Parkinson's Disease (Shaking Palsy) - Clinical Presentation and Pathophysiology
Summary
TLDREste video trata sobre la enfermedad de Parkinson, un trastorno neurodegenerativo que afecta al 0.3% de la población mayor de 40 años. Se analizan los síntomas principales, como los temblores, la rigidez, la bradicinesia y la inestabilidad postural. Además, se profundiza en la anatomía y el papel de los ganglios basales en la coordinación del movimiento, explicando cómo la disminución de dopamina afecta este proceso en los pacientes con Parkinson. También se mencionan los factores de riesgo genéticos y ambientales, así como los factores protectores, como el ejercicio y el café.
Takeaways
- 🧠 El Parkinson es una enfermedad neurodegenerativa que afecta aproximadamente al 0.3% de la población mayor de 40 años, con unos 7.5 millones de personas afectadas en todo el mundo.
- 🫵 Los síntomas cardinales del Parkinson incluyen temblores, rigidez, bradicinesia e inestabilidad postural.
- 👤 Otros síntomas incluyen hipomimia (falta de expresión facial), disfagia, hipofonía y problemas visuales como visión borrosa y dificultad para abrir los párpados.
- 🧠 El daño ocurre en el núcleo basal o ganglios basales, que son responsables del control del tono muscular y de los movimientos suaves y aprendidos.
- 🔄 El movimiento normal implica una señal del córtex cerebral a los ganglios basales, que luego envían señales de vuelta al córtex motor para coordinar un movimiento controlado.
- ❌ En la enfermedad de Parkinson, la falta de dopamina impide que las señales sean transmitidas correctamente, lo que causa movimientos no suaves y descoordinados.
- 💡 La patología incluye la degeneración de las neuronas dopaminérgicas en la sustancia negra, provocada por apoptosis, estrés oxidativo o disfunciones mitocondriales.
- ⚠️ Factores de riesgo incluyen genética, exposición a pesticidas, mientras que fumar, el café y el ejercicio vigoroso pueden ser factores protectores.
- 🧬 Las mutaciones en genes como GBA, SNCA, LRRK2 y PINK1 están asociadas a un mayor riesgo de desarrollar Parkinson.
- 🔬 La presencia de cuerpos de Lewy, compuestos principalmente de proteínas mal plegadas como alfa-sinucleína, es un marcador patológico clave de la enfermedad.
Q & A
¿Qué es la enfermedad de Parkinson y cuánta gente la padece?
-La enfermedad de Parkinson es una enfermedad neurodegenerativa que afecta al 0.3% de la población mayor de 40 años, lo que equivale a unas 7.5 millones de personas en todo el mundo.
¿Cuáles son los cuatro síntomas cardinales de la enfermedad de Parkinson?
-Los cuatro síntomas cardinales son: temblores, rigidez, bradicinesia (lentitud en los movimientos) e inestabilidad postural.
¿Qué otras características pueden observarse en personas con Parkinson?
-Algunas características adicionales incluyen hipomimia (falta de expresión facial), disfagia (dificultad para tragar), hipofonía (voz débil), problemas visuales como visión borrosa y dificultades para abrir los párpados, además de alteraciones en la marcha, como pasos cortos y congelación.
¿Qué parte del cerebro está afectada en la enfermedad de Parkinson?
-La enfermedad de Parkinson afecta principalmente los ganglios basales, una región del cerebro que regula el tono muscular y facilita movimientos suaves y controlados.
¿Qué función tienen los ganglios basales en el movimiento?
-Los ganglios basales ayudan en el control subconsciente del tono muscular y en la coordinación de patrones de movimientos aprendidos. Reciben señales del cortex cerebral y, tras procesarlas, las devuelven para ejecutar movimientos suaves y controlados.
¿Cómo afecta el Parkinson a la señalización entre los ganglios basales y el córtex cerebral?
-En el Parkinson, la señal de salida desde los ganglios basales hacia el tálamo y luego de vuelta al córtex cerebral está alterada, lo que impide que los movimientos sean suaves y coordinados.
¿Qué sucede en la vía dopaminérgica en los pacientes con Parkinson?
-En el Parkinson, las neuronas dopaminérgicas de la sustancia negra se degeneran, lo que reduce la liberación de dopamina. Esto afecta los receptores de dopamina D1 y D2, alterando la inhibición y activación necesarias para el control del movimiento.
¿Qué teorías explican la muerte de las neuronas dopaminérgicas en el Parkinson?
-Las teorías sobre la muerte de las neuronas incluyen el mal plegamiento de proteínas, agregación y toxicidad, disfunción mitocondrial, estrés oxidativo y proteólisis defectuosa.
¿Qué cambios patológicos se observan en el cerebro de una persona con Parkinson?
-En la enfermedad de Parkinson, se observa pérdida de mielina, pérdida neuronal y gliosis en la sustancia negra. También se encuentran cuerpos de Lewy, que son inclusiones intracelulares formadas principalmente por proteínas alfa-sinucleína.
¿Cuáles son algunos factores de riesgo y factores protectores en la enfermedad de Parkinson?
-Entre los factores de riesgo se incluyen predisposición genética, exposición a pesticidas y mutaciones en genes como GBA, SNCA y LRRK2. Entre los factores protectores están el consumo de café, el tabaquismo, el ejercicio vigoroso y el uso de antiinflamatorios no esteroideos.
Outlines
🧠 Introducción a la enfermedad de Parkinson y sus síntomas
El video comienza con una introducción a la enfermedad de Parkinson, una enfermedad neurodegenerativa que afecta al 0,3% de la población mayor de 40 años, con 7,5 millones de personas afectadas a nivel mundial. Los síntomas clave incluyen temblores, rigidez, bradicinesia (lentitud de movimiento) e inestabilidad postural. También se describen otros síntomas que afectan el rostro, como la disminución de la expresión facial (hipomimia), problemas visuales y dificultades en la marcha, que están relacionados con daños en los ganglios basales del cerebro.
🧬 Estructura cerebral implicada en el Parkinson
Se explica la anatomía básica del cerebro, destacando estructuras como el hipocampo y la amígdala, pero enfocándose en los ganglios basales, que controlan el tono muscular y los movimientos suaves. El Parkinson afecta esta área del cerebro, interrumpiendo las señales entre la corteza cerebral y el cuerpo, lo que lleva a problemas con el control del movimiento. La falta de señales adecuadas desde los ganglios basales hacia la corteza cerebral es la raíz de los movimientos no controlados en la enfermedad de Parkinson.
🧪 El papel de la dopamina en la enfermedad de Parkinson
Los ganglios basales funcionan enviando señales de ida y vuelta entre la corteza cerebral y el cuerpo, con la dopamina desempeñando un papel clave. En el Parkinson, la producción de dopamina se reduce, lo que interfiere con la capacidad de iniciar movimientos suaves. Se describe cómo la dopamina actúa sobre los receptores D1 y D2, y la importancia de estas interacciones en el control de los movimientos musculares. En el Parkinson, la falta de dopamina conduce a una actividad inhibitoria excesiva que bloquea la capacidad de la corteza cerebral para controlar el movimiento.
Mindmap
Keywords
💡Enfermedad de Parkinson
💡Ganglios basales
💡Temblores
💡Bradicinesia
💡Rigidez
💡Hipomimia
💡Substancia nigra
💡Dopamina
💡Corteza motora
💡Apoptosis
Highlights
Parkinson's disease affects 0.3% of the population over the age of 40, amounting to approximately 7.5 million people worldwide.
The four cardinal features of Parkinson's disease are tremors, rigidity, bradykinesia, and postural instability.
Other symptoms include hypomimia (reduced facial expressions), dysphasia, hypophonia (lowered voice volume), blurred vision, and eyelid opening problems.
Gait abnormalities in Parkinson's include shuffling steps, festination, and freezing of movement.
Parkinson's disease is caused by problems in the basal ganglia, a brain region responsible for muscle tone and smooth movement.
The basal ganglia help coordinate learned movement patterns and ensure smooth, controlled movements by processing signals from the cerebral cortex.
Parkinson's disease disrupts the normal output of signals from the basal ganglia, resulting in abnormal, uncoordinated movements.
Key components of the basal ganglia involved in Parkinson's disease include the caudate nucleus, putamen, globus pallidus, subthalamic nucleus, and substantia nigra.
Dopamine produced in the substantia nigra plays a critical role in facilitating movement by interacting with receptors in the basal ganglia.
In Parkinson's disease, the loss of dopaminergic neurons in the substantia nigra leads to reduced dopamine levels, affecting movement control.
Reduced dopamine affects both excitatory and inhibitory pathways in the brain, resulting in abnormal output from the basal ganglia to the thalamus and cortex.
The hallmark pathological features of Parkinson's disease include demyelination, neuronal loss, and gliosis in the substantia nigra, along with the presence of Lewy bodies in neurons.
Lewy bodies are intracytoplasmic inclusions made up of proteins such as alpha-synuclein and ubiquitin, commonly found in neurons of Parkinson's patients.
Risk factors for Parkinson's include genetic mutations (GBA, SNCA, LRRK2, PINK1) and exposure to pesticides.
Protective factors against Parkinson's disease include smoking, coffee consumption, vigorous exercise, and the use of non-steroidal anti-inflammatory drugs.
Transcripts
hello in this video we're going to talk
about Parkinson's disease um which is a
neurodegenerative disease about 0.3% of
the population over the age of 40 um has
this um disease it's about 7.5 million
people
worldwide so let's look at the firstly
signs and symptoms of Parkinson's and
here I'm drawing a patient um who shows
who presents with tremors
shaking and he presents like this due to
a condition called Parkinson's disease
that affects the brain the Cardinal
features of Parkinson's disease there
four these include Tremors rigidity
Brady kinesia postural
instability there are other features
which affect the cranial facial areas
which include hypomimia which is
basically decrease in facial expression
dysphasia hypophonia reduction in uh
basically the tone of the voice volume
Vis uh other features include visual
problems such as blurred vision and
eyelid opening
aaia um other features also include gate
you can have shuffling festations and
freezing so all these signs and symptoms
are a result of um uh problems that
occur within the brain particularly in
an area of the brain known as the basil
ganglia so let's just quickly revise
some important anatomical structures of
the brain so here we have the phonic
which is an important part of the lyic
system we have the hippocampus which is
for memory the amydala for emotions but
we will mainly concentrate on this
yellow uh structure here which is known
as the basil ganglia or the basil
nucleus medially to the basil ganglia is
the thalamus which essentially is a
connection between the cortex and the
brain stem spinal cord
so again Parkinson's disease is a result
of problems that occur within the basil
ganglia or the basil nucleus because
this area is responsible for um muscle
tone as well as the ease of um movement
so to it helps in a smooth movement and
learned movement patterns so let's just
take a cross-section chronal section of
the brain here and look at the basil
gangle in a bit more details and it's
comp components so here we looking at a
section of the brain here in green is
the thalamus just to orientate where we
are all these structures in yellow here
they are part of the basil
ganglia so basil ganglia is made up of
the C nucleus C pamin pamin the Globus
paladis of which we have an external and
internal
part we also is made up of the nucleus
accumbens which I have not drawn here um
and we have also have the subthalamic
subthalamic nucleus and the substantia
which is consists of two parts and
just to complete this image we all we
have the amig um the amydala here as
well as the
hippocampus so we will mainly Focus
again on the basil ganglia which is
disrupted in Parkinson's disease so what
does the basil ganglia do so let's just
have a quick General overview of what it
does
so here again we have the brain and this
yellow structure is a basil ganglia
essentially what happens is um the
cortex when it wants to in when it when
it wants to initiate a movement it will
send signals first to the basil ganglia
and the basil ganglia will send signals
back to the CeX particularly the Moto
cortex and then when the signals are
sent back to the Moto cortex the M
cortex can then you know initiate these
signals uh send the signals down the
spinal cord um and then you know out
through the ventral Horn of the spinal
cord to that skeletal muscle to you know
initiate a smooth controlled movement
okay now let's uh look at that in a bit
more detail so again the cerebral cortex
um is it wants to initiate a voluntary
movement it will it will first send
signals to the Bas Bas ganglia and the
basil ganglia will help in the
subconscious control of sub skeletal
muscle tone as well as the coordination
of learned movement
patterns this information will then be
sent back to the cereal cortex through a
loop it will be sent to the thalamus
first and then the thalamus will send
this info to the cerebral cortex the
cerebral cortex will then um send the
movement signals the smooth controlled
movement signals down the spinal cord to
the skeletal muscle and thus we have a
normal movement
pattern two important parts in this
diagram the input from the cerebral
cortex to the basil ganglia and the
output from the basil ganglia to the
thalamus back to the cortex in
Parkinson's disease the output number
two there's a problem in the output and
thus we do not have a normal controlled
movement pattern it is not smooth so now
let us go back to the big diagram and
learn about the interconnection that
occur within the basil ganglia and how
and the disruption that occurs and how
this results in Parkinson's
disease so in this diagram um we're
going to look at all the components of
the basil ganglia so to start the kodate
nucleus and kodate pamin is also known
as the kodate striatum so here the
rectangular structure I'm drawing is the
cordate striatum this is the cortex and
all these other structures here are part
of the basal ganglia we have the
substantial nigras compacta the Globus
palus internal the substantial Nigro
pars reticula the Globus paladis
external the subthalamic nucleus and the
thalamus now I'm going to start drawing
the interconnections that occur within
this region but firstly I I want to I
want you to uh learn three main points
the input from the cortex to the basil
ganglia is uh to the striatum to the
cordate striatum first so the input is
is to the cordate strium the output from
the basil ganglia occurs in the Globus
paladis interna that's point two so the
Globus palus interna is the output from
the baso ganglia to the thalamus and
then the thalamus will then send this
information to the cortex back to the
cortex in that Loop and this is three
the cortex will then send
this information to the skeletal muscle
down the spinal cord to to you know to
cause a smooth movement
pattern coordinated movement pattern so
those are the three main points the
input to the basil ganglia the output
from the basil ganglia and then the
output from the from the cortex again to
the
muscle now within the basil ganglia
there's a lot of interconnections
happening between the glutaminergic
neurons which are the excited
neurons as well as the gabanergic
neurons which are your inhibitory
neurons but the most important thing in
uh in this diagram are is within the
substantial nraas compacta because here
we have dopaminergic neurons that
arise and these dopaminergic neurons
they release dopamine
into the cordate
striatum so dopamine can bind onto two
types of receptor D1 dopamine 1 or
dopamine 2 and depending on which
receptor it binds to it it is either
excitatory or inhibitory so if dopamine
binds onto D1 receptor it is
excitatory if so it will stimulate that
neuron if dopamine binds to dd2
receptors dopamine will inhibit that
neuron so if we were to follow it step
by
step uh the dopamine nergic neurons
releases do dopamine dopamine binds onto
the D1 receptor which is
excitatory so it will stimulate the
gabanergic neuron here and it will
directly inhibit this gab gabanergic
neuron allowing the thalamus to send
signals to the cortex so thus the cortex
can um you know um send signals to the
skeletal muscle for a controlled
movement pattern
so that is what occurs normally but
unfortunately in pinson's disease there
is there's not much dopamine the
dopamine nergic neurons die so in
Parkinson's disease you have a reduced
uh dopamine in the substantial
and the pathogenesis probably
involves apoptosis or necrosis of
dopaminergic
neurons and it is it is a result of the
death of these neurons can be due to uh
protein misfolding AG aggregation and
toxicity it can be due to defective
proteolysis it can be due to
mitochondrial dysfunction or oxidative
stress these are all
theories regardless of the cause the
result is that we have reduced dopamine
in the in this area in the basil
ganglia okay now let's go back to the
diagram and look at what happens if we
have reduced dopamine if we have reduced
dopamine dopamine does not bind onto the
D2 receptor which normally inhibits this
gabanergic
neuron thus the gabanergic neuron here
is now overactive and secretes Gaba
which inhibits the second gabanergic
neuron because this gabanergic neuron is
now inhibited it cannot inhibit the
glutaminergic neuron in the subthalamic
nucleus and so the subthalamic nucleus
glutaminergic neuron neuron will secrete
glutamate which will
stimulate this gabanergic neuron in the
Globus palus
interna similarly because we have no
dopamine the dopamine does not bind onto
the D1
receptor and so the gabanergic neuron
that normally inhibits uh the globous
paladis interna neuron is not
stimulated and as a result we have a
overactive um gabanergic neuron from the
Globus palus interna to the
thalamus so we have excessive inhibitory
input to the thalamus Thalamus
inhibition
causes
suppression um of the theal corticos
spinal pathway and because of
this um the signals that the basil
ganglia should have sent back to the
cortex
doesn't doesn't really happen and so as
a result when the when you want to
initiate a movement it's not smooth
coordinated controlled and and thus you
result in thus it results in the
clinical manifestations of Parkinson's
disease I hope that all made sense now
let's look at the pathology of
Parkinson's disease so let's zoom into
the substantial area here which is
which can be which is basically located
on the midbrain here's a cross-section
of the midbrain
and let's compare pinson's disease um uh
substanti nagra to the one of a normal
patient what we see in Parkinson's
disease is we see demyelination neuronal
loss and gliosis within the substantial
another pathological Hallmarks is
uh the presence of Louis bodies within
the Soma of the neuron so here we have
the S of the neuron and this blue
structure here are Louis
bodies and Louis IES are round eopc
intracytoplasmic occlusions in the
nucleus uh in the nuclei of the neuron
um the Louis bodies are made up of
mainly um Alpha sincan proteins
ubiinsulin now let's talk about the risk
factors as well as the protective
factors of Parkinson's
disease so the risk factors of
Parkinson's disease um include um family
risk factors there are genetic risk
factors which include GBA
cnca um lurk to park 2 and pink one as
well as there's shown that pesticides
can cause Parkinson's disease protective
factors include smoking coffee vigorous
exercising as well as the use of
non-steroidal anti-inflammatory Dr
drugs so that concludes this video on
Parkinson's disease we looked at the
signs and symptoms we looked at the some
neuro anatomy of the basil ganglia we
looked at the function of the basil
ganglia as well as what occurs in
Parkinson's disease and then we looked
at the the pathophys as well as the
pathology and the risk factors and
protective factors thank you for
watching I hope you enjoy this video
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