Does cbd oil work for sca 2
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Volume 10, Number 6, December 2020, pages 245-247
Successful Treatment of Super-Refractory Status Epilepticus With Cannabis Oil in a Patient With Neuronal Ceroid Lipofuscinosis
Athena Michaelides a, b , Spyridon Bekas a , Antigoni Papaioannou a , Athina Lazaridou a , Paola Nicolaides a
a University of Nicosia Medical School, Engomi 2408, Cyprus
b Corresponding Author: Athena Michaelides, University of Nicosia Medical School, Engomi 2408, Cyprus
Manuscript submitted August 11, 2020, accepted November 19, 2020, published online December 9, 2020
Short title: Treatment of Status Epilepticus With Cannabis Oil
Herein we describe a case of a 25-year-old man diagnosed with the “variant late infantile-onset” neuronal ceroid lipofuscinosis (NCL) who has a novel mutation in the CLN6 gene located on chromosome 15. The patient developed seizures at the age of 10 years along with progressive symptoms of ataxia, spasticity, cognitive decline and visual difficulties. At the age of 25 years, the seizures were drug-resistant, and the patient was put in an anesthesia-induced coma until the use of cannabis oil in combination with Food and Drug Administration (FDA)-approved anti-seizure drugs proved to be lifesaving. Treatment for NCL currently consists of symptomatic relief of seizures, and supportive therapies for associated symptoms of behavior, language and visual difficulties. Although limited, recent data on the efficacy of cannabinoids for treatment-resistant epilepsy have been published. Since cannabis oil is not currently FDA approved for most formulations, its use in drug-resistant epilepsy is anecdotal and remains highly controversial.
Keywords: Epilepsy; Drug-resistant seizure; Neuronal ceroid lipofuscinosis; CLN6
Neuronal ceroid lipofuscinosis (NCL) is a group of genetically inherited neurodegenerative disorders. There are 14 genetically distinct types that have been identified and are classified as CLN1 to CLN14. Most NCLs have an autosomal recessive pattern of inheritance and share clinical characteristics. The childhood types are more common and manifest as progressive vision loss, epileptic seizures, mental and motor deterioration, and premature death [ 1 ].
The management of NCL is challenging, and often requires different treatment regimens for the range of presenting symptoms. A prominent feature reported across the literature is epilepsy [ 2 – 5 ]. Since different anti-seizure drugs are not always beneficial in reducing seizures, an alternative treatment that has recently been recognized to be efficacious is cannabis oil in differing ratios of cannabidiol (CBD) and tetrahydrocannabinol (THC) [ 6 , 7 ]. Apart from Epidiolex (purified form of nearly 100% CBD), cannabis oil is not currently Food and Drug Administration (FDA) approved, so its use is controversial [ 6 ].
We describe a case of a 25-year-old man, who presented with drug-resistant epilepsy due to variant late infantile neuronal ceroid lipofuscinosis (vLINCL).
The patient described is the third son of healthy non-consanguineous Cypriot parents with no known family history of neurological disease. He was born following a full-term normal delivery and reached his early developmental milestone. There were no concerns until the age of 8 years when he developed mild learning difficulties thought to be related to impaired memory and concentration. A diagnosis of attention deficit hyperactivity disorder (ADHD) was made, and methylphenidate (ritalin) was prescribed.
At the age of 10 years, he developed his first focal motor seizure. A few months later, he had a second brief right-sided focal motor seizure with an electroencephalogram (EEG) pattern suggestive of benign childhood epilepsy with centrotemporal spikes (BCECTS), also known as benign rolandic epilepsy. At that point, ritalin was withdrawn and sodium valproate (depakine) was added.
Over the course of the year, he developed a progressive loss of motor skills and coordination – he experienced frequent falls, increasing difficulty with walking and climbing stairs, tremor and ataxia. His speech became slower and dysarthric. A brain magnetic resonance imaging (MRI) showed moderate dilation of the ventricles and extra-axial cerebrospinal fluid (CSF) spaces with minimal periventricular hyper intensities. The corpus collosum, brain stem and cervical spinal cord appeared normal. Genetic testing for spinocerebellar ataxia (SCA) excluded a diagnosis of SCA types 1, 2, 3, 6, 7, 8, 12 and 17, as well as dentatorubral-pallidoluysian atrophy (DRPLA).
His symptoms were progressive still and at the age of 14 years he was found to have proximal muscle weakness in the upper and lower limbs, and increased tone in the lower limbs with brisk reflexes and ankle clonus. He had a spastic gait ataxia with early development of scoliosis and some asymmetry at the pelvis. He also had obvious dysarthria with frequent choking episodes. On ophthalmic examination, he had failure of binocular convergence and nystagmus that was elicited on lateral gaze. Repeat MRI showed diffuse hypomyelination in the cerebrum in conjunction with cerebellar atrophy. The thalamus and globus pallidi were not thought to be atrophic.
His seizures continued to progress and remained drug-resistant requiring the use of a number of anti-seizure medications including a combination of levetiracetam, lamotrigine, lacosamide and piracetam. At the age of 22 years, genetic testing confirmed two novel variations in the CLN6 gene: a c.407G>A in exon 4 and a c.884 A>G in exon 7 resulting in the p. Arg136His and p. Tyr295Cys amino acid changes at the protein level.
The above variations were not listed in either the CLN6 gene mutation database or single nucleotide polymorphism (SNP) databases. Upon genetic testing of both parents and brothers, only the mother was found to be a carrier of the CLN6 gene c407G>A mutation with a 50% chance of transmitting the mutation to her offspring. The c.407G>A mutation was thus inherited from the mother and the c.884A>G variation appeared de novo in the proband.
No curative treatments exist for the NCLs, so despite a formal diagnosis of vLINCL, no definitive treatment could be administered. The seizures progressed to super-refractory status epilepticus (SRSE) resistant to phenobarbital, clobazam, sodium valproate, phenytoin, levetiracetam and zonisamide. The patient was admitted to the intensive care unit (ICU) and put in an anesthesia-induced coma using midazolam and propofol and remained so for a period of several weeks. Any attempt to reduce or reverse the anesthesia-induced coma resulted in the re-emergence of status epilepticus. At this point, a trial of cannabis oil was initiated with improvement in the clinical and electrographic seizures. Over the following 2 weeks, he was trialled on a combined form of CBD and THC. A significant reduction in epileptic seizures was observed within a few days of adding the CBD/THC combination. Following a further increase and after 50 days of being in the induced coma, the sedation medication was withdrawn completely, and the patient opened his eyes following a week without epileptic episodes. The patient was discharged home 4 weeks following a reduction of the anti-seizure drugs and daily intake of CBD/THC.
Currently 8 months on, the patient experiences a significantly reduced number of seizures. He has come off clobazam and zonizamide but continues taking the cannabinoid oil drop combination in addition to low dose phenobarbitone, sodium valproate and levetiracetam.
The NCLs are caused by a number of CLN gene mutations. These genes encode proteins that are involved in the secretory and/or endo/lysosomal pathways [ 8 , 9 ]. When these genes are mutated, auto-fluorescent lipopigments accumulate in various tissues contributing to the signs and symptoms seen in NCL [ 9 ].
CLN6 encodes an endoplasmic reticulum (ER) membrane protein [ 9 ]. The CLN6 mutation described in the case occurs on chromosome 15q21-23 on gene CLN6 [ 8 ].
Spectrum and symptoms
Different types of NCLs are described based on the ultrastructure of membrane-bound inclusions, genetic molecular defect and clinical phenotype [ 10 ]. Compared to the classical forms, the age of onset in vLINCL tends to be later with symptoms presenting as late as 6 years of age. Seizures, ataxia, irritability and progressive mental deterioration present early on. Loss of speech occurs at around 3 years, visual impairment at 4 years and loss of motor skills between 4 and 10 years [ 10 ]. The rate of disease progression may vary, but usually leads to severe disability by mid-adolescence and death by the end of the second decade in life [ 4 , 5 , 9 ].
The CLN6 variant of vLINCL was first identified in 2002 in Costa Rican and Venezuelen patients [ 9 ]. Since then, other cases have been reported that describe a disease course and progression similar to our case. Sun et al reported the first case of a CLN6 mutation in China – a male patient who initially presented with language articulation problems and uncoordinated movements from age 4 which went unrecognized until the patient had repeated seizure episodes [ 2 ]. Sato et al reported a male patient from Japan diagnosed with moderate mental retardation and hyperactivity disorder by the age of 6 years. Epilepsy followed, along with weakness, ataxia, and MRI findings of atrophy. Genetic testing at the age of 12 years revealed a heterozygous mutation in the CLN6 gene [ 3 ]. Al-Muhaizea et al reported four cases across three families in Saudi Arabia where a similar disease course was reported: signs of language and behavior regression between the ages of 2 and 4 years followed by gait deterioration, ataxia, seizures and brain atrophy at around 6 years of age [ 4 ]. Chin et al reported similar findings due to novel CLN6 mutations found in two patients of Caucasian and mixed native American/Northern European descent, respectively [ 5 ]. The cases describe a consistent pattern of disease progression; however, a differentiating feature amongst the reported cases is the presence of visual impairment – although it is described amongst the typical features of vLINCL, it only presents as a feature of the disease in certain cases [ 4 ].
Treatment for NCL due to a CLN6 mutation currently consists of symptomatic relief of seizures, and supportive therapies for associated symptoms of behavior, language and visual difficulties.
Although limited, recent data on the efficacy of cannabinoids for treatment-resistant epilepsy have been published. Hausman-Kedem et al prospectively investigated the use of CBD/THC (ratio 20:1) in children and adolescents aged 1 – 20 years with drug-resistant epilepsy to at least four anti-seizure drugs, a ketogenic diet and vagal nerve stimulation. A significant reduction in mean monthly seizure frequency was noted with a higher CBD dose and patient age < 10 years at treatment-onset being associated with a better outcome. The most significant adverse event recorded was somnolence which led to cessation in some cases [6 ]. Porcari et al conducted a retrospective study that analyzed seizure frequency after the addition of CBD to anti-seizure drugs in treatment-resistant epilepsy in a cohort aged < 18 years. Results showed a significant reduction in overall seizure frequency. Although no patients had monotherapy with CBD, weaning of other anti-seizure drugs was reported as an achievable outcome [7 ].
The mechanism of cannabis in treating epilepsy remains unclear, and except for Epidiolex, FDA approval for most formulations has not yet been achieved. This forces acquisition of the drug through marijuana dispensaries which creates discrepancies in dosing and CBD/THC ratios [ 6 ].
Recent developments for the management of drug-resistant epilepsy report on the use of cannabis oil in combination with anti-seizure drugs. Since cannabis oil is not currently FDA approved other than for specific epilepsy syndromes (Dravet and Lennox Gastuax), its use in drug-resistant epilepsy is anecdotal and remains highly controversial. Although this case has shown that it is beneficial in reducing the seizures in NCL, future studies are required to test the efficacy and safety of cannabis oil as well as to define a recommended ratio of CBD/THC to be trialed in drug-resistant status epilepticus.
None to declare.
The University of Nicosia provided funding to support the publication of this manuscript.
Conflict of Interest
None to declare.
Informed consent was obtained from the patient and the patient’s family for the undertaking of this study. Informed consent was obtained from all family members who underwent investigational gene testing during the work up of the patient’s case. Informed consent was obtained from each family member at the time of testing. In addition, the patient and the patient’s family have consented to the publication of this manuscript.
AM, SB, AL and AP were responsible for the data collection, writing, analysis and submission of the manuscript; PN contributed to supervising and reviewing at all stages.
The authors declare that data supporting the findings of this study are available within the article.
- Haltia M, Goebel HH. The neuronal ceroid-lipofuscinoses: a historical introduction. Biochim Biophys Acta. 2013;1832(11):1795-1800.
- Sun G, Yao F, Tian Z, Ma T, Yang Z. A first CLN6 variant case of late infantile neuronal ceroid lipofuscinosis caused by a homozygous mutation in a boy from China: a case report. BMC Med Genet. 2018;19(1):177.
- Sato R, Inui T, Endo W, Okubo Y, Takezawa Y, Anzai M, Morita H, et al. First Japanese variant of late infantile neuronal ceroid lipofuscinosis caused by novel CLN6 mutations. Brain Dev. 2016;38(9):852-856.
- Al-Muhaizea MA, Al-Hassnan ZN, Chedrawi A. Variant late infantile neuronal ceroid lipofuscinosis (CLN6 gene) in Saudi Arabia. Pediatr Neurol. 2009;41(1):74-76.
- Chin JJ, Behnam B, Davids M, Sharma P, Zein WM, Wang C, Chepa-Lotrea X, et al. Novel mutations in CLN6 cause late-infantile neuronal ceroid lipofuscinosis without visual impairment in two unrelated patients. Mol Genet Metab. 2019;126(2):188-195.
- Hausman-Kedem M, Menascu S, Kramer U. Efficacy of CBD-enriched medical cannabis for treatment of refractory epilepsy in children and adolescents – An observational, longitudinal study. Brain Dev. 2018;40(7):544-551.
- Porcari GS, Fu C, Doll ED, Carter EG, Carson RP. Efficacy of artisanal preparations of cannabidiol for the treatment of epilepsy: Practical experiences in a tertiary medical center. Epilepsy Behav. 2018;80:240-246.
- Mole SE, Cotman SL. Genetics of the neuronal ceroid lipofuscinoses (Batten disease). Biochim Biophys Acta. 2015;1852(10 Pt B):2237-2241.
- Wheeler RB, Sharp JD, Schultz RA, Joslin JM, Williams RE, Mole SE. The gene mutated in variant late-infantile neuronal ceroid lipofuscinosis (CLN6) and in nclf mutant mice encodes a novel predicted transmembrane protein. Am J Hum Genet. 2002;70(2):537-542.
- Teixeira CA, Espinola J, Huo L, Kohlschutter J, Persaud Sawin DA, Minassian B, Bessa CJ, et al. Novel mutations in the CLN6 gene causing a variant late infantile neuronal ceroid lipofuscinosis. Hum Mutat. 2003;21(5):502-508.
This article is distributed under the terms of the Creative Commons Attribution Non-Commercial 4.0 International License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
CBD For Neurodegeneration: How CBD Protects The Brain As We Age
Neurodegeneration is an umbrella term used to describe any progressive loss of neuron function.
CBD helps protect the brain from natural degeneration in four key ways — antioxidant, anti-inflammatory, immune-modulation, and sleep-support.
Neurodegenerative disorders are conditions involving a loss of neuron function in the brain and spinal cord. 
As neurons are lost, brain function begins to suffer. This produces problems with memory, concentration, attention, muscle coordination, and language. There are many causes of neurodegeneration, but the main risk factor is age.
Can CBD offer support for chronic neurodegenerative disorders?
Learn how CBD is used to support neurodegenerative disorders, and what the research says about its efficacy.
MEDICALLY REVIEWED BY
Carlos G. Aguirre, M.D., Pediatric Neurologist
Updated on October 20, 2021
Table of Contents
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The Benefits of CBD Oil For Brain Health
Neurodegenerative disorders are characterized by a gradual loss of neurons in particular regions of the nervous system. This cell loss causes a decline in cognitive ability and accounts for most of the symptoms experienced with this condition.
How CBD Protects the Brain & Neurons
- Reducing brain inflammation
- Preventing T-cell migration across the blood-brain barrier (prevents autoimmunity)
- Antioxidant support (protects the DNA from damage)
- Alleviates anxiety
- May relieve depression
- May improve muscle control & alleviate muscle tremors
- My promote recovery of damaged neurons
CBD For Degenerative Brain Disorders
Cannabis may support neurodegenerative disorders including:
- Alzheimer’s disease
- Parkinson’s disease
- Multiple sclerosis (MS)
- Huntington’s Disease
- Prion disease (minor improvement)
- Lou Gehrig’s Disease (ALS)
- Spinocerebellar Ataxia (SCA)
- Spinal Muscular Atrophy (SMA)
1. Alzheimer’s Disease
Alzheimer’s disease is the most common form of neurodegeneration. It involves the buildup of toxic metabolites (TAU proteins or beta-amyloid plaque) around the neurons. Eventually, this results in neuron death and gradual cognitive debility. Alzheimer’s disease, like most other neurodegenerative disorders, is associated with excessive neuroinflammation [11, 12].
CBD offers benefits to this condition primarily through its anti-inflammatory effects.
2. Parkinson’s Disease
Parkinson’s disease is a neurodegenerative disorder affecting the basal ganglia where dopamine is manufactured. The result is a gradual loss of dopamine in the brain, causing muscle tremors, mood changes, and a gradual loss of cognitive function.
Like Alzheimer’s disease, Parkinson’s is considered to rely on excessive inflammatory processes in the brain [11, 12].
CBD, therefore, offers relief from this condition through its anti-inflammatory and neuroprotective actions.
3. Multiple Sclerosis (MS)
Multiple sclerosis is an autoimmune-driven neurodegenerative disorder. Widespread neuroinflammation causes immune cells to attack the myelin sheath on the nerve cells, causing a gradual loss of neuron function.
CBD is very beneficial to this condition through its immunomodulatory and anti-inflammatory effects — both of which are primary factors involved with the progression of MS .
Additionally, CBD may provide direct benefits to some of the most common side-effects of MS, including muscle spasticity  and loss of bladder control .
4. Huntington’s Disease
Huntington’s disease is a neurodegenerative disorder with similar characteristics to Alzheimer’s disease. It’s a genetic disorder involving dysfunction in the gene encoding for a protein called huntingtin. People with Huntington’s disease manufacture huntingtin proteins that are too long. They fracture into smaller pieces and become tangled around the neurons — leading to their gradual death. As Huntington builds up, it causes widespread inflammation throughout the brain and loss of cognitive function over time.
There is no cure for Huntington’s disease, but CBD has been shown to offer significant benefits — slowing progression and alleviating many of the most common symptoms .
5. Creutzfeldt-Jakob Disease (CJD) and Other Prion Diseases
Prion diseases such as CJD aren’t common but bring devastating side effects as the disease progresses. It involves a misfolded, protease-resistant protein (PrPres) entering the brain and replicating. Being resistant to protease means that the brain cells cannot break down and remove this protein from the brain. Therefore, as these proteins replicate and build up in the brain, they begin to interfere with healthy brain function. Currently, there’s no cure for prion diseases.
Although inflammation is a primary factor involved with prion disease progression, CBD has only been shown to have minor benefits on the condition by resisting the buildup of PrPres .
6. Amyotrophic Lateral Sclerosis (ALS)
Lou Gehrig’s Disease (ALS) is a neurodegenerative disease causing gradual — and ultimately fatal — disruption in signals controlling voluntary muscles throughout the body.
There is no cure for ALS, but CBD has been shown to offer significant benefits.
7. Spinocerebellar Ataxia (SCA)
SCA is a progressive, inherited neurodegenerative disease affecting the cerebellum — the part of the brain associated with coordination and muscle movement. There is no cure for the disease, and it’s often fatal.
Treatment is focused on alleviating symptoms such as muscle tremors, depression, and insomnia — all of which CBD is well-known to help.
8. Spinal Muscular Atrophy (SMA)
SMA is a rare neurodegenerative disorder affecting the motor neurons controlling the muscles. Eventually, the disease causes loss of muscle function and muscle wasting. Like many other neurodegenerative disorders, the condition is caused by a dysfunction in producing a particular protein in the brain. Over time, these dysfunctional proteins build-up, resulting in the death of the neurons. There is no cure for this condition.
It’s unclear whether CBD is beneficial to those with SMA. The majority of side-effects of this condition involve muscle weakness — something CBD isn’t thought to improve.
How to Use CBD Oil For Brain Health
Tips for Getting the Most Out of Using CBD for Neurodegenerative Disorders:
- Use a full-spectrum extract (THC also offers benefits for these conditions)
- Incorporate improvements of diet and lifestyle choices at the same time as CBD supplementation
- If there is an environmental cause (such as heavy metal exposure), make sure this is removed immediately
- Be consistent with dosing — it can take up to three months before any changes are experienced when it comes to neurodegenerative disorders
What’s Are The Best CBD Products For Brain Health?
Neurodegenerative disorders are a combination of many different neurological and systemic issues working together to produce a gradual loss of neurons.
Therefore, treating these conditions isn’t as straightforward as just addressing one of these issues at a time — it relies on addressing several of them at the same time.
CBD oils and other cannabis products should, therefore, be combined with other treatments and lifestyle and dietary changes for best results.
So, when searching for the best oils for neurodegenerative disorders, there are two things to consider:
- Has the CBD product been proven to be free from contaminants such as heavy metals or pesticides?
- Does the potency of the CBD product match the recommended dose? In the case of neurodegenerative disorders, this usually means using a high-potency extract.
It’s also useful to opt for a full-spectrum CBD extract rather than an isolate if you want to leverage the neuroprotective benefits of some of the other cannabinoids. However, if this isn’t possible, or you’ve decided you like a company selling CBD isolates, that’s okay. It will still work but just isn’t the best CBD oil for the job.
What Dose Of CBD Should I Use For Neurodegenerative Disease?
Most of the research involving CBD and other cannabinoids for neurodegenerative disorders involve very high doses — usually in the realm of around 500 mg per day.
Although it may not be totally necessary to use a dose this high, it does suggest that the heavy end of the dosage range is the most beneficial.
Use our CBD oil dosage calculator below to find the best dose for you based on your weight.
Remember to start low and build up over time. Everyone reacts differently to CBD, so it’s therefore important that you take a conservative approach to find the right dose to avoid any negative side effects.
Recommended strength for neurodegenerative disorders: medium to high strength
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How Long Will It Take To Notice Improvement?
Neurodegenerative disorders are long-term medical conditions — and most of them have no cure. CBD can be used to slow the progression of the disease and alleviate common side effects but isn’t going to cure the condition.
Therefore, it’s helpful to track the progress of the disease over time to identify whether the CBD is working or if the dose needs to be increased.
You can do this by taking detailed notes about your symptoms. Then, you can go back and see if there have been any improvements over time. Additionally, in the case of progressive neurodegenerative disorders, you can track the rate of progression of the disease.
What Is Neurodegenerative Disease?
Neurodegeneration is an umbrella term for a series of unrelated medical conditions that result in a loss of neuron function.
The primary cause for this condition is dementia, including Alzheimer’s disease — accounting for up to 70% of cases around the world, according to JPND Research.
These disorders are generally progressive, worsening in severity and rate of degeneration over time. This can take any time from a few months to a few decades. However, the process of neurodegeneration usually begins long before symptoms start to appear.
Evidence in recent years has pointed the finger at inflammation in the brain as one of the primary drivers of neurodegeneration . The problem with this is that it’s also necessary for resisting neurological damage — prompting researchers to regard neuroinflammation as the “double-edged sword” of neurodegeneration.
When something causes damage to the neurons in the brain — for which there are too many potential causes to count — local immune cells start the inflammatory process.
In the early stages, this is beneficial — even necessary — for eliminating toxic materials. This is because inflammation speeds the recovery of the neurons by boosting blood flow to the area and bringing in defensive immune cells to remove any infectious materials.
The problem is that, in many cases, this inflammation goes out of control, causing a cascade of devastating, long-term inflammation in the brain. Excessive inflammation causes the microglia to release toxic substances into the brain, ultimately leading to the death of the neurons. These microglia are tasked with keeping the neurons safe [9, 10].
The whole process goes from a typical inflammatory response to a devastating, self-perpetuating process of degeneration and loss of neurons.
What Causes Degenerative Brain Disease?
When to Avoid Using CBD or Cannabis-Related Products
Even though CBD is very safe, there are some instances when you must first consult with an experienced medical professional before taking it:
- If you have psychosis
- If you have bipolar disorder (caution advised)
- Whenever taking antipsychotics or certain antidepressants
Key Takeaways: How Does CBD Support Brain Health?
Researchers are still disputing exactly how CBD and other cannabinoids are effective for slowing the progression of neurodegenerative disorders.
The interaction between CBD and the nervous system is complex — involving multiple separate processes going on at the same time.
However, the general idea is that CBD supports the homeostasis of the nervous system. This means it supports the balance of various factors involved with neurological function, including inflammation, pain transmission, nerve excitability, and immune function.