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Keywords:

  • stuttering;
  • migraine;
  • aphasia

Abstract

  1. Top of page
  2. Abstract
  3. CASE HISTORY
  4. COMMENTS
  5. REFERENCES

Stuttering is an abnormality in the fluency of speech, which is characterized by interruption of the normal rhythm due to involuntary repetition and prolongation, or arrest, of uttered letters or syllables.

The aphasic syndrome and dysarthria can be associated with classic migraine, but, to our knowledge, no study has so far described stuttering as the only neurological symptom accompanying an attack.


CASE HISTORY

  1. Top of page
  2. Abstract
  3. CASE HISTORY
  4. COMMENTS
  5. REFERENCES

A 26-year-old, right-handed woman presented to the emergency room because of frontal and temporal bilateral headache and stuttering.

The patient had been well until three hours before when she developed a severe headache and right arm and perioral paresthesia with a progressive disturbance in the fluency of her speech with stuttering.

She had never stuttered previously, and there was no family history of developmental stuttering. The patient reported having had insulin-dependent diabetes mellitus since the age of six years and only had one or two episodes of headache per year in the past; these headaches had the same features as the current episode except for the stuttering. There was no history of hypertension; use of tobacco, alcohol, or illicit drugs; auditory symptoms, vertigo, or dysarthria; neck pain; night sweats; or weight loss.

Her temperature was 36.5°C. Her pulse was 88 beats per minute, and the respirations were 16 breaths were minute . Her blood pressure was 115/80 mm Hg.

The results of the general physical examination were normal. On neurological examination, her muscle strength, sensation of pinprick, vibration, temperature, and joint position were normal; cranial nerve functions were preserved; and the visual fields were intact. Coordination and gait were normal, and Romberg's test was negative. The deep or tendon reflexes were ++ and equal in both arms and legs. Babinski's sign was not present.

The fluency evaluation revealed severe stuttering characterized by multiple repetitions or blocks, or both, with 20 or more repetitions per word during both conversational speech and oral reading. No starters or secondary stuttering characteristics, and no specific word fears or avoidance, were exhibited. No deficit in naming, spontaneous speech, comprehension, repetition, reading, and writing was observed.

Blood glucose levels and other hematological and chemical values, including the level of angiotensin-converting enzyme, were normal.

The results of a CT examination of the brain, performed during the attack, were normal, and EEG findings did not show abnormalities or focal or generalized paroxysmal activity.

Ketoprofen was administered with only a slight improvement in the patient's symptoms, but stuttering, headache, and right arm and perioral paresthesia promptly and completely disappeared after subcutaneous administration of sumatriptan, 6 mg.

One week later, a repeated CT and MRI of the brain performed after the intravenous injection of contrast material did not show any abnormality. A serological test for syphilis and a test for rheumatoid factor and antinuclear and antineutrophil cytoplasmic antibodies were also negative. Anxiety and personality disorders, including somatization and conversion and mood disorders, were ruled out on the basis of clinical history and psychiatric examination, including testing with the Minnesota Multiphasic Personality Inventory (MMPI). Scores for anxiety and depression were normal when the patient was tested with the use of visual analog scales for those disorders.

COMMENTS

  1. Top of page
  2. Abstract
  3. CASE HISTORY
  4. COMMENTS
  5. REFERENCES

The only language disturbance this patient had during the migraine attack was stuttering with no other features of aphasia, which is a pervasive impairment of linguistic processing (eg, structure of sentences, assembly of phonemes in a word, and retrieval of words from lexicon), or dysarthria, which is a defective articulation of speech sounds without compromise of linguistic processing.

The neural network of language is composed of a distributed network centered in the perisylvian region of the left hemisphere. The posterior pole is Wernicke's area, which transforms sensory input into word neural representations so that the words can enter the distributed associations that lead to meaning. 1 The anterior pole of this network is Broca's area that transforms neural word representations into their articulatory sequences, so that the words can be uttered in the form of spoken language. 1 Wernicke's and Broca's areas are interconnected with each other and with additional perisylvian, temporal, prefrontal, and posterior parietal regions, making up a neural network subserving the various aspects of language function. 1 Damage to any one of these components or to their interconnections can give rise to aphasia with various degrees of deficit in naming, spontaneous speech, comprehension, repetition, reading, and writing in relation to the site(s) of lesion in language areas. 1 This results in “central” aphasic syndromes, which arise from damage to either Broca's or Wernicke's areas, and “disconnection” syndromes, which arise from lesions interrupting the connections of these centers with each other and with the other components of the language network. 1

Onset of stuttering in adulthood is rare, though there are some reports of fluent people who developed this disturbance after a brain injury, whether cortical or subcortical, 2–5 or after drug administration. 6 Stuttering is occasionally observed in adults as a result of left hemisphere injury in Broca's area 7 and can be an integral part of the aphasic syndrome, 8 though the two disorders seem to be independent. Acquired stuttering is transitory in many cases or permanent if the lesions are bilateral. 9 The actual site(s) of lesion(s) have been documented usually by association of symptoms, EEG findings, and neuroimaging studies, but in at least one reported case lesion(s) would have been missed without the use of SPECT testing. 10 In our patient, EEG findings were normal, and brain CT and MRI scans failed to reveal any abnormality.

With no prior history of stuttering or demonstrable neurological insult, onset of stuttering in adulthood is often a conversion reaction of patients who begin stuttering purportedly secondary to psychological stress. We considered the possibility of a conversion reaction in this young woman, but both the patient and her relatives did not report any psychological stress, and the patient had no situational fears. Furthermore, psychiatric consultation and testing with MMPI ruled out anxiety and personality disorders, and scores for anxiety and depression were normal on visual analog scales. In addition, the disturbance in language fluency closely paralleled the course of her migraine attack, and the stuttering promptly resolved when migraine was abated by treatment with sumatriptan.

The mechanism responsible for such severe, although transient, stuttering is unclear. Stuttering is a disorder affecting the multiple neural systems used for speaking. Association with hyperactivity of the premotor cortex, either directly or through connectivity with the thalamus and basal ganglia, and overactivation of the motor system in both the cerebrum and cerebellum with right cerebral predominance have been implicated in stuttering, as well as lack of left-lateralized activation of the auditory systems, which are thought to support the self-monitoring of speech and selective deactivation of the frontal-temporal system implicated in speech production. 11 Furthermore, in patients who stutter significant decreases in regional glucose metabolism in Broca's area, Wernicke's area, and the frontal lobe have been shown compared with when they are not stuttering and with nonstuttering subjects. 12 The reasons why lesions or altered metabolism and function in cerebral areas controlling speaking can result in either the classic aphasic syndrome, with or without stuttering, or stuttering alone without any of the additional characteristics of aphasia, remain to be understood. It is likely that the onset of stuttering in the young woman considered here represented a focal deficit, just as aphasia can occur as an aura or as part of a migraine attack. 13 Imbalances in neurotransmitter systems triggered by the attack could have a role and, accordingly, the prompt disappearance of stuttering after sumatriptan injection supports the involvement of serotoninergic circuits.

We suggest that acquired transient stuttering should be included in the list of neurological symptoms that can accompany a migraine attack.

REFERENCES

  1. Top of page
  2. Abstract
  3. CASE HISTORY
  4. COMMENTS
  5. REFERENCES
  • 1
    Mesulam MM. Aphasias and other focal cerebral disorders. In: FauciAS, BraunwaldE, IsselbacherKJ, et al, eds. Harrison's Principles of Internal Medicine, 14th ed . New York, NY: McGraw Hill; 1998:134-142.
  • 2
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    Lanoe Y, Pedetti L, Lanoe A, et al. Aphasia caused by isolated lesion of the semi-oval centre. Rev Neurol (Paris). 1994;150:430-434.
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    Rosenbeck J, Messert B, Collins M, et al. Stuttering following brain damage. Brain Lang. 1975;82:103-138.
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  • 10
    Heuer RJ, Sataloff RT, Mandel S, Travers N. Neurogenic stuttering: further corroboration of site of lesion. Ear Nose Throat J. 1996;75:161-168.
  • 11
    Fox PT, Ingham RJ, Ingham JC, et al. A PET study of the neural systems of stuttering. Nature. 1996;382:158-161.
  • 12
    Wu JC, Maguire G, Riley G, et al. A positron emission tomography [18F] deoxyglucose study of developmental stuttering. Neuroreport. 1995;6:501-505.
  • 13
    Raskin NJ. Migraine and the cluster headache syndrome. In: FauciAS, BraunwaldE, IsselbacherKJ, et al, eds. Harrison's Principles of Internal Medicine. 14th ed. New York, NY: McGraw Hill; 1998:2307-2310.