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.

fluids in space

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.

Neurology and Skiing

ski crash
We’re mostly talking about orthopedic, spinal cord and head injuries.

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Spinal Cord Injuries:

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The incidence of spinal cord injury (SCI) is around 1 per 100,000 visits (mostly thoracolumbar spine), usually caused  caused by a simple fall, followed by hitting a tree.

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The incidence of SCI for snow boarders is higher, around 4 per 100,000 visits (mostly cervical), and usually caused by a backward fall during a jump (>75%) or other tick.

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Most SCIs in skiers and snow boarders occur in 15-25 years olds.

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Head trauma:

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The incidence of head trauma is 3.8 per 100,000 ski visits, usually from direct collision with trees.  The incidence of head trauma is higher for snow boarding, around 6.5 per 100,000 visits, more often caused by falling backwards.  Most head traumas result in concussions, but 14% are severe head trauma, and 4% are fatal.

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Others

I came across this case report of another unusual neurologic skiing complication: 
A 45-year old woman first developed distorted vision in the left eye, like looking through a kaleidoscope while skiing.  Soon afterwards, her right leg started jerking, causing her to fall. 
It turned out that she had sustained a left carotid artery dissection causing high grade stenosis during skiing.
There are a few other reports of cervical artery dissection from skiing.

Christmas Neurolgy

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Christmas Ornament from Cafe-Press

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The Christmas Tree Sign

Keyoumars Ashkan and Adrian Casey

J Neurol Neurosurg Psychiatry 1999;67:824

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Back pain and sciatica in patients with neurofibromatosis may result from a multitude of pathological processes which include scoliosis, degenerative diseases of the spine, and spinal tumors. Neurofibroma, schwannoma, meningioma, and glioma can all occur. When specific tumors are responsible for the symptoms, surgical excision can offer effective treatment. Many patients, however, have widespread disease. We recently treated a patient with multiple neurofibromas which involved several nerve roots and the cauda equine (figure). The extensive distribution of the tumors produced an MRI picture resembling a Christmas tree. In patients with “the Christmas tree sign” the challenge is in the correct diagnosis of those tumors which produce the symptoms if surgery is to remain a realistic management option.

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A Christmas Tree Cataract

E Obi and C Weir

BMJ 2010; 341, (Published 8 December 2010)

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A 73 year old woman referred for cataract surgery had on examination a left Christmas tree cataract (fig 1A). Highly reflective, iridescent, polychromatic crystals were noted within the lens. Their colours varied according to the angle of the incident light, (fig 1B, C). We postulate that Christmas tree cataracts result from the accelerated breakdown of membrane associated proteins. The peptides and amino acids accumulate in the lumen of the reticular meshwork, and cystine is concentrated beyond the level of crystallisation, giving rise to growing crystals.

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A Christmas Carol: A memorable patient

Stephanie Davies

BMJ. 1998 December 19; 317(7174):1732.

It was a few weeks before Christmas on a dull, chill November morning when Jason and his parents came to see me. As I listened to the, alas, too familiar tale of a young boy, difficult and unreasonable at home who was misbehaving at school, my heart sank and I began to feel as depressed and hopeless as everyone in the room. Jason sat quietly, certainly not demonstrating the hyperactivity suggested by his teacher. Assessment and examination showed that he was a normal and intelligent boy, so was this attention deficit hyperactivity disorder and would the magic pill help?

We discussed strategies to help based mainly on the premise of rewarding good behavior and ignoring the bad coupled with praise and appreciation. Unfortunately, at this time, there did not seem to be any good behavior to reward or any achievements to praise.

The review took place some time shortly before Christmas. I sat with prescription pad at the ready, prepared to offer methylphenidate if there was no other way. Jason came in like spring sunshine and his parents were glowing with pride and happiness. What could have wrought this transformation? It seemed unlikely that our previous consultation could have had such a dramatic effect.

I was correct. The magic had been woven by the muse of drama and Charles Dickens. Jason had starred as Scrooge in the school production of A Christmas Carol and was a smash hit. He had even saved the day by playing the part when a less intrepid thespian was incapacitated by stage fright.

Eight months passed before I saw Jason and his father again. With bated breath I inquired about progress. With delight I heard that it had been maintained, culminating in an excellent school report at the end of the academic year.

How important it is for us all to have some measure of success and how I wish all my patients could be a star for a day. I was certainly grateful that Jason and his parents allowed me to share his success. It has been one of my most memorable Christmas presents.

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The Christmas “Clacker”

David Strachan

BMJ. 1994 December 24; 309(6970): 1747.

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A 44 year old occasional drinker presented to the accident and emergency department at 5 30 am on New Year’s Day. A sensation at the back of his throat was causing a slight discomfort on breathing. On examination his uvula was found to be swollen. He had suffered the same problem on Christmas Day morning the previous year, the common factor being alcohol consumption during the previous evening. It is well known that alcohol consumption triggers or worsens snoring. Overindulgence causes muscle hypotonia and depression of the arousal mechanisms, leading to many people sleeping flat on their backs rather than on their sides. This narrows the airway and leads to a tendency to obstruction. If a kick in the back from a disgruntled partner does not rectify the situation and the “comatose” state persists then forced inspiration through a narrowed airway causes repeated trauma of the uvula and swelling.

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Convulsions at Christmas

S Kirker

BMJ. 1992 December 19; 305(6868): 1580.

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A healthy 26 year old butcher described convulsions without warning or focal onset between 11 am and noon on Christmas Eve in 1987, 1988, 1989, 1990, and 1991. He had no other convulsions or episodic symptoms that could be epileptic in origin and he had no relevant medical history. His usual working day was from 7 am to 6 pm but for the 14 days before Christmas he worked until at least 10 pm and as late as 1 am, seven days a week. He worked all through the night of 23 December. He did not miss any meals, and ate through the night as well. His usual alcohol consumption was 35 units a week but he drank less during these weeks. Results of examination and computed tomography were normal. Electroencephalograms in 1989 and 1992, each three months after the period of sleep deprivation, showed paroxysmal generalized spike and wave activity at 8 Hz, with a normal background rhythm. The patient was not prepared to change his working hours during the busiest time of year so we prescribed phenytoin over the second half of December. His electroencephalogram suggested he had an underlying tendency to have seizures, which only became apparent when his “seizure threshold” was lowered by sleep deprivation.

Musher Medicine


While I am lucky enough to be spending a few days this week dog sledding in Maine, I got to thinking about the neurology (or at least the medicine) of mushing.

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I guess most people have already heard of the famous annual Iditarod dog sled race which has become Alaska’s most popular sporting event.

However, many are unaware of the historical importance of dog sledding, and in particular the 1925  Serum run to Nome  (sometimes referred to as the “Great Race of Mercy”).

In the winter of 1925 there was a diphtheria epidemic in the isolated Alaskan city of Nome.  The city had 8,000 units of diphtheria antitoxin on hand, but it had all expired the previous summer. They had ordered a new supply, but the port had closed for the winter before the serum arrived.  The doctors were afraid to use the expired medicine.  The nearest supply of antitoxin was in Anchorage, but it might as well have been a million miles away, as the only available planes were water cooled WW1 that could not be flown in winter.  A deadly epidemic was expected.

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Sepalla in Nome, 1925

However, in a daring plan, the antioxin was moved by train from Anchorage to Nenana, and then carried another 630 miles to Nome by dog sled teams running in relay.   Gunnar Kaasen and his lead dog Balto arrived on Front Street in Nome with the antitoxin on February 2 at 5:30 a.m., just five and a half days later. The two became media celebrities, and a statue of Balto was erected in Central Park in New York City in 1925.  However, most mushers consider Leonhard Seppala and his lead dog Togo to be the true heroes of the run – they covered the most hazardous stretch of the route, and carried the serum 91 miles, the single farthest of any team.


A reenactment of the serum run was held in 1975 to mark the 50th anniversary of the “Great Race of Mercy,” and participants included descendants of many of the original mushers.  Since 1997, the event been commemorated by bi-annual “Serum Run” from Nenana to Nome, which includes stops at villages along the way to promote childhood inoculations.

“Frozen Addicts” – An Unusal Twist on Drug-Induced Parkinsonism

The term “frozen addicts” was coined by Californian neurologist Dr William Langston after he had encountered an outbreak of akinetic rigid Parkinsonism in 6 drug users in Santa Clara County California:
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The story actually starts in 1947 with Hoffman-La-Roche chemist Dr Albert Ziering, who first synthesized synthetic opioid  Desmethylprodine 1,3-Dimethyl-4-phenyl-4-propionoxypiperidine (MPPP).  The drug was never developed or marketed.

The story continues with chemist Barry Kidston, who in the 1970s synthesized MPPP using Dr Ziering’s recipe and a home chemistry set.  However, a few days after injecting himself with a sample from a newly synthesized batch of drug, Kidston became frozen, unable to speak or walk.  He was taken to the hospital by his parents, misdiagnosed with catatonic schizophrenia, and treated with electroconvulsive therapy for months.  He was ultimately diagnosed him with Parkinson’s disease, and improved with L-dopa treatment.  Soon after, researchers analyzed the tainted drugs, and concluded that it was comprised of both MPPP and a similar compound, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).  Kidston died of cocaine overdose shortly afterwards.  His autopsy showed loss of dopaminergic cells in the substantia nigra, the hallmark of Parkinson’s disease.  The case was written up in the Journal Psychiatry Research in 1979.

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In July 1982, a 42 year old named George Carillo was hospitalized in San Jose frozen like a statue in a bent twisted position.

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Then a neurologist in Watsonville, only 30 miles away, reported 2 drug-addict brothers in their 20s  both with advanced symptoms of Parkinson’s.

Ultimately seven addicts came down with these same symptoms.

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A sample of tainted heroin was ultimately analyzed, and one of the toxicologists involved remembered reading about the Kidston case in Psychiatry Research.

William Langston, the neurologist who first treated Carillo, looked the case report up and found that Kidston had prepared drugs based on a 1947 paper by Albert Ziering.  But when Langston he went to the Stanford University library to read that original paper, he found that it had been cut out of the journal.  Some enterprising college chemist was cooking up MPPP and selling it as heroin, but like Kidston had made a mistake in his recipe and produced MPTP instead.

Once inside the brain, MPTP is metabolized into 1-methyl-4-phenylpyridinium which is toxic to dopamine producing neurons in the substantia nigra.

Since then MPTP has been used to develop an animal model of Parkinson’s disease, and this has allowed researchers to investigate surgeries to repair the injured region of the brain, new techniques using electrical stimulation, and more recently stem cell replacement of damaged cells.

These Frozen Addicts have also posed a question that we have yet to answer. If a street-drug impurity can trigger on form of Parkinson’s, could other “idiopathic” cases also have a chemical source? Recent studies have found that ingestion of the pesticide Rotenone can bring on Parkinson-like symptoms in mice. Loss of motor control, stiffening of muscles, and even loss of facial expression have been noted among the rare side effects of the high blood pressure medication, Reserpine, and the heartburn drug, Metoclopramide.

Telemedicine on the ICU, Saves lives and $$s

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We have already bogged about the value of telemedicine for the evaluation of acute stroke patients in the emergency room.

Telemedicine can be valuable in any hospital department, including the Intensive Care Unit (ICU).  ICU telemedicine involves a combination of videoconferencing technology, telemetry, and electronic medical records in order to allow off-site intensivists and critical care nurses to assist in the treatment of critically ill patients.

A 2011 metanalysis of studies published from 1950 to 2010 had found that telemedicine in the ICU was associated with a significant reduction in ICU mortality and length of stay.

A more recent prospective study published in Chest last week showed that tele-ICU care improved adherence to ICU best practices, reduced the response times to alarms, leading to lower mortality and length of stay.

Keep in mind that the cost of 1 day in the ICU can be as high as $6,000-$10,000.

Lytico-Bodig Syndrome, You Might Get it From Eating Bats

Posted by Daniel Rubio, Drexel University College of Medicine Class of 2014

“A man” obsessing over “bats”…

“A man” eating “bats”…


The patients above are displaying symptoms resulting from a disease known as Lytico-Bodig Syndrome (LBS), a neurologic disease resembling amyotrophic lateral sclerosis (ALS/Lou Gehrig’s Disease), Parkinson’s disease, and Alzheimer’s disease.  The country with the greatest number affected is the US territory of Guam.  In fact, between the 1940-1960 it was the leading cause of death among the Chamorro people, a tribe found on the island of Guam.  The afflicted were usually between the ages of 25-40 years of age.

What’s up with the bats?

Although yet to be proven, it is believed that the high incidence of LBS is due to the consumption of fruit bat, a cultural delicacy on the island.  These fruit bats feed on specific fruits containing high concentrations of an altered amino acid called beta-N-methylamino-L-alanine (BMAA). BMAA is a known neurotoxin and is believed to be the cause of LBS.  BMAA is a protein building block that is incorporated into neuronal proteins to produce an abnormal form that creates clumps with neurons resulting in their dysfunction and death.

I don’t eat bat though?

I addition to the high concentrations found in the fruit bats on the island of Guam, multiple sources have been proposed leading to BMAA exposure within the United States.  Certain bacteria in fresh and salt waters produce BMAA; and, fish and crustaceans will concentrate BMAA within their tissues when they consume the bacteria as part of their normal diet.  It is believed that human consumption of fish and crustaceans in at-risk areas might increase the incidence of neurodegenerative diseases, like Alzheimer’s, Parkinson’s, and Lou Gehrig’s.  This association has been seen in many areas within the United States, especially around the gulf regions and around large bodies of water.  Click here for more details about this.

Am I more lytico or bodig?

Presenting symptoms exist along the continuum of lytico-bodig.  Patients on the lytico spectrum present more like ALS/Lou Gehrig’s disease.  These patients have muscle wasting/atrophy and accompanying weakness, paralysis of mouth and tongue, and an inability to swallow resulting in choking to death.  Over time, paralysis involves the breathing muscles requiring mechanical ventilation to help the patient breath and to prevent choking on secretions.  Lytico patients remain aware of their deterioration.  The form of LBS is fatal in all cases.

On the other end of the spectrum, patients with bodig presentations look more like Parkinson’s disease and Alzheimer’s disease patients.  Bodig patients present with “freezing” with progressive immobility with loss of starting purposeful movement and loss of spontaneous movement.  Progressive dementia with loss of speech and irrational behavior, including violence and rapid fluctuations in mood, are common.  Over time, patients are left in stiff and immobile postures with inability to speak and swallow.

How would I know if I had LBS?

Currently Lytico-Bodig syndrome is diagnosed based upon appropriate history and physical exam by a neurologist.  Definite LBS is declared in post-mortem autopsy.  However, there is research being done to develop rapid tests using cerebral spinal fluid analysis.

What can I do if I have LBS?

Treatment is mainly supportive as is based upon symptoms present, whether it’s Parkinson’s, Alzheimer’s, ALS, or a combination of the three spectrums of diseases.   The more the symptoms resemble Lytico, the greater the mortality: in patients with predominantly lytico-type symptoms the disease is practically 100% fatal.