Inflammatory trigeminal nerve and tract lesions associated with inferior alveolar nerve anaesthesia.

Inferior alveolar nerve blocks are commonly performed for dental anaesthesia. The procedure is generally safe with a low rate of complications. We report a patient with a reproducible, delayed-onset sensory deficit associated with contrast-enhancing lesions in the trigeminal nerve, pons and medulla following inferior alveolar nerve local anaesthesia. We propose that this previously undescribed condition is a form of Type IV hypersensitivity reaction.

Isolated reversible hypoglossal nerve palsy as the initial manifestation of pre-eclampsia.

Isolated hypoglossal nerve lesions often reflect sinister neoplastic or vascular pathology. Rarely, reversible lesions occur, perhaps via mechanisms similar to Bell's palsy. We report a patient with reversible isolated hypoglossal nerve palsy as the first and predominant early manifestation of pre-eclampsia and speculate on the pathogenesis behind this abnormality.

Massive astrocyte destruction in neuromyelitis optica despite natalizumab therapy.

Auto-antibody mediated astrocyte injury is implicated as a primary event in neuromyelitis optica (NMO) by biomarker, post-mortem and experimental studies that differentiate the condition from multiple sclerosis. We describe the clinical, radiological and neuropathological features of a severe cerebral attack in a natalizumab-treated patient with relapsing myelitis and serum aquaporin-4 antibodies. Our findings support autopsy evidence that abrupt astrocyte destruction precedes demyelination in NMO, and emphasize the importance of serological testing in patients with limited disease. Adherence to current NMO diagnostic criteria may delay treatment, or lead to inappropriate therapy with beta-interferon or natalizumab.

MS: is it one disease?

Neuropathological studies of early multiple sclerosis (MS) tissue have shaped prevailing views of the pathogenesis of the disease. The hallmark of the acute MS lesion, inflammatory demyelination, has been largely accepted as evidence of a macrophage-mediated attack on normal myelin, driven by perivascular and parenchymal autoreactive CD4+ Th1 cells primed in the periphery by an unknown self or foreign antigen(s). Predicated largely upon comparisons with experimental allergic encephalomyelitis, this paradigm has, in recent years, been recognized as a simplification of the events that constitute and perhaps presage lesion formation in the human disease; and the importance of the innate immune cells of the central nervous system, humoral factors, cytotoxic CD8+ T-cells and regulatory T-cells has been emphasized. An influential series of publications by one group, based on histopathological examination of actively demyelinating lesions in selected autopsy and biopsy MS tissue, defined four early lesion subtypes. In a given individual, these subtypes were reported to be mutually exclusive, suggesting that disparate pathogenetic pathways separate patients with clinically indistinguishable syndromes. This schema, which has considerable therapeutic implications, has not been independently verified and has recently been questioned by the finding of a uniform pre-phagocytic pathology and overlap of lesion subtypes in individual patients with typical relapsing and remitting disease. The latter findings would suggest that the heterogeneous features observed in active MS lesions sampled at different time-points are a reflection of the evolution of a single pathophysiological process, perhaps modified in part by genetic factors in individual cases.