Neuropsychiatric manifestations of Lyme disease

Lyme disease is a multisystem illness that may affect the central nervous system and subsequently produce mild to severe psychiatric disorders. Physicians who treat patient with Lyme disease need to be aware of its neuropsychiatric symptoms, which may emerge months to years after the initial infection. Prompt diagnosis and effective treatment are needed to avoid the debilitating and possibly irreversible mental illness associated with the neurologic involvement of this spirochetal infection. The author reviews the neuropsychiatric manifestations of Lyme disease and provides diagnostic and therapeutic approaches for the management of the central nervous system disease that may cause them.     

Primary intraocular lymphoma

Primary intraocular lymphoma can arise as an isolated clinical entity or in combination with lymphomas in the central nervous system. The symptoms are usually floaters in the visual field and reduced visual acuity. The condition is commonly misdiagnosed as chronic uveitis in spite of unresponsiveness to corticosteroids. The authors discuss a case of primary intraocular lymphoma diagnosed in a 65 year old male patient. He had bilateral intraocular lesions in addition to two brain tumours. He went into complete remission after radiation therapy, but experienced later a recurrence in one eye. A course of chemotherapy using cytarabin (cytosine arabinoside) intravenously has kept the patient in remission for four months. The authors also discuss the diagnostic and therapeutic problems connected with this rare condition.     

Ophthalmoplegia-ataxia-areflexia in pediatrics. Three new patients and review of the literature

OBJECTIVE: The objective of this study was to investigate if pediatric patients with benign brainstem encephalitis (Bickerstaff Syndrome) or with Miller-Fisher Syndrome are the extremes of the same nosological entity which, in adults, has been named ophalmoplegia-ataxia-areflexia syndrome. PATIENTS AND METHODS: The subjects included in the study were three patients of our institution and 24 patients found in the revision of the English and Spanish pediatric literature who fulfilled the diagnostic criteria of ophtalmoplegia-ataxia-areflexia syndrome. The topographical location of the lesion in the nervous system was based on previously established criteria by using clinical and complementary studies. RESULTS: Of the 27 patients included in the study we were able to reach an accurate topographical diagnosis in 9. None had an exclusive involvement of the peripheral nervous system, (6) had exclusively central nervous system involvement and 2 showed involvement of both system. In 12, the topographical location of the lesion could be only ascertained as probable; 3 of them in the peripheral nervous system, 2 in the central nervous system and mixed involvement in 7. In the remaining 7 patients there were insufficient clinical data to allow topographical classification. CONCLUSIONS: The ophtalmoplegia-ataxia-areflexia syndrome can also be found in pediatric patients. The lesion in the majority of patients in this age group is located in the central nervous system, either alone or combined with peripheral nervous system involvement.     

Establishment and preliminary characterization of human malignant mesothelioma cell lines

In this retrospective study, 47 patients with clinical diagnosis of central nervous system metastases of breast cancer were evaluated by computerized tomography (CT), magnetic resonance imaging (MRI) and cerebrospinal fluid (CSF) examination. The patients were divided in 2 groups: 1, without leptomeningeal neoplasm and 2, with leptomeningeal neoplasm. In the group 2, the time interval between the primary disease and the central nervous system metastasis as well as the survival time were shorter than in group 1 (40 and 4.3 months in group 2 versus 57 and 10 months respectively, in group 1). In both groups the most common neurological symptoms and signs were intracranial hypertension and motor deficits. The most sensitive diagnostic methods were CT and MRI in group 1, and the CSF examination in group 2. The use of the tumor markers CEA and CA-15.3 in the routine examination of CSF showed promising results, mainly in leptomeningeal forms.     

Fibrinolytic treatment with ultra-high streptokinase infusion via the dorsalis pedis vein offers no advantage over systemic infusion via the brachial vein in patients with deep vein thrombosis of the leg

BACKGROUND: Diagnosis of intraparenchymal brain lesions has usually required invasive diagnostic procedures, because too few cells are shed into cerebrospinal fluid to permit cytologic diagnosis. Polymerase chain reaction technology makes it possible to identify cell populations that are present at a much lower frequency than traditional techniques. CASE REPORT: A young woman presented with multiple brain lesions raised the question of primary central nervous system lymphoma. Polymerase chain reaction analysis of cerebrospinal fluid showed evidence of a monoclonal B-cell population heightening suspicion of lymphoma. Brain biopsy showed acute demyelination most consistent with multiple sclerosis. CONCLUSION: Although T-cell restriction has been demonstrated in multiple sclerosis lesions, the finding of a monoclonal B-cell population was unexpected and to our knowledge has not been previously reported. This case emphasizes that monoclonality is not always indicative of a neoplastic process, particularly in the central nervous system.     

Spontaneous and induced remyelination in multiple sclerosis and the Theiler's virus model of central nervous system demyelination

Remyelination in the central nervous system, originally thought to occur rarely, if ever, is now an established phenomena in multiple sclerosis patients. However, the extent of myelin repair is incomplete and limited. Experimental models of central nervous system demyelination provide an opportunity to study the cellular and molecular events involved in remyelination. These models may provide some clue to why remyelination in multiple sclerosis is incomplete as well as suggest potential methods to stimulate central nervous system repair. In this review we examine the morphological aspects of central nervous system remyelination and discuss both spontaneous and induced remyelination in multiple sclerosis and experimental models of central nervous system demyelination. We give special emphasis to the Theiler's virus model of central nervous system demyelination and its usefulness to identify therapeutic agents to promote remyelination. The role of immunoglobulins in promoting remyelination in both the Theiler's model system and in multiple sclerosis is discussed. Finally, we examine the potential physiological role of demyelination and remyelination and its relationship with clinical manifestations of central nervous system disease.     

Lower extremity manifestations of neuromuscular diseases

Neuromuscular disorders must be considered when a patient presents with a pes cavus deformity; lower extremity weakness; difficulty in walking; or cramps, stiffness, fatigue, pain, or paresthesia in the extremities. In those instances in which a neurologic disease is considered, distinctions between central and peripheral nervous system origin, focal versus generalized pathology, and static versus progressive course are critical in the diagnosis and treatment of the disorder. The complexities of the nervous system often result in missed or delayed diagnosis of these syndromes. Patients affected with neurologic diseases often require diagnostic and therapeutic interventions from various specialists. This article presents a systematic approach to the patient with a neurologic disorder, with special emphasis on neuromuscular manifestations in the lower extremities. Key observations to aid in the recognition of neuromuscular dysfunction are presented, along with an approach to diagnostic evaluation and management for these patients.     

Cerebral palsy: a comprehensive review

Cerebral palsy is a broad range of static, nonprogressive motor disabilities that present from birth or early childhood as a result of injury to neuromotor components of the central nervous system. Motor performance is normally coordinated via communication between the cerebral cortex, thalamus, basal ganglia, brain stem, cerebellum, spinal cord, and communicating sensori-motor pathways. This complex network lends itself to injury at many different levels. Etiologies are numerous and can occur during the prenatal, perinatal, and postnatal periods. The severity of the neurologic deficit and the clinical manifestations are varied depending on the time, location and nature of the original injury. In order to approach cerebral palsy systematically, the primary health care practitioner must be prepared to recognize neuromotor deficits, diagnose and classify the type of disorder, and implement a methodical treatment plan. The purpose of this article is to review the etiology, pathophysiology, diagnostic classification (Swedish system), clinical manifestations, and therapeutic management of cerebral palsy and prepare the advanced practice nurse to care for the individual and family.     

Primary non-Hodgkin's lymphoma of the brain

Between 1980 and 1993, 26 patients were treated for primary lymphoma in the central nervous system at the Norwegian Radium Hospital. This is a rare disease with poor prognosis and thus represents a great therapeutic challenge. Immunocompromised, e.g. AIDS patients, are a group at high risk, but the incidence has increased among immunocompetent patients as well. Median patient age was 64 years; and none of the patients had any signs of immunodeficiency. 23 of the patients received radiation therapy. 13 of the patients received some form of chemotherapy. The overall median survival was 19 months. WHO performance status 0-2, unifocal lesion, absence of steroid dependency and normal serum levels of LDH were all associated with longer survival. Although complete remissions were achieved in most patients, relapses in the central nervous system were frequent.     

Tumors of the central nervous system

Neoplasia of the central nervous system (CNS) can be divided into two main categories: nonpituitary CNS neoplasia and pituitary adenomas. Nonpituitary CNS neoplasias are generally compressive in nature, although some are also invasive. The majority of reported CNS tumors are secondary with only a few originating from nervous tissue. Pituitary adenomas predominantly occur in the pars intermedia of the older horse. Clinical signs, diagnostic testing, and possible treatments are discussed.     

General pharmacology of loracarbef in animals

Loracarbef ((6R, 7S)-7-[(R)-2-amino-2-phenyl-acetamido]-3-chloro-8-oxo-1- azabicyclo [4.2.0]oct-2-ene-2-carboxylic acid, monohydrate, LY 163892, CAS 121961-22-6) is a carbacephem antibiotic targeted for use in the treatment of infectious disease. The potential pharmacological effects of this agent were examined on cardiovascular, respiratory, gastrointestinal, central nervous and autonomic nervous systems. Also examined were local anesthetic activity, effects on platelet aggregation, circulating blood glucose, primary antibody production, renal function, blood coagulation, ocular irritation, and the acute inflammatory response. Doses of 100, 1000, and 2000 mg/kg given by the oral route were selected for most in vivo studies. Concentrations up to 3 x 10(-3) mol/l were used in vitro. Loracarbef was essentially inactive in the tests of central and autonomic nervous system function, platelet aggregation, renal function, blood hemolysis, primary antibody production, blood coagulation, and ocular irritation. It had no local anesthetic activity. At high oral or intravenous doses, representing significant multiples of the therapeutic dose, loracarbef caused changes in gastrointestinal (decrease in gastric acid production and gastric fluid volume; increased biliary output), cardiovascular (increased mean pressure, cardiac output, heart rate, and femoral flow), blood glucose (increased glucose levels), and anti-inflammatory tests (suppressed acute inflammatory response). In summary, loracarbef exhibited minimal activity in these pharmacodynamic studies. These results indicate loracarbef has a low potential to produce adverse effects at therapeutic doses.     

-Anesthesia and analgesia practice patterns in French obstetrical patients-

OBJECTIVES: To review current management of individuals with metastases to the central nervous system and brachial nerve plexus, and to provide a scientific basis for nursing management of the effects of the disease and treatment. DATA SOURCES: Published articles, book chapters, clinical trial data, and experience from nursing literature. CONCLUSIONS: Central nervous system metastases are events that may create oncologic emergencies with neurologic impairment and pain. Treatment of patients with central nervous system metastases is generally palliative regardless of the type of the primary cancer. Early diagnosis and treatment improve the chances for optimal recovery of neurologic function and pain management. IMPLICATIONS FOR NURSING PRACTICE: Central nervous system metastases may develop in patients with systemic disease. Disease and treatment effects present challenges to patients, family, and care providers. Nurses have a responsibility in educating the patient/family and in providing supportive care.     

Malignant giant cell tumour of the distal femur treated by excision, allografting and ligamentous reconstruction: an 18-year follow-up

Technical progress made in neuroradiology, and focal external and internal radiation therapy, have allowed the development of a series of local therapeutic modalities both in primary and in metastatic brain tumours. Eligibility criteria and results obtained with these new techniques are compared. Experimental studies with implications for radiation therapy, particularly boron neutron capture therapy, and for chemotherapy are reviewed. The possible use of chemotherapy as first-line treatment in non-Hodgkins lymphomas of central nervous system is stressed.     

Neurogenic pulmonary edema. Pathogenesis, clinical picture and therapy

Neurogenic pulmonary edema (NPE) is a rare but always life-threatening complication in patients with central nervous system lesions. NPE is evident if patients shortly after cerebral lesions suddenly develop pulmonary edema and other causes of the symptoms, such as aspiration of gastric content, congestive heart failure and direct toxic exposure, are ruled out. METHODS: The current body of literature, partially obtained by computer-guided search (Winspirs) regarding epidemiology, pathophysiology and therapy of NPE was reviewed. Additionally, the case of a patient who developed a sudden pulmonary edema after an episode of tonic-clonic seizures is analyzed. We first provide information about history, definition, incidence and mortality of NPE. Second, a case report of a postictal NPE is presented to illustrate the clinical picture of NPE, and the applied therapeutic strategies are discussed. Third, recent pathophysiologic concepts about symptoms and possible therapeutic principles are reviewed. Fourth, a rational therapeutic plan for the prehospital emergency therapy of NPE is outlined. RESULTS: The different etiologies all have one characteristic feature: an acute emergency which causes increased intracerebral pressure (ICP). NPE is known in patients after cerebral trauma, intracranial hemorrhage, stroke, intracranial tumor or seizures. The incidence is estimated at around 1% after cerebral trauma, at 71% after cerebral hemorrhage and at 2% after seizures. Mortality is appraised to lie between 60 and 100%, independent of etiology. There is a definite pathophysiologic sequence leading to NPE: a central nervous system lesion causes a sudden increase in ICP which triggers an upregulation of sympathetic signal transduction to assure brain perfusion. Increased tonus of venous and arterial vessels and of myocardial function are the immediate consequences. However, if systemic vascular resistance (SVR) increases excessively, left ventricular failure and finally pulmonary edema (NPE) may result. Additionally, the protein-rich edema fluid points to an increased endothelial permeability within the pulmonary circuit. This is thought to be caused by the acute pressure increase and by neurohumoral mechanisms, possibly similar to those described for the systemic inflammatory response syndrome (SIRS). The most important central nervous system structures involved in NPE are the medulla oblongata and the hypothalamus. CONCLUSION: NPE is always a life-threatening symptom after increased ICP, where immediate therapeutic interventions are imperative. A rational therapeutic approach needs to be focused on decreasing ICP as primary goal. Additionally, attempts should be made to optimize body oxygenation, decrease pre- and afterload and increase myocardial contractility. Postictal patients suspicious for incipient ventilation problems must be admitted to hospital for further evaluation.     

Primary Langerhans' cell histiocytosis of the central nervous system with fatal outcome. Case report

An unusual case of primary parenchymal Langerhans' cell histiocytosis of the central nervous system is reported. The definitive diagnosis was obtained by ultrastructural detection of Birbeck granules and by immunohistochemical evidence of CD1a expression. Despite complete surgical resection, there was an early recurrence with multiple central nervous system metastases leading to a fatal outcome.     

PET in cardiology: current status and clinical expectations

The development of positron emission tomography (PET) in the clinical environment along with the synthesis of biologically active molecules and tracer kinetic principles has provided a diagnostic tool for in vivo tissue characterization in humans. Moreover, based on the growing knowledge of cellular function on the molecular level of diseases PET biological imaging has stimulated the synthesis of numerous metabolic compounds labelled with the four primary positron-emitting radioisotopes C-11, F-18, N-13 and O-15. While the concept of biological imaging has gained attraction for probing both the central nervous system and neoplastic tissues, current diagnostic benefit from PET is probably best defined in cardiovascular medicine.     

Preventing firearm injuries

Fifty four cerebrospinal fluid samples obtained from as many immunocomponent patients with disorders of the central nervous system were investigated for the presence of herpesvirus DNA by nested polymerase chain reaction in order to determine an etiological diagnosis. Four of these samples proved positive for the presence of Epstein-Barr virus DNA (7.4%). The result of this diagnostic study is reported to draw insiders' attention to the possible presence of EBV in cerebrospinal fluid from patients with central nervous system diseases.     

Lymphomas in the immunocompromised patient

Lymphoma is a common opportunistic complication of immunosuppression. Lymphomas in patients with the acquired immunodeficiency syndrome (AIDS) may broadly be divided into four major types: intermediate- or high-grade systemic lymphoma, primary central nervous system (CNS) lymphoma, Hodgkin's disease (HD) and primary effusion lymphoma. Multiple active regimens have been identified for patients with AIDS-related systemic lymphoma. However, despite high initial complete response rates, most studies have reported a median survival of less than 1 year for these patients, with approximately half of the patients dying from lymphoma and half from opportunistic infections or other AIDS-related complications. The standard therapeutic approach for patients with AIDS-related primary CNS lymphoma is radiotherapy, although recent studies using combinations of chemotherapy with radiotherapy may offer an improvement in therapy for this group of patients who have very poor overall prognosis. Lymphoproliferative disease in patients after solid organ or bone marrow transplantation represents with a spectrum of disorders. No standard approach for therapy in this group of patients has been clearly established.     

Sympathetic neuron survival and proliferation are prolonged by loss of p53 and neurofibromin

This review will discuss studies demonstrating that activation of opioid receptors within the central nervous system alters various immune system parameters. Specifically, natural killer cell cytolytic activity and lymphocyte proliferative responses to mitogen appear to be modulated predominantly, if not exclusively, through central opioid receptors. The potential mechanisms by which central opioid receptors appear to modulate these peripheral immune functions will be examined by evaluating the role of both the hypothalamic-pituitary-adrenal (HPA) axis and the autonomic nervous system. The studies discussed below indicate that acute administration of morphine or related compounds appears to primarily alter peripheral immune function through the sympathetic nervous system, while more prolonged exposure to opioids alter the immune system predominantly by activation of the HPA axis. Finally, the potential clinical relevance of these observations are discussed in relationship to both the therapeutic use, as well as the abuse of opioid compounds.     

Neurologic manifestations of primary Gougerot-Sj?gren syndrome

Primary Sj?gren's syndrome is one of the commonest autoimmune connective tissue diseases. Neurological complications occur in about 20 p. 100 of primary Sj?gren's syndrome patients. It most frequently involves the peripheral nervous system, predominantly sensorimotor and sensory polyneuropathy. Sensory neuronopathy and trigeminal nerve involvement are less frequent but quite suggestive of primary Sj?gren's syndrome. Among central nervous system involvements, focal or multifocal lesions of the brain or the spinal cord are the most frequent. Diffuse encephalic involvement may present either as an aseptic meningoencephalitis or as a cognitive impairment. It is not clear whether psychiatric manifestations (mostly mood and personality disturbances) have an organic substratum or are the psychological consequence of the disability induced by a chronic disease such as Sj?gren's syndrome. The response to corticosteroids or immunosuppressive therapy is unpredictable in neurological complications of primary Sj?gren's syndrome. The pathophysiology of these complications remains unknown. Different mechanisms could be assumed depending on the neurological manifestations: vasculitis in polyneuropathies and multiple mononeuropathies, humoral and/or cellular mediated immune response against neurones in sensory neuronopathy. In central nervous system involvement, each of these mechanisms could occur.