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Opsoclonus-Myoclonus-Ataxia Syndrome
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In children, this syndrome is usually a manifestation of neuroblastoma, but it is more common and occurs in adults in relation to breast cancer and small-cell lung cancer The unique feature of the neuroblastoma form is a response to corticosteroids and ACTH in most children and in some adults, and resolution of the neurologic signs when the neuroblastoma is removed A subgroup of breast cancer patients produce an antibody that has the neuronal nuclearbinding characteristics of the anti-Hu (antineuronal antibody type 1) antibody discussed below, but it is directed at a different RNAbinding antigen within the cell It has therefore been termed antiRi (antineuronal antibody type 2) This antibody is not found in the opsoclonus-ataxic syndrome of neuroblastoma and is present only rarely with small-cell lung cancer There have also been a limited number of positive serologic tests in children with opsoclonus, apparently without an underlying tumor A few such patients have had a mild pleocytosis in the CSF; the MRI is usually normal More complex syndromes have been reported with the antiRi antibody, manifest by rigidity and intense stimulus-sensitive myoclonus in addition to the core features of opsoclonus and ataxia The neuropathologic ndings have not been distinctive; mild
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Figure 31-21 Paracarcinomatous cerebellar degeneration MRI showing subtle diffuse enhancement of the cerebellar cortex
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INTRACRANIAL NEOPLASMS AND PARANEOPLASTIC DISORDERS
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cell loss has been described in the Purkinje cell layer, inferior olives, and brainstem, with mild in ammatory changes (Luque et al) Besides breast cancer, we have observed the opsoclonusmyoclonus syndrome in a middle-aged woman with bronchial carcinoma and also in a man with gastric carcinoma Similar cases occur with both cerebellar ataxia and an irregular tremor, which we have interpreted as myoclonic in character These patients were found to have marked degeneration of the dentate nuclei The prognosis in this syndrome is somewhat better than that for the other paraneoplastic diseases, but besides a trial of ACTH, there is little that can be done but search for the tumor and resect it if possible
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Encephalomyelitis Associated with Carcinoma
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The occurrence of regional and bilateral encephalomyelitic changes in association with carcinoma has been described by several authors (Corsellis et al, Henson and Urich, Posner) In most of the reported cases, the encephalitic process has been associated with carcinoma of the bronchus, usually of the small-cell type but all types of neoplasm may be implicated Histologically, this group of paraneoplastic disorders is characterized by extensive loss of nerve cells, accompanied by microglial proliferation, small patches of necrosis, and marked perivascular cuf ng by lymphocytes and monocytes Foci of lymphocytic in ltration have been observed in the leptomeninges as well These pathologic changes may involve the brain and spinal cord diffusely, but more often they predominate in a particular part of the nervous system, notably in the medial temporal lobes and adjacent nuclei ( limbic encephalitis, Fig 3122), the brainstem (particularly in the medulla), the cerebellum (see above), and the gray matter of the spinal cord The symptoms will, of course, depend on the location and severity of the in ammatory
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Figure 31-22 Coronal FLAIR MRI from a woman with paraneoplastic limbic encephalitis associated with lung cancer and a mild pleocytosis but no detectable autoantibodies The hippocampi and adjacent regions are involved Pathologically there proved to be gliosis and a minimal in ammatory in ltrate in these regions
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changes and may overlap Most cases are subacute, meaning speci cally a progression over a few weeks or months, but often the main symptoms in mild form become apparent in a matter of days Rare instances of remission have been reported Anxiety and depression, a confusional-agitated state, hallucinations, retentive memory defect (Korsakoff syndrome), and dementia singly or in various combinations are the principal manifestations of so-called limbic encephalitis (Gultekin et al) Vertigo, nystagmus, ataxia, nausea and vomiting, and a variety of ocular and gaze palsies re ect the presence of paraneoplastic brainstem encephalitis As indicated above, these symptoms may be joined with cerebellar ataxia, and another group has a sensory neuropathy We have seen instances of this condition involving only the midbrain and others involving the medulla, the latter with unusual breathing patterns including gasping, inspiratory breathholding, and vocal-respiratory incoordination, and yet others with chorea and additional basal ganglionic features The great variety of clinical presentations can be appreciated from the series by Graus and colleagues of 200 patients: sensory neuropathy, 54 percent; cerebellar ataxia, 10 percent; limbic encephalitis, 9 percent; and others including multiple sites in 11 percent In most of these cases, MRI shows T2 signal changes in affected regions; in severe cases, zones of focal necrosis may be seen Odd seizures, including epilepsia partialis continua, have been observed with this disorder, but they must be rare Sensory symptoms may be related to neuronal loss in the posterior horns, traced to the commonly associated loss of neurons in the dorsal root ganglia (sensory neuronopathy and sensory neuropathy) as mentioned above and discussed further on All attempts to isolate a virus in these cases have failed There may be a slowly progressive, symmetrical or asymmetrical amyotrophy of the arms and less often of the legs, traced in two of our patients to poliomyelitic lesions in the anterior horns of the spinal gray matter (see further on) A form characterized mainly by corticospinal degeneration is also reported but has not been found in our clinical material Pathologic studies have not entirely clari ed these forms of paraneoplastic disorder In some cases, no changes were demonstrable in the brain, even though there had been a prominent dementia during life Contrariwise, widespread in ammatory changes may be found without clinical abnormalities having been recorded during life We believe that these seemingly paradoxical ndings may have to do with the thoroughness of the clinical and pathologic examinations Most patients with small-cell lung cancer and any of the types of paraneoplastic encephalomyelitis have circulating polyclonal IgG antibodies (anti-Hu, or antineuronal antibody, type 1) that bind to the nuclei of neurons in many regions of the brain and spinal cord, dorsal root ganglion cells, and peripheral autonomic neurons The antibodies are reactive with certain nuclear RNA-binding proteins Cancers of the prostate and breast and neuroblastoma may rarely produce a similar antibody The antibody titer is higher in the CSF than in the serum (as it is for anti-Yo with cerebellar degeneration), indicating production of antibody within the nervous system Low titers of anti-Hu are found in many patients with small-cell cancer who are neurologically normal, probably because these tumors have expressed only low levels of antigens that are recognized by anti-Hu Recently, antibodies to voltage-gated potassium channels have been identi ed in patients with limbic encephalitis without cancer (Vincent et al) Despite a few reports of improvement with plasma exchange or intravenous gamma globulin, the results of treatment have been
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