INTRODUCTION: The incidence of alterations of the central and/or peripheral nervous system in a patient with Crohn s disease (EC) is 33.2%. Casual association may occur in 19.3% of the cases. The disorder of the nervous system may precede the diagnosis of EC. DEVELOPMENT: We review the main neurological complications of EC. The predominant cerebral vascular pathology is arterial although cases of venous thrombosis have been reported. One of the mechanisms involved is the state of hypercoagulability secondary to thrombocytosis and increase in the factors V, V111 and fibrinogen. In other cases there was confirmation of the presence of antiphospholipid antibodies and lupus anticoagulant, and therefore of an autoimmune mechanisms being involved. Other neurological features include peripheral neuropathy (axonal, demyelinating and autonomic), myopathies, pseudotumor cerebri, papilloedema, psychiatric disorders (anxiety, phobias, depression) and association with syndromes such as multiple sclerosis, Cogan s syndrome, Melkersson Rosenthal syndrome, connective tissue disorders and vasculitis. CONCLUSION: As well as hypercoagulability being one of the pathogenic mechanisms of cerebral ischaemia, there is alteration of humoral and cellular immunity in patients with EC. This justifies this and other neurological manifestations, and explains its association with other immunity disorders.
INTRODUCTION: The incidence of alterations of the central and/or peripheral nervous system in a patient with Crohn s disease (EC) is 33.2%. Casual association may occur in 19.3% of the cases. The disorder of the nervous system may precede the diagnosis of EC. DEVELOPMENT: We review the main neurological complications of EC. The predominant cerebral vascular pathology is arterial although cases of venous thrombosis have been reported. One of the mechanisms involved is the state of hypercoagulability secondary to thrombocytosis and increase in the factors V, V111 and fibrinogen. In other cases there was confirmation of the presence of antiphospholipid antibodies and lupus anticoagulant, and therefore of an autoimmune mechanisms being involved. Other neurological features include peripheral neuropathy (axonal, demyelinating and autonomic), myopathies, pseudotumor cerebri, papilloedema, psychiatric disorders (anxiety, phobias, depression) and association with syndromes such as multiple sclerosis, Cogan s syndrome, Melkersson Rosenthal syndrome, connective tissue disorders and vasculitis. CONCLUSION: As well as hypercoagulability being one of the pathogenic mechanisms of cerebral ischaemia, there is alteration of humoral and cellular immunity in patients with EC. This justifies this and other neurological manifestations, and explains its association with other immunity disorders.