Over the past few years, ischemic stroke associated with cannabis use has been reported in the literature. Typically, this accident concerns young, frequent cannabis smokers and usually occurs following cannabis consumption with simultaneous intake of alcohol, which is also thought to play a role in the cerebrovascular event [1]. In most case reports, the outcome of the neurovascular event was favorable and the patients rapidly recovered from stroke within hours or a few days.

Here we report the case of a young man who presented to our hospital with stroke that led to four days of deep coma, followed by neuropsychiatric sequelae. Moreover, this stroke occurred in the absence of alcohol intoxication.

Case presentation

A 24-year-old Caucasian French man with no specific medical history was discovered in a deeply comatose, non-reactive state approximately 12 hours after he had fallen from a first-floor balcony under unknown circumstances. His blood pressure was 110/70 mmHg. During the physical examination, the mobile medical emergency team observed conjugate deviation of the eyes and concluded that the patient was having seizures. He was immediately treated with intravenous diazepam 10 mg, which had no impact on his level of consciousness, so he was intubated while on his way to our hospital.

The initial medical check-up conducted on admission to the medical intensive care unit did not reveal any biological anomalies related to his coma (electrolytes, glucose, ammonia level, liver and renal function tests, as well as arterial blood gas and carboxyhemoglobin levels). His electrocardiogram (ECG) and serum troponin I level were normal. His whole-body computed tomographic (CT) scan revealed thorax injuries due to the fall and excluded dissection of either the abdominal or thoracic aorta. His cerebral CT scan was unremarkable. Electroencephalography (EEG) (spot 20-minute recording) showed bilateral triphasic slow waves. Alcohol intoxication was excluded on the basis of a normal blood alcohol level. Urine toxicology (including tests for opioids, cocaine, amphetamines and psychotropic drugs) were negative except for the benzodiazepines administered by the emergency team before his hospital admission and for cannabis.

As the patient had not regained consciouness by day four, magnetic resonance imaging (MRI) of his brain was perfomed and revealed infarcts in the insular mantle and the lenticular and caudate nuclear structures (Figure 1), which were not consistent with traumatic contusions. A thorough evaluation did not reveal the cause of the stroke. EEG showed generalized slowing but did not give information on the patient's status epilepticus. Unfortunately, a transesophageal echocardiogram could not be performed secondary to the patient's behavioral condition. However, other studies were performed to help exclude cardioembolism, including ECG and transthoracic echocardiography. The examinations also excluded large-artery atherosclerosis (Doppler examination, magnetic resonance angiography and angiography scan) and hematological disorders (deficiencies in C and S proteins, resistance to activated C protein, dysfibrinogenemia, hyperhomocysteinemia, elevated factor VIII and D-dimer). Other causes of stroke in young adults, such as infectious or immunological disorders, were also excluded on the basis of virology tests, lumbar puncture, circulating anti-coagulant antibodies, cryoglobulins and monoclonal gammopathy.

Figure 1 T2-weighted magnetic resonance imaging scan showing bilateral superficial and deep to the right ischemic infarcts which concern different vascular territories in a young adult four days after he smoked cannabis. Full size image

Figure 2 Electroencephalographic (EEG) recording obtained within 24 hours after the patient's sixth generalized tonic-clonic seizure. The EEG tracing shows brief pseudorhythmic θ activity that predominated bifrontally. Full size image

The patient had been a regular cannabis smoker (up to five cigarettes a day) for four years. According to the patient and his close relations, on the night before admission to our hospital, he had smoked more than 10 cannabis cigarettes. We thus concluded that the patient had experienced multiple arterial cerebral infarcts after cannabis use.

From day five, and for the following four weeks, the patient's cognitive function slowly improved, but he still presented behavioral disorders, with a loss of social awareness, sexual disinhibition manifesting as masturbation and genital exposure, emotional instability and impulsiveness. He was therefore referred to the psychiatric department for one month and was treated with an anti-psychotic (levomepromazine). He discharged himself from our hospital as a result of lack of judgment, blunted affect and poor insight. During the one and a half years following this hospitalization, the patient was readmitted to the hospital on seven occasions because of the occurrence of generalized tonic-clonic seizures. The patient received valproic acid as the anti-epileptic drug, but his adherence to treatment was probably poor. The patient did not exhibit symptoms of another stroke, even though he admitted that he occasionally smoked cannabis.