Acute severe spinal cord dysfunction in bacterial meningitis in adults: MRI findings suggest extensive myelitis.
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Biomedical subjects
Publications and source records attributed to K L Roos.
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In the past 10 years the epidemiology of bacterial meningitis has changed, with a decreased incidence of meningitis caused by Haemophilus influenzae and an increasing incidence of meningitis caused by penicillin- and cephalosporin-resistant strains of Streptococcus pneumoniae. Meningococcal meningitis has become an increasing threat to college students. Successful outcome from meningitis requires not only eradication of the bacterial pathogen but also management of the neurological complications of raised intracranial pressure, stroke, and seizure activity. In this article, the pathophysiology, etiology, clinical presentation, differential diagnosis, and management of acute bacterial meningitis are reviewed. The present recommendations for the use of dexamethasone in the treatment of this infection, the use of chemoprophylaxis, and the indications for vaccinations are included.
Mycobacterium tuberculosis is one of the most common infectious agents in the world. It causes an insidious form of meningitis characterized by headache, low-grade fever, stiff neck and cranial nerve palsies, and an acute meningoencephalitis characterized by coma, raised intracranial pressure, seizures, and focal neurological deficits. This review focuses on the diagnosis and therapy of the insidious form of tuberculous meningitis and discusses the differential diagnosis of infectious and noninfectious etiologies of the aseptic meningitis syndrome.
Encephalitis is an acute infection of brain parenchyma characterized clinically by fever, headache, and an altered level of consciousness. There may also be focal or multifocal neurologic deficits, and focal or generalized seizure activity. This article discusses the clinical presentation, diagnosis, and treatment of herpes simplex virus (HSV) encephalitis, the arthropodborne viral encephalidities, Rocky Mountain spotted fever, viral encephalitis in the immunocompromised patient, and postinfectious encephalomyelitis.
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Laboratory techniques for the diagnosis of central nervous system (CNS) infections are rapidly improving but at present have limitations that necessitate our guarded enthusiasm. Enteroviruses are the most common infectious agents of viral meningitis for which an etiology can be determined, and it is anticipated that the use of the reverse transcriptase polymerase chain reaction (RT-PCR) technique should significantly improve the identification of the etiologic agent of aseptic meningitis. The combination of the polymerase chain reaction technique with laboratory methods for the determination of intrathecal antibody production to herpes simplex virus and varicella-zoster virus have improved the rapidity with which these viral infections can be diagnosed. The pearls and pitfalls of the use of these laboratory techniques in the diagnosis of viral meningitis, recurrent meningitis, and focal encephalitis are included. Recommendations for the empiric therapy of bacterial meningitis in children and adults have changed because of the emergence of penicillin and cephalosporin-resistant pneumococcal organisms. The currently recommended antibiotics and their dosages are included. The evidence for the efficacy of dexamethasone therapy in bacterial meningitis is provided. Meningitis due to Mycobacterium tuberculosis is increasingly recognized, and the initiation of empiric antituberculous chemotherapy should not await the results of CSF cultures. Toxoplasma encephalitis and primary CNS lymphoma are the most common cause of mass lesions in patients with HIV, and the diagnostic techniques to distinguish between these two infections is reviewed. A short discussion of the best test for the diagnosis of neurosyphilis is provided.
Intravascular lymphomatosis (i.v.l.) is a rare condition in which neoplastic cells preferentially infiltrate blood vessels of the central nervous system. Nonspecific symptoms associated with i.v.l. include dementia, seizures, and multifocal cerebrovascular events. i.v.l. was discovered at autopsy of a patient whose neurological deficits were predated by a particularly aggressive form of Mycobacterium marinum soft-tissue infection. It is speculated that i.v.l. may have had an occult effect on the patient's cell-mediated immunity that predisposed him to this normally innocuous mycobacteria.
PURPOSE AND METHODS: To describe the clinical and histopathologic features of a patient with viral retinitis secondary to subacute sclerosing panencephalitis. RESULTS: The patient was a human immunodeficiency virus-negative intravenous drug abuser with an acute retinitis that later progressed to encephalitis despite aggressive treatment for possible viral, protozoal, bacterial, and rickettsial infections. The patient had many of the characteristic findings of subacute sclerosing panencephalitis, including a history of measles in early childhood, myoclonus, periodic complexes on electroencephalographic testing, persistently elevated serum and cerebrospinal fluid antimeasles immunoglobulin G (IgG) titers, and a cerebrospinal fluid oligoclonal IgG gammopathy. Ultrastructural examination demonstrated numerous filamentous microtubular intranuclear viral inclusions in the nuclear layers of the retina consistent with the measles virus. This case is unusual in that our patient developed subacute sclerosing panencephalitis later in life and because there was an 8-year period between presumed viral infections in the two eyes. CONCLUSIONS: An acute retinitis in an intravenous drug abuser is not always caused by human immunodeficiency virus-related infections; not all viral retinitis responds to therapy; and mortality as well as the usual morbidity may be associated with viral retinitis. One might consider the diagnosis of subacute sclerosing panencephalitis in a young person with an acute retinitis with little or no vitreal inflammation and lack of response to anticytomegalovirus and antitoxoplasmosis therapy.
The inflammation in the subarachnoid space (SAS) that develops in the course of bacterial meningitis may have a role in eradicating the infection, but also, ultimately, is the cause of the neurological sequelae associated with this infection. The presence of an inflammatory exudate in the SAS leads to alterations in the blood-brain barrier, altered cerebrospinal fluid dynamics, cerebral edema and increased intracranial pressure, and loss of cerebral auto-regulation. Our increasing understanding of the pathophysiology of meningeal inflammation has led to therapeutic interventions to limit the degree of meningeal inflammation and neurologic sequelae. The inflammatory cascade that leads to alterations in central nervous system physiology will be reviewed as well as the experimental evidence and clinical trials demonstrating the efficacy of adjunctive therapy in reducing meningeal inflammation and decreasing the incidence and severity of neurological sequelae in bacterial meningitis.
The neurofibromatoses are defined by the presence of café-au-lait macules and neurofibromas and are associated with central and peripheral nervous system tumors. Individuals with neurofibromatosis 1 are at risk for optic nerve gliomas, nerve root and plexi neurofibromas and schwannomas, spinal cord tumors, benign and malignant peripheral nerve sheath tumors, and pheochromocytomas. Individuals with neurofibromatosis 2 are at risk for presenile cataracts, vestibular schwannomas, intracranial and intraspinal meningiomas, and intramedullary spinal cord ependymomas.
Over the last several years, the therapeutic approach to bacterial meningitis has been changing. The neurological complications of bacterial meningitis result from an inflammatory process that is initiated by the lysis of bacteria in the subarachnoid space by antibiotics; to alter the pathophysiologic events initiated by this lysis, adjunctive therapy to antimicrobial therapy has been investigated in experimental and clinical trials. This article reviews our present understanding of bacterial meningitis, the efficacy of dexamethasone in treatment, and the potential use of leukocyte monoclonal antibodies, pentoxifylline, nonsteroidal antiinflammatory agents, and anticytokine antibodies.
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The neurofibromatoses are two distinct entities with different genetic origins. The phenotypic expressions and required treatments are different. The devastating nature of neurofibromatosis-2 may be more effectively controlled through the application of advanced imaging techniques and contemporary neurotologic procedures. The most common manifestation of neurofibromatosis-2 is that of bilateral acoustic neuromas. The eventual total bilateral sensorineural deafness associated with this condition can be obviated in selected cases if the diagnosis is established early. Follow-up data are reported for three patients in whom hearing was preserved in at least one ear. When removal with hearing preservation is not possible, subtotal tumor removal with decompression of the internal auditory canals may delay progression of hearing loss. A new approach to tumors of the pterygomaxillary fossa that have extended to the middle cranial fossa has been successfully applied and is described.
A 50-year-old woman with systemic lupus erythematosus was admitted in an obtunded state. An EEG recorded while she was unconscious demonstrated one episode of rhythmic sharp wave activity in the left occipital area that lasted for 5 minutes and was followed later in the same recording by an episode of high amplitude sharp wave discharges in the right posterior temporal and occipital areas. When the patient regained consciousness, she had an Anton's syndrome of cortical blindness with denial. When she recovered light perception only, the EEG demonstrated synchronous and independent right and left occipital-posterior temporal periodic lateralized epileptiform discharges (PLEDs). Cortical blindness (Anton's syndrome) associated with abnormal electrical activity in the occipital areas has only rarely been reported. Our case is significant for the following reasons: 1) PLEDs maximal right and left occipital areas associated with bilateral visual loss has not previously been observed; 2) abnormal electrical activity in the occipital lobes may be a reversible cause of Anton's syndrome.