Synthetic cannabinoids refer to a wide variety of chemicals engineered to bind cannabinoid receptors (CB1 and CB2) and mimic the effects of delta-9-tetrahydrocanabinol. The potential for severe toxicity and limited in vivo data make synthetic cannabinoid intake an important public health and safety concern. Neurologic toxidromes associated with their use include mental status changes, panic attacks, memory distortions, acute psychosis (e.g. paranoia, delusional thoughts), disorganized behavior, and suicidal and homicidal thoughts. Systemic complications include vomiting, sinus tachycardia, myocardial infarction, and acute kidney injury. Seizures are common; however, status epilepticus is not widely reported. In this case report, we describe a patient who developed acute psychosis and new-onset refractory status epilepticus necessitating emergent neurological life-support and prolonged admission to an intensive care unit following abuse of synthetic cannabinoids. We include a brief review of the literature to prepare the treating clinician for the broad clinical spectrum of this increasingly common intoxication.

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Spontaneous intracerebral hemorrhage (SICH) is the most lethal type of stroke. Half of these deaths occur within the acute phase. Frequently observed deterioration during the acute phase is often due to rebleeding or peri-hematomal expansion. The exact pathogenesis that leads to rebleeding or peri-hemorrhagic edema remains under much controversy. Numerous trials have investigated potential predictor of peri-hemorrhagic edema formation or rebleeding but have yet to come with consistent results. Unfortunately, almost all of the “classical” approaches have failed to show a significant impact in regard of significant clinical outcome in randomized clinical trials. Current treatment strategies may remain “double-edged swords,” for inherent reasons to the pathophysiology of sICH. Therefore, the right balance and possibly the combination of current accepted strategies as well as the evaluation of future approaches seem urgent. This article reviews the role of disturbed autoregulation following SICH, surgical and non-surgical approaches in management of SICH, peri-hematoma edema, peri-hematoma expansion, and future therapeutic trends.

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Objective: We describe border-zone territory infarctions without evident hypotension or vascular stenoses in a case of hypereosinophilic syndrome (HES). We review the spectrum of neurological changes associated with HES and explore about its relationship with the observed infarction pattern. Methods: This is a case report. A PubMed literature search was conducted searching clinico-radiographic findings of neurological complications associated with HES. Results: A previously healthy 47 year old man presented with progressive encephalopathy, weight loss and general malaise over three weeks. MRI head revealed bilateral hemispheric watershed infarcts at the junction of the anterior and posterior circulations. No intracranial or extracranial vascular stenoses were found and cardiac evaluation via transesophageal echocardiography, telemetry, and cardiac computed tomography (CT revealed no clear cardiac source of emboli. Persistently elevated eosinophil (>5,000/ μL) led to a bone marrow biopsy and diagnosis of eosinophilic leukemia with CHIC-2 mutation. Treatment with Imatinib and high dose prednisone was undertaken with significant clinical improvement. Conclusion: This case highlights a very rare cause of bilateral watershed cerebral infarction in non-hemodynamic stenoses. We hypothesize that the particular pattern of infarct observed in this setting may be explained on the basis of the lower capacity of hypoperfused vessel (borderzone) to eliminate emboli related to in situ-thrombosis from degranulation of eosinophils: "Impaired Wash-Out Theory".

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5 fluorouracil (5-FU)-related neurotoxicity is a rare and severe complication of 5-FU administration. Dihydropyrimidine dehydrogenase (DPD) deficiency is associated with an increased risk of serious adverse reactions due to its role in 5-FU metabolism. We report a case of acute reversible neurotoxicity with global areas of diffusion restriction in a patient with colorectal adenocarcinoma being treated with leucovorin calcium, 5-fluorouracil, and oxaliplatin (FOLFOX) without DPD deficiency following uridine triacetate administration.