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)

A case of multiple myeloma forming an intracranial mass which invaded the skull base was reported. A 72-year-old woman was admitted to the hospital because of left oculomotor paresis. Plain craniograms showed multiple punched out lesions. A CT scan demonstrated a mass lesion, which was homogeneously slightly enhanced with contrast medium, in the middle cranial fossa. MRI, both T1 and T2 weighted images, showed an isodensity mass. In the carotid angiograms the tumor was fed by the right branches of the cavernous portion of the internal carotid artery and the maxillary artery. Laboratory data were as follows: ESR: 132mm/30min, serum TP: 9.0g/dl, IgG: 4670mg/dl, IgA: 430mg/dl, and urinary Bence-Jones protein was detected. Bone marrow biopsy of the illiac bone demonstrated myeloma cells. During hospitalization oculomotor paresis disappeared, and the patient was treated with intramuscular interferon-alpha. Multiple myeloma which invades the skull base is rare, and only 10 cases have been reported since 1977. Moreover, the biclonal type is only 0.5% of all multiple myelomas.
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PMID:[A case of multiple myeloma (biclonal type) associated with an intracranial mass invading the skull base and oculomotor palsy]. 176 45

Studied were the acute and subchronic toxicity of monensin-Na in pigs. The investigations were carried out with elancoban-100, containing 10 per cent monensin-Na. A total of 46 pigs were used, weighing 15 to 60 kg. The preparation was applied individually via the nose or with the feed. It was found that nasally at 5 mg/kg the preparation did not lead to intoxication; rates of 10 and 20 mg/kg proved toxic, and a dose of 30 mg/kg was lethal. Feed containing 300 ppm of monensin-Na given but once led to intoxication and death with part of the animals. Pig tolerated well continuous (33 days) intake of feed that contained the sodium salt of monensin in concentrations of 120 and 240 ppm - no changes in the general status and behaviour were observed, nor were there any deviations in the morphologic and biochemical composition of the blood. It was demonstrated that the low amounts of monensin stimulated the weight gain of pigs. On the other hand, the clinical picture of the intoxication consisted in going off feed, higher pulse and respiration rates, involvement of the nervous system (depression of the nociceptive, eye closure, and ear reflexes, paresis of the hind limbs, and in severe cases - of the forelimbs too), hematuria in most of the animals, higher SGPT activity, and delayed ESR. Morphologically, there were vascular and slightly manifested degenerative changes in the parenchymal organs, red to brown urine in the bladder, strongly enlarged gallbladder, and catarrhal and hemorrhagic gastroenteritis. Histologically, there was granular and fatty degeneration of the kidneys, liver, and heart, hyperemia, perivascular and pericellular edema and degenerative changes in the glial cells of the berebrum, cerebellum, and medulla oblongata.
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PMID:[Toxicity of sodium monensin for pigs]. 734 Jan 8

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

Sixteen patients (8 female, 8 male) with primary angiitis of the CNS (PACNS), were followed prospectively in a vasculitis clinic. Diagnosis was by angiography in patients without underlying disease. Median age at diagnosis was 36.5 years, and median duration of follow-up was 28 months. Onset was acute in 14 patients (88%), with 3.5 weeks (median) from onset symptoms to diagnosis. Three women developed symptoms within 3 weeks postpartum. The most frequent symptoms were severe headaches (12, 75%), stroke (6, 30%), transient ischaemic attack (TIA) (4, 28%), seizures (7, 44%), visual aberration (3, 19%), and cognitive impairment (5, 31%). Laboratory data included high ESR (2, 13%), leucocytosis (8, 80%), thrombocytosis (1, 6%), positive antinuclear antibody titre (3, 15%), and high levels of complement (5, 31%). Lumbar puncture was performed in 12 patients (75%). CSF analysis was abnormal in five patients (42%). EEG was abnormal in 5/9 patients. The major CT/MRI scan findings were cerebral haemorrhage (4, 25%), brain infarcts (5, 31%), brain atrophy (2, 13%) and non-specific lesions (2, 13%). Four patients had normal studies. All patients received corticosteroids (CS), and five were treated with oral cyclophosphamide. Two patients relapsed despite CS and cyclophosphamide therapy. All patients are alive, and at the last assessment, eight had a permanent neurological deficit, which included paresis (3, 19%), neurocognitive abnormalities (2, 13%), visual loss (2, 13%) and seizure activity (5, 31%). Our data suggest a non-progressive, non-fatal course in those PACNS patients diagnosed angiographically and treated with CS with or without cyclophosphamide.
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PMID:Primary angiitis of the CNS diagnosed by angiography. 804 67

A 22-year-old female noted a low grade fever and swelling of the cervical lymph nodes in May 1997, and later developed a dry cough. She was diagnosed to have interstitial pneumonitis, and then administration of corticosteroids alleviated her symptoms. On February 6, 1998, however, a high fever recurred and her swollen cervical lymph node on the right side was biopsied on February 9, 1998. A histological examination revealed an increased number of histiocytes and karyorrhexis of the lymphocytes in the paracortical areas, and she was therefore diagnosed to have histiocytic necrotizing lymphadenitis. She could not fully elevate her arm on February 16, 1998. On admission, her cervical lymph node was swollen on the left side. A neurological examination revealed a marked weakness of the right deltoid muscle, moderate weakness of the right latissimus dorsi, triceps and brachioradialis muscles and also a mild weakness of the serratus anterior, supra- and infra-spinatus, and biceps brachii muscles. The muscle power of the other muscles were normal and no muscle atrophy was evident. Winging of the right scapula was observed. The deep tendon reflexes were normal in all four limbs, and her sensation was also normal. No cerebellar sign was found. The Jackson, Spurling, Allen, Morley and Adson tests were all negative. ESR was mildly elevated to 18 mm/hr, but CRP was negative. RF, ANA and anti-SS-A and SS-B antibodies were positive, whereas LE-test, direct and indirect Coombs tests and other autoantibodies were negative. Needle EMG disclosed fasciculation potentials in the right triceps muscle and polyphasic waves in the right deltoid muscle. MRI showed gadolinium-enhancement of the right brachial plexus. Although an abnormal accumulation of gallium was detected in the right parotid and bilateral submandibular glands, no sicca symptoms were found and the Schirmer test findings were normal. Oral prednisolone (50 mg/day with gradual tapering) alleviated both her symptoms and the gadolinium-enhancement of the right brachial plexus. As a result, her right upper limb paresis was thus considered to have been caused by right brachial plexus neuritis, which was probably associated with histocytic necrotizing lymphadentis. Although acute cerebellar ataxia and meningitis have previously been reported to be complicated with histiocytic necrotizing lymphadenitis, this is the first report to describe the complication of peripheral neuritis with this condition.
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PMID:[A case of subacute necrotizing lymphadenitis complicated with brachial plexus neuritis]. 1020 79

A 15-year-old girl presented with headache in the left retro-orbital area associated with double vision. She had a history of migraine headaches since the age of 9, and her mother also had suffered from migraine. The patient had experienced a similar episode at the age of 13, which resolved without any treatment in a day. On examination, two days after the onset of diplopia the patient had left ptosis and paresis of inwards and downwards in the left eye. Her pupils were isocoric, and the light reflex was prompt. MRI of the brain showed thickening and enhancement of the left third nerve through the cistern portion, especially at the oculomotor midbrain exit. No cavernous sinus involvement was noted. Results of the hemogram, ESR, and CSF were normal. The oculomotor palsy resolved spontaneously within six days. A follow-up MRI two months later demonstrated a marked lessening of enhancement at the oculomotor nerve but did not completely disappeared. These serial MRI abnormalities are thought to be important and typical findings seen in the patients of ophthalmoplegic migraine.
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PMID:[MRI abnormalities of the oculomotor nerve in a case of ophthalmoplegic migraine]. 1450 56

Churge-Strauss Syndrome belongs to systematic, necrotic inflammation of medium and small vessels diseases. In this paper it is presented a case of 63 years old man with benign asthma, recognized six month earlier. Later occurs fever, difficulties with breathing, cough, fast progressing paresis of tree limbs, thinning and nephrotic syndrome with fast growing renal failure. Base for recognition was clinical picture and laboratory tests which showed elevetion of inflammation parameters (CRP, ESR), eosinophilia (18%) and p-ANCA antibodies. Treatment with glucocorticosteroids and cyclophosphamide was started. After six month proteinuria decreased. Paresis regressed and patient's movement abilities were improved. Renal failure stayed in fourth stadium of chronic renal disease. The aim of this paper is presentation diagnostic difficulties of Churge-Strauss Syndrome of atypical course with fast growing renal failure with neurological complications.
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PMID:[Rapid course of Churge-Strauss syndrome--since appearance of asthma till development of renal failure and neurological complication]. 2256 82