Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe a case of pathologic jealousy (Othello syndrome) in a patient with Parkinson disease, which abated after discontinuing amantadine. We indicate that early recognition and treatment of the syndrome in this disease may avert physical violence. We also believe that our report further suggests a link between this specific behavioral disorder and dopaminergic activity.
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PMID:Reversible pathologic jealousy (Othello syndrome) associated with amantadine. 195 68

We have studied 97 patients with dementia who have been discharged from our hospital and 106 inpatients with dementia who have been admitted during last two years in our hospital. The diagnosis of dementia was done according to the criteria of DSM-III. Based on their clinical course, neurological signs, Hachinski's ischemic score and neuroradiological findings, we divided patients into 4 groups, [senile dementia of the Alzheimer type (SDAT), vascular dementia (VD), unclassified dementia and other dementias which includes dementia with Parkinson's disease or motor neuron disease, etc.]. Concerning 70 demented patients who died during hospitalization, the average age of onset and the duration of illness of SDAT were 80.5 years old and 4.6 years respectively and those of VD were 77.6 years old and 2.7 years respectively. The common causes of death were pneumonia (50%) and cardiac failure (24%). Recurrence of cerebral vascular accident (CVA) was also another frequent cause of death in VD. The most common behavioral problems causing admission in patients of SDAT were aimless wandering, nocturnal delirium, illusion and hallucination. In VD, nocturnal delirium, aimless wandering, violence and abnormal monologue were most common causes of admission. The important causes degrading ADL of inpatients were fracture, especially fracture of the hip joint, pneumonia, intestinal bleeding and CVA. Concerning the increase of the population of over 75 years old, it will be suggested that the care and treatment of demented patients in this age group will become a major social problem.
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PMID:[Clinical and epidemiological studies on inpatients with dementia]. 238 92

mental retardation: timing and thresholds; (italic)b(/italic)) endocrine dysfunction and developmental disabilities: dose and target implications; (italic)c(/italic)) attention-deficit disorder-ADHD and learning disabilities; and (italic)d(/italic)) new horizons: extending the boundaries. Support for the Rochester conference came from both public and private sources. The National Institute of Environmental Health Sciences (NIEHS), the National Institute of Child Health and Human Development, and the EPA represented the federal government. The conference also received grants from several foundations: the Jennifer Altman Foundation, the Heinz Family Foundation, the National Alliance for Autism Research, the Violence Research Foundation, the Wacker Foundation, and the Winslow Foundation. The second of these conferences helped launch a new Center for Children's Health and the Environment at the Mount Sinai School of Medicine. It was held in New York City on 24-25 May 1999, and was convened specifically to consider the intersection between neurodevelopmental impairment, environmental chemicals, and prevention. Over 300 health scientists, pediatricians, and public health professionals examined the growing body of evidence linking environmental toxins to neurobehavioral disorders. The conference title was Environmental Influences on Children: Brain, Development, and Behavior. The conference began by reviewing well-known examples of deleterious effects of environmental chemicals, including lead and PCBs, on children's brains. The conferees then considered the potential impact of environmental chemicals on neurological disorders with particular focus on ADHD, autism, and Parkinson's disease. The inclusion of Parkinson's disease was intended to signal the notion that exposures in early life may have an influence on the evolution of neurological disease in later life. Support for the Mount Sinai conference came from the Superfund Basic Research Program (NIEHS); The Pew Charitable Trusts; the Institute for Health and the Environment at the University of Albany School of Public Health; the Agency for Toxic Substances and Disease Research (ATSDR); the Ambulatory Pediatric Association; Myron A. Mehlman, PhD; the National Center for Environmental Assessment (EPA); the National Center for Environmental Health (CDC); the National Institute of Child Health and Human Development; the Office of Children's Health Protection (EPA); Physicians for Social Responsibility; The New York Academy of Medicine; The New York Community Trust; and the Wallace Genetic Foundation. The impact of environmental toxins on children's health has become a topic of major concern in the federal government. Eight new research centers in children's environmental health have been established in the past 2 years with joint funding from EPA and NIEHS. Clinical units that specialize in the treatment of children with environmentally induced illness have been developed across the nation with grant support from ATSDR. The American Academy of Pediatrics has just published its (italic)Handbook of Pediatric Environmental Health (/italic)((italic)17(/italic)), the "Green Book," which is available to pediatricians throughout the Americas. Children's environmental health has climbed to a critical position as we launch the new millennium. This monograph marks a significant milestone in the evolution of this emerging discipline.
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PMID:The developing brain and the environment: an introduction. 1085 30

At the Department of Neurology and Internal Medicine at our hospital, there are 22 outpatients who are nursed at home. Their diseases are Parkinson's disease, spinal cerebellar degeneration, dementia and other diseases. The problem is how we should care for and support these patients in the future, now that the official Care Insurance System has started. We discuss how we could support such patients, through the case of a patient suffering from Parkinson's disease. The patient was a 69-year-old female. In 1991, she developed Parkinson's disease, accompanied with trembling in her right upper limb. Her condition was controlled at our hospital. Is April 1999, she lost strength in her right thigh without any previous notice, so she was hospitalized for treatment. For a period, she became aggressive from hallucinations and delusions and she had to be taken care of all day. Her only daughter lived apart and her 72-year-old husband was also suffering from Parkinson's disease. In spite of such conditions, she hoped to receive home care and her husband accepted that. We asked what they would want us to do. We had meetings together with the staff of the local administration, doctors, nurses, and pharmacists. The report from our hospital staff says, "It may be difficult for only her family to support her. She needs other supporting systems." She came to our hospital twice a month. We made an effort to understand her condition with the help of the report of a visiting nurse. However, her illusions and delusions made it difficult even to utilize the short-stay. Her husband sometimes uses violence and says. "I can't stand this any more--her unrest, micturition at night and refusal to eat." Nevertheless, she continues to say "I want to stay at home." They have had considerable trouble. The following are necessary for home care of some patients. 1. Understanding what a patient and her family want to do. Cooperating with the staff of the administration, in consideration of the Care Insurance System. 2. Studying with incurable neurology patients using pamphlets or other materials and supporting them, 3. Discussing how to act in concert with patients at home and outpatients at the hospital involving a risk without MSW.
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PMID:[Continuous nursing of incurable patients at home--the case of a patient with Parkinson's disease]. 1119 Mar 7

Manganese is an essential nutrient that also may be toxic at high concentrations. Subjects chronically exposed to manganese-laden dust in industrial settings develop neuropsychological changes that resemble Parkinson's disease. Manganese has been proposed as an additive to gasoline (as a replacement for the catalytic properties of lead), which has generated increased research interest in the possible deleterious effects of environmental exposure to manganese. Low-level exposure to manganese has been implicated in neurologic changes, decreased learning ability in school-aged children, and increased propensity for violence in adults. However, a thorough review of the literature shows very weak cause-and-effect relationships that do not justify concern about environmental exposure to manganese for most of the North American population.
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PMID:Does environmental exposure to manganese pose a health risk to healthy adults? 1514 30

Peripheral nerve injury is a common clinical problem, and the development of novel strategies to enhance peripheral nerve regeneration is important. Traumatic events, including motor vehicle accidents, sports-related injuries, violence, and falls, lead to significant numbers of peripheral nerve lesions. Traumatic nerve injuries are often associated with life-threatening injuries, which must be treated first. During the delay in nerve repair, the transected nerves undergo Wallerian degeneration. Therefore, delay before surgical treatment is critical, but care must also be taken to ensure that nerve reapposition is performed in a manner that will result in a therapeutic benefit. Peripheral nerve repair after transection injury combined with transplantation of myelin-forming glia cells, for example, Schwann cells (SCs) or olfactory ensheathing cells (OECs), may facilitate the regenerative process. Cell-based therapies are being considered in clinical trials for a number of neurological diseases, including multiple sclerosis, spinal cord injury, Parkinson's disease, and stroke. The rationale is that transplanted cells may provide neuroprotection by production of chemokines and neurotrophins or could serve as a replacement therapy. A number of cells derived from adult peripheral tissues for cell therapies are also being actively investigated. These cells include SCs from peripheral nerve, olfactory OECs from the olfactory system, and stromal cells from bone marrow (mesenchymal stem cells, MSCs). In principle, these cells could be derived autologously, and used acutely or expanded in culture and used for cell-based therapies. Here, we review experimental work demonstrating the potential of one of these cells, the OEC, as an experimental tool for promoting recovery in peripheral nerve injury.
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PMID:Chapter 22: Transplantation of olfactory ensheathing cells for peripheral nerve regeneration. 1968 51

Parasomnias are sleep-related abnormal behaviors. They are frequent and overlooked causes of nocturnal disruptive behavior in the elderly, especially when patients are cognitively impaired. Confusion and violence can result in sleep disruption, injuries for the patients or their bed partners, caregivers distress, and they can be a motive for institutionalization. Parasomnias include the NonREM sleep disorders of arousal (sleepwalking, sleep terrors, confusional arousals and sleep-related eating disorder), the REM sleep behavior disorder (RBD) and more rarely the parasomnia overlap syndrome, which associates both NREM and REM parasomnias. Patients with NREM sleep parasomnias are confused, eyes open, with a glazed look during their nocturnal behaviors, and they have a post-episode amnesia. They shout and bolt from the bed (night terrors), look about in a confused manner, walk and speak (sleepwalking), and eat peculiar or inedible food (sleep-related eating disorders). These behaviors, which are frequent in young adults, may be triggered by short-half live hypnotics in elderly. During the parasomnia, the brain is partially awake (enough to perform complex motor and verbal action), and partially asleep (without conscious awareness or responsibility). RBD is characterized by a loss of the normal muscle atonia that accompanies REM sleep. Patients have excessive motor activity such as punching, kicking, or crying out in association with dream content. RBD are frequent in Parkinson's disease and dementia with Lewy bodies and may precede the cognitive or motor symptoms of these diseases by 5 to 10 years. RBD can also be promoted by antidepressants. When combined with thorough clinical interviews, the video-polysomnography is a powerful tool, especially for discriminating the parasomnia from nocturnal frontal lobe epilepsy, sleep apneas and periodic leg movements. Ensuring safety and withdrawing deleterious treatments are useful in patients with violent activities, potential injurious or bothersome to other household members. Clonazepam and melatonin (3-12 mg) are highly effective for treating RBD.
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PMID:[Disruptive nocturnal behavior in elderly subjects: could it be a parasomnia?]. 2052 41

Clozapine is the best treatment option in several clinical circumstances, including treatment-resistant schizophrenia, non treatment-resistant schizophrenia, suicide risk in schizophrenia spectrum disorders, aggressiveness or violence in psychiatric patients, psychosis in Parkinson's disease, prevention and treatment of tardive dyskinesia. However, clozapine is associated with many serious side effects. Furthermore, monitoring requirements, i.e., frequent blood draws and frequent visits, discourage clozapine use. Therefore, the drug is underused. The only way to avoid the underuse of clozapine is full awareness of its side effects and competence to minimize them. The aim of the paper is reviewing the safety profile of clozapine and the suggested strategies in the management of its side effects, including neutropenia, eosinophilia, seizures, myocarditis, weight gain, diabetes, metabolic syndrome, hypersalivation, fever, constipation, ileus, urinary incontinence, sweating. The neuropsychiatric side effects of clozapine are not discussed in this review.
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PMID:Clozapine safety, 35 years later. 2212 92

In Parkinson's disease, rapid eye movement sleep behaviour disorder is an early non-dopaminergic syndrome with nocturnal violence and increased muscle tone during rapid eye movement sleep that can precede Parkinsonism by several years. The neuronal origin of rapid eye movement sleep behaviour disorder in Parkinson's disease is not precisely known; however, the locus subcoeruleus in the brainstem has been implicated as this structure blocks muscle tone during normal rapid eye movement sleep in animal models and can be damaged in Parkinson's disease. Here, we studied the integrity of the locus coeruleus/subcoeruleus complex in patients with Parkinson's disease using combined neuromelanin-sensitive, structural and diffusion magnetic resonance imaging approaches. We compared 24 patients with Parkinson's disease and rapid eye movement sleep behaviour disorder, 12 patients without rapid eye movement sleep behaviour disorder and 19 age- and gender-matched healthy volunteers. All subjects underwent clinical examination and characterization of rapid eye movement sleep using video-polysomnography and multimodal imaging at 3 T. Using neuromelanin-sensitive imaging, reduced signal intensity was evident in the locus coeruleus/subcoeruleus area in patients with Parkinson's disease that was more marked in patients with than those without rapid eye movement sleep behaviour disorder. Reduced signal intensity correlated with the percentage of abnormally increased muscle tone during rapid eye movement sleep. The results confirmed that this complex is affected in Parkinson's disease and showed a gradual relationship between damage to this structure, presumably the locus subcoeruleus, and abnormal muscle tone during rapid eye movement sleep, which is the cardinal marker of rapid eye movement sleep behaviour disorder. In longitudinal studies, the technique may also provide early markers of non-dopaminergic Parkinson's disease pathology to predict the occurrence of Parkinson's disease.
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PMID:The coeruleus/subcoeruleus complex in rapid eye movement sleep behaviour disorders in Parkinson's disease. 2380 36

Clozapine is, and will remain in the coming years, an irreplaceable drug in psychiatry which has elective indication in treatment-resistant schizophrenia, suicide risk in schizophrenia spectrum disorders, aggressiveness or violence in psychiatric patients, psychosis in Parkinson's disease, prevention and treatment of tardive dyskinesia. Unfortunately, the drug is largely underused for many and serious side effects. Only a good knowledge of these side effects and of the main strategies to prevent their occurrence or minimize their impact can allow overcoming the underutilization of this valuable therapy. The article describes the clinical and epidemiological features of the non-motor side effects of clozapine including blood dyscrasias, constipation, diabetes, enuresis, fever, hepatitis, hypersalivation, ileus, myocarditis, nephritis, priapism, seizures, serositis, weight gain and metabolic syndrome. The paper suggests several strategies, supported by scientific evidence, in the management of these side effects. The neuropsychiatric side effects of clozapine are not discussed in this review.
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PMID:Clozapine safety, 40 years later. 2480 63


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