Nausea and vomitting, It’s not always what you think.

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Posted by Sara Ghotb, MD PGYIII Internal Medicine, Monmouth Medical Center

Case history:

This 74 y/o African American male presented to the emergency department with a 1-week history nausea ad intractable vomiting.

His past medical history included surgery for esophageal cancer in 2012 and hypertension.

He was admitted to the hospital for a gastrointestinal evaluation.  His symptoms did not improve with antiemetics and he also began to complain of headache and dizziness.  He was scheduled for an upper GI endoscopy.

What would you do next?

A.  Go ahead and do the upper GI endoscopy

B.  Order a brain imaging study

C.  Do a more detailed examination

D.  Prescribe more antiemetic medication

Surgery for Migraine? Keep your scalp on!

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An excerpt from the Boston Globe April 2012

Debra Haining lay in a hospital bed at Massachusetts General Hospital, awaiting surgery. Both eyelids were colored purple, and blue dots were drawn on her forehead, including one on each temple, and one above her left eye.

The dots indicated the location where she feels the migraine, the trigger points, where the pain strikes. She is 57 years old and says that she never had a headache until five years ago, when she woke up feeling as if she’d been shot through the head.

She was forced to spend nearly every day in bed with the curtains drawn. She could not tolerate light, smell, or sound. Typically she rose only to see her 12-year-old son off to school in the morning and in the afternoon when he returned. Until recently, she had an ice pack to her head and could not drive a car.

A half-dozen medications, four different pain clinics, a variety of headache cocktails and injections, and numerous neurologists didn’t provide relief. Haining, who lives in Pawtucket, R.I., searched the Internet until she found Dr. W.G. (Jay) Austen Jr., of plastic and reconstructive surgery at Massachusetts General Hospital.

Haining says she was tired of doctors who suggested that she learn to accept a lifetime of pain, pills, and shots, and was relieved to find a doctor who offered to treat the cause of the migraine and not just the symptoms. “When you are debilitated and life comes to a halt, you are willing to try what’s out there.’’

In the operating room at Mass. General, Austen began surgery on Haining by making an incision in one of her eyelids in what would appear to be a routine blepharoplasty, a cosmetic surgery known as an “eyelid lift.”

Haining would benefit cosmetically by removal of this globular flat that settles into each eyelid with age. But the point, Austen says, is that this particular procedure provides “easy access” to the critical sensory nerves around her eyes that he believes were causing migraine pain.

This was just one of the three trigger points that Haining identified prior to surgery, and as he operated, Austen would be seeking a structural reason for that pain, a nerve compressed or impinged by surrounding bone or soft tissue.

This surgical approach was developed 12 years ago by Dr. Bahman Guyuron, chairman of the plastic surgery department at University Hospitals Case Medical Center in Cleveland, after several of his plastic surgery patients reported that their migraines improved after a cosmetic procedure known as a forehead lift.

A study published in the journal Plastic and Reconstructive Surgery in 2009 — led by Guyuron and submitted by Case Western Reserve University, the American Migraine Center, and the Center for Headache and Pain, Cleveland Clinic — found that just under 85 percent of patients who underwent the nerve decompression surgery reported at least a 50 percent reduction in migraine, calculating pain, frequency, and duration. Nearly 60 percent (28 of 49 patients) reported a complete elimination of pain. This compared with only 1 of 26 patients who had a sham surgery, in which the surgery was limited to exposure of the nerve but muscle and attachments were left intact. Reported side effects included forehead numbness, temporary hair loss and itching, a slight hollowing of the temple, and small change in eyebrow movement.

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Sound too good to be true?

Dr. Paul Mathew, neurologist at Harvard Medical School and fellow graduate of the 2014 AAN Palatucci Advocacy Leadership Program says yes….

In his recently published review on the subject, Dr Mathew explains that these surgeries are unproven, risky, expensive ($10,000-15,000) and are often not covered by medical insurance.  “Many patients have no or temporary benefits from the surgery and still wind up on long term narcotics”, he says,  and furthermore “These procedures have made their way into mainstream medicine without adequate investigation”.  This is why he has decided to make this subject the focus of his future advocacy efforts.

Click here to read the paper.

Click here to find out more about migraine.

Neurologic Complications of Space Flight

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Space Sickness

Space (“motion”) sickness was an expected complication of space flight, that was the reason for all those crazy astronaut training machines:

However, the syndrome was unknown in the first manned space flights – none of the 26 astronauts who flew in the 16 Mercury and Gemini space trips experienced disorientation or motion sickness.

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However, this changed with the Apollo missions, where there were 11 incidents of inflight motion sickness, ranging from mild to severe, in as many flight missions.  This was attributed to the increased opportunity for movement by the crewmen within the relatively large volume of the combined Apollo command and lunar modules compared to the very confined crew compartments of the Mercury and Gemini spacecraft.

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The problem got even worse with Skylab, where 5 of 9 astronauts experienced symptoms of motion sickness during the initial days of the flight, 2of them severe including vomiting.

Anti-motion sickness drugs used by the Skylab 3 and 4 crewmen were not completely effective in ameliorating symptoms.

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Interestingly, these symptoms of motion sickness were temporary, and all resolved within a few days.

In fact, in-flight experiments conducted on or after day 8 showed that all crewmen had adapted to weightlessness, and did not experience any adverse symptoms in a spinning chair (30 rpm) sufficient to cause vertigo on Earth.

We have already blogged about how the vestibular system detects head movements.

Maintaining an awareness of the relative location of our body parts requires the precise integration of visual, vestibular, and proprioceptive (touch, pressure, and stretch receptors in our skin, muscles, and joints) sensory inputs.

If your head moves in space, your eyes see the movement, but in zero-gravity the vestibular otolith doesn’t move and there is no proprioceptive input from the feet against the floor.

Space sickness is felt to be the result of “sensory conflict” or sensory mismatch.

It didn’t occur in the early Mercury and Gemini flights, because the astronauts spent the whole flight strapped into a seat inside a small capsule with limited opportunity for movement and minimal exposure to conflicting visual, motor, and vestibular sensory messages.

However, space sickness has affected >50% of astronauts since Apollo, beginning within the first hour of transition from Earth gravity to microgravity, and persisting for 2 to 3 days.  It’s so predictable that no space walks were scheduled for the first 3-days of any Space Shuttle missions.

Recent research has suggested that virtual reality training can simulate specific effects of microgravity and may prove to be an effective countermeasure against space motion sickness through a process of habituation.

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Space Headache

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Space flights can also trigger headaches. In a 2009 study 71% of astronauts reported headaches – occurring during launch, flight, activities outside the space station and landing.  None had a history of recurrent headache on earth.  There was little to no association with the main symptoms of space motion sickness, such as nausea, vomiting or vertigo.

Asked to describe the headache, the astronauts mostly said the symptoms were “exploding” or “heavy feeling.”

We know that blood volume gets redistributed to the brain and upper body when the astronaut floats in zero gravity.

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This shift of blood towards the brain causes a painful increase in pressure within the skull:

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Click here to find out more.

Petadolex for Migraine Prophylaxis: The Facts

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Posted by Sonia Jasuja, MSIV Drexel University College of Medicine

As a current student of traditional Western Medicine, I have been trained to turn towards modern pharmacology and away from natural remedies, for the most part.  However, as someone who has suffered from severe skin allergies all my life, I know how desperate patients can get in order to find something that really works! When Western Medicine fails us, where can we turn?

During my clinical Neurology rotation at Monmouth Medical Center, I saw another issue that plagues patients: Migraine.  While there have been great advances in the prevention and treatment of migraine, some patients are still left with debilitating pain. It was during this rotation that I first heard about Petadolex, or Petasites hybridus (aka Butterbur).

What is it? Butterber is an herbal plant that has been used for medicinal purposes, including migraine and headache, allergies, asthma, and many more. Most herbal remedies use the root extract in the form of a pill. It has properties that relieve spasms and decrease inflammation.1

Is it safe? Yes- studies have determined that Petasites is safe to use for the prophylaxis of migraine. The dose that was cited to have moderate efficacy is 150mg daily.2

Side effects are very mild and include burping, stomach upset, diarrhea, fatigue and itching.3

One important thing to keep in mind- make sure to only buy Petasites hybridus that is certified and labeled, “PA free”. “PA” stands for pyrrolizidine alkaloids, which cause adverse effects in the liver, lungs and circulatory system. PA’s can cause cancer.3

You should not take Petasites if you are pregnant or breast-feeding, have liver disease, or if you are allergic to ragweed, marigolds, daisies or other related herbs. 3

Does it work? Probably, but we still need more information! In 2006, Agosti et al. published “Effectiveness of Petasites hybridus preparations in the prophylaxis of migraine: A systematic review”. Of the two studies that were looked at, the systematic review showed that there is only moderate evidence for the effectiveness of Petasites at the dose of 150mg/day for a period of 3-4 months. The review also thoughtfully pointed out that confounding factors still need to be accounted for. These factors would include things like which migraine treatments have been successful or unsuccessful in the past, and any use of addictive or hormonal substances, such as nicotine or estrogens.2

The review article states that the overall effect size of the 150mg extract dose is approximately 15% percent lower migraine frequency rate per month compared to placebo.2

The bottom line.  If you have frequent or debilitating headaches, you should see you doctor for an evaluation.  You may need some diagnostic testing, and there are probably some very effective conventional medications you can try.  However, if you are still having frequent headaches despite that, Petasites might be worth a try.

REFERENCES

1. Brind’Amour, Katie. “Migraine Herbal Home Remedies From Around the World.”Healthlines RSS News. Healtline Editorial Team, 16 Apr. 2013. Web. 16 Nov. 2013.

2. R. Agosti, R.K. Duke, J.E. Chrubasik, S. Chrubasik, Effectiveness of Petasites hybridus preparations in the prophylaxis of migraine: A systematic review, Phytomedicine, Volume 13, Issues 9–10, 24 November 2006, Pages 743-746, ISSN 0944-7113, http://dx.doi.org/10.1016/j.phymed.2006.02.008.

3. “Butterbur Information | Evidenced-Based Supplement Guide.” MedicineNet. MedicineNet.com, n.d. Web. 16 Nov. 2013.

High altitude sickness and the size of your brain?

Posted by David Cuthbert, MSIV, Drexel University College of Medicine

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Every year thousands of people flock to several world locations with one common goal in mind – to push their bodies well beyond what nature has so far intended by climbing to dangerously high altitudes.

For whatever reason this appeals to some people.  Those people are eager to overcome the restrictions set by Mother Nature, despite the obvious dangers.

As a kid I loved the move Cliffhanger with Sylvester Stallone.  I remember watching that film and thinking that the only real dangers associated with extreme altitude were obvious – falling (please see video clip # 1), Slyvester Stalone wanting to use you as a human sled (watch video clip #1 again), the cold, or John Lithgow going crazy and wanting to use a helicopter to kill you for money (please see video clip #2).

But apparently those aren’t the only dangers, and medical school has taught me some pretty interesting stuff.

In fact there are a whole variety of medical syndromes that can occur at high altitude that don’t involve John Lithgow, and being that this is a neurology blog, this piece will focus on the neurological high altitude medical syndromes.  And in particular, will place emphasis on one terribly interesting study.

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Elevated intracranial pressure at high altitude may be a function of brain size?

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The “Tight Fit Hypothesis”, and the story of one extremely curious neurosurgeon.

The neurological syndromes of high altitude sickness are thought to be a spectrum of illness ranging from high altitude headache (HAH), to acute mountain sickness (AMS), to the most severe – high altitude cerebral edema (HACE).

The exact pathophysiologic mechanisms leading to these conditions are still somewhat unclear but several theories have been proposed and tested – all of which related to hypoxia and elevated intracranial pressure (ICP).

It is thought that in the milder end of this spectrum (HAH) the symptoms are solely contributed from hypoxia, and as disease severity progresses, and the patient comes closer to HACE – the pathogenesis is more attributable to raised ICP.

But what I find even more interesting than just the development of these syndromes – is the fact that there is great variability between who develops them.  For some people, no matter how acclimatized they are they simply cannot go to a certain altitude without great risk of HACE and subsequent death.  While others require little acclimatization, and are capable to trekking to the summit of Mt. Everest without necessitating the use of supplemental oxygen.  This leads one to ask, what are the factors present that allow someone this ability to tolerate high altitude?

One answer (with considerable evidence to support it) lies within their genetics.  The discovery of a transcription factor called “Hypoxia Inducible Factor”, or HIF, confirmed this.  HIF is a transcription factor that contributes to the regulation of several metabolic pathways, and allows both production of a higher concentration of hemoglobin, and greater sensitivity of the carotid body to hypoxia.  Another older, and forgotten theory looks to further explain this increased altitude tolerance through anatomic differences.

In 1985 Ross suggested that the “random nature of cerebral mountain sickness” can be explained by “more compliant systems”.  In other words, if a person has larger sized ventricles, and/or more atrophic brain, they will in turn be less susceptible to altitude sickness because the compliance will leave them better equipped to tolerate the raise intracranial pressure.

Interestingly enough, there existed someone crazy enough to test this hypothesis.  Someone not only willing to hike to these ungodly altitudes, but also willing to screw a bolt in his head to measure his own intracranial pressure.  This person was Brian Cummings, an avid outdoorsman, who also just so happened to be a neurosurgeon.

Cummings and a team of ten undertook an expedition to the Kishtwar region of northern India to try to put this hypothesis to the test.  However the data obtained from the experiment was destroyed in a fire.  Or so everyone thought!  Then recently Cummings wife (Cummings has since passed away) found the data from the experiment, allowing it to have since be published.

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Mountain rage within Kishtwar region of northern India.

In this experiment the “tight fit” hypothesis was tested by using 10 subjects.  These subjects had computed tomographic scans of their brains to measure their ventricular size.  After which a scoring system was used to measure symptomatology related to high altitude neurological syndromes while at high altitudes.  Also, three lucky volunteers had their intracranial pressures measured – allowed via screwing a pressure monitor through a burr hole in their heads .  This stayed in place while trekking through Northern India Himalaya’s.  Cummings himself participated in the study, and also had a pressure monitor placed.

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Dr. Cummings manipulating ICP monitor

The results of the study showed that the three subjects with the smallest ventricles suffered the most from Acute Mountain Sickness, and reported the worst headaches of the group.  Meanwhile patients with larger to normal sized ventricles reportedly had significantly less clinical findings related to AMS:

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Regarding the intracranial pressure monitoring, of the 3 subjects to be observed, one had large ventricles, one with normal size, and one with small ventricles.  The only one to experience headache, was the patient with the highest observed rise in ICP, and was also the subject with the smallest ventricles.

Therefore the results of this experiment support Ross’s “tight fit” hypothesis, and provide a potential anatomic explanation to compliment other genetic mechanisms to explain why some people are more prone to developing high altitude neurologic syndromes.

Obviously, the small study size cannot definitively explain this susceptibility, nor can it exclude other mechanisms as contributing as well. Nevertheless this experiment is considerably important to those who wish to conquer the hypoxic environment of Mother Nature’s higher altitudes.

It allows an explanation for those that are less able to adapt, and maybe even one day provide a means of testing their ability to acclimatize prior to their summit attempt.  And while that very well may never happen, this study at the very least is a great story about the incredible strength of the human spirit.

Dr. Cummings showed incredibly determination while searching for answers regarding the human ability to adapt to their environment, and fortunately now his work can live on.

A ripping yarn – a tale of cervical artery dissection

Case Summary:
This 46-year-old woman was healthy except for a history of occasional migraine headaches and cigarette smoking. On the day of admission she had fallen down a short flight of steps carrying a heavy box. About 2 hrs later she complained of some neck pain.  Then later that evening developed abrupt onset left sided weakness. She arrived at the emergency room within 1.5 hrs of the onset of weakness. On examination, she was alert, but she had a right gaze deviation (she wouldn’t look to the left side) and the left side was completely paralyzed. She had a normal brain CT scan.

The stroke team was notified, and she was given intravenous thrombolytic (“clot busting”) drug therapy within 1/2 hr of her arrival at the hospital and 2 hrs since the onset of her symptoms.

Carotid ultrasound subsequently showed no flow in the right internal carotid artery, and carotid arteriography subsequently showed near occlusion of the artery from an arterial dissection (see image below, red arrow):

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What is cervical artery dissection?

Cervical artery dissection is caused by bleeding inside the wall one of the major arteries in the neck.

This process is thought to be triggered by local injury to the inside layer of the vessel wall.

Cervical artery dissections occur from blunt trauma:

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Cervical artery dissection can also occur after minor trauma, particularly in someone with a genetic predisposition:

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What diseases predispose to arterial dissection?

There are some specific syndromes such as Marfan syndrome, Pseudoxanthoma elasticum and Ehlers- Danlos syndrome type IV that are associated with a weakness in the arterial wall making an arterial dissection more likely:

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In other cases, the specific cause of arterial weakness is unknown, but there is ongoing research to try to identify genetic links.

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What happens after a cervical artery dissection?

Symptoms can be caused from the damaged arterial wall itself (local symptoms) and some affected patients will later develop strokes.

Local symptoms include neck pain, unusual headache and/or Horner’s syndrome.

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L Horner’s syndrome (small pupil and drooping eyelid) caused by damage to the sympathetic nerve fibers in the arterial wall from carotid dissection. Click here to find out more about Horner’s syndrome and other causes of unequal pupils.

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What about stroke?

Stroke symptoms only occur in 25-30% dissections and can occur several days after the neck trauma and/or onset of local symptoms.

The arterial dissection narrows the space inside the blood vessel (the lumen), so less blood flow gets to the brain:

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A carotid artery dissection with blood clot inside the arterial wall (left) leading to narrowing of the vessel lumen and less blood flow (right).

Cervical arterial dissections can also cause stroke when pieces of blood clot break off and move with the blood flow only to block small arteries further inside the brain (cerebral thromboembolism), or if the dissection tracks across (and blocks off) an arterial branch (see below):

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How is arterial dissection diagnosed?

Magnetic resonance imaging is probably the easiest way to make the diagnosis:

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MR angiogram (left) showing tapered occlusion of the left internal carotid (white arrow) from dissection. Fat suppressed T1 weighted MR axial image through the dissected cervical artery (right) showing bright blood within it’s wall (black arrow) from dissection.

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How is it treated?

In most cases the arterial dissection ultimately heals on its own without any surgical intervention.  There has been some controversy surrounding the use of anticoagulant vs anti-platelet drugs for stroke prevention after cervical artery dissection, but most current data favors the use of the anti-platelet drug aspirin:

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Of course, for patients presenting with symptoms of acute stroke, throbolytic therapy is also an option, and can improve outcome without increased risk in stroke from dissection:

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Click here to find out more about cervical artery and dissection and stroke.

Click here to find out what to do if you think your having a stroke.

Click here to find out more the certified stroke center at Monmouth Medical Center.

Poor migraine control leads to chronic daily headache

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Many patients manage their infrequent migraine headaches with triptan medications, such as sumatriptan.

We call these “abortive” medications – you take them as needed whenever you have a headache to make it go away.

These medications set off an “explosion” of chemicals inside the brain, “extinguishing” the migraine just like an explosion of dynamite can put out an uncontrolled oil rig fire:

However, sometimes, that “chemical explosion” doesn’t put the fire out completely, and it comes right back.

We call this “rebound” headache, and we have already blogged about how taking too much abortive medication (including over the counter medications like Excedrin Migraine) for migraines can lead to  headache all the time, chronic daily headache, because of analgesic rebound.

Data from a new study has recently confirmed this:  The large American Migraine Prevalence and Prevention (AMPP) study showed that patients with very poor headache control were 4 times more likely to progress into chronic migraine during the following year than those with better control.

Clearly, poor headache control leads to more and more headaches, presumably because of analgesic rebound.

The solution?  Obtaining more sustained migraine control by starting a daily preventative medication for migraine like topiramate, valproic acid or botulinum toxin.

If your headaches are getting more frequent or out of control, seek the help of a board certified neurologist sooner rather than later!