Progressive systemic sclerosis (PSS) is a multi-systemic disorder characterized by abundant fibrosis of the skin, blood vessels, and visceral organs. But it rarely affects the peripheral nervous system. We report a 36-year-old man of painful trigeminal neuropathy as a complication of PSS. He was referred from Rheumatology for the evaluation of abruptly developed bilateral facial pain. He had facial hyperesthesia and paresthesia on neurologic examinations. In the blink reflex, ipsilateral and contralateral R1 and R2 responses were not detected during bilateral supraorbital stimulation. But normal latency and CMAP amplitude of facial NCV were found. Under the impression of trigeminal neuropathy caused by PSS, steroid therapy was tried, and his clinical symptoms and electrophysiologic findings were improved. PSS could be the cause of the painful trigeminal neuropathy.

Trigeminal sensory neuropathy is a clinical diagnosis in which the main feature is facial numbness limited to territory of one or more sensory branches of the trigeminal nerve. We describe a 46-year-old woman who presented with left facial numbness in the territories of maxillary nerve and mandibular nerve. MRI disclosed a lesion in left trigeminal nerve root entry zone. In Blink test stimulating infraorbital foramen, ipsilateral R1 was delayed compared with contralateral R1. Lesion in pons or medulla can present as trigeminal sensory neuropathy.

Blink reflex could be a useful tool to differentiate facial synkinesis as one of complications of facial neuropathy, from volitional associated movements. We had performed applied blink reflex test for 23 patients with objective evidence of hemifacial weakness in which orbicularis oculi muscle(zygomatic branch) and mentalis muscle(mandibular branch) areelectrophysiologically evaluated in response to supraorbital stimulation of trigeminal nerve. For an unaffected side of face there is no evidence of positive blink reflex from the mentalis muscle. We concluded that a positive blink reflex from mentalis muscle is almost always suggestive of chronic facial neuropathy even in clinical silence of facial synkinesis, or an aberrant reinnervation after peripheral facial neuropathy, and does not electrophysiologically correlate with the severity of facial palsy.