Volume 1, Issue 3 (Summer 2020)                   J Vessel Circ 2020, 1(3): 40-42 | Back to browse issues page


XML Print


Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:

Mozhdehipanah H, Gorji R. Subarachnoid Hemorrhage as a Manifestation of Magic Mushroom Abuse: A Case Report and Review Literature. J Vessel Circ 2020; 1 (3) :40-42
URL: http://jvessels.muq.ac.ir/article-1-62-en.html
1- MD, Assistant Professor, Department of Neurology, Bu-Ali Sina Hospital, Qazvin University of Medical Sciences, Qazvin, Iran
Full-Text [PDF 776 kb]   (727 Downloads)     |   Abstract (HTML)  (18251 Views)
Full-Text:   (3517 Views)
Introduction
 
Psilocybin mushrooms, known as magic mushrooms or shrooms, are classified as a polyphyletic group of fungi containing psychedelic compounds, such as psilocybin, psilocin, and baeocystin. The popularization of psilocin as a new substance for abuse was evinced worldwide by Valentina Pavlovna Wasson in early 1970 (1, 2).
Psilocybin effects appear over 20 min which mostly include nausea, vomiting, muscle weakness, cognitive and emotional changes lasting up to 6 h based on individuals’ metabolism in which the mind-altering effects could be even longer up to 8 h (3). Additionally, psilocybin is considered as a hallucinogen product altering the subjective experience of time as a result of interaction with cognitive dimensions of temporal processing via 5-HT2A receptor stimulation. There are also reports of visual, auditory, and sensory hallucinations; feelings of detachment; inability to discern fantasy from reality; spiritual experiences; and panic reactions. Notably, drug-induced psychosis could persist beyond the acute period in which the patient experiences flashbacks of previous perception impairment (3-6).
Similar to other psychedelics as lysergic acid diethylamide, the experience or trip can be positive or negative as an unpleasant experience, predominantly in higher dosages (4, 5).
This study aimed to describe a rare manifestation of magic mushroom, which is usually seen with amphetamine drugs, focusing on a
20-year-old man presenting with thunderclap headache as a result of subarachnoid hemorrhage (SAH) following magic mushroom abuse.
 
Case Report
The patient was a 20-year-old man with no significant medical history referring to the emergency department with an episode of thunderclap headache. The subject reported the consumption of an unknown quantity of mushroom in the form of tea for the first time at a party 4 h
 
 
                                                                        
 
Figure 1.  Evidence of parietal, temporal, and occipital cortical subarachnoid hemorrhage (mostly on the left side) and a thin rim in left perimesencephalic cistern subarachnoid hemorrhage without intraventricular hemorrhage
 

before admission. He noticed the strange feeling of extraordinary spiritual ability to soul summoning. Following the fantasy, theosophical ceremony, and visual hallucination of the soul summoned, suddenly he suffered a severe thunderclap headache accompanied by nausea and vomiting leading to his referral to our emergency department.
On examination, he was conscious and oriented; however, he had disorganized thought and delusion of considerable mystical ability. The vital sign evaluation revealed a blood pressure of 185/110 mmHg, pulse rate of 90, the temperature of 37°C, and respiratory rate of 16. No evidence of meningeal signs was obtained, and other systemic and neurologic assessments were unremarkable.
The patient underwent brain computed tomography (CT) without contrast, which revealed subarachnoid hemorrhage along the parietal, temporal, occipital convexities without evidence of intraventricular hemorrhage or hydrocephalus (Figure 1).
The patient was admitted to the intensive care unit and subjected to standard medical treatment. Intravenous labetalol was used to control blood pressure. The laboratory findings were all within normal limits. Subsequently, the patient underwent CT angiography which was unrevealing. Brain magnetic resonance imaging did not show a more considerable finding than the brain CT.
The neurosurgery and clinical toxicology consult were requested, which all suggested conservative treatment. In the next days, the patient improved gradually with no complaint of headache and disorganized thought. The controlled brain imaging revealed the resolution of the hemorrhage. Taking into account all considerations, the patient was diagnosed with SAH associated with magic mushroom abuse. The patient was transferred to the neurology ward and discharged with a good general condition and normal physical examination.
 
Discussion
Psilocybin mushroom is a potentially illegal substance belonging to a subclass of hallucinogens. Historical evidence suggests the consumption of psilocybin mushrooms in ancient religious rites and ceremonies over 7,000 to 9,000 years ago, which is still one of the most recreational psychedelics in the United States and Europe (6). Brande reported the hallucinogenic effect of mushrooms for the first time in 1799 and described a family who served Psilocybe semilanceata mushrooms for breakfast leading to an uncontrollable laugh in one of the members of the family (7).
In the 1960s, psilocybin mushroom was adopted in the counterculture and soon was listed as an illegal drug in 1971. Currently, they are the most commonly used psychedelics among the youth. Based on the results of a survey conducted by Hallock et al. (2012), 30 % of the participants had tried mushrooms at least once (8).
A typical trip on a moderate dose of magic mushroom (1-2.5 g) comprises a dreamy state accompanied by perceptual, emotional change, and distorted sense of time. Furthermore, such side effects as vital sign instability, nausea and vomiting, tremor, and increased tendon reflexes have been reported (3-6).
The correlation between headache and magic mushroom administration is controversial. There are reports of psilocybin-induced migraine-like headache, as the double-blind study conducted by Johnson et al, which disclosed headache as an adverse event of non-medical exposure with psilocybin. On the other hand, a few preclinical trials are suggesting a promising role of psilocybin in the treatment of cluster headache (9-11). Psilocybin increases the expression of several genes, including Iκβ-α, the main inhibitor of NFκβ. Expression of inducible nitric oxide synthase enhancing NO release is dependent on NFκβ, which is directly suppressed by psilocybin. Nonetheless, there is no convincing evidence to confirm this hypothesis as the main mechanism of headache induced by psilocybin. In addition, psilocybin might trigger headache through an increase in brainstem serotonergic activities via influence on 5-HT1A, D, 5-HT2A, C, 5-HT5, 5-HT6, and 5-HT7 receptor (12, 13).
On the other hand, SAH is a rare type
of cerebrovascular accident, which is mainly aneurysmal and accounts for 5% of strokes occurring at a relatively young age. Compared to other cerebrovascular accidents, SAH has a poorer outcome. The overall mortality rate ranges from 32%-67% with 10%–20% of patients with long-term dependence due to brain damage. Regarding the increasing rate of stroke-related deaths and disability-adjusted life years, compared to all diseases, the early diagnosis and consequent appropriate treatment are of paramount importance and special attention should be dedicated toward SAH associated with drug abuse (14-16).
To the best of our knowledge, there is no report of subarachnoid hemorrhage as a consequence of psilocybin in the literature. Our research is the first report of subarachnoid hemorrhage induced by psilocybin products.
 
Conclusion
Our report is unique as it highlights the diversity of neurologic side effects of this common substance. This research focused on subarachnoid hemorrhage as a rare manifestation of psilocybin.
 
Conflict of interest
The authors declare that they have no conflict of interests.
Type of Study: case report | Subject: vascular neurological diseases
Received: 2021/03/7 | Accepted: 2021/03/13 | Published: 2020/11/30

References
1. 1. Guzmán G. Hallucinogenic mushrooms in Mexico: an overview. Econ Bot 2008;62(3):404-12. DOI: 10.1007/s12231-008-9033-8 [DOI:10.1007/s12231-008-9033-8]
2. Rush JA. Entheogens and the development of culture: the anthropology and neurobiology of ecstatic experience. Berkeley, California: North Atlantic Books; 2013. P. 488. Link
3. Carter OL, Burr DC, Pettigrew JD, Wallis GM, Hasler F, Vollenweider FX. Using psilocybin to investigate the relationship between attention, working memory, and the serotonin 1A and 2A receptors. J Cogn Neurosci 2005;17(10):1497-508. DOI: 10.1162/089892905774597191 [DOI:10.1162/089892905774597191]
4. Samorini G. The oldest representations of hallucinogenic mushrooms in the world (Sahara Desert, 9000-7000 BP). Integration 1992;2(3):69-78. Link
5. Studerus E, Kometer M, Hasler F, Vollenweider FX. Acute, subacute and long-term subjective effects of psilocybin in healthy humans: a pooled analysis of experimental studies. J Psychopharmacol 2011;25(11):1434-52. DOI: 10.1177/026 9881110382466 [DOI:10.1177/0269881110382466]
6. Passie T, Seifert J, Schneider U, Emrich HM. The pharmacology of psilocybin. Addict Biol 2002;7(4):357-64. DOI: 10.1080/1355621021000005937 [DOI:10.1080/1355621021000005937]
7. Brande E. Mr. E. Brande, on a poisonous species of agaric. Med Phys J 1800;3(11):41-4. Link
8. Hallock RM, Dean A, Knecht ZA, Spencer J, Taverna EC. A survey of hallucinogenic mushroom use, factors related to usage, and perceptions of use among college students. Drug Alcohol Depend 2013;130(1-3):245-8. DOI: 10.1016/j. drugalcdep.2012.11.010 [DOI:10.1016/j.drugalcdep.2012.11.010]
9. Sewell RA, Halpern JH, Pope HGJ. Response of cluster headache to psilocybin and LSD. Neurology 2006;66(12):1920-2. DOI: 10.1212/01.wnl.0000219761.05466.43 [DOI:10.1212/01.wnl.0000219761.05466.43]
10. Schindler EA, Gottschalk CH, Weil MJ, Shapiro RE, Wright DA, Sewell RA. Indoleamine hallucinogens in cluster headache: results of the clusterbusters medication use survey. J Psychoactive Drugs 2015;47(5):372-81. DOI: 10.1080/02791072.2015.1107664 [DOI:10.1080/02791072.2015.1107664]
11. Johnson MW, Sewell RA, Griffiths RR. Psilocybin dose-dependently causes delayed, transient headaches in healthy volunteers. Drug Alcohol Depend 2012;123(1-3):132-40. DOI: 10.1016/j.drugalcdep.2011.10.029 [DOI:10.1016/j.drugalcdep.2011.10.029]
12. Czyrak A, Czepiel K, Mackowiak M, Chocyk A, Wedzony K. Serotonin 5-HT1A receptors might control the output of cortical glutamatergic neurons in rat cingulate cortex. Brain Res 2003;989(1):42-51. DOI: 10.1016/s0006-8993(03)03352-3 [DOI:10.1016/S0006-8993(03)03352-3]
13. Gonzalez-Maeso J, Yuen T, Ebersole BJ, Wurmbach E, Lira A, Zhou M, et al. Transcriptome fingerprints distinguish hallucinogenic and nonhallucinogenic 5-hydroxytryptamine 2A receptor agonist effects in mouse somatosensory cortex. J Neurosci 2003;23(26):8836-43. DOI: 10.1523/JNEUROSCI.23-26-08836.2003 [DOI:10.1523/JNEUROSCI.23-26-08836.2003]
14. Paybast S, Ashraf A, Sarshad H, Shakiba M, Moadabi Y. Propagating relationship of cerebral oximetric volume and the clinical outcome of recombinant tissue plasminogen activator (r-TPA) therapy on acute cerebral ischemic stroke patients. Adv J Emerg Med 2019;4(1):e7. DOI: 10.22114/ajem.v0i0.174
15. Grasso G, Alafaci C, Macdonald RL. Management of aneurysmal subarachnoid hemorrhage: state of the art and future perspectives. Surg Neurol Int 2017;8:11. DOI: 10.4103/2152-7806.198738‌ [DOI:10.4103/2152-7806.198738]
16. Aghamiri H, Paybast S, Lima BS, Mansoori B. New advances in acute ischemic stroke management. Int Clin Neurosci J 2020;7(2):55-60.‌ Link [DOI:10.34172/icnj.2020.02]

Add your comments about this article : Your username or Email:
CAPTCHA

Send email to the article author


Rights and permissions
Creative Commons License This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

© 2025 CC BY-NC 4.0 | Journal of Vessels and Circulation

Designed & Developed by : Yektaweb