Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028738 (nystagmus)
 7,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of primary position downbeating nystagmus due to an occult breast carcinoma in a 57-year-old woman with progressive oscillopsia and truncal ataxia. Acute nausea and vomiting precipitated hospitalization. Magnetic resonance imaging of the brain was normal, though a sterile mononuclear cerebrospinal fluid pleocytosis was present. Search for an occult malignancy disclosed an adenocarcinoma of the breast. Radical mastectomy and oral corticosteroid therapy did not alter the clinical course of the paraneoplastic syndrome in our patient. Primary position downbeating nystagmus is an uncommon manifestation of an occult malignancy. Our report and review of the literature suggests that investigations necessary for the diagnosis of occult malignancies of the lung, breast, uterus, and ovary be included in the search for cryptic causes of downbeating nystagmus.
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PMID:Paraneoplastic downbeating nystagmus. A sign of occult malignancy. 285 13

Invasive tumors of the pituitary gland were diagnosed in 8 dogs. Seven of the dogs had been treated for pituitary-dependent hyperadrenocorticism before the onset of neurologic signs. All 8 dogs had behavior abnormalities and similar neurologic signs: 6 dogs had rotary nystagmus and 7 dogs had symmetric tetraparesis. Once neurologic signs developed, the clinical course in all 8 dogs had a mean duration of 4.7 +/- 2.0 months before death or euthanasia; 5 dogs had a clinical course of less than or equal to 2 months. Necropsy was performed in 7 dogs. The histologic diagnosis was malignant pituitary adenocarcinoma in 2 dogs and pituitary adenoma in 5 dogs.
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PMID:Neurologic, endocrinologic, and pathologic findings associated with large pituitary tumors in dogs: eight cases (1976-1984). 319 68

Clinicopathological correlations are reported in a case with bilateral isolated infarcts in the posterior part of the parietal lobes, due to nonbacterial thrombotic endocarditis accompanying pancreatic adenocarcinoma. The initial left-sided infarct induced right visual neglect, impairment of right-beating optokinetic nystagmus (OKN), optic ataxia, Gerstmann's syndrome and apraxia. After the right-sided infarct, which occurred six weeks later, bilateral visuo-oculomotor disturbances were observed, including peripheral visual inattention, disorder of visually guided saccades, severe impairment of foveal smooth pursuit and OKN slow phase. The lesion on the left involved the upper part of the angular gyrus and a part of the adjacent superior parietal lobule (SPL). That on the right involved the supramarginal gyrus and extended posteriorly into the superoanterior extremity of the angular gyrus, into both margins of the adjacent intraparietal sulcus and into a small part of the SPL. As the oculomotor deficits and the peripheral visual inattention were bilateral after the second infarct, they probably resulted from the lesion of homologous areas in both cerebral hemispheres. The zone damaged in common included a small part of the SPL, the superoanterior extremity of the angular gyrus, and the adjacent intraparietal sulcus and a small portion of the subcortical white matter. This restricted cerebral zone could therefore, in man, be implicated both in the control of all visually guided eye movements and in visual attention. It is further suggested that two corticofugal pathways are implicated in visually guided saccades, the first arising from the frontal eye fields and projecting directly onto the premotor structures in the brainstem, the second arising from the posterior parietal cortex (probably mainly the intraparietal sulcus adjacent to the angular gyrus) and including a relay in the superior colliculus before reaching the premotor structures. Lastly, the findings support the hypothesis that optic ataxia results from interruption of direct and/or crossed occipitofrontal pathways coursing in the deep white matter of the parietal lobe.
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PMID:Infarcts of both inferior parietal lobules with impairment of visually guided eye movements, peripheral visual inattention and optic ataxia. 394 58

Paraneoplastic cerebellar degeneration (PCD) is a rare manifestation of cancer, characterized clinically by subacute progressive ataxia, dysarthria and nystagmus. The pathological hallmark of PCD is a severe, diffuse loss of Purkinje cells. PCD occurs most frequently in association with small cell carcinoma of the lung and adenocarcinoma of the ovary, but it has also developed in patients with carcinoma of the breast, malignant lymphoma, and various cancers. Autoantibodies against cerebellar Purkinje cells have been frequently observed in the serum or cerebrospinal fluid (CSF) from patients with PCD. The cause of PCD is unknown, but the presence of these autoantibodies in some patients suggests that the pathogenesis may be immune mediated. The potential role of the autoantibody in the pathogenesis of PCD is discussed.
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PMID:[Paraneoplastic cerebellar degeneration]. 799 1

Paraneoplastic cerebellar degeneration is a rare remote effect of ovarian and breast carcinoma especially, and is characterised clinically by rapidly evolving pancerebellar symptoms. A woman aged 83 developed progressive vertigo, cerebellar ataxia, nystagmus and dysarthria. The cerebrospinal fluid showed slight mononuclear pleocytosis, elevated total protein and IgG concentrations, and oligoclonal bands. A magnetic resonance investigation performed within the first month of symptoms was normal. A left pelvic mass was found, possibly a carcinoma of the colon or the left ovary. Cancer antigen 125 was elevated in the serum and antibodies against Purkinje cells (anti-Yo antibodies) were demonstrated in the serum and cerebrospinal fluid. These results suggested a carcinoma of the ovary as primary site of cancer. Autopsy revealed a left ovarian adenocarcinoma and marked loss of Purkinje cells in the cerebellum. The case illustrates that anti-Yo antibodies may serve as a marker not only for paraneoplastic cerebellar degeneration, but also for the nature of the neoplasm that caused it.
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PMID:[Paraneoplastic cerebellar degeneration. A case report]. 934 Aug 52

We report a 65-year-old woman with paraneoplastic cerebellar degeneration (PCD) who showed reduced cerebellar metabolism with preserved blood flow. She was admitted to Gunma University Hospital because of progressive gait and speech disturbances. Neurologic examination revealed nystagmus, dysphagia, explosive speech, reduced muscle tone in limbs, and marked truncal and limb ataxia, and mild hypesthesia in hands and feet. Cranial MRI demonstrated slight cerebellar atrophy. Laboratory findings disclosed high levels of serum CA19-9 and other tumor markers, and positive anti-Yo antibody, indicating that she had PCD. A specimen obtained from an axillary lymph node revealed metastasis of poorly differentiated adenocarcinoma, although systemic and vigorous checkup failed to find its origin. Cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) were measured using positron emission tomography (PET) 15 months after the onset. CMRO2 was clearly decreased in the cerebellum, while CBF was almost normal. Moreover, PET with 2 18F-fluoro-2-deoxy-D-glucose (FDG) revealed that glucose metabolism was also reduced in the cerebellum. Single photon emission tomography using 99mTc-ethyl cysteinate dimer (ECD) showed a normal blood flow pattern in the whole brain. These results indicated that uncoupling of circulation and metabolism in the cerebellum of this patient. There are several reports showing uncoupling of cerebral perfusion and metabolism in ischemic disorders, encephalitis, mitochondrial diseases, brain tumors, epilepsy and Gaucher disease, although its pathophysiology is not elucidated. Because anti-Yo antibody evidently gives a suppressive influence on the cerebellar neurons, understanding the way the autoantibody acts may give a clue to the mechanism of reduced cerebellar metabolism with preserved perfusion in PCD.
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PMID:[Uncoupling of cerebellar blood flow and metabolism in paraneoplastic cerebellar degeneration: report of a case]. 936 81

A 65-year-old woman was operated for gastric adenocarcinoma in 1989. Six years later, peritonitis carcinomatosa, swelling of periaortic lymphnodes and high serum CA-125 were discovered. She received chemotherapy with 5-FU and cisplatin resulting in reduction of ascites. In September, 1998, the swelling of left supraclavicular lymphnodes and the elevation of serum CA-125 reappeared. Pathological diagnosis of supraclavicular lymphnodes was adenocarcinoma. Serum CA-125 was normalized by chemotherapy using cisplatin, farumorubicin and endoxan. However, unsteadiness appeared since December 10, 1998 followed by dysarthria and involuntary movement of neck and upper limbs. These symptoms progressed subacutely. The physical examination on admission revealed swelling of left suraclavicular lymphnodes, nystagmus on lateral gaze, saccadic eye movement on smooth pursuit and severe cerebellar ataxia. In addition, resting tremor of 3-4 Hz was observed at right hand, left wrist and neck which tended to increase amplitude by calculation. Similar movements were seen in the left first toe, though the frequency was lower. Brain MRI revealed mild cerebellar atrophy. She was diagnosed as paraneoplastic cerebellar degeneration (PCD) by serum anti Yo antibody and clinical course. The study of HLA showed positive link to A4 without A24. The primary focus of adenocarcinoma in cervical lymphnodes was suggested to be ovary rather than stomach due to the pattern of immunostaining for cytokeratin, CEA and CA125, although no carcinoma was found in ovarium clinically. The feature of this case is a PCD with resting tremor of frequency of 3-4 Hz and negative link to HLA-A24 in Japanese.
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PMID:[A case of paraneoplastic cerebellar degeneration with resting tremor]. 1143 63

We report a 71-year-old man presenting with paraneoplastic cerebellar degeneration (PCD) associated anti-Yo antibody after surgery for gastric adenocarcinoma. Seven months after partial gastrectomy, he deviated to the right on walking. Furthermore, a feeling of dysarthria appeared and he was unable to sit after 2 months. When he was hospitalized, he showed a disturbance of his eye movement on lower gaze, a nystagmus on lateral gaze, saccadic eye movement on smooth pursuit, cerebellar ataxia, and decreasing of muscle tonus in his extremities. However, no atrophic findings of the brainstem and cerebellum were revealed by brain MRI. He responded poorly to treatment with high-dose methylprednisolone, high-dose immunoglobulin, double filtration plasmapheresis and rehabilitation. There was a strong anti-Yo immunohistochemical staining of the cytoplasm in both the patient's tumor cells and normal cerebellar Purkinje cells. These findings suggest that PCD associated with anti-Yo antibody triggered by adenocarcinoma might occur in this male patient.
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PMID:[Anti-Yo antibody associated paraneoplastic cerebellar degeneration with gastric adenocarcinoma in a male patient: a case report]. 1661 40

We report a case of lung cancer with multiple metastases to the brain and internal auditory canal. A 59-year-old man complained about persistent and progressive vertigo for 3 weeks with rapidly developing left-sided hearing loss and tinnitus. Bilateral intact eardrums and unsteady gait were noted on physical examination. There was no nystagmus. Pure tone audiometry showed left-sided sensorineural hearing loss. Magnetic resonance imaging of the brain revealed multiple intracranial tumors, including of the left-side internal auditory canal, which were interpreted as seeding of metastatic malignancy. Computed tomographic and bronchoscopic biopsy identified an asymptomatic primary pulmonary adenocarcinoma in the right upper lobe of the lungs. This was a rare case of asymptomatic primary pulmonary adenocarcinoma with brain metastases presenting with sudden hearing loss and vertigo.
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PMID:Brain metastasis of non-small cell lung cancer presenting as sensorineural hearing loss and vertigo. 1958 Nov 46

We present a case of a papillary tumour at the cerebellopontine angle in a 41-year-old man. He presented with left-sided facial and ear pain associated with dizziness, nystagmus and hearing loss. CT scan of the temporal bone showed a destructive tumour at the left cerebellopontine angle. Surgical excision was performed and the diagnosis of the endolymphatic sac tumour was made. Endolymphatic tumour is a low grade adenocarcinoma that originates from the endolymphatic sac. The definitive diagnosis requires a combination of clinical features, radiological finding and pathological correlation.
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PMID:Endolymphatic sac tumour. 2287 May 99


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