Unmasking of the trigemino-accessory reflex in accessory facial anastomosis
- aDepartment of Clinical Neurophysiology, Hospital General Universitario Gregorio Marañón, C/ Dr Esquerdo 46, 28007 Madrid, Spain, bDepartment of Morphological Sciences and Physiology, Universidad Europea, C/ Tajo s/n, Villaviciosa de Odón, 28670 Madrid, Spain
- Dr A Esteban, Department of Clinical Neurophysiology, Hospital General Gregorio Marañón, C/ Dr Esquerdo 46, 28007 Madrid, Spain.
- Received 27 July 1998
- Revised 26 January 1999
- Accepted 5 March 1999
Abstract
OBJECTIVE To evaluate the possible blink reflex responses in facial muscles reinnervated by the accessory nerve.
METHOD Eleven patients with a complete facial palsy were submitted to a surgical repair by an accessory facial nerve anastomosis (AFA). In this pathological group, blink reflex was studied by means of percutaneous electrical stimulation of the supraorbital nerve and recording from the orbicularis oculi muscle. A control group comprised seven normal people and seven patients with a complete Bell’s facial palsy; in this group, responses on the sternocleidomastoideus (SCM) muscles were studied after supraorbital nerve stimulation.
RESULTS All the patients with AFA showed a consistent degree of facial reinnervation. Ten out of the 11 patients with AFA showed reflex responses; in six, responses were configured by a double component pattern, resembling the R1 and R2 components of the blink reflex; three patients had an R1-like response and one patient showed a unique R2 component. Mean values of latencies were 15.2 (SD 4.6) ms for the R1 and 85.3 (SD 9.6) ms for the R2. In the control group, eight out of 14 people had evidence of reflex responses in the SCM muscles; these were almost exclusively configured by a bilateral late component (mean latency 63.5 (SD15.9) ms) and only one of the subjects showed an early response at 11 ms.
CONCLUSION The trigemino-accessory reflex response in the pathological group was more complex and of a significantly higher incidence than in the control group. These differences could be tentatively explained by a mechanism of synaptic plasticity induced by the impairment of the efferent portion of the reflex. This could unmask the central linking between the trigeminal and the accessory limbs of the reflex. The findings described could be a demonstration of neurobionomic function in the repairing process of the nervous system.
