Wednesday, October 22, 2014

Death By Haunted House


Halloween is a time when fear is invited. The rush of
adrenaline in a controlled environment is life-
affirming. Not much else to comment on here,
except that he seems to have excellent oral hygiene
for a chainsaw-wielding maniac.
A big man with the chainsaw and the gaping wound on his face jumps out from around the corner and growls. You leap backward and scream, your heart pounding in your ears. You’re ready to either take that power tool and teach him a lesson or to run like the kid from Home Alone. Sure you're scared, but could it kill you?

Haunted houses are great examples of stimuli that induce the fight or flight response. The name suggests that two mechanisms are fighting it out, but there is really only one biologic pathway. Whether an animal tries to escape or tries to defend itself, its muscles and mind need to be ready.

In response to a threat, the brain triggers the release of epinephrine and cortisol from your adrenal glands into the blood. As a result, your heart beats faster and stronger, your blood vessels dilate to move more blood, and your lung vessels dilate to exchange more oxygen for carbon dioxide. Equally as important, your liver breaks down glycogen (a sugar storage molecule) to glucose and dumps it into your bloodstream.

All these processes work together to increase your alertness and increase the power of your muscles for a short time - like when mothers who lift cars off their small children. You are now ready to respond to the threat; however, there is an exception – you may do nothing at all.

One of the major control mechanisms of the fight or flight response is the autonomic nervous system. This is part of the peripheral nervous system (PNS, outside the brain and spinal cord) and transmits information from the central nervous system to the rest of the body. The autonomic system controls involuntary movements and some of the functions of organs and organ systems.

Parts of the autonomic system acts like a teeter-totter, it's their relative balance that controls the outcomes. In the fight or flight response, the sympathetic system predominates and your heart rate increases and your blood vessels dilate.

The autonomic nervous system is divided into sympathetic
and parasympathetic. Much of the sympathetic innervation
comes from the thoracic and lumbar regions, while most
parasympathetic innervation is carried by the vagus nerve.
You can see that the two systems have largely opposite effects.
But what if the parasympathetic system gained an upper hand for a short time? The parasympathetic system controls what is sometimes called the rest and digest response – the opposite, get it? The heart slows, the blood vessels constrict in the muscles, blood moves from muscles to the gut, and glycogen is produced from glucose. Remember the old adage - don’t swim after your dine; eating puts you in a parasympathetic state of mind! (O.K., I just made it up)

Many people have had the experience of parasympathetic domination coincident to a threat, for some folks it proceeds long enough to have an observable result – they faint. The vagus nerve (a primarily parasympathetic cranial nerve) controls much of this response, so it may be called the vasovagal response. The parasympathetic-mediated reduction in blood oxygen and glucose do not spare the brain - and when your brain is starved of oxygen and glucose, you pass out. Fighting or fleeing is difficult when you are unconscious.

Lower animals will faint as well, but they have additional defenses along these lines. Mammals, amphibians, insects and even fish can be scared enough to fake death – ever hears of playin’ opossum?

There are overlapping mechanisms for feigned death, from tonic immobility (not moving) to thanatosis (thanat = death, and osis = condition of, playing dead). When opossums employ thanatosis, they fall down, stick their tongue out, and even emit a foul smelling odor from glands around their anus. One study in crickets showed that those who feigned death the longest were more likely to avoid being attacked, so this is definitely a survival adaptation – except for the opossums scared by cars and decide to play dead in the street.

Feigned death deters predation, so being scared ain’t all bad. Many predators won’t eat something that is already dead, so not moving could protect them from attack. Another theory is the clot formation hypothesis; it contends that slowing the heart and blood flow forces blood clots to form faster. This will reduce the amount of blood lost during an attack, improving chances for survival.

New evidence is suggesting that even humans undergo tonic immobility. Post-traumatic stress patients asked to relive their trauma show definite signs of tonic immobility, although first they show signs of "attentive immobility," which is more voluntary then the tonic form.

I highly recommend this new book for popular
biology and medicine readers. Zoobiquity explores
a powerful reality. No disease--whether physical or
psychiatric--is uniquely  human. We have much to
learn from animal patients and from the doctors who
care for them.  The impact on human medicine
will be significant.
We have discovered one exception to the rule; instead of fight or flight, it is really fight, flight or faint – but can we take it further? Should it be fight, flight, faint, or fatality? The answer is yes, but it's very rare. Sometimes animals (including us) don’t just feign death when afraid – they actually die.

In their book, Zoobiquity, What animals can teach us about health and the science of healing, Barabara Natterson-Horowitz and Kathyrn Bowers talk about capture myopathy in animals. Small traps that limit movement, cause pain, or are associated with loud noises can cause spontaneous death in live-trapped animals. Several decades ago it was not unusual for 10% of trapped animals to die. In birds, the death rate often rose to 50%! More humane methods of live trapping have reduced the death rate, but point is made – these animals were scared to death.

A human analogy of capture myopathy may have been identified. People that have had a sudden emotional shock, perhaps the death of a loved one, some other tragic occurrence, or crippling fear can undergo something that looks a lot like a heart attack, even if they have no history of heart disease.

This sudden loss of heart rhythm has been called broken-heart syndrome, but is more accurately termed stress cardiomyopathy (SCM). In these cases, the heart actually changes shape! The part of the heart that pumps blood out to the body (left ventricle) balloons out and loses the ability to pump efficiently. Dramatically less efficient pumping leads to symptoms just like a heart attack.

In the normal left ventricle of the heart (left image), the muscle is
thick around the space (in red) and contracts strongly. In SCM, the
space is ballooned at the based (middle image) and the muscular wall
is thin, giving a weak contraction. The change in shape can be seen in
the superimposed images on the right, as is the octopus trap (tako-tsubo)
that the original Japanese describers thought the lesion looked like,
hence the early name takotsubo cardiomyopathy.
In most cases, SCM and the change in heart shape resolve after a time and there is little left to show they were present, but if they go too far for too long, they can cause death – called sudden cardiac death. There are many causes for sudden cardiac death, but emotion and fear are definitely among them.

I was wondering if there was a link between SCM in humans and capture myopathy in animals, so I asked Dr. Natterson-Horowitz. She told me that those studies have not been done yet; we don’t know if there is a heart shape change in captured animals. I think it would be hard to get approval for studies that would intentionally scare animals to death.

One interesting connection amongst fight or flight, capture myopathy, and SCM is the catecholamine dump involved. Epinephrine and norepinephrine control all three responses, and in humans they control even more. Recent evidence shows that catecholamines mediate the production of fear memories.

You remember fearful events more readily and more vividly as a survival adaptation. Strong memories help you to avoid dangerous situations in the future. In this way, your mind can affect how your body responds to a threat. We will see this again in just a bit.

All babies have an exaggerated startle reflex until
they are several months old, but in some cases it may
contribute to SIDS. An exaggerated startle can lead to
apnea (temporary breathing cessation) and this can be
compounded by a depressed heart rate if the baby is
sleeping on its stomach. Some clinicians also theorize
that swaddling may contribute by exaggerating the startle
due to confinement stress, but by far the greatest
association with SIDS is stomach sleeping.
However, dying or nearly dying from fright isn’t all in your head either; some conditions can predispose you to dying from a sudden shock. One unfortunate condition is called hyperekplexia, or startle disease of the newborn. Newborns with one or more of several mutations in the glycine receptor (an inhibitory receptor in the brain used in neuron signal transmission) can lead to these babies dying from loud noises or a sudden touch.

The startle reflex involves squinting to protect the eyes, raising the arms, hunching the body to protect the back of the neck, as well as inducing the fight or flight response. With the loss of inhibitory signaling, the signals that ramp up a startle response are unchecked and can lead to uncontrolled beating of the heart (ventricular fibrillation, VF) and sudden cardiac death.

Just as some cases of the fight or flight response going too far, the startle can sometimes lead to VF. A recent study has shown that the bigger the perceived threat, the bigger the startle reflex will be. Also, if there is a fearful environment prior to the threat, then the startle will be bigger. Once in a long while, it goes too far.

Similar to hyperekplexia, there is another condition that could lead to VF and death in the environment of fear. Long QT syndrome can either be inherited or acquired later in life, and affects the time between beats of the heart. In long QT, the interval is variable and longer, and can lead to inefficient beating and VF.

On echocardiogram tracings a heartbeat has a certain shape, and 
each point has a corresponding name which is represented 
by a letter. If the time between the Q point and the T point 
is too long, the heart rhythm is subject to disintegrating 
into chaos. In the 1990’s, the antihistamine Seldane was 
taken off the market due to QT interaction when it was 
given with the antibiotic erythromycin.
Highlighting our circle of fear and the body, evidence presented here and here suggest that SCM can cause acquired long QT syndrome. Dr. Natterson-Horowitz said today many patients with long QT may have implantable defibrillators. In earlier days, however, these patients were warned not to use alarm clocks or to jump into cold water – they could startle themselves to death.

Long ago we talked about premature burial. It would be easy to envision a person waking up inside a coffin, and then dying from the fright of being buried alive! Does this mean that you are putting yourself in peril every time you visit a haunted house at Halloween? Probably not, remember that deaths from fright are exceedingly rare. Maybe you could just feign death, and the horrible monster will leave you alone.

For the next couple weeks - back to the science of flagella. Undulipodia are present in many phylums, except for where they aren’t. On the other hand, some types of organisms don’t have undulipodia - except for those that do.


Greek, R. (2012). Zoobiquity: What Animals Can Teach Us About Health and the Science of Healing. By Barbara Natterson-Horowitz and Kathryn Bowers. Knopf Doubleday Publishing: New York, NY, USA, 2012; Hardback, 320 pp; $16.23; ISBN-10: 0307593487 Animals, 2 (4), 559-563 DOI: 10.3390/ani2040559

Volchan, E., Souza, G., Franklin, C., Norte, C., Rocha-Rego, V., Oliveira, J., David, I., Mendlowicz, M., Coutinho, E., Fiszman, A., Berger, W., Marques-Portella, C., & Figueira, I. (2011). Is there tonic immobility in humans? Biological evidence from victims of traumatic stress Biological Psychology, 88 (1), 13-19 DOI: 10.1016/j.biopsycho.2011.06.002


For more information or classroom activities, see:

Fight or flight –

Autonomic nervous system –

Thantosis/tonic immobility –

Stress cardiomyopathy –

Hyperekplexia –

Long QT syndrome -