Adalimumab Induced or Provoked MS in Patient with Autoimmune Uveitis: A Case Report and Review of the Literature

Table 1

Date	Authors	Title	Summary
1994	Baker et al.	“Control of Established Experimental Allergic Encephalomyelitis by Inhibition of Tumor Necrosis Factor (TNF) Activity within the Central Nervous System Using Monoclonal Antibodies and TNF Receptor-Immunoglobulin Fusion Proteins” [10]	They suggested that anti-TNF-α were effective in ameliorating demyelination process in several transgenic mouse models of experimental autoimmune encephalomyelitis.
1995	Selmaj et al.	“Prevention of Chronic Relapsing Experimental Autoimmune Encephalomyelitis by Soluble Tumor Necrosis Factor Receptor” [11]
1996	Van Oosten et al.	“Increased MRI Activity and Immune Activation in Two Multiple Sclerosis Patients Treated with the Monoclonal Anti-Tumor Necrosis Factor Antibody cA2” [12]	It reported both radiological and laboratory deterioration in two patients with rapidly progressive MS treated with intravenous infusions of a humanized mouse monoclonal TNF-α antibody.
2001	Mohan et al.	“Demyelination Occurring during Anti-Tumor Necrosis Factors α Therapy for Inflammatory Arthritides” [13]	It conducted cases of 19 patients with neurologic events suggestive of demyelination following either Etanercept or Infliximab infusion. These cases were identified by searching of the AERS database.
2013	Andreadou et al.	“Demyelinating Disease following Anti-TNFa Treatment: A Causal or Coincidental Association?” [14]	It reported four cases of suspected MS after treatment with anti-TNF-α.
2013	Seror et al.	“Pattern of Demyelination Occurring during Anti-TNF-α Therapy: A French National Survey” [15]	A research about the pattern of demyelination in 33 patients developing demyelinating disorders after treatment with anti-TNF-α.
2014	Kaltsonoudis et al.	“Neurological Adverse Events in Patients Receiving Anti-TNF Therapy: A Prospective Imaging and Electrophysiological Study” [16]	A study included 75 patients who were treated with anti-TNF-α. These patients were followed up for an average period of 13 months and three of them developed neurological symptoms; single patient had CNS demyelination lesions, another one had optic neuritis, and the third patient developed peripheral demyelination.