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Trigeminal sensory neuropathy related to interferon‐alpha treatment

TRIGEMINAL SENSORY NEUROPATHY RELATED TO INTERFERON-ALPHA TREATMENT A 53-year-old man with chronic hepatitis C virus infection was treated with interferon-alpha-2a between January and December 2001. He was given 5 million units of recombinant interferon-alpha weekly by subcutaneous injection. One month after commencing therapy, he began to experience episodes of paresthesias and dysesthesias associated with numbness involving all three branches of the left trigeminal nerve, but especially V2 and V3. These episodes began about 48 h after each injection and abated 24–48 h before the next interferon dose. This pattern persisted for 4 months when the sensory disturbances became continuous. Interferon therapy was stopped in late December 2001, without neurological improvement. Three years later, the patient’s primary care physician, concerned about the chronic course of the illness, requested neurological consultation. On examination, there was decreased pain and temperature sensation, and altered light touch sensation in the distribution of the three branches of the left trigeminal nerve. Motor function, corneal reflex, and the jaw jerk were all normal. Neurological examination was otherwise normal. Electromyographic (EMG) study of the blink reflex confirmed an afferent type defect (delay in all components but with normal latencies on stimulation of the contralateral supraorbital nerve; Fig. 1). Needle EMG of the masseter and temporalis muscles was normal. Routine laboratory examinations, chest X-rays, and computed tomography of the paranasal sinuses were normal. Computed tomography and magnetic resonance imaging of the brain and cervical spine were normal. Liver function was normal, and blood hepatitis C virus RNA was negative. Immunoglobulins and complements were normal. Antinuclear antibody, and anti-SS-A/-B antibodies were negative. Cerebrospinal fluid (CSF) analysis was normal without oligoclonal bands on electrophoresis and no growth on bacterial or viral cultures. We examined a variety of antibacterial and antiviral antibodies in the serum or CSF, but they showed no remarkable change. He was diagnosed as having trigeminal sensory neuropathy and was given pregabaline (150 mg/12 h) with complete improvement of dysesthesias, but hypoesthesia and numbness persisted. The temporal relationship between symptoms and dosing with interferon-alpha, and the lack of an alternative etiology suggests an immune-based mechanism induced by interferon alpha. The interferons are associated with numerous adverse reactions including various neuropsychiatric manifestations and neurological syndromes. There are several reports of cranial nerve palsies occurring during interferon-alpha therapy and, in all of them, immune mechanisms are suggested. The occurrence and exacerbation of autoimmune disorders (sarcoidosis, thyroiditis, hemolytic anemia, psoriasis, thrombocytopenia) in patients treated with interferon-alpha has been reported previously.1 Trigeminal sensory neuropathy may be associated with scleroderma, primary © 2005 Wiley Periodicals, Inc. FIGURE 1. Recordings of the blink reflex confirm an afferent left lesion. The left ipsilateral early wave (R1) was absent and bilateral late wave (R2) was delayed when the left side was stimulated, whereas the blink reflex was normal when the right side was stimulated.