Journal of the Neurological Sciences 354 (2015) 140–141

Contents lists available at ScienceDirect

Journal of the Neurological Sciences
journal homepage: www.elsevier.com/locate/jns

Letter to the Editor
Deterioration of pre-existing hemiparesis
due to an ipsilateral internal capsule
infarction after a contralateral stroke

Dear Sir,
Although hemiparesis due to an ipsilateral brain lesion is rare in
clinical practice, various pathomechanisms related to this condition
have been reported [1–7]. Above all, deterioration of pre-existing
hemiparesis due to an ipsilateral brain infarction after a contralateral
stroke has been reported in two studies [1,2]. Ago's patient [1], who
had left hemiparesis associated with right putaminal hemorrhage,
presented with deterioration of the left hemiparesis related to left
corona radiata infarction. Song's patient [2], who had left hemiparesis
associated with right thalamic hemorrhage, developed worsening of
the left hemiparesis due to left corona radiata infarction. In these
cases, functional MRI demonstrated activation of the ipsilateral motor
cortex during paretic hand movement, suggesting that reorganization
of the unaffected hemisphere had occurred after the first stroke, and
that a new lesion in the reorganized area resulted in the deterioration
of hemiparesis. On the other hand, these studies included no data of
motor evoked potentials (MEP) following transcranial magnetic stimulation (TMS).
A 79-year-old male noticed the deterioration of the pre-existing
left hemiparesis, and was admitted to our hospital the next day. His
past medical history included hypertension and right pontine
infarction, for which he had been taking a depressor and aspirin.
While the right pontine infarction at the age of around 60 had resulted in mild left hemiparesis, he became able to walk with a T-cane
during recovery and needed no aid for activities of daily living. A
neurological examination on admission demonstrated mild left
hemiparesis. There was no visual field defect, facial palsy, dysarthria,
sensory disturbance, or muscle weakness of the right limbs.
Diffusion-weighted brain MRI showed an acute infarction in
the posterior limb of the left internal capsule (Fig. 1A), and
T2-weighted MRI demonstrated a previous infarction in the right
ventral pons (Fig. 1B).
MEP were recorded from the first dorsal interosseus (FDI) muscle
using a pair of Ag-AgCl surface electrodes with a standard bellytendon arrangement. TMS was performed by Magstim 2002 (The
Magstim Co., Ltd. UK) with a figure-of-8 coil of each loop of 7 cm in
diameter (2.2 T) with 100% stimulator output. We placed the center of
the coil over the scalp at 7 cm lateral to Cz to stimulate the finger area.
We compared areas of the MEP with those of the compound muscle
action potentials (CMAP) of the FDI muscle evoked by supramaximal
ulnar nerve stimulation at the wrist. We obtained clear MEP of the
right FDI muscle when stimulating the left motor cortex. Areas of the
MEP were 40.2% of the areas of the CMAP (Fig. 1C). There were no
clear MEP of the left FDI muscle when stimulating the left motor cortex

http://dx.doi.org/10.1016/j.jns.2015.05.015
0022-510X/© 2015 Elsevier B.V. All rights reserved.

(Fig. 1C). Similarly, clear MEP could not be obtained in the left or right
FDI muscles when stimulating the right motor cortex (Fig. 1D). The
poor responses of the left FDI muscle when stimulating the right
motor cortex were thought to be associated with the right pontine
infarction.
While most corticospinal tract (CST) fibers decussate at the level of
the pyramidal decussation of the caudal medulla oblongata, 10 − 30%
of the fibers continue to descend as the ipsilateral ventral CST. Although
rare, the congenital absence of decussation has been reported to be associated with hemiparesis due to an ipsilateral brain lesion [3–6]. In
our case, however, the previous infarction involving the right ventral
pons had caused left hemiparesis. In addition, TMS of the left motor
cortex produced clear MEP in the right FDI muscle. Because of the
presence of these contralateral innervations of the motor system, the
congenital absence of decussation is unlikely to have caused the ipsilateral hemiparesis in our case.
So far, deterioration of pre-existing hemiparesis due to an ipsilateral brain infarction after a contralateral stroke has been reported in
two studies [1,2]. Similar to the mechanisms described in these reports [1,2], the new internal capsule infarction in the reorganized
area might have caused deterioration of hemiparesis in our case.
The poor responses of the left FDI muscle when stimulating the left
motor cortex were thought to be associated with the new internal
capsule infarction.
Similarly to the two previous cases [1,2], our case showed
ipsilateral hemiparesis alone, which was not accompanied by contralateral paresis. In accordance with this clinical finding, TMS of the left
motor cortex in our case produced clear MEP in the right FDI muscle.
These findings indicate that the crossed and uncrossed fibers run
separately within the CST even before the pyramidal decussation,
and that the uncrossed fibers alone could be affected by brain infarction [2].
The limitation of our study was that the reorganization of the left
hemisphere could not be confirmed by functional MRI. Further,
because there was no data of MEP obtained before the onset of the
internal capsule infarction, it remains uncertain whether the poor
MEP reflecting the left uncrossed innervation (shown in Fig. 1C)
were truly due to the internal capsule infarction. These issues should
be resolved by future studies. Finally, clinicians should remember
the fact that the deterioration of hemiparesis could be caused by an
ipsilateral brain infarction in patients with previous contralateral
brain lesions involving the CST.
Disclosure
The authors report no conflict of interest.
Acknowledgment
The authors thank Chika Nakazawa (occupational therapist) for
helpful comments.

Letter to the Editor

141

References
[1] T. Ago, T. Kitazono, H. Ooboshi, J. Takada, T. Yoshiura, F. Mihara, et al., Deterioration of
pre-existing hemiparesis brought about by subsequent ipsilateral lacunar infarction, J
Neurol Neurosurg Psychiatry 74 (8) (2003) 1152–1153.
[2] Y.M. Song, J.Y. Lee, J.M. Park, B.W. Yoon, J.K. Roh, Ipsilateral hemiparesis caused by a
corona radiata infarct after a previous stroke on the opposite side, Arch Neurol 62
(5) (2005) 809–811.
[3] S. Hosokawa, S. Tsuji, T. Uozumi, K. Matsunaga, K. Toda, S. Ota, Ipsilateral hemiplegia
caused by right internal capsule and thalamic hemorrhage: demonstration of
predominant ipsilateral innervation of motor and sensory systems by MRI, MEP,
and SEP, Neurology 46 (4) (1996) 1146–1149.
[4] H. Terakawa, K. Abe, M. Nakamura, T. Okazaki, J. Obashi, T. Yanagihara, Ipsilateral
hemiparesis after putaminal hemorrhage due to uncrossed pyramidal tract,
Neurology 54 (9) (2000) 1801–1805.
[5] A.S. Ng, Y.Y. Sitoh, Y. Zhao, E.W. Teng, E.K. Tan, L.C. Tan, Ipsilateral stroke in a patient
with horizontal gaze palsy with progressive scoliosis and a subcortical infarct, Stroke
42 (1) (2011) e1–e3.
[6] K. Kang, N.C. Choi, Ipsilateral hemiparesis and spontaneous horizontal nystagmus
caused by middle cerebral artery territory infarct in a patient with agenesis of the
corpus callosum, Neurol Sci 33 (5) (2012) 1165–1168.
[7] F. Saada, N. Antonios, Existence of ipsilateral hemiparesis in ischemic and hemorrhagic stroke: two case reports and review of the literature, Eur Neurol 71 (1-2) (2014)
25–31.

Zen Kobayashi⁎,1
Miho Akaza1
Department of Neurology, JA Toride Medical Center, 2-1-1 Hongo, Toride,
Ibaraki 302-0022, Japan
⁎Corresponding author. Tel.: +81 297 74 5551; fax: +81 297 74 2721.
E-mail address: zen@bg7.so-net.ne.jp (Z. Kobayashi).
Hiroshi Endo
Department of Rehabilitation, JA Toride Medical Center, 2-1-1 Hongo,
Toride, Ibaraki 302-0022, Japan
Yoshiyuki Numasawa
Department of Neurology and Neurological Sciences, Graduate School,
Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, Tokyo,
113-8510, Japan
Hiroyuki Tomimitsu
Shuzo Shintani
Department of Neurology, JA Toride Medical Center, 2-1-1 Hongo, Toride,
Ibaraki 302-0022, Japan
28 March 2015

Fig. 1. (A) Diffusion-weighted brain MRI showed a high intensity area in the posterior limb
of the left internal capsule. (B) T2-weighted MRI demonstrated atrophy and a high
intensity area in the right ventral pons. (C and D) MEP of the FDI muscles when
stimulating the left and right motor cortex, respectively.

1

The first two authors contributed equally to this work.