Multiple sclerosis is an immune-mediated inflammatory demyelinating disease
of the central nervous system clinically characterized by relapses and rem
issions of neurological disturbance. A typical relapse, exemplified by opti
c neuritis, increases in severity over a week or two and after approximatel
y one month begins to remit. Resolution takes place over the course of two
to three months. In the early stages, clinical recovery is virtually comple
te, though persistent abnormalities of conduction can usually be detected b
y evoked potential techniques and persistent structural abnormalities can b
e detected by magnetic resonance imaging (MRI). These techniques, together
with cerebrospinal fluid examination for oligoclonal IgG, provide supportin
g evidence for the diagnosis which, in the absence of a specific test, neve
rtheless remains primarily clinical. The course of the disease is very vari
able, but after a number of years neurological deficit begins to accumulate
after each relapse. In most patients, the relapsing and remitting phase of
the disease is followed by a phase of continuous progression of disability
. Cognitive disturbances can be detected in many patients even quite early
in the course of the illness. Deficits in attention, memory and executive s
kills may he prominent and tend to become increasingly prominent as neurolo
gical deficit increases, although this is not always the case. There is som
e correlation between the extent of MRI abnormalities in the cerebral white
matter and the severity of cognitive deficit. Depression and anxiety are c
ommonly experienced but, are poorly correlated to the lesion load seen on M
RI. In contrast, the much rarer psychotic symptoms, euphoria and emotional
lability are closely linked to the severity of white matter disease.