Parkinson disease merupakan penyakit dengan gangguan gerak yang berhubungan dengan degenerasi

neuron dopamine di substansia nigra.1 Telah dikenal neuropatologi yang mendasari PD, meliputi berbagai area
otak sebagai sistem nigrostriatal dopaminergik, meliputi area yang secara langsung mengandung kontrol
motorik,seperti locus careolus, nucleus vagal dorsal, raphe nuclei batang otak, hypothalamus, tuberculum
olfactorii, dan bagian besar kortek limbik dan neocortex. Patologi juga berkembang ke sistem saraf otonom
perifer, meliputi ganglia simpatis, cardiac simpathetis efferent, pleksus mienterikus usus. Oleh karena itu, tidak
mengherankan bahwa pasien dengan PD memiliki gejala nonmotorik bervariasi. Disfungsi nonmotor pada PD
dapat mendahului tanda dan gejala motor yang nyata, dan hipotesis sekarang tentang tahap neuropatologi PD
memperkirakan bahwa patologi Lewy bodies pada sistem nigrostriatal hanya berkembang setelah area batang otak
dan sistem olfaktorius terkena. 2
Pasien PD sering memperlihatkan gangguan non motor yang meliputi, gangguan neuropsikiatri, gangguan
tidur, gangguan sensorik dan gangguan otonom. Disfungsi genitourinaria merupakan salah satu gangguan otonom
yang sering terjadi. Beberapa penelitian memperlihatkan bahwa disfungsi ini memiliki hubungan signifikan
dengan kualitas hidup dan ekonomi kesehatan. Secara khusus penting dicatat, tidak seperti gangguan otonom,
disfungsi ini sering tidak berespon dengan levodopa, diperkirakan bahwa hal ini terjadi melalui patomekanisme
yang komplek. Untuk alasan ini, penambahan terapi dibutuhkan untuk memaksimalkan kualitas hidup pasien. 1
Stimulasi elektrik pada substansia nigra pars kompakta menghambat reflek berkemih, dan tingkat/ level
dopamine striatal meningkat signifikan pada fase penyimpanan urin pada percobaan binatang. Reflek berkemih
berada dalam pengaruh dopamine ( penghambatan di D1 dan fasilitasi di D2 ) dan GABA ( penghambat). Kedua
firing neuron SNc dan pelepasan dopamine striatal terlihat mengaktifkan jalur langsung yaitu D1-GABAergik
dopamine, yang tidak hanya menghambat nuklei output ganglia basal tetapi juga dapat menghambat reflek
berkemih melewati GABAergik yang berdekatan dengan sirkuit berkemih. Pemberian dopamine
intraserebroventrikuler akan menghambat reflek berkemih dan stimulasi frekuensi tinggi pada nucleus
subthalamik menyebabkan penghambatan kandung kemih pada percobaan binatang. Pada pasien PD, terputusnya
jalur tersebut dapat menyebabkan overaktivitas dopamin dan urgensi/frekuensi berkemih.
Sebagai tambahan untuk serat nigrostriatal, area tegmental ventral (VTA) serat dopaminergik mesolimbik
mungkin terlibat dalam kontrol berkemih. Pada binatang, lesi VTA menyebabkan overaktivitas kandung kemih
yang berat daripada lesi di SNc. Stimulasi VTA menyebaban fasilitasi dan terminasi reflek berkemih. Disamping
itu, DO pada PD mungkin tergantung oleh degenerasi VTA-saraf mesolimbik pada PD.

Epworth kantuk skala

Skala menunjukkan kecenderungan untuk tidur siang hari seperti yang dirasakan oleh pasien. Skala ini
dikembangkan oleh para peneliti di Australia
GABISA BUKA HARUS BAYAR KUESIONERNYA

ANALISIS REGRESI LOGISTIK BINER

Analisis regresi logistik biner digunakan untuk menjelaskan hubungan antara variabel respon yang berupa
data dikotomik/biner dengan variabel bebas yang berupa data berskala interval dan atau kategorik

Symptoms of Restless Legs Syndrome

Restless legs syndrome (RLS) is a disorder of the part of the nervous system that causes an urge to move the
legs. Because it usually interferes with sleep, it also is considered a sleep disorder.

People with restless legs syndrome have uncomfortable sensations in their legs (and sometimes arms or other
parts of the body) and an irresistible urge to move their legs to relieve the sensations. The condition causes an
uncomfortable, "itchy," "pins and needles," or "creepy crawly" feeling in the legs. The sensations are usually worse at
rest, especially when lying or sitting.

LEVODOPA

Farmakodinamik
  Degenerasi basal ganglia pada otak penderita Parkinson menganggu fungsi neuron dopaminergik di
substansia nigra yang menyebabkan penurunan konsentrasi neurotransmiter dopamin. Oleh karena itu, perlunya
pengganti dopamin dari luar tubuh untuk mengatasi defisiensi dopamin ini. Levodopa diambil oleh neuron
dopaminergik melalui proses dekarboksilasi pada terminal presinaptik yang kemudian menghasilkan dopamin.
Levodopa dapat melewati sawar darah otak, sedangkan dopamin tidak dapat melewati sawar darah otak. Maka
levodopa disebut juga obat prekursor dopamin.[1,2,10]
Agonis dopamine dapat menimbulkan kesulitan tidur akibat eksitasi,karena naiknya kadar DA di otak.
Efek kejiwaan dapat terjadi juga , seperti rasa takut,depresi dan gejala psikosis pada overdose. Obat-obat ini dapat
juga bekerja terhadap hipotalamus dan hipofisis,maka menghambat produksi prolaktin.

What is REM sleep?

The brain cycles through five distinct phases during sleep: stages 1, 2, 3, 4, and rapid eye movement (REM)
sleep. REM sleep makes up about 25% of your sleep cycle and first occurs about 70 to 90 minutes after you fall
asleep. Because your sleep cycle repeats, you enter REM sleep several times during the night.
During REM sleep, your brain and body are energized and dreaming occurs. 1 REM is thought to be
involved in the process of storing memories, learning, and balancing your mood,2 although the exact mechanisms
are not well understood.
REM sleep begins in response to signals sent to and from different regions of the brain. Signals are sent to
the brain's cerebral cortex, which is responsible for learning, thinking, and organizing information. Signals are
also sent to the spinal cord to shut off movement, creating a temporary inability to move the muscles ("paralysis")
in the arms and legs. Abnormal disruption of this temporary paralysis can cause people to move while they are
dreaming. For example, this type of movement while dreaming can lead to injuries that could happen when a
person runs into furniture while dreaming of catching a ball.3
REM sleep stimulates regions of the brain that are used for learning. Studies have shown that when people
are deprived of REM sleep, they are not able to remember what they were taught before going to sleep. 3 Lack of
REM sleep has also been linked to certain health conditions, including migraines.2

Apa itu Polisomnografi?

Polisomnografi adalah tes kesehatan yang digunakan untuk diagnosis gangguan tidur. Tes in i
dirancang untuk merekam aktivitas gelombang otak, kadar oksigen dalam darah, detak jantung dan
pernapasan, serta pergerakan mata dan kaki selama pasien tidur. Tes yang mampu mengenali gangguan
terhadap kondisi tidur normal pasien ini membantu dokter dala m mendiagnosis kelainan sehingga
memudahkan rancangan program pengobatan yang diperlukan.

The Apnea–Hypopnea Index or Apnoea–Hypopnoea Index (AHI) is an index used to indicate the
severity of sleep apnea. It is represented by the number of apneaand hypopnea events per hour of sleep.
The apneas (pauses in breathing) must last for at least 10 seconds and be associated with a decrease in blood
oxygenation.

Since hyperphosphorylation of tau may specifically occur in neurodegenerative diseases associated with
neurofibrillary changes, we hypothesized that the phospho-tau (P-tau)/total tau ratio in CSF may be a useful
marker to discriminate CJD from other neurodegenerative disorders.

This term often refers to biomedical factors known to influence or predict health outcomes. These are
taken into account in clinical practice, when estimating a patient’s prognosis. Additionally, clinical predictors
are considered in clinical research, when trying to test new etiological or prognostic factors, and there is a need
to statistically control for known or previously established clinical predictors, which could possibly explain the
role of the new tested factors. In behavior medicine, this is often the common approach, when testing the effects
of a psychosocial factor on health outcomes. Often, it is crucial to control for the effects of clinical predictors
in behavior medicine, as clinical risk factors are either important in predicting prognosis
 Gejala Penyakit Parkinson
Secara umum, tanda atau gejala penyakit Parkinson dapat dikelompokkan menjadi gejala motorik dan gejala
non-motorik.

1. Gejala Motorik Parkinson

Gejala motorik penyakit Parkinson dikenal dengan singkatan TRAP, yaitu: tremor, rigidity,
akinesia/bradykinesia, dan postural instability.
Tremor
Tremor pada Parkinson sering muncul pada tangan, dimulai dari satu sisi, saat pasien istirahat dan menghilang
bila pasien menggerakkan tangan tersebut. Gerakannya seperti menghitung uang logam, atau dikenal dengan
istilah pill-rolling. Tidak setiap tremor adalah gejala Parkinson. Tremor pada pasien Parkinson berbeda dengan
tremor yang sering muncul pada orang tua, dimana tremor pada orang tua sering muncul ketika tangan digerakkan
dan menghilang saat tangan beristirahat/diam.

Rigiditas
Pada pasien Parkinson akan muncul kekakuan pada otot anggota gerak akibat peningkatan tonus otot dimana
ketika digerakkan secara pasif maka akan menunjukkan tahanan seperti fenomena roda bergigi.

Akinesia/Bradykinesia
Akinesia atau bradikinesia merupakan hallmark penyakit Parkinson berupa melambatnya reaksi dan gerakan
dalam menjalankan aktivitas sehari-hari. Gambaran lain bradikinesia dapat berupa nada bicara yang monoton,
berkurangnya ekspresi wajah atau sering digambarkan sebagai wajah topeng, dan berkurangnya ayunan lengan
ketika berjalan. Pasien akan mengeluh kesulitan untuk memasang kancing baju. Salah satu tanda yang juga sering
dikeluhkan pasien Parkinson adalah tulisannya menjadi lebih kecil dari biasanya.

Postural instability
Pasien Parkinson memiliki postur tertentu dan mudah jatuh. Gaya berjalan dengan langkah kecil-kecil, badan agak
membungkuk, kepala sedikit menunduk, dan ayunan tangan berkurang. Pasien akan kesulitan untuk menghentikan
langkahnya secara tiba-tiba.

2. Gejala Non-motorik Parkinson

Banyak penelitian menyebutkan gejala non-motorik pada pasien Parkinson muncul jauh sebelum gejala motorik
disadari. Namun gejala non-motorik ini sering diabaikan dan luput dari perhatian. Adapun gejala non-motorik
Parkinson antara lain:
 berkurangnya indera penciuman
 kelelahan
 sulit buang air besar dan berkemih
 nyeri pada leher
 gangguan mood atau perubahan suasana hati
 gangguan tidur
 berkurangnya daya ingat
 berkeringat secara berlebih

UK Parkinson’s Disease Society Brain Bank Diagnostic Criteria

STEP 1. Diagnosis of Parkinsonian syndrome

Bradykinesia (slowness of initiation of voluntary movement with progressive reduction in speed and amplitude
of repetitive actions).
And at least one of the following:
a. muscular rigidity
b. 4–6 Hz rest tremor
c. postural instability not caused by primary visual, vestibular, cerebellar or proprioceptive dysfunction.
STEP 2. Exclusion criteria for Parkinson’s disease
History of repeated strokes with stepwise progression of Parkinsonian features.
History of repeated head injury.
History of definite encephalitis.
Oculogyric crises.
Neuroleptic treatment at onset of symptoms.
More than one affected relative.
Sustained remission.
Strictly unilateral features after three years.
Supranuclear gaze palsy.
Cerebellar signs.
Early severe autonomic involvement.
Early severe dementia with disturbances of memory, language and praxis.
Babinski sign.
Presence of a cerebral tumour or communicating hydrocephalus on CT scan.
Negative response to large doses of levodopa (if malabsorption excluded).
MPTP exposure.

STEP 3. Supportive prospective positive criteria for Parkinson’s disease. Three or more required for diagnosis
of definite Parkinson’s disease
Unilateral onset.
Rest tremor present.
Progressive disorder.
Persistent asymmetry affecting the side of onset most.
Excellent response (70–100%) to levodopa.
Severe levodopa-induced chorea.
Levodopa response for 5 years or more.
Clinical course of 10 years or more.

The MDS-UPDRS features sections that require independent completion by people affected by Parkinson's and
their carers, and sections to be completed by the clinician.

 Part 1: non-motor experiences of daily living

 Part 2: motor experiences of daily living
 Part 3: motor examination
 Part 4: motor complications
Modified Hoehn and Yahr Scale
The Hoehn and Yahr scale is used to describe the symptom progression of Parkinson disease. The scale was
originally described in 1967 and included stages 1 through 5. It has since been modified with the addition of stages
1.5 and 2.5 to account for the intermediate course of Parkinson disease.
The modified Hoehn and Yahr scale is as follows: [1]
 Stage 0: No signs of disease
 Stage 1.0: Symptoms are very mild; unilateral involvement only
 Stage 1.5: Unilateral and axial involvement
 Stage 2: Bilateral involvement without impairment of balance
 Stage 2.5: Mild bilateral disease with recovery on pull test
 Stage 3: Mild to moderate bilateral disease; some postural instability; physically independent
 Stage 4: Severe disability; still able to walk or stand unassisted
 Stage 5: Wheelchair bound or bedridden unless aided

Standardised Mini-Mental State Examination (SMMSE)

The MMSE was designed as a screening test for the purpose of evaluating cognitive impairment in older
adults.
BAYAR

Frontal assessment battery

The FAB consists of 6 subtests exploring different functions related to the frontal lobes and correlated with frontal
metabolism, as measured with the regional distribution of fludeoxyglucose F 18 in a positron emission
tomography study of patients with frontal lobe damage of various causes. 12 The 6 subtests of the FAB explore the
following: (1) conceptualization and abstract reasoning (similarities test); (2) mental flexibility (verbal fluency
test); (3) motor programming and executive control of action (Luria motor sequences); (4) resistance to
interference (conflicting instructions); (5) inhibitory control (go–no go test); and (6) environmental autonomy
(prehension behavior). Each subtest is scored from 3 (better score) to 0, for a maximum score of 18. The FAB has
shown a good validity (correlation of ρ = 0.82 with the Mattis Dementia Rating Scale) and interrater reliability (κ
= 0.87).8

The Beck Depression Inventory (BDI) is a 21-item, self-report rating inventory that measures characteristic
attitudes and symptoms of depression (Beck, et al., 1961).

Hamilton Rating Scale for Depression (HRSD),[1] also called the Hamilton Depression Rating
Scale (HDRS), abbreviatedHAM-D, is a multiple item questionnaire used to provide an indication of depression,
and as a guide to evaluate recovery.[2] Max Hamilton originally published the scale in 1960 [3] and revised it in
1966,[4] 1967,[5] 1969,[6] and 1980.[7] The questionnaire is designed for adults and is used to rate the severity of
their depression by probing mood, feelings of guilt, suicide ideation, insomnia, agitation or
retardation, anxiety, weight loss, and somatic symptoms.

SEAD
100% – Completely independent. Able to do all chores without slowness, difficulty or impairment.
Essentially normal. Unaware of any difficulty. 90% – Completely independent. Able to do all chores with some
degree of slowness, difficulty and impairment. Might take twice as long. Beginning to be aware of difficulty. 80%
– Completely independent in most chores. Takes twice as long. Conscious of difficulty and slowness. 70% – Not
completely independent. More difficulty with some chores. Three to four times as long in some. Must spend a
large part of the day with chores. 60% – Some dependency. Can do most chores, but exceedingly slowly and with
much effort. Errors; some impossible. 50% – More dependent. Help with half, slower, et cetera. Difficulty with
everything. 40% – Very dependent. Can assist with all chores, but few alone. 30% – With effort, now and then
does a few chores alone or begins alone. Much help needed. 20% – Nothing alone. Can be a slight help with some
chores. Severe invalid. 10% – Total dependent, helpless. Complete invalid. 0% – Vegetative functions such as
swallowing, bladder and bowel functions are not functioning. Bed-ridden.

ROC SOFTWARE PENELITIAN.