The relapse in early relapsing-remitting MS has a typical pathology irrespective of its location. The first visible event is the orderly, local, mass death of oligodendrocyctes, the cells which support myelin. The myelin associated with these cells then degenerates. Degenerating myelin activates an inflammatory process. When this is over, young oligodendrocytes mature and make new myelin. The clinical counterpart to this pathology (unless it occurs in a silent area) is a loss of function which worsens over several hours to two days. The loss of function remains in place until the inflammation is over and remyelination begins. It will thus be seen that the relapse has a definite pattern and timescale.

Some people experience strange new sensations on beginning antibiotics and are often afraid that these are relapses. While relapses can occur during the first few months of antibiotics, probably initiated by virus infections, these sensations do not fulfil the timescale criteria of true relapses and tend to change their form within a week. Sometimes, in fact, they herald a return of function. What causes these 'pseudo-relapses' I do not know, but I suspect it is rebudding of neurones which make trial-and-error connections. Synaesthesia (crossover of the senses) can sometimes result; as an example, the seeing of flashes of light when hearing a loud noise. They can be quite troubling even when improvement is taking place. Repair takes place at a cellular level; function has to be re-learned at a much higher level.

A number of people with chronic infection with Chlamydia pneumoniae, whether or not they have MS, may, on treatment, experience a deep, grinding bone pain; it has a crushing quality. It does not correspond to any recognised area supplied by a sensory nerve, and it can travel along a limb, one moment being in the shoulder and the next in the fingers. It can suddenly go, and just as suddenly return. In its more severe form it is accompanied by a redness of the limb, dilation of the superficial veins and an increase in sweating in the limb. Use of the limb may be limited. There is often an exaggerated perception of skin stimuli; a light breeze over the limb may be felt as painful. Fortunately it seems transient.

This pain is typical of damage to a large peripheral nerve; it is called Reflex Sympathetic Dystrophy. It is caused by injuries - often quite minor - to a nerve; it may occur after a virus infection, particularly shingles.

In chronic Chlamydia pneumoniae infection Reflex Sympathetic Dystrophy may be caused by acute inflammation associated with the destruction of a local bacterial collection.

The mechanism of the pain is not fully understood, but is thought to involve stimulation of the thalamus, an area of grey matter deep in the brain. The pain is thus generated in the brain. It is common in those with a chronic Chlamydia pneumoniae infection, and many people develop it during bacterial killing. Its severity seems to depend on bacterial load and placement. Fortunately it is usually mild and often does not last long, though the limb can remain red or mottled for some months. In my experience complete resolution is the rule.

Severe thalamic pain of central origin can also occur in MS and is usually long-lasting. Pain as described above which goes after a week or so, and which is related to a bacteria-killing agent (when metronidazole, for instance, is added to protein-synthesis inhibitors) is more likely to be due to transient inflammation in a peripheral nerve rather than a relapse.

Other transient phenomena seen during chronic infection with Chlamydia pneumoniae include painful tics. Muscle fasciculations may also occur.