Motor nerve conduction study (NCS) of the median, ulnar, tibial and common peroneal nerves showed prolonged motor terminal latencies and F-wave latencies, and decreased compound muscle action potential (CMAP) amplitudes, sensory nerve action potential (SNAP) amplitude and nerve conduction velocity (NCV) (Table?1). appendiceal CD after surgical resection of a periappendiceal abscess. His neurologic symptoms and electrophysiologic findings recovered without any maintenance therapy. Conclusions CIDP-like neuropathy can be an initial presentation of CD, and recovery of the CIDP symptoms may result from resection of the CD. Clinicians should be aware of the possibility of CD in patients with intractable CIDP symptoms. strong class=”kwd-title” Keywords: Chronic inflammatory demyelinating polyneuropathy, Crohns disease Background Crohn’s disease (CD) is a relapsing, transmural inflammatory disease of the gastrointestinal mucosa that can affect the entire gastrointestinal tract form mouth to anus . It is considered a systemic disease because extraintestinal manifestations such as uveitis, arthritis, pleuritis, myocarditis, primary sclerosing cholangitis, pancreatitis, ankylosing spondylitis and tendinitis can develop . Neurologic manifestations can also occur, the most common being myelopathy, arterial stroke, myopathy, multiple sclerosis and epilepsy [2-4]. Peripheral neuropathy is also reported to be a neurologic complication, and it can be associated with immune-mediated inflammation, micronutrient deficiencies (e.g., vitamin B12, vitamin D, copper) and iatrogenic causes (e.g., metronidazole, TNF- antagonists) [3,5-8]. A few cases of chronic inflammatory demyelinating polyneuropathy (CIDP) have been reported [7-11], but in those cases the patients developed their symptoms after CD FAS-IN-1 had been established during various treatments, making it difficult to determine if they were caused by the disease or were treatment-related. Here, we describe a CIDP-like neuropathy patient who had 3 episodes of motor weakness as the initial presentation of concealed appendiceal CD. The neurological symptoms and abnormal electrophysiologic findings gradually improved after FAS-IN-1 surgical resection of the appendiceal CD, without CIDP treatment. Case presentation A 17-year-old male without any medical history was admitted with ascending weakness of both lower extremities that FAS-IN-1 had progressed for about two weeks. He had upper respiratory FAS-IN-1 infection one week ago. At the time of admission, his upper respiratory infection was improved and physical examinations in neck, chest and abdomen were unremarkable. On neurologic examination, he had symmetric weakness of both lower extremities (MRC grade 4) with paresthesia of both hands and feet. Deep tendon reflexes were absent in the upper and lower extremities. Routine laboratory findings, including serum complete blood count, biochemistry, urine analysis and C-reactive protein, were normal. Cerebrospinal fluid (CSF) protein level was elevated at 72?mg/dL without pleocytosis and immunoglobulin G levels in serum (3370?mg/dL) and CSF (13.8?mg/dL) were increased. Extensive laboratory investigations including, thyroid function, anti-nuclear antibodies, anti-ganglioside, myelin-associated glycoprotein and viral markers, were all negative. Motor nerve conduction study (NCS) of the median, ulnar, tibial and common peroneal nerves showed prolonged motor terminal latencies and F-wave latencies, and decreased compound muscle action potential (CMAP) amplitudes, sensory nerve action potential (SNAP) amplitude and nerve conduction velocity (NCV) (Table?1). Conduction block and temporal dispersion were also seen in the NCS, compatible with demyelinating polyneuropathy (Figure?1A). With the impression of AIDP, we started intravenous immunoglobulin (0.4?g/kg per day) for 5?days and the patient was discharged after subjective improvement of neurological symptoms. Table 1 Serial nerve conduction study findings thead th rowspan=”1″ colspan=”1″ Nerve /th th rowspan=”1″ colspan=”1″ 1st admission (2012.5.15) /th th rowspan=”1″ colspan=”1″ 2nd admission (2012.7.19) /th th rowspan=”1″ colspan=”1″ 3rd admission (2012.11.28) /th th rowspan=”1″ colspan=”1″ After appendectomy (2013.6.18) /th /thead Median motor, right?CMAP amplitude (mV)6.1 2.5 4.6 5.1?Distal latency (m/s) 4.92 11.4 15.3 5.8 ?NCV (m/s) 32.2 16.9 14.5 20.7 ?F-wave latency (m/s) 40.1 33.4 Absent 61.9 Ulnar motor, right?CMAP amplitude (mV)9.46 3.8 5.3?Distal latency (m/s) 3.27 8.4 9.89 4.8 ?NCV (m/s) 32.7 21.3 12 17.8 ?F-wave latency (m/s) 33.6 41.4 Absent 64 Peroneal motor, right?CMAP amplitude (mV) 0.62 No response No response 0.37 ?distal latency (m/s) 9.43 No response No response 9.9 ?NCV (m/s) 27.3 CD178 No response No response 17.7 ?F-wave latency (m/s) 80.4 Absent Absent Absent.