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Biomedical subjects

N E Anderson

Publications and source records attributed to N E Anderson.

At least 55 records · Page 3Linked to original sources
PubMed1988

Expression of an antigen in small cell lung carcinoma lines detected by antibodies from patients with paraneoplastic dorsal root ganglionpathy.

We have identified an autoantibody that reacts with a neuronal nucleoprotein in the serum of patients with small cell lung carcinoma (SCLC) and the paraneoplastic syndrome, subacute sensory neuronopathy (SSN). A similar antigen has been found in the tumor from one of these patients. To determine the distribution of this antigen, immunoblots of a homogenate from the SCLC of another patient with SSN, six SCLC cell lines from patients without SSN, five non-SCLC cell lines, and one ovarian carcinoma cell line were reacted with serum from five patients with SCLC and SSN. Control sera were obtained from two patients with SSN without cancer, two patients with SSN associated with tumors other than SCLC, two patients with paraneoplastic cerebellar degeneration, and five patients with SCLC but no SSN. The sera from all five patients with SCLC and SSN identified a Mr 35,000 to 40,000 antigen in neurons, in all of six SCLC cell lines and in the SCLC tumor homogenate. The antigen was not detected in other tumor cell lines. Control sera did not react with these bands, in either neurons or SCLC cell lines. Bound IgG was eluted from the blot of one SCLC cell line after reaction with SSN serum. Eluates from the Mr 35,000 to 40,000 area reacted with neuronal nuclei in the cerebral cortex by an immunoperoxidase technique; eluates from other areas of the blot were negative. These findings support the hypothesis that the autoantibody in SSN arises in reaction to an antigen shared between SCLC and neuronal nuclei.

Antibodies, Neoplasm↗
PubMed1988

An antineuronal autoantibody in paraneoplastic opsoclonus.

Sera from 7 patients with paraneoplastic opsoclonus were examined for antineuronal autoantibodies. An antibody against neuronal nuclei was found in serum from a patient with breast cancer, opsoclonus, and ataxia. This antibody recognized 53- to 61-kDa and 79- to 84-kDa antigens in immunoblots of neurons. Antineuronal antibodies were not found in other patients with paraneoplastic opsoclonus.

Adult↗
PubMed1988

The metabolic anatomy of paraneoplastic cerebellar degeneration.

Eleven patients with acquired cerebellar degeneration (10 of whom had paraneoplastic cerebellar degeneration [PCD]) were evaluated using neuropsychological tests and 18F-fluorodeoxyglucose/positron emission tomography to (1) quantify motor, cognitive, and metabolic abnormalities; (2) determine if characteristic alterations in the regional cerebral metabolic rate for glucose (rCMRGlc) are associated with PCD; and (3) correlate behavioral and metabolic measures of disease severity. Eighteen volunteer subjects served as normal controls. Although some PCD neuropsychological test scores were abnormal, these results could not, in general, be dissociated from the effects of dysarthria and ataxia. rCMRGlc was reduced in patients with PCD (versus normal control subjects) in all regions except the brainstem. Analysis of patient and control rCMRGlc data using a mathematical model of regional metabolic interactions revealed two metabolic pattern descriptors, SSF1 and SSF2, which distinguished patients with PCD from normal control subjects; SSF2, which described a metabolic coupling between cerebellum, cuneus, and posterior temporal, lateral frontal, and paracentral cortex, correlated with quantitative indices of cerebellar dysfunction. Our inability to document substantial intellectual impairment in 7 of 10 patients with PCD contrasts with the 50% incidence of dementia in PCD reported by previous investigators. Widespread reductions in PCD rCMRGlc may result from the loss of cerebellar efferents to thalamus and forebrain structures, a "reverse cerebellar diaschisis."

Adolescent↗
PubMed1988

Paraneoplastic cerebellar degeneration: clinical-immunological correlations.

Four different antineuronal autoantibodies have been identified in 23 of 47 patients with paraneoplastic cerebellar degeneration (PCD). The most common, an antibody against 34- to 38-kDa and 62- to 64-kDa protein antigens in the cytoplasm of Purkinje cells, was found in 18 patients. It is a highly specific marker for a severe stereotypical subacute pancerebellar syndrome of truncal and appendicular ataxia, dysarthria, and nystagmus in women with cancer (usually ovarian or breast carcinoma). Different anti-Purkinje cell antibodies (APCA) were found in 2 other patients with PCD. With two possible exceptions, an APCA was not found in patients with other neurological diseases, with cancer not associated with neurological symptoms, or in normal subjects. Antibodies reactive with neuronal nucleoproteins were identified in 3 other patients with PCD: an antibody that recognized 35- to 40-kDa neuronal antigens was found in 2 women with small-cell lung carcinoma, while an antibody in a woman with breast carcinoma identified 53- to 61-kDa and 79- to 84-kDa antigens. Detection of an antineuronal antibody in a patient without known cancer should prompt a careful search for a tumor at a site appropriate to the antibody type.

Adult↗
PubMed1988

Opsoclonus, myoclonus, ataxia, and encephalopathy in adults with cancer: a distinct paraneoplastic syndrome.

The clinical and pathological findings in 4 adults with cancer and opsoclonus were compared with those of 15 other patients described elsewhere. The clinical syndrome of paraneoplastic opsoclonus is characterized by the acute onset of opsoclonus and truncal ataxia, often accompanied by encephalopathy, myoclonus and a cerebrospinal fluid pleocytosis. Unlike most other paraneoplastic syndromes, the course is often remitting and relapsing. Neuropathological examination in 3 of our patients showed lymphocytic cuffing of occasional blood vessels throughout the central nervous system, associated with a mild, diffuse proliferation of microglia in 1 patient. Apart from a mild, patchy loss of Purkinje cells in 1 patient, there was no loss of neurons from the cerebellum, brainstem, cerebral hemispheres, or spinal cord. These patients differ from those with the more common paraneoplastic cerebellar degeneration by the predominance of truncal over limb ataxia, the presence of myoclonus, the absence of severe dysarthria, a tendency for remission, and the preservation of Purkinje cells.

Ataxia↗
PubMed1988

A variant of the anti-Purkinje cell antibody in a patient with paraneoplastic cerebellar degeneration.

An anti-Purkinje cell antibody was found in the serum and CSF of a man with adenocarcinoma of the lung and paraneoplastic cerebellar degeneration (PCD). This antibody differed from the autoantibodies found in patients with gynecologic cancer and PCD in that it produced a different pattern of Purkinje cell cytoplasmic staining, did not react with PCD antigens in Purkinje cell Western blots, and the antigen had a different species distribution. Unlike the antinuclear antibody found in patients with PCD and small-cell lung carcinoma, the antigen was restricted to the cytoplasm of Purkinje cells. If autoantibodies are important in the pathogenesis of PCD, this case illustrates that they can recognize different antigenic epitopes in the nervous system, but cause similar clinicopathologic syndromes.

Adenocarcinoma↗
PubMed1988

Autoantibodies in paraneoplastic syndromes associated with small-cell lung cancer.

An antineuronal autoantibody has been identified in serum from 14 patients, 8 women and 6 men, with small-cell lung carcinoma (SCLC) and a neurologic disorder. Neurologic symptoms began prior to diagnosis of the SCLC in 12 patients. The dominant neurologic disorder was a subacute sensory neuronopathy (SSN) in eight patients, SSN plus lower motor neuron weakness (2 patients), SSN plus autonomic neuropathy (1 patient), cerebellar ataxia (1 patient), myelopathy (1 patient), and multifocal nervous system disease (encephalomyelitis) in one patient. The presence of the same autoantibody in patients with SSN, encephalomyelitis, and autonomic neuropathy suggests that these diseases are different manifestations of the same nosologic process. With one exception, treatment of the tumor, immunosuppressive drugs, and plasmapheresis did not influence the course of the neurologic illness. The autoantibody was not identified in sera from more than 400 controls subjects, including patients with SSN associated with other tumors, SSN without malignancy, other paraneoplastic syndromes, and SCLC without neurologic symptoms. The autoantibody is a highly specific marker of the paraneoplastic syndromes associated with SCLC and its detection in a patient not known to have cancer should prompt a careful search for SCLC.

Aged↗
PubMed1987

Infarction of the conus medullaris.

We describe 5 patients who presented with an acute cauda equina syndrome, which we believe was due to infarction of the conus medullaris. In 3 patients, the onset was spontaneous, and in 2 patients it was secondary to temporary occlusion of the distal aorta during medical manipulation. Pain in the buttocks and posterior thighs was a prominent initial symptom in the 3 patients with unprovoked attacks. The main clinical features were profound impairment of bowel and bladder function and of perianal and perineal sensation (S3 to S5 segments). There was sensory and motor impairment in the legs of variable extent, most marked in the S1 and S2 segments, but extending as high as L4 in 2 patients. In 1 patient, ischemic changes in the conus medullaris were confirmed post mortem. Ischemia confined to the caudal tip of the spinal cord is rare, and an underlying anomaly of the pattern of arterial supply is a likely predisposing factor. Four patients had partial return of function over a period of weeks.

Aged↗
PubMed1987

Autoimmune pathogenesis of paraneoplastic neurological syndromes.

"Remote effects" of cancer on the nervous system (paraneoplastic syndromes) are disorders of the nervous system of unknown cause that occur almost exclusively, or with greatly increased frequency, in patients with identifiable or occult cancer. There are several hypotheses concerning the pathogenesis of these rare disorders. One hypothesis is that the underlying tumor and portions of the nervous system share antigens and that an autoimmune response generated against the tumor causes the nervous system disorder. Evidence supporting this hypothesis includes the ability to transmit the Lambert-Eaton Syndrome (a paraneoplastic syndrome involving the neuromuscular junction) to experimental animals by infusing IgG from patients with the disorder, the presence of autoantibodies against Purkinje cell neurons in some patients with paraneoplastic cerebellar degeneration, and the presence of autoantibodies against many neurons in patients with sensory neuronopathy and encephalomyelitis. Other evidence supporting the hypothesis is presented in this review.

Antibodies, Monoclonal↗
PubMed1987

Chronic meningitis without predisposing illness--a review of 83 cases.

Eighty-three previously healthy patients with chronic meningitis presenting to a general hospital were reviewed. The single most common cause was tuberculosis (40 per cent) with cryptococcosis (7 per cent), malignancy (8 per cent) and other definable causes much less frequent. In one-third of patients (34 per cent) no cause was found although most appeared to respond to treatment either with anti-tuberculosis drugs or steroids. There were some differences in clinical presentation, the clinical picture being most characteristic in tuberculous meningitis and malignant meningitis. However, there were frequent exceptions to any general rule and, particularly in adults, the clinical features and changes in cell count, protein and glucose in the cerebrospinal fluid (CSF) did not reliably distinguish one form of chronic meningitis from another. Cerebral and meningeal biopsy produced disappointing results with respect to practical guidance in management. It is often necessary to begin treatment before a cause has been identified. Important points in management include the early use of anti-tuberculosis treatment and the difficulty in deciding on a trial of treatment with corticosteroids or amphotericin B. Not emphasised in previous reports is a subgroup of patients with idiopathic chronic meningitis who are responsive to treatment with steroids. Those patients tend to follow a more prolonged indolent course and often require long-term immunosuppression to control symptoms.

Chronic Disease↗
PubMed1986

Activation of epileptiform activity by mental arithmetic.

Activation of epileptic seizures or electroencephalographic epileptiform discharges by mental calculation is rare. We report the case of a 34-year-old right-handed accountant with a 20-year history of generalized tonoclonic seizures. Although clinical seizures were unrelated to performance of mental arithmetic, epileptiform activity appeared when she attempted difficult mental arithmetic. Apart from one occasion, epileptiform discharges did not impair her ability to provide accurate answers to mathematical problems.

Adult↗
PubMed1986

Somatosensory evoked potentials in syringomyelia.

The two types of upper limb somatosensory evoked potential abnormality observed in nine patients with syringomyelia were reduced amplitude or absent cervical potentials and an abnormal central conduction time. Although this pattern of abnormalities resembles that observed in other intrinsic spinal cord lesions, it differs from peripheral nerve diseases and cervical radiculopathy in which the central conduction time is normal.

Adolescent↗
PubMed1986

The natural history of syringomyelia.

A retrospective analysis was made of the clinical course in 24 patients with syringomyelia who had not been treated surgically. 5 patients died during follow-up, and the survivors were followed for 1 to 37 (median 9) years after diagnosis. 8 of the 19 survivors followed a slowly progressive course over 4 to 46 (median 27) years but only 3 were severely disabled. 3 patients had an intermittent progression of symptoms, often with long intervening periods of stability. 8 patients had no progression in symptoms after presentation; none of these patients was severely disabled at last follow-up. It is concluded that the natural history of syringomyelia is unpredictable. Some patients have no further progression in symptoms for many years after onset. Prolonged survival is usual even among those patients with a slowly progressive deficit. The uncertain progression of the clinical course presents considerable difficulties in the timing of surgical intervention and in interpretation of the results.

Adolescent↗