PRESENTACION Parkinson_disease__1740492093.pdf

PatriciaAcevedoAranc 9 views 24 slides Feb 25, 2025
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About This Presentation

Parkinson_disease


Slide Content

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Introduction to
Parkinson's Disease
Parkinson's disease (PD) is a progressive neurodegenerative disorder that affects
movement, coordination, and other bodily functions. It is characterized by the loss
of dopamine-producing neurons in the substantia nigra, a region of the brain that
controls movement. Symptoms typically develop gradually, starting with a tremor
in one hand.
DR. NAINKY
BHALLA

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Epidemiology of Parkinson's
Disease
1Prevalence
Parkinson's Disease affects approximately 1-2% of individuals over the age
of 60. The prevalence increases with age, and it's estimated that about 1 in
100 people over the age of 60 have Parkinson's Disease.
2Incidence
The incidence rate is estimated to be 10-20 cases per 100,000 person-
years. There is a higher incidence in males compared to females.
3Geographical Variation
PD prevalence varies geographically, with higher rates observed in Europe
and North America compared to Asia.

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Etiology of Parkinson's Disease
Genetic Factors
While most cases are sporadic, around 5-10% of cases are familial. Several
genetic mutations have been associated with familial Parkinson's, such as
those in the SNCA, LRRK2, PARK2, PARK7, and PINK1 genes.
Environmental Factors
Exposure to certain environmental toxins, such as pesticides and heavy
metals, has been linked to an increased risk of Parkinson's. Traumatic brain
injury has also been implicated.
Aging
Aging is the most significant risk factor, with the majority of cases occurring
in individuals over 60.

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Anatomy and function of the
basal ganglia
The basal ganglia are a group of interconnected brain structures that play a crucial role in motor control,
learning, and cognitive functions.
1
Caudate Nucleus
The caudate nucleus is involved in planning and initiating movements.
2
Putamen
The putamen is involved in the execution of movements.
3
Globus Pallidus
The globus pallidus is involved in the control and refinement of movements.
4
Substantia Nigra
The substantia nigra produces dopamine, a neurotransmitter essential for smooth and
smooth and coordinated movements.

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Pathophysiology of the basal
ganglia in Parkinson's Disease
In PD, the loss of dopamine-producing neurons in the substantia nigra disrupts the balance of
neurotransmission in the basal ganglia, leading to the characteristic motor symptoms.
Dopamine Depletion
The loss of dopamine-producing neurons in the substantia nigra leads to a depletion of
depletion of dopamine in the basal ganglia.
Imbalance in Basal Ganglia Activity
The depletion of dopamine disrupts the balance of activity between the direct and indirect
and indirect pathways, leading to excessive inhibition of movement.
Motor Symptoms
The disruption of basal ganglia function leads to the characteristic motor symptoms of PD,
such as tremors, rigidity, slow movements, and postural instability.
DR. NAINKY
BHALLA

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The direct pathway in the basal
ganglia
The direct pathway in the basal ganglia is a neural circuit that promotes movement.
movement. It involves the caudate nucleus, putamen, globus pallidus internal
internal segment, thalamus, and motor cortex.
Caudate/Putam
en
Globus Pallidus
Pallidus
Internal
Segment (GPi)
(GPi)
Thalamus Motor Cortex
Dopamine Inhibition Excitation Movement
DR. NAINKY
BHALLA

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The indirect pathway in the basal
ganglia
The indirect pathway in the basal ganglia is a neural circuit that inhibits movement. It involves the
caudate nucleus, putamen, globus pallidus external segment, subthalamic nucleus, globus pallidus
internal segment, thalamus, and motor cortex.
Caudate/Putamen
The caudate and putamen project to the globus
pallidus external segment (GPe).
GPe
The GPe projects to the subthalamic nucleus
(STN).
STN
The STN projects to the globus pallidus internal
segment (GPi).
GPi
The GPi projects to the thalamus.
DR. NAINKY
BHALLA

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Disruption of the direct and indirect pathways in
Parkinson's Disease
In PD, the loss of dopamine neurons disrupts the balance between the direct and indirect pathways, leading to excessive inhibition of movement.
movement.
Direct Pathway
Dopamine depletion in the direct pathway leads
pathway leads to reduced activation of the
the motor cortex.
Indirect Pathway
Dopamine depletion in the indirect pathway
pathway leads to increased inhibition of the
the motor cortex.
Overall Effect
The net effect of dopamine depletion is a
suppression of movement, leading to the
characteristic symptoms of PD.
DR. NAINKY
BHALLA

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Pathophysiology of the Basal Ganglia
Basal Ganglia Structure
The basal ganglia are a group of
nuclei deep within the cerebral
hemispheres, including the
striatum (caudate nucleus and
putamen), globus pallidus,
substantia nigra, and subthalamic
nucleus.
Dopaminergic Pathways
Parkinson’s Disease primarily
affects the dopaminergic neurons
in the substantia nigra pars
compacta. The loss of these
neurons leads to a reduction in
dopamine levels in the striatum.
Motor Control
The basal ganglia are crucial for
regulating motor control. The loss
of dopamine disrupts the balance
between the direct and indirect
pathways of the basal ganglia,
leading to impaired motor function
and the characteristic symptoms of
Parkinson's.
DR. NAINKY
BHALLA

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Pathophysiology of Parkinson's
Disease
1
Dopaminergic Neuron Degeneration
Loss of dopamine-producing neurons in the substantia nigra.
2
Lewy Body Formation
Abnormal protein aggregates accumulate in the brain cells.
3
Neuroinflammation
Inflammation in the brain contributes to neuron death.
4
Oxidative Stress
Damage to cells from free radicals leads to neuronal dysfunction.

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Dopaminergic Neuron Degeneration
Causes
Genetics, environmental toxins, oxidative
oxidative stress, mitochondrial dysfunction,
dysfunction, and inflammation.
Effects
Loss of dopamine production leads to
impaired movement control, coordination,
and cognitive function.
Treatment
Dopamine replacement therapy, deep brain
brain stimulation, physical therapy, and
and lifestyle modifications.
DR. NAINKY
BHALLA

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Lewy Body Formation
Alpha-Synuclein
Accumulation
Misfolded alpha-synuclein protein
aggregates to form Lewy bodies.
Ubiquitin Accumulation
Lewy bodies are characterized by
the presence of ubiquitin, a
protein that tags misfolded
proteins for degradation.
Neurotoxicity
Lewy bodies disrupt normal cell function, leading to neuronal death.
DR. NAINKY
BHALLA

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Symptoms and clinical manifestations of Parkinson's
Disease
The symptoms of PD are typically slow-onset and progressive, with severity varying from person to person.
Tremors
Involuntary shaking, often in the
the hands and feet, that worsens
worsens during rest.
Rigidity
Stiffness and resistance to
movement, particularly in the
the limbs.
Bradykinesia
Slowness of movement, affecting
tasks such as walking, writing,
and eating.
Postural Instability
Difficulty maintaining balance
and an increased risk of falls.
DR. NAINKY
BHALLA

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Clinical Manifestations of
Parkinson's Disease
Motor Symptoms Non-Motor Symptoms
Tremor: Resting tremor, often
starting in one hand.
Cognitive Decline: Impairments in
memory and executive function.
Bradykinesia: Slowness of
movement.
Mood Disorders: Depression and
anxiety.
Rigidity: Increased muscle tone,
leading to stiffness.
Autonomic Dysfunction: Problems
with blood pressure regulation,
sweating, and gastrointestinal
motility.
Postural Instability: Impaired
balance and coordination, leading
to falls.
Sleep Disturbances: Insomnia and
REM sleep behavior disorder.

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Indirect Impairments and Complications
1Falls and Fractures
Due to postural instability and gait disturbances.
2Speech and Swallowing Difficulties
Dysarthria (speech problems) and dysphagia (difficulty
swallowing).
3Motor Fluctuations
Such as on-off phenomena and dyskinesias (involuntary
movements) related to long-term use of levodopa.
4Freezing of Gait
Sudden, temporary inability to move.
DR. NAINKY
BHALLA

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Investigations for Parkinson's
Disease
1
Clinical Diagnosis
Diagnosis is primarily clinical, based on the presence of motor
symptoms and response to dopaminergic medications.
2
Neuroimaging
MRI and CT scans are used to rule out other conditions, though they
don’t typically show specific changes in PD. Dopamine transporter
(DAT) scans can be used to assess dopaminergic function.
3
Laboratory Tests
Blood tests are used to exclude other causes of parkinsonism, but
there are no specific biomarkers for PD.
DR. NAINKY
BHALLA

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Neuroimaging Techniques in
Parkinson's Disease
SPECT/PET Imaging
Evaluates dopamine transporter function in the substantia nigra.
MRI
Identifies structural changes in the brain related to Parkinson's
Parkinson's disease.
DaTSCAN
Provides detailed visualization of the substantia nigra and dopamine
dopamine transporter density.

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Laboratory Investigations for
Parkinson's Disease
Blood Tests
Exclude other conditions that mimic Parkinson's, such as thyroid disorders, vitamin deficiencies, or infections.
deficiencies, or infections.
Cerebrospinal Fluid Analysis
Measure levels of alpha-synuclein and other biomarkers, providing insights into the presence and severity of
and severity of Parkinson's disease.
Genetic Testing
Identify specific mutations associated with an increased risk of developing Parkinson's disease.
DR. NAINKY
BHALLA

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Diagnostic Criteria for
Parkinson's Disease
Clinical
Features
BradykinesiaResting
Tremor
Rigidity Postural
Instability
Neuroimagin
g
Dopamine
Transporter
SPECT/PET
MRI for rule
rule out
other causes
causes
DaTSCAN for
substantia
nigra
visualization
Laboratory
Tests
Blood tests
for rule out
other causes
Cerebrospina
l fluid
analysis
Genetic
testing for
specific
mutations

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Differential Diagnosis of Parkinson's Disease
Essential Tremor
A tremor that primarily affects the hands and
can worsen with movement, unlike the
resting tremor in Parkinson's.
Multiple Sclerosis
An autoimmune disease that affects the
central nervous system, causing a wide range
of symptoms, including motor impairments.
Progressive Supranuclear Palsy
Palsy
A neurodegenerative disorder characterized
by eye movement problems, rigidity, and
falls, often mimicking Parkinson's disease.
DR. NAINKY
BHALLA

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Pharmacological Treatment of Parkinson's Disease
Levodopa
The most effective medication,
often combined with carbidopa
to enhance efficacy and reduce
side effects.
Dopamine Agonists
Such as pramipexole and
ropinirole, which mimic
dopamine.
MAO-B Inhibitors
Such as selegiline and
rasagiline, which help to
prolong the effects of
dopamine.
COMT Inhibitors
Such as entacapone, which
prolong the effect of levodopa.
Anticholinergics
Useful for controlling tremors,
though they are less commonly
used due to side effects.
DR. NAINKY
BHALLA

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Surgical Treatment of
Parkinson's Disease
Deep Brain Stimulation (DBS)
Implantation of a device that stimulates specific brain
regions, which can be effective in reducing motor
symptoms.
DR. NAINKY
BHALLA

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Rehabilitation for
Parkinson's Disease
Physical Therapy
To address gait, balance, and mobility issues.
Occupational Therapy
To assist with daily living activities and adaptive strategies.
Speech Therapy
For speech and swallowing difficulties.

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Conclusion and Future
Directions
Parkinson's disease remains a complex and challenging condition. Understanding
the underlying pathophysiology is crucial for developing effective treatments.
Future research focuses on gene therapies, stem cell transplantation, and
neuroprotective strategies to slow or prevent the progression of Parkinson's
disease.
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