IATROGENIC NEUROLOGICAL DISEASES. NEUROLOGICAL COMPLICATIONS OF PSYCHIATRIC TREATMENT.
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Antidepressive Agents↗
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Respiratory aspects of neurological disease.
Neurological disease may result in respiratory dysfunction; however the manifestations of respiratory dysfunction in such patients may be atypical because of wider effects of their underlying condition. In the present review we have considered separately acute neuromuscular respiratory disease (as well as aspects of respiratory muscle function relevant to intensive care), chronic neuromuscular respiratory disease, sleep related disorders, respiratory consequences of specific neurological diseases, and neurological features of respiratory disease. Approaches to specific clinical problems are discussed; in many instances this can be expedited by close cooperation with a respiratory physician. We suggest that management of respiratory dysfunction in neurological disease depends critically on three factors: firstly, knowledge of when respiratory dysfunction is likely to occur; secondly, maintaining a high index of clinical suspicion (specifically apparently vague symptoms should not be uncritically attributed to the underlying neurological condition); and, thirdly, the pursuing of appropriate investigations.
Brain Diseases↗
Hypothalamic-pituitary-adrenal axis, glucocorticoids, and neurologic disease.
Neurologic diseases often are accompanied by significant life stress and consequent increases in stress hormone levels. Glucocorticoid stress hormones are known to have deleterious interactions with neurodegenerative processes and are hypersecreted in neurologic disorders and comorbid psychiatric conditions. This review highlights the current state of knowledge of mechanisms controlling activation and inhibition of glucocorticoid secretion, outlines signalling mechanisms used by these hormones in neural tissue, and describes how endogenous glucocorticoids can mitigate neuronal damage in models of neurologic disease. This review highlights the importance of controlling stress and consequent stress hormone secretion in the context of neurologic disease states.
Animals↗
Physical rehabilitation in neurologic diseases.
Neurologic diseases, particularly those affecting the central nervous system, are the focus of an immense amount of research. Although only a small part of that research is directly relevant to rehabilitation, many findings published during the last year have implications for practice. Strategies to affect neglect, sensory loss, paresis, and functional performance have been examined. Approaches as diverse as exercise, feedback, electrical stimulation, patient and environment adaptations, orthotics, and task practice have been advocated.
Brain Injuries↗
[The neurologic diseases].
Neurologic diseases have important social and economic repercussions. The economic cost related to medications, caretakers, and therapists is evident, as well as the impact the disease may cause on the family. Epilepsy is the most frequent cause of medical care at the out-patient service of the Manuel Velasco Suárez National Institute of Neurology and Neurosurgery (NINN), in Mexico City and the estimated annual prevalence of this disease is 5.9 per 1,000 inhabitants. Parkinson's disease, the most representative of movement disorders, affects 20% of the populating aged > 65 years. Depression and dementia are complex and heterogeneous neuropsychiatry disorders, representing the fifth cause of morbility after accidents, cardiovascular disease, liver cirrhosis and diabetes mellitus. During the last decades, encephalic trauma has been the first cause of mortality: among brain tumors, glioblastomas have the greatest impact. Among infectious disease of the central nervous system (CNS), which are relatively infrequent as compared to gastrointestinal or respiratory infections; viral encephalitis, AIDS-associated toxoplasmosis, and tuberculous meningitis are the most frequent discharge diagnoses at the NINN. The need for a national registration system of neurologic diseases is unquestionable. Such a system would provide accurate data regarding the magnitude of problems related with such disease and help design adequate care and prevention programs.
Central Nervous System Infections↗
Quinolinic acid and kynurenine pathway metabolism in inflammatory and non-inflammatory neurological disease.
Neurological dysfunction, seizures and brain atrophy occur in a broad spectrum of acute and chronic neurological diseases. In certain instances, over-stimulation of N-methyl-D-aspartate receptors has been implicated. Quinolinic acid (QUIN) is an endogenous N-methyl-D-aspartate receptor agonist synthesized from L-tryptophan via the kynurenine pathway and thereby has the potential of mediating N-methyl-D-aspartate neuronal damage and dysfunction. Conversely, the related metabolite, kynurenic acid, is an antagonist of N-methyl-D-aspartate receptors and could modulate the neurotoxic effects of QUIN as well as disrupt excitatory amino acid neurotransmission. In the present study, markedly increased concentrations of QUIN were found in both lumbar cerebrospinal fluid (CSF) and post-mortem brain tissue of patients with inflammatory diseases (bacterial, viral, fungal and parasitic infections, meningitis, autoimmune diseases and septicaemia) independent of breakdown of the blood-brain barrier. The concentrations of kynurenic acid were also increased, but generally to a lesser degree than the increases in QUIN. In contrast, no increases in CSF QUIN were found in chronic neurodegenerative disorders, depression or myoclonic seizure disorders, while CSF kynurenic acid concentrations were significantly lower in Huntington's disease and Alzheimer's disease. In inflammatory disease patients, proportional increases in CSF L-kynurenine and reduced L-tryptophan accompanied the increases in CSF QUIN and kynurenic acid. These responses are consistent with induction of indoleamine-2,3-dioxygenase, the first enzyme of the kynurenine pathway which converts L-tryptophan to kynurenic acid and QUIN. Indeed, increases in both indoleamine-2,3-dioxygenase activity and QUIN concentrations were observed in the cerebral cortex of macaques infected with retrovirus, particularly those with local inflammatory lesions. Correlations between CSF QUIN, kynurenic acid and L-kynurenine with markers of immune stimulation (neopterin, white blood cell counts and IgG levels) indicate a relationship between accelerated kynurenine pathway metabolism and the degree of intracerebral immune stimulation. We conclude that inflammatory diseases are associated with accumulation of QUIN, kynurenic acid and L-kynurenine within the central nervous system, but that the available data do not support a role for QUIN in the aetiology of Huntington's disease or Alzheimer's disease. In conjunction with our previous reports that CSF QUIN concentrations are correlated to objective measures of neuropsychological deficits in HIV-1-infected patients, we hypothesize that QUIN and kynurenic acid are mediators of neuronal dysfunction and nerve cell death in inflammatory diseases. Therefore, strategies to attenuate the neurological effects of kynurenine pathway metabolites or attenuate the rate of their synthesis offer new approaches to therapy.
Aged↗
[Intractable neurological diseases and neurology].
In intractable neurological diseases, there are often no appropriate treatment methods even after admission and the course is frequently chronic. Therefore treatment at home is a major choice. In particular, in Parkinson's disease and amyotrophic lateral sclerosis, care at home while symptoms are stable is appropriate in terms of extension of ADL and the QOL of the patient and family. We have performed continuous treatment at home according to our plan for the previous 9 years. This treatment was favorably accepted by the patient and family without major problems. It is important to organize network to support patient with intractable neurological diseases. By virtue of the care insurance system established in 2000, services of medical care, health and welfare are being collectively provided at present. But, there still remain many issues awaiting solution on the support to advanced intractable neurological diseases. A pending problem about suction of sputa for the ALS patients serving at home are being allowed to non-medical profession like home helper.
Activities of Daily Living↗
Innate differences between simian-human immunodeficiency virus (SHIV)(KU-2)-infected rhesus and pig-tailed macaques in development of neurological disease.
Neurological disease associated with HIV infection results from either primary replication of the virus or a combination of virus infection and replication of opportunistic pathogens in the CNS. Recent studies indicate that the primary infection is mediated mainly by viruses that utilize CCR5 as the coreceptor; it is not known whether the syndrome can be mediated by viruses that use the CXCR4 coreceptor. The macaque model of the disease using simian immunodeficiency virus (SIV) has confirmed that CCR5-using viruses such as SIV(mac)251 can cause primary disease in the CNS. In this report we have examined the role of simian-human immunodeficiency virus (SHIV)(KU-2), a CXCR4 virus which replicates productively in rhesus macrophages, in causing CNS disease. A survey of archival brain tissues from SHIV(KU-2)-infected rhesus and pig-tailed macaques that succumbed to AIDS showed productive viral replication in the CNS of 10 of 14 rhesus animals. Eight of these 10 had additional infections with opportunistic pathogens. In contrast, 21 of 22 pig-tailed macaques had no evidence of productive viral infection in the brain. In an earlier study we had shown that inoculation of SHIV-infected rhesus macaques with eggs of Schistosoma mansoni, a potent inducer of IL-4, resulted in enhanced replication of the virus in tissue macrophages. In the present study, we compared the replication of the virus in macrophages from normal rhesus and pig-tailed macaques and determined further whether exogenous IL-4 could cause enhancement of virus replication in these cells. These studies showed that the virus replicated productively in rhesus macrophages, and this was enhanced significantly after recombinant macaque IL-4 was added to the medium. IL-4 also caused enhancement of virus production in macrophages isolated from virus-infected animals. In contrast, the virus replicated only minimally in pig-tailed macaque macrophages and supplemental IL-4 had negligible effects. The data thus suggested that failure of pig-tailed macaques to develop encephalitis was due to the innate resistance of macrophages from this species of macaque to support replication of SHIV(KU-2). The ability of the virus to replicate in the brains of rhesus macaques was dependent on coinfection in the brain with opportunistic pathogens which presumably induced both macrophages and IL-4 in the CNS microenvironment. A supportive role for IL-4 in the CNS disease was suggested by the presence of IL-4 RNA in the encephalitic brains of rhesus macaques and reduced levels of this cytokine in the brains from pig-tailed macaques.
Acquired Immunodeficiency Syndrome↗
Lipids and neurological diseases.
Neurological diseases, such as multiple sclerosis (MS), Sjögren-Larsson syndrome, Reye's syndrome, and Refsum's syndrome (herediopathica atactica polyneuroformis), and many others afflict millions of persons yearly and have no successful treatment available. A common aspect of these diseases appears to be a lipid imbalance involving the essential fatty acids (EFA), linoleic and linolenic, and trace fatty acids which result from faulty lipid metabolism. It is proposed that treatments for these diseases should be sought through diet and metabolic enzymes rather than drugs.
Fatty Acids, Essential↗
Disorders of gastrointestinal motility in neurologic diseases.
Neurologic diseases can affect the bowel at several levels of innervation--by altering the electrical activity that controls smooth muscle, the enteric nervous system, or the extrinsic neural pathways to the gut. This review concentrates on disorders of motility that occur in conjunction with diseases of the extrinsic neural supply (from the level of the brain to the postganglionic fibers) and those generalized disorders that affect gut smooth muscle. Modern technology, such as gastrointestinal scintigraphy and manometric techniques that measure esophageal, gastroduodenal, and anorectal motility (intraluminal pressures), has provided better methods to study the pathophysiologic aspects of gut motility in diseases of the nervous system. Distinguishing the neuropathies of the extrinsic nervous system from those of the intrinsic (enteric) nervous system is not always possible because the available techniques evaluate only the end-organ--that is, the motor function of the gut. Degenerative or infiltrative (myopathic) disorders of gut smooth muscle, however, can be distinguished from such neuropathies, and careful and systematic evaluation of autonomic function can often identify the level of disordered function in the neural-gut axis.
Autonomic Nervous System Diseases↗
The eye in neurological disease.
Neurological disease can involve the eye in many ways. Every structure--the conjunctiva, cornea, anterior chamber, iris, lens, vitreous humour, retina, choroid, and optic nerve--can be affected. In many cases, ocular involvement is the first manifestation of the underlying disease. In such cases, the ability of the physician to recognise the nature and significance of the ocular abnormality can lead to early diagnosis and successful treatment of the underlying condition. In other cases, recognition of the ocular abnormality can prevent permanent visual dysfunction.
Eye↗
[Sleep in neurologic diseases].
Neurological diseases may induce alterations in sleep which are difficult to interpret owing to the multiple interferences introduced by treatments, associated somatic symptoms and time-related changes in causal lesions. The consequences of vascular or traumatic lesions observed in man confirm the data obtained from experimental lesions created in animals, thereby throwing some light on the roles played by the cerebral cortex, the thalamus and the brain stem nuclei. In degenerative diseases polygraphic recordings show subclinical signs of extension which are exceptionally specific of any particular type of degeneration. In epileptic patients recordings have determined the distribution of intercritical activities in the various waking and sleep stages: an increase of the activities during sleep appears to be a fairly independent constitutional feature. To sum up, one may say that the various sleep and waking control systems may be diversely affected by diseases of the nervous system. States of vigilance modulate some critical pathologies, such as epilepsy, according to modalities and a physiopathology that have not yet been fully elucidated.
Brain Injuries↗
Evaluation and management of the urologic consequences of neurologic disease.
Neurologic disorders create important functional urinary tract abnormalities. Loss of bladder reflex inhibition and coordination due to neurologic disease or injury to higher centers may lead to morbidity such as recurrent urinary tract infection, hydronephrosis, urinary tract stones and loss of renal function. This paper discusses neurogenic bladder disease using a descriptive urodynamic format. The importance of detrusor hyperreflexia and internal and external sphincter dyssynergia are discussed in detail. Finally, a practical clinical management plan is discussed for patients with urologic dysfunction due to cerebrovascular accident, Parkinson's disease, multiple sclerosis, spinal cord injury, and peripheral neuropathy.
Cerebrovascular Disorders↗
Increasing role of telehomecare in treating of neurological diseases.
Neurological disorders, such as Alzheimer's disease, Parkinson's disease and stroke recovery, strike an estimated 50 million Americans each year, costing billions of dollars in medical expenses each year, not to mention the countless personal losses and the immeasurable emotional impact on families and patients that such diseases inflict. Due to the complex nature of neurological diseases, the treatment of these diseases often requires two types of care: neurological care and mental health care.
Home Care Services↗
[HTLV-I in patients from Barcelona with connective tissue diseases, neurologic demyelinating diseases and lymphoproliferative syndromes].
The presence of antibodies against HTLV-I was investigated with ELISA and Western blot techniques in 76 patients with lymphoproliferative syndromes (n = 53), idiopathic subacute myelopathies (n = 4), chronic T-lymphocytosis (n = 3) and collagen vascular diseases (n = 16) diagnosed in the Barcelona area. 9 HIV seropositive patients were included: 7 with lymphoma, 1 with chronic T-lymphocytosis and 1 with polymyositis. Although 3 samples were repeatedly positive with ELISA, none was confirmed with Western blot. These results suggest that in our country, contrasting with areas where HTLV-I infection is endemic, acute and chronic lymphoproliferative diseases, collagen vascular diseases and demyelinating neurologic diseases are not associated with HTLV-I infection. The development of lymphoma in patients seropositive for HIV also could not be related with HTLV-I infection.
Adult↗
Neuro-ophthalmologic manifestations of systemic disease and neurologic disease.
Neuro-ophthalmology is a difficult and challenging field for ophthalmologists, orthoptists, and neurologists. Unfortunately, signs and symptoms of these patients can be very subtle and easily overlooked. Although neuro-ophthalmologic cases are rare in the practice of a general ophthalmologist, missing the diagnosis can have severe impact on the patient's health. The authors review last year's publications of neuro-ophthalmologic manifestations of systemic and neurologic disease.
Brain Neoplasms↗
Neuro-ophthalmologic manifestations of systemic disease and neurologic disease.
Neuro-ophthalmology is a difficult and challenging field for both ophthalmologists and neurologists. Unfortunately, signs and symptoms of these patients can be very subtle and easily overlooked. Although neuro-ophthalmologic cases are rare in the practice of a general ophthalmologist, missing the diagnosis can have a severe impact on the patient's health. This paper reviews the past year's publications of neuro-ophthalmologic manifestations of systemic and neurologic disease.
Brain↗
IATROGENIC NEUROLOGICAL DISEASES. SOME NEUROLOGICAL COMPLICATIONS OF SURGICAL TREATMENT.
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Brain↗