D S Molenaar1, M Vermeulen, R de Haan. 1. Department of Neurology, Academic Medical Center, University of Amsterdam, The Netherlands. D.MOLENAAR@AMC.UVA.NL
Abstract
OBJECTIVE: To investigate the additional diagnostic value of sural nerve biopsy of 64 patients in whom chronic inflammatory demyelinating polyneuropathy (CIDP) was considered, as sural nerve biopsy is recommended in the research criteria of an ad hoc subcommittee to diagnose CIDP. METHODS: Firstly, the additional diagnostic value of sural nerve biopsy was analysed with multivariate logistic regression. Six clinical features (remitting course, symmetric sensorimotor neuropathy in arms and legs, areflexia, raised CSF protein concentration, nerve conduction studies consistent with demyelination, and absence of comorbidity or relevant laboratory abnormalities) were entered into a logistic model. Afterwards, all significant features identified from this model, as well as the results of sural nerve biopsy were forced into a second logistic model. Secondly, the diagnostic performance of a neurologist experienced in diagnosis of peripheral nerve disorders was studied by receiver operating characteristics (ROC) curve analysis. RESULTS: The results of the first logistic analysis showed that CSF protein concentration >1 g/l (odds ratio (OR)=38.5) and neurophysiological studies consistent with demyelination (OR=51.7) were strong predictors of CIDP. When forcing the significant features and the sural nerve biopsy data into the model, an independent predictive value of sural nerve biopsy could not be found. The neurologist was able to discriminate patients with and without CIDP (area under the curve (AUC)=0.95). His diagnostic performance did not improve significantly by offering him the results of sural nerve biopsy. CONCLUSION: Any additional diagnostic value of sural nerve biopsy in the diagnosis of CIDP could not be shown.
OBJECTIVE: To investigate the additional diagnostic value of sural nerve biopsy of 64 patients in whom chronic inflammatory demyelinating polyneuropathy (CIDP) was considered, as sural nerve biopsy is recommended in the research criteria of an ad hoc subcommittee to diagnose CIDP. METHODS: Firstly, the additional diagnostic value of sural nerve biopsy was analysed with multivariate logistic regression. Six clinical features (remitting course, symmetric sensorimotor neuropathy in arms and legs, areflexia, raised CSF protein concentration, nerve conduction studies consistent with demyelination, and absence of comorbidity or relevant laboratory abnormalities) were entered into a logistic model. Afterwards, all significant features identified from this model, as well as the results of sural nerve biopsy were forced into a second logistic model. Secondly, the diagnostic performance of a neurologist experienced in diagnosis of peripheral nerve disorders was studied by receiver operating characteristics (ROC) curve analysis. RESULTS: The results of the first logistic analysis showed that CSF protein concentration >1 g/l (odds ratio (OR)=38.5) and neurophysiological studies consistent with demyelination (OR=51.7) were strong predictors of CIDP. When forcing the significant features and the sural nerve biopsy data into the model, an independent predictive value of sural nerve biopsy could not be found. The neurologist was able to discriminate patients with and without CIDP (area under the curve (AUC)=0.95). His diagnostic performance did not improve significantly by offering him the results of sural nerve biopsy. CONCLUSION: Any additional diagnostic value of sural nerve biopsy in the diagnosis of CIDP could not be shown.