Journal of the Neurological Sciences 231 (2005) 81 – 83
www.elsevier.com/locate/jns

Short communication

Putaminal hemorrhage disrupts thalamocortical projection to
secondary somatosensory cortex: case report
Akiyuki Hiraga*, Ryuji Sakakibara, Keiko Mizobuchi, Masato Asahina, Satoshi Kuwabara,
Yuhoko Hayashi, Takamichi Hattori
Department of Neurology (D3), Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan
Received 16 July 2004; received in revised form 9 November 2004; accepted 11 November 2004
Available online 23 December 2004

Abstract
Putaminal hemorrhage presenting pure sensory stroke is rare. We describe a case of left putaminal hemorrhage presenting contralateral
hemisensory disturbance without hemiparesis. A 52-year-old man developed analgesia and thermoanesthesia in the right half of his body, but
deep sensation was relatively well preserved. Neuroradiological and somatosensory evoked potential findings suggested that thalamocortical
sensory pathways to the secondary somatosensory cortex (S2) were involved, whereas those to the primary somatosensory cortex (S1) were
spared. In experimental animals, spinothalamic projections from the thalamic nucleus input directly to S2. In humans, thalamocortical
pathways are still a subject of debate, but results of recent functional imaging studies suggest that the pathway of pain inputs directly to S2
and that of tactile sensation to S2 via S1. Our findings support these reports.
D 2004 Elsevier B.V. All rights reserved.
Keywords: Putamen; Intracerebral hemorrhage; Sensation; Secondary somatosensory cortex

1. Introduction
Pure sensory stroke (PSS) usually is caused by a small
infarct involving the lateral thalamus, brainstem, cerebral
cortex, or internal capsule [1–3] but also may be caused by
a small hemorrhage occurring at the thalamus, pons,
internal capsule, or cerebral cortex [3,4], and rarely by a
larger lenticulocapsular hemorrhage [5]. PSS caused by
thalamic stroke produces mild sensory disturbance of both
the spinothalamic and medial lemniscal types [3]; PSS
caused by an infarct in the internal capsule or corona radiata
may produce the same sensory disturbance as thalamic
stroke [3] or only spinothalamic type sensory disturbance
[2], whereas pontine PSS shows medial lemniscal type
sensory disturbance [3].
We report a patient with a left medium-sized putaminal
hemorrhage, who presented with contralateral hemi-anal-

* Corresponding author. Tel.: +81 43 226 2129; fax: +81 43 226 2160.
E-mail address: hiragaa@mail3.alpha-net.ne.jp (A. Hiraga).
0022-510X/$ - see front matter D 2004 Elsevier B.V. All rights reserved.
doi:10.1016/j.jns.2004.11.049

gesia and hemi-thermoanesthesia with very mild, deep
sensory symptoms, without hemiparesis. The possible site
in the thalamocortical pathways to the sensory cortex is
discussed.

2. Case report
A 52-year-old, right-handed man with a 5-year history of
hypertension experienced thermoanesthesia in his right hand
when he handled a cup of hot tea the morning of 12 January
2004. He was a skilled maker of takoyaki (fried dough balls
with octopus inside), a common snack food in Japan. When
he cooked takoyaki on a hot plate, he felt no sense of
hotness in his right hand and burned himself. These sensory
symptoms persisted, and he developed mild dysarthria but
not headache, dysphagia, limb weakness, or gait disability.
Two days later, he was admitted to our hospital. On
admission, his blood pressure was 210/142 mm Hg, and
he was alert and cooperative. No aphasia, apraxia, agnosia,
or cranial nerve dysfunction was found. Tendon reflexes in

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A. Hiraga et al. / Journal of the Neurological Sciences 231 (2005) 81–83

his four extremities were normal. Medical Research Council
(MRC) grades of muscle power for all four limbs were 5/5,
but there was very mild pronation of the right arm when
both arms were raised simultaneously. There was no
Babinski sign. Coordination was normal, and he could run
well. A sensory examination showed analgesia of his right
side; the face, arm, trunk, and leg, tested by pin-prick.
Thermal sensation was absent tested by both cold and hot
water in test-tube. No difference in severity of analgesia and
thermoanesthesia was seen in his body parts. Joint position
sense of his right upper and lower extremities tested by the
ability of the patient to identify flexion or extension of
fingers with his eyes closed were very mildly disturbed. A
proprioception examination, called the thumb-localizing
tests [6] (testing limb localization with the patient’s eye
closed; the examiner positioned one of the patient’s upper
limbs and asked him to pinch the thumb of that limb with
the opposite thumb and index finger) were intact on both
sides. Brain computed tomography (CT) on admission
showed a subacute hemorrhage in the posterior left putamen
(Fig. 1A). Brain perfusion by N-isopropyl-p-[123I] iodoamphetamine single photon emission computed tomography
(123I-IMP-SPECT) on day 9 after onset showed hypoperfu-

sion of the left cerebral cortex surrounding the Sylvian
fissure and left thalamus (Fig. 1B). Short latency somatosensory-evoked potentials (SEPs) after electrical stimulation
of the median nerve on day 11 showed normal scalp N20
latencies on both sides. Cranial magnetic resonance imaging
(MRI) done 1 month after onset showed T1-weighted spin
echo images of hyperintense lesions in the left putamen
(Fig. 1C, D). After hypotensive therapy with oral nifedipine,
there was no disease progression. Joint position sensation
was ameliorated, becoming normal on day 10, and he was
discharged on day 12. His thermoanesthesia, however,
remained unchanged on examination 1 month after onset.

3. Discussion
This patient presented with contralateral hemi-analgesia
and hemi-thermoanesthesia but without motor deficit caused
by hypertensive putaminal hemorrhage. An interesting
observation was that his sensory symptoms were so severe
for pain and thermal sensations that he did not sense hand
burns, whereas they were very mild for deep sensation. The
findings indicate that thalamocortical sensory pathways

Fig. 1. (A) Brain computed tomography (CT) on admission showed a subacute hemorrhage in the posterior left putamen. (B) Coronal slice of 123IMP-SPECT
on the 9th day of illness showing hypoperfusion in the inferior parietal cortex, including the secondary somatosensory area, but normal perfusion in the parietal
cortex, including the primary somatosensory area. Axial (C) and coronal (D) T1-weighted MRI of the brain (repetition time/effective spin echo time/
excitations; 400/22/3 mm) 1 month after onset showing a high intense lesion in the left putamen. Panel (D) also showed the lesion and its association with the
primary and secondary sensory areas. S1—primary somatosensory cortex; S2—secondary somatosensory cortex.

A. Hiraga et al. / Journal of the Neurological Sciences 231 (2005) 81–83

mainly were involved in spinothalamic sensation, whereas
the corticospinal tract was spared.
In a previous study of three patients who had large
putaminal hemorrhages presenting PSS, sensory symptoms
had both superficial and deep modalities and were more
marked and persistent in the legs than in other body parts
[5]. Neuroradiological data suggested that the hemorrhage
might involve the dorsolateral thalamus and/or the most
posterior part of the posterior limb of the internal capsule
adjacent to the thalamus, which might reflect somatotopy
[5]. In contrast, our patient showed the diffuse analgesia in
the right half of his body, and only analgesia and
thermoanesthesia with preserved deep sensation were
present. In view of a thalamocortical projection seen at the
internal capsule or corona radiata, a pathological study of a
patient with PSS suggested that thalamocortical sensory
radiations were located in the most posterior part of the
posterior limb of the internal capsule, and that they probably
were adjacent to the thalamus [7]. In contrast, the differences in disturbed sensory modalities in our patient suggest
that the pathways of the spinothalamic and medial lemniscal
sensory modalities might be separate.
In addition, brain SPECT showed hypoperfusion of the
left cerebral cortex, including the secondary somatosensory
cortex (S2) and normal perfusion of the primary somatosensory cortex (S1) (Fig. 1B). If we assume that putaminal
hemorrhage involves thalamocortical pathways, hypoperfusion in the ipsilateral S2 could be the result of diaschisis.
SEPs showed no laterality of N20 latency, which corresponds well to the presentation of S1 in the SPECT study in
our investigation.
A study of the monkey showed that S2 can receive
spinothalamic tract information directly through connections within the thalamic nuclei [8]. Functional data from
human electrophysiology correspond to the anatomical data
of the monkey that nociceptive input mostly reaches S2 by
direct projection from the ventroposterior inferior nucleus of
the thalamus, whereas tactile input reaches it by a projection
pathway via S1 [9,10]. However, in the other report, S1 and
S2 were activated by laser with very similar time course,
although S1 activation to painful stimuli is smaller and more
restricted than tactile stimuli [11]. Thalamocortical projection to the human somatosensory cortex, in particular to S2,
is still under debate. Previously, a patient with PSS caused

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by a cerebral infarction in S2 showed moderate contralateral
hemi-hypaesthesia for the senses of light touch, pain, and
temperature. In that patient, deep sensation as well as
stereognosis and graphaesthesia were preserved [12]. The
sensory features in our patient were similar. Fig. 1D shows
the location of the hemorrhage and its association with the
sensory area.
In conclusion, our patient developed hemi-analgesia and
thermoanesthesia because of a putaminal hemorrhage.
These symptoms may reflect a lesion in the thalamocortical
pathways to S2.

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