Pupil abnormality

Unlikely Umbal infiltrates, corneal neovascularization, keratoconus, activation of herpes simplex, exophthalmos, pupil abnormalities, vitreous disturbance, glaucoma. 

Syphilis Myoclonus (increased reflexes), abnormality of pupils on eye exam... 

If the lesion of Horner s syndrome is postganglionic, indirectly acting sympathomimetics (eg, cocaine, hydroxyamphetamine) will not dilate the abnormally constricted pupil because catecholamines have been lost from the nerve endings in the iris. In contrast, the pupil dilates in response to phenylephrine, which acts directly on the a receptors on the smooth muscle of the iris. 

Abnormal movements Tremors, convulsions Pupil function ... 

The pupillary light reflex may help differentiating metabolic cause from structural brainstem lesion in comatose patients (Tokuda et al. 2003). The light reflex is very resistant to metabolic dysfunction. An abnormal light reflex, especially when unilateral, points to a midbrain lesion. Bilateral diencephalic lesions or metabolic coma may cause bilateral small pupils well reacting to light ( diencephalic pupils ). 

Seizures/convulsions, awareness reaction, startle response, vocalization, irritability, decreased abdominal tone, increased secretion, body tremors, decreased grip strength, immobility, motor activity, ataxia, abnormal posture, stereotypy, excretion, decreased respiration, piloerection, loss of righting, pupil size, nociceptive (pain) response, corneal reflex, and pinnal reflex... 

Dilated episcleral vessels are a clue to abnormal anastamoses between branches of the external carotid artery and orbital branches of the internal carotid artery, distal to severe internal carotid artery disease. With extreme ischemia, ischemic oculopathy may develop, with impaired visual acuity, eye pain, rubeosis of the iris (dilated blood vessels), fixed dilated pupil, low-pressure glaucoma, cataract and corneal edema. 

Patients who have had cataract extraction with implantation of an intraocular lens (lOL) often have pupils that dilate less well than they did preoperatively.The poorer pupillary response probably relates to the amount of iris trauma occurring at surgery. The difference in mydriatic response may affect evaluating and treating peripheral retinal abnormalities in aphakic and pseudophakic eyes. However, even with maximally dilated pupils often the capsulotomy is the limiting fector. 

When anisocoria is greater in bright illumination, the dilated pupil is considered abnormal until proven otherwise. The differential diagnosis of this dilation includes... 

In tests of the response to direct light, a pupil that responds poorly clearly indicates the abnormal pupil.The differential diagnosis includes third-nerve palsy, anticholinergic mydriasis, Adie s pupil, or local iris disease. If each eye exhibits a good pupillary light reaction, differential diagnosis includes Horner s syndrome and physiologic anisocoria (Table 22-1). 

Disorders that are most easily evaluated pharmacologically, in which usually only one pupil is abnormal. 

Of patients with Adie s pupil, 50% to 90% demonstrate significantly impaired or absent deep tendon reflexes, and this sign serves as a helpful clinical confirmation of the diagnosis. Most patients have tendon reflexes that are abnormal throughout the body, but the ankles and triceps... 

The volunteers evacuated from the field exercise were flushed and had hoc, dry skins, parched lips and tongues, dilated pupils, tachycardia, and exaggerated deep tendon reflexes. After treatment with physostlgmine salicylate (55 >ig/kg Intramuscularly), these volunteers were restored to lucidity within 20 min. After Institution of maintenance doses of physostlgmine salicylate by mouth, the subjects were able to return to the field exercise and to perform their duties capably. When the maintenance doses of ptyrsosclgmine salicylate to the volunteer who had been given EA 3834 at 12 )ig/kg were discontinued after four such doses, he became delirious again within about 3 h and remained In that state for 5 or 6 h. No abnormalities of renal and hepatic functions were detectable In any subject 24 h and 7 d after the Injections of EA 3834. 

A 51-year-old woman took 87 tablets of carisoprodol (350 mg each) over 13 days and developed lethargy and abnormal speech. She was confused and her Glasgow Coma Score was 9/15. Her pupils were small and reactive. Two boluses of naloxone 2 mg were administered with no effect. After flumazenil 0.2 mg she became more alert but was still mildly somnolent. After a second dose of flumazenil 0.2 mg all signs of intoxication... 

An 8-year-old boy complained of abnormal facial movements and hallucinations. One day before these symptoms, he had been given his sister s Cordec DM droplets (carbinoxamine maleate 2 mg, pseudoephe-drine hydrochloride 25 mg, and dextromethorphan 4 mg) for a cold. He had facial dyskinesia, dilated pupils, pyrexia, tachycardia, and reduced bowel sounds and responded to a benzodiazepine. 

Acute overdosage with antimuscarinics produces both peripheral and CNS symptomatology. The quaternary ammonium compounds do not readily penetrate the CNS and thus exhibit minimal central effects even at toxic doses. Patients with anticholinergic toxicity will typically show peripheral symptoms including dry mouth, thirst, fixed dilated pupils, flushed face, fever, hot, dry, red skin, urinary retention, hyperthermia, hypotension, tachycardia, and increased respiratory rate. In addition to tachycardia, cardiac manifestations may include EKG abnormalities similar to those produced by quini-dine. Speech and swallowing may be impaired in association with blurred vision. Other peripheral signs and symptoms may include nausea and vomiting. 

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