Amusia due to Right Temporoparietal Infarct
H. Richard McFarland, MD, David Fortin, MD

\s=b\ An
accomplished organist, who
could neither read nor write music, suddenly lost his ability to play familiar melodies as the result of an infarction of the
right superior temporal and supramarginal
gyri. Although the patient had minor difficulty recognizing familiar melodies and
coordinating his hands, he had mainly an
expressive instrumental amusia. This
case provides further evidence of right
hemispheric dominance for musical execution, relatively independent of musical
knowledge and training.
(Arch Neurol 1982;39:725-727)

second CT scan on July 11 demonstrated a
cerebral infarct in the region of the right
superior temporal and supramarginal gyri
(Figs 1 through 3). A complete speech and
language evaluation on July 2 revealed no
dyspraxia or dysarthria. Results of the
Boston Diagnostic Aphasia Examination
were normal. He was able to recite rhymes,
sing a song, and imitate rhythm. He had
mild difficulty drawing figures in perspec¬
tive and copying stick figures. An audiometric screening test was given in a nonsound-treated room, and his hearing sensi¬
tivity was within normal limits for his age.
On Oct 1, the patient was tested (by
H.R.M.) at the organ using the Dorgeuille

test battery.3 He had considerable difficul¬

ty reproducing rhythmic patterns of sim¬
ple and universally familiar melodies on
the organ. Although he perceived the mel¬
ody in his mind, he could not make his
hands correctly reproduce the melody.
What he produced was garbled and did not

sound correct to him. He also had some
difficulty identifying familiar melodies,
but no difficulty discriminating sounds or
identifying types of music or musical
instruments. He did recognize his favorite
melodies as familiar. He was able to play
his favorite melodies at this time, albeit
with numerous missed notes and chords
and poor syncopation. One year after his

Amusia is an impaired capacity for
musical activity.1 Sensory (recep¬
tive) amusia comprises an inability to
hear, read, or understand music (mu¬
sical agnosia), whereas motor (expres¬
sive) amusia is difficulty in singing or
writing music or in instrumental per¬
formance.2 The patient described
herein was not trained in theory or
sight reading but was able to repro¬
duce on the organ melodies he heard.
He experienced expressive, instru¬
mental amusia as the result of a right
temporoparietal lobe infarct.
REPORT OF A CASE

78-year-old, right-handed man en¬
joyed good health until June 4, 1980, when
without warning he sneezed eight times in
A

succession and thereafter was unable to

play the organ. Although he could still
strike notes and form some chords, he
could neither place them into a melodious
sequence nor make his right and left hands
coordinate properly. Two weeks later,
when he was seen in neurologic consulta¬
tion, he admitted to being less alert, for¬
getting familiar names, and enunciating
improperly. On neurologic examination he
was alert, oriented, and had a mild degree
was 165/90 mm Hg
of dysarthria. His
and his pulse was irregular. Minimal astereognosis was found in the left hand. He
had a fine action tremor and a hesitancy in
walking. The remainder of the neurologic
examination results were normal. The
EEG showed focal slowing in the right

temporoparietal region. Computed tomographic (CT) scan of the head June 20
showed an acute right temporoparietal
cerebral infarct with luxury perfusion. A
Accepted for publication Dec 31, 1981.
From the Departments of Neurology (Dr
McFarland) and Radiology (Dr Fortin), St Luke's
Hospital, Kansas City, Mo, and the Department
of Neurology, University of Kansas Medical Center, Kansas City (Dr McFarland).
Reprint requests to 4320 Wornall Rd, Suite 620,
Kansas City, MO 64111 (Dr McFarland).

Fig 1.—Non-contrast-enhanced images from 55 to 70 mm above orbitomeatal line obtained July
11, 1980, showing irregular, radiolucent lesion in right temporoparietal region adjacent to sylvian
fissure involving superior temporal and supramarginal gyri.

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Fig 2.—Coronal reconstruction, July 11,
1980. Note prominent area of diminished
absorption superficial to circular sulcus on
right that represents infarction of temporal
operculum (ie, superior temporal gyrus).

patients with right hemispheric dis¬
ease who could not identify melodies.
Right hemispheric lesions have
resulted in difficulty with musical
perception and rhythm apprecia¬
tion.810 Following right carotid amobarbital injection into right-handed
subjects, Gordon and Bogen11 ob¬
served transient expressive amusia.
Benton's3 analysis of the clinical liter¬
ature suggests that pure expressive
amusia with preservation of receptive
functions and without aphasia is most
likely to be associated with lesions of
the right hemisphere. Recently Da¬
masio and Damasio12 accepted the
right hemisphere as dominant for
musical execution and perception,
independent of musical knowledge
and training.
Conversely, left temporoparietal
lesions may not produce amusia.5
Assai13 described a pianist who suf¬
fered from Wernicke's aphasia and
word deafness following an embolie
lesion of the left temporoparietal
region who did not have any defect in
his musical ability. (For a recent
review of this subject, see Brust.14)
The patient was a "naive" musician
and not musically educated. Beaver

and Chiarello15 called attention to the
possibility that, according to the sub¬
ject's contact with music, different
nervous structures may be engaged in
the processing of musical stimuli and
that a melody, regardless of its being
composed by a series of isolated notes,
may be either perceived in terms of its
overall melodic contour or as an orga¬
nized arrangement of components.
Beaver and Chiarello concluded that
naive listeners and musicians do, in
fact, perceive melodies in a gestalt
fashion and that the processing is
predominantly in the right hemi¬

sphere.

In conclusion, lesions of the right
hemisphere may cause both motor

and sensory amusia. The case
described provides further evidence
that the right hemisphere is dominant
for musical execution.
Fig 3.—Schematic localization of four slices of examination of July 11, 1980 (shown in Fig 2);
stippled area represents lesion. IPG indicates inferior parietal gyrus; PCG, posterior central
gyrus; SK/IG, supramarginal gyrus; and STG, superior temporal gyrus.

stroke, he refrains from playing the organ
because his production is inaccurate and
not melodious.
COMMENT

Penfield and Perot" found that
musical hallucinations were evoked
with stimulation of the superior or
lateral surface of the first temporal
convolution on either side, but more
on the right than on the left. Follow-

ing right temporal lobectomy for
epilepsy, Milner5 recognized an im¬
pairment of certain kinds of auditory
discrimination, comparison of tonal
patterns and judgment of tonal quali¬

ty. This pattern did not occur after
left temporal lobectomies. After right
temporal lobectomy, Shankwieler6
noted deterioration of melody recog¬
nition. Grison7 described a number of

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References
1. Werthheim N: Is there an anatomical localization for musical faculties? in Critchley M,
Henson PA (eds): Music and the Brain. London,
William Heinemann Medical Books Ltd, 1977, pp
282-297.
2. Henson RA: Neurological aspects of musical
experience, in Critchley M, Henson PA (eds):
Music and the Brain. London, William Heinemann Medical Books Ltd, 1977, pp 3-21.
3. Benton AL: The amusias, in Critchley M,
Henson PA (eds): Music and the Brain. London,
William Heinemann Medical Books Ltd, 1977, pp
378-397.
4. Penfield W, Perot P: The brain's record of
auditory and
visual experience. Brain

1963;86:595-696.

5. Milner B: Laterality effects in audition, in
Mountcastle VB (ed): Hemispheric Relations and
Cerebral Dominance. Baltimore, Johns Hopkins
Press, 1962, pp 107-195.
6. Shankweiler D: Effects of temporal lobe
damage on perception of dichotically presented
melodies. J Comp Physiol Psychol 1966;62:115\x=req-\
119.
7. Grison B: Une etude sur les alterations
musicales au cours des lesions hemispheriques,
thesis. Paris, 1972.
8. Kohl GF, Tschabitscher H: Uber einen Fall
von Amusie. Wein Z Nervenheilkd Grenzgebiste

PA (eds): Music and the Brain. London, William
Heinemann Medical Books Ltd, 1977, pp 141\x=req-\

1953;6:219-230.

9. Pittrich H: Sensorische Amusie mit paramusie nach rechtsseitger Temporalverlitzung,
film. G\l=o"\ttingen,Germany, G\l=o"\ttingenInstitute
fur den Wissenchaften Film, 1956.
10. Potzl 0: Zur Pathologie der Amusie.
Z Gesamte Neurol Psychiatr 1939;165:187-195.
11. Gordon HW, Bogen JE: Hemispheric lateralization of singing after intracarotid sodium
amylobarbitone. J Neurol Neurosurg Psychiatry

155.
13. Assal G: Aphasie de Wernicke sans, amusie chez un pianiste. Rev Neurol 1973;129:251\x=req-\
256.
14. Brust JCM: Music and language: Musical
alexia and agraphia. Brain 1980;103:367-392.
15. Beaver TJ, Chiarello RJ: Cerebral dominance in musicians and non-musicians. Science

1974;37:727-738.

1974;185:537.

12. Damasio H, Damasio AR: Musical faculty
and cerebral dominance, in Critchley M, Henson

Hypermagnesemic Periodic Paralysis
Treatment With Digitalis and Lithium Carbonate
Wendelin Emser, MD
\s=b\ An 18-year-old man suffering from a
hereditary hyperkalemic periodic paralysis showed, in addition, a hypermagnesemic periodic paralysis with a 2.5-fold
increase in serum magnesium level. All
other serum electrolyte levels were normal. The hypermagnesemic periodic
paralysis seems to have been caused by a
disturbance of the renal tubular system.
Thus, magnesium-stimulated paralysis
was prevented by treatment with lithium
carbonate and digitalis, which blocked
the active ion transport.
(Arch Neurol 1982;39:727-730)

An 18-year-old man was ordered to
report to an army recruiting sta¬
tion but sought medical advice

because he believed himself to be unfit
for military service. The young man,
his mother, brother, and sister, and
other relatives (Fig 1) had a hyper¬
kalemic periodic paralysis1·2 with
myotonic signs. This combination has
also been reported in other pa¬
tients.36
The short-lasting hyperkalemic
weakness did not bother the young
man. It was the occurrence of longerlasting and severe paralyses that wor¬
ried him, since none of the other fam¬
ily members showed these symp¬
toms.
REPORT OF A CASE

The patient had his first attack of peri¬
odic paralysis at the age of 6 years. The
attacks were mild, lasted ten to 20 minutes,
started with lingual myotonia, lid-lag, and

Accepted for publication Feb 15, 1982.
From the Department of Neurology, University Hospital, Homburg, Saar, West Germany.
Reprint requests to Neurologische Universit\l=a'\tsklinik,Universit\l=a"\tdes Saarlandes, 6650
Homburg/Saar-FRG (West Germany) (Dr Emser).

myotonic signs in the face, and sometimes
spread to limb muscles before the actual
paresis occurred. The attacks were hyper-

kalemic.
When the patient was 12 years old,
another type of periodic paralysis began. It
was much more prolonged and more
severe, had no preceding myotonic symp¬
toms, occurred every four to six weeks, and
lasted six to eight days. Typically, the
weakness started without other symptoms
when he awoke; the patient noticed a weak¬
ness of the distal muscles of the lower
extremities, especially of those muscles
responsible for foot elevation; this resulted
in a foot-slapping gait.
During the course of one to two days and
in conjunction with the increasing serum
magnesium level, the weakness spread to
the forearm muscles such that the patient
had difficulty making a fist. Often the
proximal leg muscles became affected, and
the patient had difficulties in walking up
stairs and in coming up from a squatting
position. The weakness thus manifested
itself for about three to four days. The
recovery from this periodic paralysis
spanned two days but the muscles first
affected were the last to improve. During
recovery, the patient believed that he had
to urinate more often. The trunk muscles
were seldom involved, being affected at the
most once a year. In this case, elevation
from a lying or squatting position was

severely impeded. Sometimes, even after

feet and hand extensors were affected, the
paralysis ceased and showed no further
signs of progression.
Respiratory, facial, and esophageal mus¬
cles were never affected. The patient never
noticed any symptoms of the developing
paralysis or any other discomfort.
Physical activities or other exogenous
factors, such as nutrition, did not provoke
this periodic paralysis. The patient was not
taking any medication. If, by chance, he
had driven a bicycle or strained his arms
shortly before the weakness appeared, the
used muscles then were affected more

severely.

During the course of the paralysis, only
weak reproducible reflexes were found
during neurological examination. The
patient could not stand on his heels or toes
(Fig 2), coming up from a squatting posi¬
tion was clearly difficult, chair climbing
was difficult, and hand strength was
strongly reduced (Fig 3). The affected mus¬
cles had a weak tone and were not sensitive
to pressure. Otherwise the neurological
findings were normal.
Relatives of the patient (Fig 1) were
available for questioning and examination.
None of them complained about experienc¬
ing the same paralysis experienced by the
patient. The relatives with hyperkalemic
periodic weakness would only allow a
serum electrolyte determination; this test
produced normal magnesium values. No
relatives were willing to subject them¬
selves to further detailed clinical examina¬
tion because they all felt well and their
mild hyperkalemic periodic paralysis did
not cause them any discomfort.
Between attacks, the patient showed no
abnormalities on neurological examina¬

tion, poorly developed reflexes, no myotonia after grasp or percussion, and no lidlag; only a percussion myotonia of the
tongue was detected.

LABORATORY FINDINGS

The ECG

was

normal between

attacks; however during attacks high
waves appeared. Between attacks
electromyography at the upper ex¬
tremities showed "pseudomyotonic"
discharges (bizarre high frequency)
for 5 to 10 s with spontaneous activity
known in patients with hyperkalemic
paralysis.7 The muscles' volitional
potentials were normal.
During hypermagnesemic periodic
paralysis, neither spontaneous activi¬
ty nor myotonic discharges could be
detected. Investigations of the ulnar
and median nerves with repetitive
stimulation8 did not show a myasthen-

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