When Words Get Stuck: The Complex Causes Behind Stuttering

Cherrie Chang

Illustrations by Iona Duncan

A king sits before a microphone, moments before addressing his entire nation. Despite his position and power, anxiety ripples through him. Sweat soaks through his suit and into the cushioning of his chair. He starts to speak: “Through the…” He falters, then continues, “…wireless… one of the marvels of…” Seated close to him, his father raises an eyebrow and advises him to take his time. The man hesitates, suffocated by fear and the tightness of his necktie. He tries to go on, “…m-modern… science…” Every word is a struggle. “Just try it!” His father barks at him in anger. The king tries to continue, but the words only form a lump in his throat. Disappointed, his father walks away.

This is how the film The King’s Speech depicts King George VI stuttering through his Christmas day speech. From his exchange with his father, we can see the overwhelming stress that many stutterers experience. While it may be tempting to ease the anxiety of a stutterer by saying “take your time, relax, you’ll get it out,” these kinds of responses misunderstand the complex mechanisms that actually drive a person’s stutter. John Hendrickson, a stutterer and senior editor at The Atlantic, explains that contrary to popular belief, stuttering is a neurological condition caused by many factors, and is not solely anxiety-induced [1]. In fact, anxiety usually follows stuttering, especially when the stutterer is being pressured by the listener through aggressive prompting like “just try it!” [2, 3] To become truly compassionate listeners to an individual who stutters, it is important to understand the neurological mechanisms underlying stuttering and how they interact with the vast network of genetic, developmental and other factors that shape a stutterer’s unique speech pattern.

What is Stuttering?

Stuttering, also known as stammering, is a speech disorder where an individual’s flow of speech is disrupted by irregular features like repeated sounds, prolonged words, and long pauses. Historically, stuttering has been primarily treated as a uniform disorder without any further subdivisions. Despite the diversity of causes behind each person’s stutter, there is currently no official classification of stuttering into subtypes in the U.S. [4, 5, 6]. In many attempts at classification, stuttering has been grouped by behavior, brain activity, and other factors [7, 8].

While classifications differ, stuttering is often divided into three subtypes: developmental, neurogenic, and psychogenic [9]. Developmental stuttering refers to the repetition of words and phrases by young children when first learning a language — imagine a flustered 4-year-old with balled up fists, howling “I-I-think-I think you’re lying!” This type of stuttering is not seen as a disorder, but simply typical in language acquisition, and it usually subsides when the child reaches the age of five [10, 11]. However, stuttering that persists beyond this age becomes a cause for concern and leads physicians to look for deeper causes. Neurogenic stuttering characterizes cases where the stutter stems from injury, disease, or dysfunction of the brain, while psychogenic stuttering is usually used to classify cases caused by psychological stress or trauma [9, 12].

A perfect classification is difficult for most stuttering cases, however, because of the complexity of its causes. For instance, it is nearly impossible to distinguish neurogenic and developmental stuttering based only on how someone speaks [13]. Case reports have also complicated classification further by showing that neurogenic stuttering can involve damage to almost any brain region, from areas associated with movement to those that process auditory information [7]. Due to the distinct nature of the damage, many clinicians treat stuttering on a case-by-case basis, customizing treatment plans for each individual [13, 14]. Some patients benefit from therapy that focuses on cultivating their in-the-moment awareness during speech; some find physical training like breathing exercises more helpful; and others develop speech strategies like circumlocution, where they replace difficult words with longer but easier sentences on the go [15]. The individualization of stuttering treatment stems from the diversity of stuttering causes. Therefore, while it is imperative to explore the neurological mechanisms behind stuttering, we should also recognize that these three categories are tentative and overlapping, demonstrating the complex nature of stuttering’s causes. 




The Neurological Mechanisms of Stuttering

The irregularities in a stutterer’s speech can be characterized into three types — repetitions, prolongations and blocks. Repetitions refer to stutters where sounds, syllables or words get repeated, like “this-this st-stutter.” Prolongations involve extending sounds or syllables in speech, like in “pro-looooooooongation” instead of “prolongation.” Blocks indicate long gaps in speech, usually occurring between the beginnings of words. In a New York Times interview about his experience with stuttering, John Hendrickson demonstrates these stuttering patterns, tripping over his description of stuttering itself: “right after a really long painful block,” he starts, “is momentary relief and exhaustion, you typically have a large… exhale.” Here, he blocks before “exhale” [1].

Several attempts have been made to determine the neurological mechanisms behind each stutter type. One highly utilized approach is to identify the areas of the brain involved in stuttering by analyzing neuroimaging data from individual patients. The findings between these cases and neuroimaging data does not always line up: there was a Vietnam War soldier who acquired stuttering after missile wounds to both sides of their brain, a 68-year old man who developed a stutter following damage to a large area in the middle of his brain, and several stroke patients who had begun to stutter after suffering cell death in a wide range of brain areas [16, 17, 18]. Stuttering, therefore, can arise from damage to almost any site in the brain [17, 19, 20]. Recently, however, more findings have shown stuttering to be more strongly correlated with damage to two brain areas — the thalamus and the basal ganglia — which are both important components of the brain’s motor pathways for producing voluntary movements [21, 22]. The connection between stuttering, the thalamus, and the basal ganglia offers a promising start to uncovering the mechanisms behind stuttering. By examining the roles played by the thalamus and the basal ganglia, we can analyze how damage to these regions could disrupt the flow of speech.

The Steps of a Stutter

One important function of the thalamus is to relay signals between brain structures involved in motor coordination. Imagine saying the word “prolongation:” first, the sequence of motor movements involved in saying “prolongation” has to be planned. This planning is done by the motor areas of your cerebral cortex, the neurons in the wrinkly outer layer of the brain that performs sophisticated cognitive functions, like decision-making and movement-planning [23]. After the motor areas of the cerebral cortex create the blueprint for a movement, they send signals to the brain structures that coordinate the sequential movements of all the muscles involved in speech, from contracting your diaphragm to pressing your lips together for the “p.” The thalamus mediates communication in this pathway by regulating how signals are relayed between the cerebral cortex and the lower structures [23]. When there is damage to your thalamus, the normal flow from planning to say “prolongation” to actually saying it is disrupted. In other words, you experience a block in speech.

Another theory of stuttering’s origin in the brain focuses on the basal ganglia and its role in controlling the sequence of motor movements in speech [21, 24]. When you try to say “prolongation,” you are not just trying to create a single motion that results in the entire pronunciation of “prolongation.” Rather, you are making a series of correctly timed movements to utter each syllable — “pro-lon-ga-tion” — smoothly and sequentially. To time pronunciation correctly, your basal ganglia generates an internal timing cue after each syllable, signaling the next one to be pronounced. If your basal ganglia could speak in your ear, it would almost sound like an in-ear monitor cueing each syllable you utter with “1, 2, 3, go!” Now imagine this is occurring rapidly in between each syllable: “pro”—  1, 2, 3, go! — “lon” — 1, 2, 3, go! — “ga”... and so on. Damage to the basal ganglia impairs the brain’s ability to provide these cues and leads you to repeat the previous syllable like a broken record [21, 24]. “Pro-” you start, but your basal ganglia fails to cue for the “-lon.” “Pro-pro-prolo…” your brain fails to find the cue for “ga,” so you are stuck “prolonging” this syllable. “Prolooooooon…gation,” you finish. Together, these two theories propose explanations for the variety of stutter types in terms of impairments to the motor pathways leading to speech. However, the wide range of brain regions that could result in stuttering when damaged suggests that not only is there room for many more explanations, but that looking at neurological explanations alone may not be enough to understand the causes of a stutter. Instead, we must understand how the neurological mechanisms of stuttering interact with its larger network of other causal factors.

Getting to the Roots of a Stutter

The complexity of the causes behind stuttering is best illustrated by stuttering that begins at a young age and persists beyond the age of five, which often involves not only a neurological component, but genetic, developmental and social components as well [25, 26, 27]. For instance, mapping the family heritage of real developmental stuttering cases has revealed patterns in stuttering’s inheritance: stuttering is more likely to be passed from a parent onto their child of the opposite sex, boys in particular. Compared to a boy with a stuttering father, a boy with a stuttering mother is more likely to develop and not recover from stuttering, and is also more likely to stutter than his sister [27, 28]. Behind this pattern are four genes that determine the process by which molecules are packaged and transported between structures within each cell, which is called intracellular transportation [29]. A mutation in one or more of these four genes affects the normal functioning of a cell [29]. This mutation can damage the intracellular transportation of many cells at once, so if this damage is concentrated in a particular brain region, the malfunctioning in its composite cells will impair the region’s overall function [30]. When this region is one involved in stuttering, such as the thalamus or basal ganglia, speech production will be compromised [21, 31]. By integrating this genetic explanation and neurological mechanisms, we may achieve a more comprehensive understanding of the causes behind stuttering.

While genetic mutations may kickstart stuttering, a stutterer’s individual developmental process plays a large role in shaping their stutter [32]. Twin studies show that shared environmental variables — such as excessive parental concern about imperfect speech, competitive families and perfectionistic household cultures — can cause stuttering to persist or make it difficult to overcome [32]. As documented in The King's Speech, King George VI was raised under the immense pressure of being a royal, and his father’s high expectations and pronounced disappointment had always been constants in his life [33]. If we imagine that the king had an identical twin living in a less stressful household, with parents who did not pressure him for smooth speech, perhaps that twin could have grown up to have a milder stutter or even none at all. Even if a stutterer carries the relevant genetic mutations for stuttering, how strongly these mutations are expressed to affect the person’s speech-production is heavily influenced by the environmental factors surrounding their childhood [32].

Stuttering Under Stress

One final important contributor to a stutter is the moment-to-moment emotional state of the person. When a stutterer is faced with a stressful situation, they may anticipate that they will stutter through their words and subsequently feel anxious [34]. This freezes some of their vocal muscles in what is called an involuntary stress response, making it even more difficult for them to speak [35]. In The King’s Speech, King George VI stutters through most of his sentences, but he struggles the most during public speeches, or whenever he is under father’s piercing gaze [33]. His stutter pattern echoes evidence suggesting that stuttering occurs more frequently when the stutterer faces increased difficulty in their linguistic task or emotional stress, especially when they are treated with impatience from their audience [2, 24, 36]. King George VI, for instance, stumbles over the long and convoluted speeches he has to give in front of thousands of people, but manages to consistently speak eloquently to his speech therapist [33].

In fact, handling stress during speech is one of many highly successful techniques stutterers use to manage stuttering [37]. Some stutterers report feeling intense urgency and fear during conversations, as they feel the need to respond to their audience in a timely manner, while predicting that they will need more time to speak without stuttering. To manage this, they try to resist the urge to respond immediately, allowing themselves to slow their rate of speech, resulting in slower, but much more fluent speech. To be able to employ this strategy in conversations on the spot, stutterers often train themselves in their own time by learning to take a broader perspective on their stutter, distancing their sense of self-worth from their self-criticism of their stuttering [37, 38]. These reports affirm the significant effect stress has on stuttering, in the form of immediate pressure during conversations but also as a pervasive anxiety stutterers face every day when their self-confidence is harmed by their disdain towards their own stutter.


How Can We Support Stutterers?

A stutterer’s speech is continually shaped from birth to death, with genes and environmental factors interacting to mold how their nervous system produces speech. Even within a single moment, a stutterer’s speech patterns fluctuate according to the difficulty of the subsequent word and stress. Because of the constant variation in stutter patterns, people studying stuttering are moving towards analyzing stuttering as a dynamic system of interacting causal factors [39]. Recognizing the complexity behind stuttering is crucial to correct any misconceptions of it. By patiently listening to those who stutter, we may be able to shatter the unwarranted stigma surrounding stuttering.


References

  1. Robinson, J. (2022, August 23). I stutter. This is what you're not hearing. The New York Times.

  2. Choi, D., Conture, E., Walden, T., Jones, R., & Kim, H. (2016). Emotional diathesis, emotional stress, and childhood stuttering. Journal of Speech, Language, and Hearing Research, 59(4). doi: 10.1044/2015_JSLHR-S-14-0357

  3. Edgren, B., Leanderson, R., & Levi, L. (1970). A research programme on stuttering and stress. Acta Oto-Laryngologica, 69(sup263), 113–118. doi: 10.3109/00016487009131533

  4. Ajdacic-Gross, V., Bechtiger, L., Rodgers, S., Müller, M., Kawohl, W., von Känel, R., Mutsch, M., Rössler, W., Seifritz, E., Castelao, E., Strippoli, M.-P. F., Vandeleur, C., Preisig, M., & Howell, P. (2018). Subtypes of stuttering determined by latent class analysis in two Swiss epidemiological surveys. PLOS ONE, 13(8). doi: 0.1371/journal.pone.0198450

  5. Cohen, J. (2014). A new name for stuttering in DSM-5. American Psychological Association, 45(7), 51.

  6. Yairi, E. (2007). Subtyping stuttering I: A review. Journal of Fluency Disorders, 32(3), 165–196. doi: 10.1016/j.jfludis.2007.04.001

  7. Jiang, J., Lu, C., Peng, D., Zhu, C., & Howell, P. (2012). Classification of types of stuttering symptoms based on brain activity. PLOS ONE, 7(6), e39747. doi: 10.1371/journal.pone.0039747

  8. Prasse, J. E., & Kikano, G. E. (2008). Stuttering: An Overview. American Family Physician, 77(9), 1271–1276. PMID: 18540491

  9. Costa, D., & Kroll, R. (2000). Stuttering: An update for physicians. CMAJ: Canadian Medical Association Journal, 162(13), 1849–1855. PMID: 10906923

  10. Lawrence, M., & Barclay, D. M. (1998). Stuttering: A brief review. American Family Physician, 57(9), 2175–2178. PMID: 9606307

  11. Reilly, S., Onslow, M., Packman, A., Cini, E., Conway, L., Ukoumunne, O. C., Bavin, E. L., Prior, M., Eadie, P., Block, S., & Wake, M. (2013). Natural History of Stuttering to 4 Years of Age: A Prospective Community-Based Study. Pediatrics, 132(3), 460–467. doi: 10.1542/peds.2012-3067

  12. Almada, A., Simões, R., Constante, M., Casquinha, P., & Heitor, M. J. (2016). Psychogenic stuttering: A case and review. European Psychiatry, 33(S1), S386–S387. doi: 10.1016/j.eurpsy.2016.01.1389

  13. Van Borsel, J., & Taillieu, C. (2001). Neurogenic stuttering versus developmental stuttering: An observer judgment study. Journal of Communication Disorders, 34(5), 385–395. doi: 10.1016/S0021-9924(01)00057-0

  14. Craig-McQuaide, A., Akram, H., Zrinzo, L., & Tripoliti, E. (2014). A review of brain circuitries involved in stuttering. Frontiers in Human Neuroscience, 8. doi: 10.3389/fnhum.2014.00884

  15. Sønsterud, H., Halvorsen, M. S., Feragen, K. B., Kirmess, M., & Ward, D. (2020). What works for whom? Multidimensional individualized stuttering therapy (MIST). Journal of Communication Disorders, 88, 106052. doi: 10.1016/j.jcomdis.2020.106052

  16. Ludlow, C. L., Rosenberg, J., Salazar, A., Grafman, J., & Smutok, M. (1987). Site of penetrating brain lesions causing chronic acquired stuttering. Annals of Neurology, 22(1), 60–66. doi: 10.1002/ana.410220114

  17. Lundgren, K., Helm-Estabrooks, N., & Klein, R. (2010). Stuttering following acquired brain damage: A review of the literature. Journal of Neurolinguistics, 23(5), 447–454. doi: 10.1016/j.jneuroling.2009.08.008

  18. Norman, R. S., Jaramillo, C. A., Eapen, B. C., Amuan, M. E., & Pugh, M. J. (2018). Acquired Stuttering in Veterans of the Wars in Iraq and Afghanistan: The Role of Traumatic Brain Injury, Post-Traumatic Stress Disorder, and Medications. Military Medicine, 183(11–12), e526–e534. doi: 10.1093/milmed/usy067

  19. Grant, A. C., Biousse, V., Cook, A. A., & Newman, N. J. (1999). Stroke-Associated Stuttering. Archives of Neurology, 56(5), 624–627. doi: 10.1001/archneur.56.5.624

  20. Lebrun, Y., Leleux, Ch., & Retif, J. (1987). Neurogenic stuttering. Acta Neurochirurgica, 85, 103–109. doi: 10.1007/BF01456105

  21. Chang, S. E., & Guenther, F. H. (2020). Involvement of the Cortico-Basal Ganglia-Thalamocortical Loop in Developmental Stuttering. Frontiers in Psychology, 10. doi: 10.3389/fpsyg.2019.03088

  22. Sherman, S. M., & Guillery, R. W. (2006). Exploring the thalamus and its role in cortical function, 2nd ed (pp. xxi, 484). MIT Press.

  23. Bosch-Bouju, C., Hyland, B., & Parr-Brownlie, L. (2013). Motor thalamus integration of cortical, cerebellar and basal ganglia information: Implications for normal and parkinsonian conditions. Frontiers in Computational Neuroscience, 7. doi: 10.3389/fncom.2013.00163

  24. Alm, P. A. (2004). Stuttering and the basal ganglia circuits: A critical review of possible relations. Journal of Communication Disorders, 37(4), 325–369. doi: 10.1016/j.jcomdis.2004.03.001

  25. Ingham, R. J., Ingham, J. C., Finn, P., & Fox, P. T. (2003). Towards a functional neural systems model of developmental stuttering. Journal of Fluency Disorders, 28(4), 297–318. doi: 10.1016/j.jfludis.2003.07.004

  26. Ludlow, C. L., & Loucks, T. (2003). Stuttering: A dynamic motor control disorder. Journal of Fluency Disorders, 28(4), 273–295. doi: 10.1016/j.jfludis.2003.07.001

  27. Kraft, S. J., & Yairi, E. (2012). Genetic bases of stuttering: The state of the art, 2011. Folia Phoniatrica et Logopaedica, 64(1), doi: 10.1159/000331073

  28. Bloodstein, O., & Ratner, N. B. (2008). A handbook on stuttering (6th ed). Thomson Delmar Learning. 

  29. Frigerio‐Domingues, C., & Drayna, D. (2017). Genetic contributions to stuttering: The current evidence. Molecular Genetics & Genomic Medicine, 5(2), 95–102. doi: 10.1002/mgg3.276

  30. 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. The New England Journal of Medicine, 362(8), 677–685. doi: 10.1056/NEJMoa0902630

  31. Andy, O. J., & Bhatnagar, S. C. (1991). Thalamic-Induced Stuttering (Surgical Observations). Journal of Speech, Language, and Hearing Research, 34(4), 796–800. doi: 10.1044/jshr.3404.796

  32. Felsenfeld, S., Kirk, K. M., Zhu, G., Statham, D. J., Neale, M. C., & Martin, N. G. (2000). A study of the genetic and environmental etiology of stuttering in a selected twin sample. Behavior Genetics, 30(5), 359–366. doi: 10.1023/A:1002765620208

  33. Hooper, T. (Director). (2010, November 26). The King’s Speech [Drama/History].

  34. Alm, P. A. (2004a). Stuttering, emotions, and heart rate during anticipatory anxiety: A critical review. Journal of Fluency Disorders, 29(2), 123–133. doi: 10.1016/j.jfludis.2004.02.001

  35. Góral - Półrola, J., Żychowska, M., Ziółkowski, A., & Pąchalska, M. (2015). Changes in gene expressions associated with cell stress in the patient with chronic preservative stuttering. Acta Neuropsychologica, 13, 417–424.

  36. Natke, U., Grosser, J., Sandrieser, P., & Kalveram, K. T. (2002). The duration component of the stress effect in stuttering. Journal of Fluency Disorders, 27(4), 305–318. doi: 10.1016/S0094-730X(02)00163-8

  37. Plexico, L., Manning, W. H., & DiLollo, A. (2005). A phenomenological understanding of successful stuttering management. Journal of Fluency Disorders, 30(1), 1–22. doi: 10.1016/j.jfludis.2004.12.001

  38. Plexico, L., Manning, W. H., & Levitt, H. (2009). Coping responses by adults who stutter: Part II. Approaching the problem and achieving agency. Journal of Fluency Disorders, 34(2), 108–126. doi: 10.1016/j.jfludis.2009.06.003

  39. Smith, A., & Weber, C. (2017). How stuttering develops: The multifactorial dynamic pathways theory. Journal of Speech, Language, and Hearing Research, 60(9), 2483–2505. doi: 10.1044/2017_JSLHR-S-16-0343


References

  1. Medvei, V. C. (1987). The illness and death of Mary Tudor. Journal of the Royal Society of Medicine, 80(12), 766–770. doi: 10.1177/014107688708001214

  2. Small, G. W. (1986). Pseudocyesis: An overview. Canadian Journal of Psychiatry. Revue Canadienne de Psychiatrie, 31(5), 452–457. doi: 10.1177/070674378603100514

  3. Azizi, M., & Elyasi, F. (2017). Biopsychosocial view to pseudocyesis: A narrative review. International Journal of Reproductive Biomedicine, 15(9), 535–542. PMID: 29662961

  4. Campos, S. J., Link D. (2016). Pseudocyesis. The Journal for Nurse Practitioners. 12, 390–394. doi: 10.1016/j.nurpra.2016.03.009

  5. Dubravko, H. (2010). Pseudocyesis in peri- and postmenopausal women. Open Medicine, 5(3). doi: 10.2478/s11536-009-0084-8

  6. Seeman, M. V. (2014). Pseudocyesis, delusional pregnancy, and psychosis: The birth of a delusion. World Journal of Clinical Cases, 2(8), 338. doi: 10.12998/wjcc.v2.i8.338 

  7. Ibekwe, P., & Achor, J. (2008). Psychosocial and cultural aspects of pseudocyesis. Indian Journal of Psychiatry, 50(2), 112. doi: 10.4103/0019-5545.42398

  8. Tarín, J. J., Hermenegildo, C., García-Pérez, M. A., & Cano, A. (2013). Endocrinology and physiology of Pseudocyesis. Reproductive Biology and Endocrinology, 11(1), 39. doi: 10.1186/1477-7827-11-39 

  9. Rawindraraj, A. D., Basit, H., & Jialal, I. (2020). Physiology, anterior pituitary. StatPearls Publishing. PMID: 29763073

  10. Ozturk, S., & Demir, R. (2010). Particular functions of estrogen and progesterone in establishment of uterine receptivity and embryo implantation. Histology and  Histopathology, 25(9), 1215–1228. doi: 10.14670/HH-25.1215

  11. Pascual, Z. N., & Langaker, M. D. (2020). Physiology, pregnancy. StatPearls Publishing. PMID: 32644730

  12. Grover, S., Sharma, A., Ghormode, D., & Rajpal, N. (2013). Pseudocyesis: A complication of antipsychotic-induced increased prolactin levels and weight gain. Journal of pharmacology & pharmacotherapeutics, 4(3), 214–216. doi: 10.4103/0976-500X.114610

  13. Freeman, M. E., Kanyicska, B., Lerant, A., & Nagy, G. (2000). Prolactin: Structure, function, and regulation of secretion. Physiological Reviews, 80(4), 1523–1631. doi: 10.1152/physrev.2000.80.4.1523

  14. Bazer, F.W. (Ed.). (1998). Endocrinology of pregnancy. Humana Press Inc. doi: 10.1007/978-1-4612-1804-3

  15. Bargiota, S. I., Bonotis, K. S., Messinis, I. E., & Angelopoulos, N. V. (2013). The effects of antipsychotics on prolactin levels and women’s menstruation. Schizophrenia Research and Treatment, 2013, 1–10. doi: 10.1155/2013/502697

  16. Maguire, G. (2002). Prolactin elevation with antipsychotic medications: Mechanisms of action and clinical consequences. Journal of Clinical Psychiatry. PMID: 11913677

  17. Majumdar, A., & Mangal, N. S. (2013). Hyperprolactinemia. Journal of human reproductive sciences, 6(3), 168–175. doi: 10.4103/0974-1208.121400

  18. Salleh, M. R. (2008). Life events, stress and illness. Malays J Med Sci, 10(4), 9-18. doi: 10.1016/j.nurpra.2016.03.009

  19. Aguilera, G. (1998). Corticotropin releasing hormone, receptor regulation and the stress response. Trends in Endocrinology & Metabolism, 9(8), 329–336. doi: 10.1016/s1043-2760(98)00079-4

  20. Froude, J. A. (1924). The reign of Mary Tudor. Dent.

  21. Ouj, U. (2009). Pseudocyesis in a rural southeast Nigerian community. The journal of obstetrics and gynecology research, 35(4), 660–665. doi: 10.1111/j.1447-0756.2008.00997.x

  22. Reblin, M., & Uchino, B. N. (2008). Social and emotional support and its implication for health. Current opinion in psychiatry, 21(2), 201–205. doi: 10.1097/YCO.0b013e3282f3ad89

Previous
Previous

Running Up That Hill: The Stranger Things About Listening to Music

Next
Next

A Little-Known Side Effect of Chemotherapy: Chemotherapy-Induced Peripheral Neuropathy