Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinicopathological and immunohistochemical studies were performed in a patient with paraneoplastic limbic encephalitis, myelitis, sensory neuropathy and cerebellar degeneration secondary to small cell lung cancer. A 67-year-old male smoker developed orthostatic dizziness 6 months prior to admission. Over the following months, his wife noticed that he became forgetful and confused. Over the next three weeks, he became unable to sit or stand unaided and admitted to our service. On admission, he was lethargic and disoriented in time and place. Neurological examination revealed marked limb weakness with distal dominant muscle atrophy. A chest radiograph demonstrated a mass in the right middle lobe and a bronchial biopsy revealed a small cell carcinoma. CT scan and MRI of the brain revealed abnormalities in the bilateral medial temporal lobes and putamen. He was treated with anti-cancer chemotherapy, but died of respiratory failure after 13 months illness. Postmortem examination showed a mass in the right middle lobe of the lung. No tumor metastases were noted in the nervous tissue. Microscopical examinations of the nervous system revealed neuronal loss, astrogliosis and perivascular and parenchymatous lymphocytic infiltration in the hippocampus, subiculum, amygdala, putamen, medulla oblongata, spinal cord and dorsal root ganglia. Loss of Purkinje cells was also seen in the cerebellum without lymphocytic infiltration. Immunohistochemical analysis of the patient's serum and CSF by the use of adult rat brain revealed immunoreactivity at the hippocampal pyramidal neurons CA3 and CA4. At the higher dilution, neuronal nuclei were specifically stained.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A clinicopathological study of a patient with paraneoplastic limbic encephalitis, myelitis, sensory neuropathy and cerebellar degeneration, associated with a unique antineuronal antibody]. 839 16

A 62-year-old man was given a diagnosis of small cell lung cancer, and received 6 courses of combination chemotherapy (PE therapy) composed of cisplatin (80 mg/m2, day 1) and etoposide (100 mg/m2, days 1, 2, 3). Multiple brain metastases were found, and whole brain irradiation (44 Gy) was given. Eleven months after radiotherapy, he suffered from dizziness and abnormal gait. Enhanced CT of the head showed slight enlargement of the lateral ventricles and markedly low density of the white matter, but no evidence of intracranial tumor involvement. A magnetic resonance scan (axial T2-weighted) showed symmetric extensive hyperintensity in the white matter. Treatment-related leukoencephalopathy caused by the PE therapy and whole brain irradiation was diagnosed. He was alive 8 months after the appearance of neurological symptoms, without recurrence of lung cancer. A search of the literature revealed no previous report of leukoencephalopathy related to PE therapy.
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PMID:[Leukoencephalopathy in a patient being treated for small cell lung cancer]. 854 87

Amifostine is a protective agent of normal tissue from adverse effects of radiochemotherapy. It is the prodrug that is dephosphorylated by alkaline phosphatase on plasma membrane into the active form named WR-1065. More than 90 per cent of the drug is cleared from plasma in 6 minutes and the peak tissue concentration is 10-30 minutes after intravenous administration. Amifostine has the selective property to protect normal tissue but not cancer cells by mainly scavenging free radicals induced by radiation and chemocytotoxic agents. Both preclinical and clinical studies of this drug provide the significant protection of hematopoietic progentitors from a broad range of cytotoxic agents such as cyclophosphamide, cisplatin, vinblastine, carboplatin, mitomycin-C, fotemustine, doxorubicin, daunorubicin and radiation as well. Moreover, this drug can protect other normal organs or tissues including kidney, salivary gland, liver, heart, lung and small intestine. Amifostine is quite safe, the two major side effects are vomiting and hypotension, and the minor effects are flushing, sneezing, dizziness, chills, metallic taste etc. The drug was approved by the FDA of U.S.A. for use as a cytoprotectant in cyclophosphamide and cisplatin treatment for advanced ovarian cancer and non small cell lung cancer.
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PMID:Amifostine and hematologic effects. 1080 97

The anti-Hu antibody (HuAb) is directed against RNA-associated neuronal proteins and is known to cause paraneoplastic encephalomyelitis/sensory neuronopathy syndrome mostly when associated with small cell lung cancer (SCLC). Paraneoplastic encephalomyelitis/sensory neuronopathy syndrome with concurrent autonomic neuropathy has been reported to occur in paraneoplastic syndromes, although its occurrence concomitant with acute pandysautonomia is less frequent. The authors describe the clinical, neuropathologic, and serologic features of two cases with an anti-Hu-related paraneoplastic syndrome presenting with progressive autonomic neuropathy. Both patients showed features of dysautonomia, including postural dizziness, abdominal pain, and diarrhea, and symptoms of sensory neuropathy. Investigations disclosed severe sensory and autonomic neuropathy and positive HuAb titers. The disease of patient 1 had a very rapid progression, and the patient died of cardiac arrest within 2 months of the onset of symptoms. The autopsy revealed SCLC. In contrast, the disease of patient 2 had a less aggressive course. An extensive tumor search disclosed SCLC only 28 months after onset of symptoms, and the patient died 1 month later of cardiorespiratory arrest. Autopsies in both cases showed inflammation involving the intermediolateral columns and the dorsal root ganglia. These two cases illustrate the association of early dysautonomia with HuAb-related paraneoplastic syndrome and the variations of clinical, neuropathologic, and serologic findings in these types of cases.
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PMID:Phenotypic and neuropathologic heterogeneity of anti-Hu antibody-related paraneoplastic syndrome presenting with progressive dysautonomia: report of two cases. 1157 Jun

Opsoclonus myoclonus syndrome, one of the paraneoplastic neurological syndromes involving several neurological symptoms that result from "remote effects" of cancer, is a rare disease characterized by opsoclonus, cerebellar ataxia and myoclonus of the trunk and extremities. A 53-year-old man was admitted with dizziness and difficulty walking. Medical examinations led to a diagnosis of opsoclonus myoclonus syndrome. CT scans showed mediastinal and cervical lymphadenopathy, and a diagnosis of small cell lung cancer was made. Steroid therapy and chemotherapy (carboplatin + etoposide) produced significant improvement in the neurological symptoms.
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PMID:[Small cell lung cancer complicated by opsoclonus myoclonus syndrome]. 1999 3

Small cell lung cancer (SCLC) is considered as a disease with poor prognosis and early metastasis with a very short survival. Endobronchial involvement is fairly common finding in SCLC and can cause respiratory symptoms. In this report we present a 47-year-old man diagnosed with small cell lung cancer. In the disease course, primary involvement of right bronchus spread to left bronchus and carina. Scheduled sessions of bronchoscopic interventions with electrocautery and argon plasma coagulation were used to maintain his large airways open. The intrabronchial interventions were accompanied by six courses of cisplatin-based chemotherapy as a standard treatment. Although patient's definite diagnosis was extensive SCLC, he remained in a good condition for 5 years. In last year of his follow up, headache and dizziness were added to his occasional respiratory symptoms. Brain MRI identified metastatic lesion in his brain. Hence, brain radiotherapy was suggested, but he refused further aggressive treatment. Seven months later, he died of brain metastatic lesion. Considering long survival of this patient with adequate and proper scheduled endobronchial interventions along with standard courses of chemotherapy, we conclude that this combined treatment strategy in patients with endobronchial involvement might increase survival.
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PMID:Long-term survival of a small cell lung cancer patient with proper endobronchial management. 2342 51

Our case report involves a Chinese patient who was presented to our hospital with the chief complaint of dizziness and double vision for one week. He was diagnosed with small cell carcinoma of lung in the past. The patient undertook various test at our hospital. His MR scan revealed an intraventricular metastasis from small cell carcinoma of lung which is very rare. We have analyzed the clinical data of this patient and related literature. We report this case to increase the awareness of this rare metastasis of small cell carcinoma of lung.
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PMID:A rare case of small cell carcinoma of lung with intraventricular metastasis. 2849 95

A 63-year-old female who developed dizziness, diplopia and subsequent gait disturbance from September X-1 year was analyzed. The first neurological findings in May X year revealed cerebellar ataxia, weakness in the proximal limbs, decreased tendon reflexes, and autonomic symptoms (ADL:mRS 3). Furthermore, an incremental phenomenon was observed in the repetitive nerve stimulation test, and she was diagnosed with Lambert-Eaton myasthenic syndrome (LEMS) based on the serum P/Q-type calcium channel (VGCC) antibody positivity. In addition, small cell lung cancer was detected by chest CT and bronchoscopy, and her cerebellar ataxia was diagnosed as paraneoplastic cerebellar degeneration (PCD). Therefore, the patient underwent chemotherapy and radiotherapy from June in X year. Six months after initiation of treatment, her cerebellar ataxia had almost disappeared and she could walk without assistance (ADL:mRS 1). The P/Q-type VGCC antibodies were also negative at that time. Cases wherein cerebellar ataxia resolved almost completely in parallel with disappearance of the serum P/Q-type VGCC antibodies are of great interest. We conducted a systematic literature review of PCD-LEMS cases in Japan reported since P/Q-type calcium channel antibody measurement was reported in 1995. As a result, 13 cases (including our study) that concurrently displayed cerebellar ataxia and LEMS were selected. The average age of the 13 patients (10 males and 3 females) was 61.5 years. Small cell carcinoma was complicated in 11 patients (10 in the lung and 1 in the oropharynx); in the other 2 patients, cancer was not found at the time of reporting (the observation period was as short as 1-2 months). The time from onset to treatment ranged between 1 week and 10 months. While 1 of the 13 patients developed cerebellar ataxia during the subsequent course of the treatment, the remaining 12 had already developed cerebellar ataxia and LEMS symptoms, although their main neurologic finding was cerebellar ataxia and they were subsequently diagnosed with LEMS after electrophysiological testing and autoantibody detection. Small cell carcinoma was found in 11 patients. We define the pathology following such a certain clinical course as PCD-LEMS. The P/Q-type VGCC antibodies were positive in 11 of the 13 cases, although their antibody titers were not necessarily very high. Treatment for the associated small cell carcinoma might have improved the neurological findings in 9 of the 11 PCD-LEMS patients. The P/Q-type VGCC antibodies were measured before and after the treatment. The PCD-LEMS symptoms improved in all patients and their antibody titers decreased. These findings indicate that P/Q-type VGCC antibodies are involved in the pathology of PCD-LEMS. Appropriate and timely treatment, at least in PCD-LEMS patients in Japan, that actively treats any associated cancer can be expected to improve not only life prognosis but also cerebellar ataxia. (Received October 15, 2018; Accepted November 5, 2018; Published January 1, 2019).
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PMID:[Paraneoplastic Cerebellar Degeneration with Lambert-Eaton Myasthenic Syndrome: A Report of an Effectively Treated Case and Systematic Review of Japanese Cases]. 3071 46