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Without hallucinations, other types of dementias should be considered, including vascular disease, Alzheimer’s disease, and frontotemporal dementia. DLBD is a condition where Lewy bodies are present in the cerebral cortex as well as in the brainstem nuclei. The heredodegenerative disease, known as frontotemporal dementia, is an autosomal dominant disorder due to mutations of the tau gene or the progranulin gene on chromosome 17; the full syndrome presents with dementia, loss of inhibition, parkinsonism, and sometimes muscle wasting.

Thus, younger patients are often started with a dopamine agonist rather than levodopa since these drugs are much less likely to cause these motor complications, but they are less effective in reversing the symptoms of PD. Other drugs that influence brain dopamine are also used. Besides being metabolized by aromatic amino acid decarboxylase (commonly known as dopa decarboxylase), levodopa is also metabolized by catechol-O-methyltransferase (COMT) to form 3-O-methyldopa. COMT inhibitors (entacapone and tolcapone) can be added to levodopa to extend the plasma half-life of levodopa, thereby prolonging the duration of action of each dose of levodopa.

Two MAO-B inhibitors are selegiline and rasagiline. These drugs have also been shown to slow the clinical progression of PD. After levodopa, the next most powerful drugs in treating PD symptoms are the dopamine agonists. Several of these are available. The ergot compounds of pergolide, bromocriptine, and cabergoline have the potential to induce fibrosis (cardiac valvulopathy and retroperitoneal, pleuropulmonary and pericardial fibrosis, so these agents are not recommended, and indeed pergolide has been withdrawn from the US market.

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Guidelines on Sterilization and Disinfection Methods by World Health Organization
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