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Parkinson’s Disease

PD is a progressive neurological disorder characterized by a large number of motor and


non-motor features that can impact on fuction to a variable degree (Jankovic, 2007).

Parkinson's disease (PD) is a neurodegenerative disorder that affects predominately


dopamine-producing (“dopaminergic”) neurons in a specific area of the brain called
substantia nigra (parkinson.org)

Parkinson disease (PD) is a progressive disorder of the CNS that typically affects its
victims around age 60 (Tortora Ed. 13).

Parkinson adalah penyakit neurodegenerative progresif yang memiliki karakteristik


tanda-tanda klinis parkinsonisme, seperti tremor saat istirahat, rigiditas, ataksia,
bradikinesia, dan instabilitas postural.

 Ataksia: failure of muscular coordination; irregularity of muscular action.


 Degenerative disease: any disease in which deterioration of structure or function
of tissue occurs.
The midbrain contains several other nuclei, including the left and right substantia
nigra, which are large and darkly pigmented.
Neurons that release dopamine, extending from the substantia nigra to the basal nuclei,
help control subconscious muscle activities.
Axons from the substantia nigra terminate in the caudate nucleus and putamen.

Globus pallidus + Putamen = Lentiform Nucleus


Lentiform Nucleus + Caudate Nucleus = Corpus Striatum

Epidemiologi
 Mempengaruhi sekitar 1% individu berusia lebih dari 60 tahun.
 Insidens dan prevalens meningkat seiring bertambahnya usia dan umur rata-rata
pasien saat awitan awal adalah sekitar 60 tahun.
 Pria 3 : 2 Wanita

Etiologi
 Sporadis: kombinasi stress oksidatif terhadap neuron dopaminergic; racun
lingkungan; penuaan yang dipercepat; genetic.
 Familial (10%): mutasi autosomal dominan pada alpha synuclein, gen autosomal
resesif Parkin atau mutasi gen DJ-1 (onset muda). MPTP (neurotoksin)

Clinical Features

4 cardinal [utama] features: TRAP


1. Tremor at rest: the most common symptom of PD
Involuntary skeletal muscle contractions often interfere with voluntary movement.
For instance, the muscles of the upper limb may alternately contract and relax,
causing the hand to shake (Tortora Ed. 13).
Tremors are unilateral, occur at a frequency between 4 and 6 Hz, and almost
always are prominent in the distal part of an extremity (Jankovic, 2007).
Rest tremor disappears with action and during sleep (Jankovic, 2007).
2. Rigidity
Muscle tone may increase greatly, causing rigidity of the involved body part.
Rigidity of the facial muscles gives the face a masklike appearance (a wide-eyed,
unblinking stare and a slightly open mouth with uncontrolled drooling).
3. Akinesia [bradykinesia]: slowness of movement
Activities such as shaving, cutting food, and buttoning a shirt take longer and
become increasingly more difficult as the disease progresses (Tortora Ed. 13).
Bradykinesia refers to slowness of movement and is the most characteristic
clinical feature of PD [also seen in other disorders, including depression]
(Jankovic, 2007).
Assessment of bradykinesia usually includes having patients perform rapid,
repetitive, alternating movements of the hand (finger taps, hand grips, hand
pronation–supination) and heel taps and observing not only slowness but also
decrementing amplitude [luas ayunan; lebar ayunan] (Jankovic, 2007).
4. Postural instability
Postural instability due to loss of postural reflexes is generally a manifestation of
the late stages of PD and usually occurs after the onset of other clinical features.
Inability to maintain equilibrium.
Inability to react to abrupt changes in position.
Postural Deformities
Postural deformities resulting in flexed neck and trunk posture and flexed elbows and
knees are often associated with rigidity. However, flexed posture generally occurs late
in the disease.
Camptocormia is characterised by extreme flexion of the thoracolumbar spine.
Freezing
Freezing, also referred to as motor blocks, is a form of akinesia (loss of movement) and
is one of the most disabling symptoms of PD.
It typically manifests as a sudden and transient (usually 10 s) inability to move.
This may include hesitation when beginning to walk (start hesitation) or a sudden
inability to move the feet during specific situations (eg, turning or walking through a
narrow passage, crossing busy streets, approaching a destination).

Non-Motor Features
1. Autonomic Dysfunction
Features include orthostatic hypotension, sweating dysfunction, sphincter
dysfunction and erectile dysfunction.
Orthostatic hypotension is defined as a decrease in systolic blood pressure of
20 mm Hg or a decrease in diastolic blood pressure of 10 mm Hg within three
minutes of standing when compared with blood pressure from the sitting or
supine position.
2. Cognitive and Neurobehavioural Abnormalities
PD related dementia is also associated with a number of other neuropsychiatric
comorbidities. Among 537 such patients, depression (58%), apathy (54%),
anxiety (49%) and hallucinations (44%) were frequently reported.
3. Sleep Disorders
Rapid eye movement sleep behaviour disorder, now considered a pre-
parkinsonian state, is characterised by an increase in violent dream content
accompanied by talking, yelling, swearing, grabbing, punching, kicking, jumping
and other dramatic, violent and potentially injurious motor activity which may also
involve the bed partner.
4. Sensory Abnormalities
Sensory symptoms such as olfactory dysfunction, pain, paresthesia, akathisia,
oral pain and genital pain are frequent but are often not recognised as
parkinsonian symptoms.
Akathisia is a movement disorder characterized by a feeling of inner
restlessness and a compelling need to be in constant motion, as well as by
actions such as rocking while standing or sitting, lifting the feet as if marching on
the spot, and crossing and uncrossing the legs while sitting.

Diagnostic Criteria
Acute challenge testing with either levodopa plus dopa decarboxylase inhibitor (DDI) or
apomorphine has been suggested as helpful in discriminating PD from other
parkinsonian syndromes or mimics.
Acute Levodopa Test
 Levodopa is administered to evaluate the improvement of symptoms.
 This test should not be used for diagnosis of PD.
 Other parkinsonian disorders may also respond to this test including multiple
system atrophy and progressive supranuclear palsy.
 Levodopa: Metabolic precursor of dopamine, a neurotransmitter depleted in
Parkinson disease; crosses blood-brain barrier to be converted by striatal
enzymes to dopamine
 Given that most patients with suspected PD will be treated with dopaminergic
therapy at some stage, there is no additional benefit with acute challenge testing,
but such challenges are associated with adverse effects and extra costs.

Diagnostic Tools
Olfactory Testing
Olfactory function is impaired in most patients clinically diagnosed with PD but is normal
or less impaired in patients with atypical syndromes and other imitators.
Anosmia and hyposmia are found more frequently in patients with PD than in controls or
patients with conditions which may imitate PD such as vascular parkinsonism,
progressive supranuclear palsy (PSP), Alzheimer’s disease and essential tremor.

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