Acquired Stuttering

About the presenter: Henny-Annie Bijleveld, Ph.D. was born in Holland 29-11-46. She studied in French language and linguistics in Holland and in German languages and linguistics in Brussels, Belgium. Post-doctoral studies in Neurolinguistics in Brussels, specialisation in Stuttering. PhD in Neurolinguistics , "A Linguistic Analysis of Acquired Stuttering", Brussels. Professor in Neurolinguistics at the ULB (Universit� Libre de Bruxelles), Brussels. Associated Professor in Applied Linguistics at the ULB, Brussels. Research in the field of developmental and acquired stuttering, in the field of stuttering therapy, and in cross-cultural influences in individual speech output (socio-linguistics). trained therapy Dr. Bijleveld trained with Hugo Gregory of Northwestern University and with Lena Rustin in London and is a member of IFA and IALP and member and representative for Belgium of APB ( Association Parole-B�gaiement), a French association for stuttering which includes stutterers and non-stutterers.

Acquired Stuttering

by Henny Bijleveld
from Belgium

Introduction

Definition: the term "acquired stuttering" is used to indicate the manifestation of stuttering after brain lesion - mostly in adults, who have acquired language. It is also called "neurogenic or neurological stuttering". When stuttering follows brain lesion in children, it is also called neurological stuttering, even if language is not completely acquired.

Compared to the huge amount of existing literature on developmental stuttering, the articles on acquired stuttering occupy a rather small place. The interest in this particular form of stuttering goes back to the end of the 19th century, when Pick (1899) analysed after Kussmaul (1877), the case of stuttering patient who manifested aphasia symptoms as well. Kussmaul had described this phenomenon as ´ aphatisches Stottern ª (aphasic stuttering). The linguistic analysis of this case by Pick revealed the following elements:

1. stuttering in the beginning of difficult words

2. repetitions of syllables and One-syllable- words

3. repetitions of parts of words in the middle of the word

4. possible repetitions of final consonants.

Pick noted the intriguing similarity between these phenomena and those observed in developmental stuttering. He also expressed the hope that they could shed light on the nature of developmental stuttering.

Pick also observed another patient who started to stutter after a lesion in the brainstem, but who did not manifest aphasic symptoms:

´ although (he) repeats his words several times before he finally speaks them, yet exhibits no trace of aphasia ´  (p.466).

Thus the existence of acquired stuttering without aphasia was given as a possibility.

In the analysis of the observed patients, Pick noted the concomitance of acquired stuttering and a lesion in the left- or right hemisphere, as well as cortical and sub-cortical lesions.

The observations of Pick concerning brain lesions and acquired stuttering with or without aphasia have gained interest in the last 30 years. Much recent research on the topic with modern techniques of investigation (CT scan and MRI and functional MRI) has confirmed and corrected Pick’s suppositions. We will see how.

Brain localisation and acquired stuttering

The following three aspects will be treated:

1. Acquired stuttering after cortical lesion in the left hemisphere (with or without aphasia)

2. Acquired stuttering after cortical lesion in the right hemisphere (with or without aphasia)

3. Acquired stuttering after sub-cortical lesion (with or without aphasia).

However, it should be mentioned that it is often hazardous to draw a strict limit between cortical and sub-cortical lesions, as large cortical lesions can easily extend to sub-cortical ones.

1. Acquired stuttering after cortical lesion in the left hemisphere (with or without aphasia).

Luchsinger and Arnold (1970) have used Pick’s terminology (´ stuttering with aphasia ª) to make a distinction between this sort of acquired stuttering (observed by Pick) and ´ aphasic stuttering ª, that they viewed as a psychological stress reaction to aphasia. In the last case, the patient who is conscious about his aphasic condition develops a stutter, because he can not find his words. In their theory, the lesions responsible for the aphasia and the stutter are located in the left hemisphere.

Some researchers like Sapir and Aronson (1990), Roth et al. (1989), Gainotti (1972) have also observed stress reactions in neurological patients with a cortical lesion in the left hemisphere. The studied patients often show a sharp awareness of their linguistic handicap and are worried about it. Besides their aphasia, they do develop depressive behaviour and anxiety. However, according to these authors, the depression and anxiety are not stress reactions to the aphasia, but the consequence of the neurological lesion itself. Sapir and Aronson (1990) give following explanation of their hypothesis:

´ Depression and anxiety have been linked to disturbances of the basal ganglia, thalamus, limbic system, and frontal lobe; These same anatomical structures are also important in voice, speech, language and non-speech motor function. These findings ... suggest that depression and anxiety are likely to coexist with voice, speech, or language disorders as a result of Central Nervous pathology ª (p.503).

Farmer (1975), Ackermann (1994), Mazzucchi et al.(1981) noticed stuttering with aphasia in their patient with a cortical lesion in the left hemisphere. A lesion in the left hemisphere is likely to impair the regions implicated in the production of speech and language, and thus it is not surprising that Farmer came to the conclusion that:

´ ...lesions to the left hemisphere resulting in inefficient language performance may reflect temporal disorganisation in the form of stuttering repetitions ª (p.395).

Acquired stuttering and aphasia can appear and develop rather independently from one another. Indeed, in the case of Rao’s (1990) patient who stuttered after an accident, the aphasic component was only noticed when the stuttering diminished, and in the case of a patient described by Lebrun et al. (1983), the stuttering appeared before the aphasia. Besides, the stuttering and the aphasic signs can develop in a similar and in an opposite way.

On the other hand several authors like Quinn and Andrews (1977), Rosenfield (1972), Helm et al. (1978). mention acquired stuttering without aphasia after cortical lesion. The last authors did not find any indication that:

´ acquired stuttering results from the emotional strain created by aphasia. Only four of ten cases developed stuttering and aphasia concurrently... Two, and possibly four of our patients were never aphasic ª (p.1163).

Through another study, Helm et al. (1980) hypothesized that transient acquired stuttering may be due to unilateral lesions, whereas non-transient stuttering might be the consequence of multiple, bilateral lesions:

´ Transient stuttering, ... was associated with multifocal lesions of the left hemisphere. In no case did the stuttering occur with the first stroke ª (p.273).

Aram et al. (1990) analysed children who started to stutter after brain lesions, but who did not manifest any aphasic symptom. They could not find any relationship between localisation of lesions and stuttering. However, the authors noticed that none of the children with a simple unilateral lesion in the left or right hemisphere had a severe stutter. They thus hypothesized that:

´ a unilateral lesion alone is not sufficient to produce the more severe forms of stuttering ª (p.118).

Unfortunately, Aram et al. did not mention the transient or non-transient nature of the stuttering in their patients.

On the other hand, it should be noted that Aram et al.’s study concerned children, in whom the brain plasticity is well known to be great, which can favourably have influenced the evolution.

Finally, when a patient wakes up from a coma, and immediately starts to stutter with his first uttered words, as it happened to one of my patients, it is hard to believe that this is a stress reaction to aphasia.

In light of the above data, it is difficult to conclude that one or more cortical lesions in the left hemisphere, in right-handed people, provoke necessarily acquired stuttering with aphasia. As a matter of fact, acquired stuttering occurs as often concomitant with aphasia as it occurs alone.

2. Acquired stuttering after lesion in the right hemisphere (with or without aphasia)

In the above mentioned study of Helm et al; (1980), the authors focus a special interest

on one of their patients, a right handed man, who had suffered a CVA in the right hemisphere, eighteen years ago. Since then, he experienced frequent epileptic attacks. After one of those attacks which was accompanied by a heart attack, he was unconscious for a time. Having recovered consciousness, he started to stutter. Fourteen years later, this situation had not changed. Besides his stutter, he showed some problems with three dimensional drawing and naming objects, but the authors were not sure about the aphasic origin of these impairments.

In a study of Horner and Massey (1983), the described patient started to stutter after an occlusion of the right carotid. And just like the patient of Helm et al,. he experienced some troubles when reading, writing, and drawing, but he was not labelled aphasic. In the case of Ardila and Lopez’ (1986) patient who began to stutter ´ when he started to recover language ª (p.240) after a cerebral accident in the right hemisphere, the stuttering persisted three years later. The same persisting stuttering without aphasia was also described by Lebrun et al; ( 1985 and 1990), and Fleet and Heilman (1985) in their patients with a CVA in the right hemisphere.

In line with the studies of Helm et al. (1980), and Horner and Massey (1983) are the case studies of Kent and Rosenbek (1982), Ardila (1984), and Blonder et al. (1985). In their patients who stuttered after a CVA in the right hemisphere, they noticed in the first place changes in prosody. Indeed, the patients could not follow a melody, and could not sing any more. Moreover, these patients manifested troubles in emotional and automatic speech. According to Bottini et al. (1994), a lesion in the right hemisphere can be responsible for the loss of metalinguistic language, as they demonstrate in their analysis.

On the other hand, transient stuttering after a parietal right hemispheric accident is reported in the study of Rosenbek et al. (1978). Their patient only stuttered for several days, and had no other language impairment. In line with this is the case of Rousey et al. (1986), whose patient also suffered a parietal right hemispheric insult, which cleared up after some months. He also had no other neurological symptoms.

From the above described cases, one can draw the conclusion, that a right hemispheric lesion (in right handed people) can be at the origin of transient or permanent acquired stuttering. Secondly, language problems can, but do not necessarily develop with the stuttering. In the third place, typical right hemispheric troubles can occur, as loss of emotional and/or automatic speech and prosody, impairments in three-dimensional drawing and spatial orientation.

In all the studied cases, there is no doubt about the neurological origin of the reported acquired stuttering, with or without aphasic troubles.

3. Acquired stuttering after sub-cortical lesion (with or without aphasia)

Several sub-cortical lesions can be responsible for the appearance of stuttering, among which is a lesion in the brainstem, or in the basal ganglia or in the cerebellum.

Indeed, Marshall and Neuburger (1987) described a right-handed patient who started to stutter after a car accident that produced a lesion in the brainstem. Seventeen years later, the stutter and the concomitant cognitive disorders were still handicapping him in every day life, in such a way that he could not live on his own. Helm et al. (1986) and Rosenfield (1980) also stress the important role of the brainstem in acquired stuttering :

"Perhaps patients who have suffered damage to their corticobulbar system may develop characteristics of stuttering as a result of deranged control over their intrinsic laryngeal reflex mechanisms"(p.183 in Rosenfield et al. (1980)

Lesions in the basal ganglia form an often-reported cause of the manifestation of stuttering in people who never stuttered before (Meyers et al (1990), Wallesch (1990), Ludlow et al. (1987), and Cipolotti et al. (1988). Besides the stuttering, Meyers et al. noted word finding problems, which could indicate an aphasic element as well. Ludlow et al. observed in their patients with lesions of the basal ganglia, troubles in hand movements, in following a rhythm and in three dimensional drawing, which make us think of difficulties described following right hemisphere lesions. In light of these observations, Ludlow et al. came to the conclusion that:

"Acquired stuttering is a motor control disorder that can occur with unilateral right- or lift sided lesions involving the basal ganglia and white matter tracts, as identified on CT scans"(p.60).

In the case of Cipolotti’s et al. (1988) patient, the clinical tableau did not mention aphasia, but he was dysarthric. Moreover, he manifested difficulties in hand movements and rhythm, just like the patient described by Ludlow et al. Nor could he stop a movement: when he was asked to press a button a single time, he could not stop as requested, but repeated the movement several times, like stuttering behaviour.

On the other hand, difficulties in initiating and terminating movements, is observed in the case of cerebellar lesions in Roulet Perez et al. (1996), Bell-Berti and Chevrie-Müller (1991), and Chevrie-Müller (1995). The described patients in their studies all manifested acquired stuttering with difficulties in hand movements. That is why the authors point to the role of the cerebellum in:

"initiating and terminating movements, as well as co-ordinating complex movements" (p.295).

Another puzzling phenomenon is the temporary disappearance of stuttering after a sub-cortical lesion, as was described by Cooper (1983), and known as "the case of Vicky". This chronic stuttering patient suffered a road accident that caused a lesion in the brainstem, after which her stuttering suddenly and completely disappeared. When the lesion healed, the stuttering returned. Miller (1985) reports a similar case. Two of his chronic stuttering patients stopped stuttering when they developed MS. In line with Miller is one of Helm's patients, (1986) who for more than one year, stopped stuttering after a sub-cortical lesion. When his stuttering returned, it was less severe than before the accident.

Opposite to these findings is what happened to one of Rosenfield's (1980) patients. This chronic stutterer manifested an aggravation of his trouble after having suffered a lesion in the brainstem. Rosenfield concludes that:

"One would anticipate patients developing "stutters" following brainstem disease that has compromised their corticobulbar system" (p.183).

Sudden manifestation of stuttering symptoms in adults can be one of the first indications of neurological problems. It can accompany sub-cortical lesions (Helm et al.1986, Quinn and Andrews 1977). It can announce Parkinson disease (Lebrun et al. 1986; Koller 1982), or it can follow the appearance of Parkinson (Downie et al. 1982, Sakai et al. 1992). Thus, Helm et al. make the careful observation that:

"Onset of stuttering in a well-adjusted adult should be regarded as a possible symptom of neurological disease" (p.201).

Finally, the importance of the thalamus in the manifestation of stuttering symptoms is clearly demonstrated by the works of Bhatnagar and Andy (1989) and Andy and Bhatnagar (1991), who could provoke stuttering thanks to electrical stimulation of frontal part of the thalamus. When the stimulation diminished, the stuttering stopped. When stimulating the lateral part of the thalamus, their patient stuttered less and experienced a relief of headaches and epileptic seizures. They thus come to the following conclusion that:

"Chronic pain and stuttering may be implicated … in reticular networks extending from the brainstem to the thalamus, and that acquired stuttering may be recruited as one component of a larger syndrome complex" (p.385).

The variety of possible lesions giving birth to acquired stuttering is strikingly demonstrated by the investigation of Market et al. (1990) concerning 81 patients with acquired stuttering. The authors found 38% of the patients with a cortical lesion in the left hemisphere, 8.6% with a cortical lesion in the right hemisphere, 9.9% with bilateral lesions, 11.1% with sub-cortical lesions and 32.1% with lesions of unknown origin.

Moreover, 32.1% from the patients were aphasic as well, 12.3% had concomitant dysarthria, 11.1% had both pathologies and 44.4% had acquired stuttering without any other language problems.

Thus, research during the last 30 years may have demonstrated and illustrated the complexity of acquired stuttering, a syndrome reflecting the complexity of the brain functioning itself.

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September 1, 2001

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