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Synthetic cannabinoids are human-made mind-altering chemicals that are either sprayed on dried, shredded plant material so they can be smoked or sold as liquids to be vaporized and inhaled in e-cigarettes and other devices.


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Try out PMC Labs and tell us what you think. Learn More. Synthetic drugs contain substances that are pharmacologically similar to those found in traditional illicit drugs.

The new classes of synthetic illicit drugs can ificantly harm the brain: a neuro imaging perspective with full review of mri findings

Some of the most commonly abused synthetic drugs include synthetic marijuana, bath salts, ecstasy, N-bomb, methamphetamine and anabolic steroids. Many of them share the same chemical properties and physiologic responses with the drugs they mimic and may exaggerate the pathologic response in the brain leading to addiction.

These drugs have detrimental and often irreversible effects on the brain and primarily affect the central nervous system by two mechanisms: 1 Neural hyper stimulation via increasing activation of certain neurotransmitters norepinephrine, dopamine, and serotonin2 Cause ificant reduction in CNS neural connectivity affecting various brain regions such as the basal ganglia, hippocampus, cerebellum, parietal lobe, and globus pallidus. Furthermore these drugs sometimes have severe, life-threatening adverse effects on the human body.

A few structural MRI studies have been conducted in synthetic drug abusers to reveal the effects of these drugs on the brain parenchyma. This review article will describe the potential brain imaging findings in synthetic drug abusers as demonstrated by several case reports and the primary literature.

Synthetic drugs contain substances that are pharmacologically similar to those found in traditional illicit drugs, such as cocaine, methamphetamine, and marijuana. Some of these synthetic counterparts are available in various forms as over the counter medications and thereby easily accessible to the general population. These particular over the counter medications are sold under various names including Jazz, Scooby Snax, Spice and Bath Salts, among others. Synthetic drug abuse is a growing epidemic worldwide.

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Many of these drugs are addictive stimulants, and their repeated use causes long term or irreversible damage to dopaminergic, adrenergic and serotonergic pathways in the brain. Some of the most commonly abused synthetic drugs include synthetic marijuana, bath salts, ecstasy, N bomb, methamphetamine and anabolic steroids. Furthermore these drugs sometimes have severe, life-threatening adverse effects on the human body, including triggering seizures, cardiac arrhythmias, acute infarction, and even sudden death.

In the meantime, recent advances in medical imaging have made it easy to study the brain parenchyma with great detail.

Evaluate the effect of commonly abused new synthetic drugs on the brain based on abnormal findings detected by Magnetic Resonance Imaging MRI. On average the US market introduces five synthetic drugs every month, which means 60 different names in a year. Synthetic marijuana has grown into the second most commonly abused drug among young males.

Synthetic cannabinoids are a combination of herbs and spices with similar effects as marijuana; however, they can be four times as potent. This drug is usually spread on herbal material before being smoked, usually in ts or pipes. This chemical regulates and binds more strongly to the same brain receptors as deltatetra hydro cannabinol THCthe psychoactive component in marijuana, which may for its stronger and more unpredictable effects.

Its psychological effects are analogous to those of marijuana including altered perception, paranoia, excessive anxiety, violent behavior and suicidal thoughts [ 2 ]. studies have found that chronic marijuana users present with a decreased brain volume in the orbito frontal cortex OFCa brain region that is related to addiction, but otherwise demonstrate increased brain connectivity [ 3 ]. Yet, limited research has been performed on the effect of synthetic cannabinoids on the brain. Especially, there are few records revealing MRI findings in patients under the influence of synthetic cannabinoids in the acute setting.

Few studies available to date have demonstrated abnormal restricted diffusion involving large portions of vascular territories or, alternatively, presenting in an embolic pattern. For instance, a prior case report about two women ages 22 and 26 with stroke like symptoms hours after having consumed synthetic marijuana demonstrated an extensive area of acute infarction within the middle cerebral artery vascular territory. Similarly, another study presenting 19 and 26 year old siblings that had used synthetic cannabis revealed multi-embolic acute infarcts within the middle cerebral artery vascular territory.

Yet, a case of a 50 year old male that was found unconscious after synthetic cannabis use the night prior to presentation demonstrated a bilateral symmetric pattern of abnormal diffusion restriction on MR diffusion imaging involving many regions of the brain, not limited to a single vascular territory.

The fact that this patient did not have other clinical manifestations or causes of embolic stroke to support these MRI findings may sustain the hypothesis that synthetic marijuana can result in direct neurotoxicity, presumably by affecting mitochondrial function similar to tetrahydrocannabinol THC [ 4 ]. This pattern is that of a global hypoxic ischemic injury. Other MRI findings reported in a 24 year old male with a first time seizure after Spice use included diffuse sulcal FLAIR hyper intensity as well as leptomeningeal enhancement on post contrast imaging Figure 3.

The spice of death: the science behind tainted “synthetic marijuana”

Such findings denote how important it is for medical physicians to consider synthetic marijuana intoxication in the differential diagnosis of a first time seizure. Identification of the aforementioned imaging findings can also be valuable for early diagnosis of synthetic marijuana toxicity, which has become an increasing issue in the emergency setting [ 5 ]. Initial T1-weighted post-contrast image shows diffuse leptomeningeal enhancement middle image. These synthetic drugs stimulate the central nervous system by inhibiting the reuptake of norepinephrine and dopamine damage to severe CNS adverse effects or even death.

Their symptoms include insomnia, depression, suicidal ideation, seizures and panic attacks as well as tachycardia that could lead to myocardial infarction heart attack and stroke. Bath salts have similar effects to other CNS stimulants such as cocaine, which is known to induce acute intraparenchymal and subarachnoid hemorrhage as well as ischemic infarction [ 2 ]. Kramer et al. Kramer, et al. In a animal research study, functional magnetic resonance imaging fMRI of male rat brains showed ificant reduction of neural connectivity, especially between the frontal cortex and striatum, including connectivity between the prelimbic prefrontal cortex and other frontal cortical regions and the insular cortex from the spice, ventral and hypothalamic striatal brains, after administration of one dose of MDPV Methylenedioxypyrovaleroneone of the most potent bath salts.

A similar disruption of brain functional connectivity has been observed in patients with psychosis and associated with cognitive dysfunction, visual and auditory hallucinations.

How harmful is k2/spice (synthetic marijuana or synthetic cannabinoids)?

These findings suggest that disruption of such neural connectivity could contribute to the harmful effects of MDPV. Sequential direct imaging of these brain alterations may represent a potential marker for future development of treatment for bath salts intoxication and understanding of their detrimental effect in humans [ 8 ].

It affects the brain by increasing the activity of dopamine, norepinephrine and serotonin. However, compared to methamphetamine, MDMA causes a greater release of serotonin, but a lesser release of dopamine.

This relative excess in serotonin release may for the mood elevating effects seen in MDMA users. Subsequent depletion in brain serotonin reserve may be involved in the long-lasting depression, confusion, and selective injury in working memory and attention activities seen in chronic MDMA users.

Imaging findings in ecstasy users include alterations in brain activity in areas that have a role in emotion, cognition and motor function, which corresponds to their euphoria, distorted perception of time and increased motor activity. Ecstasy is primarily administered orally [ 9 ]. A prior study by Watkins et al. Particularly, the right superior parietal lobule and left precuneus exhibited the highest activation including regions within Brodmann Areas 7, 39 and Such ificant findings were not found within the left hemisphere. This may indicate the right hemisphere could be more vulnerable to the prolonged neurophysiological brains observed after ecstasy use.

This study supports prior records associating lifetime use of ecstasy with disrupted functional neural connectivity. Congruent findings have been demonstrated in Alzheimer patients during semantic object naming activity. Additionally, the behavior of ecstasy polydrug users was not affected in the face of increased brain activity, which supports the hypothesis that ecstasy polydrug users have decreased cortical efficacy in the process of semantic encoding, probably due to neurotoxicity of 5-HT by ecstasy.

A possible drawback of the aforementioned study was the difference in polydrug exposure between subjects and controls. Additionally, unrecognized factors, such as socioeconomic, genetic or environmental, other than ecstasy could have played a role on the observed MRI findings.

Further studies on brain activity are encouraged to support these findings and identify from this augmented cortical damage after ecstasy use has ificant clinical implications, such as cognitive decline, seizures or lower excitability threshold, and whether similar alterations in brain activity are observed after incident MDMA use [ 10 ]. These findings agree with those of studies proposing that the globus pallidus is especially susceptible to the spices of ecstasy [ 11 ].

What are synthetic cannabinoids?

N-bomb is another phenethylamine with potent central nervous system stimulant and hallucinogenic properties mimicking LSD or mescaline a hallucinogen derived from a cactus plant that acts as a full agonist of the serotonin receptor, 5-HT 2A.

Some of its adverse effects include confusion, agitation, seizure, hyperpyrexia, clonus, visual and auditory hallucinations, rhabdomyolysis and even death. It is more commonly administered via the oral or sublingual route [ 12 ]. LSD users have shown decreased connectivity within brain networks and increased connectivity between brain networks that do not usually interact on brain fMRI. Particularly, the visual cortex has exhibited more communication with other brain regions, ing for the vivid hallucinations experienced by LSD users [ 13 ].

Yet, N-bomb may have a permanent deleterious effect on the central nervous systems as suggested by a case study of a year-old boy presenting with seizure like activity and hallucinations, severe ataxia, left sided weakness, difficulty with activities of daily living and higher executive dysfunction after ingesting N-bomb about 18 months prior to his admission.

Even though there are few treatment options, prompt recognition of cerebral structural alterations by this drug as demonstrated by MRI could hasten rehabilitation depending on the extent of damage [ 14 ]. Ketamine is a dissociative anesthetic with some hallucinogenic properties that cause dissociation, sedation, hallucinations and amnesia.

It is available in powder or liquid form and is usually injected, mixed into drinks, snorted or smoked by young adults [ 1 ]. Chronic ketamine use causes damage to many organs such as the brain.

Yet there is only one study documenting brain changes via MRI in 21 chronic ketamine addicts of 0. Such changes included cortical atrophy in the frontal, parietal or occipital cortices. The initial lesions on T2-weighted imaging appeared as patchy hyper intense foci throughout the subcortical white matter after only one year of ketamine addition Figure 6. By 3 years of addiction, these lesions extended into the internal capsule.

After 4 years of addiction, similar hyper intense foci appeared to spread to the more inferior cerebral hemispheres, cerebellum, and the brainstem. During this period, areas of abnormal diffusion restriction correlated with FLAIR hyper intensities in the insula and parahippocampal gyrus. Yet, after 5 years of addiction, al abnormality involving the parahippocampal gyrus was also evident. By 6 years, the striatum exhibited hyper intense lesions. After 7 years of addiction, cortical atrophy had extended to the frontal, parietal and occipital regions.

One of the patients of this study was taking ecstasy and amphetamine in addition to ketamine and showed early cortical atrophy involving the rectus gyri after only 0. Similar findings were observed in another patient that had consumed a high dose of ketamine 3 g per during 3 years.

In the rest of the patients, lesions in the midbrain appeared after 7 years of addiction. The aforementioned lesions persisted after 10 to 12 years Table 1.