Hyperintense lesions of the middle cerebellar peduncle and beyond: a pictorial essay.

INTRODUCTION

The middle cerebellar peduncle (MCP) is the largest afferent system of the cerebellum
and consists of fibres from the cortico-ponto-cerebellar tract ( Figure 1 ). Lesions in this structure can be detected by brain
magnetic resonance imaging (MRI) as hyperintensity on T2-weighted/fluid-attenuated
inversion recovery (T2/FLAIR) sequences.

Figure 1 Coronal and axial views (A and B, respectively) showing the
cortico-ponto-cerebellar pathways.

Coronal and axial views (A and B, respectively) showing the
cortico-ponto-cerebellar pathways.

Several aetiologies may present with FLAIR hyperintensity in the MCP: demyelinating
diseases-multiple sclerosis (MS), acute disseminated encephalomyelitis (ADEM),
neuromyelitis optica spectrum disorder (NMOSD) and progressive multifocal
leucoencephalopathy (PML); toxic-metabolic diseases-hepatic encephalopathy (HE) and
osmotic demyelination syndrome (ODS); a degenerative disease-multiple system atrophy
(MSA); genetic diseases -fragile X-associated tremor/ataxia syndrome (FXTAS),
megalencephalic leucoencephalopathy with subcortical cysts (MLC) and spinocerebellar
ataxias (SCAs); a vascular disease-hemi-pontine infarct with trans-axonal
degeneration; and a neoplastic disease-diffuse midline H3K27M-mutated glioma.

The purpose of this pictorial review is to discuss the imaging findings that are
relevant for the differential diagnosis of diseases presenting with T2/FLAIR
hyperintensity in the MCP on T2-weighted imaging (T2WI). Such knowledge is of utmost
importance for the practicing radiologist.

DISEASES OF ADULTHOOD

Demyelinating diseases

MS

A chronic autoimmune disease of the central nervous system (CNS), MS presents
with inflammation, demyelination and axonal loss. The female-to-male ratio
in MS is approximately 3:1, and the average age at onset is 20-40
years ( 1 ) .

With regard to MRI findings, the lesions are usually isointense to
hypointense on T1-weighted imaging (T1WI) and hyperintense on T2/FLAIR
sequences ( Figure 2 ). The McDonald
criteria for MS include dissemination in time and space that can be
identified with MRI. Specifically, dissemination in space requires one or
more lesions that are hyperintense on T2WI in two or more of the following
locations: periventricular; cortical or juxtacortical; infratentorial; or in
the spinal cord. Dissemination over time requires either new lesions that
are hyperintense on T2WI when compared with a previous MRI or the
simultaneous presence of gadolinium-enhancing and non-enhancing
lesions ( 2 ) . A
classic T2/FLAIR finding consists of lesions oriented perpendicular to the
lateral ventricles and that are well-depicted on parasagittal images ( Figure 2A ). These alterations are
referred to as Dawson’s fingers. Active MS lesions show contrast enhancement
and usually form an incomplete pattern around the periphery to create an
open ring sign. Such lesions are frequently infratentorial, periventricular
or juxtacortical ( Figure 2 ). Mixed
white and grey matter lesions can also be identified. The MCP is an
important tract of white matter and is one of the most commonly affected
structures in MS ( 1 , 3 ) , as depicted in Figure 2B and detailed in Table 1 .

Table 1 Epidemiology and imaging characteristics of the various diseases
affecting the MCP. Group Disease Usual age at presentation
(years) Most commonly affected gender Distinguishing
characteristics in imaging MS 20-40 Female T2/FLAIR hyperintense lesions
oriented perpendicular to the lateral ventricles ADEM 5-8 Male Bilateral, asymmetric, poorly
marginated, multifocal lesions, presenting with T2
hyperintensity Demyelinating diseases NMOSD Approximately 40 Female Characteristically involving
the optic chiasm and retrochiasmatic regions, with lesions
typically found in aquaporin 4-rich areas such as the
periependymal regions abutting the ventricles PML Depends on the specific cause
leading to immunosuppression; most commonly seen in patients
with AIDS, with CD4 counts of 50-100 cells/pL; potentially
related to immunosuppressive monoclonal antibody
therapy Discrete multifocal, asymmetric,
periventricular and subcortical involvement, with no
significant mass effect or contrast enhancement Toxic metabolic diseases HE Depends on the
aetiology of liver dysfunction and portal hypertension T2/FLAIR symmetric
hyperintensity in the insula, thalamus and posterior limb of
the internal capsule; hyperintensity on T1WI in the globus
pallidus and anterior midbrain ODS Depends on the
aetiology of the osmotic stress affecting oligodendroglial
cells Restricted diffusion in the pons;
hyperintense signal on T2/FLAIR in the central portion of
the pons, sparing the periphery Degenerative diseases MSA 54-61 Male Hot cross bun sign in the pons on T2;
disproportionate atrophy in the olivary nuclei and MCP FXTAS Approximately 60 for tremor and
ataxia Male T2/FLAIR hyperintense lesions
in the MCPs and in the splenium of the corpus callosum Genetic diseases MLC 5 Male Subcortical cysts, permanence
of the cavum septum pellucidum, symmetric signal alteration
of white matter SCA3 5-70 (median, 40) Male Pontine and cerebellar atrophy; atrophy of
the globus pallidus atrophy in some patients with
long-standing disease Vascular diseases PI with Wallerian degeneration Depends on the
stroke aetiology Paramedian pontine
hyperintensity on T2WI Neoplastic diseases Diffuse midline H3K27M-mutated glioma 5-11 No difference T2 hyperintense lesion in the
pons, thalamus or spinal cord

Epidemiology and imaging characteristics of the various diseases
affecting the MCP.

Figure 2 MS. A: Sagittal FLAIR sequence showing callosal lesions
perpendicular to the ventricular wall. Note also the lesions in
the occipital and cerebellar white matter. B: Axial T2WI showing
bilateral hyperintense lesions (more conspicuous on the left
side) involving the MCPs.

MS. A: Sagittal FLAIR sequence showing callosal lesions
perpendicular to the ventricular wall. Note also the lesions in
the occipital and cerebellar white matter. B: Axial T2WI showing
bilateral hyperintense lesions (more conspicuous on the left
side) involving the MCPs.

NMOSD

One CNS autoimmune disease that causes multifocal inflammation, mostly in the
optic nerves and spinal cord, is NMOSD. The median age at onset is 40 years,
with 20% of patients being children or adults > 65 years old. Most
anti-aquaporin-4-positive patients are female, whereas the male-to-female
ratio is closer to 1:1 in those who are seronegative. Clinically, NMOSD has
six core presentations-area postrema syndrome, acute brainstem syndrome,
diencephalic syndrome, symptomatic cerebral syndrome, optic neuritis and
myelitis-all of which can be seen during acute attacks and
relapses ( 4 ) .

When NMOSD is suspected, the imaging modality of choice is MRI. Specifically
in acute phases, orbit MRI can show hyperintense lesions in the optic
nerves, with chiasmatic and retrochiasmatic involvement ( Figure 3A ). A T2WI scan of the brain
often reveals hyperintense lesions around the ventricles and in the MCP
( Figure 3B ), areas that are rich in
aquaporin-4. In addition, MRI of the spinal cord typically shows
longitudinally extensive myelitis involving three or more contiguous
medullary segments. There can be associated cord swelling, and central grey
matter involvement is usual. After contrast administration, T1WI of the
spinal cord can show patchy cloud-like enhancement of lesions that appeared
as bright spots on T2WI. There can be involvement of the MCP ( 3 , 4 ) , as illustrated in Figure 3B and described in Table
1 .

Figure 3 NMOSD. A: Contrast-enhanced coronal T1WI of a patient with
symptoms of acute optic neuritis of the left eye showing a
contrast-enhanced lesion in the intraorbital portion of the left
optic nerve. B: Axial FLAIR sequence showing a hyperintense
confluent lesion in the pons and in the MCPs. Note the
involvement of the periventricular regions adjacent to the
fourth ventricle in aquaporin-4-rich areas of the periependymal
tissue.

NMOSD. A: Contrast-enhanced coronal T1WI of a patient with
symptoms of acute optic neuritis of the left eye showing a
contrast-enhanced lesion in the intraorbital portion of the left
optic nerve. B: Axial FLAIR sequence showing a hyperintense
confluent lesion in the pons and in the MCPs. Note the
involvement of the periventricular regions adjacent to the
fourth ventricle in aquaporin-4-rich areas of the periependymal
tissue.

PML

The CNS demyelinating disease known as PML is caused by the John Cunningham
virus. This virus is typically dormant in healthy individuals but can be
reactivated by impaired cellular immunity, as seen in patients infected with
HIV or who are using drugs such as natalizumab. Usually progressing over the
span of a few months, PML results in neurological impairment and dementia.
Common symptoms include paresis, language disorders and ataxia ( 5 , 6 ) .

The MRI lesions can be seen as T2/FLAIR hyperintense multifocal, bilateral,
and asymmetric alterations ( Figure 4 )
that are usually located in the cerebral white matter (most often
subcortically), cerebellum and brainstem. Crescent-shaped cerebellar lesions
are characteristic findings. The lesions can also affect the basal ganglia
or thalamus but do not usually present oedema, nor do they present a mass
effect or enhance with contrast. This pattern of T2 hyperintensity, with no
mass effect or contrast enhancement and restricted patchy peripheral
diffusion, is also observed in the MCP ( 6 ) , as indicated in Figure 4B , Figure 4C , and
Table 1 .

Figure 4 PML. A: Axial FLAIR sequence showing periventricular and
subcortical white matter lesions, with no mass effect. T1WI
after contrast (not shown) revealed no enhancement. Axial FLAIR
sequence (B) and T2WI (C) showing pontine and cerebellar white
matter lesions, as well as hyperintensities in both MCPs.

PML. A: Axial FLAIR sequence showing periventricular and
subcortical white matter lesions, with no mass effect. T1WI
after contrast (not shown) revealed no enhancement. Axial FLAIR
sequence (B) and T2WI (C) showing pontine and cerebellar white
matter lesions, as well as hyperintensities in both MCPs.

Toxic metabolic diseases

HE

Acute or chronic liver failure can cause the brain dysfunction known as
HE ( 7 ) , which
frequently presents as personality alterations, as well as changes in
cognition, consciousness and motor function. The pathophysiology of this
condition is complex and involves blood-derived factors that alter the
normal working of the brain and blood-brain barrier ( 8 ) .

Neuroimaging with T2/FLAIR shows symmetric hyperintensity in the insula,
thalamus, cingulate gyrus and posterior limbs of the internal capsule. In
more severe cases, there is diffuse cortical oedema and T2/FLAIR
hyperintensity. Diffusion-weighted imaging (DWI) can show alterations and
distribution similar to those found on T2/FLAIR. On T1WI, hyperintensity is
commonly observed in the globi pallidi because of manganese deposition
( Figure 5A ). The MCP can show
bilateral symmetrical involvement ( Figure
5B ,C; Table 1 ).

Figure 5 HE. A: Axial T1WI showing hyperintensities in the globus
pallidus. Axial FLAIR sequence (B) and axial T2WI (C) showing
asymmetrical hyperintensities in the MCPs.

HE. A: Axial T1WI showing hyperintensities in the globus
pallidus. Axial FLAIR sequence (B) and axial T2WI (C) showing
asymmetrical hyperintensities in the MCPs.

ODS

The metabolic disease known as ODS consists of cell shrinkage and
demyelination in response to osmotic stress. Brain areas that are rich in
oligodendrocytes and myelin tend to be the most affected. It frequently
follows rapid correction of hyponatremia but can also be related to
hypokalemia, hypophosphatemia, malnutrition, harmful alcohol use and liver
dysfunction. Clinical features include impaired vigilance, dysphagia,
dysarthria and limb weakness ( 9 ) .

The diagnostic modality of choice is brain MRI, with the areas of
demyelination showing hyperintensity on T2/FLAIR and hypointensity on T1
( Figure 6 ). Characteristically, ODS
involves the central pons and spares the corticospinal tract, peripheral
pons and tegmentum, thereby creating a trident pattern signal in the
anterior pons. In some acute cases, there is restricted diffusion ( Figure 6D ), although this differs from
ischemic lesions that extend to the periphery of the pons while sparing the
midline. The lesions can extend to the MCP ( 10 ) ( Figure
6 ; Table 1 ).

Figure 6 ODS. Axial T2WI (A,B) and axial FLAIR sequence (C), showing
confluent hyperintensity involving the pons while sparing its
anterior peripheral aspect and extending into the MCPs. D: DWI
showing restricted diffusion

ODS. Axial T2WI (A,B) and axial FLAIR sequence (C), showing
confluent hyperintensity involving the pons while sparing its
anterior peripheral aspect and extending into the MCPs. D: DWI
showing restricted diffusion

Degenerative diseases

MSA

The neurodegenerative disorder MSA is an α-synucle-inopathy that
presents with a combination of parkinsonism, cerebellar ataxia, autonomic
nervous system dysfunction and cognitive deficits, as well as pyramidal and
extra-pyramidal signs. The mean age of onset is 54-61 years. It can be
divided into two clinical subtypes ( 11 ) : MSA with parkinsonism as the predominant
manifestation; and MSA with cerebellar ataxia as the predominant
manifestation.

On MRI, atrophy of the pons, cerebellum and MPC can be seen ( Figure 7B ). In addition, the
characteristic “hot cross bun” sign, which consists of cruciform T2
hyperintensity in the pons, can be seen ( Figure 7A ). However, this sign is not specific for MSA as it
occurs in other cerebellar degenerative disorders. Other alterations include
lateral putaminal rim hyperintensity on T2WI and T2 hyperintensity in the
posterior putamen in MSA with parkinsonism as the predominant
manifestation ( 11 ) .

Figure 7 MSA with cerebellar ataxia. A: Axial T2WI showing a hyperintense
cross in the form of a hot cross bun. B: Sagittal T1WI showing
flattening of the anterior aspect of the pons and cerebellar
atrophy. C: Axial FLAIR sequence showing cerebellar and MCP
atrophy, together with hyperintensities in the MCPs.

MSA with cerebellar ataxia. A: Axial T2WI showing a hyperintense
cross in the form of a hot cross bun. B: Sagittal T1WI showing
flattening of the anterior aspect of the pons and cerebellar
atrophy. C: Axial FLAIR sequence showing cerebellar and MCP
atrophy, together with hyperintensities in the MCPs.

Genetic diseases

SCAs

The group of genetic diseases known as SCAs consists of neurodegenerative
diseases that frequently manifest as cerebellar ataxia, slurred speech,
ocular motor abnormalities and a wide range of other neurological
features ( 12 , 13 ) . The prevalence is
estimated to be between 1 and 5 per 100,000 population ( 12 ) . They can be caused by
dynamic repeat expansion mutations and non-repeat mutations ( 13 ) , with the most common
forms being caused by repeat expansions, including SCA1, SCA2, SCA3, SCA6,
SCA7 and SCA17 ( 13 ) . The
most common of those is SCA3, also known as Machado-Joseph
disease ( 13 ) .

The MRI findings for SCA3 include atrophy of the infraand supra-tentorial
structures, with brainstem and cerebellar volumetric reductions ( Figure 8 ) being common
findings ( 14 ) . In
the cerebellum, atrophic changes in the vermis and superior peduncle are
noticeable, whereas pontine atrophy is more conspicuous in the
tegmentum ( 15 , 16 ) . Other sites of atrophy
include the frontal and temporal lobes, the globus pallidus, the dentate
nucleus and the red nucleus ( 16 ) . As noted in Table
1 , T2 hyperintensity of the transverse pontine fibres and MCP is
also observed ( 16 ) .

Figure 8 SCA3 in a 29-year-old man. Axial and sagittal T2WIs (A and B,
respectively) demonstrating atrophy of the cerebellar
hemispheres, as well as of the vermis, pons and MCPs. C: Axial
T1WI showing atrophy of the cerebral cortex.

SCA3 in a 29-year-old man. Axial and sagittal T2WIs (A and B,
respectively) demonstrating atrophy of the cerebellar
hemispheres, as well as of the vermis, pons and MCPs. C: Axial
T1WI showing atrophy of the cerebral cortex.

Vascular diseases

Pontine infarction with Wallerian degeneration

Pontine infarction (PI) is a consequence of vascular obstruction hampering
proper blood flow to the pons. Clinically, PI can present with
manifestations ranging from pure motor/sensory contralateral deficits,
ipsilateral cranial nerve palsy associated with contralateral motor and/or
sensory impairment or even locked in syndrome ( 17 ) . There are no precise epidemiological
studies of this condition, and PIs of different aetiologies show different
epidemiological profiles; they can be caused by small vessel disease,
cardiac emboli or large artery atherosclerosis ( 17 ) . After the ischemic insult, Wallerian
degeneration occurs in axons distal to the site of neuronal lesion, leading
to demyelination and disintegration ( 18 ) . This, in turn, leads to morphological alterations
of the MCP. These demyelination events result in hyperintensity on T2/FLAIR
MRI sequences of the affected structures. As previously mentioned, the MCP
contains fibres of the cortico-ponto-cerebellar tracts that originate in the
contralateral pontine nuclei. Unilateral pontine lesions affect the
ipsilateral cortico-pontine fibres and the crossing contralateral
ponto-cerebellar fibres ( 19 ) .

Imaging findings for PI and posterior Wallerian degeneration depend on the
specific phase of the process. Specifically, in the first few minutes of the
ischemic process, there is an increase in the intensity of the signal on DWI
and a decrease in the apparent diffusion coefficient in the MCP,
inferolateral portion of the pons, flocculus, and anteroinferior surface of
the cerebellum. At 6 h after symptom onset, T2/FLAIR hyperintensity is
detectable ( Figure 9A ). As it
progresses, there is symmetric, bilateral T2/FLAIR hyperintensity of the
MCP, albeit without gadolinium enhancement, although there can be volume
loss ( Figure 9B ; Table 1 ).

Figure 9 Wallerian degeneration. A: Axial T2WI showing hyperintensity
(suggestive of sequelae of infarction) in the right hemi-pons.
B: Axial FLAIR sequence showing hyperintensity in both MCPs.
These findings are suggestive of Wallerian degeneration caused
by a PI.

Wallerian degeneration. A: Axial T2WI showing hyperintensity
(suggestive of sequelae of infarction) in the right hemi-pons.
B: Axial FLAIR sequence showing hyperintensity in both MCPs.
These findings are suggestive of Wallerian degeneration caused
by a PI.

DISEASES OF CHILDHOOD

Demyelinating diseases

ADEM

One immune-mediated demyelinating CNS disorder, known as ADEM, which is most
commonly diagnosed in boys between 5 and 8 years of age, has been associated
with previous infection ( 20 , 21 ) . It is also a common
manifestation of anti-myelin oligodendrocyte glycoprotein disease.

Neuroimaging on T2/FLAIR frequently reveals multiple, bilateral, poorly
delimitated hyperintense lesions with surrounding oedema ( Figure 10 ). These lesions are usually
located in subcortical and central white matter regions, as well as in the
thalami, brainstem, cerebellum, basal ganglia and grey-white matter junction
( Figure 10 ). Typically, the brain
lesions in a given case of ADEM all show a similar stage of development. In
this regard, most lesions show similar degrees of enhancement in response to
contrast, resulting in a ring pattern. This finding is useful in
distinguishing ADEM from MS, in which focal lesions that show gadolinium
enhancement coexist with lesions without enhancement ( 22 ) . In addition, DWI can
reveal restricted diffusion at the periphery and there can be involvement of
the MCP ( 3 ) , as illustrated
in Figure 10B and described in Table 1 .

Figure 10 ADEM. A: Axial FLAIR sequence demonstrating supratentorial
lesions involving the white and grey matter (basal ganglia and
left thalamus). B: Axial FLAIR sequence depicting bilateral
hyperintense MCP lesions. C: Contrast-enhanced T1WI showing no
enhancement in the MCP lesions.

ADEM. A: Axial FLAIR sequence demonstrating supratentorial
lesions involving the white and grey matter (basal ganglia and
left thalamus). B: Axial FLAIR sequence depicting bilateral
hyperintense MCP lesions. C: Contrast-enhanced T1WI showing no
enhancement in the MCP lesions.

Genetic diseases

FXTAS

Fragile X-associated conditions include several diseases associated with
pathogenic variants of the FMR1 gene, with the most common form being the
fragile X syndrome caused by more than 200 CGG repeats in FMR1. Fragile X
syndrome usually presents with intellectual disability, developmental delay,
autism spectrum disorder and seizures ( 23 ) . In contrast, FXTAS is caused by 55-200 CGG
repeats of the FMR1 gene and manifests as kinetic tremor, gait ataxia,
executive dysfunction and neuropathy ( 23 ) ; this condition is more common in men ( 24 ) .

There are two major neuroimaging findings in FXTAS ( 24 ) : T2 hyperintensity in the MCP ( Figure 11 ), which is seen in 60% of
males and 13% of females; and T2 hyperintensity in the corpus callosum, the
male-to-female ratio of which is similar to that reported for T2
hyperintensity in the MCP ( 25 ) . Other imaging findings in FXTAS include T2
hyperintensity in the pons, insula and periventricular region, as well as
generalised brain and cerebellar atrophy ( Table 1 ).

Figure 11 FXTAS. Axial T2WI showing MCP hyperintensity and cerebellar
atrophy.

FXTAS. Axial T2WI showing MCP hyperintensity and cerebellar
atrophy.

MLC

Another genetic disorder of childhood is MLC, which manifests as cerebral
white matter oedema. There are two different forms of the disease. The first
form, known as classic MLC, presents with a deteriorating phenotype and is
mostly associated with MLC1 mutations, whereas the second form presents with
a remitting phenotype and is associated with GLIALCAM gene mutations.
Patients with the deteriorating form present with macrocephaly, ataxia,
spasticity and epilepsy, whereas those with the remitting form present with
neurological deterioration ( 18 ) . In either form, MLC predominantly affects males, with
the initial motor deterioration being detected at a median age of 5
years ( 26 ) .

In many patients with MLC, one can notice oedema and signal abnormalities in
the cerebral and cerebellar white matter. With optic radiation sparing, the
MCP can also be altered ( Figure
12B ,C). As the disease progresses, there can be enlargement of the
ventricles and subarachnoid spaces ( 26 ) . On DWI, abnormal white matter can show increased
diffusion ( 27 ) . In
addition, subcortical cysts, with or without near-cyst rarefaction of
subcortical white matter, primarily in the anterior temporal lobe and
frontoparietal regions, are common ( Figure
12A ). There can be persistence of the cavum septum pellucidum.
Reversal of the MRI abnormalities can occur in patients with the remitting
form of MLC ( 26 ) , as
described in Table 1 .

Figure 12 MLC. A: Axial T1WI showing cysts in the white matter frontal
lobes and persistence of the cavum septum pellucidum. Axial
FLAIR sequence (B) and axial T2WI (C) showing a mildly
hyperintense signal in the cerebellar white matter (and in the
MCPs), together with diffuse white-matter abnormalities in the
temporal and occipital lobes.

MLC. A: Axial T1WI showing cysts in the white matter frontal
lobes and persistence of the cavum septum pellucidum. Axial
FLAIR sequence (B) and axial T2WI (C) showing a mildly
hyperintense signal in the cerebellar white matter (and in the
MCPs), together with diffuse white-matter abnormalities in the
temporal and occipital lobes.

Neoplastic diseases

Diffuse midline H3K27M-mutated glioma

Gliomas are the most common form of primary CNS tumours ( 28 ) . Among them, diffuse
midline H3K27M-mutated gliomas form a group of high-grade neoplastic lesions
that arise from midline structures such as the thalamus, brainstem and
spine ( 28 ) . These
tumours are most commonly identified in the paediatric population, with a
median age at presentation of 5-11 years ( 29 ) ; males and females are equally
affected ( 29 ) .
Patients usually present with cerebrospinal fluid obstruction, with or
without brainstem dysfunction that can include ataxia, pyramidal signs and
cranial nerve abnormalities; thalamic lesions can lead to motor weakness and
gait disturbance ( 30 , 31 ) .

Neuroimaging commonly reveals lesions not only in the pons but also in the
brainstem, thalamus and spinal cord. These lesions are usually hypointense
on T1WI, hyperintense on T2WI, and can present with hyperintensity in the
MCP ( Figure 13 ). There can be minimal
or no gadolinium enhancement. Tumour size, infiltrative appearance on FLAIR
sequences, the mass effect, contrast enhancement characteristics, the
presence of necrosis, and the pattern of disease recurrence are similar
between wild-type and histone H3K27M-mutated gliomas ( 32 ) .

Figure 13 Diffuse midline H3K27M-mutated glioma. Sagittal FLAIR sequence
(A) and axial T2WI (B), showing an expansile hyperintense lesion
in the pons, and flattening of the fourth ventricle floor
involving the medulla oblongata and the MCPs.

Diffuse midline H3K27M-mutated glioma. Sagittal FLAIR sequence
(A) and axial T2WI (B), showing an expansile hyperintense lesion
in the pons, and flattening of the fourth ventricle floor
involving the medulla oblongata and the MCPs.

CONCLUSION

A proper imaging investigation is essential for the diagnosis of several neurological
diseases, including those described here, which cause alterations specifically in
the MCP. Knowledge of the imaging patterns associated with these diseases can help
the practicing radiologist make an informed analysis that, in turn, will lead to a
more accurate diagnosis by the neurologist and, potentially, better treatment. As
such, an adequate understanding of the imaging patterns associated with MCP lesions
is essential knowledge for radiologists.