The Diagnosis

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The main risk is of underestimating these manifestations. They are indeed transient, and often have an original, if not odd, expression; also, many patients are reluctant to report them spontaneously, as they are afraid to describe disorders that could seem too extraordinary to be true. The clinician himself may be tempted to consider these manifestations as the expression of fatigue, which is often present in multiple sclerosis. He may find it difficult to individualize these paroxysmal manifestations when they develop within a chronic neurological deficit syndrome.

The diagnosis itself may be discussed with regard to three main syndromes. This is notably the case when the paroxysmal manifestations correspond to the onset of multiple sclerosis. This may also be the case in overt multiple sclerosis, as an intercurrent disease may always appear. A first alternative diagnosis is migrainous aura. The aura is visual in most cases, which is exceptional in multiple sclerosis-related paroxysmal manifestations. It may also be sensory, hemicorporeal or facial, which often leads to misdiagnosis. It may be dysphasic, which is also exceptional for a paroxysmal manifestation of multiple sclerosis, the latter being usually limited in that case to dysarthria. The motor manifestations, so frequent in the paroxysmal manifestations of multiple sclerosis, are not present in migrainous aura. Positive signs and subacute development over a few minutes until a plateau is reached and maintained for about 10 min are other characteristics of migrain-ous aura. Remission is also subacute on a few minutes' scale. The overall duration of migrainous aura is much greater than that of the paroxysmal manifestations of multiple sclerosis. It is usually followed by a typical headache.

Transient ischaemic attacks (TIAs) may cause many difficulties with their sudden occurrence and short duration. In fact, they differ from the paroxysmal manifestations of multiple sclerosis in several respects. They involve negative signs instead of positive ones. The episode may last several minutes to several hours. It rarely recurs with such a high frequency and symptomatic stereotypy as is the case with paroxysmal manifestations of multiple sclerosis.

Epileptic attacks are usually even more misleading. Generalized epilepsy is perfectly well documented in multiple sclerosis, with a frequency similar to that observed in the general population (0.5-1%). More specifically, focal epileptic attacks in multiple sclerosis may correspond to a cortical or subcortical plaque. Neurological symptoms may then be similar to those of a paroxysmal manifestation. It is the localization of the concerned plaque which makes the difference: cortical or subcortical in epilepsy, subcortical or clearly distant from the cortex in paroxysmal manifestations. This being said, there is obviously a clear continuum between epileptic attacks and paroxysmal manifestations in multiple sclerosis. In some cases, electroencephalography may allow us to see the difference. According to the available literature, the overall rate of epilepsy may reach 4% of the patients with multiple sclerosis. In the Lyon MS Cohort, 46 cases with epilepsy out of 2926 patients with multiple sclerosis have been traced (1.5%).

None of the paroxysmal manifestations which have been reported in multiple sclerosis has a specific diagnostic value. This is obvious for trigem-inal neuralgia. Clinically, nothing may distinguish the multiple sclerosis-related and the idiopathic trigeminal neuralgia. As explained above, the Lhermitte sign has been reported in cases of radiation myelopathy, cord compression, acute combined degeneration of the cord, and other conditions. Tonic seizures have been described in neuro-Behqet, systemic lupus erythematosus and many other collagene diseases.

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