In 1934, Greenfield initially described two cases of subacute cerebellar degeneration occurring with carcinoma outside the nervous system . Thirteen years later in 1947, Denny-Brown reported two patients with primary sensory neuropathy and muscular changes associated with bronchial carcinoma .
R. Zand, MD
Department of Neurology, University of Tennesse, Geisinger Health System,
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A. Minagar, J.S. Alexander (eds.), Inflammatory Disorders of the Nervous System, Current Clinical Neurology, DOI 10.1007/978-3-319-51220-4_8
In 1954, Henson et al.  published a series of 19 cases with various types of carcinomatous neuropathy and myopathy. Eight of these patients had proximal atrophic weakness of limbs and involvement of ocular and bulbar muscles. Four patients also exhibited myasthenic features with a favorable response to neostigmine in some cases. Later in 1956, Chartan et al.  described episodes of severe mental disturbance in three male patients with bronchial carcinoma. In all of those, the mental disorder either preceded or overshadowed the presence of cancer.
In 1968, Corsellis et al.  reported autoimmune limbic encephalitis associated with small-cell lung cancer. For years, it was believed that “limbic encephalitis” was almost always associated with a form of neoplasia mainly lung, thymic, or testicular tumors. In 2001, it was shown that voltage-gated potassium channels (VGKC) were associated with reversible limbic encephalitis . Four years later, other antibodies to the cell surface or synaptic proteins were detected in six patients with subacute limbic encephalitis and involvement of additional brain regions . Further studies of those patients with immunotherapy-responsive encephalitis resulted in the characterization of the antigen as the NR1 subunit of the N-methyl-D-aspartic acid receptor (NMDA receptor) and the definition of its clinical characteristics [10-12], since many other neuronal cell surface antigens have been detected and introduced in patients with autoimmune encephalitis.