Combined central and peripheral demyelination: Clinical features, diagnostic findings, and treatment

MOG antibodies in combined central and peripheral demyelination syndromes

“… 1 – 3 Spinal cord lesions of variable length and abnormal visual evoked potentials with and without clinical optic neuritis have been commonly described in CCPD series and single reports, but AQP-4 antibodies were detected in a minority of patients. 1 – 4 MOG antibodies have not been reported in CCPD cases, and their role in CCPD is largely unknown. The clinical relevance of previously suggested antigens, such as neurofascin-155 (NF-155), expressed both in peripheral and central myelin, remains controversial.…”

Charcot-Marie-Tooth Disease Type 1A and Inflammatory-Demyelinating Lesions in the Central Nervous System

“…This combination is clinically heterogeneous and usually triggered by an infectious event. Its onset can be central or peripheral, with a monophasic or recurrent course, poor response to treatment with corticosteroids and immunoglobulins, and a prognosis which is generally poor [9]. Although the pathogenesis has not been fully elucidated, in the context of CIDP, it has been linked to the presence of anti-neurofascin 155 antibody, and it would seem that in this case, it could constitute an entity of its own with specific clinical characteristics initiated with dexamethasone, which led to resolution of the symptoms.…”

Peripheral neuropathy in limbic encephalitis with anti‐glutamate receptor antibodies: Case report and systematic literature review

“…Besides, anticipating Guillain–Barré syndrome (GBS) had also been reported in patients with anti‐NMDA receptor encephalitis (Tojo et al., ; Pruss et al., ). Moreover, GBS may also develop concurrently with acute disseminated encephalomyelitis (Bernard, Riou, Rosenblatt, Dilenge, & Poulin, ), Bickerstaff's brainstem encephalitis (Odaka et al., ; Han et al., ), and combined central and peripheral demyelination (Ogata et al., ; Cortese et al., ). In clinical practice, peripheral symptoms may be masked by severe CNS dysfunctions (Joubert et al., ).…”