The British Journal of Radiology, 74 (2001), 458–467 E 2001 The British Institute of Radiology

Pictorial review
Trigeminal nerve: anatomy and pathology
P WOOLFALL, FRCR and A COULTHARD, FRCR
Department of Radiology, Royal Victoria Infirmary, Queen Victoria Road, Newcastle-Upon-Tyne NE1 4LP,
UK

Abstract. MRI is the imaging modality of choice when trigeminal nerve pathology is suspected.
Most lesions are readily recognizable if appropriate imaging sequences are performed. Routine
cranial MRI sequences augmented by a three-dimensional gradient echo sequence such as FISP
(fast inflow with steady-state precession) are sufficient to demonstrate most pathological processes
involving the trigeminal nerve and nucleus. Intravenous gadolinium-DTPA occasionally provides
additional diagnostic information. MRI is particularly useful in planning the management of
those conditions where surgical or medical intervention can result in improvement or resolution
of symptoms. In this review, examples of a range of pathologies involving the trigeminal nerve
and nucleus are presented.

The trigeminal nerve is the largest of the cranial
nerves. It carries motor supply to the muscles of
mastication and transmits sensory information
from the face, oral and nasal cavities, and most of
the scalp. Disease within or local to the nerve can
cause trigeminal neuralgia or loss of sensory or
motor function in the distribution of the nerve.
MRI has greatly increased the role of imaging in
the diagnosis of trigeminal disorders. This review
describes the radiological anatomy of the trigem-
inal nerve and illustrates some of the pathological
conditions involving the trigeminal nerve that
might be demonstrated on MRI. For diagnostic
clarity, pathology involving the trigeminal nerve
can be subdivided according to anatomical loca-
tion (nucleus, pre-pontine cistern, Meckel’s cave/
cavernous sinus and extracranial).
trigeminal nerve exits the anterolateral (ventral)
aspect of the pons as a large sensory root and
a much smaller motor root and traverses the
pre-pontine cistern (Figure 1). As it exits the
pons, the point of change from central to
peripheral myelin is known as the root entry
zone (REZ). It is at this point that the nerve is
thought to be most susceptible to compression by
tortuous branches of the posterior circulation
vessels, an important cause of trigeminal neur-
algia. The nerve continues anteriorly to the apex
of the petrous temporal bone. Here it traverses a
defect in the dura to enter Meckel’s cave, a CSF-
filled space lying immediately lateral to the
cavernous sinus. The nerve trunk then expands
to form the trigeminal (Gasserian) ganglion, from
which the three branches of the trigeminal nerve
arise (Table 1) [1].

Radiological anatomy
MRI technique
The trigeminal nerve arises from one motor
There are no specific clinical features allowing
nucleus and three sensory nuclei, which extend
confident localization of pathology affecting the
throughout most of the length of the brain stem.
pre-ganglionic trigeminal nerve. In addition, the
The principal sensory nucleus is situated within
trigeminal nerve is often involved in generalized
the lateral aspect of the pons. The spinal
neurological conditions such as cerebrovascular
trigeminal nucleus extends through the medulla
disease and primary demyelination, which are
and reaches the upper cervical cord. The mesen-
multifocal in nature. It is therefore essential that
cephalic nucleus extends from upper pons to the
the whole brain is imaged routinely to ensure that
midbrain. The motor nucleus lies medial to the
all significant pathology is demonstrated.
principal sensory nucleus in the upper pons. The
All patients with symptoms involving the
Received 23 March 2000 and in revised form 14 June trigeminal nerve are imaged using a standardized
2000, accepted 7 July 2000. brain MRI protocol. This consists of T1 weighted

458 The British Journal of Radiology, May 2001

Pictorial review: Trigeminal nerve anatomy and pathology
spin echo sequences and proton density and T2
weighted fast spin echo sequences acquired in the
axial plane, with a turbo STIR (short tau
inversion recovery) sequence acquired in the
coronal plane. Patients with trigeminal neuralgia
are also imaged using a T1 weighted 3D-FISP
(three-dimensional fast inflow with steady-state
precession) sequence acquired axially. 3D-FISP is
a gradient echo technique that shows flow within
small vessels as high signal intensity, and also
returns sufficient signal from the adjacent soft
tissues to enable vessels to be accurately
localized. The 3D dataset may be reformatted
in any plane. Routinely, 1 mm thick sagittal
oblique reformations are constructed for each
trigeminal nerve (Figure 1) along with 1 mm
reconstructions in the coronal plane from brain
stem to Meckel’s cave (Figure 8). In addition to
these reconstructions parallel to and perpendi-
cular to the course of the trigeminal nerve, axial
plane reconstructions and maximum intensity
projections are occasionally useful. Both the
3D-FISP and T1 weighted sequences may be
repeated following intravenous (iv) gadolinium-
DTPA if appropriate.
Pathology
The pathological processes affecting the tri-
geminal nerve may be most usefully considered
according to the anatomical part of the nerve
affected.
Lesions involving the trigeminal nuclei
Cerebrovascular disease is a common cause of
sensory loss within the distribution of the
trigeminal nerve (Figure 2). Patients usually
have other clinical signs and so an isolated
trigeminal neuropathy is uncommon. Additional
Table 1. Divisions of the trigeminal nerve
Branch Course
Ophthalmic (V1) Anteriorly through cavernous sinus.
Accompanied by III, IV, VI and V2
cranial nerves. Exits skull through
superior orbital fissure and enters orbit
Maxillary (V2) Accompanies V1 through cavernous sinus.
Exits skull through foramen rotundum
and enters pterygopalatine fossa
Mandibular (V3) Immediately exits skull through foramen
ovale
The British Journal of Radiology, May 2001
lesions are often demonstrated in other parts of
the brain.
Primary demyelination often affects the brain
stem (Figure 3). Patients may present with
trigeminal neuralgia or sensory loss. Other
sensory or motor signs are frequently present.
Cranial MRI demonstrates high signal intensity
plaques on T2 weighted images. Similar lesions
may also be identified in other parts of the brain,
for example the corpus callosum and the periven-
tricular white matter.
Brain stem neoplasms in adults are most
commonly metastases from an extracranial pri-
mary neoplasm. They are usually manifested as
strongly enhancing solid lesions with an asso-
ciated mass effect. There may be additional
lesions in other parts of the brain. Primary
intraaxial tumours arising in the brain stem are
usually gliomas. If a mass lesion suspicious of a
neoplasm is demonstrated on pre-contrast images,
T1 weighted sequences after iv gadolinium-DTPA
are mandatory. Pontine hamartomas or gliomas
may occur in patients with Type I neurofibroma-
tosis [2] (Figure 4).
Vascular malformations of the brain stem, such
as arteriovenous malformations (AVMs) and
cavernous haemangiomas, may become sympto-
matic following an episode of haemorrhage.
AVMs are usually manifested as a collection of
flow voids. Cavernous haemangioma has a fairly
typical appearance on MRI, particularly if there
has been previous haemorrhage. Central hetero-
geneous signal hyperintensity corresponding to
methaemaglobin is seen on both T1 and T2
weighted sequences. A circumferential ring of
markedly hypointense signal intensity is usually
present, indicating haemosiderin deposition
(Figure 5). There is no mass effect or oedema,
and feeding or draining vessels are not identified
[3].
Viral rhombencephalitis is an uncommon life-
threatening infection of the brain stem and may
Function
Sensory to nose, paranasal sinuses and upper face
Sensory to middle third of face and upper teeth
Sensory to lower face tongue, jaw and lower teeth.
Motor to muscles of mastication, and mylohyoid
and other small muscles
459

involve the trigeminal nucleus and nerve [4]
(Figure 6).
Syringobulbia may present with cranial neuro-
pathies and is often secondary to previous trauma
or pre-existing anomalies such as Arnold–Chiari
malformation. It appears as a lesion within the
brain stem of similar signal intensity to CSF on
all imaging sequences, usually contiguous with a
spinal cord syrinx (Figure 7).
Pathological processes, for example neoplasm,
demyelinating disease, may affect the extension of
the spinal trigeminal nucleus into the upper
cervical spinal cord.
Lesions involving the trigeminal nerve in the
pre-pontine cistern
Neurovascular compression is now accepted as
being the commonest cause of trigeminal neur-
algia unresponsive to medical therapy. Tortuous
branches of the posterior circulation vessels,
particularly the superior cerebellar artery, may
impinge upon the trigeminal nerve at its REZ. The
resultant compression of the nerve leads to
intractable trigeminal neuralgia. The aberrant
vessels are usually small and are best demon-
strated on the 3D-FISP sequence (Figures 8–10).
Intravenous gadolinium-DTPA improves visuali-
zation of the smaller pre-pontine vessels.
Detection of these vessels is important, as micro-
vascular decompression usually leads to remission
or improvement of symptoms [4–8]. Less commonly
than trigeminal nerve compression secondary to
aberrant small branch vessels, the pre-pontine
trigeminal nerve may be compressed by ectatic
vertebral or basilar arteries (Figure 11).
Cerebellopontine angle neoplasms may cause
trigeminal neuralgia or neuropathy by extrinsic
compression of the nerve. Some metastatic
tumours may spread perineurally along the
trigeminal nerve itself (Figure 12). Acoustic
Figure 1. 3D-FISP image reconstructed in the sagittal
oblique plane (TR/TE 30/7; flip angle 20 ˚). The
normal root entry zone (REZ) and the cisternal
course of the right trigeminal nerve are demonstrated
(asterix). Flow within blood vessels is shown as very
high signal intensity using the 3D-FISP sequence. A
small cisternal vessel lying inferior to the REZ
(arrow) is well clear of the nerve and is of no patho-
logical significance (compare with Figures 8–10).
460
P Woolfall and A Coulthard
neuromas occasionally present with trigeminal
symptoms. Meningiomas (Figure 13), arachnoid
cysts (Figure 14) and epidermoid cysts (Figure 15)
are sometimes found in this location.
The latter two pathologies may be difficult to
differentiate, as epidermoid cyst may show very
similar signal intensities to CSF. Pointers to the
diagnosis of epidermoid cyst include signal
intensity greater than CSF on T2 weighted
sequences, slight signal heterogeneity due to cyst
debris and occasional lobulated appearance [9].
Meckel’s cave and cavernous sinus
Neoplasms within Meckel’s cave, for example
meningioma, epidermoid tumour and trigeminal
neuroma, may cause trigeminal nerve symptoms
(Figure 16). Tumours arising from the pituitary
or the skull base may also cause trigeminal nerve
symptoms, but only rarely do these symptoms
occur in isolation. Granulomatous or inflamma-
tory disease, such as neurosarcoid, may involve
the nerve or ganglion at this site (Figure 17).
Carotid aneurysms may cause trigeminal
symptoms, particularly cavernous aneurysms
(Figure 18). In this situation, trigeminal nerve
symptoms are most often found in association
with other clinical features.
Extracranial involvement of trigeminal nerve
divisions
Any local pathology, most commonly head
and neck neoplasms and metastatic tumour
deposits, may affect the three divisions of the
trigeminal nerve. Inflammatory conditions such
as orbital pseudotumours, abscesses and sinusi-
tis may affect one or more branches of the
trigeminal nerve.
The British Journal of Radiology, May 2001
Pictorial review: Trigeminal nerve anatomy and pathology
(a)
(b)
Figure 2. (a) T2 weighted axial plane FSE image
from a 43-year-old woman presenting with sudden
onset of facial numbness and hemianaesthesia. There
is diffuse signal hyperintensity within the right side of
the pons. (b) T1 weighted sagittal image acquired 8
months later shows a mature pontine infarct (arrow).
The British Journal of Radiology, May 2001
(a)
(b)
Figure 3. (a) Coronal plane STIR image through the
brain stem of a 41-year-old woman with multiple
sclerosis, presenting with a short history of altered
facial sensation. There is a high signal intensity
plaque of demyelination within the right brachium
pontis (arrow). (b) Axial plane T2 weighted FSE
image at the level of the centrum semiovale. Typical
ovoid lesions of primary demyelination in the periven-
tricular and subcortical white matter.
461

(a)
(b)
Figure 4. (a) Axial T2 weighted FSE image at mid
pontine level from a 29-year-old patient with Type I
neurofibromatosis and recent onset of facial pain.
There is an ill defined mass within the pons on the
right (arrow). (b) An image from a FLAIR sequence
acquired in the coronal plane confirms the diffuse
mass. The diagnosis was pontine glioma. Such
tumours tend to run a relatively benign course in
patients with neurofibromatosis.
462
P Woolfall and A Coulthard
(a)
(b)
Figure 5. Cavernous haemangioma of the midbrain in
a 29-year-old woman presenting with vague facial
sensory disturbance and ataxia. (a) Axial plane T2
weighted FSE image and (b) coronal plane FLAIR
image. Both sequences show the typical MRI appear-
ances of a cavernous haemangioma: central high
signal intensity (methaemaglobin) surrounded by a
rim of very low signal intensity (haemosiderin deposi-
tion).
The British Journal of Radiology, May 2001
Pictorial review: Trigeminal nerve anatomy and pathology

(a) (b)

Figure 6. Viral rhombencephalitis in a 20-year-old

woman who presented with headache, vertigo and
photophobia and went on to develop left-sided paraes-
thesia and left facial weakness. (a,b) Axial plane T1
weighted SE images after iv gadolinium-DTPA. There
is marked enhancement of the left trigeminal nerve
(a) and nucleus (b). (c) Repeat examination after 4
months. Axial plane T1 weighted SE image after iv
gadolinium-DTPA. The trigeminal nerve and nucleus
now appear normal. Herpes simplex virus is the com-
monest cause of viral rhomboencephalitis, although
often (as in this case) no specific pathogen can be
isolated.

(c)

The British Journal of Radiology, May 2001 463


Figure 7. Syringobulbia and syringomyelia in a 20-
year-old man presenting with horizontal diplopia and
left facial sensory loss. Sagittal T2 weighted FSE
image showing a large syrinx extending cranially
through the foramen magnum to involve the brain
stem. The foramen magnum is stenosed. Parasagittal
sections showed a Chiari I malformation.
Figure 8. Neurovascular compression of the trigem-
inal nerve in a 63-year-old woman with severe right
trigeminal neuralgia. 3D-FISP sequence reconstructed
in the coronal plane. There is a small high signal
intensity vessel in close contact with the right trigem-
inal nerve (small arrow). On the left side there is a
vessel lateral to but not in contact with the trigeminal
nerve (arrowhead).
464
P Woolfall and A Coulthard
(a)
(b)
Figure 9. Neurovascular compression and trigeminal
neuralgia in a different patient. (a) 3D-FISP sequence
reconstructed in the sagittal oblique plane to show
the right trigeminal nerve. There are two vessels in
contact with the upper and lower aspects of the nerve
(arrows). (b) An axial reconstruction may occasion-
ally be helpful. One of the vessels shown in (a) is in
contact with the lateral surface of the right trigeminal
nerve (arrow). The other vessel seen in (a) lies postero-
lateral to the arrowed vessel on this section.
Figure 10. Neurovascular contact with the trigeminal
nerve in an asymptomatic 31-year-old male subject.
Sagittal oblique reconstruction from a 3D-FISP study
shows a vessel crossing the left trigeminal nerve at
the root entry zone (arrow). Vascular compression is
the cause of trigeminal neuralgia in many patients
with symptoms unresponsive to medical treatment,
but it is important to remember that small vessels
may also be found in the vicinity of the trigeminal
nerve in up to 27% of normal subjects [8].
The British Journal of Radiology, May 2001
Pictorial review: Trigeminal nerve anatomy and pathology
(a)
(b)
Figure 11. Dolichoectasia of the vertebral or basilar
arteries may result in vascular compression of the tri-
geminal nerve. (a) Coronal plane STIR image at the
level of the pons. The ectatic basilar artery is seen as a
flow void (long arrow) displacing the left trigeminal
nerve superiorly and laterally (short arrow). (b)
Parasagittal reconstruction of a 3D-FISP sequence in
the plane of the left trigeminal nerve. The ectatic
vessel is shown as a high signal intensity structure
(long arrow) impinging on the trigeminal nerve
(arrowhead).
Figure 13. Cerebellopontine angle meningioma in a
64-year-old man with trigeminal neuralgia. Axial T1
weighted SE image after iv gadolinium-DTPA. There is
a mass within the left cerebellopontine angle, which
enhances strongly.
The British Journal of Radiology, May 2001
Figure 12. Perineural metastasis from a malignant
melanoma in a 77-year-old woman. Axial T1 weighted
SE image after iv gadolinium-DTPA. There is an
enhancing metastatic deposit spreading along the
right trigeminal nerve and invading the pons. The
right orbital apex is also involved.
Figure 14. Arachnoid cyst in the cerebellopontine
angle in a 28-year-old woman with trigeminal neural-
gia. Axial T2 weighted FSE image showing a well
defined lesion of similar signal intensity to CSF
within the left cerebellopontine angle.
465
 P Woolfall and A Coulthard

(a)

(b) Figure 16. Neuroma of the trigeminal ganglion in a

Figure 15. Epidermoid cyst in the left cerebellopon-
tine angle, CSF signal intensity. (a) Axial plane T1
weighted SE section at the level of upper medulla.
Apparent widening of the cistern on the left side
(arrow). (b) Coronal plane T1 weighted SE image.
Apparent asymmetry of the cisterns is due to the pres-
ence of an epidermoid cyst. The left trigeminal nerve
is displaced superiorly (arrow).
31-year-old woman. Axial T1 weighted SE image after
iv gadolinium-DTPA. There is an enhancing mass
within Meckel’s cave on the right (arrow). The
patient presented with altered sensation in the distri-
bution of the right trigeminal nerve.

(a) (b)
Figure 17. Transient enhancing lesion in Meckel’s cave. The 29-year-old female patient presented with left facial
pain and numbness. (a) Coronal plane T1 weighted SE image after iv gadolinium-DTPA. An enhancing mass in
Meckel’s cave on the left (arrow). Initial diagnosis was trigeminal neuroma. (b) Repeat examination 14 months
after (a). Complete resolution of the enhancing mass lesion corresponding with disappearance of the patient’s
symptoms. In retrospect, the mass was presumably inflammatory in aetiology.

466 The British Journal of Radiology, May 2001

Pictorial review: Trigeminal nerve anatomy and pathology
(a)
(b)
Figure 18. Internal carotid artery aneurysm arising
within the cavernous sinus. (a) Coronal plane T1
weighted image at the level of the cavernous sinus in
a patient presenting with symptoms including left V1
and V2 distribution sensory disturbance. The caver-
nous aneurysm is arrowed. (b) Maximal intensity
projection reconstruction of a time-of-flight MR
angiography sequence confirming the left cavernous
carotid aneurysm (arrow).
The British Journal of Radiology, May 2001
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