Stuttering and sleep: Some speculation

out 22, 2012 | por Sandra Merlo | Gagueira, Sono
Este texto foi originalmente publicado na Conferência Online Mundial relativa ao Dia Internacional de Atenção à Gagueira do ano de 2012. Veja a publicação original aqui.



This paper examines a possible relationship between stuttering and sleep. My interest in this topic came from my own experience: some years ago, I realized my stuttering became worse after several nights of poor sleeping. When I ask this question to my patients, they usually answer they have never observed if their sleep affects their speech. However, after some weeks of observation, they usually report their stuttering becomes worse when they sleep poorly.

In my clinical practice, I have seen three situations. First, I have seen cases of childhood stuttering with total recovery of stuttering after sleep hygiene measures were taken. However, it is not possible to say if sleep hygiene measures really acted to improve stuttering or if these cases were just cases of spontaneous recovery. Second, I have seen cases of persistent stuttering with significant improvement of speech after sleep hygiene measures were applied. And third, I have seen cases of persistent stuttering with no observed improvement of speech after sleep hygiene measures were applied.


What is a bad night of sleep? Sleep hygiene measures

There are several answers to this question. I will specify below the ones I see more frequently in my clinical practice.

1) It is a night when one sleeps fewer hours than necessary. What is necessary changes from person to person but it is possible to rely on what is more commom to each age groups (O’Brien, 2009):

  • Hours of sleep for preschool children: 14 hours
  • Hours of sleep for school children: 10-11 hours
  • Hours of sleep for teenagers and adults: 8 hours

2) It is a night when one sleeps out of phase. What is “out of phase”? There are people who prefer to go to bed earlier and there are others who prefer to go to bed late at night. When people lie down some hours earlier or later than their natural need, the feeling of rest will not be the same the next day. This occurs because his/her sleep was in a different phase in regards to his/her biological clock. Therefore it is also important to observe the preferable hour to go to bed and try to follow the natural rhythm of one’s biological clock (Benca et al, 2009).

3) It is when one has a very irregular sleep schedule. For example, there are nights when he/she goes to sleep at 10 PM and wakes up at 6 AM, while there are nights when he/she goes to sleep at 1 AM and wakes up at 9 AM. Irregular sleep schedules are considered risk factors for mental diseases, such as anxiety and depression (Benca et al, 2009).

4) It is when one takes a long time to fall asleep or wakes up several times during the night. This typically occurs with everybody but it is a problem when it becomes a habit. It is suggested to see a neurologist, who may indicate exams (like polysomnography) or medication (like a sleep hormone). The physician may also refer the patient to a psychiatrist or a psychologist (if he/she concludes, for example, the sleep disorder is due to anxiety or depression) or even to a nutritionist (if he/she concludes the sleep disorder is due to bad food habits, such as coffee or alcohol abuse).

Thus, some sleep disorders are related to difficulties with sleep itself: sleeping a few hours, taking a long time to fall asleep, waking up several times during the night, or waking up too early in the morning. These situations are called “primary sleep disorders”.

5) A bad night of sleep is also when one cannot adequately breath. This may be something temporary (like an upper respiratory infection) or a persistent respiratory disorder (like mouth breathing, snoring, rhinitis, sinusitis, nasal septum deviation, adenotonsillar hypertrophy, sleep obstructive apnea, or asthma) (Simmons & Clark, 2009).

Those who cannot adequately breath when asleep, wake up several times during the night to try to breath better not only impairing sleep by the breathing problem but also by the frequent awakenings.


Sleep deprivation, muscle relaxation, and self monitoring

One of the consequences of sleep deprivation may be increasing of muscle tension.

Sleep consists of four different stages, which cyclically alternate during the night. In a complete night of sleep:

  • 50% is light sleep
  • 25% is deep sleep. It is this kind of sleep that favours the feeling of rest. The occurrence of heavy sleep is longer at the beginning of the night (Guyton & Hall, 1996a). As soon as one is rested, the occurrences of deep sleep decreases.
  • 25% of sleep is called REM (rapid eye movement) sleep. While deep sleep decreases, REM sleep increases over the course of the night. So, sleeping fewer hours than necessary primarily interferes with REM sleep. It is during this stage of sleep that intense muscle relaxation occurs (Guyton & Hall, 1996a). The following day, with the potential of greater muscle tension in the speech musculature (lips, tongue, and vocal folds), stuttering may become worse.

Another consequence of sleep deprivation may be the impairment of cognitive function that suppports speech. After a bad night of sleep, attention and executive functions become worse on the following day (Schmidt et al., 2007) and this may affect speech fluency. Attention and executive functions are necessary abilities to apply speech strategies to improve fluency.


Insomnia and brain damage

Altena et al. (2010) analyzed the brain anatomy of adults with and without persistent insomnia. The group with insomnia consisted of 24 patients, from 52 to 74 years old, both genders. Results showed reduction in grey matter in the orbitofrontal cortex and also in the precuneus in the brain of patients with persistent insomnia when compared to the control group.

The precuneus is the posterior parietal cortex (Brodmann area 7). Lesions on this area may have negative consequences in speech therapy. The posterior parietal cortex is related to the conscious perception of somatic sensations (Guyton & Hall, 1996b). With some stuttering patients, one of the objectives of speech therapy is learning to use a smaller degree of muscle tension during speech (smooth movements strategy). For those who stutter more frequently on consonants, it is essential to perceive different degrees of tension of the lips and tongue. For those who stutter more frequently on vowels, it is essential to perceive different degrees of tension in the vocal folds. Therefore damage to the posterior parietal cortex may have negative consequences in speech therapy because it may impair the ability to consciously perceive muscle tension along the vocal tract which may ultimately impair the ability to programme smoother articulatory gestures.

By the other hand, the orbitofrontal cortex (Brodmann areas 10, 11, and 47) is related to assigning affective values to experiences (Kringelbach & Rolls, 2004). That is why it connects virtually the entire the brain, including the secondary auditory cortex, premotor cortex, and basal ganglia, areas directly related to stuttering. The fact that sleep deprivation damages the orbitofrontal cortex may help to explain why some people who stutter show very negative emotional reactions to speech related experiences. Some are very sensitive to experiences of social punishment; others are not particularly sensitive to success and positive reinforcement experiences. These two kinds of emotional behaviors usually delay progress in therapy.

Altena et al. (2010) showed that persistent sleep deprivation damages the brains of adults’. However, persistent sleep deprivation is even more harmful in childhood because their brains are still developing. It is estimated that 80% of children with some kind of neurodevelopmental disorder present sleep disorders, which makes rehabilitation more difficult (Blunden & Beebe, 2006).

But exactly how would persistent sleep deprivation cause brain damage? Two mechanisms have been studied: oxidative stress and gene expression (Jan et al., 2010).

One of the functions of sleep is to detoxify the brain. It is believed free radicals that were produced over the day are removed during sleep. The excessive number of free radicals in cells is called “oxidative stress”. Oxidative stress is dangerous because it damages the cells. The structural damage to neurons can occur in different areas: the cell membrane, the organelles inside the neuron, or the DNA can be damaged (Delwing, 2003). If the neuron structure is damaged, it will no longer function properly. This mechanism resembles the functions of GNPTAB, GNPTG, and NAGPA genes, the first gene mutations discovered to be related to stuttering. These three genes are involved in the production of two enzymes associated to the cell’s garbage disposal system (Kang et al., 2010).

Persistent sleep deprivation can also damage the brain through changing gene expression. There are genes activated just at wakefulness, others are activated just at sleep, and still others are activated by sleep deprivation. In the mouse brain, for example, about 2,000 genes are turned on and off from wakefulness to sleep. So, it is possible that sleep disorders may precipitate childhood stuttering by turning on genes related to stuttering in children that carry those genes.


Sleep, breathing, and brain damage

Breathing problems during sleep reduce oxygen levels to the brain (Blunden & Beebe, 2006). The brain is the body organ most sensitive to the lack of oxygen. Reductions from 4 to 10% in the saturation level of arterial oxygen causes hypoxia to the brain (Barbosa et al., 2006). Repetitive reductions in the level of oxygen to the brain causes an increase of free radicals due to a specific biochemical reaction in mitochondrias (Barbosa et al., 2006; Blunden & Beebe, 2006). Mo< The lack of oxygen causes neuron death if it persists for 30 minutes or longer (Barbosa et al., 2006). When it lasts less than that (as in the case of sleep-disordered breathing), the neuron can be reoxygenated. On one hand, reoxygenation prevents neuron death but, on the other hand, it damages the neuron due to several biochemical reactions that release free radicals (Barbosa et al., 2006). Thus both lack of oxygen and reoxygenation start a biochemical reaction that releases free radicals, increasing oxidative stress in neurons.

So, the first consequence of oxidative stress is neuron damage. The second consequence is impairment in neuronal function. One of the impaired functions is “long-term potentiation”, which is related to learning (Blunden & Beebe, 2006). Children with sleep-disordered breathing have worse performance in intelligence, memory, and executive function tests, show vocabulary and verbal fluency deficits, and have worse school performance in comparison to children without sleep-disordered breathing (Blunden & Beebe, 2006; Gottlieb et al., 2004). These differences in performance may be detected even in children as young as five years old (Gottlieb et al., 2004). But what kind of breathing problems can cause such differences in performance? Only more serious ones, like obstructive sleep apnea? Sleep obstructive apnea certainly can, but also simple breathing problems (like snoring and noisy breathing) may cause such deficits (Gottlieb et al., 2004). Moreover, children from the ages of 6 to 16 years old with sleep obstructive apnea have a higher probability of damage to hippocampus and frontal cortex The first is related to long-term memory and the second, to language and executive functions (Halbower et al., 2006).

The conclusion is clear: sleep-disordered breathing should be identified and treated as soon as possible (Simmons & Clark, 2009). This prevents, or at least stops, potential brain damage.


On the other hand.. . .

Macey et al. (2002) analyzed brain morphology of 21 men with and 21 men without sleep obstructive apnea. They found brain lesions (loss of grey matter) in the group with apnea. Some of the lesions were localized only in one side of the brain. The authors concluded that unilateral brain damages could not be caused by advent of apnea. All unilateral lesions were related to somatic sensations, motor function, or breathing control. <0> One of the unilateral lesions was in Broca’s area (Brodmann 45), which also is a brain area affected in people who stutter. The authors discovered that 8 of the 21 adults with apnea had a stuttering history (compared to only 2 of the 21 subjects in the control group). The authors suggested that stuttering may be a predisposing factor for developing sleep apnea.

Other lesions occurred in both sides of the brain. In this case, they were considered consequences of repetitive episodes of lack of oxygen. One of these lesions was to the posterior parietal cortex (Brodmann 7), which may have negative consequences to speech rehabilitation (see above).

Therefore, this research showed a vicious cycle. On one hand, brain damage in people who stutter increases the chances of developing sleep apnea. On the other hand, brain damage caused by sleep apnea increases difficulties in remediation in speech therapy.



It is well established that sleep disorders are risk factors for mental disorders (O’Brien, 2009). It may be the case they are also risk factors for the beginning and persistence of stuttering.

Sleep disorders may worsen stuttering through several mechanisms:

  1. Impairment of removal of free radicals, increasing oxidate stress in brain cells.
  2. Turning on genes related to stuttering.
  3. Increasing muscle tension in the vocal tract.
  4. Impairment of cognitive functions that support speech fluency.
  5. Damaging the posterior parietal cortex, which impairs the ability to consciously perceive somatic sensations related to speech production.
  6. Damaging the orbitofrontal cortex, which impairs the assignment of affective values of speech related experiences.

In conlusion, it is necessary to include sleep hygiene measures as basic procedures of speech therapy and when it is necessary, referring to a neurologist or otorhinolaryngologist.




Altena, E.; Vrenken, H.; Van Der Werf, Y.; Van den Heuvel. O. A. & Van Someren, E. J. W. (2010). Reduced Orbitofrontal and Parietal Gray Matter in Chronic Insomnia: A Voxel-Based Morphometric Study. Biological Psychiatry, 67 (2), 182-185.

Barbosa, L. F.; Medeiros, M. H. G. & Augusto, O. (2006). Danos oxidativos e neurodegeneracao: o que aprendemos com animais transgenicos e nocautes? Quimica Nova, 29 (6). Link.

Bencaa, R.; Duncanb, M. J.; Frankc, E.; McClungd, C.; Nelsone, R. J. & Vicenticf, A. (2009). Biological rhythms, higher brain function, and behavior: Gaps, opportunities, and challenges. Brain Research Reviews, 62 (1), 57-70.

Blunden, S. L. & Beebe, D. W. (2006). The contribution of intermittent hypoxia, sleep debt and sleep disruption to daytime performance deficits in children: Consideration of respiratory and non-respiratory sleep disorders. Sleep Medicine Reviews, 10 (2), 109-118.

Delwing, D. (2003). Estudo do papel do estresse oxidativo em cortex cerebral de ratos submetidos ao modelo experimental de hiperprolinemia tipo II. Master’s dissertation. Federal University of Rio Grande do Sul (Brazil). Link.

Gottlieb, D. J.; Chase, C.; Vezina, R. M.; Heeren, T. C.; Corwin, M. J.; Auerbach, S. H.; Weese-Mayer, D. E. & Lesko, S. M. (2004). Sleep-disordered breathing symptoms are associated with poorer cognitive function in 5-year-old children. The Journal of Pediatrics, 145 (4), 458-464.

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Guyton, A. C. & Hall, J. E. (1996b). Somatic sensations: I. General organization; the tactile and position senses. In: Textbook of medical physiology (pp. 595-607). 9th ed. Philadelphia: W.B. Saunders.

Halbower, A. C.; Degaonkar, M.; Barker, P. B.; Earley, C. J.; Marcus, C. L.; et al. (2006). Childhood Obstructive Sleep Apnea Associates with Neuropsychological Deficits and Neuronal Brain Injury. PLoS Medicine 3(8): e301. Link.

Kang, C.; Riazuddin, S.; Mundorff, J.; Krasnewich, D.; Friedman, P.; Mullikin, J. C. & Drayna, D. (2010). Mutations in the Lysosomal Enzyme-Targeting Pathway and Persistent Stuttering. New England Journal of Medicine, 362, 677-685.

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Jan, J. E.; Reiter, R. J.; Bax, M. C. O.; Ribary, U.; Freeman, R. D. & Wasdell, M. B. (2010). Long-term sleep disturbances in children: A cause of neuronal loss. European Journal of Paediatric Neurology, 14 (5), 380-390.

Macey, P. M.; Henderson, L. A.; Macey, K. E.; Alger, J. R.; Frysinger, R. C.; Woo, M. A.; Harper, R. K.; Yan-Go, F. L. & Harper, R. M. (2002). Brain Morphology Associated with Obstructive Sleep Apnea. American Journal of Respiratory and Critical Care Medicine, 166 (10), 1382-1387.

O’Brien, L. M. (2009). The Neurocognitive Effects of Sleep Disruption in Children and Adolescents. Child and Adolescent Psychiatric Clinics of North America, 18 (4), 813-823.

Schmidt, C.; Colletteab, F.; Cajochenc, C. & Peigneuxd. P. (2007). A time to think: Circadian rhythms in human cognition. Cognitive Neuropsychology, 24 (7), 755-789.

Simmons, M. S. & Clark, G. T. (2009). The Potentially Harmful Medical Consequences of Untreated Sleep-Disordered Breathing: The Evidence Supporting Brain Damage. The Journal of the American Dental Association, 140 (5), 536-542.


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