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.