Preserved motor-evoked potentials but without good motor recovery in a patient with decerebrate rigidity.
ABSTRACT The corticospinal tract is not incriminated in decerebrate rigidity (DR). However, this has not yet been proven in humans. We applied transcranial magnetic stimulation (TMS) in a decerebrate patient to support the hypothesis. A patient suffering from pontine hemorrhage with the fourth ventricular extension was admitted unconscious and in a decerebrate posture. Five days later, she regained consciousness but remained in a decerebrate posture. Motor-evoked potentials (MEPs) to TMS were measured 1 week after she had regained consciousness, and this provoked muscle responses in her hands and feet bilaterally. During the follow-up, the patient's muscle tone became persistently flaccid, although her strength increased to varying degrees in different body and limb muscles. She remained bedridden for 3 years after the stroke and could neither turn on the bed by herself nor perform skilled movements using her hands. The findings of TMS confirmed the animal studies in that the mechanism of decerebrate rigidity did not come through a damage of the corticospinal pathway. This also implies that a preserved corticospinal tract function cannot guarantee a good motor recovery in a stroke patient.
[show abstract] [hide abstract]
ABSTRACT: By definition, transient ischemic attacks (TIAs) do not leave a neurological deficit beyond 24 hours after onset. However, a subgroup of TIA patients is characterized by persistent perfusion defect on single photon emission computed tomogram or infarction on brain computerized tomogram and magnetic resonance imaging. Here, we applied transcranial magnetic stimulation (TMS) to study whether TIA could produce persistent subclinical dysfunction for more than 24 hours. The study included 23 TIA patients who had the criteria of hand weakness as one of their clinical manifestations. TMS was done twice in each TIA patient. The first time was during the period of 24-48 hours after onset and the second 7 days after onset. We studied the cortical motor threshold, the latencies and the amplitudes of the motor evoked potentials, the central motor conduction time, and the cortical silent period at the intensity of 1.5 times motor threshold with maximal voluntary isometric contraction. The recording was at the first dorsal interosseous muscle. There was no significant difference between the whole group of TIA patients and normal control. However, in the subgroup of TIA patients who had hand weakness more than 1 hour, they had increased motor threshold and prolonged cortical silent period during the first test. Both improved 1 week after onset. On the contrary, in TIA patients who had hand weakness less than 1 hour, their data were all within normal limits during the first and the second studies. Our results indicate that the motor function of TMS study will recover to full if the motor symptoms subside within 1 hour in TIA patients. Subclinical motor deficits may persist in TIA patients who have motor symptoms more than 1 hour.Journal of the Chinese Medical Association 06/2004; 67(5):229-34. · 0.79 Impact Factor
Article: Prognostic value of motor evoked potential obtained by transcranial magnetic brain stimulation in motor function recovery in patients with acute ischemic stroke.[show abstract] [hide abstract]
ABSTRACT: The early prognostic application of transcranial magnetic brain stimulation (TMS) for assessing motor and functional recovery in ischemic stroke patients has yielded contradictory results. We performed a prospective study of patients with acute ischemic stroke and motor deficit to evaluate the early prognostic value of TMS in motor and functional recovery. Fifty patients with different degrees of hemiparesis were studied in the first week after ischemic stroke and evaluated by clinical scales (Medical Research Council Scale, Canadian Neurological Scale, Barthel Index), with clinical follow-up over 6 months. TMS (Magstim 200) was performed at the same time, recording the motor evoked potential (MEP) in the thenar eminence muscles, with facilitation by voluntary contraction. Of the total group of 50 patients, MEP was absent in 20 and present in 30 (17 with normal and 13 with delayed central conduction time [CCT]). The patients with MEP showed better motor and functional recovery than those without. The MEP provided information on patient recovery, regardless of the initial strength and/or Barthel values. The degree of recovery was better in those patients with normal CCT than in those with delayed CCT. MEP obtained by TMS in patients with hemiparesis after acute ischemic stroke is useful as an early prognostic indicator of motor and functional recovery. This technique would allow the early identification of those patients who will have a good recovery, particularly among those with severe initial paresis.Stroke 10/1998; 29(9):1854-9. · 5.73 Impact Factor
The Journal of Physiology 03/1898; 22(4):319-32. · 4.72 Impact Factor
Preserved motor-evoked potentials but without good motor recovery in
a patient with decerebrate rigidity*
Chuen-Der Kaoa,b,c, Kon-Ping Lina,b, Jen-Tse Chena,b,d, Jiun-Bin Changa,b,e, Wan-Yuo Guob,f,
Yung-Yang Lina,b,g, Kwong-Kum Liaoa,b,*
aDepartment of Neurology, Taipei Veterans General Hospital, Taipei, Taiwan, ROC
bDepartment of Neurology, National Yang-Ming University School of Medicine, Taipei, Taiwan, ROC
cDepartment of Neurology, Taichung Hospital, Taichung, Taiwan, ROC
dDepartment of Neurology, Cathay General Hospital, Taipei, Taiwan, ROC
eDepartment of Neurology, Chie-Mei Liouying Hospital, Tainan, Taiwan, ROC
fDepartment of Radiology, Taipei Veterans General Hospital, Taipei, Taiwan, ROC
gDepartment of Medical Research and Education, Taipei Veterans General Hospital, Taipei, Taiwan, ROC
Received 1 March 2010; accepted 10 June 2010
The corticospinal tract is not incriminated in decerebrate rigidity (DR). However, this has not yet been proven in humans. We applied
transcranial magnetic stimulation (TMS) in a decerebrate patient to support the hypothesis. A patient suffering from pontine hemorrhage with the
fourth ventricular extension was admitted unconscious and in a decerebrate posture. Five days later, she regained consciousness but remained in
a decerebrate posture. Motor-evoked potentials (MEPs) to TMS were measured 1 week after she had regained consciousness, and this provoked
muscle responses in her hands and feet bilaterally. During the follow-up, the patient’s muscle tone became persistently flaccid, although her
strength increased to varying degrees in different body and limb muscles. She remained bedridden for 3 years after the stroke and could neither
turn on the bed by herself nor perform skilled movements using her hands. The findings of TMS confirmed the animal studies in that the
mechanism of decerebrate rigidity did not come through a damage of the corticospinal pathway. This also implies that a preserved corticospinal
tract function cannot guarantee a good motor recovery in a stroke patient.
Copyright ? 2011 Elsevier Taiwan LLC and the Chinese Medical Association. All rights reserved.
Keywords: Decerebrate state; Mobility limitation; Stroke; Tegmentum mesencephali; Transcranial magnetic stimulation
The technique of transcranial magnetic stimulation (TMS)
in patients with motor disabilities as a result of cerebrovascular
disorders. TMS is also of prognostic utility, and a preserved
TMS response usually indicates a better outcome.2
The term “decerebrate rigidity” (DR) was first used in 1898
by Sherrington3in describing posture after a prepontine tran-
section. He also concluded that the corticospinal tract could
not be incriminated in either causing or reversing decerebrate
posture after a series of animal studies. To our knowledge,
TMS has not been applied in the study of corticospinal tracts
in DR patients. Here, we report a patient with DR because of
a brainstem hemorrhage. She failed to execute voluntary
movement of her limbs, although her consciousness was clear
and the function of the corticospinal tract was preserved after
the acute stage of DR had passed. We reviewed the mechanism
of DR and the phenomenon of poor motor control even with
preserved function of the corticospinal tract.
*The authors declare no conflicts of interest.
* Corresponding author. Dr. Kwong-Kum Liao, Department of Neurology,
Taipei Veterans General Hospital, 201, Sec. 2, Shih-Pai Road, Taipei 112,
E-mail address: email@example.com.
1726-4901/$ - see front matter Copyright ? 2011 Elsevier Taiwan LLC and the Chinese Medical Association. All rights reserved.
Available online at www.sciencedirect.com
Journal of the Chinese Medical Association 74 (2011) 37e39
2. Case report
A 48-year-old woman suffering from pontine hemorrhage
with the fourth ventricular extension was admitted because of
a sudden change of consciousness. The Glasgow Coma Scale
on admission was 4, the best motor response was 2 (decere-
brate posture), the best verbal response was 1 (no response),
and the eye-opening response was 1 (no response). Neuro-
logical examination revealed a normal light reflex, an absence
of right-eye corneal reflex, and oculocephalic reflex. A
mechanical ventilator was used to support her respiration. DR,
which developed extension of her four limbs with internal
rotation of bilateral arms and plantar flexion, clenching of jaws
and opisthotonos, had been noted since admission, and these
findings were enhanced by pain or pressure stimulations on her
limbs. She regained consciousness 5 days after the stroke
onset and was able to obey simple orders (such as opening and
closing her eyes). Limb movement was limited, and she could
only move the right upper limb slightly. Motor-evoked
potentials (MEPs) to TMS 1 week after she had regained
consciousness showed preserved corticospinal tract responses,
although the onset latencies were delayed and the peak
amplitudes were decreased (Fig. 1).
Three months later, there were residual neurological defi-
cits, with right abducens palsy, right facial and crossed left
hemibody sensory impairment, poor hand dexterities, and
truncal unsteadiness. The patient was able to follow
commands to execute simple tasks, such as moving her
shoulders and flexing and extending her wrists or elbows. She
could not perform some tasks, such as using her hands to write
or to eat with chopsticks, a fork, or a spoon. She could not
maintain a steady sitting position without support, not to
mention an upright posture with support. The muscle response
to TMS became larger along with her muscle strength
improvement, although her muscle tone decreased as hypo-
tonia. She remained in flaccid weakness and did not have
a significant improvement in motor function after 3 years of
Series of animal studies have revealed that the integrity of
reticular, cerebellar, vestibular, and cortical descending neural
systems is responsible for the development of DR.4Our TMS
findings confirmed these animal studies in that the DR mecha-
nism did not come through a damage of the corticospinal
of a lesion involving the rubrospinal pathway and an indirect
disinhibition of vestibulospinal and reticulospinal effects.5
Preserved MEPs to TMS usually indicate a good motor
recovery of stroke patients. However, our patient has remained
bedridden for 3 years after the stroke. In a general sense, the
control of posture and locomotion is based on a spinal central
pattern generator influenced by supraspinal structures and
peripheral afferents. From the original concepts of Kuypers,6
the supraspinal control is divided between two systems:
a fine control of locomotion (the lateral system, including the
corticospinal and rubrospinal tracts) and a provision of
postural support for the fine control (the medial system,
including the reticulospinal and vestibulospinal tracts). During
the control of goal-directed locomotion, selection of a motor
program is performed in the basal ganglia and then reaches the
command centers in the diencephalic locomotion region and
the mesencephalic locomotion region, which can modulate the
spinal central pattern generator for locomotion via the retic-
ulospinal neurons.7In our patient, preserved MEP might
represent certain integrity of the corticospinal tracts. The poor
control of posture and fine voluntary movement might have
come through a locomotion dysfunction by disruption of the
rubrospinal or in part reticulospinal tracts involving the loco-
motion command center at the brainstem level. However,
locomotion failure has been used to describe gait disorders in
humans, and it may not account for the loss of hand dexterity
in our patient.
The concept of incomplete lesion was first proposed by
Dimitrijevic et al,8describing a preserved electrophysiological
function of the corticospinal tract but clinically exhibiting
complete paralysis in spinal man. He supposed that a sub-
stantial number of nerve fibers can survive the trauma but
insufficient to elicit effective contraction of muscles. A similar
concept can be applied to our case, where the lesion involved
the brainstem instead of the spinal cord. The TMS study of our
patient showed residual connectivity of the corticospinal tract,
but she did not have any voluntary movement of the hands and
had poor motor recovery later. This may in part share a similar
“incomplete” mechanism of spinal man.
Loss of dexterity and prolonged flaccid weakness were
noted in our patient. Brainstem lesions may produce cerebellar
diaschisis,9,10which may last 20 years after stroke.11Although
single photon emission computed tomography or positron
emission tomography was not done in our patient, we infer
that she had cerebellar dysfunction because of diaschisis.
Cerebellar dysfunction may decrease human muscle tone and
Fig. 1. The motor-evoked potentials of a 48-year-old patient, who presented
with decerebrate rigidity because of a pontine hemorrhage during the acute
stage and 3 months after stroke onset. Recordings: abductor pollicis brevis and
38 C.-D. Kao et al. / Journal of the Chinese Medical Association 74 (2011) 37e39
disturb human motor control. Hence, persistent cerebellar
dysfunction because of diaschisis might in part account for her
hypotonia and clumsiness.
In conclusion, DR may occur following a massive, bilateral
cerebral trauma, anoxic damage, or midbrain destructive
lesion, such as the hemorrhagic stroke in our case. Although it
is rare, preserved MEP can occur in humans with DR. Our
case also emphasizes that preserved MEP does not always
indicate a good voluntary movement and motor recovery.
This study was supported, in part, by Taipei Veterans
General Hospital (grant no. V99C1-027).
1. Wong WJ, Chen JT, Kao CD, Shan DE, Lin YY, Hu HH, et al. Trans-
cranial magnetic stimulation in patients with transient ischemic attacks.
J Chin Med Assoc 2004;67:229e34.
2. Escudero JV, Sancho J, Bautista D, Escudero M, Lopez-Trigo J. Prog-
nostic value of motor evoked potential obtained by transcranial magnetic
brain stimulation in motor function recovery in patients with acute
ischemic stroke. Stroke 1998;29:1854e9.
3. Sherrington CS. Decerebrate rigidity and reflex coordination of move-
ments. J Physiol 1898;22:319e32.
4. Davis RA, Davis L. Decerebrate rigidity in animals. Neurosurgery 1981;9:
5. Kao CD, Guo WY, Chen JT, Wu ZA, Liao KK. MR findings of decere-
brate rigidity with preservation of consciousness. AJNR Am J Neuroradiol
6. Kuypers HG. The organization of the “motor system”. Int J Neurol 1963;
7. Mori S, Matsuyama K, Kohyama J, Kobayashi Y, Takakusaki K. Neuronal
constituents of postural and locomotor control systems and their interac-
tions in cats. Brain Dev 1992;14:s109e20.
8. Dimitrijevic MR, Dimitrijevic MM, Faganel J, Sherwood AM. Supra-
segmentally induced motor unit activity in paralyzed muscles of subjects
with established spinal cord injury. Ann Neurol 1984;16:216e21.
9. Jacobs A, Herholz K, Pietrzyk U, Wurker M, Wienhard K, Heiss WD.
Diaschisis of specific cerebellar lobules: pontine haematoma studied with
high-resolution PET and MRI. J Neurol 1996;243:131e6.
10. Fazekas F, Payer F, Valetitsch H, Schmidt R, Flooh E. Brain stem
infarction and diaschisis: a SPECT cerebral perfusion study. Stroke 1993;
11. Shih WJ, Huang WS, Milan PP. F-18 FDG PET demonstrates crossed
cerebellar diaschisis 20 years after stroke. Clin Nucl Med 2006;31:
39C.-D. Kao et al. / Journal of the Chinese Medical Association 74 (2011) 37e39