| dc.description.abstract | Trigeminal neuralgia (TGN, tic douloureux) refers to sudden severe paroxysms of severe
lancinating pain on one side of the face involving one or more branches of the trigeminal
nerve (CN V) which usually lasts a few seconds to a few minutes. Attacks of excruciating
lancinating pain, which usually lasts a few seconds to about two minutes, and often
triggered by stimuli such as talking, drinking, brushing teeth, shaving, chewing and
touching the face but occur spontaneously. There is often a trigger point which elicits
pain.
The cause of trigeminal neuralgia is multi-factorial, with about 10% of cases being due to
local lesions such as tumors, arachnoid cysts, on a demyelinating plaque affecting the pons at the root entry zone. In 1934, an American Neurosurgeon, Walter Dandy, suggested that idiopathic trigeminal neuralgia might be due to compression of the fifth cranial nerve at the pons by a pulsating blood vessel based on his observations at exploratory craniotomy in a patient with TGN in whom he expected to find a tumour but instead observed arterial compression of the nerve by a looping artery and no other cause. This area where the trigeminal nerve enters the pons is referred to as the root entry zone and the theory
suggests that pulsatile irritation of the nerve at the pons results in damage to the nerve
and, subsequently pain. The theory was not widely accepted, even after the publication of
Jannetta s large series of surgical exploration of the posterior fossa in which neurovascular compression of the fifth cranial nerve was seen in 96% of cases of recalcitrant trigeminal neuralgia. Prior to the publication of our method and papers NVC could not be demonstrated by imaging.
Purpose: To determine whether high resolution MRI with a Time-Of-Flight Magnetic Resonance
Angiographic approach could reliably depict the vascular anatomy of the posterior fossa in
the region of the pons and trigeminal nerves, and determine whether neurovascular
compression of the nerve (NVC) was present in TGN patients but not in controls.
Methods: High-resolution 3D MRA was carried out with the imaging volume centred over the pons in patients with TGN, controls and patients with multiple sclerosis. Imaging was conducted in a superconducting 1 .5-T magnet (Siemens Magnetom, Erlangen, Germany) with the patient positioned in the head coil. A standard sagittal localizer (250/15, [TR/TE], two excitations) yielding seven 5-mmthick slices with a 2.5 mm inter-slice gap was obtained.
An FISP 3D sequence [35/7, flip angle 15deg, 55mm slab, 64 partitions, 22 cm field of view, 256 x 256 matrix] centered axially over the pons was prescribed from the midline slice. A parallel saturation slab was placed superiorly to eliminate venous flow. The effective slice thickness and in-plane resolution were both 0.9 mm. Intravenous contrast agent (Gadopentate dimeglumine, 0.1mmol/kg) was administered to patients in whom arterial
contact was not confirmed on unenhanced MRA, to delineate the veins as veins which are
saturated on non-contrast MRA.
Sagittal and coronal mean-planar-reconstructions (MPRs) were constructed along with
axial oblique MPRs when necessary.
Results: MR images vascular contact with the trigeminal nerve at the pons was identified in 70% of 40 nerves on unenhanced imaging in patients with idiopathic trigeminal neuralgia and in a further 15% following injection of contrast medium. Contact between the nerve and two vessels at the pons was seen In 10% of cases, and deformity of the nerve was present in 30% of cases. In the control group, vascular contact with the nerve was identified in 8% of 114 nerves. NVC was also identified in the majority of patients with TGN associated with multiple sclerosis, in whom demyelinating plaques along the trigemino-thalamic tract
were absent. There was excellent correlation with surgical findings.
Conclusion: NVC of the trigeminal nerve can be reliably demonstrated in patients with TGN, most commonly by the superior cerebellar artery. Vascular contact between the nerve and an
adjacent artery is not specific for TGN, occurring in 7-14% of the population although
distinct differences between vascular compression in TGN and vascular contacts in
asymptomatic subjects are evident. Surprisingly, NVC was also present in the majority of
patients with multiple sclerosis and trigeminal neuralgia, indicating that MS must not be
accepted as the cause of TGN in symptomatic patients with an MS history. | en |
