ABSTRACT
Subarachnoid hemorrhage is the most common cause of cerebral salt wasting syndrome. There are few reports of this condition in infectious meningitis. We describe a patient with hyponatremia and bacterial meningitis. Hyponatremia rapidly improved after administration of sodium chloride. The purpose of this report is to alert clinicians to the fact that hyponatremic patients with central nervous system disease do not necessarily have a syndrome of inappropriate secretion of antidiuretic hormone (SIADH), but may have cerebral salt wasting syndrome. By contrast with SIADH, the treatment requires saline administration.
Subject(s)
Brain Diseases/diagnosis , Hyponatremia/drug therapy , Meningitis, Bacterial/diagnosis , Sodium Chloride/therapeutic use , Streptococcal Infections/diagnosis , Wasting Syndrome/etiology , Aged, 80 and over , Female , Humans , Hyponatremia/etiologyABSTRACT
INTRODUCTION: Familial occurrence of progressive systemic sclerosis is unusual. The occurrence of conjugal scleroderma is exceptional. EXEGESIS: We report here a case of systemic sclerosis in a wife and husband who both developed the onset of illness within a 10-year period. Solvent exposure was noted. CONCLUSION: The etiology of systemic sclerosis remains unknown. Environmental factors may play role in its pathogenesis.
Subject(s)
Scleroderma, Diffuse/physiopathology , Aged, 80 and over , Echocardiography , Female , Humans , Hypertension, Pulmonary/complications , Male , Scleroderma, Diffuse/chemically induced , Scleroderma, Diffuse/diagnosis , Solvents/toxicityABSTRACT
INTRODUCTION: Primary Sjogren syndrome is considered as the most frequent connective tissue disease. Neurological complications may affect the peripheral nervous system and to lesser extent the central nervous system. Autonomic system nervous dysfunction and epilepsy have been rarely reported. EXEGESIS: We present on case of Sjogren's syndrome with epilepsy and autonomic nervous system dysfunction. The epilepsia respond to valproate. CONCLUSION: Autoimmune investigations for Sjogren's syndrome should be initiated in any patient presenting with unexplained neurologic manifestations.
Subject(s)
Autonomic Nervous System Diseases/etiology , Epilepsy/etiology , Polyneuropathies/etiology , Sjogren's Syndrome/complications , Aged , Anti-Inflammatory Agents/administration & dosage , Anti-Inflammatory Agents/therapeutic use , Anticonvulsants/administration & dosage , Anticonvulsants/therapeutic use , Autonomic Nervous System Diseases/diagnosis , Electromyography , Epilepsy/diagnosis , Epilepsy/drug therapy , Female , Fludrocortisone/administration & dosage , Fludrocortisone/therapeutic use , Humans , Hypotension, Orthostatic/drug therapy , Magnetic Resonance Imaging , Midodrine/administration & dosage , Midodrine/therapeutic use , Polyneuropathies/diagnosis , Sjogren's Syndrome/diagnosis , Sympathomimetics/administration & dosage , Sympathomimetics/therapeutic use , Treatment Outcome , Valproic Acid/administration & dosage , Valproic Acid/therapeutic useABSTRACT
INTRODUCTION: Hereditary hemochromatosis is inherited as an autosomal recessive trait. It is characterized by increased absorption of dietary iron. The association between pernicious anaemia and hereditary hemochromatosis has never been described. EXEGESIS: We report a case of paradoxical association of hereditary hemochromatosis and pernicious anaemia. CONCLUSION: It seems that pernicious anaemia may prevent manifestations of hemochromatosis. We suppose that this protective role is due to atrophic body gastritis with iron malabsorption.
Subject(s)
Anemia, Pernicious/complications , Hemochromatosis/complications , Aged , Anemia, Pernicious/blood , Anemia, Pernicious/diagnosis , Anemia, Pernicious/drug therapy , Bloodletting , Ferritins/blood , Follow-Up Studies , Hemochromatosis/blood , Hemochromatosis/diagnosis , Hemochromatosis/genetics , Humans , Male , Mutation , Time Factors , Transferrin/analysis , Treatment Outcome , Vitamin B 12/administration & dosage , Vitamin B 12/blood , Vitamin B 12/therapeutic useABSTRACT
INTRODUCTION: Tolosa-Hunt syndrome is characterized by painful ophthalmoplegia due to idiopathic granulomatous inflammation of the cavernous sinus. Steroid therapy dramatically reverses the symptoms and clinical signs. Because they also may respond to steroids, tumors such as lymphoma and meningioma and orbital tumors can make differential diagnosis difficult. EXEGESIS: We report the case of a 78-year-old male patient in whom systemic lymphoma associated with inflammation of the cavernous sinus was uncovered by painful, gradually progressing, ophthalmoplegia mimicking Tolosa-Hunt syndrome. CONCLUSION: When faced with a clinical picture suggestive of the existence of Tolosa-Hunt syndrome clinical workup is mandatory and should lead to diagnosis of exclusion.
Subject(s)
Cavernous Sinus , Leukemia, Lymphocytic, Chronic, B-Cell/diagnosis , Tolosa-Hunt Syndrome/diagnosis , Aged , Anti-Inflammatory Agents/therapeutic use , Biopsy, Needle , Bone Marrow Examination , Diagnosis, Differential , Diplopia/etiology , Disease Progression , Giant Cell Arteritis/diagnosis , Humans , Inflammation , Leukemia, Lymphocytic, Chronic, B-Cell/complications , Leukemia, Lymphocytic, Chronic, B-Cell/therapy , Magnetic Resonance Imaging , Male , SteroidsABSTRACT
INTRODUCTION: Progressive multifocal leukoencephalopathy is a demyelinating disease resulting from an opportunistic infection of the central nervous system by JC papovavirus. It mostly occurs in patients with an underlying immunosuppressive disorder. In the era of acquired immunodeficiency syndrome it is observed with increasing frequency. EXEGESIS: We report the case of a non-HIV-infected patient who presented chronic lymphocytic leukemia with progressive multifocal leukoencephalopathy uncovered by both imaging and the presence of JC virus in the cerebrospinal fluid. CONCLUSION: Due to the lack of specific treatment, the disease is still rapidly progressive and fatal.
Subject(s)
JC Virus/isolation & purification , Leukemia, Lymphocytic, Chronic, B-Cell/complications , Leukoencephalopathy, Progressive Multifocal/complications , Aged , Humans , Leukemia, Lymphocytic, Chronic, B-Cell/cerebrospinal fluid , Leukemia, Lymphocytic, Chronic, B-Cell/diagnosis , Leukoencephalopathy, Progressive Multifocal/cerebrospinal fluid , Leukoencephalopathy, Progressive Multifocal/diagnosis , Magnetic Resonance Imaging , MaleABSTRACT
Herpes zoster is uncommonly followed by cerebral infarction. The pathophysiological mechanism remains uncertain. Outcome is favorable after early specific treatment. We report the case of a 70-year-old woman who developed right hemiparesis with aphasia 15 days after thoracic herpes zoster. The herpes zoster induced cerebral vasculitis was hypothesized as no other etiology could be identified after detailed assessment of the cerebral infarction including brain MRI and cerebrospinal fluid study, and as the clinical course responded to antiviral therapy.
Subject(s)
Brain Ischemia/etiology , Herpes Zoster/complications , Vasculitis, Central Nervous System/etiology , Acyclovir/therapeutic use , Aged , Anti-Inflammatory Agents/therapeutic use , Antiviral Agents/therapeutic use , Aphasia/etiology , Cerebral Angiography , Drug Therapy, Combination , Female , Herpes Zoster/drug therapy , Humans , Magnetic Resonance Imaging , Methylprednisolone/therapeutic use , Paresis/etiology , Vertebrobasilar Insufficiency/complications , Vertebrobasilar Insufficiency/diagnostic imagingABSTRACT
We report on two new patients with both rheumatoid arthritis and multiple sclerosis. In one patient, the first manifestations of multiple sclerosis occurred eight years after onset of seronegative rheumatoid arthritis without extraarticular manifestations. The other patient had a 20-year history of multiple sclerosis when she developed seropositive, nodular rheumatoid arthritis. Neither patient had evidence of systemic lupus erythematosus. A lip biopsy was done in one patient, with normal results; the other patient was free of clinical symptoms of sicca syndrome and had a negative Schirmer's test. The paucity of similar cases in the literature is surprising since multiple sclerosis and rheumatoid arthritis are both autoimmune diseases and share many pathophysiologic and etiologic features. Although chance alone may explain the occurrence of both conditions in the same patient, the existence of shared etiologic factors should in theory increase the likelihood of the association.