients with excessive intake, but only quinine produces blindness. Cinchonism consists of abdominal pain and vomiting, ringing in the ears (tinnitus), and confusion. Visual loss after quinine overdose is due to direct retinal toxicity, although until recently it was believed to be due to spasm of the arterial blood supply to the retina. Treatment is difficult, but limited evidence suggests charcoal hemoperfusion may be beneficial (hemoperfusion is similar to hemodialysis, except in place of a semi-permeable membrane to filter the toxin from the blood, charcoal is used to bind the toxin). 

Inquire specifically about dose-by-dose effects of medication, wearing off of medication, inadequate response to a single dose of medication, "freezing," abnormal involuntary movements, cramps or spasms, hallucinations (particularly visual hallucinations), and nausea, vomiting, or light-headedness. Offer suggestions to help alleviate these. 

One prevalent neurological disease among human adults is multiple sclerosis (MS), usually characterized by spasms and weakness in one or more limbs, bladder dysfunction, local sensory losses, and visual disturbances. This disorder—the prototype demyelinating disease—is caused by patchy loss of myelin in areas of the brain and spinal cord. In MS patients, conduction of action potentials by the demyellnated neurons is slowed, and the... 

HEALTH SYMPTOMS inhalation (pulmonary edema, drowsiness, dizziness, visual disturbances, muscle twitching, painful muscle spasms, shortness of breath) skin absorption (nausea, headache, dizziness, vertigo) skin contact (inflammation, blisters, redness, swelling, rapid release of compressed gas may cause frostbite). 

B. Drugs Used for Acute Muscle Spasm Many drugs are promoted for the treatment of acute spasm due to muscle injury. Most of these drugs are sedatives or act in the brain stem or spinal cord. Cyclobenzaprine, a typical member of this group, is believed to act in the brain stem, possibly by interfering with polysynaptic reflexes that maintain skeletal muscle tone. The drug is active by the oral route and has marked sedative and antimuscarinic actions. Cyclobenzaprine may cause confusion and visual hallucinations in some patients. It is not effective in muscle spasm due to cerebral palsy or spinal cord injury. 

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

C. Retinal toxicity occurs 9-10 hours after ingestion and includes blurred vision, impaired color perception, constriction of visual fields, and blindness. The pupils are often fixed and dilated. Fundoscopy may reveal retinal artery spasm, disk pallor, and macular edema. Although gradual recovery occurs, many patients are left with permanent visual impairment. 

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