draft parkinson

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Hidrosefalus bertekanan normal - Gejalanya mirip yaitu : Walking problems Unsteadiness Leg weakness Sudden falls Shuffling steps Difficulty taking the first step, as if feet were stuck to the floor "Getting stuck" or "freezing" while walking - Ada symp otonom juga : Inability to hold urine Inability to hold stool, or feces (less common) -Tapi pas di CT scan : show ventricular enlargement or other changes that suggest NPH. Newer techniques can actually measure the flow of CSF in the brain. -Cisternography: It highlights absorption of the CSF. -Di LP utk remove csf di area spinal cord lowerback dan diambil yg banyak utk kurangin tekanan di otaknya, usually helps. Lanjutannya bisa d pertimbangkan shunt. Tremor esensial Tremor is more likely to be noticed in the hands. The arms, head, eyelids, or other muscles may also be affected. The tremor rarely occurs in the legs or feet. A person with essential tremor may have trouble holding or using small objects such as silverware or a pen. Tremor nya lebih dr 5 x per detik Tremornya muncul saat gerakan dan kurang tampak saat istirahat, terbalikan parkinson. Etiologinya bsa krn hipertiroid, brti ada gejala hipertiroid lain, ada alcohol withdrawal, too much caffeine.. Hasil ct mri lab smua normal.

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Draft Parkinson

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Page 1: Draft Parkinson

Hidrosefalus bertekanan normal- Gejalanya mirip yaitu :

Walking problemsUnsteadinessLeg weaknessSudden fallsShuffling stepsDifficulty taking the first step, as if feet were stuck to the floor

"Getting stuck" or "freezing" while walking- Ada symp otonom juga :

Inability to hold urine Inability to hold stool, or feces (less common)-Tapi pas di CT scan : show ventricular enlargement or other changes that suggest NPH. Newer techniques can actually measure the flow of CSF in the brain.-Cisternography: It highlights absorption of the CSF.-Di LP utk remove csf di area spinal cord lowerback dan diambil yg banyak utk kurangin tekanan di otaknya, usually helps. Lanjutannya bisa d pertimbangkan shunt.

Tremor esensialTremor is more likely to be noticed in the hands. The arms, head, eyelids, or other muscles may also be affected. The tremor rarely occurs in the legs or feet. A person with essential tremor may have trouble holding or using small objects such as silverware or a pen.Tremor nya lebih dr 5 x per detikTremornya muncul saat gerakan dan kurang tampak saat istirahat, terbalikan parkinson.Etiologinya bsa krn hipertiroid, brti ada gejala hipertiroid lain, ada alcohol withdrawal, too much caffeine..Hasil ct mri lab smua normal.

Penyakit Bingswanger : subcortical vascular dementia, karena adanya damage pd deep layers of white matter di otak. The damage is the result of the thickening and narrowing (atherosclerosis) of arteries that feed the subcortical areas of the brain. Atherosclerosis (commonly known as "hardening of the arteries")

The most characteristic feature of BD is psychomotor slowness - an increase in the length of time it takes, for example, for the fingers to turn the thought of a letter into the shape of a letter on a piece of paper. Other symptoms include forgetfulness (but

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not as severe as the forgetfulness of Alzheimer's disease), changes in speech, an unsteady gait, clumsiness or frequent falls, changes in personality or mood (most likely in the form of apathy, irritability, and depression), and urinary symptoms that aren't caused by urological disease. Brain imaging, which reveals the characteristic brain lesions of BD, is essential for a positive diagnosis.Narrowed vessel keliatan di ct scan

Progresif supra nuklear palsi - Cardinal manifestations:

Supranuclear ophthalmoplegiaNeck dystoniaParkinsonismPseudobulbar palsyBehavioral and Cognitive impairmentImbalance and Difficulties walkingFrequent falls

- Clinical features that distinguish from idiopathic Parkinson’s disease include

symmetrical onset, a lack of or irregular resting tremor, and a reduced response to

dopaminergic drugs (including levodopa).[3]

Degenerasi striatonigra - What is Striatonigral Degeneration?Striatonigral degeneration is a neurological disorder caused by a disruption in the connection between two areas of the brain-the striatum and the substantia nigra. These two areas work together to enable balance and movement. Striatonigral degeneration is a type of multiple system atrophy (MSA). Symptoms of the disorder resemble some of those seen in Parkinson's disease, including rigidity, instability, impaired speech, and slow movements.- Is there any treatment?There is no cure for striatonigral degeneration, and treatments for the disorder have variable success. Treatments used for Parkinson's disease are recommended. However, unlike Parkinson's disease, striatonigral degeneration is not responsive to levodopa. Dopamine and anticholinergics provide some benefit. Generally, treatment is reevaluated as the disorder progresses.

Parkinson plus syndrome

Parkinson-plus syndromes, also known as disorders of multiple system degeneration, is a group of neurodegenerative[1] diseases featuring the classical features of Parkinson's disease (tremor, rigidity, akinesia/bradykinesia, postural

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instability) with additional features that distinguish them from simple idiopathic Parkinson's disease. Some consider Alzheimer's disease to be in this group.[2] Parkinson-plus syndromes are either inherited genetically or occur sporadically.[3]

The atypical parkinsonian or Parkinson Plus syndromes are often difficult to differentiate from Parkinson's disease and each other. They include multiple system atrophy (MSA), progressive supranuclear palsy (PSP), and corticobasal degeneration (CBD). Dementia with Lewy bodies (DLB), may or may not be part of the PD spectrum, but it is increasingly recognized as the second most common type of neurodegenerative dementia after Alzheimer's disease. These disorders are currently lumped into two groups, the synucleinopathies and the tauopathies.[4] They may coexist with other pathologies.[5]

Additional Parkinson-plus syndromes include Pick's disease and olivopontocerebellar atrophy (OPCA).[6] The latter is characterized by ataxia and dysarthria, and may occur either as an inherited disorder or as a variant of multiple system atrophy. MSA is also characterized by autonomic failure, formerly known as Shy-Drager syndrome.[7]

Clinical features that distinguish Parkinson-plus syndromes from idiopathic Parkinson’s disease include symmetrical onset, a lack of or irregular resting tremor, and a reduced response to dopaminergic drugs (including levodopa).[3] Additional features include bradykinesia, early-onset postural instability, increased rigidity in axial muscles, dysautonomia, alien limb syndrome, supranuclear gaze palsy, apraxia, involvement of the cerebellum including the pyramidal cells, and in some instances significant cognitive impairment.[3]

Accurate diagnosis of these Parkinson-plus syndromes is improved when precise diagnostic criteria are used.[3] Since diagnosis of individual Parkinson-plus syndromes is difficult, the prognosis is often poor. Proper diagnosis of these neurodegenerative disorders is important as individual treatments will vary depending on the condition. Nuclear medicine SPECT procedure using 123I-IBZM, is an effective tool in the establishment of the differential diagnosis between patients with Parkinson's disease and Parkinson-Plus syndromes.[8]

FISIOLOGI Substansia nigra yg bikin dpoamin. Neurin di SN pelan2 mati, dopamine jd dikit di produksinya.Imbalans ach dan dopamine bkin Parkinson,Movement dia tur extrapyramidal syst, yaitu sn, st, bsl ganglia, tahalmus.Promote inhibit movement jgBasal ganglia: caudate putamen glibus palidus,.Caudat dan putamen bentus c.striatum.Sn pars kompata produce dopamine to striatum : nigrostriatal pathway.Normalnya ach dan dopamine balance di stiatumPd Parkinson, SN produce less dopamine, shg yg masuk ke striatum jg sedikit, 60-80% dopamine producing cell damage, extrapyramidal syst kehilangan fungsinya utk promote movement, shg muncul gejala2 prkinson.Terapi: icnerease dopamine level di brain

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Direct pathway tugasnya untuk excitatory movement, jd dopamine sent to striatum dan thalamus utk bisa mempercepat gerakan kita pd Parkinson ga ckup dopamin1 utk excitatory shg jd slowingSdgkn indirect pathway tugasnyah utk inhibitory, saat kt pgn pelan2, butuh banayk dopamin2 yg sifatnya inhibitory, tp ga ada, shg yg available mc ach/glutamate aja yg sifatnya excitatory, jdnya gagal allowing down tp malah rigid,stiff, tremor dan akhirnya loss movement

ALCOHOL – PARKINSONAlcohol has been suggested to be either protective of, or not associated with Parkinson's disease (PD). However, experimental animal studies indicate that chronic heavy alcohol consumption may have dopamine neurotoxic effects relevant for PD. We studied the association between diagnosed alcohol use disorders and PD.Conclusions: A history of an alcohol use disorder conferred an increased risk of admission with a diagnosis of Parkinson's disease in both women and men. In particular, the risk seemed higher at lower ages of first admission with Parkinson's disease

SIDE EFFECT:Levodopa ; dizziness, drowsiness, blurred vision, nausea, vomiting, dry mouth, loss of appetite, heartburn, diarrhea, constipation, sneezing, stuffy nose, cough, other cold symptoms, muscle pain, numbness or tingly feeling, trouble sleeping (insomnia or strange dreams), skin rash, itching

Pramipexole: dizziness when standing (postural hypotension), nausea, dry mouth, stomach pain, vomiting, constipation, headache, dizziness, spinning sensation, drowsiness, swelling in your hands and feet, appetite or weight changes, blurred vision, sleep problems (insomnia

Gabapentin: dizziness, drowsiness, unsteadiness, memory loss, lack of coordination, difficulty speaking, viral infections, tremors, double vision, fever, unusual eye movements, and jerky movements.

Ada dua jalur dalam Basal ganglia - jalur langsung dan jalur tidak langsung. Jalur langsung sifatnyah excitatory; memfasilitasi gerakan yang diinginkan dan jalur tidak langsung sifatnyah inhibitory; menghambat gerakan yang tidak diinginkan.

Direct pathway dimulai dari striatum yang terexcitacy oleh cortex striatum inhibit GPinternal dan SNpars retikulata menggunakan GABA. Ketika struktur ini di inhibisi maka mereka tidak bisa meng-inhibit thalamus dan menyebabkan thalamus utk mengirimkan excitatory input ke kortex, yang tugasnya memfasilitasi gerakan.

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Indirect pathway dimulai dari striatum yang di eksitasi oleh kortex, kemudian neuron di striatal mengirim inhibitory outout ke GPexternal menggunakan GABA. GPexternal biasanya mengirimkan inhibitory input ke Subtalamic nucleus menggunakan GABA, tp karena ini di inhibit oleh striatum, maka gagal unruk inhibit subtalamic nucleus sehingga mereka hanya mengirimkan excitatory input ke basal ganglia pathway GP interna dan SN par reticulate. Struktur2 ini akhirnya inhibit Thalamus dan membuat utk gagal mengirimkan inpus excitatory ke kortex, sehingga secara tdk langsung menginhibisi motor cortex dan membatasi gerakan.

Pada Parkinson, terjadi kerusakan atau degenerasi 60% neuron dopamine sehingga efeknya sangat menonjol pda indirect pathway-lah yang menyebabkan gejala pada Parkinson muncul. Yaitu akibat dari over-activity indirect pathway. Dimana dopamine yang dikirimkan oleh SNparskompakta kurang, shg aefek inhibisinya meningkat dn sangat membatasi gerakan