Shingles is a viral infection of an individual nerve and the skin surface that is supplied by the nerve. Shingles is caused by the varicella-zoster virus — the same virus that causes chickenpox. After you’ve had chickenpox, the virus lies inactive in nerve tissue near your spinal cord and brain. Years later, the virus may reactivate as shingles.
Varicella-zoster virus belongs to a group of viruses called herpes viruses, which is why shingles is also known as herpes zoster. All herpes viruses can hide in the nervous system where they can remain almost indefinitely. Given the right conditions, the herpes zoster virus can “reactivate” (or wake up from hibernation) and travel down nerve fibers to cause a new active infection.
While it isn’t a life-threatening condition, shingles can be very painful. Some of the signs and symptoms include:
- Pain, burning, numbness or tingling
- Sensitivity to touch
- A red rash that begins a few days after the pain
- Fluid-filled blisters that break open and crust over
Some people also experience:
- Sensitivity to light
A Patients Guide for Using Medical Marijuana for Shingles
Shingles is a painful condition that originates from the same virus that causes chickenpox, called varicella zoster. For reasons that are poorly understood, decades after contracting chickenpox, the virus can “wake up” in some individuals, causing shingles. Unlike chickenpox, shingles is not contagious, but it does cause painful symptoms such as headache, sensitivity to light, rashes, blistering, and trouble thinking clearly. There is no cure for shingles, but there are treatments that can reduce the pain and symptoms associated with it, including medical marijuana.
How Medical Marijuana Helps Patients with Shingles
Shingles causes pain in part by attacking nerve cells. Traditional painkillers like morphine do not work well since shingles damages the receptors that would ordinarily allow traditional painkillers to provide relief. However, the receptors for cannabis and cannabinoids are located throughout the body and are not attacked by the shingles virus allowing medical marijuana to provide pain relief to shingles patients. Medical marijuana can also reduce inflammation, one of the major symptoms of shingles. Several studies have investigated the actions that allow medical marijuana to provide these types of relief:
- The natural endocannabinoid system present in the human body, which cannabinoids in medical marijuana can activate, has neuro-protective functions that can fight nerve inflammation and damage. By activating the CB1 receptor in the body, cannabinoids from medical marijuana can encourage these neuro-protective actions (Regulatory Role of Cannabinoid Receptor 1 in Stress-Induced Excitotoxicity and Neuroinflammation, Silvia, Z., et al.)
- Painkillers such as morphine can have a detrimental effect on the body’s ability to fight against pain on its own. Chronic or long term use of opioid painkillers has been shown to interfere with the action of the body’s natural endocannabinoids, especially once tolerance to opioids has developed (Chronic Morphine Modulates the Contents of Endocannabinoid, 2-Arachidonoyl Glycerol, Viganò, D., et al.)
- There are two known cannabinoid receptors in the body, CB1 and CB2. CB1 is more frequently found in the nervous system, particularly in the cerebellum and basal ganglia [where the pain caused by shingles primarily originates]. Activating the CB1 receptor causes significant reduction in neuroinflammation (Inflammation and aging: can endocannabinoids help, Marchalant, Y., et al.)
Medical marijuana can help relieve the symptoms of pain caused by shingles as well as potentially reduce inflammation and protect nerve cells no matter how patients choose to take their medication. This means that shingles patients have many options of how to medicate using medical marijuana according to what feels most comfortable. These options include:
- Vaporizing medical marijuana using vaporizer equipment to inhale medical marijuana’s cannabinoids as steam
- Smoking medical marijuana through more traditional means, such as pipes or cigarettes
- Ingesting medical marijuana prepared in food, liquids or tinctures
As research continues, scientists are learning more about how medical marijuana can help shingles patients, as well as coming closer to a cure for this painful disease. Many patients with shingles have found relief through cannabis, which is approved for chronic pain in most medical marijuana states. Speak with your doctor to find out if medical marijuana might be right for you.
Regulatory role of cannabinoid receptor 1 in stress-induced excitotoxicity and neuroinflammation.
- Department of Pharmacology, Faculty of Medicine, Universidad Complutense de Madrid, Madrid, Spain.
Exposure to stress elicits excitoxicity and neuroinflammation in the brain, contributing to cell death and damage in stress-related neurological and neuropsychiatric diseases. The endocannabinoid system is present in stress-responsive neural circuits and has been proposed as an endogenous neuroprotective system activated in some neuropathological scenarios to restore homeostasis. To elucidate the possible regulatory role of cannabinoid receptor 1 (CB1) in stress-induced excitotoxicity and neuroinflammation, both genetic and pharmacological approaches were used alternatively: (1) wild-type (WT) and CB1 knockout mice (CB1-KO) were exposed to immobilization/acoustic stress (2 h/day for 4 days) and (2) to specifically activate CB1, the selective CB1 agonist Arachidonyl-2′-chloroethylamide (ACEA) (2.5 mg/kg) was intraperitoneally administered daily to some groups of animals. Stress exposure increased CB1 mRNA and protein expression in the prefrontal cortex of WT mice in a mechanism related to N-methyl-D-aspartate glutamate receptor activation. Daily ACEA pretreatment prevented stress-induced: (1) upregulation of CB1 mRNA and protein, (2) decrease in glutamate uptake and glutamate astroglial transporter excitatory amino acid transporter 2 expression, (3) increase in consecutive proinflammatory molecules, such as cytokines (tumor necrosis factor-α and MCP-1), nuclear factor kappa B, and enzymatic sources, such as inducible nitric oxide synthase (NOS-2) and cyclooxygenase-2 (COX-2), (4) increase in lipid peroxidation; although having no effect on plasma corticosterone. Interestingly, a possible related mechanism could be the positive ACEA modulation of the antiinflammatory pathway deoxyprostaglandin/peroxisome proliferator-activated receptor γ (15d-PGJ(2)/PPARγ). Conversely, KO animal experiments indicated that a lack of CB1 produces hypothalamic/pituitary/adrenal (HPA) axis dysregulation and exacerbates stress-induced excitotoxic/neuroinflammatory responses. These multifaceted neuroprotective effects suggest that CB1 activation could be a new therapeutic strategy against neurological/neuropsychiatric pathologies with HPA axis dysregulation and an excitotoxic/neuroinflammatory component in their pathophysiology.
Cannabinoids as pharmacotherapies for neuropathic pain: from the bench to the bedside.
- Neuroscience and Behavior Program, Department of Psychology, University of Georgia, Athens, Georgia 30602, USA.
Neuropathic pain is a debilitating form of chronic pain resulting from nerve injury, disease states, or toxic insults. Neuropathic pain is often refractory to conventional pharmacotherapies, necessitating validation of novel analgesics. Cannabinoids, drugs that share the same target as Delta(9)-tetrahydrocannabinol (Delta(9)-THC), the psychoactive ingredient in cannabis, have the potential to address this unmet need. Here, we review studies evaluating cannabinoids for neuropathic pain management in the clinical and preclinical literature. Neuropathic pain associated with nerve injury, diabetes, chemotherapeutic treatment, human immunodeficiency virus, multiple sclerosis, and herpes zoster infection is considered. In animals, cannabinoids attenuate neuropathic nociception produced by traumatic nerve injury, disease, and toxic insults. Effects of mixed cannabinoid CB(1)/CB(2) agonists, CB(2) selective agonists, and modulators of the endocannabinoid system (i.e., inhibitors of transport or degradation) are compared. Effects of genetic disruption of cannabinoid receptors or enzymes controlling endocannabinoid degradation on neuropathic nociception are described. Specific forms of allodynia and hyperalgesia modulated by cannabinoids are also considered. In humans, effects of smoked marijuana, synthetic Delta(9)-THC analogs (e.g., Marinol, Cesamet) and medicinal cannabis preparations containing both Delta(9)-THC and cannabidiol (e.g., Sativex, Cannador) in neuropathic pain states are reviewed. Clinical studies largely affirm that neuropathic pain patients derive benefits from cannabinoid treatment. Subjective (i.e., rating scales) and objective (i.e., stimulus-evoked) measures of pain and quality of life are considered. Finally, limitations of cannabinoid pharmacotherapies are discussed together with directions for future research.