Anatomy and Pathology of the Cerebellar Peduncle

Toshio Moritani MD, PhD, Akio Hiwatashi MD, Henry Z Wang MD, PhD,
Yuji Numaguchi, MD, PhD, Leena Ketonen MD, PhD,
Sven E Ekholm 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
 E-mail: moritani2001@yahoo.com

Introduction

Lesions in the cerebellar peduncle include various pathological conditions: infarction,

various primary or secondary degeneration, demyelinatiing disease, toxic metabolic
disease, 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 anatomy (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 cerebellar peduncles; the rostral 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).
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-ponto-cerebellar
pathway, composed of the corticopontine tract and the pontocerebellar tract, is major
afferent fibers through the middle cerebellar peduncle. It arises from the cerebral cortex
and enters the ipsilateral pontine nucleous and almost entirely crossed to the
contralateral cerebellum. Olivocerebellar fibers form the largest 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 colliculus. 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 anatomy (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).
Infarction (Figures 2-5)
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 large involvement of the cerebellar hemisphere, and can be associated with
the involvement of pons, midbrain, thalamus and occipital lobe (Figure 4) (4). Bilateral
AICA territory infarcts are very rare (Figure 5), and can occur due to hypoperfusion in
the watershed area between the AICA and the SCA (6).
Wallerian degeneration of the pontocerebellar tracts 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).
Osmotic myelinolysis (Figure 7).
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.
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
primary or secondary degeneration.
Herpes encephalitis (Figure 9)
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 (Figure
6G) (11).
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 cortico-ponto-cerebellar
pathways (middle cerebellar peduncle) or other pathways such 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).
Olivopontocerebellar atrophy (OPCA) and other primary degenerative diseases
(Figure 12).
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 dominant spinocerebellar atrophy
(16), Wilson’s disease, non-Wilsonian hepatocerebral degeneration (17), and fragile X
syndrome (18).
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).
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).
Tumor (Figures 17 and 18).
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 multiforme also occur in the
cerebellar peduncle. Tumors involving the ventricular portion or the cerebellar portion
of the middle cerebellar peduncle can be removed by surgery (3).
Neurofibromatosis (Figure 19)
Hamartomatous lesions are observed 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.
Diffuse axonal injury (DAI) (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).

Conclusion

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.

References

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Figure Legends

Figure 1. Normal anatomy.

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.
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 2. An infarct in the inferior cerebellar peduncle. 72-year-old man with

vertigo.
A, B. FLAIR image and DWI show a hyperintense lesion, representing a small acute infarct in
the left inferior cerebellar peduncle.

Figure 3. An infarct in the inferior cerebellar peduncle. 57-year-old man with ataxia
and diplopia.
A, B. T2WI and DWI show a hyperintense lesion, representing an acute infarct in the right
middle cerebellar peduncle.

Figure 4. infarcts involving the superior cerebellar peduncle. 58-year-old man with
loss of consciousness.
A, B. FLAIR image and DWI show hyperintensity lesions in the left cerebellar hemisphere, and
the midbrain including the left superior cerebellar peduncle.

Figure 5. Bilateral infarcts in the middle cerebellar peduncle. 80-year-old man with
ataxia and 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.

Figure 6. Wallerian degeneration in the middle cerebellar peduncle. 50-year-old

man with quadriparesis and loss of consciousness after chiropractic.
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 (red 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
(red 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 1998;4:171-177. Toshihiro O'uchi MD with permission).
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.
 
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 7. CPM. 50-year-old female presenting with loss of consciousness after rapid
correction of hyponatremia.
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 (red arrows).
These lesions maybe due to myelinolysis itself or secondary degeneration.

Figure 8. Solvent encephalopathy. 38-year-old man presenting with blurred vision,

ataxic 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 (red arrows).

Figure 9. Herpes encephalitis. 40-year-old male presenting with a seizure.

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 (red arrows) and the temporal lobes.

Figure 10. Crossed cerebellar diaschisis. 27-year-old male, presenting with status
epilepticus. He has a history of recurrent generalized seizures.
A. FLAIR image shows hyperintensity lesions in the right cerebellar hemisphere (red arrows)
and contralateral diffuse cerebral hyperintensity associated with status epilepticus.
B, C. FLAIR images at the level of the brain stem show a hyperintense lesion in the right
superior cerebellar peduncle (red arrows). These findings suggest that crossed cerebellar
diaschisis of this case is related to retrograde transneuronal degeneration through the
cerebello-rubro-thalamic tract.
Figure 11. Crossed cerebellar atrophy. 19-year-old female. She had a history of
recurrent seizures and perinatal intracranial hemorrhage.
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 (blue arrow) and hemisphere. Wallerian degeneration of ipsilateral brain
stem is also seen (red arrow).

Figure 12. Olivopontocerebellar atrophy (sporadic type). 54-year-old woman

presenting with dysarthric speech and dizziness.
A, B. Axial and sagittal FLAIR images show hyperintensity in the middle (red arrows) and
inferior cerebral peduncles (blue 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 (light blue arrows) and the
pyramidal tracts (green arrows) are spared.

Figure 13. Leukoencephalopathy with vanishing white matter. An 11 year-old boy.

A. T2WI shows diffuse white matter signal abnormalities similar to CSF intensity.
B. T2WI also shows hyperintense lesions in the central tegmental tracts (blue arrows),
pyramidal tracts (teal arrows), and inferior and middle cerebellar peduncles with atrophy (red
arrows).

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 (red arrows) cerebellar hemispheres, and in the deep white matter, which is
characteristic of MS.

Figure 15. MS. 57-year-old man presenting with speech disturbance and ataxia.
A, B. T2WI and FLAIR image shows hyperintense lesions in the pons, and inferior cerebellar
peduncles (red arrows), and in the callosomarginal interface in the deep white matter, which is
characteristic of MS.
C, D. Hyperintense lesions are also seen in the midbrain, and the superior cerebellar peduncle
(red arrows).

Figure 16. PML. 25-year-old man presenting with right-sided weakness and headache.
He has had a history of HIV infection.
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 enhancement.

Figure 17. Low grade astrocytoma. 4-year-old boy presenting with autism.
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.
Figure 18. Acoustic schwannoma. 17-year-old female presenting with hearing loss
and progressive ataxia.
A, B. Axial T2WI and sagittal T1WI show an extra-axial cerebellopontine angle mass lesion
which deviates the left middle cerebellar peduncle posteriorly and superiorly (red arrows).

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 cerebellum.

Figure 20. DAI. 29-year-old woman with DAI, presenting with loss of consciousness
after motor vehicle accident.
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.