Toxic Leukoencephalopathy in a Teenager Caused by the Recreational Ingestion of 25I-NBOMe: A Case Report and Review of Literature

Abstract

Over the past 5 years, the designer drug classification of illicit substances has gained the attention of law enforcement agencies, healthcare providers, and concerned parents around the world. These drugs are often marketed as safe and legal alternatives to their already banned counterparts and are easily acquired online, at "head" shops or behind the counter at local convenient stores. This new drug class includes synthetic cathinones, synthetic cannabinoids, and phenylethylamine derivatives of the 2C class of hallucinogens. Many of these drugs were created for animal research purposes only and were never intended for human consumption. As such, little is known about their pharmacokinetic, pharmacodynamics, and adverse effect profile. Variability in preparation may further alter the already unpredictable safety profile. We report an otherwise healthy 16-year-old adolescent who presented to the emergency department for worsening left-sided weakness, new onset seizure activity, changes in mental status, and an overall decline in health. He self-reported the recreational ingestion of 25I-NBOMe prior to admission. Magnetic resonance imaging and a brain biopsy performed during the course of his admission confirmed the diagnosis of toxic leukoencephalopathy secondary to synthetic hallucinogenic drug use. The basic pharmacology and end-organ effects of 25I-NBOMe are reviewed, their adverse effect profile is presented, and potential anesthetic implications are postulated.

Neuroimaging features of psilocybin-induced toxic-metabolic encephalopathy in an adolescent

“…A report of an adult presenting with a similar clinical presentation after psilocybin ingestion demonstrated no significant findings on MRI 7. Notably, a case report of an adolescent with neurological changes after 25I-NBOMe ingestion, a synthetic hallucinogen that acts through a similar mechanism to psilocybin, demonstrated diffuse white matter changes on imaging 8. In our case, signal abnormalities localised to the splenium of the corpus callosum.…”

NBOMes–Highly Potent and Toxic Alternatives of LSD

“…NBOMes produce an array of adverse effects (Hill et al, 2013;Rose et al, 2013;Bersani et al, 2014;EMCDDA, 2014;Forrester, 2014;Grautoff and Kähler, 2014;Lawn et al, 2014;Stellpflug et al, 2014;Suzuki et al, 2014;Tang et al, 2014;World Health Organization, 2014a,b;Hieger et al, 2015;Nikolaou et al, 2015;Poklis et al, 2015b;Srisuma et al, 2015;Wood et al, 2015;Gee et al, 2016;Kristofic et al, 2016;Hermanns-Clausen et al, 2017;Humston et al, 2017;Madsen et al, 2017;Rajotte et al, 2017;Schetz et al, 2017;Wiergowski et al, 2017;Zygowiec et al, 2017;Marchi et al, 2019;Erowid.org); for comprehensive reviews see Suzuki et al, 2015;Halberstadt, 2017).…”

“…Patients with hematological disturbances require transfusion(s) of blood preparations (frozen plasma, frozen erythrocytes, or platelet concentrate). Severely aggressive patients may require antipsychotic drugs in addition to benzodiazepines (Hill et al, 2013;Rose et al, 2013;Forrester, 2014;Stellpflug et al, 2014;Hieger et al, 2015;Gee et al, 2016;Humston et al, 2017;Schetz et al, 2017;Wiergowski et al, 2017). Some emergency interventions are specifically intended to treat rhabdomyolysis, which may lead to severe complications, particularly acute kidney injury/failure and metabolic acidosis.…”

Acute pharmacological profile of 2C-B-Fly-NBOMe in male Wistar rats—pharmacokinetics, effects on behaviour and thermoregulation

“…Highly intoxicated individuals can suffer from anxiety, confusion, panic attacks and paranoia, they can also manifest aggressive and bizarre behaviour. In terms of adverse somatic effects, intoxications with NBOMes can cause seizures, kidney failure, toxic leukoencephalopathy, or show clinical features associated with serotonergic toxicity, such as tachycardia, hypertension, breathing difficulties, convulsions, sweating and overheating, rhabdomyolysis, acute multiorgan failure, heart arrhythmia, fibrillation, and cardiac arrest ( Hill et al, 2013 ; Poklis et al, 2014 ; Stellpflug et al, 2014 ; Humston et al, 2017 ; Richeval et al, 2017 ). Most frequent fatal poisonings involve 25I-NBOMe, 25B-NBOMe and 25C-NBOMe ( Andreasen et al, 2015 ; Kueppers and Cooke, 2015 ; Nikolaou et al, 2015 ; Shanks et al, 2015 ; Al-Imam, 2018 ).…”