Download Anatomy And Pathology Of The Cerebellar Peduncle

Introduction
Lesions in the cerebellar peduncle include variou s pathological
conditions: infarction, various primary or secondary degeneration,
demyelinatiing disease, toxic metabolic diaease, trauma, and benign
and malignant tumors. Their differential diagnoses are occasionally
difficult. We illustrate the anatomy, pathology and imaging findings of the
cerebellar peduncle.
Anatomy
Gross anatom y (Figure 1A-F).
The cerebellum is connected to the brainstem by three cerebellar
peduncles: 1) the inferior cerebellar peduncle (restiform body and
juxtrarestiform body) 2) the middle cerebellar peduncle (brachium
pontis), and 3) the superior peduncle (brachium conjunctivum) (1). The
wall and lateral roof of the 4th ventricle are formed by the inner surfaces
of the ce rebellar pedun cles; the rost ral portion by the superior
peduncles; and the caudal portions by the inferior peduncles (Figure
1A -F). The middle cerebellar peduncle is lateral to inferior and superior
peduncles and is not directly exposed to the cavity of the 4th ventricle.
The middle cerebellar peduncle can be divided into three portions: brain
stem portion, ventricular portion, and cerebellar portion (Figure 1E).
This classification can be a useful application in surgery (2).
Toshio Moritani MD, PhD, Akio Hiwatashi MD, Henry Z Wang MD, PhD, Yuji Numaguchi
Numaguchi,, MD, PhD, Leena Ketonen MD, PhD, Sven E Ekholm MD,PhD
MD,PhD,, Per-Lennart A Westesson MD, PhD, DDS
Division of Diagnostic and Interventional Neuroradiology, Department of Radiology, University of Rochester Medical Center, Rochester NY F E-mail: [email protected]
G. Cerebellar connections. The cortico-ponto-cerebellar pathway
(corticopontine tract and pontocerebellar tract) is major afferent fibers
through the middle cerebellar peduncle. Olivocerebellar fibers (afferent
fibers) are through the inferior cerebellar peduncle. Efferent fibers
mainly arise from the dentate nucleus to the red nucleus through the
superior cerebellar peduncle (cerebello-rubro-thalamic tract).
Figure 6. Wallerian degeneraion in the middle cerebellar
peduncle. 50-year-old man with quadriparesis and loss of
co nsciousness after chiropract ic.
A
Solvent encephalopathy (Figure 8)
There have been a few case reports of middle cerebellar peduncle lesions
in solvent encephalopathy (chronic toluene intoxication) in which the
cerebral and cerebellar white matter, thalamus, basal ganglia, internal
capsule, and brain stem are also involved (9, 10) (Figure 8). These
patients' symptoms are usually composed of pyramidal tract and cerebellar
signs. The middle cerebellar peduncle lesions can be p rimary or
secondary degeneration.
B
Figure 8. Solvent encephalopathy. 38year-old man presenting with blurred
vi sion, ataxi c speech and bilateral
pyramidal signs.
T2WI shows diffuse hyperintense lesions in
the white matter of both temporal lobes and
mildly hyperintense lesions in the pons and
bilateral middle cerebellar peduncles (arrows).
Cerebellar connections (Figure 1G).
The cerebellum is linked to other parts of the brain by numerous efferent
and afferent fibers that are grouped together on each side of the
cerebellum in three peduncles (1). Most of the afferent tracts enter the
cerebellum via the inferior and middle cerebellar peduncles. A few enter
via the superior cerebellar peduncle. Afferent fibers are far more
numerous that efferent fibers by a ratio of 40:1 (3). The cortico-pontocerebellar pathway, composed of the corticopontine tra ct and the
pontocerebellar tract, i s major affe rent f ibers through the middle
cerebellar peduncle. It arises from the cerebral cortex and enter the
ipsilateral pontine nucleous and almost entirely crossed to the
contralateral cerebellum. Olivocerebellar fibers form the large st
component of the inferior cerebellar peduncle. Most of efferent tracts of
the cerebellum are via the superior cerebellar peduncle. They mostly
arise from dentate nucleus and decussate at the levels through the
inferior collicu lus. Most of the fibers enter the contralateral red nucleus
and project the cerebral cortex via the thalamus.
Symptomatology
Lesions of the cerebellar peduncle result in variable clinical symptoms,
ranging from vertigo or vomiting as the only clinical presentation to facial
palsy, ataxia, nystagmus, diplopia, dysphagia, dysarthria, deafness,
contralateral motor weakness, trigeminal sensory loss, dysmetria of the
limb, loss of pain and temperature sense, Horner's syndrome, and
"locked-in" syndrome (1,4,5).
Imaging of normal anatom y(Figure 1F).
The posterior fossa is difficult to evaluate on CT because of poor
contrast resolution and artifacts. MRI more clearly demonstrates the
anatomy and pathology of the middle cerebellar peduncle in the
posterior fossa than does CT. FLAIR images occasionally show a slight
increase in signal intensity in normal middle cerebellar peduncles
(Figure 1F).
s
s
i
i
m
s
B
A, B, FLAIR image and
DWI show a
hyperintense lesion,
representing a small
acute infarct in the left
inferior cerebellar
peduncle.
D
m
B
V
C
F
A
m
i
B
Figure 3. An infarct in the inferior cerebel lar peduncle. 57year-old man with ataxia and diplopia.
A
B
Figure 4. infarcts involving the superior cerebellar peduncle. 58year-old man with loss of consciousness.
i
A. Coronal FLAIR image. B,C,D, Sagittal T1WI. E, Axial T2WI.
F. FLAIR image occasionally shows slightly high signal intensity in the
normal superior (not shown), inferior and middle cerebellar peduncles.
middle cerebellar peduncle (m), superior cerebellar peduncle (s),
inferior cerebellar peduncle (i).
brain stem portion (B), ventricular portion (V), and cerebellar portion (C)
of the middle cerebellar peduncle.
E
A, B. DWI and T2WI shows hyperintense lesions in the right cerebellar
hemisphere and the left side of the pons at 10 days after onset, which
represents subacute hemorrhagic infarcts.
C, D. On follow-up MRI at 8 months after onset, old infarcts show very high
intensity on T2WI and low intensity on FLAIR image as CSF. Symmetrical
round hyperintense lesions in bilateral middle cerebellar peduncles are seen
on T2WI and FLAIR image (arrows). These lesions represent wallerian
degeneration of the pontocerebellar tracts secondary to pontine infarction.
E. T2WI at the level of the medulla demonstrates symmetric hyperintense
lesions corresponding to the bilateral olivary nuclei, representing hypertrophic
olivary degeneration (arrows).
F. On the pathological
specimen of another
patient, wallerian
degeneration of the
pontocerebellar tracts
is recognized as
symmetric rounded
lesions (arrows) in
bilateral middle
cerebellar peduncles
and extends out to the
mossy fibers in the
cerebellar cortex
(open arrows)
(Ref. 3. Int J Neuroradiol
Figure 2. An infarct in the inferior cerebellar peduncle. 72-year-old
man with vertigo.
A,B. T2WI and DWI at 24
hrs after onset clearly
reveal homogenous
round hyperintensity
areas representing acute
infarcts in the bilateral
middle cerebellar
peduncles and both
cerebellar hemispheres.
i
E
The inferior cerebellar peduncle is mainly supplied by the posterior
inferior cerebellar artery (PICA). The middle cerebellar peduncle is
supplied by the anterior inferior cerebellar artery (AICA) and partly by the
superior cerebellar artery (SCA). The superior cerebellar peduncle is
mainly supplied by the SCA. These arteries vary greatly in origin, size,
course, and supply area, the aera of infarction are variable in extent and
location, ranging from a small infarct localized into the cerebellar
peduncle (Figure 2 and 3) to la rge involvement of the cerebella r
hemisphere, and can be associated with the involvement of pons,
midbrain, thalamus and occipital lobe (Figure 4) (4). Bilateral AICA
territory infarcts a re very rare (Figure 5), and can occur due to
hypoperfusion in the watershed area between the AI CA and the SCA (6).
D
1998;4:171-177.
Toshihiro O'uchi MD
with permission).
F
G. Wallerian degeneration
in bilateral middle
cerebellar peduncles
The lesion involving the
pontine nucleus can also
involve the pontocerebellar tract from the
contralateral pontine
nucleus, which results in
wallerian degeneration in
bilateral middle cerebellar
peduncles.
B
B
Walle rian degenera tion of the pon tocerebella r trac ts
secondary to pontine hemorrhage or infarction (Figure 6).
Wallerian degeneration secondary to pontine hemorrhage or infarction is
usually bilateral. Differentiating from infarction is important. This is because
of damage to both ipsilateral pontine nuclei (which deliver axons to the
contralateral cerebellar hemisphere) and the ipsilateral axons (which
originate from the contralateral pontine nuclei and course into the ipsilateral
cerebellar hemisphere) (Figure 6G) (3). The T2 prolongations were first
recognized from 26 days to 4.5 months after insult Theoretically, the
wallerian degeneration of the pontocerebellar tracts should extend out to
the mossy fibers in the cerebellar cortex, as seen on the pathological
specimen; however this is beyond the resolution of MRI(3). Hypertrophic
olivary degeneration occasionally coexists with these lesions, because the
lesion can also involve the area in the Guillain-Mollaret triangle (Figure 6H)
(7).
Bilateral middle cerebellar peduncle lesions were present in a patient with
herpes encephalitis with bilateral temporal lobe involvement (Figure 9).
The cause of these lesions is unknown. Secondary transneuronal
degeneration via bilateral cortico-ponto-cerebellar pathways may be one of
the possible explanations for these lesions (F igure 6G) (11).
Figure 9.
Herpes
encephalitis
A. T2WI shows diffuse hyperintense lesions in the cortex and white matter
in bilateral temporal lobes, which represents herpes encephalitis.
B. Coronal FLAIR image shows hyperintense lesions in the bilateral middle
cerebellar peduncles (arrows) and the temporal lobes.
Crossed cerebellar diaschisis and atrophy (Figures 10 and 11)
Crossed cerebellar diaschisis and atrophy presumed to be associated with
transneuronal metabolic depression in the cerebellum through corticoponto-cerebellar pathways (middle cerebellar peduncle) or other pathways
su ch as cerebello-rubro-thalamic tract (superior cerebellar peduncle)
(Figure 10) (12,13) Unilateral atrophy of the middle cerebellar peduncle
and cerebellar hemisphere occurs as a sequela of ischemic or destructive
injury of the contralateral cerebral hemisphere (14). These findings are
found in children with a history of extreme prematurity, perinatal
intracranial hemorrhage, and recurrent seizures (Figure 11).
C
A. FLAIR image shows hyperintensity lesions in the right cerebellar
hemisphere (arrows) and contralateral diffuse cerebral hyperintensity
associ ated with status epilepticus.
B,C. FLAIR images at the level of the brain stem show a hyperintense
lesion in the right superior cerebellar peduncle (arrows). These
findings suggest that crossed cerebellar diaschi sis of this case is
related to retrograde transneuronal degeneration through the
cerebello-rubro-thalamic tract.
Figure 11. Crossed
cerebellar atrophy
B
A. B. T2WI shows a hyperintense lesion in the central pons representing CPM.
T2WI also shows symmetrical round lesions in the bilateral middle cerebellar
peduncles (arrows). These lesions maybe due to myelinolysis itself or
secondary degeneration.
Leukodystrophy and leukoencephalopathy (Figure 13).
Some kinds of leukodystrophy and leukoencephalopathy can also involve in
the cerebellar peduncles. This leukoencephalopathy with vanishing white
matter is an autosomal recessive disorder with chronic and progressive
episodes of rapid deterioration, provoked by fever and minor head trauma.
This is primarily an axonopathy, with myelin being secondarily affected (19)
(Figure 13).
A. T2WI shows diffuse white
matter signal abnormalities
similar to CSF intensity.
B. T2WI also shows
hyperintense lesions in the
central tegmental tracts
(arrows), pyramidal tracts
(arrows), and inferior and
middle cerebellar peduncles
with atrophy (arrows).
A
B
Demyelinating disease: multiple sclerosis (MS), acute
disseminated encephalomyelitis (ADEM) and progressive multifocal
leukoencephalopathy (PML) (Figures 14-16)
Brain stem and cerebellar involvement including cerebellar peduncles is
common in patients with MS and ADEM. Cerebellar symptoms and signs
are commonly seen in 50-80% in MS patients. On MRI brainstem lesions
in 68% and cerebellar lesions in 49%-88% were detected (20). These
lesions in MS or ADEM are often bilateral but asymmetric (Figures 14 and
15). In PML involvement of the posterior fossa including the cerebellar
peduncles is also common (32%). Isolated disease in the posterior fossa is
in 10% of PML patients (21) (Figure 16).
Figure 14. MS. 40-year-old woman with multiple sclerosis, presenting
with speech disturbance and ataxia.
A, B.T2WI shows multiple
asymmetric hyper-intense
lesions in the pons, middle
cerebellar peduncles
(arrows) cerebellar
hemispheres, and in the
deep white matter, which is
characteristic
of MS.
A
B
A, B.T2WI and FLAIR
image shows
hyperintense lesions in
the pons, and inferior
cerebellar peduncles
(arrows), and in the
callosomarginal
interface in the deep
white matter, which is
characteristic of MS.
A. T2WI shows right cerebral atrophy with ventricular dilatation representing
a sequela of perinatal intracranial hemorrhage.
B. T2WI through the posterior fossa shows atrophy of the contralateral
cerebellar middle cerebellar peduncle (arrow) and hemisphere.
Wallerian degeneration of ipsilateral brain stem is also seen (arrow).
A,B A mass lesion is located
in the ventricular portion to
the cerebellar portion of
the left middle cerebellar
peduncle. It is high signal
on T2WI and low signal
on T1WI and with no
enhancement (not
shown). This lesion can
be removable by surgery.
B
B
17-year-old female
presenting with
hearing loss and
progressive ataxia
A
B
A,B Axial T2WI and sagittal T1WI shows an extra-axial cerebellopontine
angle mass lesion which deviates the left middle cerebellar peduncle
posteriorly and superiorly (arrows).
Neurofibrom atosis (Figure 19)
Hamarto matous lesions are obse rved in 80% of all patients with
neurofibromatosis type 1. Multiple lesions in the basal ganglia, optic
radiation, brainstem, and cerebellar peduncles are common (Figure 19).
Pathologically, these lesions are foci of hyperplastic or dysplastic glial
proliferation and considered malformations rather than neoplasms.
Figure 19. Neurofibromatosis type 1. 4-year-old girl presenting
with developmental delay.
A,B T2WI and FLAIR
image show
multiple asymmetric
lesions in the pons,
middle and inferior
cerebellar
peduncles, and
A
cerebellum.
B
Diffuse axonal injury (DA I) (Figure 20)
The gray-white matter interface, the corpus callosum, and dorsal aspect
of the upper brainstem including the superior cerebellar peduncle are
three specific areas for the occurrence of DAI. Other less frequent
locations include the caudate nuclei, thalamus and internal capsule.
Cerebellar involvement including the middle cerebellar peduncle is
uncommon (Figure 20).
Figure 20. DAI. 29-year-old woman with DAI, presenting with loss of
consciousness after motor vehicle accident.
A
B
A. FLAIR image shows a
hyperintense lesion in the left
middle cerebellar peduncle to
cerebellar hemisphere due to
DAI.
B. DWI shows hyperintense
lesions in the corpus callosum
and bilateral internal
capsules, which is typical
findings of DAI.
Conclusion
1) Carpenter MB. Cerebellum. In, Core Textbook of Neuroanatomy. 5th edition. Baltimore, MD: Williams &Wilkins, 1996;583-623.
2) Tomita T. Surgical management of cerebellar peduncle lesions in children. Neurosugery 1986;18:568-575.
3) O'uchi T. Wallerian degeneration of pontocerebellar tracts after pontine hemorrhage. Int J Neuroradiol 1998;4:171-177.
4) Amenco P, Rosengart A, DeWitt D, Pessin MS, Caplan LR. Anterior inferior cerebellar artery teritory infarcts. Mechanisms and clinical
features. Arch Neurol 1993;50:154-161.
C, D. Hyperintense
lesions are also seen
in the midbrain, and
the superior cerebellar
peduncle (arrows).
A. T2WI shows an isolated
hyperintense lesion in
the right middle
cerebellar peduncle
extending into the
cerebellar hemisphere.
B. Gd-enhanced T1WI
shows this lesion as
hypointensity with no
A
enhancement.
A
Figure 18.
Acoustic
schwannoma.
Re feren ces
A
5) Milandre L, Rumeau C, Sangla I, Peretti P, Khalil R. Infarction in the territory of the anterior inferior cerebellar artery: report of five cases.
Neuroradiology 1992;34:500-503.
6) Akiyama K, Takizawa S, Tokuoka K, Ohnuki Y, Kobayashi N, Shinohara Y.Bilateral middle cerebellar peduncle infarction caused by
traumatic vertebral artery dissection. Neurology 2001;56:693-694.
7) Kitajima M, Korogi Y, Shimomura O, Sakamoto Y, Hirai T, Miyayama H, Takahashi M.Hypertrophic olivary degeneration: MR imaging and
pathologic findings. Radiology 1994;192:539-543.
8) Mangat KS, Sherlala K. Cerebellar peduncle myelinolysis: case report.
Neuroradiology 2002;44:768-769.
D
Figure 16. PML. 25-year-old man presenting with right-sided
weakness and headache. He has had a history of HIV infection.
B
Figure 17. Low grade astrocytoma. 4-year-old boy presenting with
autism.
Lesions in the middle cerebellar peduncle include various pathological
conditions, ranging from infarction, tumor, infection, trauma and
demyelination to primary and secondary degeneration. Understanding
the anatomy, pathology, imaging characteristics is important for the
differential diagnosis of lesions in the middle cerebellar peduncle.
C
A
Benign tumors such as astrocytoma or cavernous angioma can involve
in the cerebellar peduncle (Figures 17). An extra-axial tumor such as
benign acoustic schwannoma occasionally displaces the middle
cerebellar peduncle (Figure 18). Malignant tumors such as metastasis
or glioblastoma multifo rme also o ccu r in the cerebellar peduncle.
Tumors involving the ventricular portion or the cerebellar portion of the
middle cerebellar peduncle can be removed by surgery (3).
A, B. Axial and sagittal FLAIR images show hyperintensity in the middle
(arrows) and inferior cerebral peduncles (arrows).
C. Axial FLAIR image also shows cruciform hyperintensity in the transverse
pontine fibers on the anterior and lateral aspect of the pons. The
tegmentum (arrows ) and the pyramidal tracts (arrows) are spared.
Figure 15. MS. 57-year-old man presenting with speech disturbance
and ataxia.
B
Tumor (Figures 17 and 18).
C
B
B
19-year-old female.
She had a history of
recurrent seizures and
perinatal intracranial
hemorrhage.
A
A
An 11 year-old boy.
A
A
Figure 7. CPM
50-year-old female
presenting with loss of
consciousness after
rapid correction of
hyponatremia.
Figure 12. Ol ivopontocerebellar atrophy (sporadic type). 54-yearold woman presenting with dysarthric speech and dizziness.
40-year-old male
presenting with
a seizure.
27-year-old male, presenting with status epilepticus. He has a history
of recurrent generalized seizures.
Symmetrical lesions in bilateral middle cerebellar peduncles without central
pontine myelinolysis (CPM) was reported as cerebellar peduncle myelinolysis
(8). However, in our case, bilateral cerebellar peduncle lesions accompanied
by CPM (Figure 7). These lesions are presumed to be due to myelinolysis
itself or secondary degeneration related to CPM.
OPCA is a degenerative disease characterized by atrophy of the pons,
middle cerebellar peduncles, and cerebellar hemispheres. There are
characteristic histologic changes, such as loss of specific fiber tracts and
the presence of gliosis in the pons, middle cerebellar peduncles and
cerebellum (15). The fibers affected in the pons are the transverse pontine
fibers, while the pyramidal tracts and tegmentum are spared (Figure 12).
Increased hyperintensity in the middle cerebellar peduncles are also
reported in other multiple system atrophy, autosomal do minant
spinocerebellar
atrophy
(16),
Wilson’s
disease,
non-Wilsonian
hepatocerebral degeneration (17), and fragile X syndrome (18).
Figure 13.Leukoencephalopathy with vanishing white matter.
Figure 10. Crossed cerebellar diaschisis
Osmotic myelinolysis (Figure 7).
A
Herpes encephalitis (Figure 9)
H. Guillain-Mollaret
triangle and hypertrophic
olivary degeneration
The lesion involving the
pontine nuclei can extend
into the areas within the
Guillain-Mollaret triangle,
which causes hypertrophic
olivary degeneration.
Figure 5. Bilateral infarcts in the middle cerebellar peduncle. 80year-old man with ataxia and vertigo.
m
C
Infarction (Figures 2-5)
A, B, FLAIR image and DWI
show hyperintensity
lesionsin the left
cerebellar hemisphre,
and the midbrain
including the left superior
cerebellar peduncle.
A
m
A
C
A, B, T2WI and DWI show a
hyperintense lesion,
representing an acute
infarct in the right middle
cerebellar peduncle.
Figure 1. Normal anatomy.
Olivopon toce rebellar atrophy (OPCA) and othe r p rimary
degenerative diseases (Figure 12).
Anatomy and Pathology of the Cerebellar Peduncle
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B
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