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IDIOPATHIC INTRACRANIAL HYPERTENSION (IIH) (PSEUDOTUMOR CEREBRI) SYMPTOMS, CAUSES, AND TREATMENTS.

@Neuralgroover

 

What Is Idiopathic Intracranial Hypertension (IIH) (Pseudotumor Cerebri) And What Causes It?

Idiopathic intracranial hypertension (IIH) was previously called pseudotumor cerebri. Pseudotumor cerebri was an old term which was often confusing to patients because this disorder is not because of a brain tumor. Brain tumors in strategic areas of the brain can block the flow of cerebrospinal fluid (CSF), which can cause back up and elevation of CSF pressure, called hydrocephalus. This is where the older term of pseudotumor cerebri was derived from. Benign intracranial hypertension was another previously used term which was changed because the disease can certainly be not so benign.

 

IIH is a completely different problem than the elevated CSF pressure from a brain tumor though, and treated much differently. The problem of IIH involves an elevation of CSF around the brain and spinal cord, without a clear reason.

 

CSF is continuously produced (by something called the choroid plexus inside the ventricles of the brain), absorbed, and transported out of the nervous system (by something called arachnoid villi) and into large draining veins surrounding the brain called the cerebral venous sinuses, and then into the jugular veins and blood where it is broken down.




There have been a number of theories and findings as to the causes of IIH. These include:

 

  • Overproduction of the CSF
  • Blockage of CSF absorption into the cerebral venous sinuses due to a faulty transport mechanism
  • Stenosis (narrowing) of the venous sinuses
  • Blot clot (thrombus) blocking the inside of venous sinuses preventing the outflow of CSF and pressure build up
  • Compression of the venous sinus from the outside (such as brain tumor, meningioma, etc.), causing narrowing on the inside
  • Sex hormones such as androgens and adipose tissue may play a potential role
  • Some medications have been associated with IIH including lithium, retinoids (such as excess vitamin A derivatives), oral contraceptives, and tetracycline antibiotics such as doxycycline and minocycline. Rebound IIH has also been reported from corticosteroid withdrawal.
  • Dural arteriovenous (AV) fistula (an artery connects to the venous sinus, allowing arterial blood flow into the venous sinus and causes much higher pressure)

 

Think of it like this…

 

Imagine the brain and spinal cord surrounded and suspended in fluid called the CSF (which cushions and keeps the brain and spinal cord afloat). To keep this fluid in place, it is surrounded by a thick lining called the dura mater. Basically, think of this arrangement like a water balloon. Now, imagine that you keep filling the water balloon with water until the pressure inside gets higher and higher. Eventually, the balloon pops. The same problem occurs in IIH. The pressure of the CSF gets higher and higher. As the pressure rises, it puts pressure on various areas of the brain and cranial nerves resulting in a variety of neurological and other symptoms. This is the basis of IIH.

Sometimes, the pressure can become high enough and you can get a CSF leak out of the surrounding membrane, similar to the balloon popping. This situation can sometimes lead to a low CSF pressure (intracranial hypotension, or CSF leak), which can cause a different type of positional headache and a different set of symptoms. We’ll discuss the problem of CSF leaks in a separate blog article and will focus here on the problem of high CSF pressure.

 

What Are IIH (Pseudotumor Cerebri) Symptoms?

Headache is the most common symptom of IIH. It typically involves the whole head, and is often worse in the morning (after lying down all night and pressure tends to build). It can commonly flare up by certain activities such as coughing, sneezing, straining, bending forward, and laughing.

 

Normal CSF pressure in adults is generally considered to be 100-200 mm CSF (10-20 cm CSF). According to criteria, IIH consists of a headache associated with CSF pressure greater than 250 mm CSF (25 cm CSF) in adults, and greater than 280 mm CSF (28 cm CSF) in children, checked by lumbar puncture (LP). The CSF pressure should be measured in the absence of treatment to lower intracranial pressure, and without sedative medications. The optimal position to check CSF pressure is lying on the left side (left lateral decubitus position) with legs extended (initially the legs/hips are flexed up towards the stomach for insertion of the LP needle to open up the spaces between the vertebrae, and then can be carefully extended out with assistance once the LP needle is in place), head in neutral position (not flexed far forwards), and the patient is breathing calmly and normally.

 

CSF pressure often varies through the day, so a single measurement may not be indicative of the average CSF pressure over 24 hours. In adults, if the pressure is 200-250 mm CSF (20-25 cm CSF), this can still be considered abnormal if they also have the associated signs, symptoms, and imaging findings consistent with a diagnosis of IIH. If there is uncertainty, prolonged lumbar or intraventricular pressure monitoring is occasionally considered. Temporary relief of the headache following lumbar puncture is often seen and can be supportive of the diagnosis, although it doesn’t confirm or exclude the diagnosis whether it happens or not.

 

IIH criteria also must have at least one of either pulsatile tinnitus (typically described as a whooshing in the ear) and/or papilledema (swelling of the optic nerve (transmits vision to the brain) in the back of the eye, seen during an eye exam).

 

Some patients report transient obscurations of vision (TVOs), which are brief (usually seconds) partial or complete loss of vision which rapidly returns to normal. This is suspected to be due to brief lack of blood flow (ischemia) in the swollen area of the optic nerve (from papilledema). Double vision is occasionally reported. It is usually from abducens nerve (cranial nerve 6) palsy (weakness) and can be 1 or both sides, but other reported nerve palsies can include cranial nerve 3, 4, and 7. Additional symptoms can include neck pain, pain radiating from the neck down the arm (cervical radiculopathy), back pain, ear fullness (such as high altitude), dizziness and unsteadiness.

 

What Tests Are Done To Diagnose IIH (Pseudotumor Cerebri)?

 

Dilated Eye Exam (Fundoscopy)

Irreversible progressive vision loss is the main concern with IIH if it continues untreated. The enlarged physiologic blind spot develops first followed by inferonasal visual defects, followed by progressive constriction of visual fields, and central vision is the last to be affected.

 

Sometimes a subtle clue of elevated CSF pressure can be picked up by observing the venous pulsations in the back of the eye on exam. If they are present, CSF pressure is likely relatively normal. If the venous pulsations are absent, this can suggest elevated CSF pressure. However, occasionally some patients can have a lack of venous pulsations normally. Another normal variant that can appear abnormal is pseudopapilledema. This looks like papilledema, but can also be normal anatomy or from causes such as optic disk drusen. With pseudopapilledema, venous pulsations are usually present, whereas in true papilledema they are absent. Additional tests to evaluate for pseudopapilledema include ultrasound and fundus autofluorescence, done with an ophthalmologist.

 

Every patient with suspected IIH should be referred (preferably) to neuro-ophthalmology to evaluate and monitor for evidence of elevated CSF pressure on a dilated eye exam and full visual field testing. They often do a test called optical coherence tomography (OCT) which is checked periodically to monitor for thinning (atrophy) of the optic nerve, and other structural damage from excess CSF pressure on the nerve. If a neuro-ophthalmologist is not available, than an ophthalmologist (not an optometrist) should be seen. The vision loss from IIH is usually a slow process that may or may not be noticed by the patient, and it is irreversible. Therefore, all IIH patients should have early detailed dilated eye exams and should be followed serially by a neuro-ophthalmologist or ophthalmologist.

 

There are a much less common (and somewhat controversial) group of patients that may have IIH without papilledema. This has been suggested to be possibly related to anatomic variations in the subarachnoid space (where CSF collects around the optic nerve) not reaching far enough to the back of the eyeball. So the part of the optic nerve that may be swollen may be further back behind the eyeball, and can’t be visualized. Another theory of this group of patients includes the episodic presence of a CSF leak, so pressure isn’t sustained long enough to cause papilledema. So, when CSF pressure reaches a certain level, the CSF leaks from a weakened area in the meninges (these keep the CSF in place around the brain and spinal cord) either in the nose (CSF rhinorrhea), the ear (CSF otorrhea), or in the spine. Rarely, some patients are felt to have alternating cycles of high pressure (IIH symptoms) and when the CSF leak reforms, cycles of low pressure (intracranial hypotension, CSF leak headache), so their complaints can vary widely between these 2 extremes of high pressure or low pressure.

 

Lumbar Puncture (LP)

This is really the most central piece of the IIH diagnosis as detailed above. If CSF pressure is high and the patient has signs, symptoms, and/or findings on MRI, then the diagnosis is confirmed. When the LP is done to check pressure, it is worthwhile to also send some CSF to the lab to analyze for signs of inflammation, infection, or cancerous (such as metastatic leptomeningeal disease) factors. Temporary relief of the headache following lumbar puncture is often seen and can be supportive of the diagnosis, although it doesn’t confirm or exclude the diagnosis whether it happens or not.

 

Brain MRI and Brain MRV

A brain MRI with contrast should be a first line test, which helps to exclude other obvious causes of papilledema and elevated CSF pressure (such as brain tumor), and results can support a diagnosis of IIH. However, a diagnosis should never be made based on MRI alone, but on the MRI in combination with a good history and clinical symptoms. Some of the supportive MRI findings include empty sella turcica, or “empty sella syndrome”. However, this is does not definitively confirm the diagnosis, and it is not uncommon to see this appearance in normal patients. Again, putting together MRI findings with the right clinical story is key. Other MRI findings that may or may not be visible include dilation/distention (due to increased CSF surrounding the optic nerves) and tortuosity of the optic nerve sheaths (more curvy and twisted appearance), flattening of the posterior sclerae (flattening of the back of the eyeball), enhancing protrusion of the swollen optic disks, pseudo-Chiari (not a true Chiari, but some cerebellar decent due to high CSF pressure pushing it down), and transverse cerebral venous sinus stenosis (narrowing).

 

Brain MRV should always be done with the MRI to ensure there is no blood clot (cerebral venous thrombosis) in the venous drainage pathways, or significant narrowing (stenosis) of the venous sinuses. It is preferably done with contrast for optimal imaging clarity, although contrast is not absolutely necessary. In most patients, if there is a significant finding, you’ll usually see it on noncontrast MRV. The contrast can add further definition of an area in question if there is uncertainty.

 

How Is IIH Treated?

 

Weight Loss for IIH (Pseudotumor Cerebri)

Weight loss is an absolute must for IIH if the patient is overweight. Research has suggested that losing 6-10% of initial body weight can cause IIH remission in many patients. Bariatric surgery is sometimes considered for morbidly obese patients who are unsuccessful in losing weight by more conservative ways.

 

What is the best IIH (Pseudotumor Cerebri) Diet?

A low-calorie, low-salt diet with mild fluid restriction generally seems to be the most helpful diet for IIH.

 

What Medications Are Used To Treat IIH (Pseudotumor Cerebri)?

The carbonic anhydrase inhibitors are the first line treatment for IIH. These medicines work for IIH because they decrease the production of CSF (and thus CSF pressure is lower because production has slowed). They also have a mild diuretic effect. The most common medications used for IIH are Acetazolamide (Diamox), Topiramate (Topamax), and Methazolamide.

 

Typical doses for Diamox start at 500 mg twice daily and can be increased to 2000 mg twice daily, although lower doses are often effective. Side effects can include tingling/numbness (paresthesias), changes in taste, and gastrointestinal symptoms such as nausea, vomiting, or diarrhea.

 

If there is any question of migraine mixed in with IIH, then Topiramate is my first choice because it is also FDA approved for migraine prevention, in addition to decreasing CSF production. I usually start Topamax with 25 mg at bed and is increase by 25 mg at bed each week until 100 mg at bedtime. If not improving by 4 weeks at the 100 mg dose, morning dosing is then added with 50 mg for 1 week and then 100 mg twice daily. Side effects often include weight loss, which would certainly be a desired side effect in obese patients with IIH. Other side effects can include mood changes, tinging/numbness, and cognitive complaints such as memory, word finding, and concentration.

 

Methazolamide is started at 25 mg twice daily and can be increased to 200 mg twice daily.

 

Other medicines sometimes used if the above options are not tolerated or working include furosemide and bumetanide. For sulfa allergic patients, spironolactone, triamterene, and ethacrynic acid are occasionally used.




Treating Other Headache Disorders That Occur With IIH (Pseudotumor Cerebri)

It is also very important to also treat other headache disorders that may be mixed in with the IIH headaches. For example, many patients with IIH also have headache flares that easily fit criteria for migraine headaches. They typically have chronic daily headache which looks like a mix of chronic migraine and chronic tension type headache. So, when there is IIH mixed in with these headache disorders, it sometimes becomes cloudy on which headache disorders are contributing to which symptoms as well as the overall chronic daily headache. Many times these patients are in rebound headache (medication overuse headache), and that issue must be treated and resolved before the headaches are able to improve. I typically treat these patients targeting both chronic migraine and IIH (if IIH has been confirmed as well) since they are most often intermingled.

 

If there are any associated headache symptoms of throbbing, pulsating, pounding (even if a low level), nausea, sensitivity to both light and sound with headache flares, then migraine should also be targeted with both an abortive and preventive treatment option. Abortive options include NSAIDs, ergots, triptansneuromodulatory devices, the ditans (Reyvow (Lasmiditan)) and the gepants (Ubrelvy (Ubrogepant) and Nurtec ODT (orally dissolvable tablet) (Rimegepant)).

 

If the migraines are happening frequently enough, then a migraine preventive treatment should be considered. Preventive migraine treatments are used to lessen the frequency and/or severity of migraine attacks. Preventive treatments include a variety of daily pill medicationsCGRP monoclonal antibodies (mAbs) (Aimovig (Erenumab), Emgality (Galcanezumab), Ajovy (Fremenazumab), Vyepti (Eptinezumab)), neuromodulation devicesBotoxNurtec ODT every other day (1st and only dually approved migraine abortive and preventive), herbal and natural supplements and vitaminsyoga and meditation, and acupuncture and acupressure.

 

What Are Surgical Treatments for IIH (Pseudotumor Cerebri) When Other Treatments Fail?

 

Optic Nerve Fenestration For IIH

Optic nerve fenestration is sometimes done for papilledema that is not improving with standard medical treatments and vision continues to worsen. This is basically a procedure which makes small slits in the optic nerve sheath, which encloses the optic nerves and keeps the CSF in place around them. By doing this, it can release the CSF pressure on the nerves (imagine it as cutting a slit in a garden hose). This procedure is only done to prevent further vision loss which isn’t responding to conservative treatment, but does not typically help the headache.

 

Venous Sinus Stenting For IIH

Stenoses of the transverse venous sinuses can sometimes be seen on MRV. This leads to increased venous pressures in these channels, as well as the superior sagittal sinus. Increased venous sinus pressures can be confirmed with catheter venography with manometry. Transverse venous sinus stenting is occasionally considered as a surgical treatment option for IIH in patients with pressure gradients of more than 8 mm Hg and refractory symptoms. One study found that a pressure gradient of 21 mm Hg or higher had the best outcomes.

 

Shunts for IIH

Ventriculoperitoneal (VP) shunts and lumboperitoneal (LP) shunts are occasionally done with a goal of surgically placing a valve and tubing device to maintain a normal pressure in the spinal fluid. VP shunting is preferred over LP shunting due to lower rates of complications. If the pressure reaches above a specific pressure setting of the valve, then CSF will drain through the tubing and into the peritoneal cavity of the body where it is then absorbed and eliminated. Shunting should always be a last resort option (outside of severe emergent cases which need rapid pressure relief) after every possible medical management option has failed. Shunts don’t tend to provide long term effectiveness for headache management and frequently require revisions. It is not uncommon for the hardware to become infected or blocked and then have to be removed. One large study found that initial improvement in headaches following shunting returned to recurrent headaches at 36 months in almost half of all patients.

 

How Do You Treat IIH (Pseudotumor Cerebri) In Pregnancy?

Acetazolamide can be used after the 1st trimester. Repeated LPs to drain some of the CSF pressure can be done if necessary. For women who have progressive papilledema and worsening vision, optic nerve fenestration may be necessary to preserve vision, although it will not typically help the headache.




IF YOU HAVE HEADACHE, MIGRAINE, OR FACIAL PAIN AND ARE LOOKING FOR ANSWERS ON ANYTHING RELATED TO IT, A HEADACHE SPECIALIST IS HERE TO HELP, FOR FREE!

FIRST, LET’S DECIDE WHERE TO START:

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR THE LATEST INFORMATION, HOT TOPICS, AND TREATMENT TIPS, VISIT OUR FREE BLOG OF HOT TOPICS AND HEADACHE TIPS HERE. THIS IS WHERE I WRITE AND CONDENSE A BROAD VARIETY OF COMMON AND COMPLEX  MIGRAINE AND HEADACHE RELATED TOPICS INTO THE IMPORTANT FACTS AND HIGHLIGHTS YOU NEED TO KNOW, ALONG WITH PROVIDING FIRST HAND CLINICAL EXPERIENCE FROM THE PERSPECTIVE OF A HEADACHE SPECIALIST.

IF YOU DON’T HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR POSSIBLE TYPES OF HEADACHES OR FACIAL PAINS BASED ON YOUR SYMPTOMS, USE THE FREE HEADACHE AND FACIAL PAIN SYMPTOM CHECKER TOOL DEVELOPED BY A HEADACHE SPECIALIST NEUROLOGIST HERE!

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR FURTHER EDUCATION AND SELF-RESEARCH ON YOUR DIAGNOSIS, VISIT OUR FREE EDUCATION CENTER HERE.

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Last updated on September 17th, 2021 at 06:46 am

LONG COVID, POST-COVID SYNDROME, POST-VIRAL SYNDROME, MECFS, PWME, AND POST-COVID HEADACHE EXPLAINED AND TREATED.

@Neuralgroover

Background

Long Covid, post-Covid syndrome, long Covid syndrome, long Covid-19, post Covid-19 syndrome, long haul Covid, and long tail Covid are some of the emerging terms for what appears to be a chronic constellation of symptoms following Covid-19 infection in some patients.

 

What are long Covid symptoms, and what is long Covid syndrome?

Here is how I want you to visualize long Covid syndrome, or any chronic post-viral syndrome. Close your eyes and imagine your body in its usual shape and form, but with no tissue or anything else except for its vast nervous system and network of nerves throughout every fraction of a millimeter of your body. Imagine this extensive network of nerves as if they are bare metal electrical wires plugged into their source of electricity, the brain, which normally regulates all of these various electrical circuits in the body. Now imagine a bucket of water dumped onto this vast connection of live electrical wires. This immediately causes short circuiting of the electricity running through the nerves, along with smoke, and a smoldering, crackling, buzzing, electrical fire (hopefully you’re getting a good visual there). This is how you can think of post-Covid syndrome, except it isn’t a bucket of water dumped onto the body’s electrical connections, but rather Covid-19 with the same end results of a nervous system meltdown, and often to a much greater degree than a typical case of chronic post-viral syndrome.

 

So essentially, think of long Covid syndrome as having gotten stuck in an extensive variety of short circuits and nervous system dysregulation because the normal regulating circuits from the brain have been injured and disrupted. The resulting long Covid symptoms are widely variable but most often include headaches, excess fatigue, exercise intolerance, shortness of breath, muscle pains, chest pain, breathlessness, muscle weakness, dizziness, imbalance, disequilibrium, tremors, cognitive fog, tinnitus, brain fog, cognitive dysfunction of memory, concentration, and attention, sleep disturbances, dysautonomia, POTS, dizziness or passing out when standing (orthostatic intolerance), temperature dysregulation, tachycardia (racing heart) with mild activity, night sweats, persistent low grade fever, depression, anxiety, gastroparesis (the gut not transporting food through the digestive tract as efficiently), and other gastrointestinal symptoms such as diarrhea and constipation. These are just a few of the reported chronic symptoms. This study of 3762 patients identified 203 symptoms of long Covid syndrome.

 

Now keep in mind, this scenario is not specific for only Covid-19. This is a syndrome well known by neurologists and seen not too uncommonly, normally called a chronic post-viral syndrome. Awareness has just become higher given the Covid-19 pandemic and amount of people infected with resultant chronic post-viral syndrome. It usually begins around the time of a nonspecific mild viral illness which you wouldn’t expect to cause any significant complications such as an upper respiratory infection, diarrheal illness, or a vague flu-like illness. Covid-19 is another virus which can also trigger this same syndrome, just as many other viruses have done historically for centuries. However, the chronic symptoms seem to often be much more severe and debilitating compared to other chronic post-viral syndromes.

 

Many of the long Covid symptoms and other chronic post-viral syndromes have symptoms which overlap with myalgic encephalomyelitis chronic fatigue syndrome (MECFS). Another term for patients with these symptoms is people with myalgic encephalomyelitis (PWME) which is commonly seen discussed on social media outlets. Patients with these disorders often report some nonspecific viral symptoms such as the common cold, runny nose, cough, or diarrhea preceding the onset of their MECFS symptoms. So, a similar mechanism causing MECFS, long-Covid syndrome, and other chronic post-viral syndromes is suspected. Many of these syndromes are also consistent with fibromyalgia syndrome, which shares many similar characteristics. All of these terms should be considered a diagnosis of exclusion, meaning other possible causes should be excluded first. Comprehensive evaluations should include cardiac (heart), pulmonary (lung), autoimmune and rheumatologic (such as lupus, multiple sclerosis, etc.), neurocognitive, sleep medicine, physical therapy, ongoing infections, medication side effects, or other metabolic disturbances depending on what constellation of symptoms the patient is dealing with.

 

What Causes long Covid syndrome?

Generally, the cause of post-Covid syndrome, similar to other chronic post-viral syndromes, has been suspected to have an immune reaction as the underlying cause of it. The way it works is that your immune system first develops antibodies against a piece of the virus which it encounters, typically a protein. Well, that piece of the virus that your immune system forms antibodies to are meant to attack and neutralize any viruses that enter your body with a similar protein so you don’t get sick from it again. The thinking is that the antibodies formed may have a similar appearance to something in your own body’s cells (such as the myelin on nerve cells or other nervous system tissue). So your immune system then erroneously attacks your own cells as well. What follows is a wide constellation of symptoms, depending on which cells and area of the body are affected. Besides this persistent immune activation and reaction, other theories of possible long-Covid syndrome causes include persistent viral replication, metabolic dysfunction, residual cellular injury from the initial viral infection, and unmasking of underlying diseases which were just under the surface and pushed over the edge by the Covid-19 infection.

 

What is the treatment for long Covid syndrome?

Treatment for Long-Covid Syndrome is the same as other chronic post-viral syndromes, as well as MECFS symptoms. Unfortunately, this treatment is typically symptomatic, meaning treating the specific individualized symptoms such as insomnia, headache, pain, etc., rather than one unifying treatment. It is important to not automatically consider these patients as “functional”, or that they are embellishing their symptoms. Many of them were highly functioning professionals suddenly stopped in their tracks with this disruptive constellation of symptoms and no one can explain exactly why to them. Thus, anxiety and depression secondary to these symptoms and associated frustration should also be considered. Some patients have reported that their long-Covid symptoms improved after receiving the Covid-19 vaccination, but this has certainly not been a consistency for everyone. Treatment involves a trial and error process of trying different medications, depending on what symptoms are being targeted. For neurological symptoms and headaches, think of it as trying to find something to help “reset” or “reboot” the system electrically. Optimizing nutrition is also important.

 

How long do long Covid symptoms last?

This is an evolving science and surely more information will come over time. This study of 3762 patients found that the most frequent symptoms after 6 months were fatigue, post-exertional malaise, and cognitive dysfunction. For the majority of patients (>91%), the time to recovery was more than 35 weeks. By 7 months, many patients had not yet recovered (mostly from systemic and neurological/cognitive symptoms), had not returned to previous levels of work, and continued to experience significant symptom burden.

 

How do you treat Covid-19 headache?

Coronavirus (Covid-19) headache is discussed in much greater detail here in terms of background, symptoms, and treatments. If this is an issue for you, I would suggest that you read that article for a better overall understanding. However, to summarize, there are a few different varieties of Covid-19 headache. Patients that have a history of migraine commonly have a flare up of their migraines related to the Covid-19 infection itself. Similarly, it has been common to see migraines flare up with the Covid-19 vaccine as well. These migraine flare ups are typically temporary and may last a few days to a week or so for some. There is also a milder nonspecific tension type headache (achy pressure tightness) that some patients get with either the Covid-19 infection, or the Coronavirus vaccine, and it is also typically a temporary headache which may last a few days at most. Then, there are the unfortunate group of patients that develop New Daily Persistent Headache (NDPH) after Covid-19 infection, and much more rarely after the Covid-19 vaccine itself. This is a much more persistent headache which begins as a daily persistent headache from the onset, and lasts for more than 3 months. It is notoriously a very resistant form of headache to many treatments. However, improvement is still possible with the combination of time and trial and error treatments until the most effective treatment is found, which can be widely variable between patients.

 

IF YOU HAVE HEADACHE, MIGRAINE, OR FACIAL PAIN AND ARE LOOKING FOR ANSWERS ON ANYTHING RELATED TO IT, A HEADACHE SPECIALIST IS HERE TO HELP, FOR FREE!

FIRST, LET’S DECIDE WHERE TO START:

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR THE LATEST INFORMATION, HOT TOPICS, AND TREATMENT TIPS, VISIT OUR FREE BLOG OF HOT TOPICS AND HEADACHE TIPS HERE. THIS IS WHERE I WRITE AND CONDENSE A BROAD VARIETY OF COMMON AND COMPLEX  MIGRAINE AND HEADACHE RELATED TOPICS INTO THE IMPORTANT FACTS AND HIGHLIGHTS YOU NEED TO KNOW, ALONG WITH PROVIDING FIRST HAND CLINICAL EXPERIENCE FROM THE PERSPECTIVE OF A HEADACHE SPECIALIST.

 

IF YOU DON’T HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR POSSIBLE TYPES OF HEADACHES OR FACIAL PAINS BASED ON YOUR SYMPTOMS, USE THE FREE HEADACHE AND FACIAL PAIN SYMPTOM CHECKER TOOL DEVELOPED BY A HEADACHE SPECIALIST NEUROLOGIST HERE!

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR FURTHER EDUCATION AND SELF-RESEARCH ON YOUR DIAGNOSIS, VISIT OUR FREE EDUCATION CENTER HERE.

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Last updated on September 17th, 2021 at 06:44 am

FOODS THAT STOP NAUSEA IN ITS TRACKS.

@Neuralgroover

Nausea is an extremely common symptom across a wide spectrum of diseases. It is one of the main symptoms in the ICHD3 diagnostic criteria for migraine. Nausea is one of the 3 “most bothersome migraine symptoms” (along with photophobia (sensitivity to light) and phonophobia (sensitivity to sound)) which most acute/abortive (as-needed) migraine medication clinical research studies assess as a primary data endpoint in trying to resolve, because it is such a disruptive symptom.

 

As the electrical activity of migraine spreads through the brainstem, it activates the nausea centers of the brainstem, and you are well aware of the misery that follows that. So, are there tricks or things that you can do to lessen nausea other than using standard antiemetics (anti-nausea) medications such as Metoclopramide (Reglan), Prochlorperazine (Compazine), Promethazine (Phenergan), and Ondansetron (Zofran)? Are there certain foods or drinks that can help lessen the nausea? I’ll give you the quick answer which is detailed below. Yes there are!!

 

You may be searching terms such as, what helps with nausea, what helps nausea, how to get rid of a stomach ache, home remedy for nausea, home remedy for stomach ache, feeling nauseous, upset stomach remedies, nausea remedies, what to eat when stomach is upset, stomach upset remedy, stomach upset home remedies, how to help nausea, home remedies for stomach upset, how to get rid of stomach ache, home remedies for stomach ache, stomach ache remedies, best foods for nausea, etc., etc.

 

Let’s talk about how to treat nausea symptoms naturally…

 

Occasionally, Virtual Headache Specialist will allow guest bloggers to write an article on a migraine related topic. How to treat nausea including natural treatments for nausea is one of those very relevant migraine associated topics. It is certainly not a symptom associated only with migraine, and has a very wide range of causes. Whatever the cause may be, it is a miserable symptom to have to deal with. So, I hope the following article gives you some additional firepower to add to your migraine treatment war chest in treating the migraine associated symptom of nausea!

 

FOODS THAT STOP NAUSEA IN ITS TRACKS.

Guest author: Kristen Seymour

 

Nausea: It’s one of those universal human experiences we can all commiserate with. In fact, it’s estimated that each year half of the adult population experiences at least one bout of nausea, which may or may not lead to vomiting. That makes sense because there are many reasons people feel nauseous.

 

WHAT TO EAT AND DRINK WHEN YOU FEEL NAUSEOUS

If you feel sick to your stomach, eating or drinking may be the last thing on your mind. And if your symptoms only last for a short time, abstaining could be the right thing to do.

However, if your symptoms persist for more than a couple of hours, not only is it important to stay hydrated (especially if you vomit or experience diarrhea) but there are some foods and drinks that can help quell your nausea, too. That said, if your symptoms persist for more than a day or are especially severe, you should contact your doctor.

 

WATER AND LIGHT OR CLEAR BEVERAGES

Even when you’re healthy, being dehydrated can leave you feeling pretty crummy. When you already feel awful, dehydration exacerbates the effect. And, if you have a fever and/or ­­struggle to keep food or drinks down, you could become dangerously dehydrated without realizing it. Water alone is a great start, but if you lose fluids through vomiting or diarrhea, you may want to incorporate sips of coconut water, clear juices, or sports drinks. Flat ginger ale can also be a good option, but be cautious with carbonation as this could upset your stomach further.

Beverages and foods that are cold may be more appealing (or less likely to turn your stomach) than warm ones because they’re typically less fragrant. Sip small amounts rather than guzzling a whole glass, and consider sucking on small ice chips or a popsicle.

 

GINGER

This ancient herb has historically been used to relieve stomach upset, and the evidence that it works isn’t only anecdotal, it’s been proven in a variety of modern scientific studies, too. Keep in mind that effectiveness is tied to the amount consumed: Most studies use ½ to 1½ grams (or the equivalent) of dried ginger daily. But many common methods of consuming ginger (ginger tea, ginger ale, candied ginger slices, ginger cookies) make it hard to measure how much you’re getting. Taking ginger capsules or using your own fresh or dried ginger for tea is probably the best way to track your intake. If you’re pregnant or breastfeeding, talk to your doctor before using ginger for nausea.

 

BROTH OR SIMPLE SOUPS

When you’re ready to venture beyond clear fluids, broth is a great next step because it provides hydration, electrolytes, and a little more flavor, which may help you ease into real food. Broth is also a versatile base you can add more nutrition to in the form of chicken (diced small), vegetables, noodles, or rice as your body becomes capable of handling heartier fare. Just be sure to keep the spices and seasonings to a minimum at first.

 

BLAND, DRY STARCHY FOODS

Bread, crackers, rice, noodles, and other similarly simple foods are sick-day staples, although interestingly, this is one nausea-fighting food group that lacks scientific research to back up its effectiveness. It’s believed that starchy foods may help absorb some of the stomach acid that contributes to feeling nauseated, and it’s well-documented that we’re more likely to experience nausea on an empty stomach than when we’ve eaten a little something. So if you’re up for it, try nibbling on a soda cracker or a little steamed rice. You can add a small amount of seasoning, such as salt (or ginger) if it sounds appetizing.

 

APPLESAUCE

Not only is applesauce a gentle, healthy source of carbs (which can help you build back your energy), but it can also benefit you if you’re experiencing diarrhea. That’s because it has high dietary pectin, which helps by binding substances in the intestine, adding bulk to loose stools. Applesauce is part of the BRAT diet (bananas, rice, applesauce, and toast), which has long been a go-to grocery list for people with nausea.

 

BANANAS

Many of the foods on this list can soothe your stomach but lack in overall nutritional value. Not so with bananas. This nutrient-dense fruit is not only soft and easy to eat, it also provides you with approximately 105 calories, 27 grams of carbs, and 12 percent of potassium and 22 percent of vitamin B6 needs for the day (for a medium banana). One tip: The riper the banana, the more fragrant, so if smells turn you off, try a greener one.

 

HERBAL TEA

We mentioned that cold drinks are often more appealing than hot, but sometimes sipping on something warm provides much-needed comfort. In that case, try a caffeine-free herbal tea. See if perhaps peppermint, chamomile, or ginger sounds like something you’d like to sip. You may find that lukewarm or iced works better for you than hot.

 

Each person—and each instance of nausea—is different, so if you’re under the weather, don’t force yourself to eat a particular food if the smell turns your stomach. Listen to your body and take it slow; you’ll be back to your regular meals before long.

 

The original article can also be seen here, as originally published on Health Perch – A Digital Health Magazine.

 

IF YOU HAVE HEADACHE, MIGRAINE, OR FACIAL PAIN AND ARE LOOKING FOR ANSWERS ON ANYTHING RELATED TO IT, A HEADACHE SPECIALIST IS HERE TO HELP, FOR FREE!

FIRST, LET’S DECIDE WHERE TO START:

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR THE LATEST INFORMATION, HOT TOPICS, AND TREATMENT TIPS, VISIT OUR FREE BLOG OF HOT TOPICS AND HEADACHE TIPS HERE. THIS IS WHERE I WRITE AND CONDENSE A BROAD VARIETY OF COMMON AND COMPLEX  MIGRAINE AND HEADACHE RELATED TOPICS INTO THE IMPORTANT FACTS AND HIGHLIGHTS YOU NEED TO KNOW, ALONG WITH PROVIDING FIRST HAND CLINICAL EXPERIENCE FROM THE PERSPECTIVE OF A HEADACHE SPECIALIST.

 

IF YOU DON’T HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR POSSIBLE TYPES OF HEADACHES OR FACIAL PAINS BASED ON YOUR SYMPTOMS, USE THE FREE HEADACHE AND FACIAL PAIN SYMPTOM CHECKER TOOL DEVELOPED BY A HEADACHE SPECIALIST NEUROLOGIST HERE!

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR FURTHER EDUCATION AND SELF-RESEARCH ON YOUR DIAGNOSIS, VISIT OUR FREE EDUCATION CENTER HERE.

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Last updated on September 17th, 2021 at 06:41 am

SYNCOPE EPISODE, SYNCOPE DEFINITION, AND AN EASY TOOL TO QUICKLY RECALL ALL CAUSES OF SYNCOPE.

@Neuralgroover

If you have ever had a syncope episode (passing out, or fainting), you know how scary it can be. It is scary not only from the event itself, but sorting out the causes of syncope can be both scary and frustrating. Syncope is not an uncommon association with migraine attacks. This is most often due to a vasovagal response related to the severe pain of the migraine or dehydration from vomiting. However, many migraineurs can also have some degree of dysautonomia during an attack. Dysautonomia is a dysfunction of the autonomic nervous system, which controls blood pressure, arterial dilation or constriction, heart rate, heart rhythm, sweating, and gastric motility. This is illustrated with migraine associated symptoms such as gastroparesis, dizziness, POTS, and complaints of cold hands and feet during an attack for some.

 

So what is syncope? Let’s first discuss the syncope definition, which is also frequently termed syncope and collapse. Syncope is a temporary loss of consciousness typically due to a brief lack of blood flow to the brain. The most common reasons are from a drop in blood pressure upon standing (orthostatic hypotension), from a vasovagal response (a form of neurocardiogenic syncope), or from the heart not pumping enough blood to the brain from an arrythmia (heart temporarily beating too fast or too low), or a weak heart muscle (such as in congestive heart failure). Near syncope is the term for “almost” having a syncope episode. This is where you feel like you “almost pass out”, and perhaps briefly get dizzy, lightheaded, woozy, and unsteady.

 

Syncope is rarely ever of a true neurologic cause. However, for some reason, this is still one of the most common reasons for neurology consults in the hospital setting. Therefore, I created a simple mnemonic tool that will help you consistently remember every possible cause of syncope to check off your differential diagnosis list of possibilities. I always teach this tool to the residents and medical students who are rotating on the inpatient neurology hospital service because syncope is such a common reason for neurological consultation. However, it can be helpful across all medical specialties since syncope is such a common event across all specialties. It can also be used by patients suffering from syncope to help them gain a better understanding of syncope and syncope causes.

 

The mnemonic tool is CONSNOC. It’s a palindrome spelled the same forwards and backwards. It’s a nonsensical word, but remembering it will quickly bring to memory every possible differential diagnosis of syncope to run through in your mind. Let’s go through each letter:

 

Cardiac: Think the SA (sinoatrial) node, and then think Structural and Arrhythmia causes. Structural can be outflow obstruction or low ejection fraction in CHF (congestive heart failure). Arrhythmia can be from the heart beating too fast (tachycardia) or too slow (bradycardia).

 

Orthostatic: This is from low blood pressure which occurs when someone stands up from a lying or sitting position. It is often seen with dehydration or blood pressure medication doses that are too high. Orthostatic intolerance is another term for this. Since this is typically such a common cause of syncope, near syncope, and dizziness, I have listed a number of treatment suggestions to help with treatment at the bottom of this page.

 

Neurocardiogenic: This is your classic vasovagal response where there is a sudden decrease in heart rate followed by an abrupt drop in blood pressure leading to syncope and collapse (passing out, or fainting). The physiologic mechanism for neurocardiogenic syncope can be triggered by several things. Vasovagal syncope classically occurs with a sudden scare (sees blood, intense pain, fright, etc.). Variants of the vasovagal response also include micturition or defecation syncope (think about the old lady who passed out after standing up from using the toilet, triggered by a large parasympathetic discharge), carotid hypersensitivity (think about the old guy shaving and becomes bradycardic by inadvertent carotid massage from pressing on the neck during shaving), and cough syncope or syncope with coughing.

 

Seizure: This is a common reason for inpatient neurological consult even though syncopal episodes are almost never from a seizure. Look for additional symptoms such as tongue biting, incontinence, and witnesses to the event for description (preceded by staring off, posturing, tonic-clonic activity, etc.). Keep in mind, you can still have convulsions during syncope called convulsive syncope (syncope with convulsions), which are not true seizures but just a manifestation of sudden drop in blood pressure and lack of blood flow to the brain. Incontinence can also occur with syncope, so it does not confirm a seizure cause. The diagnosis of seizure is best made by the company it keeps (associated symptoms with the syncopal event).

 

Neuropathic: This correlates to dysautonomia, also known as autonomic neuropathy. This is neuropathy involving the small nerve fibers that control heart rate, heart rhythm, blood pressure, gastrointestinal motility, sweating, and other things. The result is often a disconnect between blood pressure and heart rate where they are not working in synchronicity together, leading to symptoms such as syncope. There are a wide variety of these disorders, but the top categories to keep in mind are from chronic/toxic autonomic neuropathy such as from diabetes, autoimmune dysautonomia (such as acetylcholine receptor (AchR) autoantibody, paraneoplastic), post-viral dysautonomia, neurodegenerative dysautonomia (such as Shy-Drager Syndrome in Parkinson’s Disease), and POTS (Postural Orthostatic Tachycardia Syndrome). These disorders are often easily diagnosed by a tilt table test, or even a good set of orthostatic vitals.

 

Other: Think additional possibilities such as mechanical (the patient simply tripped or lost their footing), glucose (hyperglycemia, hypoglycemia)

 

Cerebrovascular: Think posterior circulation and vertebrobasilar ischemia. This is the other most common reason for inpatient neurology consultation in terms of TIA (transient ischemic attack) or stroke, but again, syncope is rarely the result of this. If this is the cause, it is typically associated with other neurological symptoms, particularly of the posterior circulation. So, assess for associated brainstem symptoms such as double vision, hemiparesis or hemisensory loss, slurred speech, vertigo, dysphagia, etc. Similar to seizures, the diagnosis of posterior circulation TIA or stroke is best made by the company it keeps (associated symptoms with the syncopal event).

 

As mentioned above, since orthostatic intolerance (orthostasis) is such a common symptom and disorder, here are some suggestions to consider to help treat it.

 

Guidelines for the Treatment of Orthostatic Intolerance (OI):

 

  1.  Make all postural changes from lying to sitting or sitting to standing, slowly.

 

  1.  Drink to 2.0 -2.5 L of fluids per day. If you have a history of congestive heart failure (CHF), you should discuss fluid intake with your cardiologist to avoid a CHF exacerbation.

 

  1.  Increase sodium (salt) in the diet to 3 – 5 g per day. If not helpful and blood pressure is stable, may try 5-7 g per day. If you have a history of high blood pressure, you should discuss these adjustments with your cardiologist or primary care physician.

 

  1.  Avoid large meals which can cause low blood pressure during digestion. It is better to eat smaller meals more often than three large meals.

 

  1.  Avoid alcohol.  Alcohol and cause blood to pool in the legs which may worsen low blood pressure reactions when standing.  This can aggravate OI.

 

  1.  Perform lower extremity exercises to improve strength of the leg muscles.  This will help prevent blood from a pooling in the legs when standing and walking.

 

  1.  Raise the head of the bed by 6 to 10 inches.  The entire bed must be at an angle.  Raising only the head portion of the bed at waist level or using pillows will not be effective.  Raising the head of the bed will reduce urine formation overnight and there will be more volume in the circulation in the morning.

 

  1.  During bad days, drink 500 cc of water quickly.  This will result in an increased blood pressure within 5 minutes of drinking the water.  The effect will last up to one hour and may improve orthostatic intolerance.

 

  1.  Use custom fitted elastic support stockings.  These will reduce a tendency for blood to pool in the legs when standing and may improve orthostatic intolerance.

 

  1.  Use physical counter maneuvers such as leg crossing, squatting, or raising and resting the leg on a chair.  These maneuvers increase blood pressure and can improve orthostatic intolerance.

 

  1. Avoid temperature extremes, particularly excessive heat.

 

  1. For activity planning involving higher levels of physical activity, try to plan for:

-Before rather than after a meal

-Afternoon rather than morning

-Avoid excess heavy lifting

-Avoid during excessively hot weather

 

 

IF YOU HAVE HEADACHE, MIGRAINE, OR FACIAL PAIN AND ARE LOOKING FOR ANSWERS ON ANYTHING RELATED TO IT, A HEADACHE SPECIALIST IS HERE TO HELP, FOR FREE!

FIRST, LET’S DECIDE WHERE TO START:

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR THE LATEST INFORMATION, HOT TOPICS, AND TREATMENT TIPS, VISIT OUR FREE BLOG OF HOT TOPICS AND HEADACHE TIPS HERE. THIS IS WHERE I WRITE AND CONDENSE A BROAD VARIETY OF COMMON AND COMPLEX  MIGRAINE AND HEADACHE RELATED TOPICS INTO THE IMPORTANT FACTS AND HIGHLIGHTS YOU NEED TO KNOW, ALONG WITH PROVIDING FIRST HAND CLINICAL EXPERIENCE FROM THE PERSPECTIVE OF A HEADACHE SPECIALIST.

 

IF YOU DON’T HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR POSSIBLE TYPES OF HEADACHES OR FACIAL PAINS BASED ON YOUR SYMPTOMS, USE THE FREE HEADACHE AND FACIAL PAIN SYMPTOM CHECKER TOOL DEVELOPED BY A HEADACHE SPECIALIST NEUROLOGIST HERE!

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR FURTHER EDUCATION AND SELF-RESEARCH ON YOUR DIAGNOSIS, VISIT OUR FREE EDUCATION CENTER HERE.

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Last updated on September 17th, 2021 at 06:39 am

MEDICAL MARIJUANA (CANNABIS) FOR MIGRAINE, HEADACHE AND PAIN. A CRASH COURSE OF EVERYTHING YOU NEED TO KNOW.

@Neuralgroover

BACKGROUND

Medical marijuana (medical cannabis) for treatment of migraine, headache, pain, and chronic pain has become an increasingly hot topic of interest. As states continue to legalize the use of medical marijuana, there are increasing discussions and questions about its medical uses. What are the best medical marijuana strains for migraine, headache, and pain? Is medical marijuana helpful for migraine, chronic migraine, headache, pain, and chronic pain? How is medical marijuana used and dosed? Is medical marijuana legal to use? What are the side effects of medical marijuana? How do you get medical marijuana? How does marijuana differ from CBD (cannabidiol)? What is the best CBD dose for pain? What is the best CBD dose for migraine? What is the best THC dose. How do you increase CBD dosing, THC dosing, or cannabis dosing?

 

Patients ask about these treatments all the time, so this blog is to provide a comprehensive overview to answer all of these questions and much more. Reading the whole blog will give you a comprehensive, yet condensed detailed education of its history and everything you need to know about cannabis, CBD, and THC for medical use, with an additional focus in the treatment of migraine and pain. Alternatively, you can skip down to find the specific topic that you are looking for information on. For example, specific suggestions for how to begin CBD or THC dosing, and a schedule of how to titrate upwards can be found below. If you would like to skip to a specific topic, here is the sequence of the topics discussed:

 

-HISTORY CRASH COURSE OF MARIJUANA (CANNABIS) IN THE TREATMENT OF MIGRAINE, PAIN, PROHIBITION, AND RETURN TO LEGAL STATUS.

-STATES WHERE MEDICAL AND RECREATIONAL (ADULT-USE) MARIJUANA (CANNABIS) ARE LEGAL.

-MEDICAL MARIJUANA (CANNABIS) USE FOR PAIN AND MIGRAINE.

-WHAT TYPES OF MARIJUANA (CANNABIS) ARE THERE AND HOW DO YOU KNOW WHICH ONE TO USE?

-WHAT IS THE EVIDENCE FOR MARIJUANA (CANNABIS) USE FOR MIGRAINE?

-GENERAL SUGGESTIONS OF HOW TO USE MEDICAL MARIJUANA (CANNABIS).

-HOW DO YOU ESTIMATE THC CONTENT, WHAT IS THE BEST THC DOSE, AND HOW DO YOU USE THC?

-WHAT IS THE BEST CBD DOSE AND HOW DO YOU USE CBD?

-SIDE EFFECTS AND ADVERSE REACTIONS OF MEDICAL MARIJUANA (CANNABIS).

-WHAT IS CANNABIS HYPEREMESIS SYNDROME AND HOW DO YOU TREAT IT?

-CANNABIS (MARIJUANA) ADDICTION AND ABUSE

 

When many people hear the term “medical marijuana”, they think of a street drug with no true medicinal qualities, used only for recreation and abuse. Their mind immediately activates the visual hippie imagery of the 1967 Summer of Love and 1969 Woodstock festival. However, this is an outdated view in the scientific research community. The term “marijuana” (sometimes spelled marihuana) is a loaded term with many negative connotations including old political and racial associations, and is associated with the plant being used recreationally as a drug of abuse. Cannabis is the scientific name of the plant and is the preferred terminology.

 

It is best to think of cannabis, as a broad class of medication. Within this medication class there are many types of cultivars (strains, breeds), or more accurately, chemovars (chemotypes). “Cultivar” is short for “cultivated variety”, while “chemovar” refers to “chemical variety”. The older cultivar classification system (Sativa, Indica, Ruderalis) has evolved to the more current, scientific, and simplified chemovar classification system. These systems are discussed in more detail further down under the treatment section.

 

Each chemovar has standardized reproducible compositions of cannabinoids and terpenes, which are the phytochemicals in cannabis that make up most of the medicinal qualities. The CBD and THC (tetrahydrocannabinol) cannabinoids and terpenes are discussed further down, and are also discussed in great detail here. Similar to a medication, there will be some variation in benefits, responses, effectiveness, and side effects between patients for each chemovar. Also similar to a medication, there are common characteristics attributed to each chemovar that the majority of users will experience.

 

For comparison of this concept, antidepressants are a broad class of medication. Within this medication class there are many types of drugs. Each drug has standardized reproducible compositions of neurotransmitter targets. Similarly, there will be some variation in benefits, responses, effectiveness, and side effects between patients for each drug, and a set of common characteristics attributed to each drug that the majority of users will experience.

 

HISTORY CRASH COURSE OF MARIJUANA (CANNABIS) IN THE TREATMENT OF MIGRAINE, PROHIBITION, AND RETURN TO LEGAL STATUS.

To understand the current legal status of cannabis, it is important to know the history of cannabis, detailed here. The use of cannabis for medicinal purposes dates back to ancient times, with a Western/Central Asian botanical origin. Medicinal uses have been documented to 4000 BC or more. Chinese physicians were using it for joint pains and analgesia in childbirth 5000 years ago. Fast forward to 1839 when Dr. William Brooke O’Shaughnessy introduced the Western world to the medicinal uses of Cannabis indica, or “Indian hemp”, after he spent a professorship in Calcutta, India and learned of its uses while there. He advocated for its use in analgesia and muscle relaxation.

 

Throughout the 1800s into the 1900s, it was being recommended by many prominent physicians of those times for numerous diseases, particularly pain, headache, chronic daily headache, migraine, and chronic migraine, and was being used both acutely and preventatively.

 

In 1890, Sir John Reynolds, President of the British Medical Association, and Physician to the Royal household, wrote a paper in Lancet on his 30 years of experience prescribing cannabis for variety of ailments, particularly migraine and neuralgia.

 

In 1915, the “Father of modern medicine”, Sir William Osler, was recommending cannabis for migraine treatment in his historic medical textbook of those times, The Principles and Practice of Medicine. He went on to suggest that when treating migraine, “Cannabis indica is probably the most satisfactory remedy. Seguin recommends a prolonged course.” Dr. E.C. Seguin whom he referenced was a well-known neurologist and was the President of the NY Neurological Society. He was a vocal proponent of cannabis for migraine.

 

Cannabis-based preparations had been listed in the US Dispensatory in 1845. In North America, some pharmaceutical companies including Bristol-Meyers Squib, Parke-Davis, and Eli Lilly were producing cannabis-based preparations, as was Burroughs-Wellcome & Co. in England.

 

In the 1930s, Harry Anslinger was leading the Federal Bureau of Narcotics, which was essentially the early DEA. He began a campaign against cannabis, attempting to associate psychosis, mental deterioration, addiction, and violent crimes to cannabis use. He claimed cannabis was a drug of abuse used by minority and low-income communities. Instead of using the term cannabis when he was pushing his prohibition bill in front of congress in 1937, he purposely would use the term “marijuana,” subtly trying to convey a racial connection since it was commonly associated with recreational use among poor Mexican immigrants who would bring it from Mexico to the USA at that time. He reportedly chose his terminology wisely to fit this agenda and distance the plant from the more scientific term cannabis along with its growing uses for medicinal and industrial purposes. Furthermore, marijuana has a general connotation of being used as an intoxicant and recreationally, whereas cannabis has more of a scientific association. For all of these reasons, cannabis should really be the preferred terminology over marijuana.

 

The Marihuana Tax Act of 1937 was passed, attributing large fines and prison time to anyone involved with cannabis. Some historians also discuss influence on this law from prominent businessmen such as Andrew Mellon and the DuPont family since the hemp industry was gaining traction in industrial uses, posing a threat to synthetic and other more common competitor products, but that is a whole different discussion. The AMA (American Medical Association) strongly opposed this law.

 

In 1938, Dr. Robert Walton argued against the new Marihuana Tax Act and published a comprehensive review of cannabis, referencing 12 experts on its effectiveness for migraine.

 

In 1941 cannabis preparations were taken off the US Pharmacopoeia and National Formulary.

 

In 1942, Dr. Fishbein, the Editor of JAMA (Journal of the American Medical Association), published his recommendations for oral preparations of cannabis over ergotamine for menstrual migraine. Other physicians also published supporting evidence for cannabis in migraine treatment.

 

Then the 1960s hit, where there was a resurgence of recreational marijuana use. This left a lasting and ongoing negative stigma of cannabis. Again, cue the visual hippie imagery of the 1967 Summer of Love and 1969 Woodstock festival. Unfortunately, many people who are not aware of cannabis history have been stuck in this mindset since…

 

The final nail in the coffin for legal cannabis use came with the Controlled Substances Act of 1970. This is what changed cannabis to its schedule 1 drug illegal status, of which it has remained since that time. The Assistant Secretary of Health, Dr. Roger O. Egeberg, stated his reason as follows, “Since there is still a considerable void in our knowledge of the plant and effects of the active drug contained in it, our recommendation is that marijuana be retained within schedule 1 at least until the completion of certain studies now underway to resolve the issue.”

 

Well, we are well past those studies Dr. Egeberg mentioned, and extensively more have been completed since then, yet cannabis remains federally illegal, despite all the evidence and vast amount of knowledge that we have gained from research. Thus, it is only a matter of time until the tide finally turns completely, and cannabis is rescheduled from Schedule 1 in my opinion.

 

So, cannabis has been a schedule 1 drug since 1970. Schedule 1 drugs also include heroin, lysergic acid diethylamide (LSD), and 3,4-methylenedioxymethamphetamine (Ecstasy). According to the United States Drug Enforcement Agency (DEA), Schedule I drugs have a high potential for abuse, and have no accepted medical treatment use. If you are saying to yourself, that cannabis doesn’t seem like it fits into this category, you are certainly part of the majority opinion, which has shifted over the years. The DEA has continued to claim that cannabis has “no accepted medicinal use”, a statement which has no evidence to support it, but rather more evidence exists that disprove that claim.

 

Interestingly, despite this claim of no medicinal benefit, the US Government’s Department of Health and Human Services was awarded a patent (US Patent #6,630,507) for “cannabinoids as antioxidants and neuroprotectants” in 2003. Furthermore, the FDA has approved 3 synthetic versions of cannabinoids for medicinal purposes. Two are synthetic forms of THC (Dronabinol (Marinol), Nabilone (Cesamet)), and one is a purified form of CBD (Epidiolex). So, these statements and facts are clear contradictions to one another…

 

The schedule 1 classification has been a huge barrier preventing US federal funding for research and the legal ability to even proceed with research, although this has loosened up in recent years. This has historically been the primary hurdle in conducting medical research needed to obtain the evidence-based medicine in support of cannabis in the US. Meanwhile, many other countries such as Israel and Canada have been researching for years and have federal cannabis programs. For example, the Canadian equivalent to the US FDA is Health Canada. They have maintained a successful federal cannabis program for years. Despite this schedule 1 hurdle in the US, there has been accumulating evidence for various therapeutic benefits of cannabis, especially in the treatment of pain disorders.

 

In 1976, the FDA began an Investigational New Drug Program, after a glaucoma patient sued the government on grounds that cannabis was helping him, and won. This program closed in 1992, and 13 patients in the program at the time of closure were allowed to continue. Most recently, there were still 2 remaining who still receive monthly government supplied cannabis; one for multiple hereditary exostoses (painful bone tumor disorder), and the other for glaucoma. Access to this government supplied cannabis has since been controlled by the National Institute on Drug Abuse (NIDA), and the only federally approved cannabis source for decades has been from a farm at the University of Mississippi, who has had an ongoing contract with the federal government since 1968.

 

Through the 1990s-2000s, there was growing commentary from leading physicians and journals supporting cannabis for medicinal purposes. This has been accompanied by a growing push by medical organizations to reschedule cannabis to allow research and for patients who need it when they have failed all conventional treatments. Some of these organizations include American Academy of Neurology (AAN), American Medical Association (AMA), Epilepsy Foundation, American Journal of Public Health, and American Academy of Pediatrics (AAP).

 

In 2013, Dr. Sanjay Gupta MD, CNN Chief Medical Correspondent, issued a public apology article retracting his previous anti-marijuana stance which can be read here. He noted that “of more than 20,000 papers published in recent times, only 6% of the studies look at potential benefits of cannabis, while all the rest investigate potential harm, leading to an inherent bias and a profoundly distorted view.” He went on to further say:

“Well, I am here to apologize. I apologize because I didn’t look hard enough, until now. I didn’t look far enough. I didn’t review papers from smaller labs in other countries doing some remarkable research, and I was too dismissive of the loud chorus of legitimate patients whose symptoms improved on cannabis. Instead, I lumped them with the high-visibility malingerers, just looking to get high. I mistakenly believed the DEA listed marijuana as a Schedule 1 substance because of sound scientific proof. Surely, they must have quality reasoning as to why marijuana is in the category of the most dangerous drugs that have “no accepted medicinal use and a high potential for abuse.” They didn’t have the science to support that claim, and I now know that when it comes to marijuana neither of those things are true. It doesn’t have a high potential for abuse, and there are very legitimate medical applications. In fact, sometimes marijuana is the only thing that works. We have been terribly and systematically misled for nearly 70 years in the United States, and I apologize for my own role in that.”

 

Dr, Gupta has done a series of documentaries on CNN about the medicinal benefits of cannabis and are very enlightening to watch. This change in Dr. Gupta’s public opinion was also occurring along with spreading anecdotal cases of children with refractory pediatric epilepsy who were improving dramatically with CBD extracts from cannabis. One of these children, Charlotte Figi, became the poster child for this movement. In fact, the cannabis strain bred and extracted for high CBD for these purposes (Charlotte’s Web), was named after her. Unfortunately, she died 4/7/20 at the age of 13, and was remembered here.

 

STATES WHERE MEDICAL AND RECREATIONAL (ADULT-USE) MARIJUANA (CANNABIS) ARE LEGAL.

The legal use of medicinal cannabis continues to increase globally, including the United States. In 1996, CA became the 1st state to pass the Compassionate Use Act, allowing the legal use of cannabis for medicinal purposes. Since that time, legalized cannabis has continued to grow. As of 11/4/20, medical use of cannabis is legal in 35 states (AK, AR, AZ, CA, CO, CT, DE, FL, HI, IL, LA, ME, MD, MA, MI, MN, MO, MS, MT, ND, NH, NJ, NM, NY, NV, OH, OK, OR, PA, RI, SD, UT, VT, WA, WV) + Washington DC. Recreational marijuana use (“adult use”) is approved in 15 states (AK, AZ, CA, CO, IL, MA, ME, MI, MT, NJ, NV, OR, SD, VT, WA) + Washington DC. Despite a number of states legalizing cannabis use at the local level, it is still illegal federally in all states.

 

States which have medical cannabis programs have a list of qualifying conditions, which vary by state. The State Medical Board certifies doctors to “recommend” medical cannabis (Certificate to Recommend; CTR). The physician then confirms the qualifying condition and signs a “recommendation” form for potential benefit from medical cannabis. The patient then takes the recommendation to the local dispensary (which are also highly regulated by the state) and the patient discusses the best options there. However, it is important to remember that under the CSA (Controlled Substances Act), cannabis remains a schedule I drug, so doctors can’t “prescribe” cannabis. They can only “recommend” it. Also, interstate travel with any amount of cannabis or plant extract (including CBD products with THC content >0.3%) violates federal law and could potentially result in federal drug trafficking charges with stiff penalties of prison time and fines.

 

In 2009, the Justice Department sent a memorandum to federal prosecutors stating that patients and their providers should not face federal prosecution if they are following state law. In 2013 the Cole Memorandum was sent to US Attorney Generals, reinforcing that the Justice Department would not enforce federal prosecution in legal states who are following their state laws. In 2018, the Cole Memorandum was rescinded by Attorney General Jeff Sessions, which sent shockwaves through the industry. However, President Trump has continued to reinforce his support in protecting states that have legalized cannabis from federal prosecution. There have been discussions of re-evaluating the rescheduling of cannabis to remove the federal schedule 1 illegality, and it is suspected to be only a matter of time until this eventually happens.

 

MEDICAL MARIJUANA (CANNABIS) USE FOR PAIN AND MIGRAINE.

In medical cannabis registries, the most commonly reported reason for cannabis use is chronic pain of various types. Because of the increasing evidence of cannabis in the treatment of pain, the Canadian Pain Society revised their consensus statement in 2014 to recommend cannabinoids as a third-level therapy for chronic neuropathic (nerve) pain based on the abundance of supporting evidence and a NNT (number needed to treat) estimated at approximately 3 (the number of patients needed to treat for 1 of them to receive benefit). In 2017, The U.S. National Academies of Sciences, Engineering, and Medicine published a statement that the use of cannabis for the treatment of pain is supported by well-controlled clinical trials and that there is substantial evidence that cannabis is an effective treatment for chronic pain in adults. In February 2019, the World Health Organization (WHO) recommended that cannabis be rescheduled and removed from the most restrictive scheduling category.

 

Cannabis works through our endocannabinoid system. The endocannabinoid system is a normal and important biological system within everyone which helps to maintain homeostasis. It plays a role in many regulatory physiological processes across all organ systems, and is widely distributed throughout the central nervous system (brain and spinal cord) and peripheral nervous system (nerves outside of the spinal canal). This system is involved in the “runner’s high” as well. Notably, it plays a very strong role in pain pathways. This system works by the interaction of our own natural endocannabinoids turning on or turning off various endocannabinoid receptors throughout our body.

 

Over 540 phytochemicals have been described in cannabis, 18 different chemical classes, and more than 100 different phytocannabinoids. THC and CBD have been the most researched and are considered the major cannabinoids. There are many additional cannabinoids referred to as minor cannabinoids. The quantities of major and minor cannabinoids are widely variable between different types of cannabis chemovars. There is evidence for analgesic and anti-inflammatory effects in many of the cannabinoids. Cannabinoids are unique to the cannabis plant, and can be thought of as the “plant equivalents” of our own endocannabinoids. So, they interact with the same endocannabinoid receptors in our body as our own endocannabinoids do. The existing literature and research on the treatment of pain have primarily studied cannabis itself with its variable and often undefined combinations of THC, CBD, other cannabinoids, terpenes, and other constituents. These compounds, especially cannabinoids and terpenes, play significant roles in influencing one another and working together. The synergy and interactions between these compounds are referred to as the “cannabis entourage effects”. Thus, the medicinal benefits of cannabis are suspected to be from the “entourage effects”, more so than any of the individual components alone.

 

THC is a major cannabinoid and the most researched in cannabis. THC causes the psychoactive qualities (“high”) of cannabis. THC has been shown to be 20 times more anti-inflammatory than aspirin and 2 times as anti-inflammatory as hydrocortisone. It is also a potent anti-emetic (anti-nausea), which is why there are two FDA-approved synthetic THC medications for chemotherapy related nausea and vomiting (Dronabinol, Nabilone). THC is the cannabinoid which is tested for in drug tests. It is important to know that most CBD products contain trace amounts of THC, although there are some varieties that do not. It is typically a negligible amount unlikely to show up on a drug test, but it is not completely risk free. You can read about the different types of CBD products here. THC can be detected by a variety of ways, although most commonly it is tested in the urine. Here are the general timeframes that it will show positive:

  • Blood:
    • Few hours to 1-2 days after a single use
    • In heavy users (multiple times a day), possibly up to a week
  • Saliva:
    • Appears in saliva an hour after use, detectable for up to 1-2 days
  • Urine:
    • 5-12 days after one-time use
    • 11-18 days when used 2-4 days/week
    • 33-48 days when used 5-6 days/week
    • Around 50-65 days if used daily (stored in adipose tissue)
  • Hair:
    • Generally 90 days, but some hair follicle tests can go back years

CBD is the other major cannabinoid and has gained a lot of attention as a therapeutic agent over the past several years given a wide range of reported anecdotal benefits. It is discussed in much greater detail here. In contrast to THC, CBD is non-intoxicating (no “high”). Furthermore, it helps to neutralize some of the negative THC side effects. CBD has been shown to be several hundred more times anti-inflammatory than aspirin. Greater than 65 molecular receptor targets and greater than 80 mechanisms of action have been identified. There have been scientific, animal models, and very limited human clinical trials documenting its anti-inflammatory and analgesic (pain-relieving) properties. However, there are no high-quality research studies to date evaluating isolated pure CBD in any pain, migraine, or other headache disorders. So, it is unclear how much benefit CBD in isolation provides outside of the presumed entourage effects that it contributes to.

 

In November 2017, The World Health Organization (WHO) concluded that CBD exhibits no evidence for abuse or dependence potential, and that there is no evidence of public health related problems associated with its use. In January 2018, the World Anti-Doping Agency (WADA) removed CBD from their prohibited list, no longer banning use by athletes. In December 2018, the Agriculture Improvement Act (Farm Bill) was signed into law. This legalized the agricultural growth and use of hemp (cannabis strains containing 0.3% THC or less) and hemp derivatives such as CBD. The Farm Bill also removed hemp from the Controlled Substances Act, making it no longer an illegal substance under federal law. Up until the Farm Bill was passed, any form of cannabis or cannabis derivatives (including CBD) have been federally illegal since the Controlled Substance Act of 1970. Therefore, it is important to remember that cannabis chemovars and CBD oils with greater than 0.3% THC are still illegal federally, require a medical cannabis card for use, and are illegal to cross state lines with. In May 2019, TSA began to allow travel with CBD products containing 0.3% or less of THC.

 

The terpenes account for many of the pharmacological properties of cannabis, as well as many medicinal herbs, plants and essential oils. They are the source of flavors, aromas, and other characteristics that help differentiate cannabis cultivars. Terpenes are often used in many household products such as limonene (citrus), pinene (pine, conifer), and linalool (lavender) to name just a few. Similar to the cannabinoids, many have anti-inflammatory and analgesic properties.

 

WHAT TYPES OF MARIJUANA (CANNABIS) ARE THERE AND HOW DO YOU KNOW WHICH ONE TO USE?

As discussed at the beginning of the blog above, there are many types of cannabis chemovars that vary widely in the composition of cannabinoids, terpenes, flavonoids, and other compounds. These components work synergistically to produce wide variations in benefits, side effects, and chemovar characteristics. Different chemovars have different ratios of these compounds, and thus have different characteristics.

 

The older cultivar (strain, breed) classification system was based on strain appearance, smell, and clinical effects. Cannabis Sativa strains were generally described by patients as uplifting, energetic, creative, euphoria, spacey, cerebrally-focused effects, and better for day use, while cannabis Indica strains were typically described as calming, relaxing, sedative, full body effects such as “body buzz”, and better for night use. Cannabis ruderalis (hemp) strains were considered predominantly or purely high CBD without any real clinical use effects.

 

However, biochemical studies of specific strain names often do not accurately distinguish CBD and THC content, which was the predominant basis for strain classification. Strain characteristics and clinical effects are dependent on varying ratios of major and minor cannabinoids and terpenes, not only from CBD:THC ratios, as there are no significant differences in CBD:THC ratios between many Sativa and Indica strains when studied chemically. Most strains used today are hybrid strains genetically cross-bred for standardized CBD, THC, terpenes, and minor cannabinoid content.

 

The older cultivar classification system has evolved to the newer and more scientific chemovar (chemotype) classification system, and is divided into type I-III chemovars. This system allows medical users to find a chemical profile better matching their pharmacological needs.

 

Type I chemovars are THC predominant. They are high THC (>0.3%, but generally >10-20%), and low CBD (<0.5%, but generally <2%). They are very intoxicating, and associated with recreational more than medical use. They are moderately-heavily psychedelic with changes in perception and sensory awareness and have the potential for significant physiological changes in heart rate and blood pressure. They can intensify relief from symptoms like nausea or pain, so terminal cancer patients may be one of the few true medical uses for these chemovars.

 

Type II chemovars are more balanced THC and CBD. They are high THC (>0.3%, but generally 3%-10%), and high CBD (>0.5%, but generally 1%- 14%). They are intoxicating to a lesser degree than Type I chemovars. They can be mildly-moderately psychedelic with milder cerebral and cognitive changes in perception and sensory awareness possible. In general, they can be more effective at treating symptoms with less negative side effects.

 

Type III chemovars are CBD predominant. They are low THC (<0.3%, but generally 0%-1%), and high CBD (>0.5%, but generally 5%-20% or more). They have low to no intoxication side effects. There is little to no cognitive impairment for most, but there can be possible mild effects in sensitive users, depending on the THC content.

 

WHAT IS THE EVIDENCE FOR MARIJUANA (CANNABIS) USE FOR MIGRAINE?

The benefits of cannabis/cannabinoids in various chronic pain disorders has been well established. These benefits are suspected to likely extrapolate to headache disorders including migraine given overlapping neurobiological pathways of pain. There are some notable interactions and synergies between the cannabinoid receptors and pathways of migraine involving the trigeminovascular system (including the same receptors that the triptans work on) and serotonergic system. A more detailed discussion of this physiology can be read here and here. The medical literature regarding treatment of headache, migraine, and facial pain disorders shows limited supporting evidence for cannabis/cannabinoids in the treatment of chronic headaches, migraine including chronic migraine, medication overuse headache, cluster headache, idiopathic intracranial hypertension, and multiple sclerosis (MS) associated trigeminal neuralgia. However, the majority of this limited supporting evidence consists primarily of case series, case studies, case reports, surveys, clinical/anecdotal reports, and one retrospective analysis. There have been no placebo-controlled studies of cannabis for headache disorders or migraine thus far. There are only two prospective trials containing a control group evaluating the use of cannabinoids in the treatment of headache disorders, both of which showed benefit. The details and references of these studies and all of the smaller case studies mentioned can be read here and here.

 

Part of the difficulty in these types of trials, besides the federal illegality and the schedule 1 status of cannabis, is that there are so many variations of chemovars. It is unknown what chemovars and varieties of cannabis might be most helpful for migraine treatment. Most likely, it is not a one size fits all. Similar to how patients have a wide variety of therapeutic responses to abortive and preventive migraine treatments (what works for one person often does not work for another, etc.), responses to chemovars is probably similar. One person may respond very well to a specific chemovar, while another may respond better to a different one. Everyone is different, so like the trial and error process of trying different medications to see which may work best, cannabis chemovars most likely have a similar process.

 

With that said, there have been a couple studies evaluating a large medical cannabis registry, in an attempt to determine what chemovars patients with migraine and headache prefer to use. In one study, which can be read here, chemovars with high THC and low CBD were most preferred. “OG Shark” was the most preferred chemovar and consisted of high THC/THCA (tetrahydrocannabinolic acid) and low CBD/CBDA (cannabidiolic acid), with predominant terpenes β-caryophyllene and β-myrcene. This could reflect the potent analgesic, anti-inflammatory, and anti-emetic properties of THC, with anti-inflammatory and analgesic properties of β-caryophyllene and β-myrcene. Notably in that study, many headache patients replaced pharmaceuticals with cannabis, most commonly opiates/opioids (43.4% in headache patients, and up to 73% in chronic pain patients), anti-depressant/anti-anxiety (39%), NSAIDs (21%), triptans (8.1%), anticonvulsants (7.7%), muscle relaxers (7%), and ergots (0.4%).

 

In a follow up study (publication pending) 6 of the top 8 preferred chemovars were again high THC/low CBD, with “Headband” (22-24% THC, <1% CBD), “Warlock CBD” (8-11% THC, 8-11% CBD), and “Master Kush” (24-26% THC, <1% CBD) all tied for the top preferred cannabis chemovar. All three of these chemovars again had β-caryophyllene as one of their top 3 predominant terpenes, along with a mix of linalool, limonene, β-myrcene, bisabolol, and humulene as one of the top 3 predominant terpenes between them. There were 2 preferred chemovars which had high CBD and lower THC. They were “Warlock CBD” (8-11% THC, 8-11% CBD) which was in a 3-way tie for top preferred chemovar as mentioned above, and “Cannatonic” (3-7% THC, 6-10% CBD).

 

GENERAL SUGGESTIONS OF HOW TO USE MEDICAL MARIJUANA (CANNABIS).

Cannabis can be used by smoked, vaporized, oral, oral-mucosal, topical, or rectal routes of administration. Oral routes cause a slower onset of action and a prolonged duration of action. Smoking and vaporizing cause the fastest onset of action and the shortest duration of action. Smoking is not recommended due to the production of unhealthy respiratory irritants and toxins. Vaporizing is a newer technique with a goal of suppressing irritating respiratory toxins by heating cannabis to a temperature where active cannabinoid vapors form, but below the point of combustion where smoke and associated respiratory toxins are produced.

 

Start low on the dose, go slow, and stay on as low of a dose as possible. This promotes tolerance to the THC psychoactive effects. Use the lowest dose THC possible, and use CBD and THC together because CBD helps to neutralize some of the negative THC side effects. Approximately 15-20% CBD with less than 1% THC is a good starting point to consider. CBD predominant preparations are better for working and daytime use, while THC predominant preparations are better for after work and at bedtime. Long acting oral formulations are better for chronic conditions and symptoms. Vaporization can be an as needed (prn) for episodic symptom exacerbations. Driving should be avoided for at least 4 hours after inhaled cannabis, 6 hours after ingested cannabis, and 8 hours if euphoria is experienced.

 

Common dosing quantities and terminology include one cannabis cigarette (“joint”) = 0.3-0.5 grams, one eighth = 3.5 grams, one quarter = 7 grams, and one ounce = 28 grams. Based on peer-reviewed literature, the majority of patients using smoked or orally ingested cannabis for medical purposes have been observed to use between approximately 10-20 grams of cannabis per week, 1-3 grams per day, and a frequency of 3-4 times daily. With that said, specific dosing recommendations are not available, and this is one area of much needed research in order to determine the best dosing for various disorders.

 

The matching of the proper chemovar to the proper patient will be widely variable based on the targeted symptoms and the patient’s experience with cannabis. The anti-pain effects of THC may need a Type I or Type II chemovar, although the side effect profile will be higher (highest with Type I). The anti-anxiety or anti-inflammatory effects of CBD may require a Type II or Type III chemovar. Type III chemovars will have the least risk of side effects. Patients new to cannabis should be started with a Type II or Type III chemovar and it can be adjusted as needed and as tolerated.

 

HOW DO YOU ESTIMATE THC CONTENT, WHAT IS THE BEST THC DOSE, AND HOW DO YOU USE THC?

For THC dosing, 1-2.5 mg is a good starting dose. For example, starting at bedtime and increase 1-2.5 mg every few days at bedtime or daytime (depending on treatment goals) until benefits or side effects are reached. At 5 mg THC, many will experience benefit without excess side-effects. At 10 mg, most will have side effects. At 15 mg or more it may cause psychiatric side effects. The total daily THC dose should be less than 20-30 mg to limit adverse effects and tolerance. In addition, THC should preferably be used with CBD as mentioned above because it helps to neutralized out some of the negative THC side effects. Use of high dose THC chemovars more than 5 grams per day of flower suggests possible tolerance or misuse, and is usually unjustified medically unless perhaps an end stage cancer patient.

The best way to estimate the mg of THC in flower to get the goal THC dose is as follows. Say that you have 1 gram (1000 mg) of flower (typical cannabis cigarette quantity) from a chemovar with 10% THC. That means 1 gram flower contains 100 mg THC (1000 mg x 10%)!! With that formula in mind, you can easily figure out the THC content by switching out those numbers of weight and THC percentage in the flower or product being used. Taking this example a step further, 30 mg would be just more than 1/3rd (30 mg THC goal / 100 mg THC), 20 mg THC would be 1/5th of the 1 gram flower quantity (20 mg THC goal / 100 mg THC), 10 mg THC would be 1/10th of the 1 gram flower quantity (10 mg THC goal / 100 mg THC), 5 mg THC would be 1/20th of the 1 gram flower quantity (5 mg THC goal / 100 mg THC), and so on. So the easiest way to fine tune your THC dose from your flower would be to divide 1 gram of flower into a specific fraction as outlined (depending on dosing goals), so you can know exactly how much to use and exactly how much THC you are ingesting.

 

WHAT IS THE BEST CBD DOSE AND HOW DO YOU USE CBD?

For CBD dosing, a good general guideline of how to begin CBD dosing with a gentle titration is as follows:

-Week 1: 5-10 mg at bedtime

-Week 2: 5-10 mg twice daily

-Weeks 3-4: 5-10 mg three times daily

-Weeks 5 onwards: 20 mg three times daily

It is suspected that high doses are likely needed for pain and inflammation disorders, but this needs to be clarified with research. There are no established dosing guidelines or max doses established. For reference, doses of 400-600 mg/day showed benefit in anxiety, doses of 600-800 mg/day showed benefit in psychosis, and doses up to 2500 mg/day (25-50 mg/kg) have been used in epilepsy studies.

 

SIDE EFFECTS AND ADVERSE REACTIONS OF MEDICAL MARIJUANA (CANNABIS).

Side effects are influenced by dose, method of administration, patient tolerance, chemovar of cannabis, ratios of THC to CBD, cannabinoids, terpenes, production quality control (toxins, fungus, bacteria, heavy metals, etc.) to name a few. Many studies have been inconclusive or contradictory in terms of association with stroke, heart attack. This publication provides the most comprehensive review of cannabis and its recognized side effects. The most common side effects (which vary depending on the chemovar) include dizziness, dry mouth, increased appetite, disturbances in concentration, and sedation/drowsiness. Less common side effects can include incoordination, euphoria, anxiety, and paranoid thinking. In the majority of trials, side effects have been well tolerated, mild to moderate, transient, and not bothersome enough that many patients withdrew from studies. Overdose can occur and is typically from high THC content and oral dosing. Signs may include tachycardia, arrhythmia, confusion, panic attack, extreme paranoia, and hallucinations.

 

From existing research, there is concern for possible long-term cognitive side effects of cannabis use during adolescent years when the brain is still rewiring, pruning, and organizing itself. Studies suggest a decline in IQ/neurocognitive function when used frequently under age 18. In adults, a larger study suggested problems in verbal memory recall after chronic cumulative use (after 5 years of cumulative frequent/chronic use, 1 in 2 people may recall 1 word less from a list of 15 words). Current users had both decreased verbal memory and processing speed.

 

According to “The Health Effects of Cannabis and Cannabinoids: The Current State of Evidence and Recommendations for Research”, published by the National Academies of Sciences, Engineering, and Medicine in January 2017, the following are conclusions regarding cannabis side effects based on existing literature reviews.

 

For cardiovascular risk, there is limited evidence of cannabis triggering an acute MI (heart attack), ischemic stroke, or subarachnoid hemorrhage. There is no evidence to support or refute chronic cannabis use and increased risk of acute heart attack.

 

For cancer risk, there is moderate evidence of no association between the incidence of lung cancer (cannabis smoking), or the incidence of head and neck cancers. There is no or insufficient evidence to support associations with other cancers.

 

For respiratory disease risk, there is substantial evidence for worse respiratory symptoms and more frequent chronic bronchitis episodes (long-term cannabis smoking).

 

For neurocognitive risk, there is moderate evidence of impairment in the cognitive domains of learning, memory, and attention with acute cannabis use, but limited evidence for persistent impairments in cognitive domains of learning, memory, and attention after sustained cannabis abstinence.

 

For mental health risk, there is substantial evidence for development of schizophrenia or other psychoses in those at risk genetically, with the highest risk among the most frequent users. There is moderate evidence for increased symptoms of mania and hypomania in bipolar disorder. There is a small increased risk of depressive disorders and an increased incidence of social anxiety disorder. There is an increased incidence of suicidal ideation and suicide attempts with higher incidence in heavier users, and an increased incidence of suicide completion.

 

For prenatal, perinatal, and neonatal exposure, there is substantial evidence between maternal cannabis smoking and lower birth weight. During lactation, the amount reaching the infant is very low, although the effects of this are unknown. Therefore, it is recommended to not use cannabis in either pregnancy or breastfeeding.

 

There is substantial evidence for an increased risk of motor vehicle crashes. There is moderate evidence for increased risk of overdose, especially among pediatric populations. There is no or insufficient evidence for all-cause mortality, and there has been no documented death exclusively attributed to cannabis overdose or use. Cannabis has been shown in toxicology studies to be 114 times less lethal than alcohol. In fact, the deadliest substances in one toxicology study in order were alcohol, heroin, cocaine, tobacco, ecstasy, methamphetamine, and lastly, cannabis.

 

WHAT IS CANNABIS HYPEREMESIS SYNDROME AND HOW DO YOU TREAT IT?

Cannabis hyperemesis syndrome (CHS) has become increasingly seen as states legalize cannabis. It presents with clinical symptoms of cyclical nausea/vomiting, diffuse abdominal pain, and the need to take frequent hot showers (this is a pathognomonic sign).

 

Episodes of these symptoms last 24-48 hours, may last 7-10 days, and often recur with re-exposure of cannabis. CHS tends to be associated with high-dose, high-THC regular cannabis use. It can be confused with CVS (cyclical vomiting syndrome), and is differentiated by a history of chronic cannabis use and frequent hot bathing which produces temporary relief. The etiology (cause) of CHS is not fully understood. It has been theorized that there is a dysregulation of the endogenous cannabinoid system by downregulation of CB1 (cannabinoid 1) receptors, and in the GI (gastrointestinal) tract this may slow gastric motility, causing hyperemesis. Genetic differences in the cytochrome P450 system (enzymes in the liver which metabolize drugs) has also been proposed. The TRPV1 receptor in our bodies interacts with the endocannabinoid system. More specifically, anandamide (our main natural endocannabinoid) works at this receptor (one of many). Interestingly, this receptor is also the capsaicin receptor, and is activated by heat such as in hot peppers (which contain capsaicin). Therefore, it has also been proposed that perhaps the fact that these patients take frequent hot showers/baths for relief is because they are indirectly activating their endocannabinoid system.

 

Treatment of CHS revolves around cannabis cessation. There is no way around it. Supportive therapy can assist with fluid resuscitation. Capsaicin 0.075% topically to areas of the abdomen, back of arms, and areas that hot water gives symptom relief have shown some benefit (not using on private areas or mucosal surfaces). Antipsychotics such as Haloperidol and Olanzapine showed some temporary benefit. Conventional antiemetics, antihistamines, serotonin antagonists, benzodiazepines have shown limited evidence for effectiveness, and opiates should be avoided.

 

CANNABIS (MARIJUANA) ADDICTION AND ABUSE

Comparative addiction rates between substances have included tobacco 32%, heroin 23%, cocaine 17%, alcohol 15%, and lastly cannabis 9% (but 17% when used in adolescence, and 25-50% in adolescents who are using daily). Tolerance develops much faster with high potency high THC chemovars.

The DSM-5 recognizes 5 cannabis-associated disorders:

-Cannabis Use Disorder

-Cannabis Intoxication

-Cannabis Withdrawal

-Other Cannabis-Induced Disorders (Cannabis Intoxication Delirium, Cannabis Induced Psychotic Disorder, Cannabis Induced Anxiety Disorder, Cannabis Induced Sleep Disorder

-Unspecified Cannabis-Related Disorder

 

An estimated 3-4% of users meet criteria for Cannabis Use Disorder. The prevalence decreases with age, with the highest ages 18-29 years old (4.4%), and lowest ages 65 and older (0.01%). Cannabis Use Disorder is divided into mild (2-3 criteria), moderate (4-6 criteria), and severe (7 or more criteria). These criteria include any of the following:

  • Cravings and urges to use cannabis
  • Failure to fulfill major role obligations (work, school or home)
  • Unsuccessful attempts to quit/cut down
  • Spends excessive time in acquisition, using or recovering from use
  • Using Cannabis in larger amounts or for longer than you meant to (tolerance)
  • Continued use despite consistent social or interpersonal problems
  • Recurrent use in hazardous situations
  • Important social, occupational, or recreational activities are given up or reduced because of cannabis use
  • Needing more cannabis to get the effect you want (Tolerance)
  • Uses despite negative effects (physical or psychological)
  • Development of withdrawal symptoms, which can be relieved by taking more of the substance

 

IF YOU HAVE HEADACHE, MIGRAINE, OR FACIAL PAIN AND ARE LOOKING FOR ANSWERS ON ANYTHING RELATED TO IT, A HEADACHE SPECIALIST IS HERE TO HELP, FOR FREE!

FIRST, LET’S DECIDE WHERE TO START:

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR THE LATEST INFORMATION, HOT TOPICS, AND TREATMENT TIPS, VISIT OUR FREE BLOG OF HOT TOPICS AND HEADACHE TIPS HERE. THIS IS WHERE I WRITE AND CONDENSE A BROAD VARIETY OF COMMON AND COMPLEX  MIGRAINE AND HEADACHE RELATED TOPICS INTO THE IMPORTANT FACTS AND HIGHLIGHTS YOU NEED TO KNOW, ALONG WITH PROVIDING FIRST HAND CLINICAL EXPERIENCE FROM THE PERSPECTIVE OF A HEADACHE SPECIALIST.

 

IF YOU DON’T HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR POSSIBLE TYPES OF HEADACHES OR FACIAL PAINS BASED ON YOUR SYMPTOMS, USE THE FREE HEADACHE AND FACIAL PAIN SYMPTOM CHECKER TOOL DEVELOPED BY A HEADACHE SPECIALIST NEUROLOGIST HERE!

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR FURTHER EDUCATION AND SELF-RESEARCH ON YOUR DIAGNOSIS, VISIT OUR FREE EDUCATION CENTER HERE.

 

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Last updated on September 17th, 2021 at 06:37 am

CBD (CANNABIDIOL) FOR MIGRAINE, HEADACHE, AND PAIN. EVERYTHING YOU NEED TO KNOW.

@Neuralgroover

BACKGROUND

CBD (cannabidiol) for migraine, headache, pain, chronic pain, arthritis, and other medical conditions are topics that patients are increasingly asking about. Why? CBD is everywhere! You can buy it at the local grocery store, supplement store, gas station, video rental store, and almost anywhere else nowadays. There are hundreds of brands. Is it right for you? Will it work? How do you take it? How do you know which products are of good quality and are safe? Are there downsides? Are there side effects? Will you test positive on a drug screen? These are a few of the many questions you likely have. Our patients ask about CBD use all the time in regard to migraine and pain. So, I decided to write this blog to provide an overview and answer these burning questions you may have!

 

There have been a multitude of studies documenting the analgesic and anti-inflammatory benefits of medicinal cannabis across many chronic pain syndromes1–4, and it has been a historical treatment for headache and migraine for centuries.2,3,5–7 An extensive discussion of medicinal cannabis, or medicinal marijuana, for chronic pain, headache, and migraine can be read here. The vast majority of supporting evidence of cannabis and cannabinoids involves various chronic pain syndromes. These benefits are hypothesized to extend to headache disorders such as migraine given overlapping neurobiological pathways of pain. Some data suggests that cannabinoids appear to work uniquely within the inherent anatomical pathways of migraine (including serotonergic triptan pathways) and pain.1,2,5–37 Unfortunately, the majority of data supporting the use of cannabis and cannabinoids in migraine and headache disorders is based on case series, case reports, surveys and anecdotal evidence.5,6,32,33,38–57 There has been one retrospective study of cannabis use in the treatment of migraine which reported strong statistically significant findings of benefit.58 There have been only two limited prospective trials of cannabinoids containing a control group in headache disorders. One reported significant benefit in chronic daily headache associated with medication overuse headache,59 and the other reported significant benefit in both the acute and preventive treatment of chronic migraine.60

 

The endocannabinoid system is a normal and important biological system within everyone. It plays a role in many regulatory physiological processes across all organ systems, and is widely distributed throughout the central nervous system (brain and spinal cord) and peripheral nervous system (nerves outside of the spinal canal). Notably, it plays a strong role in pain pathways. This system works by the interaction of our own natural endocannabinoids turning on or turning off various endocannabinoid receptors throughout our body.

 

Cannabidiol (CBD) and delta-9-tetrahydrocannabinol (THC) are the two predominant cannabinoids found in cannabis (marijuana). Cannabinoids are unique to the cannabis plant, and can be thought of as the “plant equivalents” of our own endocannabinoids. So, they interact with the same endocannabinoid receptors in our body as our own endocannabinoids do. Given the growing evidence of cannabis and cannabinoids in the treatment of chronic pain and other medical conditions, in February 2019 The World Health Organization (WHO) recommended that cannabis be rescheduled and removed from the most restrictive scheduling category. In January 2017, the National Academies of Sciences, Engineering, and Medicine concluded that the use of cannabis for the treatment of pain is supported by well-controlled clinical trials and that there is substantial evidence that cannabis is an effective treatment for chronic pain in adults. In 2014, the Canadian Pain Society revised their consensus statement to recommend cannabinoids as a third-level therapy for chronic neuropathic pain based on the abundance of supporting evidence and a NNT (number needed to treat) estimated at approximately 3 (the number of patients needed to treat for 1 of them to receive benefit). So naturally, there has been a quickly growing public interest in these potential therapies for a variety of reasons, especially in pain disorders.

 

THC causes the psychoactive qualities (“high”) of cannabis. THC has been shown to be 20 times more anti-inflammatory than aspirin and 2 times as anti-inflammatory as hydrocortisone. It is also a potent anti-emetic (anti-nausea), which is why there are two FDA-approved synthetic THC medications for chemotherapy related nausea and vomiting (Dronabinol, Nabilone). The existing literature and research on the treatment of pain have primarily studied cannabis itself with its variable and often undefined combinations of THC, CBD, other cannabinoids, terpenes, and other constituents. The medicinal benefits of cannabis are suspected to be from the “entourage effects” from synergistic action (working together) between various cannabinoids such as THC and CBD, and terpenes.1,61

 

In contrast to THC, CBD is non-intoxicating (no “high”). CBD has been shown to be several hundred more times anti-inflammatory than aspirin. Greater than 65 molecular receptor targets and greater than 80 mechanisms of action have been identified. There have been scientific, animal models, and very limited human clinical trials documenting its anti-inflammatory and analgesic (pain-relieving) properties. However, there are no high-quality research studies to date evaluating isolated pure CBD in any pain, migraine, or other headache disorders. So, it is unclear how much benefit CBD in isolation provides outside of the presumed entourage effects that it contributes to.

 

In November 2017, The World Health Organization (WHO) concluded that CBD exhibits no evidence for abuse or dependence potential, and that there is no evidence of public health related problems associated with its use. In January 2018, the World Anti-Doping Agency (WADA) removed CBD from their prohibited list, no longer banning use by athletes. In December 2018, the Agriculture Improvement Act (Farm Bill) was signed into law. This legalized the agricultural growth and use of hemp (cannabis strains containing 0.3% THC or less) and hemp derivatives such as CBD. The Farm Bill also removed hemp from the Controlled Substances Act, making it no longer an illegal substance under federal law. To review, up until the Farm Bill was passed, any form of cannabis or cannabis derivatives (including CBD) have been federally illegal since the Controlled Substance Act of 1970, which is when cannabis was changed to a Schedule 1 drug of which it has remained since. Therefore, it is important to remember that cannabis chemovars (strains) and CBD oils with greater than 0.3% THC are still considered marijuana, and thus are illegal federally, require a medical marijuana card for use, and are illegal to cross state lines with. In May 2019, TSA began to allow travel with CBD products containing 0.3% or less of THC.

 

Thus, the use of CBD products has been exponentially increasing for a wide variety of uses, including pain and headache, and anecdotal benefits are commonly reported. Although the various CBD companies provide guidance on dosing, there are no standardized dosing guidelines on optimal dosing, and strengths and frequencies used are widely variable. Some cannabinoid experts feel that most over the counter bought CBD products have too low of milligram content to have true physiological effects based on the high dose needed to enter the central nervous system through the blood-brain barrier. On the other hand, some suggest that “micro-dosing” with the lower CBD doses found in many products is enough to help replace endocannabinoid deficiencies. These dosing uncertainties have yet to be clarified and confirmed scientifically. Pure isolated CBD has never been evaluated prospectively in a randomized controlled trial in the treatment of migraine, headache, or pain to date. So, its use in the treatment of pain disorders including migraine remains primarily anecdotal at this time, but we anticipate future trials will provide more objective scientific data. The FDA is currently gathering and assessing available objective scientific data in anticipation of providing general dosing guidelines and recommendations of use.

 

WHAT IS THE BEST CBD DOSE AND HOW DO I INCREASE THE DOSE?

For CBD dosing, a good general guideline of how to begin CBD dosing with a gentle titration is as follows:

-Week 1: 5-10 mg at bedtime

-Week 2: 5-10 mg twice daily

-Weeks 3-4: 5-10 mg three times daily

-Weeks 5 onwards: 20 mg three times daily

 

SAFETY AND SIDE EFFECTS OF CBD

CBD is generally very well tolerated, and pure CBD is not felt to be sedating. Actually, low to moderate doses are often more alerting.62 Early anecdotal literature involved CBD with sedating components (full spectrum products) including trace THC, other cannabinoids, and terpenes. For example, myrcene is a terpene often attributed to the “couch lock” phenomenon of some cannabis chemovars (strains). So, the sedation was not from the CBD, but actually from these other associated components. More recent studies (up to 600 mg pure CBD) have reported no sedative side effects.

 

There is one FDA approved form of CBD called Epidiolex, and these trials are what most of the known CBD safety data comes from. This is a purified cannabis derived form of CBD which was FDA approved in June of 2018 for some forms of refractory pediatric epilepsies.63 Dosing ranges from 5 to 20 milligrams per kilogram body weight total daily dose, which is divided between a morning and evening dose. These does are significantly higher than any form of over the counter non-prescription forms of CBD commonly sold. CBD is metabolized (broken down) in the liver. So, patients with liver disease many need to be more cautious with their dosing. In the Epidiolex studies, there was a slight elevation in liver enzymes in some patients. However, the vast majority of these liver enzyme elevations were in patients using the highest 20 milligram per kilogram daily dose and particularly when CBD was also being used with other anti-seizure medications, especially valproate and clobazam. This risk was much lower in patients outside of these categories. None the less, caution should be used when CBD is used with other medications that are metabolized by the same liver enzyme systems to avoid causing high or low levels of other medications. For example, high doses of CBD (such as those in the Epidiolex trials) may increase levels of certain medications such as warfarin, macrolide antibiotics, calcium channel blocker blood pressure medications, benzodiazepines, cyclosporine immunosuppressants, sildenafil, antihistamines, antidepressants, antipsychotics, antiretrovirals (such as HIV meds), and some antiseizure medications (such as clobazam), to name a few. With that said, the more commonly used doses bought over the counter are nowhere near the high doses of CBD in Epidiolex, so the clinical relevance of CBD use with these liver interactions is unclear at much lower doses. For example, Sativex studies (a whole plant CBD rich sublingual spray) found no interactions with liver enzyme systems with 40 mg CBD. The bottom line is that there are still many uncertainties so it is better to use caution until future studies can help clarify these questions.

 

In the Epidiolex studies, the most common adverse effects in a minority of patients were somnolence, lethargy, drowsiness, fatigue, diarrhea, decreased appetite, and nausea/vomiting. However, these side effects were in patients who were also using other anti-seizure medications (virtually all of which have drowsiness as a universal side effect). In addition, Epidiolex is about 98% pure CBD, but still contains 0.15% or less of THC, traces other cannabinoids and terpenes at a dose of 10 milligrams per kilogram per day. Therefore, these side effects are most likely to be related to these other factors rather than from the CBD content itself.

 

DIFFERENCES IN CBD PRODUCT TYPE, QUALITY, AND SAFETY

CBD has a wide variety of formulations from oral (primarily oils), tinctures, vaporization, and topical creams. Full spectrum or “whole plant” oral CBD products are the most popular. They are most likely to provide the “entourage effects” of cannabis. They contain everything the cannabis plant contains including CBD, trace THC (should be ≤0.3% per Federal law), terpenes, and flavonoids. Broad spectrum CBD products can be thought of as full spectrum without the trace THC. CBD isolate products consist of CBD isolated from all plant contents, without trace THC. It is important to know that use of these products may have a risk of testing positive on a marijuana drug test (which tests for THC). Although this risk is very low and can also be influenced by differing metabolisms between people, it is still a risk to be aware of. The risk of this correlates with the presence of trace THC and this risk would be highest in full spectrum, followed by broad spectrum, followed by CBD isolate products. Lastly, there is a misconception that CBD converts into THC in the human body. This is not true, and there is no evidence of this happening in the human body, and actually more evidence that it does not happen.62 This notion was based on an old lab-based experiment which involved acids and conditions which are not reflective of normal human physiology.

 

CBD products chosen should include independent 3rd party laboratory testing for content and quality. The reason is because there are so many CBD companies and products, and many of them are of low quality. In 2017, there was a study published in the Journal of the American Medical Association (JAMA) which evaluated 84 CBD products analyzed from 31 different companies, including 40 oils, 24 vaporization liquids, and 20 tinctures.64 Only about 30% of the products were labeled accurately with what they claimed to contain, while about 70% of the products were inaccurately labeled based on actual CBD content (43% had higher than advertised CBD, 26% had lower than advertised CBD). In addition, 21.4% had high levels of THC, above legal limits.

 

Another study looked at 13 CBD products tested across Los Angeles and New Jersey.65 Five of them (almost half) had no traceable CBD, and only 1 had an accurately advertised amount of CBD! Two had high THC (3 mg), 1 CBD gel cap product was contaminated with a deadly strain of E. Coli (shiga toxin), and 2 had potentially dangerous levels of ethanol.

 

In 2017, 5 patients in Utah developed seizures, confusion, coma, and hallucinations with a labeled “CBD” product, and 52 patients were harmed through 2018 with this product. This “CBD” product actually contained a synthetic cannabinoid and no CBD at all. The International Cannabis and Cannabinoid Institute in the Czech Republic assessed 29 CBD products and found that 69% exceeded the recommended levels of polycyclic aromatic hydrocarbons. These are known carcinogens and genotoxic mutagens according to International Agency for Research on Cancer. Unregulated CBD products may contain pesticides or heavy metal contamination as well.

 

CONCLUSIONS

In summary, CBD shows analgesic and anti-inflammatory effects in scientific and animal models, but there is limited data involving human studies. However, this should be changing soon now that CBD is federally legal with easier access to research. None the less, there may be a wide variety of tremendous therapeutic potential to be harnessed. Non-FDA approved forms of CBD may have inconsistent levels of CBD, THC, and contamination. Therefore, non-FDA approved forms of CBD should be from companies using independent 3rd-party lab analysis to confirm quality and contents until FDA regulations are available. It is important to know that CBD involves drug interactions with some common liver enzyme metabolism systems, but dosing threshold to interfere with other medications being metabolized in these same pathways is unclear and needs to be further clarified.

 

IF YOU HAVE HEADACHE, MIGRAINE, OR FACIAL PAIN AND ARE LOOKING FOR ANSWERS ON ANYTHING RELATED TO IT, A HEADACHE SPECIALIST IS HERE TO HELP, FOR FREE!

FIRST, LET’S DECIDE WHERE TO START:

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR THE LATEST INFORMATION, HOT TOPICS, AND TREATMENT TIPS, VISIT OUR FREE BLOG OF HOT TOPICS AND HEADACHE TIPS HERE. THIS IS WHERE I WRITE AND CONDENSE A BROAD VARIETY OF COMMON AND COMPLEX  MIGRAINE AND HEADACHE RELATED TOPICS INTO THE IMPORTANT FACTS AND HIGHLIGHTS YOU NEED TO KNOW, ALONG WITH PROVIDING FIRST HAND CLINICAL EXPERIENCE FROM THE PERSPECTIVE OF A HEADACHE SPECIALIST.

 

IF YOU DON’T HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR POSSIBLE TYPES OF HEADACHES OR FACIAL PAINS BASED ON YOUR SYMPTOMS, USE THE FREE HEADACHE AND FACIAL PAIN SYMPTOM CHECKER TOOL DEVELOPED BY A HEADACHE SPECIALIST NEUROLOGIST HERE!

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR FURTHER EDUCATION AND SELF-RESEARCH ON YOUR DIAGNOSIS, VISIT OUR FREE EDUCATION CENTER HERE.

 

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