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Tumor necrosis factor–α (TNF-α) blockers are a popular therapeutic choice in a number of inflammatory diseases. Thus far, five TNF- α blockers have been approved for clinical use (etanercept, infliximab, adalimumab, golimumab. and certolizumab). Despite being considered relatively safe, serious side effects associated with immune suppression have been reported, including central and peripheral nervous system (CNS) demyelinating disorders. It is still elusive whether these events are mere coincidence or a side effect of anti-TNF-α use. In this paper, we review the published case reports of CNS demyelination associated with anti-TNF-α therapy and present the follow-up of our 4 previously reported patients who developed neurologic symptoms suggestive of CNS demyelination after having received anti-TNF-α treatment. We also discuss the possible role of TNF-α blockers in demyelination. © 2017, The Author(s).

Ocular motor cranial nerve palsies of viral etiology are uncommon and, when accompanied by skin lesions, zoster ophthalmicus is the most frequent diagnosis. We describe the case of a 68-year-old woman who developed fourth and sixth nerve palsies 3 days after appearance of a painful vesicular skin rash on the left side of her forehead. Neuroimaging was normal but polymerase chain reaction (PCR) testing of the cerebrospinal fluid was positive for Herpes Simplex 1 and negative for Varicella Zoster. The patient was treated with intravenous acyclovir, and the cranial nerve palsies resolved over 7 weeks. Although the similarity of the cutaneous vesicular eruption in our patient to that seen with zoster might have led to an incorrect diagnosis, acyclovir seems to be safe and effective for both viral etiologies. © 2014 by North American Neuro-Ophthalmology Society.

Glycogen storage disease type II (Pompe disease) affects mainly proximal skeletal muscles. Despite older histological evidence of extraocular muscle involvement, ocular motor palsies or other eye movement abnormalities are not considered part of the clinical picture.We investigated the dynamics of saccadic eye movements of five patients suffering from late-onset Pompe disease and compared their performance to that of age matched healthy controls. Horizontal rightward and leftward saccades were recorded binocularly, while subjects looked at LED targets placed at ±5°, 10° and 15° eccentricities.No differences in saccade amplitudes, peak velocities or durations were observed between controls and patients. More specifically, for 5° saccades, patients had a mean peak velocity of 146°/s with duration of 76. ms. For 10° and 15° saccades these values were 258°/s, 86. ms and 324°/s, 101. ms respectively, thereby lying well within one standard deviation of the mean of normal data. Moreover, saccadic amplitude accuracy was also unimpaired.These results indicate that patients with late onset Pompe disease perform fast and accurate horizontal saccades without evidence of muscle paresis or other ocular motor abnormalities. Reported histological abnormalities of extraocular muscles do not appear to have a phenotypic impact. © 2014 Elsevier B.V.

Tumor necrosis factor antagonists (anti-TNFa) are an established therapeutic option for several autoimmune and inflammatory bowel diseases. Despite their clinical effectiveness, neurological adverse events have been reported and literature data suggest a potential role of anti-TNFa in the induction of demyelination of the CNS. We present four patients treated with anti-TNFa who developed symptoms suggestive of CNS demyelination. The first patient, a 17-year-old male who received etanercept for psoriatic arthritis for eight months, presented with dysesthesias up to T4 level. The second patient, a 30-year-old male treated with adalimumab for three years due to ankylosing spondylitis, presented with right unilateral tinnitus. The third case, a 47-year-old female, received etanercept for four years because of psoriatic arthritis and developed persistent headache and left-sided face and head numbness. Finally, the fourth patient, a 57-years-old female treated with etanercept for six years due to ankylosing spondylitis, presented with difficulty in speech, swallowing, and ptosis of the right corner of the mouth. In all cases, brain MRI showed lesions suggestive of demyelination, while positive oligoclonal bands were detected in the CSF. Anti-TNFa treatments were discontinued and patients showed clinical improvement with pulsed intravenous corticosteroid therapy. CNS demyelination following anti-TNFa treatment represents a relatively rare but potential serious complication. Close follow-up and MRI monitoring of these patients is mandatory to elucidate whether the clinical manifestations represent adverse events occurring during anti-TNFa therapy or a first demyelinating episode.

Tumor necrosis factor antagonists (anti-TNFa) are an established therapeutic option for several autoimmune and inflammatory bowel diseases. Despite their clinical effectiveness, neurological adverse events have been reported and literature data suggest a potential role of anti-TNFa in the induction of demyelination of the CNS. We present four patients treated with anti-TNFa who developed symptoms suggestive of CNS demyelination. The first patient, a 17-year-old male who received etanercept for psoriatic arthritis for eight months, presented with dysesthesias up to T4 level. The second patient, a 30-year-old male treated with adalimumab for three years due to ankylosing spondylitis, presented with right unilateral tinnitus. The third case, a 47-year-old female, received etanercept for four years because of psoriatic arthritis and developed persistent headache and left-sided face and head numbness. Finally, the fourth patient, a 57-years-old female treated with etanercept for six years due to ankylosing spondylitis, presented with difficulty in speech, swallowing, and ptosis of the right corner of the mouth. In all cases, brain MRI showed lesions suggestive of demyelination, while positive oligoclonal bands were detected in the CSF. Anti-TNFa treatments were discontinued and patients showed clinical improvement with pulsed intravenous corticosteroid therapy. CNS demyelination following anti-TNFa treatment represents a relatively rare but potential serious complication. Close follow-up and MRI monitoring of these patients is mandatory to elucidate whether the clinical manifestations represent adverse events occurring during anti-TNFa therapy or a first demyelinating episode.