Background Chronic inflammatory demyelinating polyneuropathy (CIDP) is an aquired, demyelinating, motor and sensory neuropathy that is presumed to be immune mediated. The classic form of CIDP is fairly symmetric and motor involvement is greater than sensory. In our study we examined atypical forms of CIDP which are more difficult to recognize because of lack of unified diagnostic criteria. Materials and methods We studied 52 patients divided into 3 groups: 20 patients with typical CIDP, 20 patients with atypical CIDP according to the EFN/PNS guideline (revised 2010) and 12 patients with sensory CIDP according to the criteria of French CIDP study group. Results Our results suggest that in group of atypical CIDP prevail multifocal sensory- motor forms called Lewis-Sumner Syndrome (LSS) -56% of cases. Upper limbs are first involved in the clinical evolution of patients with LSS and not lower limbs as in typical CIDP. NCS show conduction blocks mostly in median and ulnar nerves in patients with LSS, but unaffected nerves are strictly normal. In typical CIDP NCS show evidence of demyelination in all nerve trunks. Anti-ganglioside antibodies were positive only in motor forms of CIDP. NCS is not a sensitive test to diagnose sensory CIDP, in 75% cases motor conduction velocities were not affected. SSEP is a high sensitive test to be used for underlying a possible CIDP from all sensory polyneuropathies. Overall Neuropathy Limitation Scale and 9 hole peg test are the most efficient tests to evaluate progression or regression of symptoms in patients with CIDP. Loss of myelin was the most prominent finding on biopsy. Nerve biopsy is used mainly when other studies fail to clearly establish the diagnosis of CIDP, particularly when electrophysiologic criteria for demyelination are not met. Nerve biopsy should be considered in patients with progressive, predominantly large fiber sensory neuropathy of otherwise unknown etiology, as they may have sensory CIDP that responds to therapy. Conclusions There is significant phenotypic variability in the clinical spectrum of CIDP suggesting that there are differint immunopathological mechanisms at play. Future research is needed to identify disease markers to improve diagnosis and to develop new therapeutic strategies