Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An episode of subarachnoid hemorrhage was seen on a 22-year-old married woman, which followed vaginal spotting and convulsive seizure. The neurological examination revealed bilateral papilledema, retinal hemorrhage, neck stiffness, Kernig's sign abducens paresis on the right. The chest X-ray film showed a spherical mass lesion in the right lung. The pelvic examination disclosed no pathological findings, however, HCG (human chorionic gonadotropin) in the urine increased significantly. Intracranial metastasis of chorioepithelioma was the tentative diagnosis at the admission and the right caroid angiography was performed, which demonstrated a fusiform aneruysm of the right middle cerebral artery beside arterial shift indicating a metastatic mass lesion in the parietal lobe. At surgery the tumor was removed and the arterial change was resected. Histologically the tumor was verified and the aneurysm was produced by metastasis of the tumor to the intima and interruption of the internal elastic membrane. She was placed on the anticarcinogenic agent and later the mass lesion in the chest was operated and irradiated. The postoperative carotid angiography showed another berry-shaped aneurysm arising from the right calloso-marginal artery. After the serial treatment with Actinomycin D the aneurysm disappeared completely and the arterial branch distal to the aneurysm was thrombosed. The patient is still alive 3 years after the onset of illness. An emphasis was placed that the neurosurgeon should be aware of cerebrovascular changes due to metastasis of the chorioepithelioma while making diagnosis of subarachnoid hemorrhage of the female patients who belong to the reproductive age. Intracranial aneurysmal change due to metastatic infiltration to the arterial wall was reported.
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PMID:[Subarachnoid hemmorrhage and aneurysmal change of cerebral arteries due to metastases of chorioepithelioma (author's transl)]. 123 92

We report a 65-year-old woman with progressive multiple cranial neuropathy. She had been suffered from bronchial asthma since 1979 for which prednisolone had been prescribed. She noted an onset of pain around her nose in October, 1989, which extended into the periorbital regions bilaterally. In February, 1990, she was treated with stellate ganglion block and trigeminal nerve block; these treatments partially alleviated her pain. In May of 1991, she noted a difficulty in swallowing solid foods. In November of the same year, she developed right facial paresis; two weeks later, she noted numbness in her left face, and was hospitalized to our service on December 16, 1991. On admission, she was afebrile and general physical examination was unremarkable except for piping rales in her both lung fields. On neurologic examination, she was alert and oriented to all spheres; higher cerebral functions were intact. In the cranial nerves, her olfactory sense was lost bilaterally; her vision was markedly diminished bilaterally only to recognize hand movements; the optic fundi appeared normal; the pupils were isocoric and reacted to light promptly. The extraocular muscles were moderately weak to most of the directions more on the left; no nystagmus was present. Facial sensation was diminished bilaterally; the jaw deviated to right; right facial paresis of peripheral type was present; her hearing was diminished bilaterally more on the right. The movement of the soft palate was diminished on the right side; dysphagia was present; her voice was horse; the gag reflex was diminished. The sternocleidomastoid muscle was weak bilaterally; the tongue appeared normal. Examination of gait was differed because of headache, however, no apparent motor weakness was present. No ataxia or involuntary movement was noted. Deep reflexes were normally elicited and symmetric. Plantar response was flexor. Sensation in the extremities was intact. Kernig's sign was positive at 70 degree leg extension; eyeball tenderness was also present bilaterally, however, no nuchal stiffness was noted. Following abnormalities were present in the laboratory examination: WBC 11,400/microliters, ESR 50 mm/hr, CRP 6.1 mg/dl. The lumbar CSF was under a normal pressure containing 29 WBC/microliters (neutrophils 7, lymphocytes 20, others 2), 67 mg/dl of protein, and 53 mg/dl of sugar; cultures for acid-fast bacilli as well as for other bacteria were negative; no malignant cells were found. A cranial CT scan revealed an isodensity mass in the orbit and ill-defined low density areas in the white matters of the frontal lobes.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 65-year-old woman with headache, facial pain, and progressive multiple cranial neuropathy]. 787 85