Ipsilateral hemiparesis after putaminal
hemorrhage due to uncrossed
pyramidal tract
H. Terakawa, MD; K. Abe, MD; M. Nakamura, MD; T. Okazaki, MD; J. Obashi, MD;
and T. Yanagihara, MD

Article abstract—Objective: Previous case reports supported the presence of the uncrossed pyramidal tract in exceptional patients. However, most of these case reports have not fully discussed involvement of the motor cortex controlling
the ipsilateral limbs. Design and Method: The authors investigated a 62-year-old man who developed right hemiparesis
after right putaminal hemorrhage by using MRI, transcranial magnetic stimulation, functional MRI (fMRI), and sensory
evoked potentials. He had moderate weakness including the face, spasticity with brisk deep tendon reflexes and Babinski
sign, and impaired vibration and position sense, all on the right side. Result: A MRI study showed hemorrhage in the right
putamen and the wedge-shaped medulla. A fMRI study during a sequential finger opposition task showed activation in the
motor cortex ipsilateral to the finger movements, but not on the contralateral side. Sensory evoked potentials showed
cortical response ipsilateral to the side of stimulation. Conclusion: The pyramidal tract and the dorsal column-medial
lemniscus pathway did not cross in the medulla in this patient. In view of the presence of the abnormal shape in the
medulla and congenital scoliosis, a congenital factor might be responsible for the uncrossed pyramidal tract and dorsal
column-medial lemniscus in this patient. Key words: Ipsilateral hemiparesis—Functional MRI—Ipsilateral innervation.
NEUROLOGY 2000;54:1801–1805

Previous neuroanatomic studies have firmly supported the notion that the primary motor cortex predominantly innervates the contralateral half of the
body. Conversely, some case reports supported the
existence of the uncrossed pyramidal tract in exceptional patients.1-3 These case reports primarily discussed the uncrossed pyramidal tract alone and have
not fully discussed the motor cortex controlling the
ipsilateral limbs. We report a patient with right
hemiparesis after hemorrhage in the right putamen
in whom we demonstrated motor control by the ipsilateral motor cortex by using functional MRI (fMRI)
and transcranial magnetic stimulation (TMS).
Case report. A 62-year-old, right-handed man with a
history of hypertension suddenly developed right hemiparesis. He was taken to a hospital by ambulance. On neurologic examination, he was drowsy and had right
hemiparesis. His muscle tone was diminished and deep
tendon reflexes were absent, but the Babinski sign was
present on the right side. A CT scan showed a hemorrhage
in the right internal capsule and basal ganglia (figure 1).
The lateral and third ventricles were of normal size without any deformity or deviation of the midbrain. On the day
of admission, he underwent stereotaxic surgery for removal of the hematoma.
Ten months later, he was admitted to our hospital for
further evaluation of residual right hemiparesis. He had a
marked congenital scoliosis in the thoraco–lumbar spine.

On neurologic examination, he was alert but had slight
dysarthria. His pupils were 2.5 mm in diameter and equal.
His pupillary responses were prompt bilaterally. Eye
movement was mildly restricted in the horizontal direction
bilaterally. He had facial weakness on the right side. The
soft palate moved normally. He had moderate weakness,
spasticity with brisk deep tendon reflexes, and Babinski
sign on the right. He did not have mirror movements. He
had subjective hypesthesia and impaired vibration and position sense on the right side, but impaired light touch and
pain sensation on the left side.
MRI study was performed using a 1.5-T MR system
(Magnetom, Siemens, Erlangen, Germany) 10 months after the hemorrhagic event, which revealed sequelae of old
hemorrhage and surgical intervention in the right putamen. With the fluid-attenuated inversion recovery (FLAIR)
image, high signal intensities were observed in the cerebral peduncle, pons, and medulla on the right side, considered to represent Wallerian degeneration following
destruction of the corticospinal tract and neuronal death in
the putamen.4 However, we could not identify Wallerian
degeneration in the cervical spinal cord due to the resolutional ability of MRI. The medulla had a wedge-shaped
notch and appeared to be separated, but there was no
abnormality in the upper cervical cord (figure 2).
fMRI was performed by the same device. The patient’s
head was positioned within the standard head coil and
head movements were restricted by using foam rubber
pads and Velcro band across the forehead. Body movements were also minimized by using the proximal arm

From the Department of Neurology (Drs. Terakawa, Hakamura, and Okazaki), Osaka Koseinenkin Hospital; the Department of Neurology (Drs. Abe and
Yanagihara), Osaka University Graduate School of Medicine; and Department of Neurosurgery (Dr. Obashi), Ohno Memorial Hospital, Japan.
Received November 9, 1999. Accepted in final form January 27, 2000.
Address correspondence and reprint requests to Dr. Kazuo Abe, Department of Neurology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka,
Suita, Osaka 565, Japan.
Copyright © 2000 by the American Academy of Neurology

1801

Figure 1. CT scan on the day of onset
(left) and MRI 10 months after intracranial hemorrhage (right). A hematoma is visible in the right putamen
with CT, which is also visible with MRI
after stereotactic surgery.
strips. Conventional T1-weighted axial images were acquired parallel to the bicommissural plane. A single shot
gradient recalled echoplanar imaging was used with interscan interval of 2 seconds, echo time of 66 msec, flip angle
of 10 degrees, matrix of 128 ⫻ 128, field of view of 24⫻32
cm, and slice thickness of 5 mm. The patient was asked to
perform a sequential finger opposition task, during which
he repeatedly touched the left four fingers with the left
thumb in a sequential order as quickly as possible with
eyes closed. The cue to begin and cease the movement was
a light tap on the knee. Pixels showing the stimulusrelated signal increase were identified by calculating the
correlation between the MR signal time course and timeshifted boxcar function. The threshold for significant activation was set at p ⬍ 0.005. The resulting binary map was

then filtered by a 3 ⫻ 3 median filter. For visualization,
the map was superimposed onto the corresponding MRI
slices. During the motor task, the functional activity was
observed in the motor cortex ipsilateral to the finger movements (figure 3).
SPECT with 99mTc-hexamethyl-propylene-amine-oxime
demonstrated hypoperfusion in the right basal ganglia and
the frontoparietal region of the right cerebral hemisphere.
An ultrasound examination of the carotid artery showed
no plaque or stenosis on either side.
TMS was performed using a magnetic stimulator (Nihon Kohden, Tokyo, Japan) with a circular electromagnetic
coil in loop with an inside diameter of 8 cm and an outside
diameter of 14 cm (10,000 A ⫽ 900 V at maximal output).
We used magnetic stimulation at the intensity ranging

Figure 2. Fluid-attenuated inversion
recovery MRI 10 months after onset.
High-intensity lesions are visible in the
right cerebral peduncle, pontine base,
and medulla, corresponding to the location of the pyramidal tract. Note the
shape of the medulla, which appeared
to be separated in the midline, and the
cervical cord, which was normal in
shape.

Figure 3. Functional MRI during motor activation. Three axial slices acquired parallel to the bicommissural
plane at 4, 8, and 12 cm below the cerebral vertex are presented. Significantly
activated pixels are visible on the left
side during left finger movements.
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May (1 of 2) 2000

Figure 4. Results of the motor evoked
potentials after stimulation of the primary motor cortex. The left abductor
pollicis brevis and anterior tibialis
muscles responded after stimulation of
the left motor cortex (top), whereas the
right abductor pollicis brevis and anterior tibialis muscles did not respond
after stimulation of the right motor
cortex (bottom).
from 800 to 900 V. We placed the center of the coil over the
scalp in the vertex to stimulate the leg area and at 2 cm
posterior to Cz to stimulate the finger area. We used counterclockwise coil current for preferential activation of the
left motor cortex and clockwise coil current for preferential
activation of the right motor cortex. EMG electrodes were
placed on the belly tendons of the abductor pollicis brevis
(APB) muscle and the anterior tibialis (TA) muscle on each
side. Stimulation of the left motor cortex evoked responses
in the left APB with a latency of 20.5 msec and in the left
TA with a latency of 32.1 msec, both of which were ipsilateral to the side of stimuli. No response was evoked in the
muscles on the right side. Stimulation of the right motor
cortex evoked no response on either side (figure 4).
Sensory evoked potentials (SEP) were recorded with a
standardized electrodiagnostic system (Neuropack4, Nihon
Kohden). Electrical stimulation with square-wave pulses
was delivered by a bipolar surface electrode with five electrical impulses per second for a duration of 0.2 msec to the
right and left median nerve at the wrist, which produced a
minimal thumb twitch. A total of 256 responses were

summed and averaged. The recording electrodes were
placed according to the international 10-20 system at 3 cm
behind C3 and C4 (cortical N20 peak). Those active electrodes were referenced to a midfrontal Fz electrode. The
ground electrode was placed on the side of stimulation 10
cm proximal to the stimulus electrode. After left median
nerve stimulation, the primary cortical response N20 was
elicited in the left central and parietal region, which was
ipsilateral to the side of stimulation. Right median nerve
stimulation elicited cortical response in the right central
and parietal region, which was also ipsilateral to the side
of stimulation (figure 5).

Discussion. The most notable clinical feature of
this patient was the development of right hemiparesis following hemorrhage in the right putamen. Because this hematoma in the right putamen did not
exert any signs of mass effect on CT, it could not
compress the left pyramidal tract, primary motor
area, or secondary motor area directly or indirectly.

Figure 5. Results of the sensory
evoked potentials after stimulation of
the median nerve. A cortical potential
(N20) was evoked in the left cerebral
cortex (C3⬘) after stimulation of the
left median nerve (left), and in the
right cerebral cortex (C4⬘) after stimulation of the right median nerve
(right).
May (1 of 2) 2000

NEUROLOGY 54

1803

Although dysfunction in the right secondary motor
area is a possible reason for right hemiparesis, there
was no lesion affecting the right secondary motor
area on MRI. We conclude that dysfunction in the
right pyramidal tract or motor cortex was the reason
for right hemiparesis.
TMS allows a simple and painless evaluation of
the human motor pathway.5 Magnetic stimulation of
the motor area usually evokes contralateral limb
movement. However, our patient showed left limb
movement after magnetic stimulation of the left motor cortex. This suggests that the pyramidal tract
might not have crossed in this patient. fMRI is another way to gather information concerning cortical
innervation for limb movements. Signals in fMRI
represent changes in the deoxyhemoglobin concentration due to activation of neurons in the underlying cortical areas.6 In our patient, the left primary
motor cortex showed significant activation after finger movements on the left side, suggesting that the
left motor cortex had control over finger movements
on the left side. The results of TMS and fMRI are
consistent with the presence of the uncrossed pyramidal tract and predominant control of movements
by the ipsilateral motor cortex in this patient.
In addition to motor impairment, our patient also
showed impairment of position and vibration sensation
on the same side as that of hemiparesis, suggesting the
presence of the uncrossed dorsal column–medial lamniscus pathway and of the dentatorubrothalamic pathway. The results of SEP support the presence of an
aberrant dorsal column–medial lamniscus pathway.
Because the light touch and pain sensation were impaired on the side opposite to the side of hemiparesis,
the spinothalamic tract appeared to have run the
ordinary course. We believe the most plausible explanation is that the pyramidal tract and the dorsal
column–medial lamniscus pathway did not cross in
the medulla in this patient. The abnormal shape of
medulla, which appeared to be separated in the midline, supports this notion.
There are controversies over ipsilateral innervation of limb movements. In animals, ipsilateral innervation by the primary motor and premotor cortex
has been reported.7-9 In humans, Penfield and Boldrey conducted a classic study of somatotopic innervation of the motor function by the primary motor
cortex and concluded that motor movements were
predominantly innervated by the contralateral motor
cortex.10 More recently, an anatomic study showed
ipsilateral projection from the primary motor cortex,11 but it was considered to have a much weaker
control over limb muscle movements than contralateral projection.12 In addition, clinicopathologic studies,13 TMS studies,14,15 and PET studies16,17 have
emphasized the critical role of the ipsilateral pyramidal tract in the recovery from hemiparesis caused by
cerebral damage.
Several case reports described ipsilateral hemiparesis following damage in the ipsilateral cerebrum.18-24
Cuatico reported a case of ipsilateral hemiparesis but
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May (1 of 2) 2000

without further anatomic discussion.1 Hosokawa et al.
reported a patient with ipsilateral hemiparesis after
putaminal hemorrhage and showed the presence of
the uncrossed pyramidal tract from the putamen to the
cervical cord by MRI, but without discussion of the
cortical contribution.3 Kudo and Uno reported a patient
with transient ipsilateral hemiparesis following compression of the secondary motor area by a hematoma.2
Schneider and Crosby reported a patient with ipsilateral motor impairment after rupture of an arteriovenous malformation in the island of Reil. They
emphasized the role of the secondary motor area located in the precentral insular cortex bilaterally innervating the muscles in the face and limbs.21 These
previous case reports failed to show control of limb
muscles by the ipsilateral motor cortex. In our patient,
we were able to demonstrate that the motor cortex on
the left side controlled the limbs on the left side by
using TMS and fMRI.
Patients without decussation of the pyramidal
tracts have been reported to have other cerebral malformations.19,20,22 Krams and colleagues described
mirror movements in Kallmann’s syndrome as the
result of abnormal development of the ipsilateral corticospinal tract.25-27 Our patient did not have mirror
movements. Our patient and a patient reported by
Hosokawa et al. had congenital scoliosis.3 These observations suggest the presence of a congenital factor
for the uncrossed pyramidal tract in some of those
patients.
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18. Brodal A. Self-observations and neuroanatomical considerations after a stroke. Brain 1973;96:675– 694.
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Poststroke depression and
emotional incontinence
Correlation with lesion location
Jong S. Kim, MD; and Smi Choi-Kwon, PhD, RN

Article abstract—Objective: To correlate the location of stroke with poststroke depression (PSD) and emotional incontinence (PSEI). Methods: The authors prospectively studied 148 patients (94 men and 54 women, mean age 62 years) with
single, unilateral stroke (126 infarcts and 22 hemorrhages) at 2 to 4 months poststroke with regard to the presence of PSD
(using Diagnostic and Statistical Manual of Mental Disorders IV criteria and Beck Depression Inventory) and PSEI. The
lesion location was analyzed by CT or MRI. Results: Twenty-seven patients (18%) had PSD and 50 (34%) had PSEI. The
presence of PSD and PSEI was not related to the nature, laterality, or size of the lesion. The frequency of PSEI, but not of
PSD, was higher in women than in men and in ischemic rather than hemorrhagic stroke ( p ⬍ 0.05). Although both PSD
and PSEI were related to motor dysfunction and location (anterior versus posterior cortex) of the lesion, location was a
stronger determinant for PSD ( p ⬍ 0.05). The prevalence of PSD/PSEI in each location was 75%/100% in frontal lobe of
anterior cerebral artery territory, 50%/0 in temporal lobe, 30%/40% in frontal–middle cerebral artery territory, 13%/0 in
occipital lobe, 19%/45% in lenticulocapsular area, 11%/16% in thalamus, 16%/53% in pontine base, 36%/55% in medulla,
and 0/22% in cerebellum. Parietal and dorsal pontine lesions were not associated with PSD or PSEI. PSEI was more
closely associated with lenticulocapsular strokes than was PSD ( p ⬍ 0.01). Conclusion: Development of PSD and PSEI is
strongly influenced by lesion location, probably associated with the chemical neuroanatomy related to the frontal/temporal
lobe– basal ganglia–ventral brainstem circuitry. Although the lesion distribution is similar, PSEI is more closely related to
lenticulocapsular strokes than is PSD. Key words: Depression—Emotion—Laughing—Crying—Cerebrovascular disease.
NEUROLOGY 2000;54:1805–1810

Many patients develop depression after the occurrence of stroke.1,2 The prevalence of poststroke depression (PSD) ranges from 12% to 64%.3-15 The wide
variation in the frequency of PSD may be related to
methodologic heterogeneity in items such as the cri-

teria for depression, the time of assessment after
stroke, and the sampled population. A main controversy regarding PSD has been the relationship between the location of stroke and PSD. Whereas some
have reported that PSD occurred more often after

From the Department of Neurology (Dr. Kim), University of Ulsan, Asan Medical Center; and Department of Nursing (Dr. Choi-Kwon), Seoul National
University, Seoul, Korea.
Received August 9, 1999. Accepted in final form January 27, 2000.
Address correspondence and reprint requests to Dr. Jong S. Kim, Department of Neurology, Asan Medical Center, Song-pa, P.O. Box 145, Seoul 138-600,
Korea; e-mail: jongskim@www.amc.seoul.kr
Copyright © 2000 by the American Academy of Neurology

1805

Ipsilateral hemiparesis after putaminal hemorrhage due to uncrossed pyramidal tract
H. Terakawa, K. Abe, M. Nakamura, et al.
Neurology 2000;54;1801-1805
DOI 10.1212/WNL.54.9.1801
This information is current as of May 9, 2000
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