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and Therapeutic Potential on Effects CBD, Sciatica, Current Research

melanzhelad
18.06.2018

Content:

  • and Therapeutic Potential on Effects CBD, Sciatica, Current Research
  • Cannabinoid Study Shows CBD can reduce Sciatica
  • What is Sciatica?
  • Get the latest news on health and wellness delivered to your inbox! . Side effects of CBD include nausea, fatigue and irritability. .. This has dramatically limited the potential for real research by real scientists to be conducted. my sacrum and sciatic nerve and whilst the chemo and radiotherapy saved my. Endocannabinoids: A Promising Impact for Traumatic Brain Injury important areas of basic research and potential therapeutic interest to treat TBI. Current treatment of major TBI is primarily managed through surgical As such CBD may be a promising future avenue of investigation in the study of. Cannabidiol Is a Potential Therapeutic for the Affective-Motivational . The present study therefore evaluates the effect of CBD, injected either .. injury of the sciatic nerve, but not an acute oral dose of CBD (20 mg/kg).

    and Therapeutic Potential on Effects CBD, Sciatica, Current Research

    Over the years the pain has gradually worsened to the point I considered surgery. There have been days I felt like I'm being punched in the junk and other days it was challenging to even walk. While I appreciate my primary care physician, he hasn't been the help I was searching for. Cortisone shots are effective for a few weeks.

    Muscle relaxers don't work and only make me feel like a zombie. Stretching is beneficial but doesn't alleviate the pain. It wasn't until I started exploring cannabis infused products that I discovered relief. Fortunately a friend of mine introduced me to a THC infused lotion from Apothecanna. At the time, this was the only product that could provide me any form of sciatic pain relief. The problem is you can't get the THC infused lotion anywhere.

    It's only available in states where medical marijuana or adult use is legal. It's because of this challenge I turned to CBD. Only surgery is seems to be the option for complete treatment. However, CBD can provide pain free days and much needed relief. How does this work? CBD is a molecule that binds with the CB1 and CB2 receptors in your endocannabinoid system , a system responsible for communicating "good and bad signals" throughout your body.

    When CBD attaches itself to these receptors, it can change the bad signal to a good one, restoring balance or homeostasis in your body. Cannabinoids have been shown to help your body heal from a variety of health issues.

    CBD is a cannabinoid that helps fight inflammation and pain. This is why CBD can help sciatica pain. Currently there's not enough medical research on treating sciatica with cannabis. The good news is anecdotal evidence is promising! It's important to state you should consult with your physician before changing any medications or using CBD with current medications.

    The two best CBD infused products are listed below. CBD tinctures are oils you place under your tongue, hold for seconds, and swallow. The CBD oil will enter your bloodstream and eventually provide you with relief. I recommend at least a mg tincture due to the strength of the CBD. Start with a lower dosage half a dropper and increase from there.

    Since cannabinoids affect each person differently, be sure to keep on a daily regiment until you find your proper dosage. CBD topicals are lotions or salves you rub onto the affected part of your body. While topicals won't provide long lasting relief, they can provide immediate relief -- usually up to two hours. Effective TBI drug therapies have yet to be proven, despite promising preclinical data Lu et al. The many biochemical events that occur in the hours and months following TBI have yielded preclinical studies directed toward a single injury mechanism.

    However, an underlying premise of the present review is an important need to address the multiple targets associated with secondary injury cascades following TBI. A growing body of published scientific research indicates that the endogenous cannabinoid endocannabinoid; eCB system possesses several targets uniquely positioned to modulate several key secondary events associated with TBI.

    Here, we review the preclinical work examining the roles that the different components of the eCB system play in ameliorating pathologies associated with TBI. Cannabinoid now more generally refers to a much more broad set of chemicals of diverse structure whose pharmacological actions or structure closely mimic that of plant-derived cannabinoids.

    Three predominant categories are currently in use; plant-derived phytocannabinoids reviewed in Gertsch et al. These three broad categories of cannabinoids generally act through cannabinoid receptors, two types of which have so far been identified, CB 1 Devane et al.

    CB 1 receptors mediate most of the psychomimetic effects of cannabis, its chief psychoactive constituent THC, and many other CNS active cannabinoids. These receptors are predominantly expressed on pre-synaptic axon terminals Alger and Kim, , are activated by endogenous cannabinoids that function as retrograde messengers, which are released from post-synaptic cells, and their activation ultimately dampens pre-synaptic neurotransmitter release Mackie, Acting as a neuromodulatory network, the outcome of cannabinoid receptor signaling depends on cell type and location.

    CB 1 receptors are highly expressed on neurons in the central nervous system CNS in areas such as cerebral cortex, hippocampus, caudate-putamen Herkenham et al. The abundant, yet heterogeneous, distribution of CB 1 and CB 2 receptors throughout the brain and periphery likely accounts for their ability to impact a wide variety of physiological and psychological processes e. Another unique property of the eCB system is the functional selectivity produced by its endogenous ligands.

    Traditional neurotransmitter systems elicit differential activation of signaling pathways through activation of receptor subtypes by one neurotransmitter Siegel, However, it is the endogenous ligands of eCB receptors which produce such signaling specificity.

    Although several endogenous cannabinoids have been described Porter et al. Additionally, their receptor affinity Pertwee and Ross, ; Reggio, and efficacy differ, with 2-AG acting as a high efficacy agonist at CB 1 and CB 2 receptors, while anandamide behaves as a partial agonist Hillard, a. As such, cannabinoid ligands differentially modulate similar physiological and pathological processes. The availability of pharmacological inhibitors for eCB catabolic enzymes has allowed the selective amplification of anandamide and 2-AG levels following brain injury as a key strategy to enhance eCB signaling and to investigate their potential neuroprotective effects.

    Endocannabinoid system cell localization by CNS cell type. Cellular level changes in eCB biosynthetic and catabolic enzymes as a result of brain injury have yet to be investigated, though morphological and molecular reactivity by cell type is well documented.

    Historically, cPLA2 was considered to be the primary rate-limiting enzyme in AA production reviewed in Buczynski et al.

    As such, 2-AG functions not only as an endogenous CB1 and CB2 receptor ligand, but also an immunomodulator by virtue of its being a major precursor for AA, making it a versatile target for the treatment of TBI related pro-inflammatory pathologies.

    Understanding the biosynthesis mechanisms of eCBs may prove useful in modulating their entry into pro-inflammatory pathways. Arrows represent known TBI-induced changes in eCBs, catabolic and downstream enzymes, and their metabolic products arrow size has no relation to magnitude of change.

    Traumatic brain injuries are heterogeneous in their etiology, clinical presentation, severity, and pathology. The sequelae of molecular, biochemical, and physiological events that follow the application of an external mechanical force produce interacting acute and delayed pathologies, described as primary and secondary injuries.

    The initial insult produces an immediate mechanical disruption of brain tissue Reilly, This primary injury consists of contusion, blood vessel disruption and brain oedema, localized necrotic cell death, as well as diffuse axonal injury producing degeneration of cerebral white matter Adams et al.

    Secondary injury mechanisms are initiated within minutes, in which necrotic and apoptotic cell death in contused areas and pericontusional penumbra continue over a period of days to months Raghupathi, Neuronal disruption spills excitatory amino acids into the interstitial space, producing glutamate-mediated excitotoxicity Bullock et al.

    Injury-induced activation of CNS resident glial cells, microglia, as well as recruitment of circulating inflammatory cells, e. Increased intracranial pressure leads to reductions in cerebral blood flow Shiina et al. Extracranial pathologies are also evident following TBI with pulmonary complications being the most common Pelosi et al. NPE often develops early after brain injury, producing hypoxemia and further aggravating secondary brain injury Brambrink and Dick, ; Oddo et al.

    These varied and interacting disease processes highlight the necessity to address the multiple targets associated with secondary injury cascades following TBI. While there are many types of CNS injury models [e. Arai and Lo, ; Titomanlio et al. While basal anandamide and 2-AG levels differ within various structures in the CNS, levels increase on demand in response to a given stimuli [e.

    Consequently, eCB signaling is enhanced by a stimulus-response synthesis and release mechanism. Endocannabinoid levels increase in selected CNS tissue following neuronal damage, which may reflect a self-neuroprotective response. NMDA excitotoxicity produces elevations of anandamide in ipsilateral cortex of rats by 4-fold at 4 h and fold at 24 h, but with no changes in 2-AG levels Hansen et al.

    Concussive head trauma in rats produces a similar pattern of findings in which modest increases of anandamide levels occur in ipsilateral cortex, and again with no change in 2-AG levels Hansen et al.

    This pattern was replicated by Tchantchou et al. In contrast, Panikashvili et al. A lack of studies systematically investigating the consequences of TBI on changes in eCB levels in specific brain regions perhaps point to the difficulty in measuring changes in the volatile eCBs, prone to rapid degradation Deutsch and Chin, ; Dinh et al. While pharmacological and genetic manipulations of the eCB system continue to be evaluated following TBI; full characterization of how eCB biosynthetic and degradative enzymes, receptors, and endogenous ligands, their precursors and catabolic products, change as a consequence of TBI remains to be fully illuminated.

    Traumatic brain injury-induced neuronal loss occurs almost immediately as necrotic cell death and continues for months following the initial insult via both necrotic and apoptotic cell death Raghupathi, From a traumatic insult, the initial contused area forms a regional primary lesion or infarct surrounding which is the pericontusional penumbra, the area immediately adjacent to the primary lesion and at risk for further neurodegeneration.

    The evolution of the pericontusional penumbra occurs largely due to secondary injury mechanisms and has long been considered a candidate for interventions to protect against, or salvage from, further injury Wang et al. The investigation of cannabinoids on traumatic CNS cell death have thus far demonstrated efficacy in two areas; attenuated neurodegeneration and reduced lesion volume.

    Neurodegeneration, commonly measured by reductions in the neuronal marker fluoro-jade C, has been found to be readily attenuated in mice by CB 2 receptor agonists Amenta et al. Additionally, FAAH inhibitors produce reductions in lesion volume, and increased production of the heat shock proteins Hsp70, known to be structurally protective, and Hsp72, a negative regulator of apoptosis Tchantchou et al. A CB 1 receptor antagonist attenuated the protective effects on lesion volume, while CB 1 and CB 2 receptor antagonists prevented the protective effects on neurodegeneration Tchantchou and Zhang, Combined, this evidence suggests that inhibitors of eCB hydrolysis offer protection against TBI-induced cell death which involve CB 1 and CB 2 receptors, though the distinction between the eCBs remains to be clarified.

    One study using a model of cerebral focal ischemia found that exogenously administered anandamide and 2-AG in combination reduced infarct size in rats, but with no facilitatory effects beyond anandamide or 2-AG alone Wang et al.

    Previous efforts to attenuate the effects of excitotoxicity following brain injury focused on NMDA receptor antagonists, presumably with the understanding that the induction of depressed NMDA receptor function would counteract TBI-induced excitotoxicity. This class of drugs showed promise in laboratory animal models of TBI Shohami et al. Research investigating manipulations of the eCB system on glutamatergic functioning following TBI have thus far focused primarily on 2-AG, and paradoxically, its effectiveness to protect the integrity of glutamate receptor function.

    Both findings were completed 30 days post injury Zhang et al. However, little overlap is found between receptor expression endpoints across papers. In an example of contradictory patterns of GluA1 expression after injury, GluA1 expression was reduced in a study that subjected mice to a daily mild CHI on three consecutive days Zhang et al.

    Endocannabinoids are known to depress glutamate release from pre-synaptic terminals, and in particular, 2-AG has been explored in its ability to influence the functioning of electrochemical neurotransmission. MAGL inhibition has been found to protect against injury-induced increases in frequency and amplitude of EPSC in pyramidal neurons at the site of injury Mayeux et al. Finally, the excitotoxicity resulting from TBI is part of the sequelae of events that lead to release of damaging ROS.

    Antioxidants are known to prevent oxidation of free radicals and thus protects against the cellular damage in response to sudden ROS elevation. Combined, these data suggest that MAGL represents a promising target to reduce the damaging effects of injury-induced excitotoxicity through complimentary molecular pathways. Hydrolytic enzymes of anandamide and 2-AG produce a shared metabolic product in the formation of free AA, the major substrate of the biosynthetic enzymes of pro-inflammatory eicosanoids Nomura et al.

    Therefore, eCB oxidation not only produces inactivation at cannabinoid receptors, but also leads to the production of bioactive lipids involved in inflammatory responses during the early stages of injury. Manipulations of the eCB system have proved effective in downregulating inflammation in many experimental models, such as inflammatory pain Ahn et al. The use of cannabinoids following TBI have thus far been linked to two predominant features of inflammation; decreased inflammatory cell activation, and decreases in pro-inflammatory cytokine production.

    Pro-inflammatory activated microglia are known to exacerbate TBI-induced neuroinflammation Kigerl et al. Thus, decreasing TBI-inductions of inflammatory cell activation is an attractive treatment strategy. A parsimonious explanation for these findings is that prevention of 2-AG hydrolysis leads to reduced levels of AA and concomitant reductions of pro-inflammatory mediators. Given the contribution of 2-AG catabolism to eicosanoid production, it is unsurprising that several studies have reported eCBs as demonstrating pro-inflammatory roles, some examples of which include models of nephropathy Mukhopadhyay et al.

    Most of such pro-inflammatory effects are attributed to 2-AG and not anandamide, likely due to its considerable abundance over anandamide. Thus, a need exists to disentangle the potential contributions of 2-AG to pro-inflammatory processes from its role as a substrate for AA production, versus anti-inflammatory effects through cannabinoid receptors, following TBI.

    Inhibition of eCB degradative enzymes has also produced decreases in TBI-induced pro-inflammatory mediators. Reductions in the expression of inducible enzymes that trigger eicosanoid production following brain injury, COX-2 enzyme which converts free AA to prostaglandins and iNos which produces the free radical nitric oxide in response to cytokine signaling , are seen in response to ABHD6 inhibition Tchantchou and Zhang, and FAAH inhibition Tchantchou et al.

    These findings seem counter-intuitive given the possibility of the rapid oxidation of 2-AG and its consequent contribution to eicosanoid production. However, exogenous 2-AG has also been shown to ameliorate TBI-induced transactivation of the nuclear factor NF-kB linked to cytokine production in wild type mice, but not in CB 1 knockout mice, suggesting that CB 1 receptors mediate the protective effects of exogenous 2-AG Panikashvili et al.

    The blood vessels which carry oxygen rich blood to the brain are lined by endothelial cells as well as astrocytes. These cells, combined with specific transport proteins and enzymes, strictly regulate movement between the general circulation and CNS extracellular fluid, and are collectively known as the BBB. TBI has been well documented in producing cerebral blood flow pathology Kelly et al. Given that cannabinoids are known to exert vascular effects, producing vasodilation as well as hypotension reviewed in Hillard, b , their manipulation may hold promise as protectants against cerebrovascular damage.

    Exogenous administration of 2-AG Panikashvili et al. However, Panikashvili et al. The mechanism by which 2-AG acts as a protectant of BBB integrity following traumatic insult is yet to be resolved. While the mechanism underlying the structural protection of the BBB was not explored following TBI, anandamide has been found to decrease BBB permeability in a model of ischaemic stroke by transient receptor potential cation channel, subfamily V, member 1 TRPV1 Hind et al.

    The exploration of how anandamide may be exerting its protective effects of BBB integrity may yet yield further novel targets for the treatment of TBI. In cerebral circulation, CB 1 receptor activation produces vasodilation. Indeed, the CB 1 receptor antagonist rimonabant inhibited hypotension induced by endotoxin shock and hemorrhagic shock, as well as increasing survival Varga et al. Though cannabinoids are yet to be explored in the context of TBI-induced changes in cerebral blood flow, CB 1 receptor antagonism may prove to be a potential target for the treatment of TBI-induced hypotension.

    The key biological idea that structure dictates function also holds true for the neurophysiology of TBI. The use of cannabinoids has thus far been linked to protection against several of the CNS structural changes associated with TBI, with 2-AG being the most frequently studied eCB in this area. While a traumatic insult can result in the rapid onset of cerebral oedema, exogenously administered 2-AG protects against TBI-induced oedema Panikashvili et al. Changes in protein physiology have also been found to occur following TBI.

    These proteins are thought to accumulate from damaged axons and as a result of a disturbed balance between genesis and catabolism Johnson et al. MAGL inhibition also decreases astrocyte activation Mayeux et al. These consistent protective effects of 2-AG across varied TBI-related structural pathologies point to its important role in maintaining cell structure and promoting remodeling.

    Protective roles played by anandamide in injury-induced structural changes are yet to be ascertained. Furthermore, eCBs may not be working alone to offer protection from TBI-induced structural impairments.

    These findings suggest that the regulatory activity of the eCB receptors in response to TBI may be mediated by endocrine as well as paracrine signaling mechanisms. Traumatic brain injury is well described to increase CB 1 and CB 2 receptor expression, which includes disruption of diurnal rhythms of CB 1 receptor expression Martinez-Vargas et al.

    Post-injury treatment with a CB 1 receptor antagonist reduces CB 1 receptor expression at 6 weeks following injury Wang et al. The exact CNS circuits involved in NPE have yet to be identified, though a sudden rise in intracranial pressure, rapid sympathetic surge, increased systemic vascular resistance and increase in hydrostatic pressure in the pulmonary vasculature, as well as release of pro-inflammatory mediators may all contribute to interstitial pulmonary oedema formation Brambrink and Dick, While at the present time there are no studies evaluating the contributions of, or protection by, the eCB system to NPE following TBI, this may prove an interesting area of future investigation.

    Specifically, the lung possesses a basal tone of 2-AG Avraham et al. The heterogeneous clinical presentation of TBI pathology in populations of survivors is reminiscent of its cellular and molecular pathophysiology described above. Most frequently investigated measures in the pre-clinical TBI literature include neurological motor, and learning and memory impairments, leaving a wide breadth of TBI clinical effects yet to be studied.

    Once again, components of the eCB system may become active to compensate for TBI symptomology given what is currently known of its regulatory effects within these areas, two examples being pain, and anxiety and depression Corcoran et al.

    Learning and memory impairments are among the most frequently reported symptoms following TBI, and are slow to recover with deficiencies reported 10 years later Zec et al. The eCB system has been shown to play a well-documented role in memory regulation reviewed in Mechoulam and Parker, , and as such its manipulation holds considerable promise to address such a profound consequence of TBI.

    The protective effects of 2-AG appear to be task specific, with ABHD6 inhibition showing learning and memory protection in a Y-maze task, but not a Morris water maze task.

    To date, only a Y-maze task has been used to evaluate the memory protective effects of FAAH inhibition, and this task-specific effect did not occur with a MAGL inhibitor. Mice are a well-used pre-clinical model organism to study the memory effects of TBI; however, they are known to perform behavioral tasks more readily, and with less error, when the task does not rely on aversive motivation Stranahan, This attribute of mice may, in some part, contribute to the task-related differences seen between the Y-maze task which uses exploratory behaviors associated with novelty and the aversively motivated escape behavior necessary in the Morris water maze.

    Moving forward, the use of behavioral tasks able to selectively assess such frontal lobe-type memory impairments might improve the translational capacity of eCB TBI pre-clinical assessments one such example being the Morris water maze Reversal Task, which evaluates cognitive flexibility. Traumatic brain injury-induced neurological motor impairments currently represent the most frequently studied behavioral outcome measure in the TBI-cannabinoid literature.

    In clinical populations, neurological motor impairments seen as a result of TBI show spontaneous improvement over time, but one third of patients continue to experience neuromotor abnormalities 2 years after injury Walker and Pickett, A variety of eCB system manipulations have thus far been found to be protective against the neurological motor deficits associated with murine models of TBI.

    Both 2-AG and anandamide elevation provide protection against TBI-induced neurological motor deficits. MAGL inhibitors Zhang et al. FAAH inhibition has produced mixed findings in neurological motor tests, such as beam-walk deficit protection Tchantchou et al. In support of anandamide being protective against TBI-induced motor deficits, exogenous anandamide has also produced improved NSS performance Martinez-Vargas et al.

    The involvement of the CB 2 receptor is further supported by rotarod deficit protection from a CB 2 receptor agonist Amenta et al. The role of entourage effects has also been evaluated in the area of TBI-induced neurological motor impairments. Co-release of endogenous fatty acid derivatives can potentiate 2-AG signaling, termed an entourage effect Ben-Shabat et al. Given FAAH is responsible for the degradation of various fatty acid amides in addition to anandamide Boger et al.

    Thus any inferences drawn about anandamide through the use of FAAH inhibition needs to consider contributions of non-cannabinoid fatty acid amides. The signs of post-traumatic anxiety have been difficult to replicate in murine models of TBI Tucker et al. Also, as there is a limited number of studies evaluating eCBs in this area, no definitive conclusions can be made.

    Thus far, only FAAH inhibition has been explored to address post-traumatic anxiety, and was found to protect against TBI-induced increases in anxiety-like behavior in mice Tchantchou et al.

    This protection in the zero maze was unaffected by either CB 1 or CB 2 receptor antagonists, suggesting that these receptors are dispensable. Modeling post-traumatic epilepsy is time consuming and faces other challenges such as a low percentage of animals that develop epilepsy Mazarati, , however, recent models that produce consistent replication of spontaneous seizure activity following a TBI are available Ping and Jin, Contrary to preclinical research demonstrating that the eCB system plays a protective roles against seizures Wallace et al.

    This nascent body of data, suggests that eCB manipulations hold promise to treat injury-induced clinical symptoms outside of the more popular areas of learning and memory and neurological motor impairments. Although currently well over one hundred phytocannabinoids have been elucidated from the Cannabis sativa plant Elsohly et al. The investigation of phytocannabinoids on TBI pathology not only holds topical relevance, but also but also holds promise as potential treatment for TBI and other disorders.

    However, clinical and pre-clinical findings provide evidence suggesting that the primary psychoactive constituent of Cannabis sativa , THC, is neuroprotective when administered prior to a traumatic insult.

    In a 3 year retrospective study of patients who had sustained a TBI, urine toxicology screen results showed decreased mortality in individuals with a positive THC screen Nguyen et al. In two mouse models of CNS injury that yield cognitive deficits, pentylenetetrazole an excitotoxic agent and carbon monoxide induced hypoxic injury, prior administration of THC provided impairment protection Assaf et al.

    Curiously, an extraordinarily a low dose of THC i. The authors explained this effect through the known biphasic effects of THC producing analgesia, acute hypothermia, and decreased locomotion at high doses 10 mg. Such low dose effects of THC have been found to potentiate calcium entry into cells in vitro Okada et al.

    Therefore, Assaf et al. Moreover, the molecular signaling cascades behind cardiac and cerebral ischaemia preconditioning include activation of ERK and Akt Dirnagl et al.

    As such, individuals may experience very low plasma THC concentrations for prolonged periods after each application. This presumed prolonged exposure of THC due to its pharmacokinetics, as well as other potentially neuroprotective cannabinoids, such as CBD Perez et al.

    A finding of increased clinical relevance, is that post-conditioning when the mildly noxious stimulus is applied after the insult with low dose THC also produced cognitive sparing effects in mice Assaf et al. These findings, however, remain controversial, and are yet to be replicated in animal models of TBI. The phytocannabinoid CBD, currently being investigated in clinical trials for its seizure reduction potential in Tuberous Sclerosis Complex Gw Research Ltd, , has known anti-inflammatory properties.

    As such CBD may be a promising future avenue of investigation in the study of neuroinflammation in response to brain injury. The eCB system, through release of its endogenous ligands or by changes in cannabinoid receptor constitutive activity, possesses promise in the treatment of diverse TBI pathology.

    An important step forward in understanding the role that the eCB system plays in TBI pathology includes not only the full characterization of ligands targeting cannabinoid receptors and eCB regulating enzymes, but also changes in cannabinoid receptors, eCB levels, and eCB regulating enzymes as a consequence of TBI.

    So too do the plant-derived phytocannabinoids represent an understudied yet promising group of compounds given the neuroprotective results obtained from other types of CNS injury. In particular, CBD as well as other phytocannabinoids which do not bind cannabinoid receptors, represent promising molecules to treat TBI. To date, the only reported cannabinoid to be specifically evaluated for the treatment of TBI in patient populations is Dexanabinol, also known as HU Although HU has been described as a cannabinoid by virtue that it is an enantiomer of the potent synthetic cannabinoid agonist HU, it does not bind or activate cannabinoid receptors.

    This therefore brings to light an important consideration of the classification of cannabinoids. One consistently overlooked area across the study of TBI is the evaluation of the central penetration of systemically administered drugs. Pharmacological treatments will need to be assessed for their ability to cross the BBB.

    Furthermore, given the often biphasic nature of cannabinoid drugs, it is critical to move away from single dose pharmacology to full dose-response assessments, which may yield an increased understanding of the mechanism and potential of cannabinoids to treat TBI. Overall, the abundant and growing pre-clinical research suggests that the eCB system possesses many promising targets for new and existing drugs that may ameliorate diverse TBI pathology.

    LS performed the literature review and composed the article; AL contributed to the composition of the article. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

    This research was funded by a Ruth L. National Center for Biotechnology Information , U. Journal List Front Pharmacol v. Published online Feb Schurman and Aron H. Author information Article notes Copyright and License information Disclaimer. This article was submitted to Experimental Pharmacology and Drug Discovery, a section of the journal Frontiers in Pharmacology. Received Oct 15; Accepted Feb 2.

    The use, distribution or reproduction in other forums is permitted, provided the original author s or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    Cannabinoid Study Shows CBD can reduce Sciatica

    As anyone who has experienced back problems like sciatica, slipped What is it about CBD that makes it potentially effective in taking on spine pain? associated with numerous side-effects, with CBD, researchers are finding offer pain relief and “suggest new therapeutic approaches to avoid central. Cannabidiol, or CBD, is a chemical compound in marijuana with a variety of uses . rat study found that oral CBD treatment significantly reduced sciatic . Research on the potential health benefits of CBD oil is ongoing, so. Mechanism of cannabidiol for safe pain relief without side effects Researchers were able to extrapolate the exact dosage of CBD pain, such as back pain, sciatica, diabetic, cancer and post-trauma pain. "This research is a new advancement for an evidence-based application of cannabis in medicine.

    What is Sciatica?



    Comments

    olkas

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    deedee12

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