Marieke van Rosmalen

Chapter 1 16 phase , are necessary to calculate the percentage of fat. The first image is acquired when water and fat have the same phase, i.e. they rotate in phase, and the total signal can be calculated by the sum of the signal of water and the signal of fat. Next, a second image is acquired when the protons are in opposed phase, i.e. they are out of phase, and the total signal contains the signal of water minus the signal of fat. In this way, the percentage of water and the percentage of fat of the total signal of a tissue can be calculated. Injured or inflamed tissue may lead to changes in the diffusion parameters, for example by increasing or decreasing AD or RD, and changes in T2 relaxation times and fat fraction. Measuring and comparing quantitative MRI parameters between groups of patients and (healthy) controls, and correlating the found differences to histology or clinical data, may help in diagnosis, pathophysiology or prognosis of disease. Combined, these quantitative techniques inform on structural nerve changes due to pathophysiological processes. CIDP, MMN & MRI Diagnosis In current clinical practice diagnosis of CIDP and MMN is predominantly based on the consensus criteria of the guideline of the European Federation of Neurological Societies/Peripheral Nerve Society and the Utrecht criteria. 4,5,7 It is important to differentiate CIDP and MMN from their clinical mimics as an early start of immunomodulatory treatment in CIDP and MMN could prevent irreversible (axonal) damage and worsening of symptoms. 1,2 Differential diagnosis of (typical and variants of) CIDP includes Guillain-Barré syndrome, motor neuron diseases, focal compression neuropathies, diabetic neuropathy and Charcot-Marie-Tooth disease. 12 MMN is an important clinical mimic of motor neuron diseases, such as amyotrophic lateral sclerosis and progressive muscular atrophy, as they all can present with an asymmetric weakness without sensory deficits. However, treatment and prognoses differ considerably and the use of diagnostic consensus guidelines may help in the differentiation. These guidelines for CIDP and MMN describe that diagnosis is primarily based on a characteristic clinical presentation and specific features on nerve conduction studies, i.e. conduction blocks. These conduction blocks are believed to be caused by demyelination, in particular in CIDP, or axolemmal changes. 13 However, diagnosing CIDP or MMN often remains challenging as nerve conduction studies require specific expertise, cost a lot of time and are often burdensome to patients. Conduction blocks could be easily missed, which compromises diagnostic accuracy. 6 In more elusive cases, supportive criteria may help in diagnosis. One of the additional diagnostic tools is laboratory examination which may show an increased protein in the cerebrospinal fluid or presence of anti-GM1 antibodies (MMN only). 4,5 Second, a good response to immunomodulatory treatment may add to diagnosis although this criterium is seriously hampered by costs, the risk of adverse events in patients and the lack of a clear definition of treatment response. MRI of the brachial