However, serum prolactin was elevated as well, which
also would suggest altered hypothalamic regulation.
Without evidence of a primary structural pituitary lesion, these hormonal changes are more likely to be
caused by interference with normal inhibitory control
exerted by corresponding hypothalamic factors.
Our patient showed a favorable biochemical and
clinical response to bromocriptine with the exception
of somatomedin C levels, which remained elevated
during treatment. Levels of growth hormone and prolactin fell to within the normal range, and carbohydrate
homeostasis was restored. Thyroid-stimulating hormone levels were unchanged. These hormonal effects
suggest that bromocriptine can restore hypothalamicpituitary feedback mechanisms produced by a primary
childhood hypothalamic disturbance.
Bromocriptine, an ergot derivative with dopamine
receptor agonistic actions, has been used to treat adult
pituitary tumors and acromegaly IS, 7, 13, 161. Although its primary site of action is believed to be in the
pituitary gland [9], a direct hypothalamic effect has also
been suggested [lb]. The efficacy of bromocriptine in
lowering serum prolactin seems well established, but
its role in inducing biochemical and clinical improvement in acromegaly recently has been questioned [GI.
Its part in reducing pituitary tumor size following bromocriptine administration is equally uncertain [ 131.
The possibility that our patient’s tumor was functionally active and secreting a growth hormone-releasing peptide is a consideration. The association between
carcinoid tumors and acromegaly has been recognized
C13, 141; in addition, a peptide has been characterized,
and its ability to stimulate growth hormone release
from human somatotrophic adenoma in vitro has been
demonstrated [ 151. However, because of the concomitant alterations in prolactin level in our patient, we
favor a “functional geographic” effect with dual action,
leading to decreased somatostatin secretion, exaggerated growth hormone release, and a decrease in “prolactin inhibiting factor.”

References
1. Costin G: Endocrine disorders associared with tumors of the
pituitary and hypothalamus. Pediatr Clin North Am 26: 15-3 1,
1979
2. Costin G, Fefferman RA, Kogut MD: Hypothalamic gigantism.
J Pediatr 83:419-425, 1973
3. Dabek JT: Bronchial carcinoid tumor with acromegaly in rwo
patients. J Clin Endocrinol Metab .38:329-333, 1974
4. Fienman NL, Yakovac NC: Neurofibromarosis in childhood. J
Pediatr 76339-346, 1970
5. Kobberling J, Blossey HC, Dirks H, Mayer G: More on bromocriptine in acroqegaly. N Engl J Med 306:748, 1982
6. Lindholm J. Riishede J, Vestergaard S, e t al: No effect of bromocriptine in acromegaly. N Engl J Med 304:1450-1454, 1981
7. McGregor AM, Scanlon MF, Hall I(,et al: Reduction in size of a
pituitary tumor by bromocriptine therapy. N Engl J Med
3001291-293. 1979
8. Parker JC, Smith JL, Reyes P, Vuksanovic MM: Chiasmal optic

304

glioma after radiation therapy. Neuro-ophrhalmologicipathologic Correlation. J Clin Neuro Ophthalmol 1:31-43, 1981
9. Parkes D: Bromocriptine. N Engl J Med 301:873-878, 1979
10. Riccardi VM: Von Recklinghausen’s neurofibromatosis. N Engl
J Med 305:1617-1627, 1981
11. Richardson RR, Noronha A, Leersma J, Siqueira EB: Multiple
neoplastic associations with central and peripheral Von Reck.linghausen’s disease. South Med J 73:1074-1077, 1980
2. Rosman NP, Pearce J: The brain in multiple neurofibromatosis
(Von Recklinghausen’s disease): a suggested neuropathological
basis for the associated mental defect. Brain 90:839-850, 196.7
3. Salti IS, Istfan N: Bromocriptine fails to stop growth of eosinophilic adenomas in acromegaly. N Engl J Med 301:386, 1979
4. Sonksen PH, Ayers AB, Braimbridge M, et al: Acromegaly
caused by bronchial carcinoid tumors. Clin Endocrinol (Oxf)
5:503-513, 1976
5. Webb CB, Thominet JL, Frohman LA: Ectopic growth hormonl:
releasing factor stimulates growth hormone release from human
somatotroph adenomas in vitro. J Clin Endocrinol Metab
56:417-419, 1982
16. Zervas NT, Martin JB: Management of hormone-secreting pituitary adenomas. N Engl J Med 302:210-214, 1980

Transfer of
Language Dominance
Henry Lee, MD, Tsutomu Nakada, MD,
Jon L. Deal, PhD, Stan Lin, MD, and Ingrid L. Kwee, MD

It has been suggested that recovery from aphasia may
depend on the ability of the nondominant hemisphere to
subserve language functions. We describe a patient who
illustrates a possible “transfer” o f language dominance.
The patients sustained two infarcts two years apart, one
in each hemisphere, involving mirror image territories
in the temporoparietal area. The clinical course of each
infarct was almost identical, consisting of an initial Wernicke’s aphasia which evolved into anomic aphasia during recovery.

Lee H,Nakada T, Deal JL,Lin S, Kwee I L
Transfer of language dominance.
Ann Neurol 15:304-307, 1984

Recovery from aphasia is a complex and mechanistically poorly understood process [4].We report a case
of recurrent aphasia following a right temporoparietal
infarct in a right-handed patient who earlier had suffered a stroke in the left hemisphere. The findings in
this patient suggest a transfer or resumption of language function in the right hemisphere.
From the Department of Neurology, University of California, Davis,
and the Veterans Administration Medical Center, Martinez, CA.
Received July 18, 1983, and in revised form Aug 12. Accepted for
publication Aug 13, 1983.
Address reprint requests to Dr Lee, Department of Neurology, University of California, Veterans Administration Medical Center, I50
Muir Rd, Martinez, CA 94553.

AUDITORY COWREHEN5ION
ronrsicd from a b y m r c
I wort M

X "

A

ARTICULATORY AGII I T Y
farditr .I phonrnu'and iyllrblr
1.111

Fig 1 . Rdting scale profile of speech characteristics on Boston
Diagnostic Aphasia Examination. (A)Initial testing, in the
first week of hospital admission, resulted in a profile compatible
with that of a patient with Wernicke's aphasia. IB) The profile
on follow-up testing, three months afrer admission, was compatible with that of a patient with anomic apha.ria.

A 57-year-old, right-handed man was admitted one week
after sudden onset of difficulty in understanding spoken and
written language. Two years earlier he had suffered a left
hemisphere stroke and aphasia. The aphasia was described as
being of a Wernicke's type initially, which evolved into mild
anomia over a six-month period.
O n neurological examination, the patient's speech was
fluent with circumlocutions and moderate word-finding
difficulty. There was no finger agnosia or right-left confusion.
Results of cranial nerve examination were within normal limits except for mild lower facial weakness on the right side.
The patient's strength was normal. H e showed a slight pronator drift on the right side of the body. Sensory examination
showed a subtle hypesthesia on the right side. Two-point
discrimination, graphesthesia, and stereognosis were intact.

The patient's gait and results of cerebellar examination were
normal, Deep tendon reflexes were normal with bilateral
flexor plantar responses.
In the first week of hospital admission the patient was
tested using the Boston Diagnostic Aphasia Examination
(BDAE) E2a). The auditory comprehension z score was
-0.5. He had particular difficulty with sequential common
and complex material. H e was able to repeat single words,
but sentence repetition, especially repetition of low probability sentences, was impaired. Numerous verbal and some literal paraphasias were noted. T h e patient experienced some
difficulty with the naming sections of the test. Ability to copy
was intact, but writing to dictation was moderately impaired.
Reading comprehension was mildly impaired. The BDAE
profile was that of a patient with Wernicke's aphasia (Fig IA).
O n follow-up examination, three months after admission,
the auditory comprehension z score was +0.75. The patient
was able to follow all but the most complex commands exactly, and comprehension of complex material had improved
notably. Sentence repetition, especially repetition of low
probability sentences, was more accurate. The frequency of
literal and verbal paraphasias had decreased markedly. Naming had improved. The patient's reading comprehension and

Case Report: Lee et al: Transfer of Language Dominance

305

writing to dictation had improved slightly. The BDAE profile
was most compatible with that of a patient with anomic
aphasia (Fig 1B).
Computed tomography (CT) on the fourth day of admission showed an old left temporoparietal infarct involving the
left angular and posterior temporal artery territories. Following infusion of contrast material, cortical enhancement was
noted in the right angular and posterior temporal artery territories, indicating a recent infarct (Fig 2).

Discussion
The role of the nondominant hemisphere in linguistic
function remains a controversial issue. It is thought to
have a minor role in language function, involving
mainly the emotional aspect, or prosody of language 19,
10, 121. However, the capacity of the nondominant
hemisphere for developing a major function in language following injury in the dominant hemisphere has
been observed [3, 5-8). Studies of patients who
underwent commissurotomy reveal that the right
hemisphere has simple vocabulary and some grammatical capability [2). It is more capable of semantic than
phonetic information processing and has some plasticity for acquiring certain language functions generally
believed to belong to the left hemisphere [ll). The
patient described by Cummings and colleagues [I} re-

306 Annals of Neurology

Vol 15 No 3 March 1984

F i g 2 . Computed tomography with contrast enhancement shou s
an old infarct in the left temporoparietalregion and an acute enhanced infarct in the right temporoparietalregion.

covered partially from global aphasia following an embolic infarct involving both Wernicke’s and Broca’s
areas as demonstrated by CT. These authors suggested
that a “transfer” of language function to the right hemisphere was the basis of the recovery observed.
Our patient presumably illustrates this transfer phenomenon. Alternately, he may be part of that 1 5 9 of
the population that apparently possesses bilateral language representation in the hemispheres. Another possible explanation is that the new infarct seen on the CT
scan was accompanied by a fresh lesion on the left that
was not seen on CT, but which was responsible for
exacerbation of the aphasia. This explanation seems
unlikely. Whether the recurrence of Wernicke’s
aphasia with a new right hemisphere lesion represents
damage to a transferred language function or to a
preexisting right hemisphere language capacity cannot
be determined, however.
A question of equal importance is the mechanism of
recovery from the second occurrence of aphasia. Several hypotheses can be derived from this case: ( 1) the

area of infarct in this patient is not the primary area for
storing the language function, but rather the secondary
area, which activates the primary language storage area;
(2) a “third” area capable of acquiring the language
function is present in this patient; or ( 3 )recovery from
the second aphasia resulted from healing of the lesion
itself. The answers to these questions await further
studies.

References
1. Cummings JL, Benson DF, Walsh MJ, Levine HL: Left-to-right
transfer of language dominance: a case study. Neurology
29:1547-1550, 1979
2. Gazzaniga MS, Volpe BT, Smylie CS, et al: Plasticity in speech
organization following commissurotomy. Brain 102:805-8 15,

1979
2a. Goodglass H, Kaplan E: The Assessment of Aphasia and Related Disorders, Philadelphia, Lea & Febiger, 1972
3 . Henschen SE: Klinische und anatomische Beitrage zur

Pathologie des Gehirns. Vols 5-7. Stockholm, Nordiska
Bokhandlin, 1922
4 Kertesz A: Recovery and Treatment. In Heilman KW, Valenstein E (eds): Clinical Neuropsychology. New York, Oxford
University Press, 1979, pp 503-524
5 Kinsbourne M: The minor cerebral hemisphere as a source of
aphasic speech. Arch Neurol 25:302-306, 1971
6.Lenneberg EH: Biological Foundations of Language. New York,
John Wiley & Sons, 1967, pp 142-158
7. Luria AR: Restoration of Function after Brain Injury. London,
Pergamon Press, 1963
8. Nielson JM: Agnosia, Apraxia, Aphasia. New York, Paul B
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9. Ross ED: The aprosodias. Arch Neurol 38:561-569, 1981
10. Ross ED, Mesulam MM: Dominant language functions of the
right hemisphere? Arch Neurol 36:144-148, 1979
11 Sidtis JJ, Volpe BT, Wilson D H , et al: Variability in right hemisphere language function after callosal section: evidence for a
continuum of generative capacity. J Neurosci 1:323-331, 1981
12. Tucker DM, Watson RT, Heilman KM: Discrimination and evocation of affectively intoned speech in patients with right parietal
disease. Neurology 27947-950, 1977

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307