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Objective: In patients with hemifacial spasm (HFS), abnormal muscle responses (AMR) are frequently present. The objective of this study was to investigate whether the afferent input of AMR is mediated by antidromic facial nerve stimulation or orthodromic trigeminal nerve stimulation. Methods: AMR in the orbicularis oris muscle were recorded in 28 patients with HFS. When AMR were present, they were recorded after subthreshold stimulation of the facial nerve and weak stimulation delivered to the skin. Results: AMR were recordable in 24 (86%) of the patients, and usually consisted of the early constant component (mean onset latency, 10.0 ms) and late variable component (35.3 ms), similar to R1 and R2 of the blink reflex. The early or late components of AMR, or both, were frequently elicited after subthreshold stimulation of the facial nerve (43%) and skin stimulation (88%). Conclusions: AMR are likely to be mediated by trigeminal afferent inputs, rather than antidromic activation of the facial nerve, and are a type of trigeminal reflex.

Background: Patients with atypical neuralgia or atypical facial pain have been surgically treated with microvascular decompression (MVD) of the trigeminal root entry zone (TREZ). There are no data regarding the sensitivity and specificity of a vessel-TREZ relationship as a cause of pain in patients with persistent idiopathic facial pain (PIFP) according to the definition given by the International Headache Society (IHS). Methods: The TREZ was visualised by 3D CISS MRI in 12 patients with unilateral PIFP according to the IHS criteria. Results: The frequency of artery-TREZ, vein-TREZ, or vessel (artery/vein)-TREZ contacts on the symptomatic and asymptomatic sides did not differ significantly. On the symptomatic side, vessel-TREZ contact was found in 58% of patients (sensitivity). On the asymptomatic side, vessel-TREZ contact was absent in 33% of patients (specificity). Conclusions: On the basis of the low sensitivity and specificity found in the present study, PIFP cannot be attributed to a vessel-TREZ contact, and therefore, pain relief after MVD cannot be expected.

Background: Since the initial report of Ford et al in 1998 no further study has evaluated radiosurgery of the trigeminal nerve in chronic cluster headache (CCH). Methods: We carried out a prospective open trial of neurosurgery and enrolled 10 patients (nine men, one woman; mean age 49.8 years, range 32–77) presenting with severe and drug resistant CCH (mean duration 9 years, range 2–33). The cisternal segment of the nerve was targeted with a single 4 mm collimator (80–85 Gy max). Results: The mean follow up was 13.2 months. No improvement was observed in two patients and three patients had no further attacks. Three patients showed dramatic improvement with a few attacks per month or very few attacks over the last six months. Two patients were pain free for only one and two weeks and their headaches recurred with the same severity as before. Three patients developed paraesthesia with no hypoaesthesia, one developed hypoaesthesia, and one developed deafferentation pain. Conclusions: The rate and severity of trigeminal nerve injury appeared to be significantly higher than in trigeminal neuralgia, and this study does not support the positive results of the study of Ford et al. We consider the morbidity to be significant for the low rate of pain cessation, making this procedure less attractive even for the more severely affected subgroup of patients.

Background and objectives: Hyperekplexia and the stiff-man syndrome (SMS) are both conditions with exaggerated startle suggesting abnormal brainstem function. Investigation of brainstem reflexes may provide insight into disturbed reflex excitation and inhibition underlying these movement disorders. Patients and methods: Using four-channel EMG, we examined four trigeminal brainstem reflexes (monosynaptic masseter, masseter inhibitory, glabella, and orbicularis oculi blink reflexes) and their spread into pericranial muscles in five patients with familial hyperekplexia (FH), two with acquired hyperekplexia (AH), 10 with SMS, and 15 healthy control subjects. Results: Both FH/AH and SMS patients had abnormal propagation of brainstem reflexes into pericranial muscles. All patients with hyperekplexia showed an abnormal short-latency (15–20 ms) reflex in the trapezius muscle with a characteristic clinical appearance (“head retraction jerk”) evoked by tactile or electrical stimulation of the trigeminal nerve, but normal monosynaptic masseter reflexes. Inhibitory brainstem reflexes were attenuated in some FH/AH patients. Four of 10 patients with SMS had similar short-latency reflexes in the neck muscles and frequently showed widespread enhancement of other excitatory reflexes, reflex spasms, and attenuation of inhibitory brainstem reflexes. Conclusion: Reflex excitation is exaggerated and inhibition is attenuated in both stiff-man syndrome and familial or acquired hyperekplexia, indicating a physiological relationship. Reflex transmission in the brainstem appears biased towards excitation which may imply dysfunction of inhibitory glycinergic or GABAergic interneurons, or both.