Lidocaine

An early report from 1934 showed that intralesional injections of procaine (Novocain®) relieved pain in six cases [1]. More recently, other types of local treatment of painful sites with lidocaine patches (5%) (Lidoderm®) [2,3] or lidocaine/prilocaine (25 mg/25 mg) cream (EMLA®) [4] have shown a reduction of pain in a few cases.  In the 1980s, treatment with intravenous infusions of lidocaine (Xylocaine®) in varying doses was reported in nine patients [5-12]. The resulting pain relief lasted from 10 hours [5] to 12 months [10]. In five of the cases, the lidocaine treatment was combined with mexiletine (Mexitil®), which is a class 1B anti-arrhythmic with similar pharmacological properties as lidocaine [7,13,14,12].

The mechanism by which lidocaine reduces pain in Dercum’s disease is unclear. It may block impulse conduction in peripheral nerves [5], and thereby disconnect abnormal nervous impulse circuits [12]. Nonetheless, it might also depress cerebral activity that could lead to increased pain thresholds [5]. Iwane et al. [5] performed an EEG during the administration of intravenous lidocaine. The EEG showed slow waves appearing 7 minutes after the start of the infusion and disappearing within 20 minutes after the end of the infusion. On the other hand, the pain relief effect was the greatest at about 20 minutes after the end of the infusion.

Based on this, the authors concluded that the effect of lidocaine on peripheral nerves most likely explains why the drug has an effect on pain in Dercum’s disease. In contrast, Atkinson et al. [10] have suggested that an effect on the central nervous system is more likely, as lidocaine can depress consciousness and decrease cerebral metabolism [10]. In addition, Skagen et al. [9] demonstrated that a patient with Dercum’s disease lacked the vasoconstrictor response to arm and leg lowering, which indicated that the sympathicusmediated local veno-arteriolar reflex was absent. This could suggest increased sympathetic activity. An infusion of lidocaine increased blood flow in subcutaneous tissue and normalised the vasoconstrictor response when the limbs were lowered. The authors suggested that the pain relief was caused by a normalisation of up-regulated sympathetic activity.

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