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same syndromes and antibodies occur rarely without an evident tumor Small-cell cancer of the lung, adenocarcinoma of the breast and ovary, and Hodgkin disease are the tumors most often associated with these disorders, but the paraneoplastic neurologic syndromes occur in only a very small proportion of these cases The mechanism(s) by which carcinomas produce their remote effects are poorly understood Perhaps the most plausible theory, as intimated above, is that they have an autoimmune basis According to this theory, antigenic molecules are shared by certain tumors and central or peripheral neurons The immune response is then directed to the shared antigen in both the tumor and the nervous system The evidence for such an autoimmune mechanism is most clearly exempli ed by the Lambert-Eaton syndrome, in which an antibody derived from a tumor binds to voltage-gated calcium channels at neuromuscular junctions (Chap 53) Furthermore, in some types of paraneoplastic disorders, there is provocative evidence that the inciting tumor has receptors for the antibody on its surface and the self-binding of the antibody may inhibit tumor growth This is said to account for the dif culty in detecting diminutive small-cell lung cancers that underlie some of the paraneoplastic syndromes It should be noted, however, that there is no evidence that suppressing or removing the antibody leads to growth of the tumor

For many years, this disorder was considered to be quite uncommon, but it is perhaps the most characteristic of the paraneoplastic syndromes In reviewing this subject in 1970, we were able to nd only 41 pathologically veri ed cases; in a subsequent review (Henson and Urich), only a few more cases were added The actual incidence is much higher than these gures would indicate At the Cleveland Metropolitan General Hospital, in a series of 1700 con-

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secutive autopsies in adults, there were 5 instances of cerebellar degeneration associated with neoplasm In the experience of Henson and Urich, about half of all patients with nonfamilial, late-onset cerebellar degeneration proved sooner or later to be harboring a neoplasm Large series of cases have been reported from the Mayo Clinic and the Memorial Sloan-Kettering Cancer Center (Hammock et al; Anderson et al) We see three or more cases yearly but have also encountered numerous instances of an identical syndrome with no cancer evident and no antibodies (Ropper) In approximately one-third of the cases, the underlying neoplasm has been in the lung (most often a small-cell carcinoma) a gure re ecting the high incidence of this tumor However, the association of ovarian carcinoma and lymphoma, particularly Hodgkin disease, accounting for approximately 25 and 15 percent, respectively, is considerably higher than would be expected on the basis of the frequency of these malignancies Carcinomas of the breast, bowel, uterus, and other viscera have accounted for most of the remaining cases (Posner) Characteristically, the cerebellar symptoms have a subacute onset and steady progression over a period of weeks to months; in more than half the cases, the cerebellar signs are recognized before those of the associated neoplasm Symmetrical ataxia of gait and limbs affecting arms and legs more or less equally dysarthria, and nystagmus are the usual manifestations Striking in fully developed cases has been the severity of the ataxia, matched by few other diseases Occasionally, myoclonus and opsoclonus or a fastfrequency myoclonic tremor may be associated ( dancing eyes dancing feet, as noted below) In addition, there are quite often symptoms and signs not cerebellar in nature, notably diplopia, vertigo, Babinski signs (common in our cases), sensorineural hearing loss, disorders of ocular motility, and alteration of affect and mentation ndings that serve to distinguish paraneoplastic from alcoholic and other varieties of cerebellar degeneration These are well emphasized in the series of 47 patients collected by Anderson.

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and colleagues and the 55 cases by Peterson et al, who tabulated the additional neurologic features The CSF may show a mild pleocytosis (up to 60 cells/mm3 in a few of our patients) and increased protein, or it may be entirely normal Early in the course of the disease, CT scanning and MRI show no abnormality, but after a few months, atrophy of the brainstem and cerebellum may appear In a few cases, T2-weighted MRIs disclose an increased signal of the cerebellar white matter (Hammock et al), but this has not been uniform in our experience (Fig 31-21) Pathologically, there are diffuse degenerative changes of the cerebellar cortex and deep cerebellar nuclei Purkinje cells are affected prominently and all parts of the cerebellar cortex are involved Rarely, there are associated degenerative changes in the spinal cord, involving the posterior columns and spinocerebellar tracts The cerebellar degeneration is frequently associated with perivascular and meningeal clusters of in ammatory cells Henson and Urich regard the in ammatory changes as an independent process, part of a subacute paraneoplastic encephalomyelitis (see below) This view is supported by the nding that the speci c antibodies that are linked to cerebellar degeneration differ from those that are found in paraneoplastic in ammatory lesions in other parts of the nervous system Anti Purkinje cell antibodies (termed anti-Yo ) can be found in the sera of about half the patients with paraneoplastic cerebellar degeneration and in the large majority of those related to carcinoma of the breast or female genital tract; the clinical syndrome and this antibody have therefore become closely linked (Hu, another paraneoplastic antibody, and Yo are taken from the names of patients in whom the antibody was rst found) For example, in the Mayo Clinic series of 32 patients with paraneoplastic cerebellar degeneration, 16 had such antibodies; all were women and most of them had mammary or ovarian cancers Anderson and colleagues.

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