Rarely, tardive dyskinesia can occur when the medication is stopped. Overdose
Symptoms of an overdose include tachycardia, agitation, dysarthria, decreased consciousness, and coma. Death has been reported after an acute overdose of 450 mg, but also survival after an acute overdose of 2000 mg. Fatalities generally have occurred with olanzapine plasma concentrations greater than 1000 ng/mL post mortem, with concentrations up to 5200 ng/mL recorded (though this might represent confounding by dead tissue, which may release olanzapine into the blood upon death). No specific antidote for olanzapine overdose is known, and even physicians are recommended to call a certified poison control center for information on the treatment of such a case. Olanzapine is considered moderately toxic in overdose, more toxic than quetiapine, aripiprazole, and the SSRIs, and less toxic than the monoamine oxidase inhibitors and tricyclic antidepressants. Interactions
Drugs or agents that increase the activity of the enzyme CYP1A2, notably tobacco smoke, may significantly increase hepatic first-pass clearance of olanzapine; conversely, drugs that inhibit CYP1A2 activity (examples: ciprofloxacin, fluvoxamine) may reduce olanzapine clearance. Carbamazepine, a known enzyme inducer, has decreased the concentration/dose ration of olanzapine by 33% compared to olanzapine alone. Another enzyme inducer, ritonavir, has also been shown to decrease the bodys exposure to olanzapine, due to its induction of the enzymes CYP1A2 and uridine 5-diphospho-glucuronosyltransferase (UGT).Probenecid increases the total exposure (area under the curve) and maximum plasma concentration of olanzapine.
The most common lissencephaly observed, consisting of frontotemporal pachygyria and posterior agyria, is Grade 3. Another malformation worth mentioning because of its connections to pachygyria is polymicrogyria. Polymicrogyria is characterized by many small gyri separated by shallow sulci, slightly thin cortex, neuronal heterotopia and enlarged ventricle and is often superimposed on pachygyria. Treatment
Because pachygyria is a structural defect no treatments are currently available other than symptomatic treatments, especially for associated seizures. Another common treatment is a gastrostomy (insertion of a feeding tube) to reduce possible poor nutrition and repeated aspiration pneumonia. Microcephalic osteodysplastic primordial dwarfism
Microcephalic osteodysplastic primordial dwarfism (MOPD) type II is an autosomal multisystem disorder including severe pre- and post-natal growth retardation, microcephaly with Seckel syndrome-like facial appearance, and distinctive skeletal alterations. Usually those affected have mild to moderate mental retardation. See also
Lissencephaly
Polymicrogyria

References
Phadke SR, Girisha KM, Phadke RV (2007). "A new autosomal recessive disorder of bilateral frontotemporal pachygyria without microcephaly: report of a case and review of literature". Neurol India. 55 (1): 57–60. doi:10.4103/0028-3886.30429. PMID 17272902. External links

Online Mendelian Inheritance in Man (OMIM): 600176