Gene/Protein Disease Symptom Drug Enzyme Compound
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A 42-year-old housewife with myasthenia gravis (MG) for 22 years, who was initially treated by radiation to the hyperplastic thymus and anti-cholinesterase therapy, developed bilateral ptosis, paresthesia of her right face and decreased taste sensation after house work at the age of 42 years. Neurological examinations revealed lateral and vertical gaze palsy, upward nystagmus, decreased taste sensation, peripheral facial palsy on the left side. She also had hypalgesia on the right face, arm and chest up to Th7 level, and urinary retention. She had hyperreflexia on the right side but no extensor toe signs. CSF study revealed 5 cells/microliters and protein of 23 mg/dl. Serum IgG anticardiolipin antibody was positive. Magnetic resonance imaging studies revealed high intensity areas in the brainstem tegmentum and periventricular white matter. Diagnosis of multiple sclerosis (MS) was made. This is the first case in which MG, MS and serum anticardiolipin antibody were present simultaneously, which may be all due to some immunological abnormality. Steroid therapy made anti-cardiolipin antibody negative, but new MS plaque developed in 7 months, which favors diagnosis of MS rather than infarction, since the activities of ACLA were not correlating to clinical symptoms. MRI was helpful in detecting MS plaques in MG patients.
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PMID:[A case of myasthenia gravis associated with multiple sclerosis and positive anticardiolipin antibodies]. 836 70

We report a 46-year-old female who presented progressive ophthalmoplegia and limb weakness. She was well until the age of 15 years when there was an onset of bilateral deafness. She became completely deaf by 20 years of age. She noted an onset of weakness in her legs when she was 27-years-old and of ptosis at 34 years of age. She was admitted to our hospital when she was 41-years-old. Neurological examination revealed near total ophthalmoplegia, bilateral ptosis, dysphagia, generalized muscle atrophy and weakness of approximately 4/5 degree, facial grimacing, athetotic movements in four limbs. Laboratory examinations revealed increase in blood lactate and pyruvate levels and diffuse low density change in the cerebral white matter in CT scans. She was thought to have a mitochondrial encephalomyopathy. She was discharged for follow-up, but her clinical course was that of a relentless deterioration. She was readmitted to our service in December 1989. She showed further progress in her weakness and muscle atrophy. Otherwise neurological examination was essentially similar to the previous one. Her cranial CT scans showed low density changes in striatum, thalamus and midbrain in addition to the white matter. Enzyme activities of the electron transport complexes revealed a moderate decrease in the succinatecytochrome c reductase activity, and the Southern blot analysis of mtDNA revealed multiple deletions in mitochondrial genomes. Two months after her admission, she developed bronchopneumonia, and expired on March 13th, 1990. Post-mortem examination revealed diffuse pallor of myeline in the cerebral white matter in K-B staining. A marked neuronal loss and gliosis were observed in putamen bilaterally. Skeletal muscles showed typical changes of mitochondrial myopathies with ragged-red fibers in Gomori-Trichrome staining, and crystalline inclusion bodies by electron microscopic observations. Some neurogenic atrophies were also seen. Oculomotor nuclei appeared intact. It was thought that she had an incomplete form of Kearns-Sayre syndrome. The patient was discussed in a neurological CPC of the departments of Neurology and Pathology of Juntendo University School of Medicine.
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PMID:[Forty-six-year-old woman with progressive external ophthalmoplegia and limb weakness]. 847 58

We report a case of mitral regurgitation caused by a total rupture of the posterior papillary muscle that had occurred after acute myocardial infarction. A 72-year-old woman was transferred to our hospital for cardiogenic shock. Echocardiogram revealed massive mitral regurgitation and prolapse of posterior mitral leaflet presumably due to a rupture of a papillary muscle. Cardiac catheterization demonstrated a total occlusion in the segment 2 of the right coronary artery. She had developed progressively increasing heart failure even though the patient had received a successful PTCA for a total occlusion of the right coronary artery. She underwent an emergency mitral valve replacement with preservation of the posterior leaflet using a SJM prosthetic valve. Intraoperative findings were confirmative of total rupture of the posterior papillary muscle. A postoperative course was uneventful. This case is the seventh case which has been reported as the successful operation of a total rupture of the papillary muscle in Japan.
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PMID:[A case of acute postinfarction mitral regurgitation and cardiogenic shock caused by a total rupture of the papillary muscle]. 847 86

Among 21 patients with left atrial myxoma treated during the past 11 years in our institute, 3 patients had associated acquired heart disease which required concomitant cardiac surgery. Two patients had atherosclerotic coronary arterial disease, and underwent single coronary artery bypass grafting (CABG) and 4 CABGs in addition to removal of myxoma, respectively. Both of them received CABGs after removal of myxoma, because the intraoperative heart protection using retrograde coronary perfusion could afford the situation. Another patient had a huge left atrial myxoma associated with mitral and tricuspid regurgitation. She suffered from sudden heart failure caused by tumor obstruction of blood flow across the mitral valve, and an emergency surgery was performed. She underwent mitral valve replacement for annular dilatation with prolapse of both leaflets and tricuspid annuloplasty for annular dilatation, in addition to removal of myxoma. All of these 3 patients went a good postoperative course and are doing well now with no local recurrence. In this paper, preoperative and intraoperative evaluation, and surgical treatment of associated heart disease with left atrial myxoma were discussed.
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PMID:[Surgical treatment of left atrial myxoma with concomitant acquired heart disease]. 851 67

A 49-year-old woman who underwent mitral valve replacement with 29 mm Mitroflow pericardial valve in 1985 started to have severe hematuria, anemia and icterus around May 1994. She was diagnosed to have mitral regurgitation with hemolytic anemia due to structural deterioration of the prosthetic valve. She underwent replacement of the prosthetic valve with 29 mm St. Jude medical mechanical valve, which alleviated the symptoms remarkably. The explanted valve showed an extensive cuspal tear and prolapse close to the commissure and poor endothelialization of the inflow surface of the frame. In our experience the rate of structural deterioration of the Mitroflow valve is so high that we discontinued using this bioprosthesis.
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PMID:[A case of failure of mitroflow pericardial valve with severe hemolytic anemia]. 853 1

A 52-year-old woman had a 14-year history of stridor attacks. Pulmonary function tests revealed reversible airway obstruction, and bronchial asthma was diagnosed. She also has bilateral ptosis, diplopia, and moderate weakness of all four limbs; a positive edrophonium test confirmed the diagnosis of myasthenia gravis. Although the parasympathetic system plays an important role in the regulation of bronchial tone, in this patient the edrophonium test did not provoke an asthmatic attack or exacerbate pulmonary function, except for increases in sputum production and in frequency of cough. The general weakness was usually worse in the afternoon. The decrease in grip strength and the shortening of arm elevation time also occurred after asthma attacks, which means that general muscle fatigue was caused by the work of breathing. Furthermore, dyspnea increased and pulmonary function worsened when an anti-cholinesterase inhibitor was discontinued, probably because of respiratory muscle weakness. Accordingly, the clinical status of bronchial asthma seemed to change in parallel with that of the myasthenia gravis.
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PMID:[Bronchial asthma complicated by myasthenia gravis]. 869 67

A 60-year-old woman with past history of perineorrhaphy due to vaginal prolapse; squamous cell carcinoma of the uterine cervix stage IIB, treated with radiation theraphy at doses of 7500 rads administered as teletherapy and brachytherapy with Cesium 137. Ten weeks later a Piver II hysterectomy was performed, her posoperative morbidity was a vaginal abscess. Twelve years later, she developed a pulmonary metastasis. One year thereafter she had vaginal discharge of cetrinous fluid and prolapse of greater omentum through the vagina. She was treated by a midle exploratory celiotomy, primary closure of the vaginal defect and the pelvic floor was covered with an omental pedicle flap. The postoperative period was unremarkable.
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PMID:[Vaginal evisceration following radiotherapy and surgery for cervico-uterine cancer. Report of a case]. 871 67

We report a 63-year-old woman who presented myotonia and parkinsonism. The patient was well until 15 years of the age when she noted that the ring finger of her left hand at times flexed when she did not intend to do so. She noted weakness in her left upper extremity at the age of 40, and difficulty in relaxing her hand grip at 45. She had an onset of tremor in her right foot at age 50, which was followed by difficulty in gait and hand writing. She was admitted to Juntendo University Urayasu Hospital when she was 63-year-old. Her mother, two sisters, and a son were affected with similar muscle weakness and myotonia. Although some of them developed stooped posture in the late stage of the disease, none of them had overt parkinsonism. General physical examination was unremarkable. Neurologic examination revealed an alert and oriented woman with some recent memory loss. She had bilateral ptosis, facial weakness, and a masked face. Myerson's sign was present. Her speech was small and monotonous. The sternocleidomastoid muscles were markedly atrophic and weak. The remaining of the cranial nerves were intact. She walked in small steps with freezing with support. She showed bradykinesia, retropulsion, and resting tremor in her right leg. Slight distal dominant weakness was noted in both upper and lower extremities more on the left. No cerebellar signs were noted. Muscle stretch reflexes were within normal limits in the upper extremities and diminished in the lower limbs. Sensation was intact. Routine laboratory findings were unremarkable. Cranial CT scan and MRI revealed slight cortical atrophy and leukoaraiosis. She responded to levodopa and she became able to walk by herself. She was transferred to another hospital one month after her admission. She had several bouts of airway obstruction with one episode of respiratory arrest. She expired six month after the transfer. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that this patient suffered from myotonic dystrophy and Parkinson's disease which set in later years. Postmortem examination on the iliopsoas muscle revealed uneven muscle fiber diameters, central nuclei, and type 1 fiber predominance; the pathologic finding was consistent with myotonic dystrophy. The substantia nigra showed marked cell loss and Lewy bodies in the remaining neurons. The finding was consistent with Parkinson's disease. In myelin stain, diffuse myelin pallor was noted in the cerebral white matter which was the pathologic substrate of leukoaraiosis in this patient. Combination of these two disorders have never been reported in the literature to our knowledge. It appears to be that the coincidence is just a by-chance phenomenon, but it seems interesting to note that accelerated aging process appears to be present in both myotonic dystrophy and Parkinson's disease.
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PMID:[A 63-year-old woman with muscle weakness, myotonia, and parkinsonism]. 886 42

A 55-year-old woman with a several-decade history of thyroid goiter is presented here as a case of myasthenia gravis complicated with hyperthyroidism and thymoma with serological evidence of systemic lupus erythematous (SLE). She had had right eyelid ptosis since July 1992, with a positive tensilon test. The acetylcholine receptor antibody titer was 4.01 nmol/L. A thyroid function test revealed T3: 162 ngidl, T4: 14.98 micrograms/dl, TSH:0.09 microIU/ml and positive anti-microsomal antibody (1:400). An MRI of the chest showed a thymoma in the left thymus. Other autoantibody screenings include ANA (1:320, speckled pattern) and anti-ds DNA (+) suggesting a serological association with SLE. After three courses of plasmapheresis, she received an extended maximal thymomectomy and a subtotal thyroidectomy. She was then treated with prednisolone, Mestinon, Eltroxin and discharged without complications. The coexistence of myasthenia gravis, hyperthyroidism, thymoma and a serological evidence of SLE have not previously been documented in the literature.
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PMID:Myasthenia gravis complicated with hyperthyroidism, thymoma and serological evidence of systemic lupus erythematosus: a case report. 887 Mar 31

A 72-year-old woman developed a sudden onset of bilateral ptosis, diplopia and gait disturbance. Neurological examination revealed bilateral oculomotor palsies, truncal ataxia, and transient slight weakness in the right upper extremity. She was diagnosed to have Nothnagel syndrome. T2-weighted MRI disclosed a high signal intensity lesion at the left paracentral portion of the upper midbrain in addition to the bilateral medial thalamic lesions, while brain CT showed only the thalamic lesions. Brain MRI was useful for detecting the small midbrain lesion.
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PMID:[A case of Nothnagel syndrome]. 895 59


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