Background: It has not previously been clarified if human facial muscles possess either typical muscle spindles, spindle-like structures or no spindles at all. Methods: Six patients from the Institute of Anatomy were used to investigate the Mm. orbiculares oculi and orbiculares oris. The age ranged from 53 to 91 years; three were males, three females. The specimens were imbedded in paraffin and examined in serial sections. Muscles were prepared for histological (H&E and Elastica van Gieson) and immunohistochemical (protein S-100, neurofilaments, and PGP 9.5) stainings. Results: All biopsies showed skeletal muscle fibers with some discrete alterations according to age. In some regions there were many small peripheral nerve fibers in close vicinity to muscle; but spindle-like structures with intrafusal fibers could not be detected. There were no signs of a sensorimotor double innervation of striated muscle fibers. Discussion: Previous investigators came to conflicting results regarding the absence or presence of muscle spindles in human facial muscles. However, in previous studies serial sections and immunohistochemical investigations had not been performed. Our observation of lacking muscle spindles in the facial muscles has several clinical and neurophysiological implications: (1) Pathological central muscle spindle afferent processing is assumed in the pathophysiology of dystonia. Although botulinum toxin leads to a denervation of muscle spindles its effect in the treatment of facial dystonias cannot be related to that. (2) A central facial paresis shows no signs of spasticity even in the chronic stage. Spasticity results in part from abnormal spinal processing of proprioceptive input mediated by Ia afferents. Thus, the absence of muscle spindles in the facial muscles may explain the lack of spasticity in these muscles. (3) In contrast to limb muscles, electrical facial and trigeminal nerve stimulations do not evoke silent periods and facial muscles show no facilitation of magnetic evoked potentials by vibration stimuli. Both phenomena are mediated by Ia afferents and their absence can be explained by the lack of muscle spindles.