These two rare neurodegenerative diseases show, side by side, what an honest reading of cannabis evidence looks like. In motor neurone disease, a randomised controlled trial of the THC:CBD spray nabiximols had a positive result on spasticity. In Huntington’s disease, a randomised trial of the same spray found nothing. And in the middle sits a much-repeated story about one woman that cannot support the weight placed on it.
Nothing here is medical advice. Neither condition is treatable with cannabis. Nothing below should displace neurological care or disease-modifying therapy where it exists (for ALS: riluzole and others; none is approved for Huntington’s). In Thailand cannabis flower is a controlled herb dispensed only on prescription form PT 33.
1. Amyotrophic Lateral Sclerosis
ALS (motor neurone disease, also called Lou Gehrig’s disease) is the death of motor neurons in the brain and spinal cord. It causes progressive loss of control of the limbs, breathing, swallowing and speech, with muscle weakness and wasting. It is fatal, and the disease-modifying drugs available slow it modestly at best.
What is commonly claimed. Cannabis may help ALS patients by reducing pain, spasticity, drooling and appetite loss. THC with other cannabinoids benefited laboratory mice with ALS. Clinical trials of cannabinoids in humans are needed.
Every part of that is a symptom claim except the mouse work, and the call for trials is the correct conclusion to draw from an animal result. So far, so honest.
What happened next: the trial. CANALS (Riva N et al., The Lancet Neurology 2019;18(2):155–164) was a multicentre, double-blind, randomised, placebo-controlled phase 2 trial of nabiximols (Sativex). Nabiximols is the roughly 1:1 THC:CBD oromucosal spray also used for spasticity in multiple sclerosis. Sixty patients with motor neurone disease were randomised and 59 were analysed. Treatment ran six weeks, and the primary outcome was spasticity on the Modified Ashworth Scale.
Result: spasticity scores improved slightly in the nabiximols group (mean −0.11), while the placebo group’s scores deteriorated (+0.16). The treatment was well tolerated, with no serious adverse events, and the authors recommended investigation in larger clinical trials.
That is a genuinely positive result in a difficult population, and it deserves to be reported as such. Note precisely what it is: a six-week phase 2 trial with spasticity as the outcome. It says nothing about survival, disease progression or motor neuron loss. It is symptom control in a disease where symptom control matters enormously.
2. The Cathy Jordan Story, and Why It Cannot Do the Work
The account that circulates is this. Cathy Jordan, a Florida medical cannabis advocate, was diagnosed with ALS in 1986 and told by her neurologist she had three to five years to live. She began using cannabis in the late 1980s and credited it with her survival. She died in July 2024, aged 74, about 38 years after her diagnosis. In a widely quoted 2014 interview, she said she had asked her doctors whether they would take a drug that was neuroprotective, antioxidant and anti-inflammatory, meaning cannabis. She also noted that ALS patient associations fight for the right to die with dignity: “But what about my right to life?”
Read as a human account, it is powerful, and her argument about the right to live is a serious one.
Read as evidence, it establishes nothing. Her diagnosis and disease course were not independently documented in the medical literature; the story rests on her own account and press coverage. And even if the diagnosis is accepted, the main problem is specific to ALS rather than a general objection.
ALS is unusual among fatal diseases in the width of its survival distribution. Most patients die within a few years, but a small minority live for decades. Stephen Hawking was diagnosed at 21 and lived a further 55 years, with no suggestion that cannabis played any part. Long survivors exist and are documented, which is why one long survivor cannot implicate whatever they happened to be taking.
Put it as a question: if a treatment had no effect whatsoever, would we still expect to find long survivors who used it? In ALS, yes, with certainty. Which means observing one tells you nothing. This is the general problem with personal testimony as medical evidence, and ALS is the sharpest specific example of it.
3. Huntington’s Disease
Huntington’s disease is an inherited neurodegenerative disorder that causes involuntary movements, cognitive decline and psychiatric symptoms. There is a specific reason to expect cannabinoids to matter: patients with Huntington’s show a marked reduction in CB1 receptors in the striatum, the brain region the disease attacks.
The animal work. Spanish groups, including Javier Fernández-Ruiz’s at Complutense University, have studied THC and CBD in Huntington’s models. The best-known THC result is Blázquez C et al. (Brain 2011;134(Pt 1):119–136). In R6/2 mice, which carry a fragment of human mutant huntingtin, THC ameliorated motor symptoms, neuropathology and molecular pathology. The authors argued that losing striatal CB1 receptors is itself a key driver of the disease. That is a strong preclinical result on a mechanistically coherent target.
The human trials.
- CBD alone: Consroe P et al., Pharmacol Biochem Behav 1991;40(3):701–708 (University of Arizona). Double-blind crossover trial in 15 patients, about 10 mg/kg/day for six weeks. CBD was neither symptomatically effective nor toxic compared with placebo.
- Nabilone: Curtis A et al., Mov Disord 2009;24(15):2254–2259. Double-blind crossover trial in 44 patients. There was no significant difference on the primary total motor score, but chorea and neuropsychiatric scores improved.
- Nabiximols: López-Sendón Moreno JL et al., J Neurol 2016;263(7):1390–1400. Double-blind crossover trial, 26 patients randomised, 12 weeks. The spray was safe but showed no difference from placebo on motor, cognitive, behavioural or functional scores.
The wider picture. A systematic review of randomised controlled trials of cannabis-based medicines in movement disorders (Oikonomou P, Jost WH, J Neural Transm 2022;129(10):1247–1256) identified these three RCTs in Huntington’s disease. Only one, using nabilone, found symptom relief. The review’s overall conclusion applies here: the small number of small, inhomogeneous trials rules out reliable conclusions.
4. Two Diseases, Two Lessons
| ALS / motor neurone disease | Huntington’s disease | |
|---|---|---|
| Mechanistic rationale | General neuroprotective and antispastic properties | Specific: striatal CB1 receptor loss |
| Animal evidence | Positive | Positive, with motor and neuropathological improvement |
| Human RCT evidence | One positive phase 2 trial on spasticity (CANALS, nabiximols) | Three small RCTs: CBD negative, nabiximols negative, nabilone partly positive (chorea) |
| What is claimed | Symptom relief: pain, spasticity, drooling, appetite | Symptom relief |
| What is not claimed | Survival benefit or disease modification | Survival benefit or disease modification |
The most honest contrast is the product itself. The same THC:CBD spray helped spasticity in motor neurone disease and showed no benefit in Huntington’s disease. The trials measured different symptoms, but the drug was the same. Huntington’s also had the stronger mechanistic story, with a documented receptor deficit in the exact brain region, and still produced the weaker clinical result. That pattern recurs across neurology and is worth internalising: a compelling mechanism is a reason to run a trial, not a substitute for one.
5. What This Means for Patients and Families
Both conditions are relentless, both have limited treatment options, and families in both often look beyond what is offered. That is understandable and it is not irrational.
What the evidence supports is narrow and real: symptom management, particularly spasticity. CANALS provides randomised evidence for this in motor neurone disease, and spasticity is where cannabinoids have their best-established role generally. Pain, sleep, appetite and drooling are legitimate targets for the same conversation.
What the evidence does not support is any effect on the disease itself. Nothing in this article slows neurodegeneration in a person.
The practical position for both: keep it inside the neurology service, target a named symptom, and set a defined trial period and a stopping rule. Do not let it displace disease-modifying therapy where it exists (for ALS: riluzole and others; none is approved for Huntington’s), respiratory support, nutritional support or palliative care. All of these have better evidence for the outcomes patients care about most.
6. In Thailand
Cannabis flower is a controlled herb under the Notification of the Ministry of Public Health Re: Controlled Herbs (Cannabis), B.E. 2568, issued 26 June 2025. It may be dispensed only against a prescription on form PT 33 from an authorised practitioner. Each prescription covers no more than 30 days and is single use (no refills), and the flower must come from a GACP-certified source. Online sale and advertising of flower are not permitted. Whether nabiximols itself is registered in Thailand is a separate regulatory question from whether flower is prescribable, and should be checked with the treating neurologist.
Huntington’s disease is also much less common in Asian populations. A meta-analysis found a pooled prevalence of 0.40 per 100,000 in Asian studies, against 5.70 per 100,000 in Europe, North America and Australia (Pringsheim T et al., Mov Disord 2012).
If you or a family member lives with motor neurone disease or Huntington’s in the region: was spasticity treated actively, and with what? The CANALS result is about spasticity specifically. Whether that symptom gets attention at all, by any means, is the question that most affects daily life.
This article is general educational information from the Asiannabis Community, not medical advice. Cannabis does not treat ALS or Huntington’s disease.