ABSTRACT
INTRODUCTION: Haloperidol is a dopamine receptor antagonist used to treat patients with psychotic disorders. Especially at high doses, haloperidol carries a higher risk of extrapyramidal symptoms (EPS) compared to second-generation antipsychotics. Few cases of haloperidol misuse are found in the medical literature. Case Presentation. We describe a patient with schizophrenia who smoked marijuana mixed with crushed haloperidol tablets. After the smoking of cannabis and haloperidol, the patient presented to the emergency department (ED) with suicidal ideation, psychosis, and acute dystonia. With the administration of intramuscular diphenhydramine at the ED, the dystonia resolved in less than an hour. To our knowledge, this is the first report on haloperidol misuse by smoking. CONCLUSION: Clinicians should be aware that patients might misuse prescribed antipsychotics via unconventional routes, potentially combined with other substances.
ABSTRACT
BACKGROUND: Newly developed white matter (WM) injury is common after cardiopulmonary bypass (CPB) in severe/complex congenital heart disease. Fractional anisotropy (FA) allows measurement of macroscopic organization of WM pathology but has rarely been applied after CPB. The aims of our animal study were to define CPB-induced FA alterations and to determine correlations between these changes and cellular events after congenital heart disease surgery. METHODS AND RESULTS: Normal porcine WM development was first assessed between 3 and 7 weeks of age: 3-week-old piglets were randomly assigned to 1 of 3 CPB-induced insults. FA was analyzed in 31 WM structures. WM oligodendrocytes, astrocytes, and microglia were assessed immunohistologically. Normal porcine WM development resembles human WM development in early infancy. We found region-specific WM vulnerability to insults associated with CPB. FA changes after CPB were also insult dependent. Within various WM areas, WM within the frontal cortex was susceptible, suggesting that FA in the frontal cortex should be a biomarker for WM injury after CPB. FA increases occur parallel to cellular processes of WM maturation during normal development; however, they are altered following surgery. CPB-induced oligodendrocyte dysmaturation, astrogliosis, and microglial expansion affect these changes. FA enabled capturing CPB-induced cellular events 4 weeks postoperatively. Regions most resilient to CPB-induced FA reduction were those that maintained mature oligodendrocytes. CONCLUSIONS: Reducing alterations of oligodendrocyte development in the frontal cortex can be both a metric and a goal to improve neurodevelopmental impairment in the congenital heart disease population. Studies using this model can provide important data needed to better interpret human imaging studies.
