Remission of Cerebellar Dysfunction after Pneumonectomy for Bronchogenic Carcinoma

Paone, Joseph F.; Jeyasingham, K.

doi:10.1056/nejm198001173020305

Cited by 66 publications

(14 citation statements)

References 5 publications

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“…Three reports in the medical literature document significant improvement in the cerebellar dysfunction, one without treatment and two following treatment. In the first patient with colon carcinoma gait and appendicular ataxia remitted one month after onset before any treatment was given, while in the second improvement followed pneumonectomy for bronchogenic carcinoma (5,6). In the second case the remission of symptoms began immediately after surgery and by seven days the patient was able to ambulate with a cane.…”

Section: Discussionmentioning

confidence: 96%

“…In the second case the remission of symptoms began immediately after surgery and by seven days the patient was able to ambulate with a cane. At eleven months there was no signs of cerebellar disease (5). In the third patient with bronchogenic carcinoma and remote effect sensory polyneuropathy, cerebellar syndrome, and long tract signs, there was improvement from poor antigravity function being unable to keep his shin on the opposite heel to walking with a walker following 4 1/2months of therapy (7).…”

Section: Discussionmentioning

confidence: 99%

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Paraneoplastic cerebellar degeneration

Greenberg

1984

J Neuro-Oncol

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Six patients developed a pancerebellar syndrome with symptoms preceding the diagnosis of neoplasia in five (median - 4 months) and following in one (2 years). In all patients, the initial cranial computed tomographic (CT) scans were normal. Five patients had repeat CTs and of these three were abnormal; cerebellar atrophy appearing 7 to 25 months following the initial CT. Median follow-up was 31 months (range 12-84 months) without evidence of CNS metastatic disease. In five of six patients the neurologic impairment did not progress. One patient's neurologic signs improved markedly with mantle radiation therapy of her Hodgkin's disease. An initially negative CT does not preclude the diagnosis of remote effect cerebellar atrophy. Paraneoplastic cerebellar degeneration is a self-limited nonprogressive process in the majority of patients.

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Paraneoplastic cerebellar degeneration

Greenberg

1984

J Neuro-Oncol

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“…In one detailed case study (Smith, Gonda and Malamud, 1958) including postmortem on a male aged 63 years, severe degeneration and cell loss from the cerebellum and its centrifugal connections together with demyelination, cell loss and gliosis of the corpus Luysi and globus pallidus in the extra-pyramidal system were found; there was no family history of cerebellar ataxia nor was tumour apparent at post-mortem. Another case is cited (Brain and Wilkinson, 1965) (Woodhouse et al, 1967 (Brain and Wilkinson, 1965) (Paone and Jeyasingham, 1980). The aetiology of the paraneoplastic neurological syndromes remains unknown, but several mechanisms, not mutually exclusive, have been suggested (Joynt, 1974;Henson, 1970).…”

Section: Discussionmentioning

confidence: 99%

Cerebellar cortical degeneration with ovarian carcinoma

Steven

Mackay

Carnegie

et al. 1982

Postgraduate Medical Journal

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A case is described of progressive cerebellar degeneration in association with ovarian carcinoma, with nearly 4 years elapsing between the onset of neurological illness and the discovery of the carcinoma. Neither treatment with prednisolone nor surgical removal of the tumour effected any improvement, CAT scanning late in the illness showed marked cerebellar atrophy. Histology at post-mortem showed complete loss of cerebellar Purkinje cells. The cerebrospinal fluid gave weak binding to multiple neural components in a solid-phase radio-immuno-assay.

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“…Although immunomodulation and immunosuppression improve the symptoms of LEMS, the concomitant cerebellar deficits are much less responsive to treatment [59][60][61]. Despite this low potential for recovery, there are reports of patients who have paraneoplastic cerebellar dysfunction whose symptoms improved after treatment of the tumor or immunosuppression [62][63][64][65]. In some of these patients, as in approximately 40% of patients who have cancer and subacute cerebellar degeneration without paraneoplastic antibodies, the CSF showed inflammatory abnormalities identical to those found in patients who have paraneoplastic antibodies, suggesting an immune-mediated pathogenesis.…”

Section: Limbic Encephalitis: a Model For Other Paraneoplastic Disordersmentioning

confidence: 99%

Clinical and Immunological Diversity of Limbic Encephalitis: A Model for Paraneoplastic Neurologic Disorders

Dalmau

Bataller

2006

Hematology/Oncology Clinics of North America

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The most important contribution to the understanding and management of paraneoplastic neurologic disorders (PND) is the discovery that many of these disorders are immune mediated. It is believed that cytotoxic T-cell responses and antibodies that target neuronal proteins usually expressed by the underlying tumor cause the neurologic symptoms [1]. The detection of these antibodies has provided diagnostic tests that allow recognition of the disorder as paraneoplastic and direct the search of the tumor to selected organs [2]. A better understanding of the function of the paraneoplastic neuronal (or onconeuronal) antigens along with modelling PND in animals results in improved treatment strategies. For the clinician who currently confronts these patients, however, the best chance to affect the neurologic outcome depends on: (1) the prompt diagnosis of the disorder, (2) the early discovery and treatment of the tumor, and (3) the use of immunotherapy. Likewise, any clinical features or tests suggesting that the patient's syndrome is not a PND are also important to prevent delays incurred by unnecessary oncologic evaluations.In 60% of patients who have PND the neurologic symptoms develop before the presence of cancer is known, so these patients are usually seen first by general practitioners or neurologists [6]. In an attempt to improve the recognition of these syndromes, the authors recently proposed a logical approach to the management of limbic encephalitis and postulated that many patients without well-characterized antibodies harbor novel immune responses [6,7]. This approach takes into consideration the type of syndrome, the neuroimaging and cerebrospinal fluid (CSF) findings, and whether the autoantigens are intracellular or are located in the cell membrane. Disorders associated with intracellular autoantigens usually associate with cytotoxic T-cell mechanisms and are less likely to improve than are disorders that associate with autoantigens in the cell membrane. This review summarizes the authors' findings of limbic encephalitis and postulate that a similar approach can be used for syndromes involving other areas of the nervous system.

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Remission of Cerebellar Dysfunction after Pneumonectomy for Bronchogenic Carcinoma

Cited by 66 publications

References 5 publications

Paraneoplastic cerebellar degeneration

Paraneoplastic cerebellar degeneration

Cerebellar cortical degeneration with ovarian carcinoma

Clinical and Immunological Diversity of Limbic Encephalitis: A Model for Paraneoplastic Neurologic Disorders

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