Chronic inflammatory demyelinating polyneuropathy associated with manic symptoms

To the Editor

Chronic inflammatory demyelinating polyneuropathy (CIDP) is an autoimmune disease involving cellular and humoral immunity. It is characterized by progressive symmetrical weakness or sensory loss in both proximal and distal muscles developing over a more than 8-week period (Vallat et al., 2010). Neuropsychiatric disorders related to CIDP rarely occur. Here, we report a case of CIDP with manic symptoms.

A 66-year-old man was referred to our hospital with progressive weakness and numbness in all limbs over the past 2 years. One year prior to presentation, he developed irritable and labile mood and manic symptoms, including exaggerated sense of self-confidence, talkativeness, spending sprees, insomnia and increased energy. Laboratory investigation showed increased erythrocyte sedimentation rate (ESR: 39 mm/h). The nerve conduction velocity showed prolonged distal latency, a slowing of the conduction velocity and prolonged F-wave latency of the median, ulnar and peroneal nerves. Although he refused lumbar puncture, cerebrospinal fluid (CSF) studies are not mandatory according to the Inflammatory Neuropathy Cause and Treatment criteria for CIDP. A clinical diagnosis of CIDP was made.

Intravenous methylprednisolone was given for 4 days and then shifted to oral prednisolone. His muscle weakness gradually improved after 1 week of steroid therapy. The mood symptoms improved with the initial Young Mania Rating Scale (YMRS) 22 and decreased to 13 after 3 weeks of steroid treatment.

To our knowledge, no cases of bipolar disorder associated with CIDP have been previously documented. In acute inflammatory demyelinating polyneuropathy (AIDP), brief reactive psychosis, anxiety, depressive episodes and rapid eye movement (REM) sleep abnormalities were observed (Chan and Gold, 2007). The possible mechanism includes potential central nervous system (CNS) targets of the disease shown by lower CSF hypocretin-1 levels, inflammation and microglial activation in CNS, and proinflammatory cytokine-induced neurotransmitter dysfunction (Chan and Gold, 2007).

Several reports have shown subclinical involvement and demyelination of the central pathways (Chan and Gold, 2007; Vallat et al., 2010). This is similar to another chronic inflammatory demyelinating disorder, multiple sclerosis (MS), which affects the CNS and could increase rates of depression and bipolar disorder that might be related to oxidative stress, autoimmunity and demyelination (Carta et al., 2014). Immune-mediated inflammation and cytokines may influence brain circuits as observed in MS and AIDP, and steroid treatment was effective for both CIDP and mania-like episode in our patient, suggesting that his manic symptoms could relate to the immunopathogenesis of CIDP.

In conclusion, we report the first case of mania-like episode associated with CIDP. More studies are needed to clarify the associations between CIDP and manic-like episode.