Neurological Stuttering a Clinical Entity?
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J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.40.7.699 on 1 July 1977. Downloaded from Journal ofNeurology, Neurosurgery, and Psychiatry, 1977, 40, 699-701 Short report Neurological stuttering a clinical entity? P. T. QUINN AND GAVIN ANDREWS From the Human Communication Laboratory, University of New South Wales Teaching Hospitals, The Prince Henry Hospital, Sydney, Australia SUM MARY Stuttering associated with neurological pathology in normal adult speakers is uncommon, has no consistent clinicopathological picture, and its significance is too easily dismissed. A case is reported showing that stuttering may be a presenting symptom of progressive neurological disease, and another case demonstrates that a speech disorder which is indistinguishable from common stuttering may follow cerebral injury in adulthood. Recent evidence that genetic factors are important There was a clear history of stutter-free speech in in the aetiology of typical stuttering (Andrews childhood, and there was no family history of and Harris, 1964; Howie, 1975) suggests that a stuttering. neurological abnormality may underlie this com- After a high-speed motorcycle accident in mon speech disorder, although the detailed which he was thrown headfirst into a speedway Protected by copyright. aetiology is still unknown. The rarer syndrome of retaining wall, he was admitted to hospital coma- stuttering after neurological pathology in pre- tose with multiple fractures of the upper limbs. viously normal speaking adults is not universally Burrholes revealed considerable extradural clot accepted as a clinical entity. Perhaps this is be- extending over the left frontal lobe. During his cause relevant case reports are frequently anec- slow rehabilitation it was noted in his medical dotal in nature, do not present a consistent records that he was disorientated in time and space clinicopathological picture, and are so rare that and had post-traumatic amnesia for more than they may represent merely a predictable back- two months, as well as expressive dysphasia and a ground rate of eccentric case reporting. tendency to perseverate in speech. He had left We know of six cases in which apparently amblyopia, left optic atrophy, right temporal permanent stuttering was either a presenting hemianopia, and nystagmus with a fast component symptom or a complication of neurological to the right. His pupils responded directly and pathology in adults. In two cases the stuttering consensually to light directed to the right eye but preceded the eventual diagnosis of presenile not to the left. He showed behavioural problems dementia, whereas it followed the onset of neuro- characterised by occasional aggression, and was logical lesions in two cases of stroke, one of easily distracted. At six months his speech was thalamotomy, and one of head injury. Two of nearly normal although he tended to perseverate http://jnnp.bmj.com/ these cases are described in some detail. when tired. Six years after the accident the patient presented Case 1 for treatment of stuttering, which he had first noticed four years earlier. It had become pro- 'STUTTERING AFTER HEAD INJURY gressively worse. Speech pathologists diagnosed This 30 year old man was intensively investigated his speech disorder as stuttering, characterised in an attempt to clarify the nature of his speech more by repetitions similar to those of childhood disorder and the associated neurological deficit. stutterers than by the hesitations and mannerisms on October 1, 2021 by guest. There was little doubt that the subject's speech of adult stutterers. had once been stutter-free since, quite fortuitously, On examination he was stuttering on 20% of his he was looked after by one of the present authors syllables and his speech rate was reduced to 108 (GA) both before and after the onset of stuttering. syllables per minute. His stuttering showed the adaptation effect (Index=68) and consistency Address for reprinL requests: Dr P. T. Quinn, Human Communica- effect (scores=3.06, 3.88, 3.19) described by tion Laboratory, The Prince Henry Hospital, Little Bay, NSW 2036, Australia. Johnson et al. (1963) as characteristic of typical Accepted 7 February 1977 stuttering. 699 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.40.7.699 on 1 July 1977. Downloaded from 700 P. T. Quinn and Gavin Andrews His intellectual and language function had, in evident that his business acumen was failing and six years since the accident, returned to virtually uncharacteristic errors of judgement were being normal levels. His WAIS intelligence score had made. improved by 24 points to 110 (Verbal 103, Per- Seven months later his stutter had become so formance 118), and aphasia was now only evident severe that he was again referred for treatment. in weakness and concrete responses in the verbal When assessed he was stuttering on 48% of his expression subtest of the Illinois Test of syllables, and his speech rate was reduced to 31 Psycholinguistic Abilities. syllables per minute. The stutter was unusual in This subject was included in an investigation that there were multiple simple repetitions on each of cerebral dominance in stutterers using the affected syllable as is common in childhood stutter- Wada intracarotid sodium amylobarbitone tech- ing and similar to that of the first case. In contrast nique (Andrews et al., 1972). This technique with the latter, the stutter was not improved when usually produces marked dysphasia after dominant the subject attempted to speak under a masking hemisphere injection, although the minority of tone, with delayed auditory feedback or with pro- left handers who showed bilateral speech repre- longed speech. By this time there was evidence of sentation also demonstrate unusually mild dys- an early dementing process, with mild expressive phasia (Milner et al., 1966). The present subject aphasia, poor concentration, and impaired judge- not only was unable to sustain speech after the ment. Six months later the stutter was still present injection of either hemisphere, but also experi- but was overshadowed by the impaired compre- enced severe dysphasia. These findings suggested hension and grossly impaired intellectual per- a post-traumatic inter-hemispheric redistribution formance. Evidence that his father and sister had of language function which may represent a pro- died from a similar rapidly progressive presenile cess of division rather than of reduplication. dementia was also obtained. Dichotic listening tests are widely employed in The most probable diagnosis for this man and Protected by copyright. the investigation of cerebral dominance. There is his relatives appears to be Alzheimer's disease. some evidence that those subjects with left hemis- Stuttering, similar in form to his earlier childhood pheric lesions who show unusually powerful stutter, was presumably the reiterative utterance 'paradoxical' right ear superiority on dichotic of parts of words which is so characteristic of testing may have lesions of a trans-callosal path- Alzheimer's disease. The condition continued to way which, under dichotic conditions, transfers be progressive and this man died 18 months after auditory information from the right hemisphere the appearance of the first symptom. Necropsy to the left (Sparks et al., 1970). The scores of the was not performed. present subject on a dichotic test used in this laboratory (Quinn, 1972) were comparable with Discussion those of the above individuals. His scores were: left ear 2; right ear 30. Six months later, his scores Lately there have been attempts (Canter, 1971) to were: left ear 4; right ear 27. establish a clinical syndrome of stuttering associ- The evidence for bilateral representation of ated with neurological insult in previously normal language in the present subject, however, con- speakers. The present report provides clinical and founds the model of Sparks et al., which pre- investigatory evidence to support such a concept. http://jnnp.bmj.com/ supposes unilateral left hemispheric language We have seen a steady trickle of adults who output. While this subject's left hemisphere may would fit this syndrome. Our experience is con- be more receptive of dichotically dispersed sistent with impressions derived from the litera- auditory information than the right, alternative ture that neurological stuttering is uncommon, has explanations for the poor report of left ear words, no consistent clinicopathological picture, and is too in a subject with proven left hemispheric injury, easily dismissed when it does occur. Since the first would include the possibility of additional neuro- two characteristics do not render a clinical entity logical lesions. invalid, and in view of evidence concerning speech on October 1, 2021 by guest. details in our first case, we would suggest that a Case 2 speech disorder which is indistinguishable from common stuttering may be evidence of specific PRESENILE DEMENTIA PRESENTING WITH STUTTERING neurological disorder. A 62 year old successful businessman presented because of the recurrence of a stutter that had References afflicted him transiently during his childhood. No neurological or psychiatric abnormalities were Andrews, G., and Harris, M. (1964). The Syndrome of noted at this time, although in retrospect it is Stuttering. Clinics in Developmental Medicine No. J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.40.7.699 on 1 July 1977. Downloaded from Neurological stuttering- a clinical entity? 701 17, Heinemann: London. (1963). Diagnostic