1152

SHORT REPORT

Deterioration of pre-existing hemiparesis brought about
by subsequent ipsilateral lacunar infarction
T Ago, T Kitazono, H Ooboshi, J Takada, T Yoshiura, F Mihara, S Ibayashi, M Iida
.............................................................................................................................

J Neurol Neurosurg Psychiatry 2003;74:1152–1153

Mechanisms of post-stroke recovery are still poorly understood. Recent evidence suggests that cortical reorganisation in the unaffected hemisphere plays an important role.
A 59 year old man developed a small lacunar infarct in the
left corona radiata, which then caused marked deterioration in a pre-existing left hemiparesis that had resulted from
an earlier right putaminal haemorrhage. Functional
magnetic resonance imaging showed that the paretic left
hand grip activated the ipsilateral left motor areas, but not
the right hemispheric motor areas. This suggests that
partial recovery of the left hemiparesis had been brought
about by cortical reorganisation of the left hemisphere and
intensification of the uncrossed corticospinal tract. The subsequent small infarct may have damaged the uncrossed
tract, thereby causing the pre-existing hemiparesis to deteriorate even further.

P

artial or complete recovery of motor function is the general rule after stroke. However, the mechanisms of
post-stroke recovery are still poorly understood.1 We
report a case where cortical reorganisation of the unaffected
hemisphere may have played a significant role in post-stroke
recovery, but where this partial recovery of hemiparesis
appears to have been damaged by a subsequent small ipsilateral infarct in the hitherto unaffected hemisphere.

CASE REPORT
A 59 year old man was admitted to our hospital because of
marked deterioration in pre-existing left hemiparesis. The
patient was an outpatient with a history of right putaminal
haemorrhage five years earlier, since when he had had a mild
left hemiparesis. Upon admission, the patient was alert. His
blood pressure was 134/70 mmHg and his pulse rate was 70
beats/min. Neurological examination showed that the preexisting left hemiparesis had deteriorated markedly, but that
the function of his face and limbs on the right side remained
intact. Cranial magnetic resonance fluid attenuated inversion
recovery (FLAIR) imaging showed a small high intensity area
in the left corona radiata (fig 1A), which was shown to be a
fresh lesion by diffusion weighted imaging (fig 1B). As no
stenotic lesions of the large carotid or cerebral arteries were
demonstrated by magnetic resonance angiography or cervical
ultrasound sonography (findings not presented), the new
lesion was diagnosed as a lacunar infarct. A functional
magnetic resonance imaging (fMRI) study—in which the
patient was scanned while doing a simple motor task consisting of five repetitions of self paced hand grip for 40 seconds

www.jnnp.com

followed by rest for 40 seconds—showed that the grip of the
non-paretic right hand activated the contralateral left sensorimotor cortex (fig 1C, upper row). On the other hand, grip of
the paretic left hand also increased the cerebral blood flow in
the ipsilateral larger areas including the sensorimotor cortex,
the supplementary motor area, and the premotor cortex, but
not in any of the motor areas of the contralateral hemisphere
(fig 1C, lower row).

DISCUSSION
We describe a case where a small lacunar infarct in the left
corona radiata caused deterioration in a pre-existing left
hemiparesis that had resulted from an earlier right putaminal
haemorrhage.
To elucidate this enigmatic phenomenon, we employed
fMRI. The fMRI study clearly showed that a significant shift in
left motor control to the ipsilateral cortex had taken place
after the first stroke. It appears that cortical reorganisation of
the left hemispheric motor areas had occurred, thereby
contributing to the partial recovery of the left hemiparesis in
this patient (fig 1C, lower row).
Various studies, including positron emission tomography2–4
and fMRI,5 6 have identified three processes related to
post-stroke motor recovery1: activation of the peri-infarction
area,5 7 increased reliance on motor areas such as the
supplementary motor area and the premotor cortex,4 8 and
cortical reorganisation within the motor areas of the
unaffected hemisphere.4–6 9 10 The present case seems to have
involved the third process.
In this case, a small lesion in the left corona radiata manifestly caused deterioration in the pre-existing left hemiparesis; however, it did not produce any right motor dysfunction. A
possible explanation for the absence of right motor dysfunction may be that the lesion was too small to produce damage
to the crossed corticospinal tract. Indeed, a small infarct in the
corona radiata is often asymptomatic. On the other hand, it
may simply be that by chance the infarct produced direct
damage to the uncrossed corticospinal tract itself.
When an initial stroke results in extensive damage to motor
function, a subsequent stroke contralateral to the first stroke
sometimes causes deterioration in the ipsilateral pre-existing
hemiparesis, as well as producing contralateral motor dysfunction. Cortical reorganisation in the unaffected hemisphere after the first stroke may be involved in the occurrence
of such symptoms. fMRI may be useful for evaluating the
pathophysiology of these patients. Further cases are necessary
to confirm our interpretation of the interesting phenomenon
seen in this case.

Deterioration of hemiparesis through further infarction

1153
Figure 1 (A) FLAIR and (B) diffusion
weighted imaging (b-factor 1000) on
the second day of hospital admission
revealed a small high intensity area
in the left corona radiata
(arrowhead), suggesting a fresh
lacunar infarct. FLAIR imaging
showed a large subcortical high
intensity area which represented an
old putaminal haemorrhage (arrow).
(C) fMRI induced by the grip task is
shown. Arrowheads point to areas
activated by hand grip. Upper row:
right hand grip activated the
contralateral left sensorimotor cortex.
Lower row: left paretic hand grip
activated the ipsilateral left
sensorimotor cortex, supplementary
motor area, and premotor cortex.
fMRI, functional magnetic resonance
imaging.

.....................

Authors’ affiliations
T Ago, T Kitazono, H Ooboshi, J Takada, S Ibayashi, M Iida
Department of Medicine and Clinical Science, Graduate School of
Medical Sciences, Kyushu University, Fukuoka, Japan
T Yoshiura, F Mihara, Department of Clinical Radiology, Graduate
School of Medical Sciences, Kyushu University,
Correspondence to: Dr Tetsuro Ago, Department of Medicine and
Clinical Science, Graduate School of Medical Sciences, Kyushu
University, Maidashi 3-1-1, Higashi-ku, Fukuoka 812-8582, Japan;
agou@intmed2.med.kyushu-u.ac.jp
Received 11 December 2002
In revised form 15 April 2003
Accepted 15 April 2003

REFERENCES
1 Johansson BB. Brain plasticity and stroke rehabilitation. The Willis
lecture. Stroke 2000;31:223–30.
2 Weiller C, Chollet F, Friston KJ, et al. Functional reorganization of the
brain in recovery from striatocapsular infarction in man. Ann Neurol
1992;31:463–72.

3 Chollet F, DiPiero V, Wise RJ, et al. The functional anatomy of motor
recovery after stroke in humans: a study with positron emission
tomography. Ann Neurol 1991;29:63–71.
4 Nelles G, Spiekermann G, Jueptner M, et al. Reorganisation of sensory
and motor systems in hemiplegic stroke patients. A positron emission
tomography study. Stroke 1999;30:1510–16.
5 Cramer SC, Nelles G, Benson RR, et al. A functional MRI study of
subjects recovered from hemiparetic stroke. Stroke 1997;28:2518–27.
6 Cao Y, D’Olhaberriague L, Vikingstad EM, et al. Pilot study of functional
MRI to assess cerebral activation of motor function after poststroke
hemiparesis. Stroke 1998;29:112–22.
7 Nudo RJ, Wise BM, SiFuentes F, et al. Neural substrates for the effects of
rehabilitative training on motor recovery after ischemic infarct. Science
1996;272:1791–4.
8 Aizawa H, Inase M, Mushiake H, et al. Reorganization of activity in the
supplementary motor area associated with motor learning and functional
recovery. Exp Brain Res 1991;84:668–71.
9 Jones TA, Schallert T. Use-dependent growth of pyramidal neurons after
neocortical damage. J Neurosci 1994;14:2140–52.
10 Green JB, Bialy Y, Sora E, Ricamato A. High-resolution EEG in
poststroke hemiparesis can identify ipsilateral generators during motor
tasks. Stroke 1999;30:2659–65.

www.jnnp.com