Discussion
The diagnosis of CIDP can be made when patients fulfil a set of
clinical, electrodiagnostic, and laboratory
criteria1,25.
However, the diagnosis can be difficult, in part because of the
extensive list of differential diagnoses that mimic
CIDP8.
Poorly performed nerve conduction studies, misinterpretation of their
findings, and non-adherence to electrodiagnostic criteria commonly lead
to misdiagnosis18,29-31.
An incorrect diagnosis can also occur in patients reporting subjective
improvement after treatment, or when minor elevation of the CSF protein
concentration (probably not exceeding 1 g/L) is considered clinically
relevant by the treating neurologist30-34.
As for this patient, she showed progressive weakness and numbness, both
of which indicate alterations in the peripheral nervous system (PNS),
confirmed for the EMG of the lower limbs, at the time she had clinical
signs of alterations of the central nervous system, and lesions in the
MRI that suggested demyelination.
The explanation of how CIDP can combine with central lesions, is still
unclear. On the point of molecular biology: the myelin consists of inner
and outer lipids and in-between myelin sheath.
Approximately 15% to 30% of myelin proteins are found in the CNS and
the PNS. At least 2 common proteins which consist of the myelin have
been found, resulting in similar autoimmune disorder in peripheral and
central nerves in theory35.
When the blood-brain and blood-nerve barriers are damaged, the
antibodies cross the damaged barrier, resulting in an immune reaction in
peripheral and central nerves. So, if there appears immune-mediated
inflammatory response, there is a certain molecular basis of the mutual
lesion. But the specific mechanism remains unclear36.