In children, overdose may also result in hallucinations. Topiramate has been deemed the primary substance that led to fatal overdoses in cases that were complicated by polydrug exposure. The most common signs of overdose are dilated pupils, somnolence, dizziness, psychomotor agitation, and abnormal, uncoordinated body movements.Symptoms of overdose may include but are not limited to:

A specific antidote is not available. Treatment is entirely supportive. Interactions
Topiramate has many drug-drug interactions. Some of the most common are listed below:

As topiramate inhibits carbonic anhydrase, use with other inhibitors of carbonic anhydrase (e.g. acetazolamide) increases the risk of kidney stones. Enzyme inducers (e.g. carbamazepine) can increase the elimination of topiramate, possibly necessitating dose escalations of topiramate. Topiramate may increase the plasma-levels of phenytoin. Topiramate itself is a weak inhibitor of CYP2C19 and induces CYP3A4; a decrease in plasma levels of estrogens and digoxin has been noted during topiramate therapy. This can reduce the effectiveness of oral contraceptives (birth control  pills); use of alternative birth control methods is recommended. Neither intrauterine devices (IUDs) nor Depo-Provera are affected by topiramate. Alcohol may cause increased sedation or drowsiness, and increase the risk of having a seizure. As topiramate may result in acidosis other treatments that also do so may worsen this effect. Oligohidrosis and hyperthermia were reported in post-marketing reports about topiramate; antimuscarinic drugs (like trospium) can aggravate these disorders. Pharmacology
The topiramate molecule is a sulfamate modified sugar, more specifically, fructose diacetonide, an unusual chemical structure for a pharmaceutical. Topiramate is quickly absorbed after oral use.
Primary juvenile glaucoma is glaucoma that develops due to ocular hypertension and is evident either at birth or within the first few years of life. It is caused due to abnormalities in the anterior chamber angle development that obstruct aqueous outflow in the absence of systemic anomalies or other ocular malformation. Presentation
The typical infant who has congenital glaucoma usually is initially referred to an ophthalmologist because of apparent corneal edema. The commonly described triad of epiphora (excessive tearing), blepharospasm and photophobia may be missed until the corneal edema becomes apparent. Systemic associations
Two of the more commonly encountered disorders that may be associated with congenital glaucoma are Aniridia and Sturge-Weber syndrome. Genetics
JOAG is an autosomal dominant condition. The primary cause is the myocilin protein dysfunction. Myocilin gene mutations are identified in approximately 10% of patients affected by juvenile glaucoma. Diagnosis
The diagnosis is clinical. The intraocular pressure (IOP) can be measured in the office in a conscious swaddled infant using a Tonopen or hand-held Goldmann tonometer. Usually, the IOP in normal infants is in the range of 11-14 mmHg. Buphthalmos and Haabs striae can often be seen in case of congenital glaucoma. Differential diagnosis
Corneal cloudiness may have myriad of causes. Corneal opacity that results from hereditary dystrophies is usually symmetric. Corneal enlargement may result from megalocornea, a condition in which the diameter of the cornea is larger than usual and the eye is otherwise normal. Treatment
The preferred treatment of congenital glaucoma is surgical, not medical.