British Journal of Radiology 74 (2001),458-467 © 2001 The British Institute of Radiology
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
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Abstract
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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.
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Introduction
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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 trigeminal 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 location (nucleus, pre-pontine cistern, Meckel's cave/cavernous sinus and extracranial).
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Radiological anatomy
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The trigeminal nerve arises from one motor nucleus and three sensory nuclei, which extend throughout most of the length of the brain stem. The principal sensory nucleus is situated within the lateral aspect of the pons. The spinal trigeminal nucleus extends through the medulla and reaches the upper cervical cord. The mesencephalic nucleus extends from upper pons to the midbrain. The motor nucleus lies medial to the principal sensory nucleus in the upper pons. The trigeminal nerve exits the anterolateral (ventral) aspect of the pons as a large sensory root and amuch 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 neuralgia. 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].
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MRI technique
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There are no specific clinical features allowing confident localization of pathology affecting the pre-ganglionic trigeminal nerve. In addition, the trigeminal nerve is often involved in generalized neurological conditions such as cerebrovascular disease and primary demyelination, which are multifocal in nature. It is therefore essential that the whole brain is imaged routinely to ensure that all significant pathology is demonstrated.
All patients with symptoms involving the trigeminal nerve are imaged using a standardized brain MRI protocol. This consists of T1 weighted 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 perpendicular 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.
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Figure 8. Neurovascular compression of the trigeminal 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 trigeminal nerve (small arrow). On the left side there is a vessel lateral to but not in contact with the trigeminal nerve (arrowhead).
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Pathology
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The pathological processes affecting the trigeminal 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 lesions are often demonstrated in other parts of the brain.
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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).
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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 periventricular white matter.
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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 periventricular and subcortical white matter.
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Brain stem neoplasms in adults are most commonly metastases from an extracranial primary neoplasm. They are usually manifested as strongly enhancing solid lesions with an associated 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 neurofibromatosis [2] (Figure 4).
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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.
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Vascular malformations of the brain stem, such as arteriovenous malformations (AVMs) and cavernous haemangiomas, may become symptomatic 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 heterogeneous 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].
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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 appearances of a cavernous haemangioma: central high signal intensity (methaemaglobin) surrounded by a rim ofvery low signal intensity (haemosiderin deposition).
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Viral rhombencephalitis is an uncommon life-threatening infection of the brain stem and may involve the trigeminal nucleus and nerve [4] (Figure 6).
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Figure 6. Viral rhombencephalitis in a 20-year-old woman who presented with headache, vertigo and photophobia and went on to develop left-sided paraesthesia 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 commonest cause of viral rhomboencephalitis, although often (as in this case) no specific pathogen can be isolated.
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Syringobulbia may present with cranial neuropathies 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).
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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.
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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 neuralgia 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 demonstrated on the 3D-FISP sequence (Figures 8–10). Intravenous gadolinium-DTPA improves visualization of the smaller pre-pontine vessels. Detection of these vessels is important, as microvascular 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).
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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 occasionally 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 posterolateral to the arrowed vessel on this section.
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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].
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Figure 11. Dolichoectasia of the vertebral or basilar arteries may result in vascular compression of the trigeminal 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).
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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 neuromas occasionally present with trigeminal symptoms. Meningiomas (Figure 13), arachnoid cysts (Figure 14) and epidermoid cysts (Figure 15) are sometimes found in this location.
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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.
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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.
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Figure 14. Arachnoid cyst in the cerebellopontine angle in a 28-year-old woman with trigeminal neuralgia. Axial T2 weighted FSE image showing a well defined lesion of similar signal intensity to CSF within the left cerebellopontine angle.
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Figure 15. Epidermoid cyst in the left cerebellopontine 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 presence of an epidermoid cyst. The left trigeminal nerve is displaced superiorly (arrow).
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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 inflammatory disease, such as neurosarcoid, may involve the nerve or ganglion at this site (Figure 17).
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Figure 16. Neuroma of the trigeminal ganglion in a 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 distribution of the right trigeminal nerve.
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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.
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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.
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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 cavernous aneurysm is arrowed. (b) Maximal intensity projection reconstruction of a time-of-flight MR angiography sequence confirming the left cavernous carotid aneurysm (arrow).
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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 sinusitis may affect one or more branches of the trigeminal nerve.
Received for publication March 23, 2000.
Revision received June 14, 2000.
Accepted for publication July 7, 2000.
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Abstract
Introduction
