Cortico-thalamic dissociation in Sleep Paralysis

Bookmark and Share

By Paul Mason

Paul Mason is a PhD student at Macquarie University and frequent contributor to Neuroanthropology.  He is well on his way to finishing his thesis, but occasionally shares his insightful columns on a wide range of topics here.  Please note that the former ‘Fattest Man in the World’ is a different Paul Mason.

Have you ever woken up and not been able to move your body? For those people who have experienced this sensation, it is unnerving, surreal, and often quite stressful. Rest assured though, that this condition is benign, harmless, and your body will wake up after a minute or two. People also report that their body wakes up when someone touches them, or even at the sound of a surprising noise. Despite the temporary sensation of uncanny paralysis upon wakening, you can ride the episode out with the knowledge that it has not been associated with any medical disorders.

This condition, known as sleep paralysis, is rare but not uncommon. Funnily enough, in the last year, three of my friends have asked me about this condition—two of them medical doctors. Sleep paralysis is a parasomnia usually associated with REM sleep. Episodes typically last one to three minutes and disappear spontaneously by themselves or by someone else’s touch. Dreams can potentially superimpose onto reality during this period. However, the condition is usually experienced as a dream state without the dreams. In other words, your body has still turned off control of its muscles as though you are dreaming, but your brain is strangely awake. In medical terms, the condition is considered a dissociated REM state where the motor atonia of REM is present in isolation. That basically means that control of your muscles has been turned off but consciousness has been switched on.

When my friends asked me what I thought about the symptoms they described, I was reminded of my undergraduate study in neuropsychology where I learnt about lesion studies in cats that disrupted areas in the brain to do with sleep, dreaming, and muscle control. In this study, researchers performed lesions to areas of the brain in cats that normally inhibit motor control during sleep. The lesion was performed to the ventral locus coeruleus of the Pons (it’s weird what you remember sometimes). This lesion caused the cats to exhibit strange sleepwalking behaviour that allowed researchers an uncanny little window into Kitty dreams.

I’m not sure, but if you google ‘dream enactment’, then you should find plenty of information on the web. Anyway, my first thought about sleep paralysis was that there must be some kind of delay in switching off the area inhibiting motor control during a hypnopomic or postdormital sleep paralysis episode. I’m not suggesting that sleep paralysis is associated with anatomical problems, merely an occasional physiological hiccup—something as simple as say pins and needles in an otherwise healthy organ. Possibly the hiccup can occur in the Pons… Possibly, as recent research indicates, it could be somewhere else…

Of my friends who shared their symptoms with me and asked me for my thoughts, one was doing shift-work, the other was suffering from severe jet-lag, and the third slept odd hours due to an erratic rotation schedule at her job. I’m not a medical doctor, but the suggestion of sucking a melatonin tablet under the tongue before bed for only a couple of nights worked wonders for my friend with jet-lag. But, you also have to consider that episodes of sleep paralysis are rare, so they probably disappeared by themselves. For my other friends I suggested potassium rich foods such as bananas, which are always yummy to eat anyway, (those friends haven’t told me of any episodes since, but then again that is anecdotal as well).

From scant research reports on the subject, it appears that sleep paralysis occasionally occurs in a familial form, affects females more often than males, and has an X-linked dominant transmission. Talking with my Indonesian friends suggests to me that the condition is not as rare as Western medical practitioners think. But then again, I have lived with Indonesians who have some extremely erratic sleeping schedules.

I am fascinated in the phenomenology and neurophenomenology of sleep paralysis episodes. One of my friends reported a hypnagogic auditory hallucination accompanying an episode of sleep paralysis. Not surprisingly, she is not the only person in her family to occasionally suffer from the condition.

In my own experience, I have had a hypnogogic visual hallucination as a child of five or six years of age. Before my teenage years, I also had an episode of what I now understand to be sleep paralysis. I woke up in the morning and could not for the life of me open my eyes. My eyelids were as heavy as lead (Pb), and then it felt like bees were performing the waggle dance all over my closed eyes. It was an overwhelming experience at the time but I can’t recall if I woke up or went back to sleep afterwards. If I’m not making stories up, I was eventually able to open my eyes, but then I shut them again and went back to sleep.

As a sidenote, the word ‘hypnagogic’ says so much to me about medical practice. A ‘hypnagogic hallucination’ is literally just a hallucination that one experiences just before or just after falling asleep. We don’t actually have an explanation for ‘hypnagogic hallucinations’, but we do have a fancy label with two lovely multi-syllabic words. On numerous occasions, friends have shared private stories about hallucinations with me. If they have been stressed by the episode then calming them simply involved asking if they were in bed at the time, which they have thus far always confirmed, and then I merely say,

“Don’t worry, you just experienced a hypnogogic hallucination. It’s not unusual in the slightest.”

On every occasion, labeling the episode makes a friend happy. I have even seen colleagues in medicine calm other acquaintances using the very same words. It’s fantastic, but it really makes me wonder how much people seek a label and how much people seek an explanation.

In research published in PNAS only in February last year (Magnin et al. 2010), researchers have made headway in describing the physiology underlying hypnagogic hallucinations. Using electrodes implanted into the brains of epileptic patients (a common pre-surgical practice to localise the origins of epileptic seizures), researchers opportunistically—but ethically—used the data to reveal what happens in the deepest parts of the brain during sleep onset. The activity of deep structures in the brain is difficult to image because MRI is too slow and EEG is too superficial. This electrophysiology research revealed a surprising finding:

The thalamus (a small but dense deep brain structure highly interconnected to body and cortical regions and involved in receiving sensory information) goes to sleep some ten minutes before the cortex.

When falling asleep, the thalamus shuts us off from the outside world, but the cortex continues to function which could explain, as the researchers hypothesise, how hallucinations can arise when we fall asleep.

A hypothesis about Sleep paralysis:

The finding that extensive cortical regions remain activated for several minutes after thalamic deactivation at sleep onset might explain forms of insomnia associated with lesions to the thalamus, and it also might be the reason that hypnagogic experiences commonly occur during the wake–sleep transition.

In the thirteen people studied, they did not find desynchronisation of the thalamus and cortex during awakening. But that was only thirteen people. If someone who experienced an episode of sleep paralysis was under observation, would we find that awareness with paralysis upon waking was associated with a desynchronisation of the thalamus and cortex? If the cortex reactivated before the thalamus could sleep paralysis be the result?

An episode of sleep paralysis typically only lasts a few minutes. Knowing that desynchronisation of the thalamus and cortex during sleep onset lasts only several minutes, then it is not implausible to hypothesise that there could be a lapse between the reactivation of the cortex and the reactivation of the thalamus in sleep paralysis that lasts only a few minutes. If the cortex wakes up before the thalamus, people might be lucid but unable to move.

The cessation of sleep paralysis by physical touch might be explained by the idea that touch might be igniting sensory systems that activate the thalamus. As an ostensibly benign condition, and one that occurs rarely and unpredictably, sleep paralysis might not be the most accessible or indeed imperative area of medical research, but as a case of dissociative consciousness it is a deeply fascinating research venture into the awareness of who we are.

References:
ResearchBlogging.org

Sudhansu Chokroverty (1999) Sleep Disorders Medicine: Basic Science, Technical Considerations, and Clinical Aspects. Butterworth-Henemann.

M.Co. (2009) Le Cerveau ne s’endort pas tout d’un coup. Science & Vie, May.

Magnin, M., Rey, M., Bastuji, H., Guillemant, P., Mauguiere, F., & Garcia-Larrea, L. (2010). Thalamic deactivation at sleep onset precedes that of the cerebral cortex in humans Proceedings of the National Academy of Sciences, 107 (8), 3829-3833 DOI: 10.1073/pnas.0909710107

Related Posts Plugin for WordPress, Blogger...

Creative Commons License
Cortico-thalamic dissociation in Sleep Paralysis by PLOS Blogs Network, unless otherwise expressly stated, is licensed under a Creative Commons Attribution 4.0 International License.

This entry was posted in Brain and tagged , . Bookmark the permalink.

Comments are closed.