Category Archives: Neurology (brain, spinal cord and nerves)

Opioids/Opiates Mechanism of Action, with Animation

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Opioids refer to a class of drugs that act via opioid receptors in the nervous system to relieve pain. The term “opioid” includes:
ENDOGENOUS opioids occurring naturally in the human body such as endorphins,
OPIATES found in the opium poppy plant such as morphine,
synthetic (methadone, fentanyl) and semi-synthetic opioids (heroin).
The major function of endogenous opioids is to modulate pain signals. They are synthesized in response to pain stimuli and exert their effects by binding to opioid receptors in the brain, spinal cord and peripheral nerves. In the brain, they also increase DOPAMINE release, producing EUPHORIC effects.
Opioid analgesics such as morphine and fentanyl mimic the action of endogenous opioids. They are powerful painkillers and are commonly used to manage severe pain. Continuous use, however, MAY lead to tolerance and dependence. Opioids slow down BREATHING and overdose can be FATAL. Their psychoactive effects also make them common drugs of abuse, with morphine being PARTICULARLY susceptible to addiction. Heroin, a semi-synthetic product made from morphine, is another drug that is highly popular among recreational users. Once administered, it is metabolized into morphine and 6-mono-acetyl-morphine, both of which are psychoactive. Heroin is rarely used in medicine.

How do opioids produce euphoric effects?
Dopamine neurotransmitter is at the basis of the brain reward pathway. Engaging in enjoyable activities causes dopamine release from dopamine-producing neurons into the synaptic space where it binds to and stimulates dopamine-receptors on the receiving neuron. This stimulation is believed to produce the pleasurable feelings or rewarding effect. Normally, GABA, another neurotransmitter, INHIBITS dopamine release in the nucleus accumbens. By binding to receptors on GABA inhibitory neurons, opioids REDUCE GABA’s activity, ultimately INCREASE dopamine release and induce pleasurable feelings.

Addiction, Dependence and Tolerance 
Continued use of opioids can result in dependence and addiction. As the body gets used to euphoric effects of the drug, it may become irritated if drug use is reduced or discontinued.
Tolerance develops following a typical sequence of events. A drug exerts its effect by INcreasing or DEcreasing a certain substance or activity in the brain to an ABNORMALLY high or low level. REPEATED exposure MAINTAINS this abnormal level for a period of time. The brain eventually ADAPTS by pulling it BACK to NORMAL level. This means the drug, at the current dosage, NO longer produces the desirable psychoactive effect; a higher dose is required to do so. This vicious cycle repeats itself and eventually leads to drug overdose.

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Brain Stroke for Patient Education, with Animation

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A stroke occurs when the blood supply to a certain part of the brain is reduced or interrupted. Without oxygen and nutrients from the blood, brain cells cannot function properly and eventually die.
There are 2 major types of strokes: ISCHEMIC stroke caused by a BLOCKED artery, and HEMORRHAGIC stroke caused by a RUPTURED artery.
Ischemic stroke happens when a blood clot OBSTRUCTS an artery. In some patients, the clot forms locally, inside the blood vessels that supply the brain. This occurs when fatty deposits in an artery, or cholesterol plaques, rupture and trigger blood clotting. In other cases, a clot may travel to the brain from elsewhere in the body. Most commonly, this happens in patients with atrial fibrillation, a heart condition in which the heart does not pump properly, blood stagnates in its chambers and this facilitates blood clotting. The clots may then pass into the bloodstream, get stuck in smaller arteries of the brain and block them.
Hemorrhagic stroke, on the other hand, occurs when an artery leaks or ruptures. This can result from high blood pressure, overuse of blood-thinners/anticoagulant drugs, or abnormal formations of blood vessels such as aneurysms and AVMs.
As a hemorrhage takes place, brain tissues located BEYOND the site of bleeding are deprived of blood supply. Bleeding also induces contraction of blood vessels, narrowing them and thus further limiting blood flow.
Stroke symptoms may include one or more of the following:
– Paralysis of muscles of the face, arms or legs: inability to smile, raise an arm, or difficulty walking.
– Slurred speech or inability to understand simple speech.
– Sudden and severe headache, vomiting, dizziness or reduced consciousness.
Cerebral stroke is a medical emergency and requires immediate attention. It is essential to determine if a stroke is ischemic or hemorrhagic before attempting treatment. This is because certain drugs used for treatment of ischemic strokes, such as blood thinners, may CRITICALLY aggravate bleeding in hemorrhagic strokes.
For ischemic strokes, emergency treatment aims to restore blood flow by removing blood clots. Medication, such as aspirin and tissue plasminogen activator, TPA, are usually the first options. TPA may be given intravenously, or, in the case the symptoms have advanced, delivered directly to the brain via a catheter inserted through an artery at the groin. Blood clots may also be removed mechanically by a special device delivered through a catheter.
Emergency treatment for hemorrhagic strokes, on the other hand, aims to stop bleeding, reduce blood pressure, and prevent vasospasm and seizures. These goals are usually achieved by a variety of drugs. If the bleeding is significant, surgery may be required to drain the blood and reduce intracranial pressure.
Preventive treatments for strokes include:
– Removal of cholesterol plaques in carotid arteries that supply the brain
– Widening of narrowed carotid arteries with a balloon, and sometimes, a stent. This is usually done with a catheter inserted at the groin.
– Various procedures to prevent rupturing of brain aneurysms, such as clipping and embolization.
– Removal or embolization of vascular malformations
– Bypassing the problematic artery

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Long Term Potentiation and Memory, with Animation

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The process of learning begins with sensory signals being transcribed in the cortex. They are then transmitted to the hippocampus where new memories are believed to form. If a signal is strong, or repeated, a long-term memory is established and wired back to the cortex for storage. Lesions in the hippocampus impair formation of new memories, but do not affect the older ones.
The brain consists of billions of neurons. Neurons communicate with each other through a space between them, called a synapse. A typical neuron can have thousands of synapses, or connections, with other neurons. Together, they form extremely complex networks that are responsible for all brain’s functions. Synaptic connections can change over time, a phenomenon known as synaptic plasticity. Synaptic plasticity follows the “use it or lose it” rule: frequently used synapses are strengthened while rarely used connections are eliminated. Synaptic plasticity is believed to underlie the process of learning and memory retention. New memories are formed when neurons establish new connections, or STRENGTHEN existing synapses. If a memory is no longer needed or rarely recalled, its corresponding synapses will slowly weaken and eventually disappear.
The strength of a synapse is measured by the level of excitability or responsiveness of the post-synaptic neuron in response to a GIVEN stimulus from the pre-synaptic neuron. High-frequency signals or repeated stimulations STRENGTHEN synaptic connections over time. This is known as long-term potentiation, or LTP, and is thought to be the cellular basis of memory formation. LTP can occur at most excitatory synapses all over the brain, but is best studied at the glutamate synapse of the hippocampus.
When a glutamatergic neuron is stimulated, action potentials travel down its axon and trigger the release of glutamate into the synaptic cleft. Glutamate then binds to its receptors on the post-synaptic neuron. The 2 main glutamate receptors that often co-exist in a synapse are AMPA and NMDA receptors. These are ion channels that activate upon binding to glutamate. When the pre-synaptic neuron is stimulated by a WEAK signal, only a small amount of glutamate is released. Although both receptors are bound by the glutamate, only AMPA is activated by weak stimulation. Sodium influx through the AMPA channel results in a SLIGHT DE-polarization of the post-synaptic membrane. The NMDA channel remains closed because its pore is blocked by magnesium ions.
When the pre-synaptic neuron is stimulated by a STRONG or REPEATING signal, a large amount of glutamate is released; the AMPA receptor stays open for a longer time, admitting more sodium into the cell, thus resulting in a GREATER DE-polarization. Increased influx of positive ions EXPELS magnesium from the NMDA channel, which NOW activates, allowing not only sodium but also CALCIUM into the cell. Calcium is the mediator of LTP induction. There are 2 distinct phases of LTP. In the early phase, calcium initiates signaling pathways that activate several protein kinases. These kinases enhance synaptic communication in 2 ways: they phosphorylate the existing AMPA receptors, thereby increasing AMPA conductance to sodium; and help to bring more AMPA receptors from intracellular stores to the post-synaptic membrane. This phase is thought to be the basis of short-term memory, which lasts for several hours. In the late phase, NEW proteins are made and gene expression is activated to further enhance the connection between the 2 neurons. These include newly synthesized AMPA receptors, and expression of other proteins that are involved in the growth of NEW dendritic spines and synaptic connections. The late phase may correlate with formation of long-term memory.

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Effect of Alcohol on the Brain, with Animation.

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Alcohol, or more specifically, ethanol, affects brain functions in several ways. Alcohol is generally known as a DEPRESSANT of the central nervous system; it INHIBITS brain activities, causing a range of physiological effects such as impaired body movements and slurred speech. The pleasurable feeling associated with drinking, on the other hand, is linked to alcohol-induced dopamine release in the brain’s reward pathway. Alcohol also increases levels of brain serotonin, a neurotransmitter implicated in mood regulation.
The brain is a complex network of billions of neurons. Neurons can be excitatory or inhibitory. Excitatory neurons stimulate others to respond and transmit electrical messages, while inhibitory neurons SUPPRESS responsiveness, preventing excessive firing. Responsiveness or excitability of a neuron is determined by the value of electrical voltage across its membrane. Basically, a neuron is MORE responsive when it has more POSITIVE charges inside; and is LESS responsive when it becomes more NEGATIVE.
A balance between excitation and inhibition is essential for normal brain functions. Short-term alcohol consumption DISRUPTS this balance, INCREASING INHIBITORY and DECREASING EXCITATORY functions. Specifically, alcohol inhibits responsiveness of neurons via its interaction with the GABA system. GABA is a major INHIBITORY neurotransmitter. Upon binding, it triggers GABA receptors, ligand-gated chloride channels, to open and allow chloride ions to flow into the neuron, making it more NEGATIVE and LESS likely to respond to new stimuli. Alcohol is known to POTENTIATE GABA receptors, keeping the channels open for a longer time and thus exaggerating this inhibitory effect. GABA receptors are also the target of certain anesthetic drugs. This explains the SEDATIVE effect of alcohol.
At the same time, alcohol also inhibits the glutamate system, a major excitatory circuit of the brain. Glutamate receptors, another type of ion channel, upon binding by glutamate, open to allow POSITIVELY-charged ions into the cell, making it more POSITIVE and MORE likely to generate electrical signals. Alcohol binding REDUCES channel permeability, LOWERING cation influx, thereby INHIBITING neuron responsiveness. GABA ACTIVATION and glutamate INHIBITION together bring DOWN brain activities. Depending on the concentration of ethanol in the blood, alcohol’s depressant effect can range from slight drowsiness to blackout, or even respiratory failure and death.
Chronic, or long-term consumption of alcohol, however, produces an OPPOSITE effect on the brain. This is because SUSTAINED inhibition caused by PROLONGED alcohol exposure eventually ACTIVATES the brain’s ADAPTATION response. In attempts to restore the equilibrium, the brain DECREASES GABA inhibitory and INCREASES glutamate excitatory functions to compensate for the alcohol’s effect. As the balance tilts toward EXCITATION, more and more alcohol is needed to achieve the same inhibitory effect. This leads to overdrinking and eventually addiction. If alcohol consumption is ABRUPTLY reduced or discontinued at this point, an ill-feeling known as WITHDRAWAL syndrome may follow. This is because the brain is now HYPER-excitable if NOT balanced by the inhibitory effect of alcohol. Alcohol withdrawal syndrome is characterized by tremors, seizures, hallucinations, agitation and confusion. Excess calcium produced by overactive glutamate receptors during withdrawal is toxic and may cause brain damage. Withdrawal-related anxiety also contributes to alcohol-seeking behavior and CONTINUED alcohol abuse.

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Anesthesia, with Animation

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Anesthesia is the use of drugs to prevent or reduce pain during a medical procedure. There are two major classes of drugs:
– Local anesthetics: these drugs block transmission of pain signals from peripheral nerve endings to the central nervous system. And
– General anesthetics: these act on the central nervous system itself to induce unconsciousness and total lack of sensation.
There are 3 major categories of anesthesia procedures:
Local anesthesia: a local anesthetic is administered directly to the site of procedure to numb a small area such as a tooth during a dental manipulation.
Regional anesthesia: a local anesthetic is injected near a cluster of nerve roots to prevent pain sensation from the area innervated by those nerves. Epidural given to women in labor is an example of this type.
General anesthesia: general anesthetics are used to suppress the entire central nervous system, resulting in loss of consciousness. A cocktail of several drugs are inhaled, given intravenously, or both. This type is used for major surgical procedures.
Apart from pain management, general anesthesia has some other goals: prevent formation of new memories, relax muscles, and suppress autonomic response to surgical injuries which could otherwise be extreme and harmful. General anesthetics are commonly used in combination with other drugs to achieve these end points.
An example of general anesthetic drug is Propofol. The exact mechanism of action of Propofol remains unclear, but it is thought to inhibit responsiveness of neurons via its binding to GABA receptor. GABA is a major inhibitory neurotransmitter in the central nervous system. Upon binding, it triggers GABA receptor – a ligand-gated chloride channel – to open and allow chloride ions flow into the neuron, making the cell hyperpolarized and less likely to fire. In other words, GABA makes the brain cells less responsive to new stimuli. Propofol binding has been proposed to potentiate GABA receptor, keeping the channel open for longer time and thus exaggerating this inhibition effect.
It is believed, however, that under anesthesia the brain does not simply shut down. Instead, the connections between different parts of the brain are lost. Using various brain imaging techniques it’s been shown that an anesthetized brain is still reactive to stimuli such as light and sounds, but somehow this sensory information is not processed resulting in no further consequences. A variety of anesthetic drugs are available, each of which may have different target molecules in the brain. However, if used at a high enough dosage, they can all cause unconsciousness. This is probably because consciousness is the result of a complex network of various brain functions, disruption of any of which could result in network dysfunction.
Emerging from unconscious state is not simply the result of drugs wearing off. As the connections between parts of the brain were lost, the brain has to somehow find the way to connect them back upon awakening. This usually happens in a certain order: the most basic and essential functions, such as respiratory and digestive reflexes, come back first, more complex brain functions return after. This may explains why older patients and people with pre-existing neurological conditions may take longer to recover all cognitive brain functions. The risk and extent of postoperative delirium – a state of mental confusion after surgery – are also higher in these patients.
The right dose of overall anesthesia is critical. It is usually calculated based on patient’s weight, age and medical history. Past or current uses of recreational drugs also have to be taken into account. Too much anesthesia results in a too deep state of unconsciousness, and consequently greater risks of postoperative complications and long-term cognitive dysfunction. On the other hand, a too low dose may cause the patient to wake up during the surgery, a phenomenon known as anesthesia awareness, which might be a traumatic experience to some patients.

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Epilepsy, Types of Seizures, with Animation.

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Epilepsy is a group of neurological diseases characterized by recurrent seizures. Seizures happen as a result of a sudden surge in the brain’s electrical activities. Depending on which part of the brain is affected, a seizure may manifest as loss of awareness, unusual behaviors or sensations, uncontrollable movements or loss of consciousness.

Mechanism

The brain is a complex network of billions of neurons. Neurons can be excitatory or inhibitory. Excitatory neurons stimulate others to fire action potentials and transmit electrical messages, while inhibitory neurons SUPPRESS this process, preventing EXCESSIVE firing. A balance between excitation and inhibition is essential for normal brain functions. In epilepsy, there is an UP-regulation of excitation and/or DOWN-regulation of inhibition, causing lots of neurons to fire SYNCHRONOUSLY at the same time.

Types of Seizures

If this abnormal electrical surge happens within a limited area of the brain, it causes PARTIAL or FOCAL seizures. If the entire brain is involved, GENERALIZED seizures will result. Partial seizures subdivide further to:

  • Simple partial: depending on the affected brain area, patients may have unusual feelings, strange sensations or uncontrollable jerky movements, but remain conscious and aware of the surroundings.
  • Complex partial seizure on the other hand involves a loss or changes in consciousness, awareness and responsiveness.

Generalized seizures subdivide further to:

  • Absence seizures: this type occurs most often in children and is characterized by a very brief loss of awareness, commonly manifested as a blank stare with or without subtle body movements such as eye blinking, lip smacking or chewing. People with absence seizures may not be aware that something is wrong for years. Kids who start having absence seizures in early years stand a good chance of outgrow them without treatment.
  • Tonic seizures are associated with stiffening of muscles and may cause the person to fall, often backwards.
  • Atonic seizures, also known as drop attacks, are characterized by a sudden loss of muscle tone, which may cause the person to collapse or drop down.
  • Clonic seizures are associated with rhythmic jerking muscle movements. Most commonly affected are the muscles of the neck, face, arms and legs. Clonic seizures are rare.
  • Myoclonic seizures are brief jerks or twitches of a muscle or a group of muscles. There can be one or many twitches occurring within a couple of seconds.
  • The most common and also most dramatic are tonic-clonic seizures, also known as convulsive seizures, which are combinations of muscle stiffening and jerking. This type is what most people relate to when they think of a seizure. It also involves sudden loss of consciousness and sometimes loss of bladder control. A tonic-clonic seizure that lasts longer than 5min requires immediate medical treatment.

Causes

Epilepsy may develop as a result of a brain injury, tumor, stroke, previous infection or a birth defect.

Generalized seizures that start in childhood are likely to involve genetic factors. Epilepsy due to a single gene mutation is rare. More often, an interaction of multiple genes and environmental factors is responsible. Hundreds genes have been implicated. Examples include genes encoding for GABA receptors – major components of the inhibitory circuit, and ion channels. Many genetic disorders that cause brain abnormalities or metabolic conditions have epilepsy as a primary symptom. The cause of epilepsy is unknown in about half of cases.

Diagnosis is based on observation of symptoms, medical history, and an electroencephalogram, or EEG, to look for abnormal brain waves. An EEG may also help in differentiating between partial and generalized seizures. Genetic testing maybe helpful when genetic factors are suspected.

Treatment

There is no cure for epilepsy but various treatments are available to control seizures.

  • Medication successfully controls seizures for about 70% of cases. Many anti-epileptic drugs are available which target sodium channels, GABA receptors, and other components involved in neuronal transmission. Different medicines help with different types of seizures. Patients may need to try several drugs to find the most suitable.
  • Dietary therapy: ketogenic diet has been shown to reduce or prevent seizures in many children whose seizures could not be controlled with medication. Ketogenic diet is a special high-fat, low-carbohydrate diet that must be prescribed and followed strictly. With this diet, the body uses fat as the major source of energy instead of carbohydrates. The reason why this helps control epilepsy is unclear.
  • Nerve stimulation therapies such as vagus nerve stimulation in which a device placed under the skin is programmed to stimulate the vagus nerve at a certain rate. The device acts as a pacemaker for the brain. The underlying mechanism is poorly understood but it has been shown to reduce seizures significantly.
  • Finally, a surgery may be performed to remove part of the brain that causes seizure. This is usually done when tests show that seizures are originated from a small area that does not have any vital function.
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Baroreflex Regulation of Blood Pressure, with Animation.

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Baroreflex, or baroreceptor reflex, is one of the mechanisms the body uses to maintain stable blood pressure levels or homeostasis. Baroreflex is a rapid negative feedback loop in which an elevated blood pressure causes heart rate and blood pressure to decrease. Reversely, a decrease in blood pressure leads to an increased heart rate, returning blood pressure to normal levels.

The reflex starts with specialized neurons called baroreceptors. These are stretch receptors located in the wall of the aortic arch and carotid sinus.  Increased blood pressure stretches the wall of the aorta and carotid arteries causing baroreceptors to fire action potentials at a higher than normal rate. These increased activities are sent via the vagus and glossopharyngeal nerves to the nucleus of the tractus solitarius – the NTS – in the brainstem.  In response to increased baroreceptor impulses, the NTS activates the parasympathetic system – the PSNS – and inhibits the sympathetic system – the SNS. 

As the PSNS and SNS have opposing effects on blood pressures, PSNS activation and SNS inhibition work together in the same direction to maximize blood pressure reduction. Parasympathetic stimulation decreases heart rate by releasing acetylcholine which acts on the pacemaker cells of the SA node. Inhibition of the sympathetic division decreases heart rate, stroke volume and at the same time causes vasodilation of blood vessels. Together, these events rapidly bring DOWN blood pressure levels back to normal.

When a person has a sudden drop in blood pressure, for example when standing up, the decreased blood pressure is sensed by baroreceptors as a decrease in tension.  Baroreceptors fire at a lower than normal rate and the information is again transmitted to the NTS.  The NTS reacts by inhibiting parasympathetic and activating sympathetic activities. The sympathetic system releases norepinephrine which acts on the SA node to increase heart rate; on cardiac myocytes to increase stroke volume and on smooth muscle cells of blood vessels to cause vasoconstriction. Together, these events rapidly bring UP blood pressure levels back to normal.

Baroreceptor reset : Baroreflex is a short-term response to sudden changes of blood pressure resulted from everyday activities and emotional states.  If hypertension or hypotension persists for a long period of time, the baroreceptors will reset to the “new normal” levels. In hypertensive patients for example, baroreflex mechanism is adjusted to a higher “normal” pressure and therefore MAINTAINS hypertension rather than suppresses it.

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Embolización Endovascular para Aneurismas Cerebrales, con Animación.

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La embolización endovascular o espiral endovascular es una técnica mínimamente invasiva que se realiza para tratar los aneurismas cerebrales. El objetivo del tratamiento es bloquear el flujo de sangre hacia el aneurisma y por lo tanto reducir el riesgo de ruptura del aneurisma.

En este procedimiento, un catéter guiado por un cable es insertado a través de la arteria femoral en la ingle y es dirigido todo el camino hacia la arteria cerebral afectada. El cable guía es retirado. Un micro-catéter que lleva una espiral de platino suave se introduce dentro del catéter inicial y es conducido hasta la abertura del aneurisma. La espiral se despliega en el saco aneurismático. Una pequeña corriente eléctrica se pasa para separar la espiral del catéter. Puede tomar varias espirales para rellenar el aneurisma. Las espirales inducen la coagulación sanguínea dentro del aneurisma y lo aíslan de la arteria.

En algunos casos, cuando el cuello del aneurisma es muy amplio, una endoprótesis puede ser usada para mantener las espirales dentro del saco aneurismático. La embolización asistida con endoprótesis consiste en colocar permanentemente una endoprótesis en la arteria antes del bobinado. La endoprótesis actúa como un andamio dentro de la arteria para ayudar a mantener las espirales en su lugar.

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Marijuana Effects on the Brain, the Goods and the Bads, with Animation Video.

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The Science of Marijuana

Marijuana, also known as cannabis, among other names, is a preparation of the Cannabis sativa plant – the hemp plant, intended for recreational and medicinal uses. Marijuana can be consumed by smoking, inhaling, or mixing with food.

The main psychoactive chemical in marijuana, responsible for most of the intoxicating effects sought by recreational users, is delta-9-tetrahydro-cannabinol, or THC. The Cannabis plant preparation also contains at least 65 other compounds that are chemically related to THC, called cannabinoids.

THC is chemically similar to a class of substances found naturally in our nervous system called endogenous cannabinoids, or endocannabinoids, of which anandamide is best known so far. The endocannabinoids are part of a newly discovered system named the Endocannabinoid system, or ECS.

How the ECS Works

A human brain contains billions of nerve cells, or neurons, which communicate via chemical messages, or neurotransmitters. When a neuron is sufficiently stimulated, a neurotransmitter is released into the synaptic cleft – a space between neurons. The neurotransmitter then binds to a receptor on a neighboring neuron, generating a signal in it, thereby transmitting the information to that neuron. Neuron communication is essential to all brain activities.

The ECS acts as a modulator of this neurotransmission. When the postsynaptic neuron is activated, endocannabinoids are produced, released, and travel back to the presynaptic neuron where they activate cannabinoid receptors. By doing so, they control what happens next when the presynaptic cell is again stimulated. The general effect is a DECREASE in the release of neurotransmitters such as GABA or glutamate. In other words, the ECS acts as a “brake”, SLOWING down neuronal activities, preventing neurons from excessive firing.

Some examples of ECS functions include:

 Pain modulation: cannabinoids SUPPRESS pain signal processing, producing pain relief effects.

 Stress and anxiety reduction: while response to stressful stimuli is necessary for an organism to react appropriately to a stressor, CHRONIC stress may be harmful. The ECS plays a role in the habituation of the body’s response to repeated exposure. It helps our body learn to restraint stress.

Mood regulation: the ECS promotes a “good feeling” by inducing dopamine release in the brain reward pathway. This explains the euphoria, or the “high”, experienced by marijuana users. THC mode of action is, however, different from other drugs: it induces dopamine release INDIRECTLY by removing inhibitory action of GABA on dopaminergic neurons.

The ECS is also involved in many other brain and bodily activities, including memory and learning, appetite and sleeping patterns, immune functions and fertility.

So how can marijuana be harmful if it does exactly what our body already does to itself?

The endocannabinoids are short-acting transmitter substances. They are synthesized on demand and their signaling is rapidly terminated by specific enzymes. The amount of endocannabinoid messengers is tightly regulated accordingly to the body’s needs. This regulation is essential for a modulator that acts to fine-tune brain activities.

Marijuana users consume a much higher amount of THC. THC is also much more stable than endocannabinoids and can persist in the body for a much longer period of time. THC overwhelms the endocannabinoid system, overriding normal brain functions. Because cannabinoid receptors are present in many parts of the brain and body, the effects of THC are wide-ranging. It can slow down a person’s reaction time, which could impair driving or athletic skills; disrupt short-term memory and higher thought processes, which could affect learning capabilities and judgment ability. Higher doses of THC may also lead to reverse effects. For example, while lower doses of cannabinoids seem to reduce stress, anxiety, and panic; higher doses may actually promote increased stressful feelings and fear. Consuming marijuana by smoking may also damage the lungs to a similar extent as smoking cigarettes.

Long – term Effects of THC

Substantial evidence from animal studies indicates that marijuana exposure can cause long-term adverse changes in the brain. Rats exposed to THC before birth, soon after birth, or during early life show significant difficulties with certain learning and memory tasks later in life. Long-term effects of marijuana in humans are still debatable mostly due to limitations of conducting research on human beings.

Medical Uses of Marijuana

While recreational use of marijuana is WITHOUT doubt harmful, the Cannabis plant may be a valuable source of medicines. Currently, the two main cannabinoids from the marijuana plant that are of medical interest are THC and cannabidiol, or CBD. These chemicals are used to increase appetite and reduce nausea in patients undergoing cancer chemotherapy. They may also be useful in reducing pain and inflammation, controlling epileptic seizures, and possibly even treating autoimmune diseases and cancers.

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Ciática, con Animación.

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La ciática o neuralgia ciática es una condición común en la cual una de las raíces nerviosas del nervio ciático es comprimida resultando en dolor lumbar, glúteo y de piernas. El nervio ciático es un gran nervio proveniente de 5 raíces de los nervios espinales: L4, L5, S1, S2 y S3. Discurre desde la columna lumbar a través del glúteo bajando por la pierna hasta el pie por la parte posterior. Hay un nervio ciático en cada lado del cuerpo. Normalmente, solo un lado del cuerpo está afectado.
Un dolor de ciática típico es descrito como un fuerte dolor agudo en la zona lumbar, bajo el glúteo, muslo y pierna en un lado del cuerpo. También puede haber sensaciones de entumecimiento, ardor y hormigueo. El dolor puede empeorar sentándose, moviéndose, estornudando o tosiendo. Los patrones de dolor dependen de la raiz nerviosa que esté comprimida y siga la distribución del dermatoma.
La causa más común de ciática es un disco espinal herniado. El disco espinal es un cojín elástico suave que se encuentra entre las vértebras de la columna. Con la edad, los discos se vuelven rígidos y pueden agrietarse; el centro gelatinoso del disco puede protuir y volverse una hernia fuera de los límites normales del disco. Una hernia de disco presiona sobre la raíz nerviosa según sale de la columna.
En la mayoría de los casos esta condición se resuelve sola tras unas semanas de descanso y tratamiento conservador. Anelgésicos, fármacos anti-inflamatorios no esteroideos y relajantes musculares pueden ser prescritos. Ejercicios de estiramientos y terapia física pueden ser recomendados.
La cirugía puede ser necesitada si el dolor no cesa después de tres meses o más de tratamientos conservadores. El disco herniado puede ser extirpado en un procedimiento llamado discectomía. O, en otro procedimiento llamado laminectomía, parte del hueso de la vértebra puede ser cortado para crear espacio para el nervio.

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