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to the left due to paresis of the left pterygoid muscle. The corneal refl ex was positive on both sides. All other neurological systems were regular. In particular, there were no sensory disturbances and no signs of polyneuropathy. Electromyography did not detect pathological spontaneous activity (most probably due to massive atrophy and chronicity of the process), but showed a single unit interference pattern during maximal voluntary contraction in the left masseter muscle and motor unit action potentials with amplitudes of 4 mV. Myopathic changes were absent. Other laboratory parameters were regular, e.g., C-reactive protein, creatine kinase, myoglobin, and blood cell count. A brain magnetic resonance imaging (MRI) scan did not detect any pathology, in particular no lesion of the pons or the mandibular trigeminal nerve branch. However, pronounced left-sided masseteric atrophy was clearly depictable on MRI images ( fi g. 1 ). Altogether, there was massive atrophy and paresis of the left jaw muscles without any sensory facial disturbances, indicating pure motor trigeminal neuropathy. Electromyography confi rmed chronic denervation of the left masseter muscle. Lumbar puncture was declined. Dear Sir, Facial asymmetry often occurs because of unilateral facial nerve paresis. Here, we report on a HIV-positive patient with progressive facial asymmetry due to unilateral motor trigeminal neuropathy.

Progressive Facial Asymmetry due to Trigeminal Motor Neuropathy