9-tetrahydrocannabinol (THC) is the primary psychoactive component in Cannabis, according to research (THC). The CB1 and CB2 receptor subtypes of selective cannabinoid receptors are seen in the brain and peripheral cells. THC primarily exerts its effects on the central nervous system by interacting with CB1 cannabinoid receptors (CNS) AEA and 2-AG seen in animal and human brain tissues.
After discovering the receptors, they constructed a reuptake mechanism and hydrolytic enzymes. Cannabinoid receptors, Delta 9 THC, synthesis, and inactivation proteins make up the endocannabinoid system.
In multiple sclerosis animal models, the endocannabinoid system regulates synaptic neurotransmission and tonically governs clinical symptoms such as stiffness and tremor (MS). Delta 9 extracts have recently been tested in clinical trials, providing more support for MS patients’ assertions that it may help with symptom management. One sees Delta 9 THC to control glutamate release, oxidant free radicals, and calcium influxes in vitro, leading to neuronal death in neuro-inflammatory illnesses when there is an overabundance.
Multiple Sclerosis and Delta 9 THC:
MS is a devastating central nervous system disease caused by the demyelination of nerve fibers. In their 20s, women are more affected than men (2:1). Fatigue, balance problems, muscle weakness, incontinence, spasms, discomfort, and tremor are symptoms. According to clinical investigations, multiple sclerosis (MS) comprises two phases: sudden relapses and gradual progression.
Hereditary and environmental factors seem to affect the disease’s progression. Relapsing-remitting MS is common (RR-MS). The number of relapses decreases over time, and most patients have gradual neurological deficits (the so-called secondary advanced phase). Primary progressive MS (PPMS) has no acute relapses.
Once patients approach the secondary advanced phase, RR-MS progresses similarly to PP-MS. In the RR-MS phase, CNS lesions tend to develop in white matter. They are commonly associated with blood-brain barrier breakdown, local edema, and demyelination, all of which are symptomatic of an inflammatory process. This sort of inflammatory activity is considerably less visible in the PP-MS phase.
Advanced stage global brain atrophy is related to disability. Despite faster impairment progression in the relapsing-remitting phase, inflammatory activity reduces. These findings suggest that disease progression reduces inflammatory activity. Active MS characterizes by T-cell, macrophage, B-cell infiltrations, myelin and axon degradation, and reactive astrocytes and microglia.
Primary demyelination is caused by inflammatory lesions that inhibit neurotransmission. MS treatments are anti-inflammatory, immunosuppressive, and immunomodulatory. These drugs are only partially effective and have adverse effects many patients can’t handle.
Anandamide (AEA), an endogenous cannabinoid, protects neurons from inflammation-induced damage by rapidly activating MKP-1 in microglial cells via the CB (1/2) receptor.
Injured CNS tissue may secrete AEA, limiting inflammatory cytokine release and immune response. Delta 9 THC is immunosuppressive, according to a study. They suppress Th1 cytokines while increasing Th2 cytokines, which have therapeutic advantages in MS.
Disease progression connects to Th1 shifts. Delta 9 THC affects IL-12 in macrophages and cerebral microglia. In primary cultures of macrophages and microglia caused by lipopolysaccharide/IFN- and Theiler’s virus, its effects on IL-12 and IL-23 mRNA and protein IL-12 p40 came in front of research. Marijuana activates CB2 receptors, reducing microglia cytokine production. Marijuana’s effects on cytokine brain function and neuroinflammatory regulation may influence MS.
Anecdotal evidence suggests that Delta 9 THC can significantly alleviate the symptoms of Multiple Sclerosis, but the comprehensive assessment of their psychotropic effects is critical for their therapeutic application. Many people with Multiple Sclerosis are self-medicating with delta 9 THC, which might help alleviate symptoms such as spasticity and discomfort.
Multiple Sclerosis (MS) spasticity treatment:
MS connects with debilitating symptoms that frequently reduce the quality of life for those who suffer from it. Swelling, tremors, and bladder incontinence are among the symptoms of this condition. Treatment of these symptoms and immune modulation and immunosuppression have gained increasing attention to manage this long-term condition.
Multiple Sclerosis (MS) sufferers often experience significant discomfort, decreased mobility, and difficulties in everyday activities as a result of muscle tone being high (tonic spasticity) or temporarily as painful cramps (phasic spasticity). Up to 90% of MS patients experience muscle spasticity and spasms at some time, among the many symptoms the disease can cause. When the spinal cord is damaged, cramps can occur.
Spasticity can also occur in children with cerebral palsy. That is especially true after a stroke or other trauma to the brain. Urinary tract infections, bladder and rectum distension, discomfort, and pressure sores contribute to spasticity development and worsening. The primary goal of antispastic treatment is to improve motor performance by lowering muscular tone; patients may benefit from learning proper posture, positioning, and weight shift strategies. Avoiding pressure sores and contractures are two further aims of spasticity treatment. There is no medication treatment plan for spasticity devices, and the available medicines are frequently unsuccessful.
Physiotherapy is the usual treatment for MS spasticity, although most patients don’t respond. Antispastics are needed. Tizanidine and baclofen are common antispastics. A recent assessment of clinical trials found that tizanidine’s efficacy and global acceptability are comparable to baclofen or diazepam.
Tizanidine with baclofen reduced spasticity in a clinical case study. According to a survey, tizanidine monotherapy can relieve spasticity. According to a case study, combination therapy helps manage spasticity and dose-dependent adverse effects. One rarely uses Dantrolene and tolperisone. Benzodiazepines are second-line antispastic drugs since they cause sleepiness and dependence. Gabapentin treats phasic spasticity.
Botulinum toxin type A
Botulinum toxin type A reduces muscular tone, although antispastic drugs are ineffective in targeted spasticity (e.g., adductor spasticity or equinovarus deviation).
Various open-label, masked, and placebo-controlled studies have proved the usefulness of intramuscular botulinum toxin injections in treating spasticity caused by MS, brain and spinal cord injury, cerebral palsy, and stroke. At least two investigations demonstrate that intrathecal baclofen, administered by an infusion pump, reduces muscle tone and spasms, but its effectiveness fades over time.
MS medicines now on the market are only partially effective and have a high risk of side effects that many patients cannot manage. Anecdotal information suggests that marijuana can help alleviate symptoms such as stiffness, discomfort, tremors, and bladder dysfunction, which is corroborated by recent scientific trials of medical Delta 9 THC extracts.
According to recent research, understanding how Delta 9 THC and novel cannabinoid-derived compounds interact with MS could create new therapeutic models to alleviate the disease’s most debilitating symptoms.
Current treatments for MS are only partially effective and have risks of side effects that patients cannot readily bear. The primary unanswered question regarding the use of Delta 9 THC as a new therapeutic medication for MS therapy is whether or not it can overcome these side effects to develop novel approaches.