Secondary Parkinsonism refers to a group of diseases which, although similar characteristics MP, but have another cause. Atypical Parkinsonism refers to a group of other neurodegenerative diseases as MP that have some features of MP, but still have some other clinical features and a different pathology. The diagnosis is made based on the clinical picture and response to levodopa. The treatment is causal aligned as far as possible.
Parkinsonism is caused by medicines; dumplings, diseases other than MP or exogenous toxins.
Secondary Parkinsonism refers to a group of diseases which, although similar characteristics MP, but have another cause. Atypical Parkinsonism refers to a group of other neurodegenerative diseases as MP that have some features of MP, but still have some other clinical features and a different pathology. The diagnosis is made based on the clinical picture and response to levodopa. The treatment is causal aligned as far as possible. Parkinsonism is caused by medicines; dumplings, diseases other than MP or exogenous toxins. In secondary parkinsonism, the mechanism consists of a blockage or malfunction of the effects of dopamine in the basal ganglia. The most common cause of secondary Parkinsonism is use of drugs which reduce the dopaminergic activity These drugs include antipsychotics (eg. B. phenothiazine, thioxanthene, butyrophenone), antiemetics (such. As metoclopramide, prochlorperazine), and drugs that degrade dopamine ( z. B. tetrabenazine, reserpine). Atypical parkinsonism includes neurodegenerative diseases such as progressive supranuclear palsy, diffuse dementia with Lewy bodies, multiple system atrophy and corticobasal degeneration. Causes of secondary and atypical parkinsonism basic observations Neurodegenerative Diseases Amyotrophic Lateral Sclerosis Guam Parkinson dementia complex Speaks poorly to anti-Parkinson’s drugs in corticobasal degeneration Begins asymmetrical, usually caused by the age of 60 cortical and basal ganglia characters, often with apraxia , dystonia, myoclonus and alien limb syndrome (movement of a limb, to be independent of the conscious control of the patient n seems) Executes after about 5 years to immobility and after about 10 years to death Speaks bad (for anti-Parkinson drugs from dementia for. As Alzheimer’s dementia, chromosome 17 associated frontotemporal dementias, diffuse dementia with Lewy bodies) Parkinsonism often typically (with prominent memory loss Alzheimer’s dementia) precedes dementia, impaired language (frontotemporal dementia) visuospatial impairment (diffuse dementia Lewy bodies) multiple system atrophy may also include prominent autonomic dysfunction may also include prominent cerebellar dysfunction Can severe Parkinson’s features include, usually with poor response to levodopa Causes often early falls and balance disorders Speaks poorly to anti-Parkinson’s drugs to Progressive supranuclear palsy first manifestations with gait and balance disturbances caused in the classical form a progressive eye paralysis that begins with an impairment of the Abblicks Speaks poorly to anti-Parkinson’s drugs to spinocerebellar ataxia (usually type 2 or type 3) Manifested usually located first with imbalance and poor coordination Speaks poorly to anti-Parkinson’s drugs to other diseases: cerebrovascular disease Manifesting with rigidity and bradykinesia or akinesia (akinetic-rigid syndrome) which extend predominantly in the lower extremities, with prominent gait disturbances and symmetrical symptoms rarely speaks for anti-Parkinson drugs to brain tumors in the vicinity of the basal ganglia Manifesting with hemiparkinsonism (d. H. Causes only on one side of the body) Repeated traumatic brain injury often dementia (caused by different mechanisms rarely caused by Liquorabflussstörung at increased CSF pressure (obstructive hydrocephalus) hypoparathyroidism as dementia pugilistica) hydrocephalus Usually characterized by normal CSF pressure (normal pressure) and causes calcification of the basal ganglia can chorea and athetosis cause Viral (z. B. West Nile) encephalitis, Can temporarily cause parkinsonism or rare autoimmune infectious or post-infectious during the acute phase, even in the long term (eg. B. postencephalitic parkinsonism after encephalitis lethargica epidemic 1915-1926) In postenzephalitischem parkinsonism consist enforced, prolonged deviations of the head and eyes (oculogyric crisis), other dystonia, autonomic instability, depression and personality changes. Medicines antipsychotics Can reversible * Parkinsonism cause meperidine analogue (N-MPTP) Can sudden, irreversible parkinsonism cause Comes with consumers of intravenous drugs before metoclopramide reserpine lithium, long-term use Can May cause reversible * Parkinsonism be dose related or associated with susceptibility are ( risk factors include older age and female gender) lithium sometimes occurs cerebellar dysfunction toxins Carbon monoxide can cause methanol used as a “contaminated moonshine” (contaminated illegal whiskey) irreversible parkinsonism cause hemorrhagic necrosis of the basal ganglia manganese may cause chronic toxicity parkinsonism with dystonia and cognitive changes If a rule in relation to activities (eg. As welding), but may be due * After discontinuation of the medication, the symptoms usually go within a few weeks back, but they can last for months and by the abuse of methcathinone (in of ephedrine produced bath salts). N-MPTP produced during unsuccessful attempts to establish meperidine for illegal use. N-MPTP = N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. Symptoms and complaints parkinsonism caused the same symptoms as MP (z. B. resting tremor, rigidity, bradykinesia, postural instability). Diagnosis Clinical assessment, response to levodopa therapy and, for the differential diagnosis, sometimes neuroradiological imaging To MP distinguishable from secondary or atypical parkinsonism, the doctor noted whether levodopa causes a dramatic improvement, which suggests MP. Causes of Parkinson’s disease can be identified as follows:. A thorough history, including labor, drug / drug and family history evaluation of neurological deficits that are characteristic of other neurodegenerative diseases as MP Neuroimaging, if indicated deficits that neurodegenerative other speak diseases as MP include views paralysis, signs of dysfunction of the corticospinal tract (z. B. hyperreflexia), myoclonus, autonomic dysfunction (if early or advanced), cerebellar ataxia, prominent dystonia, ideomotor apraxia (inability hand movements imitate), early dementia, early falls and wheelchair duty. Therapy treatment of the cause, the cause of secondary Parkinsonism is corrected, or should, wherever possible, sometimes leading to a clinical improvement or resolution of the symptoms. Drugs for the treatment of MP are often ineffective or provide only temporary benefit. However, amantadine or an anticholinergic (z. B. benztropine) can ameliorate the symptoms of a secondary parkinsonism caused by antipsychotic use. Physical measures to maintain mobility and independence are useful (as MP). These include physical and occupational therapy, training and the use of adaptive devices. Good nutrition is essential. Important points Parkinsonism may be caused by drugs, toxins, neurodegenerative diseases and other disorders that affect the brain (eg., Stroke, tumor, infection, trauma, hypoparathyroidism). Go out on the basis of clinical evaluation of Parkinsonism and differentiate this from MP by lack of response to levodopa; a neuro-radiological imaging may be required. Check for gaps that speak for another neurodegenerative disease as MP. Correct or treat if possible the cause and recommend physical measures to maintain mobility.