Expert opinion on screening, diagnosis and management of diabetic peripheral neuropathy: a multidisciplinary approach.

The proposed expert opinion aimed to address the current knowledge on conceptual, clinical, and therapeutic aspects of diabetic peripheral neuropathy (DPN) and to provide a guidance document to assist clinicians for the best practice in DPN care. The participating experts consider the suspicion of the disease by clinicians as a key factor in early recognition and diagnosis, emphasizing an improved awareness of the disease by the first-admission or referring physicians. The proposed "screening and diagnostic" algorithm involves the consideration of DPN in a patient with prediabetes or diabetes who presents with neuropathic symptoms and/or signs of neuropathy in the presence of DPN risk factors, with careful consideration of laboratory testing to rule out other causes of distal symmetric peripheral neuropathy and referral for a detailed neurological work-up for a confirmative test of either small or large nerve fiber dysfunction in atypical cases. Although, the first-line interventions for DPN are currently represented by optimized glycemic control (mainly for type 1 diabetes) and multifactorial intervention (mainly for type 2 diabetes), there is a need for individualized pathogenesis-directed treatment approaches for DPN. Alpha-lipoic acid (ALA) seems to be an important first-line pathogenesis-directed agent, given that it is a direct and indirect antioxidant that works with a strategy targeted directly against reactive oxygen species and indirectly in favor of endogenous antioxidant capacity for improving DPN conditions. There is still a gap in existing research in the field, necessitating well-designed, robust, multicenter clinical trials with sensitive endpoints and standardized protocols to facilitate the diagnosis of DPN via a simple and effective algorithm and to track progression of disease and treatment response. Identification of biomarkers/predictors that would allow an individualized approach from a potentially disease-modifying perspective may provide opportunities for novel treatments that would be efficacious in early stages of DPN, and may modify the natural course of the disease. This expert opinion document is expected to increase awareness among physicians about conceptual, clinical, and therapeutic aspects of DPN and to assist them in timely recognition of DPN and translating this information into their clinical practice for best practice in the management of patients with DPN.

Visual Evoked Potentials in Patients With Vitamin B12 Deficiency.

PURPOSE: The aim of this study was to investigate the subclinical involvement of the optic nerve in asymptomatic patients with vitamin B12 deficiency using visual evoked potentials. METHODS: This study included 40 asymptomatic patients diagnosed with vitamin B12 deficiency (considered as serum levels below 150 pg/mL) and a control group of 40 healthy individuals. All participants underwent a visual evoked potential examination. Routine screening for homocysteine was performed for patients with vitamin B12 deficiency. The levels of vitamin B12 and homocysteine and the presence of megaloblastic anemia were analyzed statistically compared with P100, N75, and N135 latencies and amplitudes. RESULTS: The mean vitamin B12 level was 96 pg/mL in the patient group and 374 pg/mL in the control group. In the patient group, 24 (60%) patients had hyperhomocysteinemia and 8 (20%) patients had megaloblastic anemia. The P100 wave latency of patients with vitamin B12 deficiency was significantly prolonged compared with the control group ( P < 0.01). There was no significant difference in the P100 amplitude between the patient group and the control group. P100 latencies were significantly longer in patients with hyperhomocysteinemia ( P = 0.002). CONCLUSIONS: Our study showed that patients with vitamin B12 deficiency may have visual evoked potential abnormalities without visual symptoms or examination findings. In addition, high homocysteine levels led to a prolonged P100 latency in the patient group independent of vitamin B12 levels.

Axon count and sympathetic skin responses in lumbosacral radiculopathy.

BACKGROUND AND PURPOSE: Electrodiagnostic studies can be used to confirm the diagnosis of lumbosacral radiculopathies, but more sensitive diagnostic methods are often needed to measure the ensuing motor neuronal loss and sympathetic failure. METHODS: Twenty-six patients with lumbar radiculopathy and 30 controls were investigated using nerve conduction studies, motor unit number estimation (MUNE), testing of the sympathetic skin response (SSR), quantitative electromyography (QEMG), and magnetic resonance myelography (MRM). RESULTS: Using QEMG as the gold standard, the sensitivity and specificity of MUNE for the abductor hallucis longus muscle were 71.4% and 70%, respectively. While they were 75% and 68.8%, respectively, when used MRM as gold standard. The sensitivity and specificity of MUNE for the extensor digitorum brevis muscle were 100% and 84.1%, respectively, when the peroneal motor amplitude as the gold standard. The SSR latency was slightly longer in the patients than in the controls. CONCLUSIONS: MUNE is a simple and sensitive test for evaluating autonomic function and for diagnosing lumbosacral radiculopathy in patients. MUNE could be used routinely as a guide for the rehabilitation of patients with radiculopathies. SSR measurements may reveal subtle sympathetic abnormalities in patients with lumbosacral radiculopathy.