Section 2 Vascular topographic syndromes
Chapter
Caudate nucleus infarcts and hemorrhages
34 Chin-Sang Chung and Louis R. Caplan
Introduction
The basal ganglia (BG) including the caudate nucleus are well
known for their motor functions. They act in concert with the
cerebral cortex to harmonize and perform goal-directed,
planned, and motivated behaviors through the motor, cogni-
tive, and limbic circuits [1]. Major studies on caudate nucleus
stroke followed the introduction and widespread use of com-
puted tomography (CT) scanning. Caudate nucleus vascular
lesions, both ischemic and hemorrhagic, rarely involve the
nucleus exclusively but affect neighboring structures like the
putamen, internal capsule, and white matter [2–14].
Anatomy of the caudate nucleus
Functional neuroanatomy: parallel frontal-striatal-
thalamic-frontal circuits
The BG nuclei are anatomically and functionally associated
with each of the frontal-striatal-thalamic-frontal circuits or
loops. Ventral regions of the basal ganglia play a key role in
reward and reinforcement and are important in the develop-
ment of addictive behaviors and habit formation. More cen-
tral basal ganglia areas are involved in cognitive functions,
such as procedural learning and working memory tasks. In
addition, the dorsolateral portion of the striatum, caudal to
the anterior commissure, is as active in the control of move-
ment [15,16].
The caudate nucleus assumes the shape of a comet, curving
along the lateral wall of the lateral ventricle. It consists of a
large head at the front, a narrow dorsal body, and a thin tail,
which follows a course passing ventrally along the temporal
horn of the ventricle, ending at the amygdala. The inferior part
of the head of the caudate nucleus is connected to the putamen
at the ventral part, at the level of the nucleus accumbens. The
demarcation of the caudate nucleus at the level of the body and
tail is easy, as it is surrounded medially by the lateral ventricle
and laterally by the internal capsule. The head of the caudate
nucleus and the putamen are connected by thin bridges of gray
matter (pontes grisei caudatolenticularis).
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The caudate nucleus controls approach-attachment behav-
ior and affect, ranging from a plain approach to a target to
romantic love, and contributes importantly to the posture of
the body and limbs as well as to the speed and accuracy of
directed movements [15,16]. In the striatum including the
caudate nucleus, there are at least five parallel, functionally
separate circuits that link the basal ganglia with the motor,
associative, and limbic systems [1]. Each circuit is defined by
the area of the cerebral cortex that projects to specified regions
of the striatum, and by the corresponding return thalamocor-
tical projection to specified areas of the frontal cortex. The
circuits remain more or less separated throughout the basal
ganglia and thalamus, and there are cross-talks between them
at various relays therein. Within each circuit, the basal ganglia
execute a similar, common function. They transform the cor-
tical input into an output signal from the internal nucleus of
the globus pallidus (Gpi) and the reticular nucleus of the
substantia nigra (SNr) to the thalamus, directed back to the
cerebral cortex and brainstem. The circuits are defined by their
source of cortical input and the zones of frontal cortex to
which their thalamic output is directed [1,2,17,18].
Because the caudate nucleus is the principal crossing area
of these circuits, vascular lesions can cause various
neurological symptoms and signs depending on the involved
circuits. The five circuits are presented diagramatically in
Figure 34.1 and include: (i) the classical motor circuit, defined
by projections from the sensorimotor cortex, supplementary
motor area, and arcuate premotor area to the putamen, and by
thalamic projections from the ventralis lateralis pars oralis and
ventralis anterior pars parvocellularis/motor cortex to the sup-
plementary motor area and precentral cortex; (ii) ocular motor
circuit, defined by input from the frontal eye fields (Brod-
mann’s area 8), dorsolateral prefrontal cortex (areas 9 and
10), and posterior parietal cortex (area 7) to the caudate
nucleus, with return thalamocortical projections from the ven-
tralis anterior pars magnocellularis and medialis dorsalis pars
paralaminaris to the frontal eye fields and supplementary eye
fields; (iii) dorsolateral prefrontal circuit, defined by input
from the dorsal prefrontal convexity (Brodmann’s areas 9
397
 Section 2: Vascular topographic syndromes

Dorsolateral Lateral Anterior

Motor Oculomotor prefrontal orbitofrontal cingulate

Cortex SMA APA,MC,SC FEF DLC,PPC DLC PPC,APA LOF STG,ITG,ACA ACA HC,EC,STG,ITG

CAUD dI-CAUD vm-caud

Striatum PUT (b) VS
(h) (h)

Pallidum vI-GPi cdm-Gpi Idm-Gpi mdm-Gin rl-Gpi,VP

Substantia
cI-SNr vl-SNr rl-SNr rm-SNr rd-SNr
nigra

VLo I-VAmc VApc m-VAmc

Thalamus MDpl MDpc Pm-MD
VLm MDmc

Figure 34.1. Basal ganglia-thalamocortical ciruits. Each circuit engages specific regions of the cerebral cortex, striatum, pallidum, substantia nigra, and thalamus.
(From Alexander et al., 1986 [1].) ACA, anterior cingulate area; APA, arcuate premotor area; CAUD, caudate nucleus, [b] body, [h] head; DLC, dorsolateral prefrontal
cortex; EC, entorhinal cortex; FEF, frontal eye fields; GPi, internal segmental of globus pallidus; HC, hippocampal cortex; ITG, inferior temporal gyrus; LOF, lateral
orbitofrontal cortex; MC, motor cortex; MDpl, medialis dorsalis pars paralamellaris; MDmc, medialis dorsalis pars magnocellularis; MDpc, medialis dorsalis pars
parvocellularis; PPC, posterior parietal cortex; PUT, putamen; SC, somatosensory cortex; SMA, supplementary motor area; SNr, substantia nigra pars reticulata; STG,
superior temporal gyrus; VAmc, ventralis anterior pars magnocellularis; VApc, ventralis anterior pars parvocellularis; VLm, mentralis lateralis pars medialis; VLo, ventralis
lateralis pars oralis; VP, ventral pallidum; VS, ventral striatum; cl-, caudolateral; cdm, caudal dorsomedial; dl-, dorsolateral; l-, lateral; ldm-, lateral dorsomedial; m-, medial;
mdm-, medial dorsomedial; pm-, posteromedial; rd-, rostrodorsal; rl-, rostrolateral; rm-, rostromedial; vm-, ventromedial; vl-, ventrolateral.

and 10) to the caudate nucleus, with overlapping projections

from the posterior parietal cortex (area 7) and arcuate pre-
motor area, return thalamic projections from the ventralis
anterior pars parvocellularis and medialis dorsalis pars parvo-
cellularis to the dorsolateral prefrontal cortex in and around
the principal sulcus; (iv) lateral orbitofrontal circuit, defined
by input from the lateral orbitofrontal cortex (Brodmann’s
area 10) to the caudate nucleus, overlapping with input from
the auditory and visual association areas from the superior and
inferior temporal gyri, respectively, and return thalamic pro-
jections from ventralis anterior pars magnocellularis and med-
ialis dorsalis pars magnocellularis to the lateral orbitofrontal
cortex; and (v) limbic circuit, defined by input from the
hippocampus, amygdala, and limbic areas of the cerebral
cortex (areas 28 and 35) projecting to the ventral striatum,
where it overlaps with inputs from the anterior cingulate
region (area 24) and widespread sources in the temporal lobe, Figure 34.2. Blood supply to the caudate nucleus. (From Kase and Caplan,
and return thalamic projections from the medialis dorsalis to Intracerebral Hemorrhage. Stoneham, MA: Butterworth Heinemann, 1994, with
the anterior cingulate area and medial orbitofrontal cortex permission.)
[1,2,18,19].

gives rise to Heubner’s arteries, a series of two to four vessels

Blood supply to the caudate nucleus
The caudate nucleus receives its blood supply mainly through
the deep penetrators arising from the anterior cerebral arteries
(ACAs) and middle cerebral arteries (MCAs) although there
are individual differences (Figure 34.2) [20–24]. The ACA
that usually arise from the A2 portions of the ACA near the
junction of the anterior communicating artery and the ACA
[25]. These vessels supply the inferior part of the head of the
caudate nucleus, the adjacent anterior limb of the internal
capsule, and the subfrontal white matter.

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 Chapter 34: Caudate nucleus infarcts and hemorrhages

(a) (b) (c)

(d ) (e) (f )

Figure 34.3. Magnetic resonance images showing an infarct limited to the medial caudate nucleus ((a)–(c)) in one patient and a large striatocapsular infarct
involving the left lateral caudate nucleus head and body ((d)–(f)) in another patient (arrows).

Direct penetrating arteries from the ACA (called medial

striate arteries or anterior lenticulostriate arteries by various
authors) supply the anterior portion of the head of the caudate
nucleus. The MCA gives rise to medial lenticulostriate arteries
that branch from the proximal M1 portion and supply a small
part of the lateral border of the caudate nucleus head and the
adjacent internal capsule.
The lateral lenticulostriate arteries branch from the mainstem
MCA or its superior division branch to supply the major portion
of the head of the caudate nucleus, as well as the adjacent internal
capsule and the anterior half of the putamen. There is consider-
able overlap between the three arteries supplying the head of the
caudate nucleus: the lateral lenticulostriate, anterior lenticulostri-
ate, and Heubner’s recurrent artery [24–26]. Anterior lenticu-
lostriate arteries supply the lateral caudate nucleus (LCN), medial
caudate nucleus (MCN), ventral caudate nucleus (VCN), and
part of the anterior limb of the capsule.
Infarcts in the territory of the anterior lenticulostriate arteries
yield only slight neuropsychological deficits, while those with
infarcts in the territory of the lateral lenticulostriate arteries
present prominent motor and neuropsychological deficits.
Caudate nucleus infarcts
Although there has been little mention of arterial territories
involved in patients with caudate nucleus infarcts, the most
commonly involved arteries in these infarcts are the lateral
lenticulostriate arteries and the anterior lenticulostriate arteries
[2,4,7–9,14]. Infarcts in the territory of the lateral lenticulostri-
ate arteries are limited to the MCN, LCN, VCN, anterior limb
of the internal capsule, and the putamen. The recurrent artery
of Heubner affects the inferior part of the caudate nucleus, the
anterior part of the internal capsule, and the nucleus accum-
bens [4].
Caudate nucleus infarcts can be divided into several
groups, according to the anatomical structures involved. In
one study, among 18 patients, infarcts were limited to the
caudate nucleus in four patients, included the caudate nucleus
and the anterior limb of the internal capsule in nine cases, and
affected the caudate nucleus, anterior limb of the internal
capsule, and anterior putamen in five patients [2]. Figure 34.3
shows MR images of an infarct limited to the caudate nucleus
and a large striatocapsular infarct involving the caudate

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 Section 2: Vascular topographic syndromes

Table 34.1. Site of lesions of caudate nucleus infarcts (49 prior reports Table 34.2. Risk factors and vascular mechanisms from combined series
and Illinois series)
Factors Patients and percentagea
Site of lesion Number (percentage)
Hypertension 92 (67%)
CN alone 22 (24%)
Diabetes mellitus 44 (32%)
CN þ anterior limb of IC þ corona 25 (28%)
radiata Large artery lesions 19 (14%)

CN þ anterior limb of IC þ putamen 44 (48%) Cardiac embolic source 18 (13%)

Total 91 Total number of patients 137

a
CN, caudate nucleus; IC, internal capsule. Some patients had more than one risk factor.
Source: adapted from Caplan & Helgason (1995) [26]. Source: adapted from references [3,4,26].

nucleus head and body. The caudate nucleus can also be Table 34.3. Symptoms and signs in caudate nucleus infarctsa
involved as part of a large striatocapsular infarct, caused by Symptoms and signs Patients and percentage
occlusion of the intracranial internal carotid artery or the
mainstem MCA. Dysarthria or dysphonia 18/21 (86%)
An analysis of the 49 previously reported cases and the 34 Motor weakness 21/21 (100%]
patients studied at the University of Illinois yielded a total of
Behavioral abnormalities 12/21 (57%)
83 patients with 91 caudate nucleus infarcts [26]. In 22
infarcts (24%), CT or MRI showed they were confined to Agitation 6 (3L, 3R)b
the caudate nucleus. The lesions involved the caudate nucleus Abulia 10 (2L, 7R, 1 bilateral)
and the adjacent anterior limb of the internal capsule or
Neglect 2 (2R)
corona radiata in 25 cases (28%). The remainder, 44 infarcts
(48%), involved the caudate nucleus, the anterior limb of the Aphasia 1 (1L)
a
internal capsule, and the putamen (Table 34.1). Cases available for clinical-neuroimaging correlation = 21; b L, left; R, right.
Source: adapted from reference [26].

Stroke mechanisms
In most of the reported patients, a full evaluation, including
angiography and cardiac evaluation, was not performed and
the data are insufficient to define the precise stroke mech-
anisms of caudate nucleus infarcts. Penetrating-branch dis-
ease has been proposed as a major mechanism because the
caudate nucleus receives its blood supply from deep pene-
trating arteries. In fact, risk factors for penetrating-branch
disease are prevalent in patients with caudate nucleus
infarcts. However, evaluation of the heart and large arteries
is essential in those without risk factors for penetrating-
branch diseases.
Echocardiography, carotid duplex ultrasound, transcra-
nial Doppler ultrasound, magnetic resonance angiography
(MRA), and computed tomography angiography (CTA)
are useful non-invasive screening tests for detection of
important occlusive vascular diseases and cardiac sources
of emboli.
The major risk factors for caudate nucleus infarcts
are: hypertension, hypercholesterolemia, diabetes mellitus,
previous myocardial infarct, and cigarette smoking [2,4].
Non-valvular atrial fibrillation (NVAF), myocardial dyskin-
esia, cardiac aneurysm with a mural thrombus, syphilis, and
Hodgkin’s lymphoma are also uncommon reported risk
factors. Table 34.2 lists the risk factors and stroke mechanisms
from the combined series of prior reports and in those patients
seen at the University of Illinois [26].
Clinical features
Caudate nucleus infarctions can cause a variety of clinical
presentations. Behavioral abnormalities including abulia, agita-
tion, and loss of executive abilities are particularly common.
Dysarthria, dysphonia, and motor weakness, are also common.
Although less common, movement disorders like hemichorea,
ballism, and tremor can occur [26].
Cognitive and behavioral abnormalities
The most prominent clinical features of caudate nucleus vas-
cular lesions are behavioral and cognitive abnormalities [2,6–
14,27]. Behavioral changes occur as a result of cortical
dysfunction caused by loss of striatal efferent projections from
the caudate nucleus, the principal crossing station of basal
ganglia-thalamocortical loops. Common behavioral features
include reduced activity and slowness, restlessness, hyperactiv-
ity, agitation, decreased attention to tasks, and defective recall
[2,9,28]. Neuropsychological tests show abnormalities in
executive functions, memory, and attention. Deficits do not
correlate with the side of the lesion, but patients with affective
abnormalities tend to have the larger infarcts.
Mendez and his colleagues divided spontaneous behavioral
symptoms into three groups: (i) apathetic, with decreased
spontaneous verbal and motor activities (dorsolateral caudate
nucleus involvement); (ii) disinhibited, inappropriate, and
impulsive (small ventromedial lesions in the caudate

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nucleus); and (iii) affective symptoms with psychotic features
(dorsolateral caudate nucleus involvement; larger and
more often extend into adjacent structures than in the first
group) [9].
Agitation
Agitation, anxiety, and talkativeness are common and restless-
ness, disinhibition, and confusion are noted. Behavioral hyper-
activity with restlessness, excitement, agitation, and shouting
may occur in infarctions of the middle or posteroinferior
temporal lobe and parietooccipital lobes [2,9].
Abulia
Patients with caudate nucleus infarcts can present with abulia,
which is defined as “apathy, disinterest, flattened affect, and
lack of initiative for usual daily activities.” Abulia is more
severe and more persistent in bilateral caudate nucleus infarcts.
Clinically, the patients show akinesia, characterized by severe
mental and affective stagnation, decreased spontaneous activ-
ity and speech, lack of initiative for action and speech, and
prolonged latency in responding to questions and other stim-
uli. They look like a patient with severe hypothyroidism. Such
akinetic attacks are often prolonged and stereotyped behaviors
are common. Patients can also show impulsivity, disinhibition,
and violent attacks [3,7]. These features have been described in
patients with bilateral globus pallidus or putaminal lesions
[29,30]. Fisher’s abulic patients had lesions in the frontal lobes
and underlying structures or in the thalamus and upper brain-
stem [31]. Interruption of the limbofrontal connection is
responsible for abulia.
Neglect
Contralateral motor and visuospatial hemineglect develop in
a quarter of the patients with a right caudate nucleus lesion,
particularly if the anterior limb of the internal capsule is also
involved [2–4]. All patients with hemineglect have involve-
ment of MCN, LCN, VCN, and neighboring structures [4].
Motor-exploratory hemineglect can develop from disruption
of the frontal-striatal-thalamic-frontal circuit that includes the
associative frontal cortical areas, striatum, and substantia
nigra.
Mood changes
Depression is observed in one-third of patients with caudate
nucleus vascular pathology but with normal cognitive function
[32]. This suggests that the caudate nucleus plays a role in
regulation of human mood.
Memory dysfunction
Unilateral lesions may cause impairment of frontal lobe func-
tions and decreased free recall of episodic and semantic items.
One-third of patients with left caudate nucleus lesions show
verbal amnesia, while patients with right caudate nucleus
lesions show visual amnesia. This suggests that the caudate
nucleus plays a role in integration of visual and verbal
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Chapter 34: Caudate nucleus infarcts and hemorrhages
memories. Verbal comprehension and verbal memory deficits
are caused by dysfunction of the corticocaudate connections
[3,4,13]. If a caudate nucleus lesion is very large, patients have
deficits in tasks requiring planning and sequencing, because of
the disconnection of the caudate nucleus from the frontal lobe
[9]. Global dementia may develop following a bilateral infarc-
tion of the heads of the caudate nuclei, because the caudate
nucleus is an essential component of basal ganglia-thalamo-
cortical circuitry and contributes to cognitive functions and
behavioral processing [33].
Other cognitive and behavioral dysfunctions
Rarely, the patients can show motor dysprosody, motor imper-
sistence in eye-closing, perseveration of hand and arm pos-
tures, and inappropriate laughing at stroke onset. Some
patients show impairment in frontal lobe testing using the
Stroop test and Luria’s conflicting tasks.
Speech and language disturbances
Dysarthria
Dysarthria is another common sign in patients with caudate
nucleus vascular lesions. Dysarthria has no side predominance
in caudate nucleus stroke. Interruption of the corticolingual
tracts to the tongue or corticostriatocerebellar loops is respon-
sible for dysarthria because these pathways play crucial roles in
uniform speech patterns [2–4,9,34].
Aphasia
Left caudate nucleus infarcts can cause minor aphasic abnor-
malities [2]. About half of the patients with a left caudate
nucleus lesion show minor and transient linguistic deficits
[4]. Different types of aphasia, such as transcortical, nonfluent
aphasia, characterized by semantic and verbal paraphasias and
perseverations without comprehension impairment, may
develop after left caudate nucleus vascular lesions [2,3,6–
14,35]. Global aphasia can also develop by intrahemispheric
diaschisis. A large striatocapsular infarct involving the caudate
nucleus, anterior limb of the internal capsule, and putamen
can result in word-finding difficulty or hesitancy without
severe aphasic abnormalities [27]. In these patients, single-
photon emission computed tomography (SPECT) imaging
may show decreased perfusion in the left frontal and temporo-
parietal lobes [4]. Acute disconnection of the linguistic path-
ways between anterior and posterior speech areas, which are
connected with the left caudate nucleus, and the anterior limb
of the internal capsule may yield a different type of aphasia.
Movement disorders
The caudate nucleus has inhibitory projections to the lateral
globus pallidus, which in turn projects to the subthalamic
nucleus. Loss of inhibitory input to the subthalamic nucleus
may provoke abnormal movements. Abnormalities of move-
ment and tone can follow acute lesions of either the striate
nuclei or the subthalamic nucleus [36].
401
 Section 2: Vascular topographic syndromes
Movement disorders following caudate nucleus infarcts
have been described but not in detail. The abnormal move-
ments usually are contralateral to the lesion and usually occur
at the time of stroke onset. These abnormal movements have
been described as ballistic, choreic, or both. Very rarely, move-
ment disorders may begin at once in all limbs bilaterally
[37,38]. In addition, onset of abnormal movements like dysto-
nia or resting tremor may be delayed for years or decades after
caudate nucleus stroke [39].
Motor abnormalities
Motor abnormality or weakness is noted in about 40% of
patients with caudate nucleus infarcts. Weakness develops
when a lesion extends into the anterior limb of the internal
capsule and putamen, interrupting the striatopontine fibers.
Lesions confined to the caudate nucleus do not cause weak-
ness. Weakness, when present, is usually slight and rarely
leaves any permanent motor disability. In some patients with
dystonia and abnormal movements, weakness may be masked
by involuntary movements and abnormal tone. The frequency
of motor involvement has likely been underestimated due to
selection bias. Most patients reported in the literature had
specific abnormalities such as behavioral disorders or abnor-
mal movements [2,4,9,28].
Treatment and prognosis
The clinical course of caudate nucleus infarction is so benign
that 60% of patients become independent. Only a few patients
with unilateral caudate nucleus infarcts in the territory of the
lateral lenticulostriate arteries or the anterior lenticulostriate
arteries have slight residual dependency needs. Rarely, patients
with unilateral caudate nucleus infarcts worsen clinically.
Those with bilateral caudate nucleus infarcts or large unilateral
infarcts in the territory of the lateral lenticulostriate arteries
can have significant residual deficits. Patients only rarely die of
underlying heart disease rather than of caudate nucleus infarc-
tion itself [4].
Because caudate nucleus infarcts can develop from
any stroke mechanisms including lipohyalinosis, branch
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Figure 34.4. Computed tomography and mag-
netic resonance images showing caudate nucleus
hematomas. They are located in the head (a) or
in the body (b) of the caudate nucleus. They
usually rupture into the lateral ventricle.
atheromatous disease, large artery atherothrombosis, or
embolism, treatment of patients with caudate nucleus
infarcts depends on the underlying stroke mechanism.
Antiplatelet or anticoagulant agent(s) and management of
stroke risk factors are given according to the mechanism of
infarction (Table 34.3).
Caudate nucleus hemorrhages
Caudate nucleus hemorrhages account for approximately 7%
of all intracerebral hemorrhages (ICH) [6] and are caused by
rupture of penetrating arteries. Hypertension is the most
common and important risk factor [4,5]. Arteriovenous mal-
formations, carotid aneurysms, and diabetes mellitus are other
important causes, but sometimes no responsible cause is found
[4,6,11,12]. Rarely, moyamoya disease and moya moya-like
atherosclerotic abnormalities of vessels secondary to hyperten-
sion and occlusive intracranial carotid artery disease can cause
caudate nucleus hemorrhage [40–45].
In an international series of striatocapsular hemorrhages,
23 patients had caudate nucleus hemorrhage, which involved
mainly the caudate nucleus head and occasionally the caudate
nucleus body [5]. The hematomas are small (less than 1 inch in
diameter), always rupture into the anterior horn of the lateral
ventricle, and occasionally extend posterolaterally into the
anterior limb of the internal capsule and anterior putamen
(Figure 34.4).
Clinical features
The clinical symptoms and signs of caudate nucleus hemor-
rhages depend on the lesion size and the neighboring struc-
tures damaged. The most common clinical presentations are
headache, nausea, vomiting, and marked meningeal irritation
signs due to rupture of the hematoma into the frontal horn of
the lateral ventricle, mimicking subarachnoid hemorrhage
(SAH) and primary intraventricular hemorrhage (IVH). Most
patients show no prominent motor, sensory, or visual abnor-
malities if the hematoma is limited to the head or body of the
caudate nucleus and dissects medially into the ipsilateral ven-
tricle causing IVH and ventricular dilatation on the ipsilateral
 Chapter 34: Caudate nucleus infarcts and hemorrhages

side [5]. When the hematoma is large enough to spread lat-
erally or posterolaterally into the putamen or anterior or
posterior limb of the internal capsule, the hemorrhage can
cause motor and neuropsychological deficits, including abulia,
frontal lobe dysfunction, and transient slight motor weakness
that clears within one week [4,5]. These patients usually
remain alert. Disconnection of the corticocaudate tract second-
ary to caudate nucleus hemorrhage can cause verbal compre-
hension and verbal memory deficits [13]. Transcortical motor
dysphasia can develop in patients with large hematomas but it
improves completely with time.
Neglect, sensory deficit, and eye movement and pupillary
abnormalities are rarely observed and are usually less severe
and transient unless the hematoma spreads across the anter-
ior limb of the internal capsule [5]. When hematomas
spread inferiorly, they may cause Horner’s syndrome,
because of thalamic involvement or compression of the
hypothalamus [4]. Rarely, a caudate nucleus hemorrhage
can cause a movement disorder like hemiballism [46].
A rare case of bilateral caudate nucleus hemorrhages has
been reported [47].
Treatment and prognosis
The long-term outcome of caudate nucleus hemorrhage is so
excellent that more than 80% of patients return to normal
activities. Less than 20% of patients remain slightly hemipar-
etic and no patient dies of caudate nucleus hemorrhage itself
[5]. There is a case report that a patient died of generalized
cerebral vasospasm following caudate nucleus hemorrhage,
but in whom no abnormality on cerebral angiography was
found [4]. Usually, surgical intervention is not required but
emergency extraventricular drainage may be necessary when
acute severe obstructive hydrocephalus develops. However,
permanent bypass surgery like ventriculoperitoneal shunt is
indicated only very rarely.

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