My medical team was quick to whip out their prescription pads and write me prescriptions for opioids in ever-increasing quantities and potency. The side effects of opiates can be really harsh, and in my case, they ended up causing more pain than relief. The havoc that they caused on my gastrointestinal system alone put me in the hospital several times. It simply wasn’t worth it, and I knew that if I kept taking those things my health would continue to decline.
After doing some more research I learned that not all CBD oil is created equal. A search for a stronger, purer product led me to Maku. Within a couple of weeks of using a higher strength product, I began noticing tangible benefits. The aches and pains were under control and brought down to a much more bearable level. I could actually sit comfortably for a couple of hours without having to be shifted and adjusted! Unless you know someone with a similar neuromuscular disease or another condition that limits mobility, you may not understand how big of a deal that is. Another symptom of my SMA, muscle tremors, also started to dissipate when they had previously been increasing in severity.
The first time I tried CBD oil I wasn’t terribly impressed. I didn’t find it to be immediately beneficial in the same way that opiates and marijuana had been. So initially, I was discouraged.
The FDA has approved the use of medical marijuana in children over the age of two for the treatment of two forms of epilepsy known as Dravet syndrome and Lennox-Gastaut syndrome (LGS). Dravet syndrome is a rare form of epilepsy that is characterized by hard to control seizures that start when the child is a baby. LGS is another rare form of epilepsy characterized by frequent, different types of seizures that start during childhood. While neither of these conditions has a cure, they can be managed with treatment. In coordination with traditional seizure medication, taking medical marijuana has been shown to reduce the frequency of seizures.
As doctors learn more about neurological conditions, more and more treatments are becoming available to help patients manage their symptoms and increase their quality of life. One relatively new treatment for neurological conditions is medical marijuana. Although medical marijuana may not be ideal for treating every neurological condition, it has proven to be especially effective in managing seizures, multiple sclerosis, and muscular dystrophy.
While this form of treatment continues to be controversial among doctors, researchers, legislators, and the public, it has been legalized in 29 states, including Florida, for medical use. Medical marijuana uses the marijuana plant and its chemicals to treat certain conditions. There are various means of delivering marijuana into the body such as: smoking, inhaling vapors, consuming it with food, placing a drop under your tongue, or applying it to the skin as a lotion, spray, oil, or cream. When considering how to take medical marijuana, it is important to note that each method takes a different amount of time to be absorbed in the body.
Now that we have a better understanding of what medical marijuana is and how it works, let’s take a look at how it can be used to treat certain neurological conditions:
Medical Marijuana for Muscular Dystrophy (MD)
Muscular dystrophy occurs when there is a lack of dystrophin, which is a protein responsible for normal muscle function. As a result, the muscles become damaged and weakened over time, which causes problems with walking, swallowing, and coordination. Medical marijuana has been used to treat muscular dystrophy and has been found to be effective against the nerve pain associated with the disease. Many people use medical marijuana as an alternative to opioid-based pain medications because it can be safely used to treat chronic pain without having to frequently increase the dosage. Medical marijuana has also been shown to decrease the length and severity of muscle spasms and cramps.
There are over 100 chemicals found in the marijuana plant, however the most commonly used chemicals for medical use are delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD). While THC is known to produce the “high” associated with marijuana use, CBD has little to no intoxicating effect. One reason why medical marjuana is so effective in treating a variety of conditions is because the chemicals it contains are similar to the chemicals found in the body that are responsible for appetite, memory, movement, and pain.
Multiple sclerosis attacks the brain and spinal cord, causing weakness, tingling, numbness, and muscle stiffness, just to name a few symptoms. There is no cure for MS, however treatment can slow the progression of the disease. Research has found that marijuana can be beneficial in the treatment of MS because it decreases muscle stiffness and spasms, as well as reducing nerve pain. Additionally, marijuana can also help people with MS to sleep better at night. Although some people also say that marjuan improves muscle tightness and eases depressive symptoms in individuals with MS, there is no substantial evidence for those claims at this time.
Medical Marijuana for Multiple Sclerosis (MS)
Dr. Kashouty, a diplomate of the American Board of Psychiatry and Neurology (ABPN), practices general neurology with fellowship trained specialization in clinical neurophysiology. Dr. Kashouty finds the form and function of the nerves and muscles the most interesting part of neurology, which is what led him to specialize in neurophysiology with more emphasis on neuromuscular conditions. He treats all neurological diseases, but his main focus is to treat and manage headaches, movement disorders and neuromuscular diseases.
Dystonias are the result of abnormal muscles tone, causing involuntary muscle contraction, and resulting in repetitive movements or abnormal posture (Breakefield et al., 2008). Dystonias can be primary, for instance paroxysmal dyskinesia, or secondary to other conditions or drug use, such as tardive dyskinesia after prolonged treatment with antipsychotic drugs (Breakefield et al., 2008).
HD is a fatal progressive neurodegenerative disease characterized by motor dysfunctions, cognitive loss and psychiatric manifestations (McColgan and Tabrizi, 2018). HD is caused by the inclusion of trinucleotides (CAG) in the exons of the huntingtin gene, on chromosome 4 (MacDonald et al., 1993; McColgan and Tabrizi, 2018), and its prevalence is 1–10,000 (McColgan and Tabrizi, 2018). Neurodegeneration in HD affects mainly the striatal region (caudate and putamen) and this neuronal loss is responsible for the motor symptoms (McColgan and Tabrizi, 2018). Cortical degeneration is seen in later stages, and huntingtin inclusions are seen in few cells, but in all patients with HD (Crook and Housman, 2011). The diagnosis of HD is based on motor signs accompanied by genetic evidence, which is positive genetic test for the expansion of the huntingtin gene or family history (Mason and Barker, 2016; McColgan and Tabrizi, 2018).
Pre-clinical studies investigating the effects of CBD on movement disorders.
Safety and side effects
CBD also antagonizes the G-protein-coupled receptor GPR55 (Ryberg et al., 2007). GPR55 has been suggested as a novel cannabinoid receptor (Ryberg et al., 2007), but this classification is controversial (Ross, 2009). Currently, the phospholipid lysophosphatidylinositol (LPI) is considered the GPR55 endogenous ligand (Morales and Reggio, 2017). Although only few studies link the CBD effect to its action on GPR55 (Kaplan et al., 2017), it is noteworthy that GPR55 has been associated with PD in an animal model (Celorrio et al., 2017) and with axon growth in vitro (Cherif et al., 2015).
Data from clinical and pre-clinical studies are summarized in Tables Tables1, 1 , ,2, 2 , respectively.
More recently, CBD was reported to act as inverse agonist of the G-protein-coupled orphan receptors GPR3, GPR6, and GPR12 (Brown et al., 2017; Laun and Song, 2017). GPR6 has been implicated in both HD and PD. Concerning animal models of PD, GPR6 deficiency was related to both diminished dyskinesia after 6-OHDA lesion (Oeckl et al., 2014), and increased sensitivity to MPTP neurotoxicity (Oeckl and Ferger, 2016). Moreover, Hodges et al. (2006) described decreased expression of GPR6 in brain of HD patients, compared to control. GPR3 is suggested as a biomarker for the prognosis of multiple sclerosis (Hecker et al., 2011). In addition, GPR3, GPR6, and GPR12 have been implicated in cell survival and neurite outgrow (Morales et al., 2018).
Huntington’s disease (HD)
The molecular mechanisms associated with CBD’s improvement of motor disorders are likely multifaceted. Data show that it might depend on CBD’s actions on 5-HT1A, CB1, CB2, and/or PPARγ receptors. Moreover, all movement disorders are in some extent linked to oxidative stress and inflammation, and CBD has been reported to display an antioxidant and anti-inflammatory profile, in vitro and in animal models for movement abnormalities.
The first study with CBD on PD patients aimed to verify CBD’s effects on the psychotic symptoms. Treatment with CBD for 4 weeks decreased the psychotic symptoms, evaluated by the Brief Psychiatric Rating Scale and the Parkinson Psychosis Questionnaire, without worsening the motor function or inducing adverse effects (Zuardi et al., 2009). Later, in a case series with four PD patients, it was verified that CBD is able to reduce the frequency of the events related to REM sleep behavior disorder (Chagas et al., 2014a). In addition, although not ameliorating PD patients’ motor function or their general symptoms score, treatment with CBD for 6 weeks improves PD’s patients quality of life (Chagas et al., 2014b). The authors suggest that this effect might be related to CBD’s anxiolytic, antidepressant and antipsychotic properties (Chagas et al., 2014b).