About the presenter: Nathan E. Lavid, M.D. is psychiatrist in private practice in Southern California. He received his bachelor of arts in microbiology and subsequently his medical degree from the University of Kansas. He completed his internship and psychiatric residency at the University of California, Irvine. He is a former faculty member at the University of Southern California School of Medicine, where he completed a forensic psychiatry fellowship at the Institute of Psychiatry and Law. He has been involved in a wide range of neuroscience research, including the first clinical trial of olanzapine for stuttering.

You can post Questions/comments about the following paper to Nathan Lavid before October 22, 2002.

The relevance of speech therapy: A physician's viewpoint from a clinical and neuroscience perspective

by Nathan Lavid
from California, USA

The purpose of this paper is to present in layman terms the relevance of speech therapy for stuttering in light of neuroscience discoveries.

Recent neuroscience research has made a significant impact on the understanding of developmental stuttering. Neuroimaging studies have revealed variations in brain areas associated with language in those who stutter. (1,2) In addition, studies of twins who stutter and families with progeny who stutter have revealed a genetic component to development stuttering. (3,4) This research has provided the foundation for the conceptualization that developmental stuttering is a genetic, brain-based phenomenon.

In line with neuroscience breakthroughs, the treatment of developmental stuttering has become more sophisticated. Even though anticipatory anxiety is a catalyst for dysfluency, research reveals that the relationship between the two is not direct. (5) That is, some individuals who have the most severe forms of stuttering do not have as much anxiety as some with mild dysfluency. This observation allows treatments to be specifically targeted at the anticipatory anxiety and at the dysfluency. This two-pronged approach best prepares the patient to respond to treatment, since these components are not directly related and treating only one does not ameliorate the other.

From a medical standpoint, there are a wide variety of medications -- that have been used safely for decades -- to successfully treat anxiety. In addition, psychopharmacological research has revealed a new class of medications, the "serotonin-dopamine antagonists," show promise in alleviating dysfluency. (6,7) These medications have side effects that can limit their use, such as affecting glucose metabolism, the conduction of the heart, and hormone secretion, but the success revealed with the preliminary data shows that dysfluency can be decreased by medications that target specific chemicals in the brain, which gives further credence to the concept that developmental stuttering is a brain-based condition.

Considering the current understanding of developmental stuttering, the question arises: What role does speech therapy have in treatment of a genetic, brain-based condition where medications can be directed at specific components?

The pragmatic answer to the aforementioned question is simply, a prominent role because it works. Sixty to eighty percent of adults show substantial improvement as a result of speech therapy. (8) As this response rate is noted in adults the efficacy cannot be attributed to spontaneous recovery, which occurs in childhood.

Considering the contemporary understanding of developmental stuttering, the efficacy of speech therapy must be attributed to its effect on brain functioning and genes. Recent advances in neuroscience research have provided an appreciation on how speech therapy accomplishes this.

In 2000, the American psychiatrist Eric Kandel was awarded the Nobel Prize for Physiology and Medicine for his contribution to the understanding of the molecular mechanisms of brain plasticity. Brain plasticity is the ability of the brain to remodel its structure and function in response to outside stimuli. In other words, the brain is not a static, "hardwired" organ, but rather a plastic, malleable organ that changes itself to perform better. (9)

Kandel demonstrated, via a series of experiments with the sea snail Aplysia, that neuronal cells (cells that comprise the brain) develop stronger connections through a molecular mechanism termed "long-term potentiation." Long-term potentiation simply means that the stronger neuronal response (potentiation) is sustained (long-term). In order to have a sustained, stronger neuronal response, their needs to be increased connections between neurons in the network -- commonly called an increase in synaptic connections -- and physical growth of the neuronal network. This increased growth and connectivity depends on new protein synthesis. Proteins are molecules that regulate the biochemical processes of life, i.e., they are the machinery for our development and metabolism. And, the only means by which the proteins necessary for long-term potentiation arise is via new gene expression.

Once conceived, one's genetic make up is set. However, how one's genes are expressed throughout life depends on a variety of influences. The remarkable aspect of Kandel's work was that genes necessary for long-term potentiation in Aplysia were expressed by repeated environmental stimuli. That is, environmental factors -- in this case repeated stimulation of the snail that modulated its gill reflex -- initiated Aplysia to turn on specific genes. This process -- a new behavior elicited by repeated stimuli -- is analogous to learning. (10) And, in short, this discovery showed that learning affected the transcription of genes and this directly changed the neuronal makeup of the snail.

Kandel's work set the stage for the understanding of the molecular mechanism of learning, and, indeed, these findings have been extended in humans. (11,12) Circuits within the hippocampus -- an area deep within each cerebral hemisphere important for the formation of memory and learning -- are highly plastic and this plasticity is mediated in part by long-term potentiation.

In addition to the new understanding of the molecular mechanisms of brain plasticity, clinical observations and experimental paradigms have revealed some other facets of the phenomenon. First, there are "critical periods" where the brain is more malleable to learning. As a critical period relates to language and possibly developmental stuttering, infants perceptually map aspects of language before they can speak, that is, children's brains change and prepare for the development of language before they have the physical means by which to express language. (13) Also, as demonstrated by the ease by which children learn second languages compared to adults, language abilities are more easily learned and developed in childhood. While current scientific query has not revealed a specific delineation of a critical period for language, the general consensus is that language development and the brain's remodeling of such development occurs during early childhood.

The second aspect noted with brain plasticity is that the phenomenon is "activity-dependent," which simply means that the brain's plastic response is dependent on the level of environmental activity, i.e., the amount and quality of information exposed to the senses. (14) The activity-dependent component of brain plasticity is analogous to the efforts of an athlete training to improve skill and strength. Over time, the athlete's efforts and practice will induce coordination and stronger muscles. Likewise, over time, a stimulated brain will become stronger and more efficient.

Even though brain plasticity is associated with critical periods and certain aspects of brain development are more plastic during childhood, the activity-dependent phenomenon occurs throughout life. In fact, recent research of the phenomenon reveals that a stimulating environment induces positive brain changes in older adults that can be detected at the molecular level. For example, adult mice raised in an enriched, stimulating environment are more active and show more improvement in learning than control mice. Autopsy of the brains of these mice raised in a stimulating environment revealed they had stronger neuronal networks than controls. (15) While autopsy investigation of human brains cannot be performed as has been done in mice, clinical medicine documents that leading an active, stimulating life benefits brain function for the aged as well as the young. (16) The appealing aspect of these clinical observations is that they can be explained at the molecular level via the activity-dependent property of brain plasticity.

Both of these components of brain plasticity have implications in the therapeutic treatment of developmental stuttering. From a conceptual viewpoint, the critical period of language development could contribute to the spontaneous recovery noted in children with developmental stuttering. Possibly, the brain of the young child who stutters adapts within this critical period of language development to learn fluency. Also, there is a body of literature that demonstrates speech therapy is of most benefit in younger children. (17) However, this observation needs to be viewed in light of high rate of spontaneous recovery noted in developmental stuttering. Even if speech therapy is of most benefit in younger children who stutter, about eighty percent of these children will recover on their own and clinicians must consider the recommendation for speech carefully in young children -- so as not to cause unneeded worry and expense to children and their parents when the stuttering may resolve on its own. Nonetheless, if the decision to engage speech therapy is made at a young age, its efficacy is most likely attributed to the critical period of language development noted in young children and increased brain plasticity at this time.

The activity-dependent aspect of brain plasticity also has clinical implications for the use of speech therapy in adults who stutter. New gene expression and subsequent brain modulation is possible throughout life. The amount of change, and hence improvement, depends on the quality and amount of stimulation and practice. Speech therapy, as revealed by its high response rate in the adult population that stutters, is the right type of positive stimulation to cause such change.

In summary, the plasticity of the brain gives credence to neurological power of teaching. Speech therapy -- verbal instruction and systematic practice -- not only induces fluency as noted clinically, but also influences the function of the brain in a mechanism revealed by cutting-edge neuroscience research. The relevance of speech therapy is not only based on its effectiveness, but also its place in a new era of neuroscience discovery.


1. Foundas AL, Bollich AM, Corey DM, Hurley M, and Heilman KM. Anomalous anatomy of speech-language areas in adults with persistent developmental stuttering. Neurology 2001; 57: 207-215.

2. Sandak R, Fiez JA. Stuttering: a view from neuroimaging. The Lancet 2000: 356: 445-446.

3. Felsenfeld S, Kirk KM, Zhu G, Statham DJ, Neale MC, Martin NG. A study of the genetic and environmental etiology of stuttering in a selected twin sample. Behavior Genetics 2000; 30: 359-366.

4. Ambrose N, Yairi E, Cox N. Early childhood stuttering: genetic aspects. Journal of Speech and Hearing Research 1993; 36: 701-706.

5. Miller S, Watson BC. The relationship between communication attitude, anxiety, and depression in stutterers and nonstutterers. Journal of Speech and Hearing Research 1992; 35: 789-798.

6. Lavid N, Franklin DL, Maguire GA. Management of child and adolescent stuttering with olanzapine: three case reports. Annals of Clinical Psychiatry 1999; 11: 233-236.

7. Maguire GA, Riley GD, Franklin DL, Gottschalk LA. Risperidone for the treatment of stuttering. Journal of Clinical Psychopharmacology 2000; 20: 479-482.

8. Conture EG. Treatment efficacy: stuttering. Journal of Speech and Hearing Research 1996; 39: S18-26.

9. Kandel ER. A new intellectual framework for psychiatry. The American Journal of Psychiatry 1998; 155: 457-469.

10. Antonov I, Antonova I, Kandel ER, Hawkins RD. The contribution of activity-dependent synaptic plasticity to classical conditioning in Aplysia. The Journal of Neuroscience 2001; 21: 6413-6422.

11. Shapiro M. Plasticity, hippocampal place cells, and cognitive maps. Archives of Neurology 2001; 58: 874-881.

12. Beck H. Goussakov IV, Lie A, Helmstaedter C, Elger CE. Synaptic plasticity in the human dentate gyrus. The Journal of Neuroscience 2000; 20: 7080-7086.

13. Kuhl PK, Tsao FM, Liu HM, Zhang Y, De Boer B. Language/culture/mind/brain. Progress at the margins between disciplines. Annals of the New York Academy of Sciences 2001; 935: 136-174.

14. van Praag H, Kempermann G, Gage FH. Neural consequences of environmental enrichment. Nature Reviews Neuroscience 2000; 1: 191-198.

15. Kempermann G, Gast D, Gage FH. Neuroplasticity in old age: sustained fivefold induction of hippocampal neurogenesis by long-term environmental enrichment. Annals of Neurology 2002; 52: 135-143.

16. Fillit HM, Butler RN, O'Connell AW, Albert MS, Birren JE, Cotman CW, Greenough WT, Gold PE, Kramer AF, Kuller LH, Perls TT, Sahagan BG, Tully T. Achieving and maintaining cognitive vitality with aging. Mayo Clinic Proceedings 2002; 77: 681-696.

17. Nicholas A, Millard SK. The case for early intervention with pre-school dysfluent children. International Journal of Language and Communication Disorders 1998; 33 Suppl(5): 374-377.

You can post Questions/comments about the above paper to Nathan Lavid before October 22, 2002.

September 14, 2002