As a life-long insomniac, I’ve always been interest in sleep at a personal level. In 1984, when I was studying for my psychology degree, the first ever research seminar I attended was one on the psychology of sleep by Dr. Jim Horne (who was, and I think still is, at Loughborough University). I found the lecture really interesting and although I never pursued a career in sleep research it was at that point that I started to take an interest more professionally. In my blog I’ve written a number of articles on various aspects of sleep including sexsomnia (engaging in sexual acts while sleeping, for instance, while sleepwalking), somnophilia (engaging in sexual acts while individuals are sleeping), Sleeping Beauty paraphilia (a sub-type of somnophilia in which individuals are sexually aroused by watching other people sleep), and lucid dreaming (where individuals are aware they are dreaming and exert some kind of control over the content of the dream),
More recently, I’ve been a co-author on a number of research papers in journals such as Sleep Medicine Reviews, Journal of Sleep Research, and Sleep and Biological Rhythms (see ‘Further reading below) but these have all involved either the effects of internet addiction on sleep or the psychometric evaluation of insomnia screening instruments rather than being about the psychology of sleep.
In a previous A-Z article on “strange and bizarre addictions” I included ‘sleep addiction’ as one of the entries. Obviously I don’t believe that sleeping can be an addiction (at least not by my own criteria) but the term ‘sleep addiction’ is sometimes used to describe the behaviour of individuals who sleep too much. Conditions such as hypersomnia (the opposite of insomnia) has been referred to ‘sleeping addiction’ (in the populist literature at least). In a 2010 issue of the Rhode Island Medical Journal, Stanley Aronson wrote a short article entitled ‘Those esoteric, exoteric and fantabulous diagnoses’ and listed clinomania as the compulsion to stay in bed. Given the use of the word ‘compulsive’ in this definition, there is an argument to consider clinomania as an addiction or at least a behaviour with addictive type elements.
In an online article entitled ‘Sleep addiction’, Amber Merton also mentioned clinomania in relation to an addiction to sleep:
“If you are obsessed with sleeping or have an intense desire to stay in bed, you could be suffering from a condition called clinomania. That doesn’t mean that there aren’t people who can experience symptoms similar to addiction and even withdrawal in association with sleep, or lack thereof”.
The reference to ‘addiction-like’ symptoms appears to have some validity based on these self-report accounts I found online. All of these individuals mention various similarities between their constant need for sleep and addiction. I have highlighted these to emphasize my assertions that some of the consequences are at the very least addiction-like:
- Extract 1: “I believe someone can become psychologically dependent on sleep. I am 47 and have used sleep for 40 years to escape from life…I typically sleep 4-6 hours too much each day. Sleep feels like an addiction to me because I crave it several times a day and am looking forward to how I can sneak it in. I don’t seem to be able to control it with will power for very long…I only have short periods when this isn’t a problem. When I am under stress it is at its worse. If I have any free or unstructured time, I can’t control how much I sleep excessively. When my time is heavily scheduled, I really struggle with keeping a full schedule and crave the time off when I can sleep for hours. If I know I’ll have a few hours in between activities free, I will find ways to sneak in some sleep. I am embarrassed about this, don’t tell the people around me the extent of the problems and devise ways to sneak in sleep without people knowing”.
- Extract 2: “I love sleeping. It feels so good I think I could even become addicted if I didn’t HAVE to wake up. I sleep about 12 hours every day and could sleep more if I didn’t have to do daily necessities. I am aware of the fact that people who generally sleep more than they are supposed to, die sooner and have other various health problems. To be honest I would rather sleep than do most things. I even choose sleep over sex a lot”.
- Extract 3: “I often sleep for 12-20 hours at a time. I have depression and am on anti-depressants. I just love sleeping. It’s so safe and comfy. I don’t know how else to explain it. It’s just amazing”.
- Extract 4: “I sleep AT LEAST 12 hours a day. But on days off I’ve been known to sleep for about 15-20 hours. [I am] addicted to sleep. I’ve cancelled social outings with friends pretending to be sick when really I just wanted to sleep in. I love sleep and I can’t get enough of it. I’ve slept through the entire weekend multiple times before, only waking up Monday morning when my alarm rang. And even after that much wonderful sleep I was still tired. The second I come home from work every day I eat, shower, and then crawl into bed and sleep the entire evening and night away. My alarm’s the only thing that can wake me up anymore…As for why I love sleep so much, I see a lot of people saying it’s an escape for them. For me it’s more, I don’t like people or going out or socializing, so sleep is my drug of choice. Is it bad? Maybe. Do I care? Not really…I more than love it, and it’s not hurting anyone if we’re being honest”.
- Extract 5: “I feel like I’m addicted to sleep. Here’s why I think though. I suffered for 13 years with depression and while I know I am still getting over it I don’t feel that’s the reason I’m addicted. During those 13 years I would have serious bouts of chronic insomnia. The doctors tried to many different sleeping medications, meditation, clinics to help me find a routine for natural sleep without meds. Nothing worked. Now I live in Thailand and my doctor here recommended melatonin tablets, all natural as your brain is supposed to produce it anyway to tell you when it’s dark it’s time to sleep and when it’s like light it’s time to wake up. She thinks my brain fails to produce certain chemicals as such with serotonin and now figured melatonin. Since I have been taking a melatonin supplement, I sleep so well, I fall asleep within 20 minutes and I sleep for AT LEAST 8 hours. When I wake up I just want to go back to sleep again because it feels amazing. I don’t feel like it’s part of my anxiety or my depression, I just think it’s because I had insomnia for so long its addictive!”
- Extract 6: “To be honest if I could I would sleep my life away. My so called normal sleeping pattern: I am awake all night. Fall asleep around 4am-8am. Sleep 12 hours. Repeat. My mind is a broken record, constantly repeating the trauma. I do suffer from depression and anxiety. Sleep is my addiction. When I sleep I feel SAFE regardless?”
- Extract 7: “I’ve been addicted to sleep (the escape from an abusive childhood, depression, and PTSD) since I was ten years old! I want to change though because my body is a mess. I’ve slept for 4 days and sometimes more with short awake periods to eat a little and use the potty. Not enough though, because now my body doesn’t work properly…Oversleeping has its consequences”.
- Extract 8: “I’m so pleased that I have found this site and other people who are addicted to sleep as this problem has plagued my adult life and I would like it to stop. Take today for instance, I woke at 5.30am and was quite awake feeling a little anxious but I could not wait to get to sleep again, so I did and stayed in bed till around 2.20 pm. I have many days like this and as the lady above the sleep state is quite lucid and I do seem to enjoy it rather than getting up and living life for real”.
Again, I reiterate that none of these individuals are addicted to sleep but in addition to the addiction-like descriptions, there is also crossover in the motivations for excessive sleep and motivations underlying addictions (most noticeably the association with depression, anxiety, psychological trauma, and using the activity as an escape). In relation to addiction, these extracts include references to salience (engaging in sleep to the neglect of everything else in their life), cravings (for sleep), the sleep being excessive, repetitive and habitual, sleep leading to negative consequences (conflict), and loss of control. The fact that many of these individuals describe their behaviour as an addiction or addictive doesn’t mean that it is.
While there is no academic paper that I know of that has ever claimed sleep can be a genuine addiction there are countless clinical and empirical papers examining excessive sleep (i.e., hypersomnia) and the different etiological pathways that can lead to hypersomnia. Although hypersomnia is not an addiction, those with the condition (like addicts) can suffer many negative side-effects from the relatively minor (e.g., low energy, fatigue, headaches, loss of appetite, restlessness, hallucinations) to the more severe (e.g., diabetes, obesity, heart disease, clinical depression, memory loss, suicidal ideation, and in extreme cases, death). In one online article I came across, the similarity between hypersomnia and addiction in relation to depression was evident:
“It’s important to note that in some cases separating cause from effect here can be muddled. For instance, does over sleeping contribute to depression or does depression contribute to oversleeping? Or are both oversleeping and depression the effect of a larger underlying cause? Furthermore, once a person is experiencing both, could they act to reinforce the other as a feedback loop?”
This observation could just as easily be made about most addictions (substance or behavioural). Finally, it’s worth noting that there are many sub-types of hypersomnia and excessive sleep. In a good review of hypersomnia [HS] in Current Neurology and Neuroscience Reports, Dr. Yves Dauvilliers notes the following hypersomnia sub-types (including narcolepsy which can include excessive sleep but isn’t usually classed as a type of hypersomnia; also note that ‘idiopathic’ means of unknown cause) which I have paraphrased below:
- Narcolepsy: This is a disabling neurologic disorder characterized by excessive daytime sleep (EDS) and cataplexy (i.e., a sudden loss of voluntary muscular tone without any alteration of consciousness in relation with strong emotive reactions such as laughter, joking).
- Narcolepsy without cataplexy: This is simply a variant of narcolepsy with cataplexy (but without the cataplexy).
- Idiopathic hypersomnia: Idiopathic HS is rare and remains a relatively poorly defined condition due to the absence of specific symptoms such as cataplexy or sleep apneas (i.e., loss of breathing while sleeping).
- Recurrent hypersomnia: This HS is characterized by repeated episodes of excessive sleep (at least 16 hours a day) lasting from a few days up to several weeks. The most well-known recurrent HS is Kleine-Levin syndrome which comprises both cognitive disturbances (feelings of confusion and unreality) and behavioural disturbances (such as overeating and hypersexual behaviour during symptomatic episodes).
- Hypersomnia associated with neurologic disorders: This type of HS causes EDS and can be a result of brain tumours, dysfunction in the thalamus, hypothalamus, or brainstem that may mimic idiopathic HS or narcolepsy.
- Hypersomnia associated with infectious disorders: This type of HS can be a result of viral infection such as HIV pneumonia, Whipple’s disease (a systemic disease most likely caused by a gram-positive bacterium), or Guillain-Barré syndrome (a rapid-onset muscle weakness caused by the immune system damaging the peripheral nervous system).
- Hypersomnia associated with metabolic or endocrine disorders: This type of HS can be a result of conditions such as hyperthyroidism, diabetes, hepatic encephalopathy (a liver dysfunction among individuals with cirrhosis), and acromegaly (a hormonal disorder that develops when the pituitary gland produces too much growth hormone).
- Hypersomnia caused by drugs: This type of HS is secondary to many different types of drug medication including hypnotics, anxiolytics, antidepressants, neuroleptics, anti-histamines, and anti-epileptics.
- Hypersomnia not caused by drugs or known physiologic conditions: This type of HS can be caused by a range of disorders such as depressive disorder, seasonal affective disorder, and abnormal personality traits.
None of these types of HS is an addiction but clearly the negative consequences can be just as serious for the individual.
Dr. Mark Griffiths, Distinguished Professor of Behavioural Addiction, International Gaming Research Unit, Nottingham Trent University, Nottingham, UK
Alimoradi, Z., Lin, C-Y., Broström, A., Bülow, P.H., Bajalan, Z., Griffiths, M.D., Ohayon, M.M. & Pakpour, A.H. (2019). Internet addiction and sleep problems: A systematic review and meta-analysis. Sleep Medicine Review, 47, 51-61.
Aronson, S. M. (2010). Those esoteric, exoteric and fantabulous diagnoses. Rhode Island Medical Journal, 93(5), 163.
Bener, A., Yildirim, E., Torun, P., Çatan, F., Bolat, E., Alıç, S., Akyel, S., & Griffiths, M.D. (2019). Internet addiction, fatigue, and sleep problems among students: A largescale survey study. International Journal of Mental Health and Addiction. doi: 10.1007/s11469-018-9937-1
Billiard, M., & Dauvilliers, Y. (2001). Idiopathic hypersomnia. Sleep Medicine Reviews, 5(5), 349-358.
Dauvilliers, Y. (2006). Differential diagnosis in hypersomnia. Current Neurology and Neuroscience Reports, 6(2), 156-162.
Domenighini, A. (2016). Can you be addicted to sleep? Vice, January 24. Located at: https://www.vice.com/en_us/article/mg7e33/can-you-be-addicted-to-sleep
Hawi, N.S., Samaha, M., & Griffiths, M.D. (2018). Internet gaming disorder in Lebanon: Relationships with age, sleep habits, and academic achievement. Journal of Behavioral Addiction, 7, 70-78.
Mamun, M.A. & Griffiths, M.D. (2019). Internet addiction and sleep quality: A response to Jahan et al. (2019). Sleep and Biological Rhythms. doi: 10.1007/s41105-019-00233-0
Merton, A. (2008). Sleep addiction. Located at: https://www.plushbeds.com/blog/sleep-disorders/sleep-addiction/
Mignot, E. J. (2012). A practical guide to the therapy of narcolepsy and hypersomnia syndromes. Neurotherapeutics, 9(4), 739-752.
Pakpour, A., Lin, C-Y., Cheng, A.S., Imani, V., Ulander, M., Browall, M. Griffiths, M.D., Broström, A. (2019). A thorough psychometric comparison between Athens Insomnia Scale and Insomnia Severity Index among patients with advanced cancer. Journal of Sleep Research. doi: 10.1111/jsr.12891.
Those that know me well often comment that I have a general inability to sit still and that I am a ‘fidget’. (This is not necessarily a bad thing and in fact there are some positives to fidgeting that I outlined in a previous blog on bad behaviours that are sometimes good for you). There is certainly some truth to the observation that I fidget but sometimes the fidgeting is out of my control. Every few weeks my right lower leg appears to take on a life of its own and I will get strange (uncomfortable) sensations (such as tingling, itching, and aching, and occasionally cramp-like feelings) that force me to move my right leg and foot around. It only happens when I am in a resting and relaxing state and usually lasts about 30 minutes (but can occasionally last much longer). On occasions it disrupts my work and sleep but I find that just getting up and moving around is sometimes enough to alleviate the uncomfortable feelings.
A few years ago I Googled my ‘symptoms’ and was surprised to find that I am not the only person who appears to experience such effects and that there is a whole medical literature on what has been termed ‘restless legs syndrome’ although in my case it would be in a singular rather than plural form). I’ve had the condition for about 15 years now and it may be related to some of the medication I take for an unrelated chronic degenerative health condition that I have. According to the Wikipedia entry on restless legs syndrome (RLS):
“The first known medical description of RLS was by Sir Thomas Willis in 1672. Willis emphasized the sleep disruption and limb movements experienced by people with RLS…The term ‘fidgets in the legs’ has also been used as early as the early nineteenth century. Subsequently, other descriptions of RLS were published, including those by Francois Boissier de Sauvages (1763), Magnus Huss (1849), Theodur Wittmaack (1861), George Miller Beard (1880), Georges Gilles de la Tourette (1898), Hermann Oppenheim (1923) and Frederick Gerard Allison (1943). However, it was not until almost three centuries after Willis, in 1945, that Karl-Axel Ekbom (1907–1977) provided a detailed and comprehensive report of this condition in his doctoral thesis, Restless legs: clinical study of hitherto overlooked disease. Ekbom coined the term “restless legs” and continued work on this disorder throughout his career. He described the essential diagnostic symptoms, differential diagnosis from other conditions, prevalence, relation to anemia, and common occurrence during pregnancy. Ekbom’s work was largely ignored until it was rediscovered by Arthur S. Walters and Wayne A. Hening in the 1980s. Subsequent landmark publications include 1995 and 2003 papers, which revised and updated the diagnostic criteria”.
As well as being referred to as RLS, it is sometimes referred to as Willis-Ekbom Disease or Willis-Ekbom Syndrome. Since being ‘rediscovered’ in the 1980s, there have been a lot of scientific papers published on the phenomenon although many of these are medical case studies (I don’t think my own experiences are extreme enough or strong enough to appear in any medical textbook. The Wikipedia entry on RLS provides a good summary of what is known medically and empirically:
“Restless legs syndrome (RLS) is a disorder that causes a strong urge to move one’s legs. There is often an unpleasant feeling in the legs that improves somewhat with moving them. Occasionally the arms may also be affected. The feelings generally happen when at rest and therefore can make it hard to sleep. Due to the disturbance in sleep, people with RLS may have daytime sleepiness, low energy, irritability, and a depressed mood. Additionally, many have limb twitching during sleep. Risk factors for RLS include low iron levels, kidney failure, Parkinson’s disease, diabetes, rheumatoid arthritis, and pregnancy. A number of medications may also trigger the disorder including antidepressants, antipsychotics, antihistamines, and calcium channel blockers. There are two main types. One is early onset RLS which starts before age 45 [years], runs in families and worsens over time. The other is late onset RLS which begins after age 45 [years], starts suddenly, and does not worsen. Diagnosis is generally based on a person’s symptoms after ruling out other potential causes… Females are more commonly affected than males and it becomes more common with age…Some doctors express the view that the incidence of restless leg syndrome is exaggerated by manufacturers of drugs used to treat it. Others believe it is an under-recognized and undertreated disorder…An association has been observed between attention deficit hyperactivity disorder (ADHD) and RLS or periodic limb movement disorder. Both conditions appear to have links to dysfunctions related to the neurotransmitter dopamine, and common medications for both conditions among other systems, affect dopamine levels in the brain”.
According to a review by Dr. Richard Allen and Dr. Christopher Earley in the Journal of Clinical Neurophysiology, RLS affects 2.5-15% of the US population. In another review on sleep disorder in the journal American Family Physician, Dr. Kannan Ramar and Dr. Eric Olson reported that RLS is typically characterized by four essential features: These are:
“(1) the intense urge to move the legs, usually accompanied or caused by uncomfortable sensations (e.g., “creepy crawly,” aching) in the legs; (2) symptoms that begin or worsen during periods of rest or inactivity; (3) symptoms that are partially or totally relieved by movements such as walking or stretching; and (4) symptoms that are worse or only occur in the evening or at night”.
Various online articles and papers report a variety of potential treatments based on the notion that RLS might be caused by a dopamine imbalance in the body. Some medics advise a regular sleep routine (such as that advised for those with insomnia), and cutting out the drinking of alcohol and the smoking of cigarettes. Pharmacological treatments include the use of drugs that are also used in the treatment of Parkinson’s disease such as L-DOPA and pramipexole, and the use of magnesium sulphate therapy (as reported in a 2006 paper in the Journal of Clinical Sleep Medicine – magnesium is known to be a natural muscle relaxant). In a 2011 issue of the journal Sleep Medicine, In an online article about RLS, Dr Michael Platt, author of the 2014 book Adrenalin Dominance, claims that RLS sufferers can be treated using a progesterone cream:
“Excess adrenalin during the night can cause restless leg syndrome. People often have associated symptoms also resulting from elevated adrenalin, such as teeth grinding, the need to urinate, and tossing and turning, and they often awaken in the morning with low back pain. Characteristically, RLS patients have an excess of adrenaline, may toss and turn all night, be quick to anger, might be workaholics, will usually have fibromyalgia (aches and pains – low back, side of the hips, and grind their teeth), they might drink too much, and will be hypoglycemic (sleepy between 3-4 p.m. or when in a car), and so on. There is an associated over-production of insulin and an under-production of progesterone…[By using a progesterone cream] I have had 100% success with eliminating RLS by getting hormones into balance, often within the first week. Patients feel more relaxed, they can sleep at night, rage disappears, and they can focus more easily”.
Dr. Luis Marin and his colleagues reported a different treatment for RLS altogether. They reported the case of a 41-year-old male RLS sufferer who after being on medication for RLS discovered his own solution – having sex. Following sex, the man reported that all RLS symptoms would disappear. Marin and colleagues speculated that the release of dopamine following orgasm might alleviate RLS symptoms. This appears to be a reasonable speculation given the findings of research published in the Journal of Neuroscience by Dr. Gert Holstege and his colleagues who examined brain activation at the point of ejaculation. In their paper they reported the similarity between ejaculation and using heroin in terms of brain activation:
“We used positron emission tomography to measure increases in regional cerebral blood flow during ejaculation compared with sexual stimulation in heterosexual male volunteers. Manual penile stimulation was performed by the volunteer’s female partner. Primary activation was found in the mesodiencephalic transition zone, including the ventral tegmental area, which is involved in a wide variety of rewarding behaviors. Parallels are drawn between ejaculation and heroin rush”.
It could well be that the increase in dopamine following ejaculation acts in a similar way to the medications that are given to RLS sufferers. Of all the treatments for RLS that I have read about, I think I know which one I would prefer!
Dr. Mark Griffiths, Professor of Behavioural Addiction, International Gaming Research Unit, Nottingham Trent University, Nottingham, UK
Allen, R.P., & Earley, C.J. (2001). Restless legs syndrome: A review of clinical and pathophysiologic features. Journal of Clinical Neurophysiology, 18(2), 128-147.
Bartell S1, Zallek S. Intravenous magnesium sulfate may relieve restless legs syndrome in pregnancy. Journal of Clinical Sleep Medicine, 15, 187-188.
Chaudhuri, K.R., Appiah-Kubi, L.S., & Trenkwalder, C. (2001). Restless legs syndrome. Journal of Neurology, Neurosurgery & Psychiatry, 71(2), 143-146.
Ekbom, K., & Ulfberg, J. (2009). Restless legs syndrome. Journal of Internal Medicine, 266(5), 419-431.
Holstege, G., Georgiadis, J. R., Paans, A. M., Meiners, L. C., van der Graaf, F. H., & Reinders, A. S. (2003). Brain activation during human male ejaculation. Journal of Neuroscience, 23(27), 9185-9193
Leschziner, G., & Gringras, P. (2012). Restless legs syndrome. British Medical Journal, 344, e3056.
Marin, L.F., Felicio, A.C., & Prado, G.F. (2011). Sexual intercourse and masturbation: Potential relief factors for restless legs syndrome? Sleep Medicine, 12(4), 422.
Ondo, W. G. (2009). Restless legs syndrome. Neurologic Clinics, 27(3), 779-799.
Ramar, K; Olson, EJ (Aug 15, 2013). Management of common sleep disorders. American Family Physician, 88, 231–238.
Satija, P., & Ondo, W. G. (2008). Restless legs syndrome. CNS Drugs, 22(6), 497-518.
For most of my life I have “suffered” from insomnia. I deliberately put the word ‘suffered’ in quotation marks as for the vast majority of the time I have always seen my lack of sleep as something positive (i.e., I had more time to do other things. In fact, when people ask me how I find the time to write so much, I usually say “Insomnia” but I don’t usually say it as a joke, it’s a matter of fact). Given my personal interest in insomnia, I’ve always enjoyed reading papers on insomnia (and no, they don’t send me to sleep!) and sexsomnia (which I looked at in a previous blog). In 1990, a Finnish man named Toimi Soini stayed awake for over 11 days (276 hours) and broke the world record for not going to sleep. However, this record no longer appears in the Guinness Book of World Records as it was withdrawn on health grounds because lack of sleep – as I’ll show in today’s blog – can lead to death.
One of the strangest (and deadliest) types of insomnia is ‘fatal familial insomnia’ (FFI). This is actually an incredibly rare genetic sleep disorder that affects around 40 families worldwide. The cause of FFI is a genetic mutation that leads to prion disease and is therefore related to bovine spongiform encephalopathy (BSE; i.e., ‘mad cow disease’), Creutzfeldt–Jakob disease (the human form of BSE), and ‘Kuru’ (the incurable and degenerative neurological disorder found in the cannibalistic tribes in New Guinea and known as the ‘laughing disease’). The (online) Medical Dictionary is a little more technical and notes:
“Fatal familial insomnia (FFI) is a very rare, autosomal dominant inherited, disease of the brain. It is caused by a mutation in a protein called prion protein (PrP): asparagine- 178 is replaced by aspartic acid. The mutation changes the shape of PrP so that it becomes a prion and makes other, normal PrP molecules change to the abnormal shape. This causes amyloid plaques in the thalamus, the region of the brain responsible for regulation of sleep patterns. The dysfunction of the thalamus results in insomnia first of all, which progresses to more serious problems over several years”
All prion diseases (known more scientifically as ‘transmissible spongiform encephalopathies’) are rare progressive neurodegenerative disorders that can affect both animals and humans. All of the prion diseases (including FFI) typically have (i) long incubation periods, (ii) a failure to induce inflammatory response, and (iii) characteristic spongiform changes that are associated with neuronal loss. The first recorded case of FFI is thought to be an Italian man who died in Venice in 1765. There are many descriptions of the disease online including case study accounts. The Wikipedia entry on FFI described the case of the American music teacher, Michael Corke from Chicago:
“He suddenly began to have trouble sleeping not long after his 40th birthday in 1991, and his health and state of mind quickly deteriorated as his sleeplessness grew worse. Eventually, he couldn’t sleep at all, and he was soon admitted to the hospital. Doctors there weren’t sure what was wrong with him, initially diagnosing multiple sclerosis; in a bid to send him to sleep in the later stages of the disease, physicians induced a coma with the use of sedatives, but they found that his brain still failed to shut down. Corke died in 1992 a month before his 41st birthday, by which time he had gone without sleep for six months”
Another 2011 online article on “bizarre brain disorders” by Anna McGann also described a family case study (which is very similar to paper published in a 2000 issue of the Journal of Neurology, Neurosurgery and Psychiatry by Dr. C. Tabernero and colleagues):
“Dr. Ignazio Rottier gained unwanted firsthand experience when he and his wife, Elisabetta, watched her family fall victim to [FFI]. First known to fall ill was Elisabetta’s grandfather. Decades later, Elisabetta’s uncle, Silviano, was 53 when he lost his ability to sleep. A few short months following initial onset, Silviano fell into a coma and died…In the 70s, an aunt of Elisabetta’s passed on, one year after her own initial onset of sleeplessness. Yet another year later, a second aunt too lost her life battling the very same affliction”.
Research has also shown that the condition (in a few cases) can result from a non-inherited genetic mutation that has been called ‘sporadic fatal insomnia’ (sFI). Less than 10 cases of sFI have ever been documented in the medical literature. As the conditions worsen, sufferers experience a wide range of symptoms including delirium, hallucinations (auditory, visual and tactile), elevated heart rate and blood pressure, hyperhidrosis (i.e., excess sweating), hyperthermia, hypertension, impotence (in men), amenorrhea (cessation of periods) and early menopause (in women), constipation, and dementia. Treating the symptoms (via vitamin therapy, meditation, use of narcoleptics) may extend the quality of life (but as noted above, there is no known cure and most interventions are purely palliative). The disease typically has four stages, and takes between half a year and a year and a half to run its course:
- Stage 1 (typically four months): Symptoms include insomnia, paranoia, phobias and panic attacks.
- Stage 2 (typically five months): Symptoms include severe hallucinations and increasing panic attacks.
- Stage 3 (typically three months): Symptoms include permanent insomnia, limited mental functioning, and rapid weight loss.
- Stage 4 (typically six months): Symptoms include dementia and general non-responsiveness leading to death.
Writing in a 2006 issue of the Medscape General Medicine journal, Dr. Joyce Schenkein outlined the etiology and characteristics of FFI. She noted that it often begins in middle age (average age of onset being 50 years) and has no cure (even ‘gene therapy has been unsuccessful to date). Unfortunately, the prognosis following initial diagnosis is poor with FFI sufferers’ only living for an average of about a year and a half (with Dr. Schenkein noting that survival ranged from 7 to 36 months from diagnosis of FFI). It originates in the form of unexplained sleeplessness before rapidly developing into a fatal insomnia. Writing in an issue of the Journal of Clinical Neuroscience, Dr. S. Collins and colleagues in a paper on prion diseases (including FFI) concluded:
“FFI [is] likely [to] remain, [a] very rare disease, [and] will be increasingly recognised as heightened clinical awareness prompts appropriate confirmatory genetic and other testing. Similarly, continued molecular biological and allied research of these less common prion diseases will undoubtedly provide fundamental insights into the pathogenesis of this group of disorders in general, disproportionate to their numerical frequency”.
Dr Mark Griffiths, Professor of Gambling Studies, International Gaming Research Unit, Nottingham Trent University, Nottingham, UK
Collins, S., McLean, C.A. & Masters, C.L. (2001). Gerstmann–Sträussler–Scheinker syndrome, fatal familial insomnia, and kuru: a review of these less common human transmissible spongiform encephalopathies. Journal of Clinical Neuroscience, 8, 387–397.
McGann, A. (2011). 5 bizarre brain disorders. Suite 101, November 25. Located at: http://suite101.com/article/5-bizarre-brain-disorders-a397906
Moody, K.M., Schonberger, L.B., Maddox, R.A., Zou, W.Q., Cracco, L., & Cali, I. (2011). Sporadic fatal insomnia in a young woman: a diagnostic challenge: case report. BMC Neurology, 11, 136.
Schenkein, J. (2006). Self-management of fatal familial insomnia. Part 1: What Is FFI? Medscape General Medicine, 8(3), 65.
Schenkein, J. & Montagna, P (2006). Self-management of fatal familial insomnia. Part 2: Case report. Medscape General Medicine, 8(3), 66.
Tabernero, C., Polo, J.M., Sevillano, M.D., Muñoz, R., Berciano, J., Cabello, A., Báez, B., Ricoy, J.R., Carpizo, R., Figols, J., Cuadrado, N., Claveria, L.E. (2000). Fatal familial insomnia: clinical, neuropathological, and genetic description of a Spanish family. Journal of Neurology, Neurosurgery and Psychiatry, 68, 774–777.
Turner, R. (2012). Fatal Familial Insomnia: The FFI Sleep Disorder. World of Lucid Dreaming. Located at: http://www.world-of-lucid-dreaming.com/fatal-familial-insomnia.html
Wikipedia (2012). Fatal familial insomnia. Located at: http://en.wikipedia.org/wiki/Fatal_familial_insomnia