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MBBS, MD (Pathology),
Sanjay Gandhi institute of trauma and orthopedics,
Bengaluru.
On Aug 2018




Dr. Mamta Gupta,
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Dr. Mamta Gupta
Consultant
(Ex HOD Obs &Gynae, Hindu Rao Hospital and associated NDMC Medical College, Delhi)
Aug 2018




Dr. Rajendra Kumar Ghritlaharey

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Salient features of the JCDR: It is a biomedical, multidisciplinary (including all medical and dental specialities), e-journal, with wide scope and extensive author support. At the same time, a free text of manuscript is available in HTML and PDF format. There is fast growing authorship and readership with JCDR as this can be judged by the number of articles published in it i e; in Feb 2007 of its first issue, it contained 5 articles only, and now in its recent volume published in April 2011, it contained 67 manuscripts. This e-journal is fulfilling the commitments and objectives sincerely, (as stated by Editor-in-chief in his preface to first edition) i e; to encourage physicians through the internet, especially from the developing countries who witness a spectrum of disease and acquire a wealth of knowledge to publish their experiences to benefit the medical community in patients care. I also feel that many of us have work of substance, newer ideas, adequate clinical materials but poor in medical writing and hesitation to submit the work and need help. JCDR provides authors help in this regards.
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Thanking you
With sincere regards
Dr. Rajendra Kumar Ghritlaharey, M.S., M. Ch., FAIS
Associate Professor,
Department of Paediatric Surgery, Gandhi Medical College & Associated
Kamla Nehru & Hamidia Hospitals Bhopal, Madhya Pradesh 462 001 (India)
E-mail: drrajendrak1@rediffmail.com
On May 11,2011




Dr. Shankar P.R.

"On looking back through my Gmail archives after being requested by the journal to write a short editorial about my experiences of publishing with the Journal of Clinical and Diagnostic Research (JCDR), I came across an e-mail from Dr. Hemant Jain, Editor, in March 2007, which introduced the new electronic journal. The main features of the journal which were outlined in the e-mail were extensive author support, cash rewards, the peer review process, and other salient features of the journal.
Over a span of over four years, we (I and my colleagues) have published around 25 articles in the journal. In this editorial, I plan to briefly discuss my experiences of publishing with JCDR and the strengths of the journal and to finally address the areas for improvement.
My experiences of publishing with JCDR: Overall, my experiences of publishing withJCDR have been positive. The best point about the journal is that it responds to queries from the author. This may seem to be simple and not too much to ask for, but unfortunately, many journals in the subcontinent and from many developing countries do not respond or they respond with a long delay to the queries from the authors 1. The reasons could be many, including lack of optimal secretarial and other support. Another problem with many journals is the slowness of the review process. Editorial processing and peer review can take anywhere between a year to two years with some journals. Also, some journals do not keep the contributors informed about the progress of the review process. Due to the long review process, the articles can lose their relevance and topicality. A major benefit with JCDR is the timeliness and promptness of its response. In Dr Jain's e-mail which was sent to me in 2007, before the introduction of the Pre-publishing system, he had stated that he had received my submission and that he would get back to me within seven days and he did!
Most of the manuscripts are published within 3 to 4 months of their submission if they are found to be suitable after the review process. JCDR is published bimonthly and the accepted articles were usually published in the next issue. Recently, due to the increased volume of the submissions, the review process has become slower and it ?? Section can take from 4 to 6 months for the articles to be reviewed. The journal has an extensive author support system and it has recently introduced a paid expedited review process. The journal also mentions the average time for processing the manuscript under different submission systems - regular submission and expedited review.
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Dr. P. Ravi Shankar
KIST Medical College, P.O. Box 14142, Kathmandu, Nepal.
E-mail: ravi.dr.shankar@gmail.com
On April 2011
Anuradha

Dear team JCDR, I would like to thank you for the very professional and polite service provided by everyone at JCDR. While i have been in the field of writing and editing for sometime, this has been my first attempt in publishing a scientific paper.Thank you for hand-holding me through the process.


Dr. Anuradha
E-mail: anuradha2nittur@gmail.com
On Jan 2020

Important Notice

Case report
Year : 2026 | Month : September | Volume : 20 | Issue : 9 | Page : OD28 - OD30 Full Version

Cannabis-associated Spontaneous Bilateral Basal Ganglia Haemorrhage: A Case Report


Published: September 1, 2026 | DOI: https://doi.org/10.7860/JCDR/2026/88094.24353
Mridula Singh, Rashmi Mishra, Aabhasha Parotra, Siddharth Maheshwari, Rajinder K Dhamija

1. Assistant Professor, Department of Neurology, Institute of Human Behaviour and Allied Sciences, New Delhi, India. 2. Senior Resident, Department of Neurology, Institute of Human Behaviour and Allied Sciences, New Delhi, India. 3. Senior Resident, Department of Neurology, Institute of Human Behaviour and Allied Sciences, New Delhi, India. 4. Assistant Professor, Department of Neurology, Institute of Human Behaviour and Allied Sciences, New Delhi, India. 5. Professor, Department of Neurology, Institute of Human Behaviour and Allied Sciences, New Delhi, India.

Correspondence Address :
Rashmi Mishra,
19/804, 8th Floor, East End Apartments, Mayur Vihar Phase 1 Extension, New Delhi, India.
E-mail: rashmi.virgo02@gmail.com

Abstract

Spontaneous Bilateral Basal Ganglia Haemorrhage (SBBGH) is an exceptionally rare entity, with fewer than sixty cases reported worldwide. Although cannabis use is a recognised risk factor for ischemic stroke, its association with Intracerebral Haemorrhage (ICH) remains uncommon and poorly characterised. A 23-year-old male with no vascular risk factors presented with acute onset right-sided hemiparesis, dysarthria, and dysphonia. Symptoms developed a few hours after cannabis ingestion. Neurological examination revealed right facial nerve palsy, vocal cord palsy, and reduced motor strength in the right upper and lower limbs. Non-contrast computed tomography of the brain demonstrated acute bilateral basal ganglia haematomas. Comprehensive evaluation, including autoimmune, infectious, coagulation, and genetic work-up, was unremarkable. Magnetic resonance angiography and venography excluded vascular malformations, aneurysms, and cerebral venous thrombosis. Urine toxicology was positive for cannabis, identifying it as the probable aetiological factor. This case represents a rare presentation of SBBGH associated with cannabis use. It expands the spectrum of cannabinoid-related cerebrovascular complications and highlights the importance of considering substance-related aetiologies in young patients with atypical ICH.

Keywords

Cannabinoids, Cerebrovascular disorders, Haemorrhagic stroke, Substance-related disorders, Young stroke

Case Report

A 23-year-old right-handed male presented with sudden onset right-sided weakness, dysarthria, and dysphonia developing over 1-2 hours. He had no symptoms to suggest sensory, cerebellar or cortical involvement. There was no preceding headache, seizure, trauma, or loss of consciousness. There was no known history of hypertension, diabetes mellitus, dyslipidaemia, or cardiovascular disease. His personal and family history was unremarkable, except for regular cannabis consumption (1-2 times per month). Notably, he had ingested approximately 4-5 grams of cannabis in the form of bhang 6-8 hours prior to the onset of neurological symptoms.

On admission, the patient was alert and oriented, with a Glasgow Coma Scale (GCS) score of 15. He was normotensive, and systemic examination was unremarkable. Neurological examination revealed right-sided facial weakness consistent with seventh cranial nerve involvement, vocal cord palsy resulting in mild dysarthria, and mild right hemiparesis with Medical Research Council grade 4/5 power in both the upper and lower limbs {National Institutes of Health Stroke Scale score of 4: mild facial palsy (1), mild dysarthria (1) and drift in right upper and lower limb (1+1)}. Sensory examination and cerebellar testing were normal.

Non-contrast computed tomography of the brain demonstrated acute hyperdense haemorrhages involving the bilateral basal ganglia, with a larger lesion on the left-side measuring approximately 4.1 cubic centimetres and a smaller right-sided haemorrhage measuring 0.8 cubic centimetres. There was no intraventricular extension, mass effect, or midline shift (Table/Fig 1).

An extensive diagnostic evaluation was undertaken to identify potential secondary causes. Routine haematological and biochemical investigations, including complete blood count, renal and liver function tests, lipid profile, erythrocyte sedimentation rate, and coagulation parameters, were within normal limits. Autoimmune screening and viral serologies were negative. Evaluation for secondary hypertension, including assessment for renal, thyroid, and adrenal disorders, did not reveal any abnormalities. Electrocardiography showed normal sinus rhythm, and transthoracic echocardiography was unremarkable.

Magnetic Resonance Imaging (MRI) of the brain with gradient echo sequences did not demonstrate cerebral microbleeds suggestive of an underlying small-vessel vasculopathy. Magnetic resonance angiography and venography excluded intracranial aneurysms, arteriovenous malformations, diffuse atherosclerotic disease, and cerebral venous thrombosis (Table/Fig 1). Digital subtraction angiography could not be performed due to financial constraints. Genetic testing did not reveal pathogenic variants associated with hereditary cerebral haemorrhage syndromes (APP, COL4A1/2, NOTCH3, HTRA1).

Urine toxicology screening was strongly positive for cannabis and negative for cocaine, heroin, amphetamines, and other commonly abused substances. There was absence of conventional risk factors like hypertension, while normal vascular imaging ruled out any aneurysm, arteriovenous malformations, and vasculitis. There was no history of fever at the onset, or any history of anticoagulant use which excluded infectious aetiology and coagulopathy. Given the temporal relationship between cannabis ingestion and symptom onset, a diagnosis of cannabis-associated SBBGH was considered most likely.

The patient was managed conservatively with close neurological monitoring (blood pressure monitoring, intravenous fluids and pantoprazole). There were no signs of raised ICP precluding the need for osmotherapy and seizure prophylaxis. His hospital course was uneventful, with gradual improvement in motor strength and speech over 4-5 days. The patient was discharged on day six with enrolment into substance cessation counselling session. He was followed-up after six weeks, had significant improvement in strength and was compliant with substance cessation. As the patient showed clinical improvement, no follow-up imaging was done.

Discussion

Spontaneous ICH involving the basal ganglia is most commonly unilateral and typically associated with long-standing hypertension or underlying small-vessel disease. SBBGH is an exceedingly rare clinical entity, with fewer than sixty cases reported in the literature. Cannabis use is a well-documented risk factor for ischemic stroke, but its association with ICH is uncommon (1). The aetiological spectrum of SBBGH includes hypertension, vascular malformations, infections, coagulopathies, and substance abuse. Hypertension is the commonest cause in elderly, while vascular anomalies are more relevant in the younger age group. Infectious causes like cerebral toxoplasmosis and fungal vasculitis occur in immunocompromised states, whereas coagulopathies also contribute. Though rare, substance abuse-primarily alcohol, cocaine and amphetamines- has been implicated as a trigger (1),(2).

Cannabis is predominantly linked to ischemic strokes, potentially due to mechanisms such as vasoconstriction, oxidative stress, vasculopathy, and cerebral autoregulation impairment, which are attributed to its psychoactive component, delta-9-Tetrahydrocannabinol (THC). Cannabis-related ICH is less common, with a prevalence of 0.3% in descriptive studies, and mainly documented through case reports (3). The probable pathophysiological hypotheses underlying cannabis-associated ICH are multifactorial and remain incompletely understood. Cannabis-induced cerebral vasospasm causes transient ischemia followed by reperfusion injury, which can damage the vascular endothelium, increasing the risk of vessel rupture and subsequent haemorrhage. Secondly RCVS-like activity is a proposed mechanism, characterised by transient, multifocal narrowing of cerebral arteries. This phenomenon, often observed in imaging studies post-cannabis use, may lead to abrupt changes in cerebral perfusion pressure (4),(5),(6).

Cannabinoids may interfere with platelet aggregation and thrombin activity, especially in the context of pre-existing microvascular stress. Transient arterial hypertension is a well-recognised acute effect of cannabis, possibly due to its sympathomimetic properties. Sudden elevations in systemic blood pressure overwhelm the cerebrovascular autoregulation, particularly in the small penetrating arteries of deep brain structures such as the basal ganglia (2),(7),(8). Despite an extensive literature search, only a limited number of case reports exists describing ICH attributed to cannabis use. Renard D et al., reported a 34-year-old Female presenting with headache after smoking four cannabis cigarettes. Imaging demonstrated a right temporal lobe haemorrhage, while angiography revealed diffuse multifocal arterial narrowing, suggesting a vasospastic mechanism (9). Similarly, Rose DZ et al., described a 31-year-old male who developed seizures, left homonymous hemianopsia, and lower limb paralysis after synthetic cannabis (“Spice”) use. Neuroimaging showed bifrontal subarachnoid haemorrhage with associated intraparenchymal haemorrhages, and DSA demonstrated multifocal vasospasm, supporting a RCVS-like process (4).

Aydin S et al., reported a 23-year-old chronic synthetic cannabis user presenting with altered consciousness (GCS 12/15). CT revealed a large right frontal haematoma, while angiography showed multiple intracranial arterial stenoses, indicating probable cannabinoid-induced vascular injury (7). Tandon R et al., described a 23-year-old male who consumed 5-10 g of “bhang” and subsequently developed altered sensorium, hypertonia, hyperreflexia, and diplopia. MRI demonstrated left thalamic and brainstem haemorrhage, with normal vasculitic and coagulation profiles, similar to our patient (6).

Atchaneeyasakul K et al., reported a 27-year-old male with sudden left hemiparesis following ingestion of a large quantity of raw cannabis. Imaging revealed a right basal ganglia haemorrhage with normal DSA findings, suggesting transient hypertension or autoregulatory dysfunction rather than structural vascular pathology (8). Ince B et al., described a 38-year-old male with right hemiplegia and aphasia after cannabis consumption with alcohol intake. Imaging revealed a large left basal ganglia bleed, while DSA showed vasospasm involving the left internal carotid artery (10). (Table/Fig 2) highlights salient features of previously reported cannabis related intracranial haemorrhage.

Conclusion

In this patient, the absence of conventional risk factors, normal vascular imaging, negative infectious and coagulation work-up, and the close temporal relationship to cannabis ingestion strongly implicate it as the causative agent. To our knowledge, this represents the first documented case of SBBGH associated with cannabis use, thereby expanding the spectrum of its recognised cerebrovascular complications. This novel association highlights the importance of a thorough substance use history in patients presenting with ICH and underscores the need for further research into the haemorrhagic potential and underlying pathophysiological mechanisms of cannabis. Clinicians should maintain a high index of suspicion for cannabis-related vascular events, especially in young patients with atypical haemorrhagic presentations and no identifiable risk factors.

Acknowledgement

No financial help or technical assistance was taken for the purpose of this case report.

References

1.
Watanabe G, Conching A, Ogasawara C, Chavda V, Bin-Alamer O, Haider AS, et al. Bilateral basal ganglia hemorrhage: A systematic review of etiologies, management strategies, and clinical outcomes. Vol. 46, Neurosurgical Review. Springer Science and Business Media Deutschland GmbH; 2023.[crossref] [PubMed]
2.
Zhao J, Chen Z, Wang Z, Yu Q, Yang W. Simultaneous bilateral hypertensive basal ganglia hemorrhage. Neurol Neurochir Pol. 2016;50(4):275-79.[crossref] [PubMed]
3.
Singh NN, Pan Y, Muengtaweeponsa S, Geller TJ, Cruz-Flores S. Cannabis- related stroke: Case series and review of literature. J Stroke Cerebrovasc Dis. 2012;21(7):555-60.[crossref] [PubMed]
4.
Rose DZ, Guerrero WR, Mokin MV, Gooch CL, Bozeman AC, Pearson JM, Burgin WS. Hemorrhagic stroke following use of the synthetic marijuana “spice”. Neurology. 2015;85(13):1177-79.[crossref] [PubMed]
5.
Alhashim A, Hadhiah K, Al-Dandan H, Aljaman M, Alabdali M, Alshurem M, et al. Spontaneous Simultaneous Bilateral Basal Ganglia Hemorrhage (SSBBGH): Systematic review and data analysis on epidemiology, clinical feature, location of bleeding, etiology, therapeutic intervention and outcome. Vasc Health Risk Manag. 2022;18:267-76.[crossref] [PubMed]
6.
Tandon R, Verma SK, Singh N. Brainstem and thalamic haemorrhage following cannabis consumption. Vol. 94, Postgraduate Medical Journal. Oxford University Press; 2018. p. 476.[crossref] [PubMed]
7.
Aydin S, Yuksel O, Aydin A, Kizilkilic O, Celik S. Intracerebral hemorrhage with multiple intracranial arterial stenoses in a synthetic cannabinoid “Spice” user. Asian J Neurosurg. 2018;13(02):522-24.[crossref] [PubMed]
8.
Atchaneeyasakul K, Torres LF, Malik AM. Large amount of cannabis ingestion resulting in spontaneous intracerebral hemorrhage: A case report. J Stroke Cerebrovasc Dis. 2017;26(7):e138-e139.[crossref] [PubMed]
9.
Renard D, Gaillard N. Brain haemorrhage and cerebral vasospasm associated with chronic use of cannabis and buprenorphine. Cerebrovasc Dis. 2008;25(3):282-83.[crossref] [PubMed]
10.
Ince B, Benbir G, Yuksel O, Koseoglu L, Uluduz D. Both hemorrhagic and ischemic stroke following high doses of cannabis consumption. Presse medicale (Paris, France: 1983). 2015;44(1):106-07.[crossref] [PubMed]

DOI and Others

DOI: 10.7860/JCDR/2026/88094.24353

Date of Submission: Feb 08, 2026
Date of Peer Review: Apr 16, 2026
Date of Acceptance: Jun 17, 2026
Date of Publishing: Sep 01, 2026

Author declaration:
• Financial or Other Competing Interests: None
• Was informed consent obtained from the subjects involved in the study? Yes
• For any images presented appropriate consent has been obtained from the subjects. Yes

PLAGIARISM CHECKING METHODS:
• Plagiarism X-checker: Mar 04, 2026
• Manual Googling: Jun 13, 2026
• iThenticate Software: Jun 15, 2026 (1%)

ETYMOLOGY: Author Origin

EMENDATIONS: 6

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