cbd oil for muscle cramps

Best CBD Oil for Cramps – February 2022

Muscle cramps or spasms are painful, involuntary contractions of the affected muscle groups. It is caused by muscle overuse and strain, dehydration, or long duration of holding a position.

Cramps can be eased within a few minutes of stretching and massage. However, severe cramps that persist for a long time and cannot be eased with stretching may be signs of a more severe condition.

Nonsteroidal anti-inflammatory drugs ( NSAIDs ), like ibuprofen and naproxen, are over-the-counter painkillers that can relieve tenderness after cramping .

However, these drugs have risks of side effects, such as gastrointestinal disorders and cardiovascular diseases (6) .

CBD may be an alternative pain and inflammation reliever for cramps because of its natural analgesic, anti-inflammatory, and anti-spasticity properties (7) . It also displayed little to no side effects when administered to humans (8) .

Cannabidiol or CBD is one of the cannabinoids present in the cannabis plant . It is the non-psychoactive compound abundant in the hemp plants. CBD oil is extracted from the said plant and mixed with carrier oils, like coconut or grapeseed oil.

Cramps can happen to the abdominal wall, arms, legs, hands, back, and feet. They may also occur due to injuries or strenuous activities.

Women are also prone to menstrual cramps or contractions of the uterus. Menstrual cramping is a common premenstrual symptom for women. It is characterized by severe discomfort and throbbing pain in the lower abdomen before or during their menstrual period.

One of the common kinds of cramps is night leg cramps. Nocturnal leg cramps are the sudden tightening of the leg muscles at night while asleep. It can also occur due to periods of inactivity within the day.

How CBD Oil Works to Help Alleviate Symptoms of Cramps

The endocannabinoid system (ECS) is the body’s system that works with cannabinoids, like CBD. Its functions include regulating pain , appetite, sleep , and memory and maintaining homeostasis (9) .

The ECS has three primary components: endocannabinoids, cannabinoid receptors , and enzymes.

Endocannabinoids are the neurotransmitters of the ECS and are spread throughout the body. These transmitters bind to receptors, which activate the functions of the bonded cannabinoids.

Cannabinoids are then broken down by the enzymes, which indicates that a successful function has been carried out.

CBD and THC (tetrahydrocannabinol), the two main components of the cannabis plant, are cannabinoids that can bond with the receptors.

THC is the psychoactive compound that can alter a person’s mind or behavior if taken in large amounts.

CBD for Menstrual Cramps

No studies have shown the direct effects of CBD on menstrual cramps. However, some researchers suggest that CBD has anti-inflammatory and pain relief activities that may help with menstrual pain management (10) .

Studies showed that CBD might inhibit prostaglandin production and improve women’s health (11) .

Prostaglandins are active substances that help in tissue damage, infection, and female reproductive system regulation. These substances control ovulation and trigger muscle contractions that cause period cramps (12) .

Period pains are also caused by secondary dysmenorrhea or other medical conditions in the female reproductive system, like endometriosis .

Endometriosis is a condition wherein the uterine lining grows outside the uterus. This condition can cause severe pain and inflammation in the affected area.

CBD is one of the effective treatments for women with endometriosis, according to a study (13) .

CBD oil reportedly reduced medication use, improved mood swings , and alleviated pain caused by the condition. The study also noted that the women used hemp oil with CBD oil.

CBD for Muscle Cramps

A study showed that CBD might reduce spasticity, pain, inflammation, and depression of multiple sclerosis patients (14) .

Multiple sclerosis is a central nervous system disorder that causes communication problems between the brain and body.

People with this condition experience spasms in the limbs that may impair their mobility.

Another study found that CBD may improve neurogenic symptoms, including pain and muscle spasms (15) .

Patients were administered CBD, THC, and combined CBD and THC extracts from cannabis plants through a mouth spray.

According to the findings, CBD has analgesic and anti-spasticity components and has minimal side effects.

The Pros and Cons of CBD Oil for Cramps

The Pros
  • Studies mentioned showed that CBD has natural analgesic, anti-inflammatory, and anti-spasticity properties that may help ease muscle cramps.
  • CBD may ease painful periods associated with menstrual cramps, a common problem for women.
  • CBD may be bought without a prescription in various states and territories in the United States where it is legal for medical use (16) .
The Cons
  • There is no approved CBD medication by the US Food and Drug Administration (FDA) besides Epidiolex, an oral solution for seizures and epilepsy (17) . CBD products in the market should be used with caution.
  • CBD products are not regulated by the FDA (18) . Hence, more products sold online and in stores are mislabeled, unstandardized, and have unproven claims (19) .
  • CBD products may be costly. As the CBD concentration increases, the price also increases.

How CBD Oil Compares to Alternative Treatments for Cramps

There are various home treatments and natural remedies that can help with cramps.

Aside from massage and stretching, muscle cramps can be eased by applying heating pads or cold compress on the affected area.

Vitamin and nutrient supplements, like vitamin B complex, magnesium, and zinc, are also recommended for cramps. Magnesium regulates the muscle and nerve function while zinc helps in muscle repair.

A study also showed that oral magnesium supplements lessened the occurrence of nocturnal leg cramps (20) . Magnesium supplements can also reduce prostaglandin levels for women with menstrual cramps (21) .

CBD oil may also be considered as an alternative treatment for cramps. It comes in different forms, like topical products (CBD balms, salves, and lotions ) for targeted pain relief and suppositories for period pain relief .

CBD oil may also be used in massages to provide pain relief.

How to Choose the Right CBD Oil for Cramps

CBD oil comes in three different types.

Full-spectrum CBD oil contains all the compounds found in hemp plants. This type includes cannabinoids, terpenes, fatty acids, and flavonoids.

Full-spectrum CBD oil also contains trace amounts of THC which is not enough to make a person high.

Like the previous type, broad-spectrum contains all the organic compounds in a hemp plant but without THC. Removing a compound from a mixture is done using a process called chromatography.

The purest among the three types is CBD isolate . This type contains only one compound, which is CBD.

Full-spectrum CBD is for those who do not worry about psychoactive effects . Meanwhile, the broad-spectrum CBD is for those who want a non-intoxicating product in their system.

Aside from these factors, choosing the right CBD oil goes beyond its spectrum. These are some ways that a user can ensure that the product is ethical and safe to use:

  • Choose brands that use third-party laboratory tests for their products. A third-party lab certificate or certificate of analysis ensures a reliable and safe manufacturing process.
  • Check the extraction method and source of hemp used in the product. The extraction method ensures the efficacy and purity of the product . The source of hemp indicates the quality of the product.
  • Read product reviews, especially when buying from an online shop. Online reviews give an insight to the user on what to expect from the product.
  • Make sure that the physical store complies with the state laws concerning the sale of CBD products. Be aware of the legalities associated with CBD use in the area where the product is bought and consumed.
  • Examine the ingredient list to see if there are any synthetic ingredients included in the formulation. The Centers for Disease Control and Prevention released a report about possible adverse effects of using synthetic cannabinoids (22) .

CBD Dosage for Cramps

There are no standard dosages in taking CBD. However, s tudies have shown that doses ranging from 1 mg to 1500 mg of CBD per day are well-tolerated by humans (23) .

It is safe to take a low dose of CBD initially, increasing it gradually until significant effects are achieved.

How to Take CBD Oil for Cramps

CBD can be taken orally, sublingually, topically, anally or vaginally (although check to make sure that the carrier component is water-soluble and not oily), and through inhalation.

Oral CBD products come in oils (CBD tinctures), gummies , and capsules.

Using a dropper, drops of CBD tincture are placed under the tongue where absorption via mucous membranes happens.

Sublingual is better than oral administration because CBD goes directly into the bloodstream.

Topical CBD products are available in lotions , creams, balms, and salves . The product can be applied to the affected area for targeted pain relief. These products are often used to address local pain, especially in the muscle and joint areas.

CBD suppositories can be inserted anally or vaginally. These products contain a specific compound that dissolves inside the vagina, for period pain relief, or rectum, for gastrointestinal problems.

Suppositories are inserted in the vagina like tampons . However, it is not advisable to apply CBD oil on tampons. Doing so may result in vaginal infections and irritations, like bacterial vaginosis, that are difficult to manage.

See also  average dose of cbd oil needed for pain relief

Vaping is also an effective method of taking CBD. As the user inhales the compound, it quickly goes through the bloodstream. Its benefits are experienced in the shortest time possible. However, there are a risk of lung damage using this method.

However, vaping is associated with lung problems (24) . Hence, individuals are advised to take caution when using CBD vape pens.


Cramps can happen to women on their menstrual cycle. Cramps can also be experienced by some people, whether active or inactive.

C hronic pain and frequency occurrence may be signs of a more severe problem that should be appropriately diagnosed.

CBD is a promising natural remedy for pain, inflammation, and spasticity. CBD oils come in different types and forms that suit a person’s lifestyle and condition.

First-time users should seek medical advice before trying any CBD product. Factors, like current medications, severity of medical conditions, and allergies, must be considered before using CBD.

  1. Russo E. B. (2008). Cannabinoids in the management of difficult to treat pain. Therapeutics and clinical risk management, 4(1), 245–259. https://doi.org/10.2147/tcrm.s1928
  2. Iffland, K., & Grotenhermen, F. (2017). An Update on Safety and Side Effects of Cannabidiol: A Review of Clinical Data and Relevant Animal Studies. Cannabis and cannabinoid research, 2(1), 139–154. https://doi.org/10.1089/can.2016.0034
  3. P Cavner, J. (2019). Is CBD A Viable Option for Menstrual Symptoms? Online Journal of Complementary & Alternative Medicine, 2(5), 1–3. https://doi.org/10.33552/ojcam.2019.02.000548
  4. U.S. Food and Drug Administration. (2020, March 11). FDA Regulation of Cannabis and Cannabis-Derived Products: Q&A. https://www.fda.gov/news-events/public-health-focus/fda-regulation-cannabis-and-cannabis-derived-products-including-cannabidiol-cbd
  5. Freedman, D. A., & Patel, A. D. (2018). Inadequate Regulation Contributes to Mislabeled Online Cannabidiol Products. Pediatric neurology briefs, 32, 3. https://doi.org/10.15844/pedneurbriefs-32-3
  6. Ong, C. K., Lirk, P., Tan, C. H., & Seymour, R. A. (2007). An evidence-based update on nonsteroidal anti-inflammatory drugs. Clinical medicine & research, 5(1), 19–34. https://doi.org/10.3121/cmr.2007.698
  7. Russo E. B. op. cit.
  8. Iffland, K., op. cit.
  9. Sallaberry, C., & Astern, L. (2018a). The Endocannabinoid System, Our Universal Regulator. Journal of Young Investigators, 48–55. https://doi.org/10.22186/jyi.34.5.48-55
  10. P Cavner, J., op. cit.
  11. Ruhaak, Lucia & Felth, Jenny & Karlsson, Pernilla & Rafter, Joseph & Verpoorte, Robert & Bohlin, Lars. (2011). Evaluation of the Cyclooxygenase Inhibiting Effects of Six Major Cannabinoids Isolated from Cannabis sativa. Biological & pharmaceutical bulletin. 34. 774-8. 10.1248/bpb.34.774.
  12. Bernardi, M., Lazzeri, L., Perelli, F., Reis, F. M., & Petraglia, F. (2017). Dysmenorrhea and related disorders. F1000Research, 6, 1645. https://doi.org/10.12688/f1000research.11682.1
  13. Armour, M., Sinclair, J., Chalmers, K. J., & Smith, C. A. (2019). Self-management strategies amongst Australian women with endometriosis: a national online survey. BMC complementary and alternative medicine, 19(1), 17. https://doi.org/10.1186/s12906-019-2431-x
  14. Rudroff, T., & Sosnoff, J. (2018). Cannabidiol to Improve Mobility in People with Multiple Sclerosis. Frontiers in neurology, 9, 183. https://doi.org/10.3389/fneur.2018.00183
  15. Wade, D. T., Robson, P., House, H., Makela, P., & Aram, J. (2003). A preliminary controlled study to determine whether whole-plant cannabis extracts can improve intractable neurogenic symptoms. Clinical Rehabilitation, 17(1), 21–29. https://doi.org/10.1191/0269215503cr581oa
  16. National Organization for the Reform of Marijuana Laws. (2020, June 30). Medical Marijuana Laws. NORML. https://norml.org/laws/medical-laws/
  17. United States Food and Drug Administration. (2018, June 26). FDA Approves First Drug Comprised of an Active Ingredient Derived from Marijuana to Treat Rare, Severe Forms of Epilepsy. U.S. Food and Drug Administration. https://www.fda.gov/news-events/press-announcements/fda-approves-first-drug-comprised-active-ingredient-derived-marijuana-treat-rare-severe-forms
  18. U.S. Food and Drug Administration., op. cit.
  19. Freedman, D. A., op. cit.
  20. Roffe, Christine & Sills, Sheila & Crome, Peter & Jones, Peter. (2002). Randomised, cross-over, placebo controlled trial of magnesium citrate in the treatment of chronic persistent leg cramps. Medical science monitor : international medical journal of experimental and clinical research. 8. CR326-30.
  21. Parazzini, F., Di Martino, M., & Pellegrino, P. (2017). Magnesium in the gynecological practice: a literature review. Magnesium Research, 30(1), 1–7. https://doi.org/10.1684/mrh.2017.0419
  22. Horth, R. Z. (2018, May 24). Notes from the Field: Acute Poisonings from a Synthetic. Centers for Disease Control and Prevention. https://www.cdc.gov/mmwr/volumes/67/wr/mm6720a5.htm
  23. Bergamaschi, M. M., Queiroz, R. H., Zuardi, A. W., & Crippa, J. A. (2011). Safety and side effects of cannabidiol, a Cannabis sativa constituent. Current drug safety, 6(4), 237–249. https://doi.org/10.2174/157488611798280924
  24. Outbreak of Lung Injury Associated with the Use of E-Cigarette, or Vaping, Products. (2020, February 25). Retrieved from https://www.cdc.gov/tobacco/basic_information/e-cigarettes/severe-lung-disease.html

CBD Clinicals is reader-supported. When you buy through links on our site, we may earn an affiliate commission. Learn more

Cannabinoids in the management of spasticity associated with multiple sclerosis

The endocannabinoid system and cannabinoid-based treatments have been involved in a wide number of diseases. In particular, several studies suggest that cannabinoids and endocannabinoids may have a key role in the pathogenesis and therapy of multiple sclerosis (MS). In this study we highlight the main findings reported in literature about the relevance of cannabinoid drugs in the management and treatment of MS. An increasing body of evidence suggests that cannabinoids have beneficial effects on the symptoms of MS, including spasticity and pain. In this report we focus on the effects of cannabinoids in the relief of spasticity describing the main findings in vivo, in the mouse experimental allergic encephalomyelitis model of MS. We report on the current treatments used to control MS symptoms and the most recent clinical studies based on cannabinoid treatments, although long-term studies are required to establish whether cannabinoids may have a role beyond symptom amelioration in MS.


Cannabis contains a series of compounds, but it has been found that the major psychoactive ingredient is Δ9-tetrahydrocannabinol (THC) ( Mechoulam and Gaoni 1967 ). Two selective cannabinoid receptor subtypes have been identified so far ( Matsuda et al 1990 ; Munro et al 1993 ), CB1 and CB2, that are expressed in nervous and peripheral cells. THC mediates the majority of its activities through stimulation of cannabinoid receptors CB1, which are expressed throughout the central nervous system (CNS) ( Matsuda et al 1990 ; Howlett et al 2002 ). Following the discovery of the receptors, fatty acid endogenous ligands, such as anandamide (AEA) and 2-arachidonoyl glycerol (2-AG), have been discovered in mammalian animal and human nervous tissues ( Devane et al 1992 ; Sugiura et al 1995 ), and a degradation system including a putative reuptake mechanism and hydrolytic enzymes has been identified ( Devane et al 1992 ; Deutsch and Chin 1993 ; Mechoulam et al 1995 ; Dinh et al 2002 ; Saario and Laitinen 2007 ). A whole endogenous signaling system consisting of cannabinoid receptors, endocannabinoids, and the proteins for their synthesis and inactivation led to the definition of the endocannabinoid system.

The endocannabinoid system functions to regulate synaptic neurotransmission ( Kreitzer and Regehr 2001 ; Ludányi et al 2008 ) and tonically controls clinical signs such as spasticity and tremor that develop in mouse models of multiple sclerosis (MS) ( Pryce and Baker 2007 ). This provides objective evidence to support the claims of MS patients that cannabis may have a benefit in symptom management ( Bifulco et al 2007 ), a claim further supported by some recent clinical trials of medical cannabis extracts ( Killestein et al 2002 ; Robson et al 2002 ; Vaney et al 2002 ). There is in vitro evidence showing that cannabinoids can also regulate glutamate release, oxidant free radicals and calcium influxes ( Kreitzer and Regehr 2001 ; Howlett et al 2002 ; Rea et al 2007 ; Lauckner et al 2008 ; Sidlò et al 2008 ), which, in excess, can cause neuronal death in neuroinflammatory disease ( Kapoor et al 2003 ).

Recent studies have suggested that cannabinoid-based treatments may be beneficial in a wide number of diseases. The pharmacological activity of AEA and 2-AG has been thoroughly examined and shown to be similar to that of some psychotropic plant cannabinoids, namely THC ( Battista et al 2006 ). In particular, they have been found to exert a neuromodulatory effect ( Navarrete and Araque 2008 ) on the synthesis, release and action of neurotransmitters. Some of these neurotransmitters, eg, dopamine, γ-aminobutyric acid, and glutamate, have been recently implicated in the genesis of experimental allergic encephalomyelitis (EAE) ( Bolton and Paul 2006 ), an animal model of inflammatory disease of the CNS myelin.

Cannabinoids and multiple sclerosis

MS is one of the most common chronic and disabling disorders of the CNS caused by demyelination (loss of insulating sheath) of nerve fibers. The disease usually begins in young adulthood and affects women more frequently than men (2:1). Common symptoms include fatigue, balance problems, muscle weakness, incontinence, muscle spasm, pain, and tremor. Clinical studies indicate that MS is characterized by at least two distinct phases, one that is dominated by acute relapses and one by steady progression. Both genetic and environmental factors seem to contribute synergistically to the manifestation and progression of the disease. MS usually starts with a relapsing – remitting course (RR-MS); over time, the number of relapses decreases, and most patients develop progressive neurological deficits that occur independently of relapses (the so-called secondary progressive phase). In a few cases, MS begins with a primary progressive course (PPMS) without acute relapses. In general, the progression rate in RR-MS is comparable with that of PP-MS as soon as the patients enter the secondary progressive phase (Malfitano et al 2005). CNS lesions, frequently detected in RR-MS phase, are usually located in areas of white matter, and are often characterized by a disturbance of the blood – brain barrier, local oedema and demyelination, features that are compatible with an inflammatory process, while in PP-MS, such inflammatory activity is much less conspicuous ( Miller et al 1998 ). Global brain atrophy, however, is more dominant in the progressive stage and seems to correlate with disability ( Losseff et al 1996 ; Fox et al 2000 ). These findings indicate that early in the disease, ongoing inflammatory activity is present in most patients and is responsible for the relapsing – remitting course, whereas a distinct process might be operative in the progressive phase of the disease, when inflammatory activity diminishes despite faster evolution of disability. Histological hallmarks of active MS include infiltrations of T cells, macrophages, and B cells, degradation of myelin, and, to a lesser extent, axons, and reactive changes of astrocytes and microglia ( Lassmann et al 2001 ). Autoimmunity is thought to drive the development of inflammatory lesions that induce the primary demyelination, which results in the inhibition of normal neurotransmission (Compston and Coles 2002). Current treatment of MS is based on anti-inflammatory, immunosuppressive, and immunomodulatory drugs, but usually the therapy is partially effective and with risks of side effects that patients are often unable to tolerate.

See also  best cbd oil for ic pain

Recently, it has been reported that during CNS inflammation, the endocannabinoid system is highly activated and the endocannabinoid an anandamide (AEA) protects neurons from inflammatory damage by CB (1/2) receptor-mediated rapid induction of mitogen-activated protein kinase phosphatase-1 (MKP-1) in microglial cell. The release of AEA in injured CNS tissue might represent a new mechanism of neuro-immune communication during CNS injury, which limits immune response after primary CNS damage (Compston and Coles 2002). Furthermore, evidence suggests that endocannabinoids have immunosuppressant and anti-inflammatory properties, they downregulate the production of T helper 1 (Th1) cytokines, enhancing the production of T helper 2 (Th2) cytokines, since a polarization of T cell response towards a Th2 phenotype has been associated with therapeutic benefit in MS, while a shift towards Th1 has been associated with disease progression ( Matsuda et al 1990 ; Hemmer 2002). A recent study showed the modulation of cytokines of the IL-12 family by cannabinoids in macrophages and brain microglia. Murine primary cultures of macrophage and microglia activated by lipopolysaccharide/ IFN-γ and Theiler’s virus were used to study the effects of cannabinoids on the regulation of IL-12 and IL-23 mRNA and protein IL-12 p40. It was observed that cannabinoids negatively regulate the production of these cytokines by microglial cells in part due to the activation of CB2 receptors. The effects of cannabinoids on cytokine brain work and on the regulation of neuroinflammatory processes may affect chronic inflammatory demyelinating diseases such as MS ( Correa et al 2007 ).

Anecdotal reports have suggested that cannabinoids significantly relieve the symptoms of MS, although a crucial point for their therapeutic application is the full assessment of their psychotropic effects. This has led some MS patients to self-medicate with cannabis, which is suggested to be beneficial in controlling symptoms such as spasticity, pain, tremor, and bladder dysfunction.

Several other plant cannabinoids, which have little or no psychoactive action, have been identified; their biosynthetic relationships have been established, and the possible contribution that they make to some of the proposed therapeutic actions of cannabis has been suggested. In particular, cannabidiol and the cannabinoic acids seem to be promising therapeutic tools, even though their sites of action are still not well understood ( Pacher et al 2006 ).

Cannabinoids and spasticity

Many studies reporting the effects of cannabinoids in in vivo models of MS have been performed. We here summarize the main findings described in literature about the antispastic properties of cannabinoids and their derived molecules. In mice with chronic relapsing experimental allergic encephalomyelitis (CREAE), an animal model of MS, evidence has been presented that both exogenous and endogenous cannabinoids, via cannabinoid receptors, alleviate spasticity and tremors ( Pryce and Baker 2007 ). Intravenous administration of THC and also R (+)− WIN55,212-2, a potent synthetic agonist of CB1 and CB2, rapidly decreased both the frequency and amplitude of tremors in limbs and hind limb spasticity of mice with this disease. Two lines of evidence suggest that these two beneficial effects are mediated by cannabinoid receptors. Firstly, the S(−)- enantiomer of WIN55,212-2, and cannabidiol, which are both very weak agonists of CB1 and CB2 receptors, did not reduce spasticity. Secondly, SR141716, which is a selective CB1 receptor antagonist, and SR144528, which is a selective CB2 receptor antagonist, prevented R(+)−WIN55,212-2 from inhibiting tremor. These findings are very important because they may lead to novel strategies for the treatment of MS-induced tremor and spasticity, for which no efficacious remedy has yet been developed. A crucial point that deserves further investigation, at least if therapeutic applications are to be developed is the full assessment of the possible psychotropic side effects of intravenous administration of cannabinoids. Methanandamide, a CB1-receptor-selective and metabolically stable analogue of the endocannabinoid anandamide ( Mechoulam et al 1998 ), was almost as potent as R (+)− WIN55,212-2 against hind limb spasticity in mice with CREAE. This finding implies that drugs based on endocannabinoids, which have been reported to have very low potential for physical dependence ( Aceto et al 1998 ), could also be used in the treatment of MS-induced spasticity. Another nonpsychoactive endogenous compound, the anti-inflammatory mediator PEA ( Lambert and Di Marzo 1999 ), also induced a significant, albeit transient inhibition of spasticity ( Pryce and Baker 2007 ); however, the mechanism of action of this compound, which does not bind appreciably to CB1 or CB2 receptors, is still a matter of speculation ( Lambert and Di Marzo 1999 ). SR141716 and with less potency SR144528, produced a significant worsening of both tremors and spasticity of hind limbs and tail of CREAE mice ( Pryce and Baker 2007 ). This finding raised the possibility that endocannabinoids such as anandamide and 2-AG ( Mechoulam et al 1998 ), might be produced during CREAE in an attempt to compensate for the spastic defect. It was shown ( Pryce and Baker 2007 ) that in normal ABH mice, whole brains and spinal cords contained similar levels of AEA, 2-AG and PEA. There was a modest increase of AEA in spastic brains compared with levels in normal brains. However, there was a marked increase of AEA, 2-AG and PEA within the spinal cord of spastic mice in comparison with normal animals. On the basis of these findings, it was suggested that augmenting the levels of endogenous AEA might have a therapeutic effect, as exogenously applied and naturally occurring cannabimimetic metabolites, in particular AEA, can limit spasticity. Furthermore, the blockade of degradation with specific inhibitors may represent an alternative to increase the bioavailability of the endocannabinoids. Spasticity could be ameliorated by injection (10 mg/kg iv) of either the competitive reuptake inhibitor AM404 ( Beltramo et al 1997 ) or the selective FAAH inhibitor, AM374 ( Deutsch et al 1997 ), both of which have been shown to enhance AEA neuromodulatory actions ( Beltramo et al 1997 ). These compounds have very low affinity for cannabinoid receptors ( Beltramo et al 1997 ; Deutsch et al 1997 ). The antispastic effect of AM374 (1 mg/kg iv) was blocked by cannabinoid receptor antagonists (SR141716 and SR144465, both 5 mg/kg iv) administered 20 min prior to AM374. These findings suggest that the inhibitory effect on spasticity by AM374, which does not directly activate CB receptors ( Deutsch et al 1997 ), is due to enhancement of endocannabinoid levels and subsequent stimulation of CB receptors. Both AEA and AM404 may also behave as vanilloid receptor (TRPV1) agonists ( Zygmunt et al 1999 ; Smart and Jerman 2000 ; Smart et al 2000 ), but the role of TRPV1, if any, in control of spasticity is yet to be demonstrated. The extremely selective anandamide transporter inhibitor VDM11 (10 mg/kg iv), which has essentially no CB or TRPV1 agonist activity ( De Petrocellis et al 2000 ), exerts a similar inhibition of spasticity. This finding, furthermore, supports the hypothesis that endocannabinoids mediate control of spasticity via CB receptors. It was observed that agonists of TRPV1 reduce bladder hyper-reactivity in MS ( Fowler et al 1992 ) and have a modest antispastic effect in EAE mice, while a substantial effect was obtained with arvanil, a synthetic compound that can activate both CB1 and TRPV1 receptors ( Melck et al 1999 ). This effect persists using antagonists of CB1 and TRPV1 and in CB1 knockout EAE mice. According to these experimental findings, it can be suggested that the antispastic effect of arvanil can be independent from CB1, CB2, or TRPV1 receptors and mediated by a different site of action.

Treatment of spasticity in multiple sclerosis

MS is associated with disabling symptoms that often impair quality of life of patients affected by this neurological disease. These symptoms include muscle stiffness, spasms, pain, tremor, bladder dysfunction. Treatment of these symptoms, along with immunomodulation and immunosuppression, is therefore important in the overall management of this chronic disease and has achieved growing attention. Of the many symptoms encountered in MS, muscle spasticity (muscle stiffness as a result of increased pyramidal tone) and spasms occur in up to 90% of patients at some point ( Ward 2008 ). This symptom often leads to considerable distress from pain, reduced mobility, and interference with activities of daily living in patients with MS; as muscle tone can be elevated persistently (tonic spasticity) or transiently as painful cramps (phasic spasticity). Spasticity develops also as a result of cerebral stroke or trauma, in children with cerebral palsy, in conditions and tumors of the spinal cord, and particularly following spinal injuries associated with spinal cord damage. The development and aggravation of spasticity is influenced by urinary tract infections, distension of the urinary bladder and rectum, pain, and pressure sores.

See also  cbd oil for crohn's disease in children

Antispastic treatment should primarily ameliorate motor function by reducing elevated muscle tone: patients may benefit from being taught techniques for appropriate posture, positioning and weight transfer. Other goals of spasticity treatment are avoiding contractures and pressure ulcers, and facilitating patient self-care. Available treatments are often rather ineffective and no protocol for drug treatment of spasticity has been developed.

Physiotherapy for the relief of spasticity in MS ( Giovannelli et al 2007 ; Pöllmann and Feneberg 2008 ), has not been extensively studied, despite being the standard approach, is insufficient alone for most patients, thus anti-spastic drugs are required. Among these antispastic drugs, the most commonly used are tizanidine and baclofen. A very recent report summarizes clinical trials demonstrating that the efficacy of tizanidine is comparable with that of baclofen or diazepam with global tolerability data favoring tizanidine. A clinical case presentation demonstrated the effective use of tizanidine in combination with baclofen as a logical avenue for improved spasticity control. A large body of evidence supports the effective use of tizanidine monotherapy in the management of spasticity. A case study demonstrates that combination therapy can effectively control spasticity while better managing dose-dependent adverse events, although additional studies need to be performed to confirm these results ( Kamen et al 2008 ). Dantrolene and tolperisone are rarely prescribed. Benzodiazepines offer sufficient antispastic effect, but are second-line drugs owing to their higher risk of side-effects such as sedation and dependence ( Paisley et al 2002 ; Shakespeare et al 2003 ). Gabapentin was shown to be effective in treating phasic spasticity ( Mueller et al 1997 ; Cutter et al 2000 ).

Antispastic drugs are often of limited value in focal spasticity (eg, adductor spasticity or equinovarus deviation), but botulinum toxin type A reduces muscle tone effectively ( Snow et al 1990 ; Hyman et al 2000 ). Numerous open-label trials as well as several masked and placebo-controlled studies in the last 10 years have demonstrated efficacy of intramuscular injections of botulinum toxin for spasticity due to MS, brain and spinal cord injury, cerebral palsy, and stroke. Introduced several years ago, intrathecal baclofen administered via an infusion pump is an expensive method, at least two studies suggest that treatment reduces elevated muscle tone and frequency of spontaneous muscle spasms ( Penn et al 1989 ; Middel et al 1997 ), although its efficacy is reduced with long-term treatment.

Current treatments of MS are partially effective and with risks of side effects that patients are often unable to tolerate. This has led some MS patients to self-medicate with cannabis, which is suggested by anecdotal evidence to be beneficial in controlling symptoms such as spasticity, pain, tremor, and bladder dysfunction, claims supported by recent clinical trials of medical cannabis extracts ( Killestein et al 2002 ; Robson et al 2002 ; Vaney et al 2002 ).

Clinical studies

The first large scale study designed to assess the hypothesis of beneficial effects of cannabinoids on MS symptoms is represented by the Cannabinoids in Multiple Sclerosis (CAMS) study ( Zajicek et al 2005 ). In a randomized, placebo-controlled trial, 630 patients with stable MS and muscle spasticity were enrolled. 630 participants were treated at 33 UK centers with oral cannabis extract (n = 211), Δ9-tetrahydrocannabinol (Δ9-THC; n = 206), or placebo (n = 213). Trial duration was 15 weeks. The primary outcome measure was the Ashworth assessment of muscle spasticity, but other MS related symptoms, disability, and safety were also evaluated.

There was evidence of a treatment effect on patient-reported spasticity and pain (p = 0.003), with improvement in spasticity reported in 61%, 60%, and 46% of participants on cannabis extract, Δ9-THC, and placebo, respectively.

The main study covered 15 weeks, with all patients discontinuing treatment during week 14. There was no evidence of treatment effects on change in Ashworth score or other measures of disability from baseline to week 13. However, there was evidence of improvement in walking time for ambulatory patients and in patient perceptions of spasticity, muscle spasms, pain, and sleep. There was evidence of patient unmasking, complicating interpretation of patient assessed outcomes. These findings are consistent with those of smaller studies, ( Petro and Ellenberger 1981 ; Ungerleider et al 1987 ; Greenberg et al 1994 ; Killestein et al 2002 ) which showed some subjective, but no observer-verified, improvement in disease-related spasticity with use of cannabinoids.

The results of the CAMS study are also consistent with a report from a crossover study ( Vaney et al 2003 ), the findings of which indicated trends in reduction of spasms and improved mobility in 50 patients who received cannabis extract. A subsequent study was performed to assess the effectiveness and long-term safety of cannabinoids in MS, in a follow-up to the main CAMS study. 630 patients with stable MS with muscle spasticity from 33 UK centers were randomized to receive oral Δ9-tetrahydrocannabinol (Δ9-THC), cannabis extract, or placebo in the main 15 week CAMS study. The primary outcome was change in the Ashworth spasticity scale. Secondary outcomes were the Rivermead Mobility Index, timed 10-m walk, UK Neurological Disability Score, postal Barthel Index, General Health Questionnaire-30, and a series of 9 category rating scales. Following the main study, patients were invited to continue medication, double blinded, for up to12 months in the follow-up study. Evidence of a small treatment effect on muscle spasticity as measured by change in Ashworth score from baseline to 12 months was observed. There was suggestive evidence for treatment effects of Δ9-THC on some aspects of disability. There were no major safety concerns. Overall, patients felt that these drugs were helpful in treating their disease. These data provide limited evidence for a longer term treatment effect of cannabinoids. Another clinical study deals with Sativex ® , a combined cannabinoid medicine constituted by THC and cannabidiol (CBD) in a 1:1 ratio ( Smith 2007 ), developed by GW Pharmaceuticals. Sativex, via an oromucosal pump spray, has proved to be well tolerated and successfully self-administered and self-titrated in both healthy volunteers and patient cohorts. Clinical assessment of this combined cannabinoid medicine has demonstrated efficacy in patients with intractable pain (chronic neuropathic pain, pain due to brachial plexus nerve injury, allodynic peripheral neuropathic pain, and advanced cancer pain), rheumatoid arthritis and MS (bladder problems, spasticity and central pain), with no significant intoxication-like symptoms, tolerance or withdrawal syndrome ( Perez 2006 ). Sativex ® was effective, with no evidence of tolerance, in select patients with central neuropathic pain and MS who completed approximately 2 years of treatment (n = 28). Ninety-two percent of patients experienced an adverse event, the most common of which were dizziness and nausea. Most adverse events were deemed to be of mild to moderate severity by the investigators ( Rog et al 2007 ). There is still concern about potential side effects associated with a prolonged treatment, thus long term studies are needed to establish whether cannabinoids may have a role beyond symptom amelioration in MS.


The emerging literature on the effects of endocannabinoids and new cannabinoid-derived molecules on MS could lead to the development of promising models for the therapy and management of disabling symptoms of the disease. Considering that current treatments of MS are partially effective and have risks of side effects not easily tolerated by patients, the development of new synthetic endocannabinoids or cannabinoid-derived drugs could represent an alternative strategy to pursue. A crucial point that deserves further investigation is the full assessment of the possible psychotropic side effects that represent the limits to the use of cannabimimetic drugs in MS therapy. The possibility of overcoming these side effects to develop novel approaches represents the main open question on the use of cannabinoids as new therapeutic drugs for the treatment of MS.


This study was supported by the Associazione Educazione e Ricerca Medica Salernitana, ERMES.

Cannabis strains for muscle spasms

Muscle spasms come in all shapes and sizes. For the most part, mild muscle spasms occur in 60% of adults. But sometimes, muscle spasms can take acute forms, disturbing sleep and the ability to exercise. While age and lifestyle can play a significant role, some people are simply more prone to muscle spasms than others. Depending on the severity of your situation, a doctor may prescribe a pain management plan that includes prescriptions ranging from over-the-counter ibuprofen to more aggressive options like prescription muscle relaxers.

However, consumers who have not found relief through traditional pain management techniques have found success using the therapeutic properties of marijuana to help combat pain from muscle spasms. While more research on this topic is needed, some consumers say marijuana strains high in CBD help relieve pain from muscle spasms. Examples of strains that may help with spasms include CBD Critical Mass, Valentine X, and Suzy Q. Use this list to discover the best marijuana strains that may help lessen muscle spasms.