Although many patients with multiple sclerosis (MS) complain of trigeminal neuralgia (TN), its cause and mechanisms are still debatable. In a multicentre controlled study, we collected 130 patients with MS: 50 patients with TN, 30 patients with trigeminal sensory disturbances other than TN (ongoing pain, dysaesthesia, or hypoesthesia), and 50 control patients. All patients underwent pain assessment, trigeminal reflex testing, and dedicated MRI scans. The MRI scans were imported and normalised into a voxel-based, 3D brainstem model that allows spatial statistical analysis. The onset ages of MS and trigeminal symptoms were significantly older in the TN group. The frequency histogram of onset age for the TN group showed that many patients fell in the age range of classic TN. Most patients in TN and non-TN groups had abnormal trigeminal reflexes. In the TN group, 3D brainstem analysis showed an area of strong probability of lesion (P<0.0001) centred on the intrapontine trigeminal primary afferents. In the non-TN group, brainstem lesions were more scattered, with the highest probability for lesions (P<0.001) in a region involving the subnucleus oralis of the spinal trigeminal complex. We conclude that the most likely cause of MS-related TN is a pontine plaque damaging the primary afferents. Nevertheless, in some patients a neurovascular contact may act as a concurring mechanism. The other sensory disturbances, including ongoing pain and dysaesthesia, may arise from damage to the second-order neurons in the spinal trigeminal complex.
Baclofen (Lioresal), a muscle relaxant, exerts a specific action on the trigeminal system by depressing excitatory synaptic transmission in the spinal trigeminal nucleus. To evaluate the effects of racemic and L-baclofen on the human trigeminal reflexes, the area of the blink reflex was measured in seven normal subjects, before and after i.v. administration of racemic baclofen (25 mg.) and oral administration of L-baclofen (15 mg.). The blink reflex is a trigeminal facial reflex consisting of two components (R1 and R2): R1 has a shorter latency and is mediated by an oligosynaptic pontine circuit; R2 has a longer latency and is believed to be relayed via a polysynaptic circuit through the lateral bulbar reticular system. Whereas the R1 response was scarcely affected by administration of racemic baclofen, it was significantly reduced by L-baclofen (P less than 0.01). R2 was depressed by both drugs (P less than 0.01). These results indicate that both racemic and L-baclofen inhibit trigeminal transmission in man, probably because they interfere with excitatory transmission through the interneurons of the lateral reticular formation. In addition, since L-baclofen reduced both R1 and R2 this form of the drug presumably has a more powerful effect than its racemic counterpart, on the few interneurons of the short latency component.
Vinorelbine (59-noranhydrovinblastine) is a new semisynthetic antineoplastic vinca alkaloid which interfers with axonal transport, inducing spiralisation of axonal microtubules and resulting in peripheral neurotoxicity. A prospective detailed neurological and electrophysiological evaluation was performed in 23 patients treated with 25 mg vinorelbine a week. All patients developed a sensory-motor distal symmetric axonal neuropathy. The neurotoxicity increased with cumulative vinorelbine doses and peripheral neuropathy was mild or moderate in most patients. After discontinuation of vinorelbine treatment, neuropathic signs and symptoms were partially reversible.
