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NEUROSURGERY
Copyright © 1986 by the Congress of Neurological Surgeons

Vol. 18, No. 4, 1986
Printed in U.S.A.

Caudate Hemorrhage

Shiro Waga, M.D., D.M.Sc., Kiyoshige Fujimoto, M.D., Masahiko Okada, M.D., Masao Miyazaki, M.D., and
Yutaka Tanaka, M.D.

Department of Neurosurgery and Neurology, Mie University Hospital and Matsusaka Central Hospital, Mie, Japan

Thirteen patients with caudate hemorrhage are described. All the hemorrhages were in the head of the caudate nucleus,
and all the hemorrhages but one ruptured in the anterior horn of the lateral ventricle. In 9 patients, the hemorrhage
was related to hypertension and the patients were older. In the other 4 patients, the hemorrhage resulted from rupture
of an arteriovenous malformation (AVM) and the patients were under 40 years old. Clinical manifestations were nearly
the same in both groups, suggestive of subarachnoid hemorrhage and including hemiparesis in most patients. In patients
with hypertension, good recovery was obtained by conservative treatment and in those with ruptured AVMs, resection
of AVMs through an anterior transcallosal approach may be safe and recommended. (Neurosurgery 18:445-450, 1986)

Key words: Arteriovenous malformation, Caudate hemorrhage, Cerebral hemorrhage, Hypertension, Ventricular

hemorrhage

The common sites of hypertensive cerebral hemorrhage are
the putamen, thalamus, cerebral hemispheric white matter,
pons, and cerebellum (1, 7). The caudate nucleus receives its
blood supply from the deep penetrating branches of the
lenticulostriate arteries, as does the putamen. Hemorrhage in
the caudate nucleus, however, has rarely been described in
association with hypertension or with arteriovenous malfor-
mations (AVMs) (2, 4-6, 8).

The present report describes 13 patients with caudate hem-
orrhage, and emphasizes its clinical and computed tomo-
graphic (CT) features, and the treatment of choice.

PATIENT POPULATION AND METHODS

From January 1977 to December 1984, we had 313 patients
with hypertensive cerebral hemorrhage. 9 of whom had hem-
orrhage in the head of the caudate nucleus. We also had 70
patients with cerebral AVMs, 4 of them in the head of the
caudate nucleus. Thus, caudate hemorrhage represents 3% of
hypertensive cerebral hemorrhages and 5.7% of cerebral
AVMs. All the hemorrhages were located in the head of the
caudate nucleus, and all the patients were diagnosed by CT
scan. All 13 patients had contrast-enhanced CT scans, and
cerebral angiography was performed in 6 out of 9 patients
with hypertensive hemorrhage and in all 4 patients with AVM.
All 9 patients classified as hypertensive had had known hy-
pertension, 2 had renal disease. and other 2 suffered diabetes
mellitus. The 4 patients with AVM were not hypertensive.
We review and analyze the case records of these 13 patients
with CT evidence of caudate hemorrhage.

REPRESENTATIVE CASE REPORTS OF
HYPERTENSION CAUDATE HEMORRHAGE

Case 5

The sleep of a 51-year-old hypertensive fisherman was
disrupted by severe headache and vomiting followed by di-
sorientation. At the time of admission, the patient was drowsy
and disoriented, but otherwise neurologically intact, except
for nuchal rigidity. CT scan disclosed hemorrhage in the head
of the right caudate nucleus with ventricular rupture (Fig. 1).
Four-vessel angiography demonstrated no vascular lesions.
He rapidly improved in the course of 1 month of conservative
treatment and returned to a fisherman’s life without deficit.

445

Case 8

A 61-year-old housewife suddenly vomited while lunching,
complained of severe headache, and then collapsed. She was
seen at a nearby hospital, where a spinal tap disclosed grossly
bloody cerebrospinal fluid (CSF). On admission to our hos-
pital, the patient was alert and cooperative. Neurological
examination revealed moderate disorientation and dyscalcu-
lia, neck stiffness, a slight right hemiparesis, and bilateral
extensor plantar responses. Her history included hyperten-
sion. CT scan demonstrated left ventricular hemorrhage (Fig.

Fic. 1. Case 5. CT scan demonstrates hemorrhage in the head of
the right caudate nucleus, with rupture in the anterior horn of the
lateral ventricle.

446 WAGA etal. Neurosurgery, Vol. 18, No. 4

Fic. 2. Case 8. .4, CT scan discloses intraventricular hemorrhage (IVH) in the left lateral ventricle. B, three weeks after the hemorrhage, the

IVH still persists. C. three months after the hemorrhage, the IVH persi although the density has decreased. The head of the left caudate
nucleus shows marked atrophy. One of reasons we conclude the I1VH originates there. D, one after the hemorrhage, the I1VH remains in the
body of the lateral ventricle and shows some enhancement after intravenous administration of iodinate contrast material.

April 1986

2A). Four-vessel angiography disclosed nothing abnormal.
She rapidly improved. and 3 weeks later she was discharged
without any sequela. Follow-up CT scan, however, demon-
strated interesting findings. At the time of discharge intraven-
tricular hemorrhage still persisted (Fig. 2B). Three months
after discharge. the hemorrhage was still seen in the left lateral
ventricle, although it decreased in intensity, and the left
anterior horn began to dilate, especially at the site of the head
of the caudate nucleus (Fig. 2C). Even | year after the hem-
orrhage, although the intraventricular hemorrhage disap-
peared in the anterior horn, it remained in the body of the
lateral ventricle (Fig. 2D), as we had observed before (9).

Case 9

A 54-year-old housewife was found unconscious on her
farm. The patient was evaluated at another hospital. She was
stuporous, with moderate nuchal rigidity and moderate right
hemiparesis. CT scan demonstrated hemorrhage in the head
of the left caudate nucleus, with ventricular rupture, and a
round mass in the left occipital region (Fig. 34). On referral
to us, she was alert and cooperative. There were right hemi-
paresis and hemihypesthesia, and right extensor plantar re-
sponse. Neurological examination revealed moderate loss of
recent memory, slight confusion, mild disorientation for time,
and moderate loss of attention span. Four-vessel angiography
demonstrated some feeding vessels to the left occipital tumor,
but did not demonstrate any vascular lesion. The tumor was
removed totally through a left occipital craniotomy. The
histological diagnosis was meningotheliomataous meningi-
oma. The caudate hemorrhage was not evacuated. Her neu-
rological symptoms and signs gradually decreased over |
month. She was discharged with only slight loss of recent
memory. CT scan demonstrated a moderate low density area
in the head of the left caudate nucleus and its adjacent region,
with dilatation of the anterior horn, and total removal of the
tumor (Fig. 3B).

CAUDATE HEMORRHAGE 447
RESULTS

Clinical and neuroradiological findings, treatment, and re-
sults are summarized in Tables | and 2.

Hypertensive caudate hemorrhage

There were seven male and two female patients: all nine
patients had known hypertension (Table 1). Five took anti-
hypertensive medication regularly and the other four took
medicine irregularly. Seven patients developed sudden severe
headache and vomiting, which was followed by unconscious-
ness in four. One was found unconscious on her farm, and
another awakened with a right hemiparesis from general
anesthesia for clipping of an aneurysm of the left middle
cerebral artery. At the time of admission no patient was
comatose; four were somnolent or drowsy, and consciousness
was nearly complete in the other five, although three of these
were moderately disoriented. Eight patients had nuchal rigid-
ity, although the degree was variable. Motor weakness was
noted in five: central facial paresis in two, moderate hemipa-
resis in 2, and moderate paresis of the upper limb in the other.
Involuntary blepharospasm-like movement of the contralat-
eral eyelids was transiently observed in one, and papilledema
was also noted in one. Hemihypesthesia was present in only
one in whom the hemorrhage extended into the anterior limb
of the internal capsule. Marked memory loss was present in
one, probably due to preceeding multiple cerebral infarcts.

According to the amount of blood within the ventricular
system, severity of intraventricular hemorrhage has been
graded as mild, moderate, and severe (3). Three had severe
hemorrhage, 3 had moderate, 2 had mild, and one did not
develop intraventricular hemorrhage. All the hemorrhages
occurred in the head of the caudate nucleus, and ventricular
rupture almost always took place in the anterior horn, when
it occurred. There was no patient with caudate hemorrhage
that ruptured in the body of the lateral ventricle. In Case 8,
the hemorrhage persisted unabsorbed in the body of the lateral
ventricle even | year after the hemorrhage, but the site of the

Fic. 3. Case 9. 4. CT scan demonstrates hemorrhage in the head of the left caudate nucleus and its adjacent region, with rupture in the
lateral ventricle and a round tumor in the left occipital region. B. 4 weeks after the hemorrhage. a moderately sized low density area in the
previously hemorrhagic region. with dilatation of the left anterior horn is observed. The occipital tumor is completely removed.

448 WAGA etal. Neurosurgery, Vol. 18, No. 4

TABLE |
Summary of Patients with Hypertensive Caudate Hemorrhage*
Patient Age Sex on Symptoms Signs cT IVH_— Angiography — Treatment Results aa
1 31 M +,renal Headache Somnolence, Hemorrhage in ++ Negative Removal of — Excellent 5% yr
collapse nuchal rigid- the head of hemor-
ity, involun- CN, ex- rhage
tary move- tended to
ment of L the anterior
eyelid, L. limb of IC
central facial (R)
paresis
2 43 M +.renal Headache Somnolence, Hemorrhage in ee Negative Supportive Excellent Syr
collapse nuchal rigid- the head of
ity, R central CN (L)
facial paresis
3 53 M +,DM Headache Nuchal rigidity, | Hemorrhage in + ND Supportive Poor (multi- Syr
(no disorienta- the head of infarct
LOC) tion, CN (L) mul- demen-
recent mem- tiple infarcts tia)
ory loss
4 59 M + Headache, Drowsiness, Hemorrhage in +t ND Supportive Dead due to
vomit- nuchal rigid- the head of DIC,
ing; gait ity, papille- CN, ex- meningi-
and dema tended to lis, and
speech the anterior broncho-
disturb- limb of IC pneu-
ance (no (L) monia
LOC)
5 51 M + Headache, Drowsiness, di- Hemorrhagein +++ Negative Supportive Excellent 4yr
vomiting sorientation the head of
(no CN, ex-
LOC) tended to
the anterior
limb of IC
(R)
6 St M  +,DM Headache, Nuchal rigidity Hemorrhage in + ND Supportive Excellent 3% yr
vomiting the head of
(no CN (R)
LOC)
7 51 M + Headache Nuchal rigidity © SAH MCA Obliteration
aneu-
rysm
R weakness —R hemiparesis Hemorrhage in = Supportive Excellent 2yr
the head of
CN (L)
8 61 F + Headache, Nuchal rigidity, | IVH (L) +++ Negative Supportive Excellent 2yr
vomit- disorientation,
ing, col- R hemipa-
lapse resis
9 54 F + Collapse, R — Nuchal, rigid- Hemorrhage in +++ Negative Supportive
weakness ity, R hemi- the head of
paresis, R CN, ex-
hemihypes- tended to
thesia the anterior
and poste-
rior limbs of
IC (L)
L occipital me- Resection Excellent 4mo
ningioma

@ Abbre’ ations: IVH, intraventricular hemorrhage; IC, internal capsule; +, mild; ++, moderate; +++, severe; CN, caudate nucleus, DM, diabetes mellitus; ND,
not done; DIC, disseminated intravascular coagulation; SAH, subarachnoid hemorrhage: MCA, middle cerebral artery.

TABLE 2
Summary of Patients with Caudate Hemorrhage Due to Ruptured AVM*
Follow-up
Patient Age Sex Hypertension Symptoms Signs IVH_— Angiography Treatment Results Period
(yr)
10 MW M = Headache. vomiting. Drowsy, nuchal ri- ++ AVM L frontal transcorti- Excellent 7
Loc gidity, R hemipa- cal
resis
iW 18 M _ LOC Drowsy, nuchal ri- ++ AVM R frontal transcorti- — Excellent 634
gidity. L hemipa- ICH cal
resis
12 37 M _ Headache, vomiting —Neurologically intact. = ++ AVM R frontal transcorti- Poor 4
cal
13 35 F _ Headache. vomiting. Drowsy, R hemipa- ++ AVM Anterior transcallosal Excellent 3

LOC resis ICH

* Abbreviations: [VH, intraventricular hemorrhage: LOC. loss of consciousness: ICH, intracerebral hemorrhage.

April 1986

original rupture into the ventricle was in the anterior horn.
In 2 patients, the hemorrhage extended to the anterior limb
of the internal capsule.

Six patients underwent four-vessel angiography, and neither
aneurysm nor AVM was demonstrated. In one patient, the
caudate hemorrhage took place during operation for intracra-
nial aneurysm, and in another an asymptomatic occipital
meningioma was found on CT scan.

No surgical treatment was given to the caudate hemorrhage,
except in one patient with a tentative diagnosis of a cryptic
AVM. The treatment given was supportive in 8. The results
were excellent in 7; one died of disseminated intravascular
coagulopathy complicated by meningitis and bronchopneu-
monia, and the other was in poor condition because of the
preceding multiple cerebral infarcts.

Caudate hemorrhage due to ruptured AVM

Three patients were men and one was a woman. They were
all under the age of 40 at onset. None was hypertensive. All
the patients had sudden severe headache; three of them then
lost consciousness. On admission, three patients were still
drowsy and presented with hemiparesis, much worse in the
upper limb than in the lower one; two had nuchal rigidity,
and only one patient was neurologically intact. CT scan
showed that three had a high density area in the head of the
caudate nucleus that was contiguous to the anterior horn and
accompanied by moderate ventricular dilatation; one had
moderate hemorrhage in the head of the caudate nucleus
extending to the internal capsule, with very slight ventricular
hemorrhage. Intravenous administration of iodinated contrast
medium did not disclose the nidus of the AVM, but clearly
demonstrated the draining veins in all 4 patients, and angiog-
raphy clearly showed the AVMs.

The AVMs were resected by a frontal transcortical approach
in three and by an anterior transcallosal approach in one. The
results were excellent in three, although transient expressive
aphasia and weakness were observed in two who were oper-
ated on by a transcortical approach. In one patient, marked
confusion and disorientation were the significant sequelae
after a right frontal transcortical resection in a right-handed
young adult. Thereafter, we selected as treatment of choice
an anterior transcallosal approach for the AVMs in the head
of the caudate nucleus. Details of the AVMs in the lateral
ventricles are described in another report (6).

DISCUSSION

Hypertensive cerebral hemorrhage occurs as a result of
rupture of such penetrating arteries as the lenticulostriate
arteries in the putamen. The rupture is generally considered
to be due to necrotic and sclerotic changes in the walls of the
arteries. The caudate nucleus is also supplied by the deep
penetrating branches of the lenticulostriate arteries, so the
hemorrhage would be expected to occur in the caudate nu-
cleus. Nevertheless, reports of caudate hemorrhage have been
rare (2, 4, 5, 8). Stein et al have reported 12 patients with
hemorrhage in the head of the caudate nucleus (4). Clinical
features included acute onset of vomiting, headache, stiff
neck, decreased consciousness and behavioral abnormalities,
including disorientation and impaired memory. Eight of 12
patients were hypertensive, and the age at onset was older
than 40 years in 10. Signs included gaze paresis, Horner’s
syndrome. and hemiparesis. Seven patients had hemiparesis,
slight and transient in 4, and much severer in 3. All 12 patients
had hemorrhage in the head of the caudate nucleus with
intraventricular rupture. The prognosis for recovery was good
in 8: | patient was dead, and other 3 left moderate sequelae.

CAUDATE HEMORRHAGE 449

Weisberg reported eight patients with caudate hemorrhage
(8). Seven initially suggested clinical symptomatology of sub-
arachnoid hemorrhage and | had initial motor weakness.
Clinical manifestation included hemiparesis, pupillary abnor-
malities, and hemihypesthesia. Four patients had internal
carotid artery aneurysms, although the exact sites were not
described, and the other 4 patients had hypertension. Two of
4 patients with aneurysms died. Two of 4 patients with
hypertension also died, and | left the hospital with hemipa-
resis and hemisensory deficit. Weisberg stressed that in cau-
date hemorrhage due to rupture of an internal carotid artery
aneurysm, CT scan showed a high density area contiguous to
the anterior horn of the lateral ventricle, and that in caudate
hemorrhage related to hypertension, a small hematoma ap-
peared contiguous with the anterior portion of the body of
the lateral ventricle with prominent intraventricular extension
(8). In contrast to Weisberg’s observation, in our series of 13
patients of caudate hemorrhage not one had an aneurysm of
the internal carotid artery. Nine patients had hemorrhage
related to hypertension, and the other 4 had hemorrhage
associated with AVM in the head of the caudate nucleus. In
patients with AVM, the age at onset is much younger than in
those with hypertension (6). The patients in both groups
almost always presented with the same clinical symptoms.
The hemorrhage in both groups was contiguous to the anterior
horn of the lateral ventricle, and none was closely associated
with hemorrhage in the anterior portion of the body of the
lateral ventricle in our series.

The prognosis of caudate hemorrhage is also controversial.
In our series, the prognosis is not as poor as it is in the
Weisberg series. Seven patients with hemorrhage related to
hypertension showed good recovery, only one died, and only
one was in poor condition, which was not related to the
caudate hemorrhage itself but to the preceeding multiple
cerebral infarcts. Three patients with AVM showed excellent
recovery, and only one was in poor condition.

There have not been sufficient data about the causes, clin-
ical symptomatology, neurological and neuroradiological
findings, treatment of choice, and results of caudate hemor-
rhage. All are still controversial. We must look forward to
further investigations.

Received for publication, August 4, 1985; accepted, November 17,
1985.

Reprint requests: Shiro Waga, M.D., Department of Neurosurgery,
Mie University Hospital, 2-174 Edobashi, Tsu, Mie, Japan 514.

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2. Fisher CM: Clinical syndromes in cerebral thrombosis, hyperten-
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3. Graeb DA, Robertson WD, Lapointe JS, Nugent RA, Harrison
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450 WAGA etal.

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COMMENT

In 9 of the 13 patients reported in this series. and the 12
reported by Stein et al. (2), caudate hemorrhage was sponta-
neous and usually due to hypertension. Most of these 21
patients presented with symptoms and signs of subarachnoid
hemorrhage due to rupture of the contiguous hematoma into
the anterior horn of the lateral ventricle. The majority also
had a hemiparesis.

In these two series, the prognosis for the patient with
caudate hemorrhage due to hypertension seems to be good
with medical therapy. I also believe these hemorrhages can

Neurosurgery, Vol. 18, No. 4

usually be treated medically following the guidelines we have
outlined for the treatment of brain hemorrhage (1).

I disagree with the authors’ last paragraph. The cause of
caudate hemorrhage has usually been established, the neuro-
radiological findings characterized, and the treatment is usu-
ally a program of medical therapy.

Robert G. Ojemann, M.D.
Boston, Massachusetts

1. Ojemann RG, Heros RC: Spontaneous brain hemorrhage. Stroke
14:468-475, 1983.

2. Stein RW, Kase CS, Hier DB, Caplan LR, Mohr JP, Hemmati
M, Henderson K: Caudate hemorrhage. Neurology (NY)
34:1549-1554, 1984.