Use of THC Concentrates and Risk of Stroke in Adults
Ibrahim Krenawi1, Mimoun Azizi*2
*Correspondence to: Mimoun Azizi, Chief Physician, Senior Consultant Neurologist and Neurogeriatrician, Klinikverbund Sudwest, Sindelfingen, Germany
Copyright
© 2026 Mimoun Azizi, This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Received: 12 October 2026
Published: 01 Nov 2026
DOI: https://doi.org/10.5281/zenodo.23907054
Abstract
The increasing availability of high-THC cannabis concentrates has raised concerns regarding their potential cerebrovascular effects; however, evidence specific to concentrated THC products remains poorly characterized and is frequently combined with general cannabis exposure. This systematic review aimed to evaluate published evidence describing ischemic or hemorrhagic stroke in adults following identifiable THC-concentrate exposure. The review was conducted in accordance with PRISMA 2020 principles. Eligible studies included adults exposed to identifiable cannabis-derived THC concentrates, including concentrated cannabis resin/hashish and extracted or processed preparations such as THC oils and vaping products, with objectively documented ischemic or hemorrhagic stroke. General cannabis exposure without separable concentrate use, synthetic cannabinoids, and cerebral vasoconstriction without stroke were excluded. Five primary reports met the eligibility criteria, comprising one clinical series and four case-based reports. Reported exposures included cannabis resin/hashish and vaporized THC or cannabis oils. Cerebrovascular presentations included ischemic infarction, subarachnoid hemorrhage, and intraparenchymal hemorrhage. Cerebral vasoconstriction, vasospasm, or reversible multifocal arterial narrowing was a recurring neurovascular finding. However, inconsistent exposure characterization, unverified THC concentrations, possible contaminants, co-exposures, and competing vascular mechanisms substantially limited causal interpretation. Overall, the available evidence remains limited and predominantly case-based. Although recurrent cerebral vasoconstriction represents a clinically relevant signal requiring further investigation, current evidence cannot establish causality or quantify stroke risk attributable specifically to THC concentrates. Prospective studies incorporating standardized assessment of product composition, THC concentration, dose, route, co-exposures, and neurovascular findings are required.
Keywords: THC concentrates; cannabis concentrates; stroke; ischemic stroke; intracranial hemorrhage; reversible cerebral vasoconstriction syndrome; cerebral vasospasm; THC vaping.
Introduction
Cannabis use has evolved considerably with the increasing availability of products containing high concentrations of Δ9-tetrahydrocannabinol (THC), the principal psychoactive cannabinoid in cannabis. THC concentrates are cannabis-derived preparations in which cannabinoids are concentrated through extraction or processing and include products such as butane hash oil (BHO), hash oil, wax, shatter, resin, and rosin. These preparations are commonly consumed through vaping or “dabbing” and may contain THC concentrations approaching 90–95%, substantially exceeding those typically found in cannabis flower. This distinction is clinically relevant because concentrated products may produce greater and more rapid THC exposure and can vary considerably in cannabinoid composition, extraction methods, and potential contaminants.
Cannabis exposure has been associated with cardiovascular and cerebrovascular complications, including ischemic and hemorrhagic stroke. However, most epidemiological studies classify exposure broadly as cannabis or marijuana use without adequately identifying product type, THC concentration, or route of administration [1]. Consequently, findings from general cannabis populations cannot be directly extrapolated to users of THC concentrates. This limitation is particularly important because concentrate-specific effects may reflect not only high THC exposure but also rapid inhalational delivery, additives, residual solvents, pesticides, or other contaminants. Existing research on high-concentration cannabis products remains heterogeneous, with important deficiencies in reporting product composition, dose, and patterns of use.
Potential mechanisms underlying cannabis-associated cerebrovascular events include alterations in cerebrovascular tone, sympathetic activation, hemodynamic instability, and cerebral vasoconstriction [2]. Nevertheless, the contribution of THC concentration, route of administration, co-exposures and contaminants remains uncertain. Concentrate-associated cerebrovascular events therefore require careful evaluation rather than attribution to THC alone.
This systematic review aimed to identify and critically synthesize published evidence describing ischemic or hemorrhagic stroke in adults following identifiable THC-concentrate exposure. Particular attention was given to concentrate formulation and route of administration, temporal relationship with stroke, cerebrovascular phenotype, neuroimaging findings, potential mechanisms, co-exposures, and alternative explanations. The review also sought to characterize the limitations of the existing evidence and identify priorities for future clinical and epidemiological research.
Methods
Study Design
This systematic review was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA 2020) reporting framework [3]. The review was designed to identify and critically synthesize published clinical evidence describing stroke following identifiable exposure to cannabis-derived THC concentrates. The review question was structured around the population of adults, exposure to THC concentrates, and objectively documented cerebrovascular outcomes.
Inclusion Criteria
Studies were eligible when they reported adults aged ≥18 years with clearly identifiable exposure to a THC-containing cannabis concentrate. Eligible products included THC oils or cartridges, cannabis/hash oil, butane hash oil (BHO), wax, shatter, dabs, resin, rosin, and other preparations explicitly described as concentrated cannabis or THC products. No restriction was applied to the route of administration.
Eligible outcomes comprised objectively documented ischemic stroke, cerebral infarction, intracerebral hemorrhage, or subarachnoid hemorrhage, supported by appropriate clinical and neuroimaging findings. Reports of reversible cerebral vasoconstriction syndrome (RCVS) or cerebral vasospasm were eligible only when accompanied by documented cerebral infarction or intracranial hemorrhage. Given the anticipated scarcity of concentrate-specific evidence, eligible primary evidence could include observational studies, case series, and case reports or conference reports providing sufficient clinical information to establish both the exposure and cerebrovascular outcome.
Exclusion Criteria
Studies were excluded when cannabis exposure was reported only as general marijuana or cannabis use and the use of a concentrate could not be established separately. Studies involving conventional cannabis flower without identifiable concentrate exposure, synthetic cannabinoids such as K2 or Spice, CBD-only preparations, or nonspecific cannabinoid-positive toxicology were excluded.
Reports describing RCVS or cerebral vasospasm without associated infarction or intracranial hemorrhage were not considered stroke cases. Studies of THC concentrates reporting only non-cerebrovascular outcomes, including psychiatric, cardiac, respiratory, or other toxicological complications, were also excluded. Reviews, systematic reviews, meta-analyses, editorials, and other secondary publications were not considered primary evidence, although their reference lists could be examined to identify potentially eligible original reports.
Search Strategy and Study Selection
A structured literature search used combinations of concentrate-related terms including THC concentrate, cannabis concentrate, marijuana concentrate, THC oil, cannabis oil, hash oil, butane hash oil, BHO, dab, dabbing, wax, shatter, resin, rosin, THC vaping, and THC cartridge. These were combined with cerebrovascular terms including stroke, ischemic stroke, cerebral infarction, intracerebral hemorrhage, subarachnoid hemorrhage, cerebral vasospasm, and reversible cerebral vasoconstriction syndrome. Reference lists of relevant reviews and eligible publications were additionally examined for potentially relevant reports.
Records were assessed against the predefined exposure and outcome criteria. General cannabis studies in which concentrate exposure could not be isolated were excluded from the primary evidence set but could be retained as contextual literature.
Data Extraction and Critical Appraisal
For each eligible report, data were extracted on publication characteristics, participant age and sex, concentrate formulation, route and pattern of exposure, temporal relationship between exposure and symptom onset, medical history, vascular risk factors, co-exposures, stroke subtype, neuroimaging and angiographic findings, proposed mechanism, treatment, and clinical outcome.
Case-based evidence was critically evaluated using the Joanna Briggs Institute (JBI) critical appraisal framework appropriate to the study design [4]. Assessment considered the adequacy of patient characteristics, clinical history, exposure ascertainment, diagnostic evaluation, intervention, follow-up, adverse-event reporting, and overall completeness of clinical reporting.
Evidence Synthesis
Because the eligible literature was expected to consist predominantly of clinically heterogeneous case-based evidence, findings were synthesized using a structured narrative approach. Evidence was organized according to THC-concentrate exposure, route of administration, stroke phenotype, neurovascular findings, temporal relationship, and proposed pathophysiological mechanisms. Particular attention was given to competing explanations, including underlying vascular risk factors, concomitant substance exposure, and possible product contaminants. Temporal associations were distinguished explicitly from causal relationships, and conclusions were restricted to the strength and limitations of the available evidence.
Results
Study Selection
Five primary reports fulfilled the predefined eligibility criteria by documenting exposure to a concentrated cannabis or THC preparation together with an objectively confirmed ischemic or hemorrhagic cerebrovascular event. The eligible evidence comprised one clinical series and four case-based reports published between 2011 and 2020. Studies were excluded when exposure was limited to general cannabis or marijuana use without identifiable concentrate exposure, when cerebrovascular injury was not objectively demonstrated, or when the publication represented secondary evidence. The final study-selection process is summarized in the PRISMA flow diagram.
Characteristics of Included Studies
The included literature encompassed both traditional concentrated cannabis resin preparations and more contemporary inhaled THC-oil products. Giray et al. reported a 35-year-old man with chronic high-dose hashish use who presented with acute right hemiplegia and an acute middle cerebral artery infarction. Toxicological analysis was positive for THC; however, cardiac akinesia and reduced ejection fraction represented an important competing vascular mechanism [5].
Wolff et al. evaluated 159 patients with ischemic stroke and identified 21 with reversible multifocal cerebral arterial stenoses and no other established stroke cause. Cannabis resin was identified as the precipitating exposure in 14 of these patients, making this the largest concentrate-specific clinical group in the eligible literature [6].
The three more recent reports involved inhaled oil-based preparations. Youn et al. described THC-oil vaporizer use preceding subarachnoid hemorrhage with reversible cerebral vasoconstriction syndrome (RCVS). Lam et al. reported daily THC vaping in a 32-year-old woman who developed multifocal acute ischemic infarctions with severe cerebral vasospasm. Kraiter and Varade described repeated vaping of cannabis oil preceding RCVS complicated by intraparenchymal hemorrhage [7, 15, 16]. The characteristics of the included reports are summarized in Table 1.
Critical Appraisal and Overall Evidence Pattern
The evidence was limited by substantial heterogeneity in exposure characterization and study design. Case-based reports generally provided detailed clinical presentation and objective neuroimaging but lacked comparator groups, standardized exposure measurement, and analytical verification of the consumed concentrate. The larger Wolff series provided stronger clinical characterization and follow-up vascular imaging but was not designed to quantify stroke risk specifically among cannabis-resin users.
Across the eligible evidence, cerebral vasoconstriction emerged as a recurrent descriptive finding accompanying both ischemic and hemorrhagic cerebrovascular injury. However, this pattern should not be interpreted as establishing a causal mechanism. Potential alternative explanations included cardiovascular abnormalities, other vascular risk factors, uncertain concentrate composition, and possible contaminants. Overall, the available literature identifies a concentrate-associated cerebrovascular safety signal, but remains insufficient to establish causality, determine incidence, or quantify the magnitude of stroke risk attributable specifically to THC concentrates.
Discussion
Principal Findings
This systematic review identified a small and clinically heterogeneous body of literature describing cerebrovascular events following identifiable THC-concentrate exposure. Across the five included primary reports, both ischemic and hemorrhagic events were documented following exposure to concentrated cannabis preparations, ranging from traditional cannabis resin/hashish to contemporary THC oils and vaporized products. The most consistent neurovascular feature was cerebral arterial vasoconstriction. Reversible multifocal stenoses, vasospasm, or RCVS accompanied several of the reported events, including ischemic infarction, subarachnoid hemorrhage, and intraparenchymal hemorrhage. Nevertheless, the available evidence is insufficient to establish that THC concentrations independently cause stroke or to estimate the magnitude of any associated risk.
The concentration-specific focus of this review is important. Most existing cerebrovascular literature categorizes exposure simply as cannabis or marijuana, without identifying formulation, potency, or route of administration [17, 18]. Such studies cannot determine whether cerebrovascular effects differ between conventional cannabis flower and concentrated products. This distinction has become increasingly relevant because contemporary concentrates can contain THC concentrations approaching 90–95%, while experimental evidence indicates that concentrate users can achieve substantially greater blood THC concentrations than flower users.
Potential Cerebrovascular Mechanisms
The recurring observation of cerebral vasoconstriction across the included reports provides a biologically plausible, although unproven, pathway linking concentrate exposure with cerebrovascular injury. RCVS involves transient dysregulation of cerebral arterial tone and may be complicated by ischemic infarction, convexity subarachnoid hemorrhage, or intracerebral hemorrhage. Cannabis is repeatedly identified among vasoactive exposures reported in the broader RCVS literature, and reversibility of cannabis-associated cerebral arterial narrowing has been described after exposure cessation.
Several mechanisms could contribute to this phenomenon. THC may influence autonomic and vascular regulation, producing changes in heart rate, blood pressure, and cerebral perfusion. Proposed pathways in the broader cannabis literature include sympathetic activation, vasospasm, impaired cerebrovascular autoregulation, endothelial dysfunction, oxidative stress, and alterations in platelet activity. These mechanisms remain hypotheses rather than demonstrated pathways specific to THC concentrates. In particular, evidence derived from general cannabis exposure should not be interpreted as direct mechanistic evidence for extracted high-THC products.
Concentrates may introduce additional considerations. Rapid pulmonary delivery through vaping or dabbing can produce substantial systemic THC exposure, while product composition may differ markedly between preparations. Concentrates may also contain residual solvents, pesticides, additives, or other contaminants depending on production and regulation. The possible myclobutanil exposure raised in the Youn report illustrates this attribution problem: a cerebrovascular event temporally following a THC cartridge cannot necessarily be attributed to THC itself when the chemical composition of the consumed product is incompletely characterized.
Interpretation in the Context of Broader Cannabis Evidence
The cerebrovascular phenotypes identified in this review are broadly compatible with those described in the larger cannabis literature. Reviews of cannabis-associated neurological complications describe ischemic stroke, intracranial hemorrhage, subarachnoid hemorrhage, and RCVS, with ischemic infarction frequently reported among cerebrovascular presentations. However, this broader literature remains difficult to apply directly to THC concentrates because exposure assessment frequently relies on self-report, diagnostic coding, or cannabinoid-positive toxicology rather than characterization of the consumed product.
This distinction also prevents the present findings from being interpreted as evidence that concentrates carry greater cerebrovascular risk than lower-potency cannabis. Although greater THC exposure provides a plausible basis for concern, a dose-response relationship for stroke has not been demonstrated. A recent systematic review of high-potency cannabis found that the available health literature remains concentrated in psychiatric and substance-use outcomes, with major gaps in other adverse-health domains. Thus, the cerebrovascular consequences of increasing THC potency remain substantially under-investigated.
Limitations of the Evidence
The principal limitation is the small and predominantly case-based evidence base. Case reports are valuable for detecting unusual clinical presentations and generating safety hypotheses, but they cannot establish incidence, relative risk, or causality. Publication bias is also likely because severe or unusual presentations following concentrate exposure are more likely to be reported than uneventful exposures.
Exposure ascertainment represents another major limitation. THC concentration, consumed dose, frequency of use, and chemical composition were inconsistently documented, and several products were not analytically tested. Consequently, the relative contributions of THC potency, route of administration, contaminants, and other cannabinoids cannot be separated. Co-exposures and competing mechanisms further complicate interpretation. For example, cardiac abnormalities in the Giray case provide an alternative mechanism for ischemic stroke, while remote substance exposure and incompletely characterized vaping products introduce additional uncertainty in other reports.
The included literature also spans markedly different products and periods. Traditional cannabis resin/hashish and modern extracted oils should not be considered chemically or pharmacokinetically interchangeable merely because both meet a broad definition of concentrated cannabis. This heterogeneity limits direct comparison across reports.
Clinical and Research Implications
Clinicians evaluating stroke in younger adults should obtain a detailed substance-use history that distinguishes conventional cannabis flower from oils, cartridges, waxes, dabs, resin, and other concentrated preparations. When concentrate exposure is reported, documenting product source, estimated THC concentration, route, frequency, timing relative to symptom onset, and potential co-exposures may improve clinical assessment and future pharmacovigilance. In presentations accompanied by severe headache or unexplained multifocal arterial narrowing, recent exposure to vasoactive substances—including cannabis products—may also be relevant to the differential diagnosis of RCVS. The broader literature supports cannabis as a repeatedly reported RCVS exposure, although direct causation in an individual patient cannot be assumed.
Future research requires prospective studies with product-specific exposure assessment rather than broad cannabis-use classifications. Analytical confirmation of THC concentration, cannabinoid profile, and contaminants would substantially strengthen exposure characterization. Studies should also record dose, route, frequency, concurrent nicotine and other drug use, conventional vascular risk factors, and standardized neurovascular imaging findings. Population-based research comparing concentrate users with appropriately characterized lower-potency cannabis users and non-users would be necessary to determine whether concentrated THC exposure is independently associated with stroke and whether any relationship varies by dose, formulation, or route.
Overall, the present literature should therefore be regarded as an early cerebrovascular safety signal requiring further investigation, rather than evidence of a quantified or causal stroke risk. The recurrent observation of cerebral vasoconstriction across otherwise heterogeneous reports provides a clinically relevant hypothesis, but appropriately designed epidemiological and mechanistic studies are required before concentrate-specific causal conclusions can be drawn.
Conclusion
This systematic review identified limited evidence describing ischemic and hemorrhagic stroke following THC-concentrate exposure. Across five primary reports, cerebral vasoconstriction was a recurring finding, suggesting a potential cerebrovascular mechanism that warrants further investigation. However, the predominantly case-based evidence, inconsistent exposure characterization, unverified THC concentrations, possible contaminants, and competing vascular factors prevent causal inference or estimation of stroke risk.
Clinicians should consider obtaining product-specific cannabis histories in patients with otherwise unexplained cerebrovascular events, particularly in younger adults. Future prospective studies with standardized assessment of THC concentration, formulation, dose, route, co-exposures, and neurovascular findings are needed to determine whether THC concentrations independently contribute to cerebrovascular risk.
References