Fight, Flight… or Freeze

TW for discussion of rape and trauma

Almost everyone has heard of the fight or flight response. When you get into a scary situation your sympathetic nervous system revs up and pumps out adrenaline and your body prepares to either fight of something or someone threatening you, or, more commonly, to run away at top speed.

The freeze response is a less well known counterpart to the classic fight or flight response, which is also called tonic immobility (TI). When an animal’s ability to fight or flee has been either blocked or exhausted the freeze response is evoked. The reflexive freeze response is believed to be a last-ditch attempt to escape a predator, because a lot of predators will drop prey that suddenly plays dead or goes limp. It is often studied in animals by immobilizing them, to simulate this. During TI animals will become very still and silent (the characteristic freeze) either stiffening up or going limp and tremble. But they also have the same sympathetic nervous response seen in the fight or flight reflex; dilated pupils, rapid heart-rate and breathing and reduced response to pain.

The freeze response has been described very thoroughly in animals, but less well in humans. In people, the freeze response was first described as “rape-induced paralysis” in victims of sexual assault. Because of this, the human freeze response has mostly been studied as a phenomenon associated with sexual assault, but it is actually a general part of the human fight or flight response and can occur in victims of all forms of trauma, including combat and other forms of interpersonal violence, natural disasters and accidents. The freeze response can be evoked in people, just like in animals in laboratory studies meant to model panic. Some people with panic disorders will also experience the symptoms of a freeze response during panic attacks.

When people experience a freeze response during trauma they also report feelings of panic and a second group of symptoms called peritraumatic dissociation which include feelings of unreality and being detached from your body. Dissociation, freeze response and panic are all closely correlated, but panic and dissociation can only be studied in people (a rat cannot tell you whether it feels a sense of unreality, for example), so it isn’t clear right now, if these are three things which often co-occur, or if dissociation and panic are actually components of the freeze response. It is possible that panic reactions occur along a spectrum with the full freeze response as the most intense or complete manifestation and other combinations of panic and dissociation representing a less intense reaction.

Discovering who experiences freezing during trauma and who doesn’t and why is important because experiencing a freeze response as well as dissociation or panic during a traumatic event is a major risk factor for going on to develop post-traumatic stress disorder (PTSD) later. Patients with PTSD report freezing during trauma at higher rates than people who have experienced similar trauma but do not have PTSD and in healthy college students have experienced trauma, those who experienced more freezing symptoms at the time also report more PTSD symptoms later. Patients who experienced freezing and subsequently developed PTSD also have more severe symptoms, on average, and do not respond as well to medication as patients who developed PTSD but did not experience a freezing response during their initial trauma. This is also the case in patients with panic disorder, patients who do have freezing responses during panic attacks have more severe symptoms and experience greater disability than those who don’t.

At least one study found that freezing predicts subsequent PTSD better than dissociation which is a more well-known and better studied risk factor. This would make sense if dissociation is, in fact, a part of the larger freeze response. However, its important to note that the most common way of measuring the occurrence of freezing, the Tonic Immobility Scale, includes questions on dissociation, which means that whether or not these two things are really part of the same neurological response people with dissociative symptoms will, necessarily receive a higher score on measures of freezing as well, which might influence this result (since dissociation by itself does predict PTSD).

Ultimately we just don’t know exactly how the freezing response relates to dissociation or to PTSD, the research is just not complete enough, but we do know a few things about how freezing relates to other factors that determine someone’s risk for PTSD after trauma. A study which attempted to evoke freezing symptoms in a laboratory test (can I just note that I have great respect for anyone who volunteers to participate on a study which aims to cause anxiety) found that people who had more anxiety-sensitivity experienced more freezing during the test. Anxiety-sensitivity is a personality trait that measures how much anxiety bothers people, and by itself it’s a risk factor for PTSD. People with good attentional control (a measure of how well you can control what you think about and focus on) have a lowered risk for PTSD in general and also had less intrusive thoughts (which is one symptom of PTSD) after they had freezing induced in a laboratory test. So the relationship that has been found between PTSD and freezing extends to other aspects of someone’s personality and cognitive skills which affect their risk for PTSD.

But there may also be a socially driven component to the effects that freezing has on developing PTSD. People who freeze during trauma are more likely to feel guilty and ashamed and they may receive less social support from people around them after their trauma, which could make them more vulnerable to developing PTSD. This is especially a problem for victims of sexual assault because victims who cannot provide evidence of fighting back are often disbelieved by the police and their friends and family.

Abrams, M. P., Carleton, R. N., Taylor, S., & Asmundson, G. J. G. (2009). Human tonic immobility: measurement and correlates. Depression and Anxiety, 26(6), 550–6. doi:10.1002/da.20462

Cortese, B. M., & Uhde, T. W. (2006). Immobilization Panic. American Journal of Psychiatry, 163(8), 1453–1454.

Fiszman, A., Mendlowicz, M. V, Marques-Portella, C., Volchan, E., Coutinho, E. S., Souza, W. F., … Figueira, I. (2008). Peritraumatic tonic immobility predicts a poor response to pharmacological treatment in victims of urban violence with PTSD. Journal of Affective Disorders, 107(1-3), 193–7. doi:10.1016/j.jad.2007.07.015

Fusé, T., Forsyth, J. P., Marx, B., Gallup, G. G., & Weaver, S. (2007). Factor structure of the Tonic Immobility Scale in female sexual assault survivors: an exploratory and Confirmatory Factor Analysis. Journal of Anxiety Disorders, 21(3), 265–83. doi:10.1016/j.janxdis.2006.05.004

Hagenaars, M. a, & Putman, P. (2011). Attentional control affects the relationship between tonic immobility and intrusive memories. Journal of Behavior Therapy and Experimental Psychiatry, 42(3), 379–83. doi:10.1016/j.jbtep.2011.02.013

Heidt, J. M., Marx, B. P., & Forsyth, J. P. (2005). Tonic immobility and childhood sexual abuse: a preliminary report evaluating the sequela of rape-induced paralysis. Behaviour Research and Therapy, 43(9), 1157–71. doi:10.1016/j.brat.2004.08.005

Pereira, M. G., Alves, R. D. C. S., Tavares, G., Lobo, I., Rego, V. R., Portella, C. M., … Oliveira, L. De. (2012). Peritraumatic tonic immobility is associated with posttraumatic stress symptoms in undergraduate Brazilian students. Rev Bras Psiquiatr, 34(1), 60–65.

Rocha-Rego, V., Fiszman, A., Portugal, L. C., Garcia Pereira, M., de Oliveira, L., Mendlowicz, M. V, … Volchan, E. (2009). Is tonic immobility the core sign among conventional peritraumatic signs and symptoms listed for PTSD? Journal of Affective Disorders, 115(1-2), 269–73. doi:10.1016/j.jad.2008.09.005

Schmidt, N. B., Richey, J. A., & Maner, J. K. (2009). Exploring Human Freeze Responses to a Threat Stressor. J Behav Ther Exp Psychiatry, 39(3), 292–304.

Volchan, E., Souza, G. G., Franklin, C. M., Norte, C. E., Rocha-Rego, V., Oliveira, J. M., … Figueira, I. (2011). Is there tonic immobility in humans? Biological evidence from victims of traumatic stress. Biological Psychology, 88(1), 13–9. doi:10.1016/j.biopsycho.2011.06.002


How Brain Cells Talk

Wow.  I just wrote a post that was almost completely about dopamine receptors, without actually explaining how neurotransmitters work.

Bruce Banner admitting that that was mean.

I’ve lost my link for this gif so I can’t cite it properly. If you know where its’ from, please let me kow.

That’s okay, I can fix it.

The first thing to know about neurotransmitters is how they fit into the electrochemical signalling between neurons.

A cartoon synapse.

Figure 1. Note how the neurotransmitters move across the synapse (the little gap) and stick to the receptors, pay attention to those. From lecture notes Dyck, R. (2010, Personal Communication).

Signalling occurs when neurotransmitter molecules bind to receptors (Figure 1).  Don’t take it to heart when magazine articles refer to neurotransmitters as having specific functions like “cuddle hormone” or “reward chemical” it’s the receptors which do all the interesting work.  This particular science article trope is one of my least favourite things; it’s meant to be a helpful simplification but it’s actually just straight up wrong.

The function of a neurotransmitter depends on which receptor it binds to and where it is in the brain.  This is why dopamine can both create and prevent attraction in voles by binding to different dopamine receptors.

Receptors can be classified based on either what they make the cell do, or how they work.

Ionotropic receptors (Figure 2A) are directly attached to ion channels so when they are activated they let ions in and out of the cell which is what generates the electrical current in the neurons

Metabotropic receptors turn on a g-protein, a member of a group of small molecules that transmit signals inside the cell.  G-proteins can open and shut ion channels just like ionotropic receptors but when they do they act more slowly and last for longer (Figure 2B).  They can also activate signalling cascades; chains of chemical reactions which alter the overall behaviour of the cell (Figure 2C).  These cascades don’t create electrical signals immediately, but they can change how the cell responds to subsequent signals.  They might, for instance, cause the cell to have a larger response to a specific neurotransmitter the next time it binds.

Different receptor types

Figure 2. Three different kinds of neurotransmitter receptor. From lecture notes: Dyck, R. (2010) Personal Communication

When receptors open or shut ion channels they can be excitatory, in which case the cell will fire a signal of its own or they can be inhibitory, in which case the cell will be prevented from firing.  The receptors which alter the cell’s behaviour in other ways, by activating different signalling cascades, they are referred to as neuromodulatory.  Neuromodulatory effects include things like changing the number or type of receptors on a cell’s surface, which doesn’t make the cell fire immediately but changes how it responds to the next round of neurotransmitter that is released; more receptors will create a bigger response to a neurotransmitter, for instance.

But those are just individual cells, what does opening ion channels have to do with adorable vole romance?  Well, these individual cells are organized into much larger networks, and it is the activity in networks in the brain, groups of cells communicating with other groups, sometimes in distant regions of the brain, that produces thoughts and behaviours.  The activity of specific cell types in specific networks is what creates behaviour.

So, to put it all together

  1. Neurotransmitters turn on neurotransmitter receptors – each neurotransmitter can bind to several different receptor types.
  2. Neurotransmitters change the way their cells behave – different receptor types create different changes, but a receptor typically only does a set thing, like making it easier for a cell to fire.
  3. The activity of big groups of cells in the brain come together to create behaviour – the same transmitter, binding to the same receptor, will create different results depending on which cell is being affected, and where it is.

Now go forth, and view lifestyle articles about neurotransmitters with the same grumpy skepticism I do, quite frankly I could use the company.