EPIDEMIOLOGY

Incidence
Parkinsons disease (Idiopathic Parkinsons) makes up 80% of cases of Parkinsonism
Mean age of onset = 55 years old (20-80)
Males:females = 3:2
(FROM DRA.BEBELETHS NOTES FEEL FREE TO EDIT OR ADD STUFF)
Prevalence - philippine setting (SEARCHING)
Etiology

Classification of Parkinsonism

PATHOPHYSIOLOGY
Parkinsons disease is a progressive illness of the central nervous system (OSullivan,
2014) where there is marked loss of specific types of neurons that produce a chemical called
dopamine. The Basal Ganglia plays a big role in this disease wherein different motor and nonmotor symptoms arise. It consists of the striatum (caudate and putamen), globus pallidus,
subthalamic nucleus and the substantia nigra (Figure 1). The degeneration of the inhibitory
nigrostriate fibers, or the neurons of the substantia nigra, result in a decrease of dopamine
within the corpus striatum (Snell, 2010)
Figure 1
Adapted
from:

http://webspace.ship.edu/cgboer/basalgangliagray.gif

The Basal Ganglia involves itself in a direct motor loop which consists of signals
transmitted from the cortex to the putamen to the globus pallidus, towards the ventrolateral
nucleus of the thalamus, and back to the cortex or the supplementary motor area (SMA). It is
said that the connection between the ventrolateral nucleus and SMA is excitatory in nature and
facilitates the discharge of cells in the SMA. The Basal Ganglia aids in the initiation of voluntary

movement through a positive feedback mechanism via activation of the cortex. Instead of
activating the thalamus, the Basal Ganglia inhibits the thalamus which cause hypokinesia in
patients with PD.

Figure 2 Direct Loop of Basal Ganglia

Adapted From Gilman, S and Newman S, 2003,10, p. 151 via O Sullivan, et al. 2014

Figure 2 describes the direct loop of the Basal Ganglia where the striatonigral fibers
arises from the putamen, although most fibers are from the caudate. It also shows the
connection of the striatum with the substantia nigra pars compacta. The different symbols
represent the following: C = caudate nucleus; cc = corpus callosum; GPe = globus pallidus pars
externa; GPi = globus pallidus pars interna; P = putamen; VL = ventral lateral nucleus of the
thalamus.
On the other hand, an indirect loop would involve the following structures: the subthalamic nucleus,
the globus pallidus interna, and substantia nigra pars reticulata which would go to the superior colliculus and
midbrain tegmentum. This loop decreases thalamocortical activation whereas the basal ganglias projection to
the superior colliculus promotes the regulation of saccadic eye movements. Likewise, the basal ganglias
connection to the reticular formation would regulate sleep, wakefulness, arousal and the trunk and limb
musculature through the extrapyramidal pathways. Other loops associated with the basal ganglia are said to be
encompassing memory as well as cognitive functions.

Figure 3 Indirect loop of Basal Ganglia

Adapted from Gilman and Newman, 2003,10, p. 152 via O Sullivan, et al. 2014
Figure 3 shows the indirect loop via the subthalamic nucleus. The efferents are also represented as
seen on the figure from the globus pallidus interna and substantia nigra pars reticulata to the
superior colliculus and midbrain tegmentum. The symbols represent the following: C = caudate
nucleus; GPe = globus pallidus pars externa; GPi = globus pallidus pars interna; ic = internal
capsule; IL = intralaminar nuclei of the thalamus; P = putamen; VA = ventral anterior nucleus of the
thalamus; VL = ventral lateral nucleus of the thalamus.
As stated earlier, Parkinsons disease is a progressive neurodegenerative disorder. The
Stages of Parkinsons disease by Baak and colleagues is used as an evidence of the continuous
progression of PD.

Stage

Areas affected

Medulla oblangata

Medulla oblangata, caudal raphe nuclei, the gigantocellular reticular

nucleus, and coeruleus-subcoeruleus complex

Medulla oblangata, caudal raphe nuclei, the gigantocellular reticular

nucleus, and coeruleus-subcoeruleus complex, nigrostriatal system

Medulla oblangata, caudal raphe nuclei, the gigantocellular reticular

nucleus, and coeruleus-subcoeruleus complex, nigrostriatal system,
cortex (temporal mesocortex and allocortex)

Medulla oblangata, caudal raphe nuclei, the gigantocellular reticular

nucleus, and coeruleus-subcoeruleus complex, nigrostriatal system,
cortex (temporal mesocortex and allocortex), sensory association
areas of the neocortex and pre-frontal neocortex

Medulla oblangata, caudal raphe nuclei, the gigantocellular reticular

nucleus, and coeruleus-subcoeruleus complex, nigrostriatal system,
cortex (temporal mesocortex and allocortex), sensory association areas
of the neocortex and pre-frontal neocortex, sensory association areas
of the neocortex and premotor areas

CLINICAL MANIFESTATIONS
The onset of Parkinsons disease is insidious, and progresses slowly. Parkinsons
disease manifests in the following ways: Rigidity or stiffness of movement, Bradykinesia or
slowness of movement, Tremors (pill-rolling), loss of dexterity/handwriting disturbances, Gait
disturbance,muscle pain, cramps, aching,and muscle weakness, Depression, nervousness and
other psychiatric problems, speech disturbance and general fatigue.
The symptoms listed above can be classified into primary motor, secondary motor and
and nonmotor disorders.
Primary motor symptoms are: Rigidity, Bradykinesia, Tremors and Postural Instability,.
Secondary motor symptoms are: decrease in motor performance (weakness and fatigue),

problems in motor function (speed-accuracy trade-off, difficulty with complex sequential,

simultaneous motions and start hesitation), and problems with gait.
Other Symptoms are:
Cognitive and Behavioral Problems such as:
o Bradyphrenia slow thought process
o Visuospatial deficits
o Perceptual motor deficits
o Decrease in attention span
o Dementia
o Depression
o Personality changes - dependent, indecisive, passive, lack of motivation
Autonomic Dysfunction
o Orthostasis orthostatic hypotension
o Increased in salivation with sialorrhea
o Cool skin
o Increased perspiration
o Seborrhea nagmamantika/sweaty
o Decreased GI peristalsis
o Poor bladder emptying
o Constipation
o Inadequate erection for males
Sensory symptoms
o Ill defined pain, burning, tingling of affected side
Other motor symptoms
o Akathesia
o Restless legs syndrome during sleep, legs jerk
Cranial nerve dysfunction
o Oculomotor nerve eye movement
o Facial nerve facial expression
o Glossopharyngeal nerve - swallowing
Secondary Problems/Complications
Muscle atrophy and weakness
Loss of flexibility/contractures
Deformity - kyphosis
Osteoporosis
Cardiopulmonary changes compromised d/t posture
o Never forget breathing and coughing exercises
Circulatory changes
Nutritional changes
Decubitus ulcers bed bound
Seborrheic dermatitis

ANATOMICAL CORRELATION
Parkinsons disease is predominantly a disorder of the basal ganglia, a group of nuclei located at the
base of the forebrain. The striatum, composed of the caudate and putamen, is the largest nuclear complex of
the basal ganglia. The striatum receives excitatory input from several areas of the cerebral cortex, as well as
inhibitory and excitatory input from the dopaminergic cells of the substantia nigra pars compacta.

Two types of spiny projection neurons receive input from the cortex and substantia nigra, neurons that
project directly to the internal segment of the globus pallidus (GPi) , the major output site of the basal
ganglia; and neurons that project to the external segment of the globus pallidus , establishing an indirect
pathway to the GPi via the subthalamic nucleus .The actions of the direct and indirect pathways regulate the
neuronal output from the GPi, which provides tonic inhibitory input to the thalamic nuclei that project to the
primary and supplementary motor areas.

Parkinsons disease is characterized by the degeneration of the neuromelanin containing

neurons (dopaminergic neurons that produce dopamine) in the brain stem, especially in the pars
compacta of the substantia nigra and locus ceruleus. The hallmark of the disease is the
presence of Lewy bodies: eosinophic cytoplasmic inclusions that appear as the disease
progresses and neurons degenerate.
When symptoms appear, there is 60% loss of dopaminergic neurons in the substantia nigra, and
80% loss of dopamine content in the striatum .

SOURCES
O'Sullivan, S., Schmitz, T., & Fulk, G. (2014). Physical Rehabilitation (6th ed.). Philadelphia,
Pennsylvania: FA Davis Company.
Snell, R. (2010). Clinical Neuroanatomy (7th ed.). Philadelphia, PA: Lippincott Williams &
Wilkins.
Hauser,R.A.,MD,MBA.(n.d.).Parkinson Disease.
Retrieved from http://emedicine.medscape.com/article/1831191