2287

Very Early Demonstration of Secondary
Pyramidal Tract Degeneration
by Computed Tomography
Seiji Kazui, MD; Yoshihiro Kuriyama, MD; Tohru Sawada, MD; Satoshi Imakita, MD

Downloaded from http://ahajournals.org by on April 11, 2024

Background While magnetic resonance imaging has revealed progressive changes in the pyramidal tract in accordance with histopathologic stages of wallerian degeneration
secondary to a supratentorial lesion, computed tomography
(CT) has only demonstrated a shrinkage of the pyramidal tract
in the midbrain or pons during the chronic stage. We present
a patient with frontoparietal subcortical hemorrhage in whom
serial CT scans clearly demonstrated wallerian degeneration
along the axis of the pyramidal tract early in the acute stage.
Case Description A 63-year-old man with a history of
hypertension suddenly developed a deterioration of consciousness, transcortical mixed aphasia, and dense hemiplegia on the
right side. CT scans revealed a massive intracerebral hematoma in the frontoparietal subcortices of the left hemisphere. Although initial CT did not detect any hypodense

areas along the left pyramidal tract below the hematoma,
ill-defined areas of decreased density appeared in the posterior limb of the internal capsule, cerebral peduncle of the
midbrain, and pontine base of the left side on day 13 after the
stroke. These areas became well demarcated on day 22 and
persisted thereafter.
Conclusions An extensive hematoma can interrupt the pyramidal tract fibers that arise not only from the motor cortex
and caudal premotor cortex but also from the somatosensory
and parietal cortices, allowing very early CT demonstration of
wallerian degeneration of the pyramidal tract. (Stroke. 1994;
25:2287-2289.)

W

ation in brain-damaged humans. Magnetic resonance
imaging (MRI) has demonstrated pyramidal tract
changes in patients with supratentorial lesion, in accordance with the histopathologic stages of wallerian degeneration mentioned above, by using T r weighted,
T2-weighted, and/or proton density-weighted images.2'7"12 In contrast, most studies involving computed
tomography (CT), the most prevalent diagnostic technique to date, have only revealed shrinkage of the
pyramidal tract in the midbrain or pons in the chronic
stage.13-14
We recently treated a patient with massive subcortical
hemorrhage in whom serial CT scans demonstrated
marked wallerian degeneration of the pyramidal tract
early in the acute stage.

allerian degeneration refers to the anterograde disintegration that affects an axon and
its myelin sheath after injury to the proximal
portion of axon or its cell body.1-2 Although Waller3
described this degenerative process observed in the
hypoglossal and glossopharyngeal nerves, the same
term has been applied to similar nerve fiber changes
occurring in the central nervous system. Abnormalities
in involved axons precede changes in the myelin sheath.
Myelin sheaths collapse, and the lamellae become
loose.1 Daniel and Strich4 studied wallerian degeneration in the spinal cord in baboons and found that myelin
sheaths break up into ellipsoids within 48 hours but
retain the staining properties of normal myelin for many
weeks. McCaman and Robins3 reported that breakdown
of myelin into simpler lipids was not observed until 100
days after section of rabbit optic nerves. The time
course of wallerian degeneration varies greatly. It occurs more rapidly in peripheral nerves than in the
central nervous system, in larger caliber fibers than in
smaller ones, in unmyelinated fibers than in myelinated
fibers, in younger animals than in older ones, and in
mammals than in cold-blooded animals.1-6
The recent advent of neuroimaging in clinical practice
has provided demonstrable proof of wallerian degenerReceived Jury 22, 1994; final revision received August 22, 1994;
accepted August 22, 1994.
From the Cerebrovascular Division, Department of Medicine,
and the Department of Radiology (S.I.), National Cardiovascular
Center, Osaka, Japan.
Correspondence to Seiji Kazui, MD, Cerebrovascular Division,
Department of Medicine, National Cardiovascular Center, 5-7-1
Fujishirodai, Suita, Osaka, 565 Japan.
O 1994 American Heart Association, Inc.

Key Words • cerebral hemorrhage
tomography • wallerian degeneration

•

computed

Case Report
This 63-year-old, right-handed Japanese man had a
history of hypertension and diabetes mellitus. He suddenly developed a deterioration of consciousness, language difficulties, and motor weakness of the right
extremities just after attending a meeting on December
1, 1993. He was hospitalized for initial care and was
diagnosed as having intracerebral subcortical hemorrhage. He was transferred to our institute on December
4, 1993.
On admission the patient was mildly drowsy. Neurological examination disclosed a transcortical mixed
aphasia, neglect for the right hemispace, and right-sided
dense hemiplegia involving the face. Muscle tonus was
flaccid on the right. The deep tendon reflexes were
exaggerated, and the plantar response was extensor on
the right.

2288

Stroke

Vol 25, No 11 November 1994

FIG 1. A, Axial computed tomographlc
scan on admission (fourth day after ictus)
showing a massive intracerebral hematoma
in the frontoparietal subcortices of the left
hemisphere. Hypodense areas consistent
with cerebral edema are observed extensively around the hematoma. B, Magnetic
resonance images. Coronal T,-weighted
spin-echo images (repetition time, 600 milliseconds; echo time, 17 milliseconds) after
intravenous injection of gadolinium-diethylenetriamine pentaacetic acid (0.1 mmol/kg
of body weight) on the sixth day demonstrate the areas of very slightly decreased
Intensity with a halo of increased Intensity.
The mass is believed to interrupt the fibers
converging to the corona radiata from the
precentral gyms and paracentral lobule of
the left side.

Downloaded from http://ahajournals.org by on April 11, 2024

CT scan using an X-force scanner (Toshiba) with a
slice thickness of 10 mm on admission (fourth day after
stroke onset) revealed a massive intracerebral hematoma in the frontoparietal subcortices of the left
hemisphere (Fig 1A). Hypodense areas consistent with
cerebral edema were observed extensively around the
hematoma. Scattered old foci of decreased density were
present in the bilateral basal ganglia or thalami. No
areas of abnormal density were found along the left
pyramidal tract (Fig 2, top row). MRI studies were
carried out on the sixth day after onset, using a 1.5-T
system (Siemens Corporation). Axial T r and T2weighted and proton density-weighted images were
obtained with spin-echo pulse sequences. T2- and proton density-weighted images revealed the mass in the
left frontoparietal subcortices to be of decreased intensity, and T r weighted images found the mass to be of

very slightly decreased intensity with a halo of increased
intensity. Postcontrast coronal T^weighted images revealed a rim of increased intensity surrounding the
mass, which appeared to interrupt the fibers converging
to the corona radiata from the precentral gyrus and
paracentral lobule of the left side (Fig IB). T2-weighted
images revealed areas of markedly decreased intensity
in the left thalamus and bilateral putamen, as well as
scattered small areas of increased intensity in the basal
ganglia and other subcortical regions. The former areas
seemed consistent with old intracerebral hematomas
and the latter ones with old foci of lacunar infarcts.
Sequential CT scans were performed on the 9th, 13th,
and 22nd days. Ill-defined hypodense areas in the
posterior limb of the internal capsule, cerebral peduncle
of the midbrain, and basis pontis on the left emerged on
the 13th day (Fig 2, second row). These areas of

day 4

day 13

day 22

day 48

FIG 2. Sequential computed tomographic
scans at the levels of the internal capsule
(right column), cerebral peduncle (middle
column), and pons (left column). No areas of
abnormal density appear along the axis of
the left pyramidal tract on the fourth day after
the initial ictus. Ill-defined hypodense areas
emerge in the posterior limb of the Internal
capsule, cerebral peduncle of the midbrain,
and basis pontis on the left side on the 13th
day. These areas of decreased density become well demarcated on the 22nd day and
are still present on the 48th day.

Kazui et al

decreased density along the left pyramidal tract became
well defined on the 22nd day (Fig 2, third row).
The patient's language disturbance gradually improved, but the dense hemiplegia was unchanged. The
patient suffered from a recurrent intracerebral hemorrhage in the right frontal opercular subcortex on January 2, 1994 (the 33rd day after the initial ictus). The
hypodense areas along the axis of the left pyramidal
tract remained, with gradual attenuations revealed on
CT scans on the 33rd, 34th, 35th, 41st, and 48th days
(Fig 2, bottom row). The patient was transferred to
another hospital on January 18, 1994 (the 49th day).

Discussion

Downloaded from http://ahajournals.org by on April 11, 2024

Sequential CT findings in our patient were quite
characteristic. As shown in Fig 2, although initial CT
did not reveal any hypodense areas along the left
pyramidal tract below the level of hematoma, ill-defined
areas of decreased density appeared in the posterior
limb of the internal capsule, cerebral peduncle of the
midbrain, and pontine base of the left side on the 13th
day after stroke onset. These areas became well demarcated on the 22nd day and persisted thereafter during
our observation period. These findings were consistent
with secondary (wallerian) degeneration of the pyramidal tract.
Wallerian degeneration can be detected as shrinkage
of the ipsilateral brain stem after damage to the supratentorial corticospinal tract in patients with chronic
hemiplegia of duration of more than 1 year.1314 Exceptionally, Kuhn and coauthors8 described a single case of
decreased attenuation in the mesencephalon and pons
on CT scans. Kameyama and associates15 reported a
patient whose CT scans demonstrated focal low densities in the cerebral peduncle and pontine base 1 month
after middle cerebral artery occlusion. To our knowledge, the present report describes the earliest demonstration of wallerian degeneration of the pyramidal tract
byCT.
Why was such an early CT change apparent in our
patient? Most of the fibers of the pyramidal tract
originate in the motor cortex and caudal premotor
cortex, but 20% stem from the somatosensory and
parietal cortices.16 Pennock and colleagues12 reported
on two adults in whom areas of increased signal intensity in the internal capsule were detected on T2weighted MRI within 2 weeks of the onset of frontoparietal infarction, and they attributed the rapid onset of
changes to the relatively sparse myelination of the
parietopontine tract. Fumeya and Hideshima11 reported
that T2-weighted MRI revealed early abnormalities of
the corticospinal tract within 1 week of ictus in patients
with spontaneous intracerebral hemorrhage. They attributed these early MRI findings to the occurrence of
acute endoneurinal edema in the corticospinal tract
fibers. Early CT changes in our patient might correspond to the above-mentioned MRI abnormalities, on
the basis of the same underlying mechanism, although
we could not obtain repeat MRI. From the present case,
we conclude that a massive hematoma, spreading out
through the frontoparietal subcortices, extensively in-

Early CT Detection of Wallerian Degeneration

2289

terrupts the fibers from the cerebral cortex to the spinal
cord, thus causing the very early manifestation of wallerian degeneration of the pyramidal tract in the internal capsule, midbrain, and pons demonstrated by CT.
Prospective studies with CT and MRI should be
conducted to detect wallerian degeneration early and to
clarify its mechanism in acute stroke patients.

Acknowledgments
This study was supported in part by grants from Japan
Cardiovascular Research Foundation and Japan Research
Foundation for Chronic Diseases and Rehabilitation. The
authors thank T. Tomosugi, MD, and K. Uetsuhara, MD
(Department of Neurosurgery, Kagoshima City Hospital), T.
Okochi, MD (Faculty of Health and Sport Sciences, Osaka
University), and N. Handa, MD (First Department of Internal
Medicine, Osaka University Medical School), for their helpful
advice.

References
1. Duchen LW. General pathology of neurons and neuroglia. In:
Adams JH, Corsellis JAN, Duchen LW, eds. Greenfield's Neuropathology, 4th ed. London, England: Edward Arnold; 1984:1-52.
2. Kuhn MJ, Mikulis DJ, Ayoub DM, Kosofsky BE, Davis KR,
Taveras JM. Wallerian degeneration after cerebral infarction: evaluation with sequential MR imaging. Radiology. 1989;172:179-182.
3. Waller A. Experiments on the section of the glossopharyngeal and
hypoglossal nerves of the frogs, and observations of the alterations
produced thereby in the structure of their primitive fibres. Philos
Trans R Soc Lond. 1850;140:423-429.
4. Daniel PM, Strich SJ. Histological observations on Wallerian
degeneration in the spinal cord of the baboon, Papio papio. Ada
Neuropathol (Bed). 1969;12:314-328.
5. McCaman RE, Robins E. Quantitative biochemical studies of wallerian degeneration in the peripheral and central nervous system,
I: chemical constituents. J Neurochem. 1959;5:18-31.
6. Thomas PK, King RHM, Phelps AC. Electron microscope observations on the degeneration of unmyelinated axons following nerve
section. JAnat. 1972;113:279-280.
7. Cobb SR, Mehringer CM. Wallerian degeneration in a patient with
Schilder disease: MR imaging demonstration. Radiology. 1987;162:
521-522.
8. Kuhn MJ, Johnson KA, Davis KR. Wallerian degeneration: evaluation with MR imaging. Radiology. 1988;168:199-202.
9. Uchino A, Imada H, Ohno M. MR imaging of wallerian degeneration in the human brain stem after ictus. Neuroradiology. 1990;
32:191-195.
10. Inoue Y, Matsumura Y, Fukuda T, Nemoto Y, Shirahata N, Suzuki
T, Shakudo M, Yawata S, Tanaka S, Takemoto K, Onoyama Y.
MR imaging of wallerian degeneration in the brainstem: temporal
relationships. AJNR Am J Neuroradiol. 1990;l 1:897-902.
11. Fumeya H, Hideshima H. Early MR abnormality indicating functional recovery from spontaneous intracerebral hemorrhage.
NeurolMed Chir (Tokyo). 1991;31:650-653.
12. Pennock JM, Rutherford MA, Cowan FM, Bydder GM. MRI:
early onset of changes in wallerian degeneration. Clin Radiol.
1993;47:311-314.
13. Stovring J, Fernando LT. Wallerian degeneration of the corticospinal tract region of the brain stem: demonstration by computed
tomography. Radiology. 1983;149:717-720.
14. Warabi T, Miyasaka K, Inoue K, Nakamura N. Computed tomographic studies of the basis pedunculi in chronic hemiplegic
patients: topographic correlation between cerebral lesion and
midbrain shrinkage. Neuroradiology. 1987;29:409-415.
15. Kameyama S, Fujii Y, Otsuka A, Morota N, Fukasaku K. A demonstration of wallerian degeneration of the descending tract in the
brain stem by means of computed tomography [in Japanese with
English abstract]. Prog Comput Tomogr. 1988;10:301-305.
16. Nieuwenhuys R, Voogd J, van Huijzen C. Motor system. In: The
Human Central Nervous System: A Synopsis and Atlas. 3rd ed.
Berlin, Germany: Springer-Verlag; 1988:247-278.