Copyright Ó Blackwell Munksgaard 2002

Acta Neurol Scand 2002: 105: 408–410
Printed in UK. All rights reserved

ACTA NEUROLOGICA
SCANDINAVICA
ISSN 0001-6314

Case report

A case of acquired stuttering resulting
from left parietal infarction
Turgut N, Utku U, Balci K. A case of acquired stuttering resulting from
left parietal infarction.
Acta Neurol Scand 2002: 105: 408–410. Ó Blackwell Munksgaard 2002.
Objective – Acquired stuttering is uncommon, and is reported
anecdotally after head injury and cerebrovascular diseases. Although
this entity is described to occur in lesions of dominant hemisphere, it is
rarely shown to occur in non-dominant hemispheric and subcortical
lesions, too. Therefore we described a case with this rare syndrome and
we discussed the possible mechanisms, lesion locations and medical
treatment of stuttering according to previous reports. Case report –
A 61-year-old right-handed man with sudden onset of right hemiparesia
and stuttering without aphasia is reported. There was a circumscribed
cortical infarction in the left parietal cortex on computerized
tomography (CT) and magnetic resonance imaging (MRI) showed a
recent infarct. Single photon emission computed tomography (SPECT)
images evidenced perfusion abnormalities in the same region. He never
stuttered before and has no family history of stuttering. He has been
maintained on antiaggregant and paroxetine treatment. Conclusion –
A rare presentation of stroke associated with stuttering is reported and
the treatment of stuttering with paroxetine is discussed.

Neurogenic (or acquired) stuttering is uncommon
and is different in some aspects from the stuttering
of developmental origin (1). Most reported cases of
acquired stuttering are described as a result of
stroke, head injury, degenerative and metabolic
brain damage (1–3). The mechanisms and location
of lesions in stuttering are poorly understood:
stroke cases with stuttering have been described
after dominant hemispheric lesions, and more rarely
after lesions affecting the non-dominant hemispheric and various subcortical structures (2–7).
A rare case of stuttering secondary to parietal
cortical infarction in the left cerebral hemisphere is
reported and the treatment of stuttering with
paroxetine is discussed.
Case report

A 61-year-old right-handed, hypertensive man
was admitted to our hospital because of acute
onset of right-sided weakness and speech disturbance since 2 days. On examination, there was a
408

N. Turgut, U. Utku, K. Balci
Neurology Department, Medical Faculty, Trakya
University, Edirne, Turkey

Key words: stroke; stuttering; therapy; paroxetine;
neuroimaging
Ufuk Utku, Neurology Department, Medical Faculty,
Trakya University, 22030 Edirne, Turkey
Tel.: +90 284 235 76 41
Fax: +90 284 235 76 52
e-mail: ufuk.utku@superonline.com
Presented in abstract form at the 9th European Stroke
Conference, Vienna, Austria, 24–27 May 2000.
Accepted for publication October 12, 2001

mild hemiparesis and sensory loss in the face and
upper limb on the right side. The patient
exhibited severe stuttering characterized by multiple clonic monosyllabic repetitions and blocks
(Table 1). Speech disturbance appeared mainly in
initial syllables with repeated reading and adaptation effect was not noted. Dysartria was not
found. A more detailed investigation of the
patient’s speech was performed using the Gülhane Aphasia Test (GAT) and the Turkish version
of the Boston Diagnostic Aphasia Examination
(BDAE) (8). GAT is the modified form of the
Mayo Clinic Aphasia Test and the BDAE, and is
in use for clinical evaluation of language disorders throughout Turkey (9, 10). The patient’s
language modalities such as auditory and reading
comprehension, naming on visual confrontation,
repetition and writing were normal. He had no
difficulty in obeying verbal commands. All in all,
the patient exhibited stuttering with no aphasia.
Severe stuttering extended to reading as well. The
medical history revealed no episodes of stuttering

A case of stroke-induced stuttering
Table 1 Examples of the normal pronunciation and the patient's actual response
Target word
Geliyorum – I'm coming
Sen – You
Rapor – Report

Patient's actual response
Ge-ge-geliyorum
S-s-s-sen
Ra-ra-rapor

Figure 3. SPECT images revealing perfusion abnormalities in
the left parietal area.

Figure 1. CT scan demonstrating hypodensity in the left
parietal cortex, consistent with subacute infarction.

third day after the onset revealed a circumscribed
cortical area of infarction in a similar location
(Fig. 2). 99m Technetium hexamethylpropylene
amine oxime (99mTc HMPAO) single photon
emission computed tomography (SPECT) results
were remarkable for perfusion abnormalities in
the left parietal area (Fig. 3). Electrocardiogram
(ECG) and echocardiogram were normal and
extracranial Doppler ultrasonography (USG)
revealed atherosclerotic plaques in the left internal carotid artery.
The patient was treated with antiaggregant therapy. After 1 week, no improvement was noted, and
paroxetine (20 mg/day) was added. Within days,
the patient’s stuttering began to improve and at the
end of 1 month, the stuttering was totally resolved.
Discussion

Figure 2. T2 weighted MRI showing left parietal cortical
infarction.

either in the patient, or in his family. Computerized tomography (CT) scans obtained on the
second day after the onset revealed an area of
hypodensity in the left parietal cortex consistent
with a subacute infarction (Fig. 1). Magnetic
resonance imaging (MRI) scans taken on the

The acquired form of stuttering is different from
the developmental form of stuttering (1). For
example, in the acquired cases, stuttering can
occur in monosyllabic as well as in longer words.
It has no adaptation effect and is rarely associated
with facial grimacing (3).
Acquired stuttering has been described more
commonly in dominant parietal lobe lesions, as
was seen in our patient. It has also been reported in
lesions of the non-dominant hemisphere, thalamus,
midbrain, pons, corona radiata and putamen (2–7).
In those cases, stuttering was sometimes associated
with a mild aphasia (1, 5). Although, our patient
had a left parietal infarction, he had no aphasia. It
is known that supplementary motor area (SMA) is
important for coordinating and planning complex
sequences of movement and this area receives
information from the posterior parietal cortex (11).
Therefore, the lesions of SMA or its connections
with cerebral cortex and basal ganglia including
409

Turgut et al.
the extrapyramidal system are possible causes of
stuttering (7, 12).
Interestingly, our case was improved after paroxetine treatment. Although a wide variety of
medication has been used in the treatment of
stuttering, only haloperidol treatment is reported
to be effective (13). Schreiber et al. (14) showed
that paroxetine (a phenyl-piperidine derivate,
potent and selective serotonin reuptake blocker)
was effective in three cases of acquired stuttering. It
has been suggested that an interaction between
serotonergic and dopaminergic systems exists in
the forebrain and paroxetine may have a serotonin
mediated indirect antidopaminergic effect in these
patients.
To summarize, our case with stroke-induced
stuttering is remarkable for his positive response to
paroxetine treatment. However, the possible confounding of spontaneous recovery cannot be
excluded and further studies are needed to examine
the role of paroxetine in the treatment of this rare
disorder.
References
1. GRANT AC, BIOUSSE V, COOK AA, NEWMAN NJ. Strokeassociated stuttering. Arch Neurol 1999;56:624–7.
2. SOROKER N, BAR-ISRAEL Y, SCHECHTER I, SOLZI P. Stuttering as a manifestation of right-hemispheric subcortical
stroke. Eur Neurol 1990;30:268–70.

410

3. HELM NA, BUTLER RB, BENSON DF. Acquired stuttering.
Neurology 1978;28:1159–65.
4. ROSENBEK J, MESSERT B, COLLINS M, WERTZ RT. Stuttering following brain damage. Brain Lang 1978;6:82–96.
5. CIABARRA AM, ELKIND MS, ROBERTS JK, MARSHALL RS.
Subcortical infarction resulting in acquired stuttering.
J Neurol Neurosurg Psychiatry 2000;69:546–9.
6. KONO I, HIRANO T, UEDA Y, NAKAJIMA K. A case of
acquired stuttering resulting from striatocapsular infarction. Rinsho Shinkeigaku 1998; 38:758–61.
7. ABE K, YOKOYAMA R, YORIFUJI S. Repetitive speech disorder resulting from infarcts in the paramedian thalamus
and midbrain. J Neurol Neurosurg Psychiatry 1993;
56:1024–6.
8. GOODGLASS H, KAPLAN E. Boston diagnostic aphasia
examination. Philadelphia, PA: Lea & Febiger, 1972.
9. TANRıDAĞ O, ÖNGEL Ç. Transcortical motor aphasia due
to a right hemisphere lesion in a right-handed man.
Aphasiology 1989;3:717–21.
10. ÖZEREN A, SARıCA Y, EFE R. Thalamic aphasia syndrome.
Acta Neurol Belg 1994;94:205–8.
11. GHEZ C. The control of movement. In: KANDEL ER et al.,
eds. Principles of neural science. New York: Elsevier Science Publishing Co., 1991;539.
12. SAKAI T, MIYAMURA M, KUZUHARA S. Palilalia and
acquired stuttering in a case of Parkinson’s disease. Rinsho
Shinkeigaku 1992; 32:859–63.
13. BRADY JP. The pharmacology of stuttering: a critical
review. Am J Psychiatry 1991;148:1309–16.
14. SCHREIBER S, PICK CG. Paroxetine for secondary stuttering: further interaction of serotonin and dopamine. J Nerv
Ment Dis 1997; 185:465–7.