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Le Touquet – Paris-Plage, France

Said G.,HOpital de la Salpetriere
Handbook of Clinical Neurology | Year: 2013

Neurological manifestations of sarcoidosis are relatively rare but constitute a treatable cause of central and peripheral neurological manifestations. Regarding the peripheral nervous system, cranial nerves are predominantly affected, and peripheral facial nerve palsy, often bilateral, is the most common neurological manifestation of sarcoidosis. Multifocal peripheral neuropathy is a rare event in sarcoidosis. In some cases, however, peripheral neuropathy is the presenting manifestation and seemingly the only organ affected. Definite diagnosis of sarcoidosis rests ideally on histological demonstration of sarcoid granulomas in tissue biopsy specimens. © 2013 Elsevier B.V. Source

de Freitas M.R.G.,Federal University of Fluminense | Said G.,HOpital de la Salpetriere
Handbook of Clinical Neurology | Year: 2013

Leprous neuropathy, which is due to infection of nerve cells by Mycobacterium leprae, still affects millions of people in many developing countries. The clinical and pathological manifestations are determined by the natural resistance of the host to invasion of M. Leprae. Failure of early detection of leprosy often leads to severe disability in spite of eradication of mycobacterium at a later date. In the lepromatous type, bacilli are easily found in the skin and in nerve cells including Schwann cells, endothelial cells, and macrophages. In the tuberculoid type, a strong cell-mediated immune reaction leads to formation of granulomas and destruction of cells harboring bacilli and neighboring nerve fibers. In many cases, treatment of patients with the multibacillary leprosy is complicated by reversal reaction and further nerve damage. Nerve lesions lead to a symmetrical, pseudo-polyneuritic pattern in most cases of lepromatous leprosy, which is usually associated with typical skin lesions, but pure neuritic forms occur in up to 10% of patients with lepromatous leprosy. In the pure neuropathic cases, only nerve biopsy permits diagnosis. The multifocal pattern is more common in tuberculoid leprosy. Treatment is currently based on multidrug therapy with dapsone, rifampicin, and clofazimine. The use of corticosteroids can reduce or prevent nerve damage in reversal reactions. It is important to remember that sequelae, especially sensory loss, are extremely common, which can lead to secondary trophic changes due to repeated trauma in painless areas. © 2013 Elsevier B.V. Source

Vrancken A.F.J.E.,University Utrecht | Said G.,HOpital de la Salpetriere
Handbook of Clinical Neurology | Year: 2013

Vasculitis is a primary phenomenon in autoimmune diseases such as polyarteritis nodosa, Wegener's granulomatosis, Churg-Strauss syndrome, microscopic polyangiitis, and essential mixed cryoglobulinemia. As a secondary feature vasculitis may complicate, for example, connective tissue diseases, infections, malignancies, and diabetes. Vasculitic neuropathy is a consequence of destruction of the vessel wall and occlusion of the vessel lumen of small epineurial arteries. Sometimes patients present with nonsystemic vasculitic neuropathy, i.e., vasculitis limited to peripheral nerves and muscles with no evidence of further systemic involvement. Treatment with corticosteroids, sometimes in combination with other immunosuppressants, is required to control the inflammatory process and prevent further ischemic nerve damage. © 2013 Elsevier B.V. Source

Pierrot-Deseilligny C.,HOpital de la Salpetriere
Handbook of Clinical Neurology | Year: 2011

In the brainstem, lateral and vertical eye movements are controlled by separate structures, the former mainly in the pons and the latter in the midbrain. The abducens nucleus (VI) in the pons controls all ipsilateral eye movements, i.e., ipsilateral saccades as well as the horizontal vestibulo-ocular reflex (VOR). This nucleus contains the abduction motoneurons, but also the internuclear neurons involved in adduction, passing through the contralateral medial longitudinal fasciculus (MLF) before relaying in the third-nerve nucleus in the midbrain. Lesions affecting the abducens nucleus result in complete ipsilateral eye movement paralysis, and lesions damaging the MLF result in internuclear ophthalmoplegia, whereas an association of these two lesions leads to the "one-and-a-half" syndrome. Ipsilateral saccades are controlled by the ipsilateral paramedian pontine reticular formation located close to the sixth nucleus, whereas the ipsilateral VOR is controlled by the contralateral medial vestibular nucleus. Vertical eye movements are controlled by the third- and fourth-nerve nuclei in the midbrain. A lesion unilaterally affecting the third-nerve nucleus results in an ipsilateral third-nerve paralysis and a contralateral upgaze paralysis because of the decussation of the superior rectus motoneurons, at the level of the third-nerve nuclei. Vertical saccades are controlled by the rostral interstitial nucleus of the MLF (riMLF) located close to the third-nerve nucleus. Downward and upward saccade paralysis results from bilateral riMLF damage whereas upgaze paralysis usually results from a unilateral lesion affecting the region of the posterior commissure, suggesting that the suprareticular control of these two types of vertical saccade is distinct. © 2011 Elsevier B.V. Source

Said G.,HOpital de la Salpetriere | Krarup C.,Copenhagen University
Handbook of Clinical Neurology | Year: 2013

Chronic inflammatory demyelinative polyneuropathy (CIDP) is an acquired polyneuropathy presumably of immunological origin. It is characterized by a progressive or a relapsing course with predominant motor deficit. The diagnosis rests on the association of non-length-dependent predominantly motor deficit following a progressive or a relapsing course associated with increased CSF protein content. The demonstration of asymmetrical demyelinating features on nerve conduction studies is needed for diagnosis. The outcome depends on the amplitude of axon loss associated with demyelination. CIDP must be differentiated from acquired demyelinative neuropathies associated with monoclonal gammopathies. CIDP responds well to treatment with corticosteroids, intravenous immunoglobulins, and plasma exchanges, at least initially. © 2013 Elsevier B.V. Source

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