ArticleJournal of neurology2026
Characteristics of patients with dropped head syndrome responsive to serotonin-norepinephrine reuptake inhibitors.
Article in Journal of neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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7 authors.
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Abstract
backgroundDropped head syndrome (DHS) is a heterogeneous disorder. DHS without any causative diseases has no established pharmacological therapy, thus current treatment is generally limited to pain management. Recently, the potential effect of duloxetine, a serotonin-norepinephrine reuptake inhibitor, has been reported in selected DHS patients. This study aimed to identify the characteristics associated with responsiveness to duloxetine in idiopathic DHS.
methods38 patients with idiopathic DHS who received duloxetine primarily for chronic pain were enrolled. Patients were classified as responders based on subjective improvement in dropped head symptoms. Demographics, clinical and laboratory data including serum monoamine levels, and radiographic parameters were measured and compared between responders and non-responders.
resultsSeventeen DHS patients were classified as responders (R group; ave. 78.2 years, 16 females) and 21 as non-responders (N group; ave. 76.1 years, 18 females). Disease duration was significantly shorter in R group compared with N group (p = 0.03). Serum serotonin levels were significantly lower in R group than that in N group (p = 0.03). C2-7 angle and C2-7 sagittal vertical axis (SVA) were significantly smaller in R group than those in N group (p < 0.01, p = 0.02, respectively). Multivariable analysis showed that lower serum serotonin levels and smaller C2-7 SVA were independently associated with duloxetine response (p = 0.04, p = 0.03, respectively).
conclusionsDuloxetine can be considered as a therapeutic option for a subset of idiopathic DHS patients, particularly those with a shorter disease duration, milder cervical deformity, and lower serum serotonin levels. Although DHS is multifactorial, disequilibrium in monoaminergic neurotransmission may contribute to its pathomechanism.
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