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Aaron Rodriguez
Aaron Rodriguez

Boala Parkinson

People with Parkinson's disease often develop a parkinsonian gait that includes a tendency to lean forward; take small, quick steps; and reduce swinging their arms. They also may have trouble initiating or continuing movement.

Boala Parkinson

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Parkinson's disease (PD), or simply Parkinson's,[10] is a chronic degenerative disorder of the central nervous system that mainly affects the motor system. The symptoms usually emerge slowly, and as the disease worsens, non-motor symptoms become more common.[1][5] Early symptoms are tremor, rigidity, slowness of movement, and difficulty with walking.[1] Cognitive and behavioral problems may occur with depression, anxiety, and apathy.[11] Parkinson's disease dementia becomes common in the advanced stages of the disease. Those with Parkinson's can have problems with their sleep and sensory systems.[1][2] The motor symptoms of the disease result from the death of nerve cells in the substantia nigra, a region of the midbrain, causing a dopamine deficit.[1] The cause of this cell death is poorly understood, but involves the build-up of misfolded proteins into Lewy bodies in the neurons.[12][5] Collectively, the main motor symptoms are known as parkinsonism or a parkinsonian syndrome.[5]

Parkinson's disease is the most common form of parkinsonism and is also called idiopathic parkinsonism, meaning that it has no identifiable cause.[19][29] The accumulation of a misfolded protein alpha-synuclein in the brain, and its spread throughout the brain makes Parkinson's disease a neurodegenerative disease classed as a synucleinopathy, and more specifically as an alpha-synucleinopathy (αsynucleinopathy).[30]

Other Parkinson-plus syndromes involve tau, rather than alpha-synuclein. These include progressive supranuclear palsy (PSP) and corticobasal syndrome (CBS). PSP predominantly involves rigidity, early falls, bulbar symptoms, and vertical gaze restriction; it can be associated with frontotemporal dementia symptoms. CBS involves asymmetric parkinsonism, dystonia, alien limb, and myoclonic jerking.[32] These presentation timelines and associated symptoms can help differentiate these similar movement disorders from idiopathic Parkinson disease.

In parkinsonism, rigidity or hypokinesia can be uniform, known as lead-pipe rigidity, or ratcheted, known as cogwheel rigidity.[19][34][39][40] The combination of tremor and increased tone is considered to be at the origin of cogwheel rigidity.[41] Rigidity may be associated with joint pain; such pain being a frequent initial manifestation of the disease.[34] In early stages of PD, rigidity is asymmetrical and tends to affect the neck and shoulder muscles before the muscles of the face and extremities.[42] With the progression of the disease, rigidity typically affects the whole body and reduces the ability to move.

Exposure to pesticides and a history of head injury have each been linked with PD, but the risks are modest. Never drinking caffeinated beverages is associated with small increases in risk of developing PD.[59] Some toxins can cause parkinsonism, including manganese and carbon disulfide.[76][77][78][79]

Medical drugs are implicated in parkinsonism. Drug-induced parkinsonism is normally reversible by stopping the offending agent,[77] such as phenothiazines (chlorpromazine, promazine, etc.); butyrophenones (haloperidol, benperidol, etc.); metoclopramide and Tetrabenazine. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is a drug known for causing irreversible parkinsonism that is commonly used in animal-model research.[77][80][81]

Other identifiable causes of parkinsonism include infections and metabolic derangement. Neurodegenerative disorders may present with parkinsonism, and are also referred to as atypical parkinsonism or parkinson plus syndromes (illnesses with parkinsonism plus some other symptoms distinguishing them from PD) including multiple system atrophy, progressive supranuclear palsy, corticobasal degeneration, and dementia with Lewy bodies.[19][83] Dementia with Lewy bodies is another synucleinopathy and it has close pathological similarities with PD, especially with the subset of PD with dementia known as Parkinson's disease dementia. The relationship between PD and DLB is complex and incompletely understood.[84] It represents a continuum with variable distinguishing clinical and pathological attributes, or it may prove to be separate diseases.[84]

Vascular parkinsonism is the phenomenon of the presence of Parkinson's disease symptoms combined with findings of vascular events (such as a cerebral stroke). The damaging of the dopaminergic pathways is similar in cause for both vascular parkinsonism and idiopathic PD, and so present with similar symptoms. Differentiation can be made with careful bedside examination, history evaluation, and imaging.[85][77][86]

Multiple causes can occur for parkinsonism or diseases that look similar. Stroke, certain medications, and toxins can cause "secondary parkinsonism" and need to be assessed during visit.[16][102] Parkinson-plus syndromes, such as progressive supranuclear palsy and multiple system atrophy, must be considered and ruled out appropriately to begin a different treatment and disease progression (anti-Parkinson's medications are typically less effective at controlling symptoms in Parkinson-plus syndromes).[34] Faster progression rates, early cognitive dysfunction or postural instability, minimal tremor, or symmetry at onset may indicate a Parkinson-plus disease rather than PD itself.[103]

Computed tomography (CT) scans of people with PD usually appear normal.[107] Magnetic resonance imaging has become more accurate in diagnosis of the disease over time, specifically through iron-sensitive T2* and susceptibility weighted imaging sequences at a magnetic field strength of at least 3T, both of which can demonstrate absence of the characteristic 'swallow tail' imaging pattern in the dorsolateral substantia nigra.[108] In a meta-analysis, absence of this pattern was highly sensitive and specific for the disease.[109] A meta-analysis found that neuromelanin-MRI can discriminate individuals with Parkinson's from healthy subjects.[110] Diffusion MRI has shown potential in distinguishing between PD and Parkinson-plus syndromes, as well as between PD motor subtypes,[111] though its diagnostic value is still under investigation.[107] CT and MRI are used to rule out other diseases that can be secondary causes of parkinsonism, most commonly encephalitis and chronic ischemic insults, as well as less frequent entities such as basal ganglia tumors and hydrocephalus.[107]

Dopamine agonists produce side effects, including drowsiness, hallucinations, insomnia, nausea, and constipation.[122][128] Side effects appear with minimal clinically effective doses giving the physician reason to search for a different drug.[122] Agonists have been related to impulse-control disorders (such as increased sexual activity, eating, gambling, and shopping) more strongly than other antiparkinson medications.[145][128] They tend to be more expensive than levodopa.[19]

Boxer Muhammad Ali showed signs of PD when he was 38, but was undiagnosed until he was 42, and has been called the "world's most famous Parkinson's patient".[27] Whether he had PD or parkinsonism related to boxing is unresolved.[201][202]

Boala Parkinson este o afectiune progresiva a sistemului nervos, care afecteaza capacitatea motorie. Simptomele apar treptat, uneori incepand prin tremurul abia perceptibil al uneia dintre maini. Tremurul este frecvent intalnit, dar boala Parkinson mai provoaca si rigiditate sau incetinirea miscarilor.

Rigiditatea picioarelor poate face imposibila ridicarea de pe scaun si mersul. Persoanele care sufera de boala Parkinson in stadiul 5 au nevoie de un scaun cu rotile sau stau la pat. Au nevoie de ingrijire non-stop, pentru orice activitate. In plus, pacientii se pot confrunta cu halucinatii.

Pe langa simptomele motorii, boala Parkinson se poate manifesta si prin simptome care nu au legatura cu miscarea. Deseori, pacientii sunt afectati mai mult de acestea din urma, si anume: apatie, depresie, constipatie, tulburari de somn, pierderea simtului mirosului si tulburari cognitive.

Desi boala Parkinson este incurabila, medicamentele specifice pot reduce semnificativ simptomele. In anumite situatii, medicul poate recomanda interventia chirurgicala pentru a regla anumite zone ale creierului si a combate simptomele. Alte optiuni de terapie includ odihna si exercitii fizice.

Exercitiile fizice sunt importante in cazul persoanelor cu boala Parkinson deoarece ajuta la mentinerea echilibrului, mobilitatii si capacitatii de a desfasura activitatile zilnice. Studiile au aratat ca pacientii care fac miscare timp de cel putin doua ore si jumatate pe saptamana reusesc sa reduca declinul calitatii vietii.

Această afecțiune neurodegenerativă debutează majoritar între 50-60 de ani. Aproximativ 1% dintre persoanele peste 65 de ani dezvoltă simptomele specifice. Numărul de bărbați diagnosticați cu boala Parkinson este de două ori mai mare, comparativ cu cel al femeilor.

Această boală neurologică prezintă un debut lent, iar primul simptom este reprezentat de tremorul de repaus. Acesta este pronunțat în repaus și se diminuează în timpul mișcărilor. Primele afectate sunt mâinile, ulterior, brațele și picioarele. Cu toate că apare în repaus, pacienții diagnosticați cu boala Parkinson nu acuză tremurat în somn.

Stadiul IÎn acest stadiu incipient, pacientul nu prezintă simptome care să interfereze cu activitățile zilnice. Cel mai frecvent simptom este prezența tremorului ușor. Pot apărea modificări ale mersului, ale posturii și ale expresiei faciale. Caracteristic acestui stadiu din boala Parkinson este că doar o parte a corpului este afectată.

Stadiul IV Pacienții diagnosticați cu boala Parkinson stadiul IV necesită, în majoritatea cazurilor, suport pentru a merge (de tipul cadrului). Activitățile zilnice sunt greu de efectuat fără ajutor. 041b061a72


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