THE

KURUME

Vol.36,

p.23-27,

MEDICAL

JOURNAL

1989

Cerebral
YOSHIHIRO

SATO,

Department

Embolism

YOUSUKE

of Internal

Received

and

Hyperthyroidism

SATO,
SHINICHI
KAKISAKO,
AND MASARO
KAJI

Medicine, Kurume University
Kurume, 830 Japan
for publication

January

17,

YOSHIAKI

HONDA

School of Medicine,

1989

Summary: Three different cases of cerebral embolism occurring in combination with hyperthyroidism are reported. Case 1; a healthy 37-year-old woman presented with sudden onset of left hemiparesis and left sided hypoesthesia
of all modalities. Embolism in area of the right middle cerebral artery was
confirmed by angiography and CT scan. Laboratory examination revealed
hyperthyroidism and anemia. Antithyroid treatment brought about euthyroid
function while slight hemiparesis remained present. Case 2; a 79-year-old
woman who suffered from hypertension for one year had sudden onset of disorientation and left hemiparesis. Electrocardiogram showed atrial fibrillation.
The CT scan indicated infarction in the right anterior and middle cerebral artery. The patient was diagnosed as having masked hyperthyroidism. Although
antithyroid medication reduced it to euthyroid condition, the patient is now
bedridden with hemiparesis. Case 3 ; a 45-year-old man who had partial thy roidectomy for Basedow's disease and had been treated with antithyroid and
antiarrhythmic therapy for 10 years. Suddenly, he was in coma with dilated
right pupil and left hemiplegia. Atrial fibrillation and hypothyroid function
were observed. CT scan indicated hemorrhagic infarction in the territory of
the middle cerebral artery with transtentorial herniation. He died on the 59th
day of hospitalization following an episode of bronchopneumonia. On the basis
of the cases presented here as well as on the basis of those described in the
literature it appears that thyrotoxic patients with atrial fibrillation exhibit
high incidence of cerebral embolism, and prophylactic anticoagualnt therapy
may be recommended.
Key words : cerebral
rial

fibrillation

-

embolism

anticoagulant

-

hyperthyroidism

-

Basedow's

disease

-

at -

therapy

Introduction

patients
of nonvalvular
atrial
fibrillation
would have a stroke during
their life time
and about 20% would face another
cerebral infarciton
within
a year
from
the
initial
ictus.

The major cardiac causes of cerebral
embolism today are nonvalvular
atrial fibrillation and mural thrombus from myocardial infarction,
as recently the general
decline in rheumatic fever and rheumatic
heart disease have reduced the incidence
and pathologic
basis for valvular
heart
disease (Scheinberg, 1988). Sherman et al.
(1984, 1986) concluded that about 35% of

Atrial fibrillation developes in 10% to
15% of patients suffering from overt hyperthyroidism
(Sandier and Wilson, 1959).
High frequency of cerebral embolism was
recorded
recently
in patients
suffering
from a combination
of hyperthyroidism
23

SATO,

24

ET

AL.

and atrial fibrillation in the U.S.A., Australia or England (Staffurth
et al. 1977;
Yuen et al. 1979; Hurley et al. 1981; BarSela et al. 1981). We report here three
cases of cerebral embolism accompanied
by hyperthyroidism.

Case Reports
Case 1;
a 37-year-old
May

11,

left-sided
of

tremor,

woman

1986

due

to

weakness.

was
a

sudden

She

had

hyperhidrosis,

admitted

on

onset
no

of

history

palpitation,

or

irritability.

Her blood pressure was 140/80mmHg.
and her pulse rate, 120 per minute, was
regular. Slight bilateral exophthalmus and
anemic conjunctiva were noted. The thyroid gland was not felt. Carotid bruits

Fig.2.
parietal

Right
and

carotid

temporooccipital

angiography
arteries.

ting

Fig.1.
A CT scan
cerebral
infarction

parietal

of Case

of Case 1, demonstrain the right
temporo-

regions.

1, showing

obstruction

of the

CEREBRAL

and

apical

ated.

systolic

murmur

Neurologic

strated
ing
thesia

left

and

tongue,

all

modalities,

of

were

auscul-

examination

alertness,
face

EMBOLISM

demon-

hemiparesis

includ-

left

hypoes-

sided
and

fine

finger

tremor.
Laboratory

tests

hypochromic

revealed

anemia

Pertinent

and

results

count

of

included

6.6g/dl;

16.5ƒÊg/dl;

total

4. 1 ng/ml

and
of

globulin

red-blood

421•~10•¬4/mm3;

hemoglobin,

Titers

microcytic,

hyperthyroidism.

serum

24%;

thyroxine

(T3)

triiodothyronine

(T4).

thyrotropine,

0.1ƒÊU/ml.

antimicrosomal
antibody

cell

hematocrit

and

were

antithyro-

1:25,600

and

1:400,

respectively.

Electrocardiogram
(ECG) revealed the
presence of sinus tachycardia;
two-dimensinal
echocardiography
revealed
no
thrombi,
chamber enlargement,
or other
abnormality.
Holter ECG did not show
any arrhythmia
in a 24-hour recording.
The plain CT scan with 360 by 360
matrix
showed a decreased
radiodensity
in an area of the right middle cerebral
artery (Fig. 1). Examination
of the patient by Seldinger's method with injection
of 10ml Metrizamide into the internal carotid artery revealed obstruction
of the
right parietal and temporo-occipital
arteries (Fig. 2). Thus, she was diagnosed
embolic cerebral
infarction
because the
site of arterial
obstruction
was distal
compared with extension
of infarct size
on CT scan.

AND

HYPERTHYROIDISM

25

Her blood pressure
was 144/66mmHg.
Pulse rate was 120 beats per minutes
and
irregular.
The
thyroid
gland
was
felt
slightly.
The
chest
and abdomen
were
normal.
The patient
was disoriented
and
hemispatial
agnosia
was suspected.
Moderate
left
hemiparesis
which
included
tongue
was present.
Sensory
impairment
was uncertain
because
of the disorder
of
consciousness.

The pertinent
laboratory
test results
were as follows: hematocrit,
38.9%; whiteblood cell count, 11,600; alkaline phosphatase (Kind-King method), high at 11.5
unit; other liver function tests revealed
no abnormalities.
Serum electrolyte
and
renal function were within normal limit.
Serum T3 was 13.7ƒÊg/dl; T4 was 0.9ng
/ml. Serum thyrotropine
was less than
0.02ƒÊU/ml. Titers of antimicrosomal
and
antithyroglobulin
antibody were both 1:
400.

After three weeks of Thiamazole
treatment
15mg
daily,
the thyroid
function
returned
to normal
(T3 8.8ƒÊg/dl,
T4 2.9
ng/ml).
Six weeks
later,
she was discharged
with slight
left hemiparesis
and
euthyroid
function.
Case

2;

a 79-year-old

ted

on

May

15,

set

of

left-sided

woman

1987

one

hypertensive

medication
hospital.

year

was

admit-

to a sudden

weakness.

hypertension
another

due

She

on-

developed

earlier

and

was

prescribed

Fig.3.

antiat

A CT

ting infarction
anterior
and

scan

of

Case

2, demonstra-

in the distribution
of the
middle cerebral
arteries.

right

SATO,

26

ET

AL.

Atrial fibrillation at a rate of 180 was
revealed in the ECG. Areas of the right
anterior and middle cerebral artery were
attenuated
in a CT scan (Fig. 3). It was
concluded that the patient suffered from
masked hyperthyroidism,
atrial fibrillation
and cerebral embolism of cardiac origin.
Following Glycerol and Thiamazole 15
mg daily, the thyroid function recovered
(T3 8.5ƒÊg/dl, T4 0.7ng/ml)
and the patient regained her consciousness. The left
hemiparesis
and atrial
fibrillation
persisted, however, and the patient was bedridden ever since.
Case 3; a 45 year-old-man
who had a
sudden
onset
of left-sided
weakness
was
admitted
on September
15, 1988. He had
been suffering
from
Basedow's
disease,
hypertension
and arrhythmia
for ten years.
Partial
thyroidectomy
was performed
and
antithyroid
and
antiarrhythmic
therapy
was instituted.

Blood pressure was 148/98 mmHg. Pulse
rate was 84 per minute and irregular.
The thyroid gland was not palpable. The
chest and abdomen were normal. The patient exhibited slight drowsiness and left
hemiplegia which included the face. On
the next day he was comatous and his
right pupil was dilated.
The laboratory test results were as follows: hematocrit, 46.2%; white-blood cell
count, 13,700; liver and renal function
were normal. Serum T3 was 2.3ƒÊg/dl, T4
0.2ng/ml
and thyrotropine
3.2ƒÊU/ml indicated hypothyroidism.
The ECG revealed presence
of atrial
fibrillation at a rate of 90 per minute. A
plain CT scan performed
on the second
day following the admission showed hemorrhagic infarction in the distribution
of
the right middle cerebral artery (Fig. 4).
The patient
was diagnosed
as suffering
from hemorrhagic
cerebral embolism with
transtentorial
herniation
caused by the
atrial fibrillation.
Although

the

patient

received

external

Fig.4.

A CT

morrhagic

scan

infarction

right middle
herniation.

cerebral

decompression

for

pressure

and

of Case
artery

died

zation

of

artificial

on

the

with

he

the

intracranial

respiration

59th

heof

transtentorial

and

were
initiated
admission,

complications

bronchopneumonia;

showing

increased

parenteral
nutrition
second
day
following
tient

3,

in the distribution

day

of

total

on
the

the
pa-

hospitali-

which

included

never

regained

consciousness.

Discussion

These three cases had different
pathologic basis. In case 1, hypertyroidism
was recognized only after the onset of
cerebral embolism. Staffurth et al. (1977)
reported three cases in which hyperthyroidism preceded the embolus. There are
no literature reports available at this time,
as to the absence of arrhythmias
in hyperthyroidism
associated
with
cerebral
embolism. Bar-Sela et al. (1981) reported
that 12 embolic complications
were found
in 30 patients presenting
with thyrotoxic

CEREBRAL

atrial
had

fibrillation,
no

episodes

while
in

sinus

other

EMBOLISM

112 patients

AND

HYPERTHYROIDISM

27

References

rhythm.

With respect to case 2, cerebral em bolism occurred in an elder patient who
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in elderly patients
with
atrial fibrillation
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Tajiri et al. 1986; Bruce et al. 1987). There
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was recognized
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