and Segarra wrote, "it is well known
that there can be some variation
among members of the same family in
pathological features of spinocerebel¬
lar atrophies."4 We believe in these
variations and are tempted to call
DSPA a variant of OPCA.
Srecko Pogacar, MD
Neuropathology Division
Medical Center General Hospital
PO Box 8269
Cranston, RI 02920
P. F. Finelli, MD
Department of Neurology
Veterans Administration
Medical Center
Providence, RI 02908

1. Pogacar S, Ambler M, Conklin WJ, et al:
Dominant spinopontine atrophy: Report of two
additional members of family WG Arch Neurol

1978;35:156-162.
2. Boller F, Segarra JM: Spinopontine degeneration. Eur Neurol 1969;2:256-373.
3. Gilroy J, Lynn GE: Computerized tomography and auditory-evoked potentials: Use in the
diagnosis of olivopontocerebellar degeneration.

Arch Neurol 1978;35:143-147.
4. Boller F, Segarra JM: Dominant spinopontine atrophy. Arch Neurol 1979;36:255.

Reemergence of Stuttering After
Focal Cerebral Insult

To the Editor.\p=m-\Therecurrence of a
childhood stutter in an adult after
cerebral insult is apparently uncommon. To our knowledge, just three
such instances have been mentioned
in the literature, although their possible importance was not discussed.1-3
Case.\p=m-\A right-$
Report of a Case.
handed, right-footed, and right-eyed man

admitted to the hospital because of
acute onset of speech difficulty. He had a
was

ten-year history of hypertension, a 25-year

history of hypothyroidism secondary to
iodine I131 therapy for hyperthyroidism, a
26-year history of insulin-dependent diabetes mellitus with associated retinopathy
and neuropathy, and a 40-pack-year history of cigarette smoking. Although he initially denied any previous history of speech
impairment, he later revealed that he had
been a "stutterer" between the ages of
about 3 and 16 years. This speech impediment had been the source of much embarrassment to him, probably explaining his
initial reluctance to discuss it. He had
never told his wife about it. He stated that
he had learned to "control" his stutter and
that it had resolved without residual
effect.
On the day before admission, he had
awakened with a dull, generalized head¬
ache. At about 10 pm that evening, he
experienced the acute onset of difficulty in
"getting his words out." He had no difficul¬
ty understanding written or spoken lan¬
guage. He denied other neurologic symp¬
toms. The next morning he went to the
emergency room because his headache and
speech difficulty had not improved.
On admission, his BP was 200/92 mm
Hg. General physical examination re¬
vealed diabetic retinopathy and peripheral

A and
illustrate extent and localization of left-parietal intracerebral hemorrhage on initial
unenhanced computed tomographic (CT) scan. C and D are comparable sections on
unenhanced scan obtained 12 weeks later. Enhanced CT scan showed no additional

abnormality.

neuropathy. There was no hemiparesis,

visual field defect, or extinction on double
simultaneous sensory stimulation. The
only neurologic deficit was dysfluent

speech characterized by frequent repeti¬

tions of initial word sounds and syllables.
Sound prolongations and frequent hesita¬
tions were also present. Associated facial
grimacing was evident with the repeti¬
tions. Some paraphasia, with occasional
neologisms, was evident in his speech.
A computed tomographic (CT) scan of
the head on the day of admission revealed
a small, left-parietal hematoma (Figure).
An EEG the next day was normal. Within
24 hours after admission, the patient's
stutter was noticeably improved. A formal
speech-language pathology evaluation 48
hours after admission found no evidence of
aphasia and only a mild degree of stutter¬
ing. No distinction could be made between
cortical or developmental stutter.
Twelve weeks later, a repeated head CT
scan was normal (Figure), and speechlanguage pathology réévaluation found no

major dysfluencies.

Comment.—Recent evidence sug¬
gests that most developmental stut¬
tering may represent a genetically

inherited neurologic disorder.4·5 If so,
the underlying defect should persist
even if the patient has learned to
"control" the stutter by any of several
treatment methods currently in prac¬
tice.6 Therefore, theoretically, a cere-

bral insult might interfere with CNS
pathways that allow the stutterer
to control the stutter, consequently
enabling clinical reemergence of the
underlying stuttering defect. Thus,
the reemergence of stuttering after
cerebral insult may indirectly support
the concept that stuttering is caused

by a genetic (permanent) abnormality
of CNS speech control systems.

Jack E. Riggs, MD
Laura Jean Nelson, MD
Department of Neurology
Joyce E. Lanham, MS
Division of Speech Pathology
Department of Otolaryngology
West Virginia University
School of Medicine
Morgantown, WV 26506

1. Quinn PT, Andrews G: Neurological stuttering: A clinical entity? J Neurol Neurosurg Psychiatry 1977;40:699-701.
2. Rosenbek J, Messert B, Collins M, et al:
Stuttering following brain damage. Brain Lang
1978;6:82-96.
3. Mazzucchi A, Moretti G, Carpeggiani P, et
al: Clinical observations on acquired stuttering.
Br J Disord Commun 1981;16:19-30.
4. Kidd KK, Reich T, Kessler S: A genetic
analysis of stuttering suggesting a single major

locus. Genetics 1973;74:s137.
5. Kidd KK, Heimbuch RC, Records MA: Vertical transmission of susceptibility to stuttering
with sex-modified expression. Proc Natl Acad Sci
USA 1981;78:606-610.
6. Van Riper C: Speech Correction: Principles
and Methods, ed 6. Englewood Cliffs, NJ, Prentice-Hall Inc, 1978.

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