Skip to main content
The Egyptian Journal of Neurology, Psychiatry and Neurosurgery
Download PDF

Synthetic cannabinoids impact on cognitive functions

The Egyptian Journal of Neurology, Psychiatry and Neurosurgery volume 59, Article number: 151 (2023) Cite this article

Abstract

Background

Synthetic cannabinoids SC are now becoming progressively popular among young people worldwide; little is known about their negative effects. Anger, anxiety, hallucinations, and perceptual changes were the most common psychoactive findings. Substance abuse causes cognitive impairment (CI). This study’s goal is to raise public awareness about the dangers that synthetic cannabinoid intoxication poses to public health. As well as the magnitude of CI in synthetic cannabinoids in comparison with healthy controls. The study included 30 synthetic cannabinoids SC addicts and 30 healthy people. The Wechsler memory scale (WMS), the Benton visual retention test (BVRT), and Trail Making Test (TMT) A and B were used to assess cognitive functions. Addiction Severity Index (ASI), Structured Clinical Interview for DSM-IV Axis I Disorder (SCID-I), and Structured Clinical Interview for DSM-IV Axis II Disorder (SCID II).

Results

Using BVRT, (96.7%) of the SC use disorder cases had more impaired performance than controls (0%) (P < 0.001). Almost three quarters of the cases had impaired performance on the trail making tests A and B compared to none of the controls (P < 0.001). Similarly, there was a high statistically significant difference between SC use disorder cases and controls in all domains of the WMS. There was no statistically significant correlation between the cognitive scales (BVRT, WMS and TMT) results in relation to age of SC use patients or duration of use.

Conclusions

Patients who used synthetic cannabinoids SC were more likely than controls to develop CI, which manifested as impaired visual, auditory, immediate, delayed, and working memory.

Introduction

Cannabinoids and synthetic cannabinoids (SC) are widely used psychoactive substances nowadays. In Egypt, nicotine is the most commonly used substance over lifetime (9%), followed by benzodiazepines (5.1%), alcohol (3.3%), and cannabis 3.1% [1]. Similar rates were found by Kabbash et al. (2022) [2].

Recently, newer psychoactive substances became popular in Europe and USA, and they are increasingly finding their way to other countries. Synthetic cannabinoids (SCs)—the focus of our research—is considered one of these new psychoactive substances (NPS) [3].

Synthetic cannabinoids (SCs) are a large family of chemically unrelated structures. Like Δ 9-tetrahydrocannabinol (THC), the active component of cannabis, they interact with cannabinoid receptors (CB1 and CB2) to exert their psychoactive effects [4].

Strox and voodoo are the most popular street names for SCs in Egypt [5, 6]. “Spice,” “K2,” “Black Mamba,” and “Scooby Snax” are some other brand names for these products [7, 8].

SCs use has many problems. First, due to lacking cannabidiol CBD (another component of cannabis, that reduces risk of psychosis) and due to their higher potency, SCs users are more prone to develop psychotic symptoms [9]. A second problem in SCs, is that the chemical components and compound concentrations varies between and within packages [10]. A third problem is that novel SCs have no urine metabolites. Therefore, SCs are undetectable by standard cannabis tests or immunoassays [11,12,13]. Finally, SC have a stronger affinity for CB1 and CB2 receptors than Δ THC. All leading to severer side effects than natural cannabis, for example, cardiovascular, gastrointestinal tract (GIT), neurological affection and more addictive properties [14, 15].

Toxicity of SC leads to life-threatening effects, including hyperarousal (19.1%), drowsiness (17.5%), hypertension (9.6%), nausea (9.3%), confusion (8.9%), dizziness, vertigo (8.1%), and chest pain (8.1%). SC can also cause ischemia, myocardial infarction, and tubular necrosis [16].

Moreover, SC has been linked to neuropsychiatric problems, such as seizures, psychosis, chronic insomnia, anxiety disorders, suicidal thoughts, or even catatonia [17,18,19,20].

On the long-term, emerging evidence show that SCs may cause cognitive decline, especially in executive functions, memory, and visuo-spatial skills. These findings were also associated with brain changes in SC users [21]. Miller et al. (2013) and Basavarajapp et al. (2014) found long-term potentiation (LTP) and white matter affection in the hippocampi of SC users [22,23,24]. A DTI study indicated that SC abusers have smaller corpus callosum and thalami than healthy controls [25]. In addition, another study demonstrated affection of the inferior fronto-occipital fasciculus (which regulates inhibition and attention), the temporal occipital fasciculus, and other social cognitive areas in SC users [26]. Given these widespread deleterious cognitive affections caused by SC, this study was set out to investigate the cognitive functions of SC-dependent male patients compared to healthy controls. This is one of the few studies discussing this important problem.

Methods

This is a cross-sectional case–control study. A convenient sample of 30 male patients with SC use disorder were included in the study. The study was conducted at the outpatient clinics of addiction unit of Ain Shams University psychiatry department, Okasha Institute, in the duration from October 2018 to August 2019.

Male patients aged between 18 and 45 years, fulfilling the diagnosis of SC-dependence disorder as outlined in the DSM-IV criteria, were included in the study. Only those who were only using SC as their main substance of abuse in the past 30 days were included (reported by the patient).

Thirty apparently healthy male smoker volunteers, aged between 18 and 45 years, were included as a control group; having no history of psychiatric diseases, substance use (except for smoking), or medical diseases. Controls were recruited from the employees and workers at the Institute of Psychiatry, Ain Shams University. They were matched for age to the case group.

Subjects were excluded from the study if they had any of the following conditions: chronic medical, or neurological disorders, or refused to sign consent.

The nature and scope of the study were discussed with each patient, and written informed consent was obtained. This study was reviewed and approved by the Ain Shams University ethics committee.

All eligible subjects (based on self-reports of drug use) were subjected to the following tools:

  1. 1.

    The psychiatric sheet of Ain Shams University, psychiatry department, including personal data and present psychiatric illness. In addition, an assessment of the concurrent medical conditions was done.

  2. 2.

    The Structured Clinical Interview for DSM-IV Axis I Disorder (SCID-I) was used for diagnosis of substance use disorder and any comorbid psychiatric disorder [27]. An Arabic version was used [28]

  3. 3.

    The Structured Clinical Interview for DSM-IV Axis II Disorders (SCID II) was used for diagnosis of Axis II personality diagnoses [29]. Arabic version was used [30].

  4. 4.

    Participants in the case group only were evaluated using the Addiction Severity Index (ASI), a semi-structured interview designed to serve as quantitative measure of symptom and functional impairment due to drug disorders, it covers demographics, alcohol use, drug use, psychiatric status, medical status, employment, legal status, and family and social issues. It is formed of 142 items, including yes–no, multiple-choice and scaled items [31]. Arabic version was used (5th ed.) [32]

  5. 5.

    Cognitive Assessment tests include:

  6. 6.

    Benton visual retention test-revised (BVRT) [33]: An individually administered test for people aged from 8 years to adulthood that was used for assessing visual perception, visual memory, and visuo-constructive abilities. BVRT test is considered impaired if the difference between obtained error score and expected error score > 4.

  7. 7.

    Trail Making Test (TMT) A and B [34, 35]. The test provides information on visual search, scanning, processing speed, mental flexibility, and executive functions. The score represents the amount of time required to complete tasks [36]. Impaired Scoring of TMT part, A: complete test > 98 s. Impaired Scoring of TMT part, B: complete test > 233 s.

  8. 8.

    Wechsler memory scale (WMS) [37]; It is a neuropsychological test designed to measure different memory functions. Anyone aged between 16 and 90 is eligible to take this test. The functions assessed include memory for verbal and visual stimuli, meaningful and abstract material, and delayed as well as immediate recall. It was applied by a trained psychologist. Scores of impaired WMS subscales: Information > 14, Verbal paired association I > 24, Visual paired association I > 18, Digit span > 19, Visual Memory Span > 21, Verbal paired association II > 8, Visual paired association II > 6

Statistical analysis

The processing of data was computed using statistical package for social Sciences (SPSS)-version 20 IBM (SPSS Inc., Chicago, Illinois, USA). Data were described in the form of number and percentage, and range and mean SD. To compare quantitative variables between two groups, the Student’s t test (T) was applied. Chi-square (X2) and Fisher’s exact test were used to compare qualitative variables. Pearson correlations was used to assess the strength of association between two quantitative variables. The correlation coefficient denoted symbolically ‘r’ defines the strength and direction of the linear relationship between two variables.

A P value of 0.05 or less was considered significant and P < 0.001 as highly significant.

Results

This study is a cross-sectional case–control study. During the study period, 32 met the eligibility criteria for the study: two patients refused to sign the consent, and there were no dropouts.

Table 1 shows the mean age of subjects were (23.6 ± 4.6) years for the SC group and (25.2 ± 3.9) years for healthy controls. There was a highly statistically significant difference between both as regard level of education, the SC group being less educated. In addition, more of SC group were single and unemployed.

Table 1 Demographic characteristics of the study group
Full size table

In SC use patients, the average duration of addiction was (1.5 ± 0.5) years and age of onset was around (20.9 ± 3.5) years.

Psychiatric disorders in the patients’ group are shown in Table 2, with schizophrenia being the most common (30%), followed by bipolar affective disorder (23.3%). The most common personality disorder in our sample was borderline personality disorder. Clinical characteristics of SC use disorder are shown in Table 3.

Table 2 Psychiatric disorders in the patients’ group by SCID-I and SCID-II scales
Full size table
Table 3 Clinical characteristics of synthetic cannabinoids use disorder cases using addiction severity index (ASI)
Full size table

Table 4 clarifies a high statistically significant difference between SC use disorder cases and controls in visual memory, visual reconstruction ability and processing and delayed memory using BVRT. The cases (96.7%) had more impaired performance than controls (0%) (P < 0.001).

Table 4 Comparing cognitive functions between tramadol group and healthy controls
Full size table

There was also statistically significant difference between SC use disorder cases and controls in attention and processing speed using trail making test (TMT) A and B. Almost three quarters of the cases had impaired performance compared to none of the controls (P < 0.001).

Similarly, a high statistically significant difference in visual, auditory, immediate, delayed and working memory using WMS between SC use disorder cases and controls in all domains.

Table 5 shows no statistically significant correlation between the cognitive scales (BVRT, WMS and TMT) results in relation to age of SC use patients or duration of use.

Table 5 Correlation between Benton visual retention test as well as Wechsler memory scale and trail making A and B in relation to age of SC use disorder cases and duration of use
Full size table

Table 6 shows a statistically significant correlation between (psychiatric dimension of ASI and Digit span of WMS) of SC use disorder cases. Otherwise, no significant correlations were found.

Table 6 Correlation between addiction severity index (ASI) of SC use disorder cases and BVRT, TMT A and B, as well as WMS
Full size table

Discussion

This study compared an age and sex matched 30 SC users to 30 healthy controls, to investigate SC impact on cognitive functioning. This is one of the few studies discussing this important problem in Egypt.

The study found that participants engaged in SC substance use were around 23 years of age, with average duration of use of 1–2 years. Seventy percent of patients were unemployed, and they were less educated than controls. This agrees with other studies showing that non-recreational SC users were less educated, and with lower socioeconomic status than controls [25, 38].

In our sample, 30% of the SC use patients had schizophrenia, (23.3%) had bipolar affective disorders, and MDD cases (3.3%). This is comparable with pervious literature investigating psychiatric effects of SC on users, which reported found that 44.3% had psychotic disorders, such as schizophrenia or unspecified psychotic disorder [39].

This implicates endocannabinoid receptors in psychosis. This receptor is strongly expressed in psychosis pathophysiology, cognition, and behavior [39]. Men with SC-induced acute psychosis demonstrated similar cognitive deficits to schizophrenics. SC-induced behavioral and cognitive impairments in animals mirror schizophrenia. The users also reported utilizing SC. For SCs, the most prevalent adverse effect is agitation, followed by irritability, restlessness, depression and psychomotor impairments [40].

SCID II showed 63.3% of SC users had Antisocial personality disorder APD and 95% of SC users had Borderline personality disorder BPD. Goretti et al. 2017 reported Between similar data, 65% and 90% of substance abusers have personality disorders (PD), with cluster B personality disorders occupying 46.7% [41]. BPD was extremely common about 76% and 12% APD. All this data conclude that addiction is a risk factor for Cluster B personality disorders [41].

Previously, another study included 120 Egyptian of substance abusers at the Menoufia University Hospitals’ Addiction Centre and Neuropsychiatry. Cluster B PDs and substance abuse were linked. Impulsivity and self-harm are important in cluster B PDs [42].

Using the ASI medical subscale, more than half of SC individuals experienced moderate to severe medical problems. SC use is associated with adverse effects [43]. Around 30% of the study population reported headache, 20% panic, 10% dizziness and fainting, 6% cardiovascular and respiratory symptoms, and 8% GIT symptoms. Substantial adverse effects and death connected to SCs were observed in the Midwest, Northeast, and West. About 11% of patients treated at the University of Mississippi Medical Center were admitted to general inpatient treatment, 10% to critical care services, and three died [43]. In April 2015, the Department of Mental Health reported 120 SC-related ED visits in a single week, six times gastrointestinal issues include hyperemesis [44, 45], severe rhabdomyolysis, hyperthermia, and seizures [46, 47].

Almost three-quarters of the patients had cognitive impairment, compared to none of the controls. Using BVRT, SC exhibited significantly worse performance than controls in visual memory, visual reconstruction ability, and delayed memory. In addition, SC users exhibited poor attention, delayed processing speed, visual, auditory, immediate, delayed, and working memory compared to controls in all domains. An increase in attention difficulties and psychiatric symptoms was found by ASI and WMS Digit span in SC group.

Two studies tested executive function, inhibition, and long-term memory [25, 48]. A study by Altinas et al. (2016) used the Frontal Assessment Battery (FAB) to assess differences in executive function [48]. They detected cognitive impairment in Israeli and Hungarian synthetic cannabinoid users. This impacted CBT outcomes, because SC users had impaired working and long-term memory and executive function.

Similarly, SC eaters have reported fine motor, memory, and long-term cognitive impairments [20]. Drug users’ response inhibition is slower. Psychomotor, visual–spatial and cognitive mistakes. A few case studies have been reported on SC’s effects on driving, including poor coordination, sedation, confusion, and motor skill impairment [49].

Many studies have explained this. In the hippocampus and prefrontal cortex, CB1 receptors are not surprising (WM). Strong cannabis agonists in SC products may impair WM function. Thalamus and left cerebellum of SC users had decreased grey matter [7].

Endocannabinoids and CB1R are known to be involved in many areas of central nervous system function and illnesses, such as addiction, memory, and schizophrenia [50]. CB1 receptors are involved in inflammation, glaucoma, cancer, liver, and musculoskeletal issues [51]. Studies on animals have indicated that activating CB1R improves memory and cognitive function [52].

Conclusions

Patients who used synthetic cannabinoids SC were more likely than controls to develop CI. The highly significant difference in cognitive performance between both groups invites for more meticulous wide-scaled study of this growing epidemic of SC use in Egypt. In addition, these results implicate that the assessment of cognitive impairment in this vulnerable group of patients may help in tailoring psychotherapeutic, academic, and vocational programs for these individuals.

Several important limitations should be borne in mind when interpreting these results: first, this sample may not represent all addiction treatment facilities in Egypt due to small sample size and non-random method of sampling. Second, the cross-sectional study design limits any causal inferences. Third, this clinical study included patients with drug-related problems with a high prevalence of comorbidities (specifically depression), which may constitute a potential confounder. As such, these findings await replication with a larger sample of synthetic cannabinoids use patients in a prospective study design.

Availability of data and materials

All data and materials are available upon request from the corresponding author.

Abbreviations

APD:

Antisocial personality disorder

ASI:

Addiction Severity Index

BPD:

Borderline personality disorder

BVRT:

Benton visual retention test

CBD:

Cannabidiol

CB1 and CB2:

Cannabinoid 1 and 2 receptors

CBT:

Cognitive behaviour therapy

CI:

Cognitive impairment

D2:

Dopamine receptor 2

DEA:

Drug Enforcement Administration

DSM-IV:

Criteria Diagnostic and Statistical Manual of Mental Disorders, fourth edition

DTI:

Diffusion tensor imaging

ECS:

Endocannabinoids

ED:

Emergency department

FAB:

Frontal Assessment Battery

LTP:

Long term potentiation

NPS:

New psychoactive substances

MD:

Doctor of Medicine

MDD:

Major depression disorder

PD:

Personality disorders

PET:

Positron emission tomography

SC:

Synthetic cannabinoids

SCID II:

Structured Clinical Interview for DSM-IV Axis II Disorder

SCID-I:

Structured Clinical Interview for DSM-IV Axis I Disorder

SCRAs:

Synthetic cannabinoid receptor agonists

SDAPA:

Synthetic Drug Abuse Prevention Act

THC:

Δ 9-Tetrahydrocannabinol

TMT:

Trail Making Test

WM:

Working memory

WMS:

Wechsler memory scale

References

  1. Rabie M, Shaker NM, Gaber E, El-Habiby M, Ismail D, El-Gaafary M, et al. Prevalence updates of substance use among Egyptian adolescents. MECP. 2020;27:4.

    Google Scholar 

  2. Kabbash I, Zidan O, Saied S. Substance abuse among university students in Egypt: prevalence and correlates. East Mediterr Health J. 2022;28(1):31–40.

    Article  PubMed  Google Scholar 

  3. Yeruva R, Mekala H, Lippmann S, Lippmann S. Synthetic cannabinoids-“spice” can induce a psychosis: a brief review. Innov Clin Neurosci. 2019;16(1–2):31–2.

    PubMed  PubMed Central  Google Scholar 

  4. Sobh ZK and Sobh HK. Strox (Novel Synthetic Cannabinoids) in Egypt: Medical and Legal Challenges, Department of Forensic Medicine and Clinical Toxicology, Faculty of Medicine, University of Alexandria, Egypt and Ministry of Health, Egypt; 2020.

  5. Oberbarnscheid CT, Miller NS. The impact of cannabidiol on psychiatric and medical conditions. J Clin Med Res. 2020;12(7):393–403.

    Article  Google Scholar 

  6. Department of Justice, Cairo. Voodoo and Strox: the synthetic drugs wreaking havoc in Cairo; 2018: access: 23/07/2018–13:22. https://observers.france24.com/en/20180723-voodoo-strox-drugs-cairo-egypt.

  7. Hess C. Pharmacological evaluation of synthetic cannabinoids identified as constituents of spice. Forensic Toxicol. 2016;34:329–43.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  8. Castaneto MS, Gorelick DA, Desrosiers NA, Hartman RL, Pirard S, Huestis MA. Synthetic cannabinoids: epidemiology, pharmacodynamics, and clinical implications. Drug Alcohol Depend. 2014;144:12–41.

    Article  CAS  PubMed  Google Scholar 

  9. Seely KA, Patton AL, Moran CL, Womack ML, Prather PL, Fantegrossi WE, et al. Forensic investigation of K2, Spice, and “bath salt” commercial preparations: a three-year study of new designer drug products containing synthetic cannabinoid, stimulant, and hallucinogenic compounds. Forensic Sci Int. 2013;233:416–22.

    Article  CAS  PubMed  Google Scholar 

  10. Mills B, Yepes A, Nugent K. Synthetic cannabinoids. Am J Med Sci. 2015;350(1):59–62.

    Article  PubMed  Google Scholar 

  11. Chimalakonda KC, Moran CL, Kennedy PD, Endres GW, Uzieblo A, Dobrowolski PJ, et al. Solid-phase extraction and quantitative measurement of omega and omega-1 metabolites of JWH-018 and JWH-073 in human urine. Anal Chem. 2011;83:6381.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  12. Hutter M, Moosmann B, Kneisel S, Auwärter V. Characteristics of the designer drug and synthetic cannabinoid receptor agonist AM-2201 regarding its chemistry and metabolism. J Mass Spectrum. 2013;48:885.

    Article  CAS  Google Scholar 

  13. Jang M, Yang W, Shin I, Choi H, Chang H, Kim E. Determination of AM-2201 metabolites in urine and comparison with JWH-018 abuse. Int J Legal Med. 2014;128:285.

    Article  PubMed  Google Scholar 

  14. Volkow ND, Swanson JM, Evins AE, DeLisi LE, Meier MH, Gonzalez R, et al. Effects of cannabis use on human behavior, including cognition, motivation, and psychosis: a review. JAMA Psychiat. 2016;73:292–7.

    Article  Google Scholar 

  15. Radhakrishnan R, Wilkinson S, D’Souza D. Gone to pot–a review of the association between cannabis and psychosis. Front Psychiatry. 2014;5:54.

    Article  PubMed  PubMed Central  Google Scholar 

  16. McKeever R, Vearrier D, Jacobs D, LaSala G, Okaneku J, Greenberg MI. K2-Not the spice of Life; synthetic cannabinoids and ST elevation myocardial infarction: a case report. J Med Toxicol. 2015;11:129–31.

    Article  PubMed  Google Scholar 

  17. Schep L, Slaughter R, Hudson S, Place R, Watts M. Delayed seizure-like activity following analytically confirmed use of previously unreported synthetic cannabinoid analogues. Hum Exp Toxicol. 2015;34:557–60.

    Article  CAS  PubMed  Google Scholar 

  18. Shanks K, Dahn T, Terrell A. Detection of JWH-018 and JWH-073 by UPLC-MS-MS in postmortem whole blood casework. J Anal Toxicol. 2012;36:145–52.

    Article  CAS  PubMed  Google Scholar 

  19. Nacca N, Vatti D, Sullivan R. The synthetic cannabinoid withdrawal syndrome. J Addict Med. 2013;7:296–8.

    Article  CAS  PubMed  Google Scholar 

  20. Musshoff F, Madea B, Kernbach-Wighton G, Bicker W, Kneisel S, Hutter M, et al. Driving under the influence of synthetic cannabinoids (“Spice”): a case series. Int J Legal Med. 2014;128:59.

    Article  PubMed  Google Scholar 

  21. Tomiyama K, Funada M. Cytotoxicity of synthetic cannabinoids on primary neuronal cells of the forebrain: the involvement of cannabinoid CB1 receptors and apoptotic cell death. Toxicol Appl Pharmacol. 2014;274:17–23.

    Article  CAS  PubMed  Google Scholar 

  22. Miller R, Thakur G, Stewart W, Bow JP, Bajaj S, Makriyannis A, et al. Effects of a novel CB1 agonist on visual attention in male rats: Role of strategy and expectancy in task accuracy. Exp Clin Psychopharmacol. 2013;21:416–25.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  23. Basavarajappa B, Subbanna S. CB1 receptor-mediated signaling underlies the hippocampal synaptic, learning, and memory deficits following treatment with JWH-081, a new component of spice/K2 preparations. Hippocampus. 2014;24(2):178–88.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  24. Lazarov O, Hollands C. Hippocampal neurogenesis: learning to remember. Prog Neurobiol. 2016;138–140:1–18.

    Article  PubMed  PubMed Central  Google Scholar 

  25. Cohen K, Weinstein A. The effects of cannabinoids on executive functions: evidence from cannabis and synthetic cannabinoids-a systematic review. Brain Sci. 2018;8(3):40.

    Article  PubMed  PubMed Central  Google Scholar 

  26. Hill SY, Wang S, Carter H, McDermott MD, Zezza N, Stiffler S. Amygdala volume in offspring from multiplex for alcohol dependence families: the moderating influence of childhood environment and 5-HTTLPR variation. J Alcohol Drug Depend. 2013; Suppl 1:001.

  27. First MB, Spitzer RL, Williams W, Gibbon M. Structured clinical interview for DSM-IV axis I disorders (SCID-I). In: Rush AJ, First MB, Blacker D, editors. Handbook of psychiatric measures. Washington: American Psychiatric Association; 1995.

    Google Scholar 

  28. Missiry A, Sorour A, Sadek A, Fahy T, Mawgoud M and Asaad A. Homicide and psychiatric illness: an Egyptian study [MD thesis]. Cairo, Egypt; Faculty of Medicine, Ain Shams University; 2004.

  29. First MB, Gibbon M, Williams J, Benjamine LS. Structured clinical interview for DSM-IV axis II Personality Disorders (SCID II). Washington: American Psychiatric Press; 1997.

    Google Scholar 

  30. Hatata H, Khalil A, Asaad T, Abo Zeid M, Okasha T. Dual diagnosis in substance use disorders (MD thesis). Faculty of Medicine, Ain Shams University, Cairo, Egypt; 2004.

  31. McLellan AT, Luborsky L, O’Brien CP, Woody GE. An improved diagnostic instrument for substance abuse patients: the Addiction Severity Index. J Nerv Ment Dis. 1980;168:26–33.

    Article  CAS  PubMed  Google Scholar 

  32. Qasem T, Beshry Z, Asaad T. Profiles of Neuropsychological Dysfunction in Chronic Heroine Users. MD degree thesis. Faculty of Medicine. Ain Shams University; 2003.

  33. Benton AL. Revised Visual Retention Test: clinical and experimental applications. 4th ed. New York: Psychological Corporation; 1974.

    Google Scholar 

  34. Reitan RM. Validity of the Trail Making test as an indicator of organic brain damage. Percept Mot Skills. 1958;8:271–6.

    Article  Google Scholar 

  35. Reitan RM, Wolfson D. The Halstead-Reitan Neuropsychological Test Battery: theory and clinical interpretation. South Tucson: Neuropsychology Press; 1985.

    Google Scholar 

  36. Rabin LA, Barr WB, Butler LA. Assessment practices of clinical neuropsychologists in the United States and Canada: a survey of INS, NAN, APA Division 40 members. Arch Clin Neuropsych. 2005;20:33–65.

    Article  Google Scholar 

  37. Axelrod BN. Administration duration for the Wechsler Adult Intelligence, Scale-III and Wechsler Memory Scale-III. Arch Clin Neuropsychol. 2001;16:293–301.

    Article  CAS  PubMed  Google Scholar 

  38. Hackman DA, Farah MJ. Socioeconomic status and the developing brain. Trends Cogn Sci. 2009;13(2):65–73.

    Article  PubMed  PubMed Central  Google Scholar 

  39. Bassir Nia A, Medrano B, Perkel C, Galynker I, Hurd YL. Psychiatric comorbidity associated with synthetic cannabinoid use compared to cannabis. J Psychopharmacol. 2016;30(12):1321–30.

    Article  PubMed  Google Scholar 

  40. Brewer TL, Collins M. A review of clinical manifestations in adolescent and young adults after use of synthetic cannabinoids. J Spec Pediatr Nurs. 2014;19:119–26.

    Article  PubMed  Google Scholar 

  41. Goretti S, Sanchez MDC, Borja PL, Rivera GB, Rodríguez L. The relationship between personality disorders and substance abuse disorders. Eur Psychiat. 2017;41:473–4.

    Article  Google Scholar 

  42. Drake RE, O’Neal EL, Wallach MA. A systematic review of psychosocial research on psychosocial interventions for people with co-occurring severe mental and substance use disorders. J Subst Abuse Treat. 2012;34:123–38.

    Article  Google Scholar 

  43. Cooper ZD. Adverse effects of synthetic cannabinoids: management of acute toxicity and withdrawal. Curr Psychiatry Rep. 2016;18(5):52.

    Article  PubMed  PubMed Central  Google Scholar 

  44. Hopkins CY, Gilchrist BL. A case of cannabinoid hyperemesis syndrome caused by synthetic cannabinoids. J Emerg Med. 2013;45:544–6.

    Article  PubMed  Google Scholar 

  45. Sevinc MM, Kinaci E, Bayrak S, Yardimci AH, Cakar E. Extraordinary cause of acute gastric dilatation and hepatic portal venous gas: chronic use of synthetic cannabinoid. World J Gastroenterol. 2015;21:10704–8.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  46. Takematsu M, Hoffman RS, Nelson LS, Schechter JM, Moran JH. A case of acute cerebral ischemia following inhalation of a synthetic cannabinoid. Clin Toxicol. 2014;52:973–5.

    Article  CAS  Google Scholar 

  47. Lapoint J, James LP, Moran CL, Nelson LS, Hoffman RS. Severe toxicity following synthetic cannabinoid ingestion. Clin Toxicol. 2011;49:760–4.

    Article  CAS  Google Scholar 

  48. Altintas M, Inanc L, Oruc GA. Clinical characteristics of synthetic cannabinoid-induced psychosis in relation to schizophrenia: a single-centre cross-sectional analysis of concurrently hospitalized patients. Neuropsychiatr Dis Treat. 2016;12:1893–900.

    Article  PubMed  PubMed Central  Google Scholar 

  49. Yeakel JK, Logan BK. Blood synthetic cannabinoid concentrations in cases of suspected impaired driving. J Analytic Toxicol. 2013;37:547–51.

    Article  CAS  Google Scholar 

  50. Kano M, Ohno-Shosaku T, Hashimotodani Y, Uchigashima M, Watanabe M. Endocannabinoid-mediated control of synaptic transmission. Physiol Rev. 2009;89:309–80.

    Article  CAS  PubMed  Google Scholar 

  51. Maccarrone M, Bab R, Biro T, Cabral GA, Dey SK, Di Marzo V, et al. Endocannabinoid signaling at the periphery: 50 years after thc. Trends Pharmacol Sci. 2015;36:277–96.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  52. Aso E, Palomer E, Juves S, Maldonado R, Munoz FJ, Ferrer I. CB1 agonist acea protects neurons and reduces the cognitive impairment of AβPP/PS1 mice. J Alzheimers Dis. 2012;30:439–59.

    Article  CAS  PubMed  Google Scholar 

Download references

Acknowledgements

Not applicable.

Funding

None.

Author information

Authors and Affiliations

  1. Psychiatry Department, Faculty of Medicine, Ain Shams University, 38 Abbaseya St., Cairo, Egypt

    Hanan Hany Elrassas, Yasser Abdel Razek Elsayed, Mai SeifElDin Abdeen, Aya Taha Mohamed & Zeinab Mohamed El Nagar

Authors
  1. Hanan Hany Elrassas
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Yasser Abdel Razek Elsayed
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Mai SeifElDin Abdeen
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Aya Taha Mohamed
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. Zeinab Mohamed El Nagar
    View author publications

    You can also search for this author in PubMed Google Scholar

Contributions

HHE study concept, critical revision of the manuscript, and design. YAE and ZME study concept, and design, and critical revision of the manuscript. ATM recruitment of cases, analysis, interpretation of data, writing and editing the manuscript. MSA, interpretation of data, and critical revision of the manuscript. All authors approved the final version of the manuscript.

Corresponding authors

Correspondence to Hanan Hany Elrassas or Mai SeifElDin Abdeen.

Ethics declarations

Ethics approval and consent to participate

This study was approved by the Ain Shams University Hospital Ethics Committee, on the 13th of May 2017. A written informed consent was obtained from participants/their guardians before participation in the study.

Consent for publication

Not applicable.

Competing interests

The authors declare that they have no competing interests.

Additional information

Publisher's Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Elrassas, H.H., Elsayed, Y.A.R., Abdeen, M.S. et al. Synthetic cannabinoids impact on cognitive functions. Egypt J Neurol Psychiatry Neurosurg 59, 151 (2023). https://doi.org/10.1186/s41983-023-00756-x

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: https://doi.org/10.1186/s41983-023-00756-x

Keywords