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Paraneoplastic Cerebellar Degeneration
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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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report a similar proportion but point out that several anti-Purkinje antibodies besides the highly characteristic one may be found by special techniques Death occurred in 4 to 18 months In an equal number of cases without antibodies, half are men with lung cancer and a few have circulating antibodies of another type ( anti-Hu ) that are more closely linked to the paraneoplastic encephalomyelitis discussed further on This leaves a proportion who have no circulating antibody but nonetheless are found to have a concealed tumor that must be sought by other ancillary tests In another small group, it must be conceded that no underlying tumor can be found despite extensive examinations and even at autopsy (Ropper) The death rate in these cases has varied widely from 6 months to several years and depends on the behavior of the underlying tumor Whether the anti-Yo antibodies are merely markers of an underlying tumor or the agents of destruction of the Purkinje cells is not known They have been found to bind to a C-myc protein that initiates a degeneration of Purkinje cells Regardless of the pathogenic signi cance of the antibodies, nding them in a patient with the typical neurologic disorder has considerable diagnostic significance As mentioned above, their presence strongly suggests that there is an underlying breast or ovarian cancer, which may be asymptomatic and small enough to be resected successfully Other antibodies besides anti-Yo and anti-Hu are found on occasion, such as those against a glutamate receptor in patients with Hodgkin disease (Smitt et al) The differential diagnosis is broad as indicated in Table 5-1 The main considerations are a variant of CreutzfeldtJakob disease, postinfectious cerebellitis, and various intoxications Treatment Little can be done to modify the cerebellar symptoms, although there are on record several cases in which there was a partial or complete remission of symptoms after removal of the primary tumor (Paone and Jeyasingham) Further, in some cases associated with Hodgkin disease, there has been spontaneous improvement of the cerebellar symptoms Preliminary reports of aggressive plasma exchange or intravenous immunoglobulin treatment early in the course suggest some bene t, but it should not be assumed that this approach will succeed in most patients, and our own experience in over 10 cases has been discouraging
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