People living near a steel plant or other source of manganese emissions have increased risk of developing Parkinson’s. One million Americans live with the degenerative disease, according to the Parkinson’s Disease Foundation. Farm pesticides increase the chance of developing it, but little is known about the effects of urban life.
“The environmental risk factors of Parkinson’s are relatively understudied, particularly in cities, where the vast majority of patients with Parkinson’s, said by e-mail Dr. Brad A. Racette, School of Medicine at Washington University in St. Louis, Missouri.
Racette’s team analyzed data from 5 million Medicare beneficiaries had not moved from county between 1995 and 2003. They then compared the number of cases of Parkinson industrial emissions of copper, lead and manganese obtained from the Environmental Protection Agency.
By 2003, less than 1 percent of city dwellers had Parkinson’s. In counties with low or no emission of metals, 274, 100,000 residents had the disease, compared with 489 residents in counties with high levels of manganese. The risk remained high after accounting for age, sex and ethnicity, published in the American Journal of Epidemiology. In areas with high levels of copper releases also reported more cases of Parkinson’s, but this increase was so slight that it could be attributed to chance.
The team known whether manganese actually made more people develop Parkinson’s. It is possible that in counties with high emissions of manganese influenced other risk factors.
Parkinsonism is a clinical syndrome that encompasses four aspects cardinal bradicinecia (slowness and lack of movement), muscle rigidity, tremor at rest (usually killed during voluntary movements) and postural balance disorders generated gait disorders and falls to soil.
The most common cause of parkinsonism is idiopathic Parkinson’s disease, first described by James Parkinson in 1816 under the name of “paralysis” agitans or shaking palsy “, who takes its current name.
The diagnosis of Parkinson’s disease should not be sure until it is known in detail all drugs that the patient, consciously or inadvertently, come take at the time of the query.
It is well known that neuroleptics (phenothiazines, butyrophenones) may trigger events and parkinsonian tremor by blocking postsynaptic dopamine receptors in the striatum. The same happens with the depleting dopamine (reserpine, tetrabenazine).
Selective blockers of calcium channels (cinnarizine, flunarizine), masked in various commercial preparations of routine administration can produce similar manifestations full or partial recovery in all patients after discontinuation of medication and within a variable.
Some authors argue that drug-induced parkinsonism may be a latent or subclinical parkinsonism revealed by antidopaminergic medication. It is noteworthy that late buccolingual dyskinesia caused by prolonged use of neuroleptics may be associated with parkinsonian manifestations but hardly reason for misdiagnosis is the presence of stereotyped slow and continuous movements that occur in the lower face (lips , jaw and tongue).
The distal parts of the body and trunk tend to show small movements of flexion and extension, while the proximal muscles are not compromised. When the patient is standing may have repetitive movements of the lower extremities (go hard). The patient often develops secondary akathisia. It is assumed that tardive dyskinesia was given to a hypersensitivity of postsynaptic receptors for dopamine and its increased secretion secondary to blockade of these receptors.
Part of parkinsonian patients develops, over time, subcortical dementia.
Although the diagnosis of Parkinson’s disease is largely clinical, can take account of hyposmia (may precede up to 20 years to your appearance), positron emission tomography showing decrease of dopamine in the striatum, markers recently biological and electromyography to show subclinical tremor.
An important chapter of this issue is that of drug-induced parkinsonism, which generally refers to the interruption but not always. Drugs that can induce are neuroleptics (phenothiazines, butyrophenones), depleting dopamine (reserpine, tetrabenazine) and calcium channel blockers (cinnarizine, flunarizine).
The clinician, before diagnosing Parkinson’s disease, should take into account the possibility cited in the preceding paragraph as well as a number of neurological disorders that are targets of specialized study.
Fustinoni (in Semiology Nervous System ) says the following signs and symptoms exclude the diagnosis of Parkinson’s disease:
Signs and Symptoms that exclude Parkinson
l buccolingual dyskinesia (parkinsonism drug)
l hyperreflexia not justified by previous stroke (Vascular parkinsonism)
l pseudobulbar syndrome (vascular parkinsonism)
l or intentional tremor predominant attitude (Essential tremor)
Since the caudate nucleus and putamen, there is a path to the black substance secreted by the inhibitory neurotransmitter GABA (gamma aminobutyric acid). In turn, a series of fibers originating in the substantia nigra send axons to the caudate and putamen, secreting an inhibitory neurotransmitter from their terminals, dopamine. This pathway maintains a degree of mutual inhibition of the two areas and the injury causes a series of neurological syndromes, among which is Parkinson’s disease.
The fibers from the cerebral cortex secrete acetylcholine, an excitatory neurotransmitter, in the neostriatum. The causes of abnormal motor activities that make up Parkinson’s disease are related to the loss of the secretion of dopamine by nerve endings in the substantia nigra on the neostriatum (nigrostriatal tract) to the left of suppression.
Thus, neurons that secrete predominantly acetylcholine, excitatory signals broadcast to all basal ganglia, responsible in whole, motor planning and some cognitive functions. It requires a loss of approximately 80% of striatal dopamine to the symptoms.
Histologically, the disease is characterized by the presence of Lewy bodies in the substantia nigra and locus coeruleus, but can also appear in other locations of the extrapyramidal system. These intracytoplasmic inclusions composed of protein, free fatty acids, sphingomyelin, and polysaccharides.
The incidence of Parkinson’s disease, assessment difficult, is variable ranging from 4.5 to 21 cases per 100,000 population per year. It is the most accurate estimate of the disease and the extent of new cases in a period of time. Prevalence is the total number of cases in a population and at the same time.
It was James Parkinson who described the disease in 1817 under the name of paralysis agitans. “The etiology is unknown but pathophysiologically related to a deficiency of dopamine in the striatum, resulting from neuronal degeneration that mainly affects the compact zone of the substantia nigra (locus niger), the locus coeruleus and other properties in catecholamine-containing which are eosinophilic inclusions known as Lewy bodies “(JC Fustinoni).
The extrapyramidal motor system is the set of motor pathways that exert a major influence on spinal motor circuits, brain stem, cerebellum and cortex. Has fibers from the motor cortex that connect with the basal ganglia, particularly the caudate and putamen, as well as bulbar nuclei (red nucleus, substantia nigra and reticular formation) or midbrain and terminate in the anterior horn of the spinal cord.
Several hypotheses attribute the disease to genetic factors (genes have been identified as responsible mutants), metabolic (oxidative stress) or environmental (pesticides, aluminum). 10% of patients exhibit genetic predisposition. One out of every thousand people with the disease is less common in blacks and Japanese.
The onset of the disease is insidious and, retrospectively, patients may report having suffered from hyposmia, pain erratic confused as arthritic origin, dysesthesias burning sensations, depression, mental or seborrheic dermatitis, which can not always be taken into account as a prodrome.
A multicenter study is published today in JAMA has identified two genes that may be risk factors for development of Alzheimer’s disease late onset, although not help quantify the risk in carriers of these alterations.
Researchers at Boston University, U.S., in collaboration with scientists from the Rotterdam Study, coordinated by Monique Breteler, the Cardiovascular Health Study, led by Oscar Lopez, AGES-Reykjavik study, coordinated by Lenore Launer, the study in May AD , directed by Steve Younkin, the European Consortium of Alzheimer’s Disease, who leads Philippe Amouyel, the ACE Foundation in Barcelona, coordinated by Merce Boada, and the Consortium for Genetic and Environmental Risk of Alzheimer’s Disease, directed by Julie Williams, have identified two genes that may be risk factors for developing Alzheimer’s disease late onset.
The work, published today in The Journal of the American Medical Association, was carried out by analysis of genome wide association. The researchers have identified two new genes in specific locations in DNA. These genes appear to be independent of those already established by its association with the disease of Alzheimer’s, such as apolipoprotein E (APOE). Continue reading