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)

Between 1965 and 1982, 52 children with acute lymphoblastic leukemia or non-Hodgkin's lymphoma were found to have central nervous system involvement of their disease. Of this group, 20 developed clinically apparent cranial nerve paresis or palsy. The cranial nerve most frequently affected was No. VII. With therapy, 16 of the patients had objective control of their central nervous system disease. Among these 16 patients, cranial nerve palsies resolved completely in 14, and only two children were left with residual cranial nerve dysfunction. Seven patients received intrathecal chemotherapy before radiation therapy was instituted in an attempt to control their cranial nerve palsies. Cranial nerve palsy resolved in only two of these seven patients. However, the addition of whole-brain irradiation in the remaining five patients reversed cranial nerve dysfunction in four of them. The combination of intrathecal chemotherapy and central nervous system irradiation was successful in reversing cranial nerve dysfunction in 11 of 13 patients in whom central nervous system disease was ultimately controlled. As cranial nerve dysfunction is associated with distressing signs and symptoms, the combination of central nervous system irradiation and intrathecal chemotherapy is important palliative therapy to initiate promptly. Intrathecal therapy alone appears to be inadequate therapy for prompt and durable reversal of symptoms in this group of patients.
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PMID:Cranial nerve involvement in children with leukemia and lymphoma. 658 24

Craniofacial malformations cause great human suffering. The purpose of the experimental studies was to investigate teratogenically induced craniofacial malformations in the rat, and to study if vitamin B6 could prevent the teratogenically induced malformations in the rat. The aim of the clinical investigation was to compare mandibulofacial dysostosis (MFD) with hemifacial microsomia (HFM) and thalidomide-induced malformations restricted to the first and second branchial arches. In the experimental studies we used two different teratogenic agents, etretinate and BAPN (beta-aminoproprionitrile). Vitamin B6 was administered one day prior to and simultaneously with the teratogenic agent. The induced malformations were observed by direct microscopy, histology, differential staining, microdissection and enzyme histochemistry. Knowledge of isoenzymic differentiation was obtained by isoelectric focusing and polyacrylamide gel electrophoresis. The clinical features of 29 patients with MFD, 26 with HFM and seven with thalidomide-induced malformations were investigated. The patients underwent clinical investigations, radiography, tomography, computed tomography, surgical exploration and audiograms. The etretinate-induced syndrome in the rat shows similarities to first and second branchial arch syndromes in man. Defective formation of Meckel's cartilage and the cartilaginous skull base, the zygoma and the middle ear ossicles were prominent features of the observed malformations. The induced malformations were accompanied by increased staining for alkaline phosphatase (APase) in the skull and skull base cartilages and Meckel's cartilage. BAPN induced cleft palate in 95% of the cases and the teratogenically induced cleft palate was accompanied by a pathological differentiation pattern that could be traced by determination of isoenzymes in the palatal shelves as well as in amniotic fluid. Vitamin B6 could prevent the teratogenic malformations induced by etretinate and BAPN in the rat. Comparing MFD, HFM and thalidomide-induced malformations, all syndromes included patients with external, middle and inner ear malformations. Cranial nerve palsy/paresis was only seen in HFM and thalidomide-induced malformations. A relationship between disturbed neural crest cell migration and defects of the first and second branchial arches seems possible.
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PMID:Teratological studies on craniofacial malformations. 920 Mar 51

Cranial nerve palsy in internal carotid artery (ICA) dissection occurs in 3--12% of all patients, but in 3% of these a syndrome of hemicranias and ipsilateral cranial nerve palsy is the sole manifestation of ICA dissection, and in 0.5% of cases there is only cranial nerve palsy without headache. We present two cases of lower cranial nerve palsy. The first patient, a 49-year-old woman, developed left eleventh and twelfth cranial nerve palsies and ipsilateral neck pain. The angio-RM showed an ICA dissection with stenosis of 50%, beginning about 2 cm before the carotid channel. The patient was treated with oral anticoagulant therapy and gradually improved, until complete clinical recovery. The second patient, a 38-year-old woman, presented right hemiparesis and neck pain. The left ICA dissection, beginning 2 cm distal to the bulb, was shown by ultrasound scanning of the carotid and confirmed by MR angiogram and angiography with lumen stenosis of 90%. Following hospitalisation, 20 days from the onset of symptoms, paresis of the left trapezius and sternocleidomastoideus muscles became evident. The patient was treated with oral anticoagulant therapy and only a slight right arm paresis was present at 10 months follow-up. Cranial nerve palsy is not rare in ICA dissection, and the lower cranial nerve palsies in various combinations constitute the main syndrome, but in most cases these are present with the motor or sensory deficit due to cerebral ischemia, along with headache or Horner's syndrome. In the diagnosis of the first case, there was further difficulty because the cranial nerve palsy was isolated without hemiparesis, and the second case presented a rare association of hemiparesis and palsy of the eleventh cranial nerve alone. Compression or stretching of the nerve by the expanded artery may explain the palsies, but an alternative cause is also possible, namely the interruption of the nutrient vessels supplying the nerve, which in our patients is more likely.
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PMID:Spontaneous carotid dissection presenting lower cranial nerve palsies. 1123 57

Four cases of schwannoma originating from the lower cranial nerves are presented. Case 1 is a schwannoma of the vagus nerve in the parapharyngeal space. The operation was performed by the transcervical approach. Although the tumor capsule was not dissected from the vagus nerve, hoarseness and dysphagia happened transiently after the operation. Case 2 is a schwannoma in the jugular foramen. The operation was performed by the infralabyrinthine approach. Although only the intracapsular tumor was enucleated, facial palsy, hoarseness, dysphagia and paresis of the deltoid muscle occurred transiently after the operation. The patient's hearing had also slightly deteriorated. Case 3 is a dumbbell-typed schwannoma originating from the hypoglossal nerve. The hypoglossal canal was markedly enlarged by the tumor. As the hypoglossal nerves were embedded in the tumor, the tumor around the hypoglossal nerves was not resected. The tumor was significantly enlarged for a while after stereotactic irradiation. Case 4 is an intracranial cystic schwannoma originating from the IXth or Xth cranial nerves. The tumor was resected through the cerebello-medullary fissure. The tumor capsule attached to the brain stem was not removed. Hoarseness and dysphagia happened transiently after the operation. Cranial nerve palsy readily occurs after the removal of the schwannoma originating from the lower cranial nerves. Mechanical injury caused by retraction, extension and compression of the nerve and heat injury during the drilling of the petrous bone should be cautiously avoided.
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PMID:Schwannoma originating from lower cranial nerves: report of 4 cases. 2251 28