This chapter addresses the following neurological conditions: cognitive decline, Alzheimer's disease, multiple sclerosis, atrophic lateral sclerosis, Parkinson's disease, Huntington's disease, epilepsy, glaucoma, restless leg syndrome, and hot flashes. Strokes are covered under Cardiovascular Conditions.
Cognitive impairment occurs in approximately 36% of older adults. Of these, roughly 14% are classified as having dementia. However, dementia prevalence increases with age, reaching 37% among individuals aged 90 and older[Graham_1997][Plassman_2007][Roberts_2013][Plassman_2008]. These percentages vary somewhat from one study to the next. The relevance of cannabis compounds for treating impairment appears not to be strongly influenced by the degree of impairment.
Several general strategies are available for fighting cognitive decline. Neurogenesis is possible in some cases.
Some of the best approaches to preventing neurodegeneration don't involve cannabis compounds. Avoiding environmental neurotoxins helps. The starting point is knowing what they are and how to avoid them. Reviewing a list of environmental neurotoxins may help. Aluminum is a neurotoxin, for example.
Toxin removal is also essential, but the most effective removal technique may be a deep, dreamless sleep. During sleep, the need for oxygen subsides, then blood volume drops and makes way for waves of cerebrospinal fluid to enter and wash away the toxins, including amyloid-beta[Harrison_2018][Fultz_2019]. Unfortunately, many people tend to suffer from insomnia. Little is known about whether sleep aids, including those listed in the Sleep Disorders discussion in the Psychiatric Conditions article, interfere with the wash cycle.
A third general strategy is to neutralize toxins instead of removing them. CBD has been found superior to both alpha-tocopherol and Vitamin C in protecting neurons of the rat cerebral cortex from toxicity[Hampson_2006]. Finally, there is the possibility of supporting the brain's microglial cells. These little scavengers are found throughout the brain and spinal cord. They eat damaged neurons, cellular debris, foreign substances, microbes, and cancer cells, among other things[WikiProjects_Physiology_2019]. BCP (β-caryophyllene), CBD, and THC can protect microglial cells by suppressing inflammation[Guo_2014][Kozela_2010].
Several degenerative neurological conditions involve prions — misfolded proteins capable of replication. They cause Creutzfeldt–Jakob disease and are implicated in several other illnesses such as amyotrophic lateral sclerosis (ALS), Alzheimer's disease, Parkinson's disease, and Huntington's disease, not to mention animal spongiform encephalopathies[WikiProjects_Molecular_and_Cell_Biology_2019]. They spread from cell to cell and throughout the brain[Hasegawa_2016]. CBD prevents prion accumulation and protects neurons against prion toxicity in animal studies[Dirikoc_2007].
Hope for reversing neurodegeneration in adults rests partly with the three areas of the brain that are capable of neurogenesis. One area dubbed the "SVZ" produces neurons that travel to the olfactory bulb, where they process smells. The second area is within the hippocampus, which is responsible for forming new long-term memories and is also involved with spatial memory and navigation. The third area is the striatum, which processes reward stimuli and performs stimulus-response learning[Prenderville_2015][WikiProject_Neuroscience_2019][WikiProject_Neuroscience_2019b][Yassa_2018][Arias-Carrión_2008][Ernst_2014].
Either acute or chronic administration of high-dose CBD has restored damaged memory in mice, possibly through neurogenesis in the hippocampus[Fagherazzi_2011]. CBD also enhanced neurogenesis in the hippocampus of young adult mice[Wolf_2010], as did CBC[Shinjyo_2013].
A chronic low dose of THC restored cognitive function in old mice, apparently due to restored hippocampal function[Bilkei-Gorzo_2017]. However, higher doses of pure THC may not be suitable. THC induces temporary memory impairment in humans, whereas THC+CBD does not[Morgan_2011]. BCP (β-caryophyllene) may stimulate neurogenesis in older mice and humans. An animal study showed that the experimental drug JWH-133 acts on the CB2 cannabinoid receptor in such a way as to promote neurogenesis. BCP stimulates the CB2 cannabinoid receptor and may promote neurogenesis as well[Goncalves_2008][Gertsch_2008].
The significance of these results in restoring hippocampal function is that, on the one hand, the hippocampus is essential to the formation of new memories. On the other, it is easily damaged by stress, Alzheimer's disease, and mental illnesses, including depression, schizophrenia, and PTSD. Patients with mild but observable cognitive impairment have 10-15% loss of hippocampus volume, those with early Alzheimer's have 15-30% loss, and in those with moderate Alzheimer's, it may reach 50%[Anand_2012].
Roughly 70% of those with dementia have Alzheimer's dementia. Of the remaining categories, 17% have vascular dementia, and 13% have some other form — in decreasing order, an undetermined form, Parkinson's dementia, normal-pressure hydrocephalus, frontal lobe dementia, alcoholic dementia, traumatic brain injury, and Lewy body dementia[Plassman_2007][What_Is_Alzheimers_2019].
Alzheimer's has understandably attracted more research interest than other types of dementia. The same is true of research into the use of cannabis compounds for dementia. While humans are the only animals that can get Alzheimer's, transgenic mice with human Alzheimer's genes have been developed. They provide some insights but do not fully replicate Alzheimer's[Cavanaugh_2914][Laurijssens_2012].
This section starts with a brief introduction to Alzheimer's, followed by research related to controlling damage from beta-amyloid and the tau protein, and lastly, controlling behavioral symptoms.
Alzheimer's develops both inside and outside of brain neurons. Inside, the tau protein, which is involved in constructing and maintaining a cell's cytoskeleton, becomes damaged. Damaged tau then forms clumps known as neurofibrillary tangles that interfere with normal cell function[Medicine_2019].
Outside of neurons, amyloid-beta proteins (Aβ proteins) become misfolded and form clumps known as plaques that are toxic to neurons. Aβ itself is an intermediary waste product formed during the metabolism of a normal protein. Unfortunately, forming plaques thwarts the successful disposal of Aβ, setting up a vicious cycle[wiki_Amyloid_precursor_protein]. Crucially, Aβ damages tau[Bloom_2014].
In the brain's learning and memory centers, the neurotransmitter acetylcholine plays an essential role in forming and preserving memories by binding to several types of acetylcholine receptors. Unfortunately, Aβ can disable and destroy some types of acetylcholine receptors[Acetylcholine_2020][Kihara_2004].
The brain's acetylcholine is mainly produced by neurons in the basal forebrain and then distributed throughout the brain and central nervous system. Unfortunately, Aβ can kill the acetylcholine-producing neurons, reducing acetylcholine levels by as much as 90%[Neuroscience_2019][Pedersen_1996][Alzheimers_2017].
Neurons dispose of used acetylcholine using the acetylcholinesterase enzyme. Acetylcholinesterase inhibitors can raise acetylcholine levels, providing symptomatic relief. Unfortunately, this does nothing to slow the progression of the disease[Georgi_2005].
As is usually the case with brain damage, dying neurons release free radicals, causing inflammation and collateral damage.
Laboratory in vitro studies show that low-dose THC reduces inflammation, is effective at lowering Aβ levels, and inhibits Aβ aggregation[Currais_2016][Eubanks_2008][Yaqiong_2014]. THC and CBN act synergistically to remove intraneuronal Aβ, reduce oxidative damage, and protect neurons from loss of energy[Schuber_2017]. An in vitro study of CBD suggests that CBD reduces Aβ-induced toxicity[Iuvone_2004].
BCP (β-Caryophyllene) can reduce Aβ plaques[Cheng_2014].
Apigenin dissolves Aβ and thus inhibits neuron death. Apigenin also protects the capillaries that maintain the blood-brain barrier, thereby preventing Aβ from robbing neurons of their blood supply[Zhao_2013][Zhao_2011].
Linalool protects against Aβ-induced cognitive deficits and damage[Xu_2017].
In vitro experiments suggest the following: CBD inhibits Aβ-induced damage to tau protein[Esposito_2005]. CBD reduces Aβ-induced neuroinflammation and promotes hippocampal neurogenesis[Esposito_2011][Hampson_2000]. CBD lowers toxicity caused by Aβ[Iuvone_2004][Esposito_2007].
Eucalyptol also mitigates inflammation caused by Aβ deposits[Hu_2017]. β-Caryophyllene inhibits neuroinflammation as well[Guo_2014]. So does trans-caryophyllene[Hu_2017].
Linalool reverses the microscopically visible
hallmarks of AD and restores cognitive and emotional functions via an
In a mouse model of the early stages of late-onset Alzheimer's, CBD+THC preserved memory and reduced learning impairment. CBD and THC had the same effect individually but were less effective[Aso_2015].
Both mice and humans make and recognize social contacts. Alzheimer's destroy this capability. The same is true in a mouse model of Alzheimer's. In the mouse model, long-term treatment with CBD preserved the capacity to recognize social contacts[Cheng_2014b][Cheng_2014a].
THC is an acetylcholinesterase inhibiter, implying that THC provides symptomatic relief[Yaqiong_2014]. It inhibits Aβ aggregation more effectively than some commercial acetylcholinesterase inhibitors[Eubanks_2008]. α-pinene is a potent acetylcholinesterase inhibitor and is anti-inflammatory as well[Miyazawa_2005][Inhibition_2012].
Multiple sclerosis is an autoimmune inflammatory disease that wreaks havoc by stripping protective insulation, known as myelin, from the surfaces of neurons in the brain and spinal cord[Multiple_sclerosis_2020].
A consensus of medical experts is that using equal parts of CBD and THC improves patient-reported spasticity symptoms[NASEM_2017].
CBD provides long-lasting protection against the harmful effects of inflammation in a viral model of multiple sclerosis. It strengthens the blood-brain barrier and inhibits the pro-inflammatory cytokine IL-1β[Mecha_2013].
One experimental model of multiple sclerosis is experimental autoimmune encephalomyelitis; CBD is effective in this model[Elliott_2018]. So are CBG[Carrillo-Salinas_2014] and BCP[Fontes_2014].
THC suppressed immune response in a mouse model of multiple sclerosis; the significance is that multiple sclerosis is believed to be an autoimmune disease[Lyman_1989][Zgair_2017].
THC has been helpful for spasticity[Vaney_2004][Petro_1981][Killestein_2014]. Whole cannabis extracts have also helped treat spasticity[Zajicek_2003][Ungerleider_1987][Wade_2004][Wade_2006].
THC and whole cannabis extracts have been helpful with urge incontinence[Freeman_2006]. THC, in combination with CBD, has also effectively reduced urinary incontinence[Brady_2004].
THC in combination with CBD effectively treats insomnia, neuropathic pain, and other neurological symptoms of multiple sclerosis[Perras_2005].
A spray preparation of CBD+THC (Sativex) directed towards the mucous surfaces of the mouth is helpful for multiple sclerosis symptoms, including neuropathic pain, dysesthesia, allodynia, spasticity, muscle spasms, and sleep disturbances[Rog_2005][Perras_2005][Barnes_2006][Collin_2007][Rog_2007][Novotna_2011].
A small anonymous survey of 112 cannabis smokers with multiple sclerosis rated the effectiveness of street cannabis against common symptoms. The results, in decreasing order of benefit, were: spasticity, chronic pain of extremities, acute paroxysmal phenomenon, tremor, emotional dysfunction, anorexia/weight loss, fatigue states, double vision, sexual dysfunction, bowel, and bladder dysfunctions, vision dimness, dysfunctions of walking and balance, and memory loss. Spasticity was improved for 92% of the patients, whereas memory loss was improved for only 30%[Consroe_1997].
A CBG metabolite alleviated neuroinflamation in an animal model of multiple sclerosis[Granja_2012].
Parkinson's disease results from the die-off of dopamine-producing neurons that supply parts of the brain involved in movement and reward, specifically, the substantia nigra[Parkinsons_2020].
BCP (β-Caryophyllene) protects against oxidative stress, neuroinflammation, and the destruction of dopaminergic neurons in the substantia nigra[Viveros-_2017][Ojha_2016][Viveros-Paredes_2017]. The positive impact of BCP may be related to the reduction of CB2 receptors[García_2017].
THCV provides symptom relief and protects against loss of neurons in the substantia nigra[García_2011]. THC, THCA, and CBD are all protective of dopamine-producing neurons in vitro[Rudolf_2012]. Most of the beneficial effects of these cannabis compounds appear to be from their value as antioxidants[García-Arencibia_2005].Given its antioxidant properties and its ability to activate CB2 but to block CB1 receptors, Δ9-THCV has a promising pharmacological profile for delaying disease progression in PD and also for lesening parkinsonian symptoms[García_2011].
CBD significantly reduced Parkinson-related psychosis in half a
dozen outpatients[Zuardi_2008]. CBD improved excessive physical movement during the rapid-eye phase of
A negative result. An orally administered cannabis extract showed no objective or subjective improvement in dyskinesias or parkinsonism[García-Arencibia_2005]. Nor did smoked marijuana[Zuardi_2008]. But in one study, cannabis did help with Parkinson's involuntary muscle movements[Carroll_2004].
Essential tremor is about ten times as common as Parkinson's. It involves shaking of hands and other extremities and is thought to be caused by a loss of fine motor control in the cerebellum. The cerebellum plays a central role in fine motor coordination and is involved in many forms of cognition[Neuroscience_2020][Neuroscience_2020]. Essential tremor is consistently associated with cognitive impairment and, in older people, dementia[Janicki_2013].
Some credible testimonials on the benefits of CBD for essential tremor have been posted in various places, including one on a Mayo Clinic site[Mayo_Clinic_2019] and several in the closed Facebook group "Essential Tremor on CBD."
Recently, a team at the University of California at San Diego has gone forward with a clinical trial based on testimonials and positive results for similar diseases such as Parkinson's. The trial uses a 20:1 CBD:THC product imported from Canada[CNBNewsnet_2019].
Huntington's is an inherited genetic illness involving mutant forms of the Huntington protein. The mutant form causes neuronal stress leading to the premature death of brain neurons, especially in the striatum, which coordinates movement, and in the frontal cortex, which controls thinking and emotions[Huntington_2020]. This is the disease that killed Woody Guthrie[Woody_Guthrie_2020].
Conventional treatments provide symptomatic relief: physical therapy and tetrabenazine for movement problems; antidepressants, mood stabilizers, and atypical antipsychotics for psychiatric symptoms[Woody_Guthrie_2020].
β-Caryophyllene and similar chemicals may protect against neuron injury and reduce neuroinflammation[Palazuelos_2009].
CBG has shown significant neuroprotection in animal models of Huntington's disease[Valdeolivas_2014].
CBD has shown neuroprotection in animal models, apparently due solely to its antioxidant properties[Sagredo_2007]. However, in human clinical trials, CBD by itself appears to be neither helpful nor harmful[Consroe_1991]. CBD+THC is neuroprotective and delays disease progression[Sagredo_2011][Valdeolivas_2012]. However, THC by itself seems to be counterproductive[Lastres-Becker_2003].
TBI patients who tested positive for THC when admitted to a Level 1 trauma center had a 2.4% mortality rate. In contrast, patients who tested negative had an 11.5% mortality rate. After adjusting for age and other confounding factors, those with THC still did better[Nguyen_2014]. This improvement could be partially due to the lowering of the TNF-α Cytokine[Mechoulam_2002].
In one case of severe TBI, a combination of CBD and essential fatty acids accompanied dramatic recovery[Klug_2019].
Several research articles report that CB2 receptor agonists help with brain injury[Zhang_2007][Amenta_2012][Amenta_2014][Braun_2018]. The same is likely true of the natural CB2 receptor agonist BCP. However, the newer synthetic CB2 agonists are progressively more potent, so adequate dose sizes could be significantly different.
Hypoxia in newborn infants. Newborns often
suffer from oxygen deprivation during delivery. The traditional treatment
is hypothermia, administered as soon after birth as possible. It is somewhat
effective. Pure CBD administered intravenously to (human) newborns was
also somewhat effective, but the two treatments combined have produced the most robust
The use of CBD alone in newborn mice allowed quantitative
measurement of improvement. Surprisingly, the therapeutic effect
was seen when treatment was delayed by as much as 18 hours[Mohammed_2017].
The available evidence supports the adjunctive use of CBD for epilepsy as accepted medical practice[Perucca_2017][Rosenberg_2015][Carlini_1981]. Much of the progress in this area is due in no small part to Charlotte Figi's success with Dravet syndrome[Maa_2014_2014][Charlotte_Figi_2020]. Cannabidiol has performed well in several clinical trials — Dravet syndrome[Devinsky_2017], Sturge-Weber syndrome[Kaplan_2017], Lennox-Gastaut[Thiele_2018], and other forms of treatment-resistant epilepsy[Devinsky_2015].
BCP inhibited seizures and protected against associated neurological damage in mouse experiments[de_Oliveira_2016][Tchekalarova_2018]. These results may be due mainly to BCP's anti-inflammatory properties.
An animal study suggests that THCV may be useful for treating epilepsy[Hill_2010]. Another study indicates that Linalool may compare favorably with diazepam (Vallium) and phenytoin (Dilantin)[De_Sousa_2010].
Restless Leg syndrome provides a recent example of how cannabis research progresses. A few desperate people experiment — with CBD, for instance. Then they get good results and post emphatic testimonials in odd places[White_2016]. Somewhere in the world, a doctor becomes intrigued and enlists colleagues to do some case studies[Megelin_2017][Ghorayeb_2018]. With good results, they recommend clinical trials.
Interest in cannabinoids for eye problems began with the observation that smoked marijuana and several individual cannabinoids can temporarily reduce intra-optic eye pressure. Marijuana may also have a neuroprotective effect in reducing the damage caused by glaucoma.
Research suggests that cannabinoids such as CBD and THC can play a direct role in slowing disease progression. Such diseases include glaucoma, diabetic retinopathy, age-related macular degeneration, and retinitis pigmentosa.
Before light can reach an eye's rods and cones, it travels through several other layers of neurons. The first is the "wires" that carry information to the optic nerve[Retinal_nerve_fiber_layer_2018]. Here is a quick summary of what's known, gleaned from a review of the research and a sample research paper[Rapino_2018][El-Remessy_2003].
The retina layers are packed with cannabinoid-sensitive receptors — the cannabinoid receptors CB1 and C2 plus four others: GPR55, TRPV1, PPARα, and PPARγ. Why would the retina be so heavily involved in cannabinoid metabolism? Endocannabinoids play a key role in protecting the retina from neurotoxins produced during retinal neurons' normal functioning.
Boosting endocannabinoid levels has decreased neurotoxic damage associated with glaucoma and other diseases. In a few animal studies, THC and CBD have also slowed disease progression.
In an animal study, chronic topical administration of either CBG or CBD significantly reduced intra-ocular eye pressure, but CBD had undesirable side effects[Colasant_1984]. THC, delta 8-THC, CBN, and CBG all reduce intraocular pressure[Elsohly_1981].
In a clinical trial, inhaled THC reduced both blood pressure and intraocular eye pressure for 3 to 4 hours. Both of these effects were greater in subjects with hypertension[Crawford_1979].
Cannabinoids are oils, and eyes are mostly water. Dabbing CBD on the outside of an eye doesn't do much. Finding a topical version of CBD for eyes is an active area of research. Options include water-miscible cannabinoid suspensions and water-soluble procannabinoids with cannabinoid metabolites.
Hot flashes involve feelings of intense heat with sweating and a rapid heartbeat. Each occurrence typically lasts from 2 to 30 minutes[wiki_hotflash]. Moderate to severe hot flashes continue after menopause for nearly five years on average but continue for ten years or more in a third of post-menopausal women[Freeman_2014].
Hot flashes involve a dysregulation of the brain's temperature control mechanism in the hypothalamus. It regulates core body temperatures between an upper threshold for sweating and a lower threshold for shivering. There is a thermoneutral zone within which the body regulates temperature without resort to sweating or shivering.
Hot flashes are associated with narrowing the thermoneutral zone coupled with the core body temperature going above the upper threshold. Among women who do not have hot flashes, the thermoneutral zone is approximately 0.72°F. In contrast, it is virtually nonexistent among women with hot flashes. High brain levels of the norepinephrine neurotransmitter shrink the thermoneutral zone. So does activation of the sympathetic nervous system, which is the portion of the autonomic nervous system responsible for the fight-or-flight response. The hypothalamus controls the autonomic nervous system[Freedman_2013].
The drug clonidine lowers norepinephrine release, raises the sweating threshold, and reduces shivering, thus reducing hot flashes. The hormone estradiol, the FDA-approved approach to hot flashes, raises the sweating threshold and lowers norepinephrine levels. A third strategy for lowering hot flashes is to go directly after the sympathetic nervous system. Slow, deep breathing calms the sympathetic nervous system and brings a 50% reduction in hot flashes (practice required)[Freedman_2013][Herbison_2000].
Finally, we come to how cannabis compounds can reduce hot flashes. To begin with, it seems they can, judging from women's emphatic testimonials[Gordon_xxx].
There has been no systematic research on how cannabis compounds affect hot flashes. However, from the above, it appears that beneficial cannabis compounds calm the sympathetic nervous system, reduce norepinephrine levels, and lower central body temperature. THC lowers central body temperature[Scott_2011]. THC may also inhibit norepinephrine in sympathetic nerves[Ishac_1996][Pfitzer_2005].
Many indica marijuana strains contain the sedative terpene d-linalool; it depresses the autonomic nervous system and may thus also widen the thermoneutral zone[Kuroda_2005].
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