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

– Piriformis syndrome
– Sciatica

Mécanisme de l’Addiction dans le Cerveau, avec Animation.

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La dépendance est un trouble neurologique qui affecte le système de récompense dans le cerveau. Chez une personne en bonne santé, le système de récompense renforce les comportements importants qui sont essentiels à la survie tels que recherche de nourriture, reproduction et l’interaction sociale. Par exemple, le système de récompense assure que vous recherchez pour la nourriture quand vous avez faim, parce que vous savez qu’après avoir mangé, vous vous sentirez bien. En d’autres termes, il rend l’activité de manger agréable et mémorable, de sorte que vous voulez la faire à nouveau chaque fois que vous avez faim. Drogues d’abus détournent ce système, transformant les besoins naturels en besoins de drogues.
Le cerveau est composé de milliards de neurones, ou cellules nerveuses, qui communiquent au moyen des messages chimiques ou neurotransmetteurs. Lorsqu’un neurone est suffisamment stimulé, une impulsion électrique appelée un potentiel d’action est générée et se déplace le long de l’axone à la terminaison nerveuse. Ici, elle déclenche la libération d’un neurotransmetteur dans la fente synaptique, un espace entre les neurones. Le neurotransmetteur se lie ensuite à un récepteur sur le neurone voisin, générant un signal en lui, transmettant ainsi les informations à ce neurone.
Les principaux circuits de la récompense impliquent la transmission de la dopamine, un neurotransmetteur, de l’aire tegmentale ventrale, l’ATV, du mésencéphale, au système limbique et au cortex frontal. L’engagement dans des activités agréables génère des potentiels d’action dans les neurones producteurs de dopamine dans l’ATV. Cela provoque la libération de dopamine par ces neurones dans l’espace synaptique. Elle se lie alors au récepteur dopaminergique se trouvant sur le neurone postsynaptique et le stimule. On croit que cette stimulation produit les sentiments de plaisir ou l’effet gratifiant. Les molécules de dopamine sont ensuite retirées de l’espace synaptique et transportées dans le neurone émetteur par une protéine spéciale appelée le transporteur de la dopamine.
La plupart des drogues d’abus augmentent le niveau de dopamine dans le circuit de la récompense. Certains drogues tels que l’alcool, l’héroïne et la nicotine excitent indirectement les neurones producteurs de dopamine dans l’ATV afin qu’ils génèrent plus de potentiels d’action. La cocaïne agit à la terminaison nerveuse. Elle se lie au transporteur de la dopamine et bloque la réabsorption de la dopamine. La methamphetamine, un psychostimulant, bloque de manière similaire la recapture de la dopamine. En outre, elle peut entrer dans le neurone, dans les vésicules contenant de la dopamine et déclenche la libération de dopamine même en l’absence de potentiels d’action.
Les différents types de drogue agissent de différentes façons, mais le résultat commun est que la dopamine accumule dans la synapse à une quantité beaucoup plus grande que la normale. Cela provoque une stimulation continue, peut-être sur-stimulation des neurones récepteurs et est responsable de l’euphorie prolongée et intense ressentie par les usagers de drogues. Des expositions répétées aux niveaux élevés de dopamine provoquées par les drogues éventuellement désensibilisent le système de récompense. Le système ne répond plus aux stimuli quotidiens; la seule chose qui est gratifiant est la drogue. Voilà comment les drogues changent la priorité de la vie de la personne. Après un certain temps, même la drogue perd sa capacité à récompenser et les doses plus élevées sont nécessaires pour obtenir l’effet gratifiant. Cela conduit finalement à une surdose de drogue.

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Action Potential in Neurons, with Animation.

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Neurons communicate with each other through their dendrites and axon. Generally, INCOMING signals are received at dendrites, while OUTGOING signal travels along the axon to the nerve terminal.  In order to achieve rapid communication over its long axon, the neuron sends ELECTRICAL signals, from the cell’s body to the nerve terminal, along the axon. These are known as nerve impulses, or action potentials. An action potential is essentially a brief REVERSAL of electric polarity across the cell membrane.

Cells are polarized, meaning there is an electrical voltage across the cell membrane. In a resting neuron, the typical voltage, known as the resting membrane potential, is about -70mV (millivolts). The negative value means the cell is more negative on the INSIDE. At this resting state, there are concentration gradients of sodium and potassium across the cell membrane: more sodium OUTSIDE the cell and more potassium INSIDE the cell. These gradients are maintained by the sodium-potassium pump which constantly brings potassium IN and pumps sodium OUT of the cell.

A neuron is typically stimulated at dendrites and the signals spread through the soma. Excitatory signals at dendrites open LIGAND-gated sodium channels and allow sodium to flow into the cell. This neutralizes some of the negative charge inside the cell and makes the membrane voltage LESS negative. This is known as depolarization as the cell membrane becomes LESS polarized. The influx of sodium diffuses inside the neuron and produces a current that travels toward the axon hillock. If the summation of all input signals is excitatory and is strong enough when it reaches the axon hillock, an action potential is generated and travels down the axon to the nerve terminal.  The axon hillock is also known as the cell’s “trigger zone” as this is where action potentials usually start. This is because action potentials are produced by VOLTAGE-gated ion channels that are most concentrated at the axon hillock.

Voltage-gated ion channels are passageways for ions in and out of the cell, and as their names suggest,   are regulated by membrane voltage. They open at some values of the membrane potential and close at others.

For an action potential to be generated, the signal must be strong enough to bring the membrane voltage to a critical value called the THRESHOLD, typically about -55mV. This is the minimum required to open voltage-gated ion channels. At threshold, sodium channels open quickly. Potassium channels also open but do so more slowly. The initial effect is therefore due to sodium influx. As sodium ions rush into the cell, the inside of the cell becomes more positive and this further depolarizes the cell membrane. The increasing voltage in turn causes even more sodium channels to open. This positive feedback continues until all the sodium channels are open and corresponds to the rising phase of the action potential. Note that the polarity across the cell membrane is now reversed.

As the action potential nears its peak, sodium channels begin to close. By this time, the slow potassium channels are fully open. Potassium ions rush out of the cell and the voltage quickly returns to its original resting value. This corresponds to the falling phase of the action potential. Note that sodium and potassium have now switched places across the membrane.

As the potassium gates are also slow to close, potassium continues to leave the cell a little longer resulting in a negative overshoot called hyper-polarization. The resting membrane potential is then slowly restored thanks to diffusion and the sodium-potassium pump.


During and shortly after an action potential is generated, it is impossible or very difficult to stimulate that part of the membrane to fire again. This is known as the REFRACTORY period. The refractory period is divided into absolute refractory and relative refractory. The absolute refractory period lasts from the start of an action potential to the point the voltage first returns to the resting membrane value. During this time, the sodium channels are open and subsequently INACTIVATED while closing and thus unable to respond to any new stimulation. The relative refractory period lasts until the end of hyper-polarization. During this time, some of the potassium channels are still open, making it difficult for the membrane to depolarize, and a much stronger signal is required to induce a new response.

During an action potential, the sodium influx at a point on the axon spreads along the axon, depolarizing the adjacent patch of the membrane, generating a similar action potential in it. The sodium currents diffuse in both directions on the axon, but the refractory properties of ion channels ensure that action potential propagates ONLY in ONE direction. This is because ONLY the unfired patch of the axon can respond with an action potential; the part that has just fired is unresponsive until the action potential is safely out of range.

An action potential generated at the axon hillock usually travels down the axon to the nerve terminal and not back to the cell body. This is because the concentrations of voltage-gated ions channels are higher in the axon than in the cell body.

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Serotonin and Treatments for Depression, with Animation.

The videos on this page can be downloaded upon purchase of a license on Alila Medical Media website. Click here!


Serotonin, or 5-hydroxytryptamine (5-HT), is a neurotransmitter involved in many brain and body functions and is commonly known as the substance of well-being and happiness.
Serotonin is produced in specialized neurons found mostly in the Raphe nuclei located along the midline of the brainstem. The axons of these neurons form extensive serotonergic pathways that reach almost every part of the central nervous system, including the cerebellum and the spinal cord. This is why it’s not surprising that serotonin is implicated in a vast array of brain functions, including sleep and wake cycle, appetite, mood regulation, memory and learning, temperature control, … among others.
Serotonin is synthesized from the amino acid tryptophan and is stored in small vesicles within the nerve terminal. When a serotonergic neuron is stimulated, serotonin is released into the synaptic cleft where it binds to and activates serotonin-receptors on the postsynaptic neuron. Serotonin action is then TERMINATED via removal of its molecules from the synaptic space. This is accomplished through a special protein called serotonin-transporter.
Low levels of serotonin in the brain have been associated with depressive disorders and current treatments for depression aim to increase these levels. The most commonly prescribed medications, called “selective serotonin reuptake inhibitors”, or SSRIs, act by blocking serotonin reuptake by the transmitting neurons. This results in elevated levels of serotonin in the synaptic space and its prolonged action on the receiving neuron. The SSRIs have developed into the drugs of choice because they produce fewer side effects thanks to their selective action on serotonin alone and no other neurotransmitters. Unfortunately, because serotonin is involved in a wide range of brain functions, the side effects remain significant and may progress to a potentially dangerous condition known as “serotonin syndrome”. This syndrome is generally caused by a combination of two or more drugs used to raise the serotonin levels in the brain. If the medications are not discontinued, the condition may become fatal.
Nonpharmacologic methods of raising brain serotonin have shown promising results in recent studies. It has been suggested that positive mood induction, either self-induced or due to psychotherapy, correlates with INCREASED serotonin synthesis in the brain. The interaction between serotonin synthesis and mood may therefore be 2-way, with serotonin influencing mood and mood influencing serotonin.
Other methods include exposure to bright light and tryptophan-rich diets. To note, however, that serotonin-rich food such as bananas would NOT work because serotonin, unlike tryptophan, can NOT cross the blood brain barrier.
Finally, although it sounds like a cliché, physical exercise maybe the most effective and safest way of improving mood. Several studies suggest that serotonin levels are increased with vigorous physical activity and that these elevated levels are maintained for several days after the exercise.

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Neuroglia – The Other Cells of the Brain, with Animation.

The videos on this page can be downloaded upon purchase of a license on Alila Medical Media website. Click here!


A human brain contains billions of neurons. Neurons are probably the most important and best-known cells of the brain as they carry out the brain’s communication function. Less known are some trillions of support cells called glia, or glial cells. The glia may not be the stars of the show, but without them, neuron functions would be impossible.
The major types of glial cells in the brain include: oligodendrocytes, microglia, and astrocytes.
Oligodendrocytes are specialized cells with arm-like processes that wrap tightly around axons of neurons to form the myelin sheath. The myelin sheath acts like an electrical insulator around a wire. It helps to speed up the electrical signals that travel down an axon. Without oligodendrocytes, an action potential would propagate 30 times slower!
Microglia are special macrophages found only in the central nervous system. They wander through the brain tissue and phagocytize dead, injured cells and foreign invaders. High concentrations of microglia are an indication of infection, trauma or stroke.
Astrocytes are the most abundant and functionally diverse glia.
These star-shaped glial cells provide supportive frameworks to hold neurons in place. They provide neuron with nutrients such as lactate. They also produce growth factors that promote neuron growth and synapse formation. There is growing evidence that astrocytes can alter how a neuron is built by directing where to make synapses or dendritic spines.
Through their numerous processes, known as perivascular feet, astrocytes induce the endothelial cells of blood vessels to form tight junctions. These tight junctions are the basis of the blood brain barrier that restricts the passage of certain substances from the bloodstream to the brain tissue.
Astrocytes help to maintain the chemical composition of the extracellular fluid. They express membrane transporters for several neurotransmitters such as glutamate, ATP and GABA, and help to remove them from synaptic spaces.
Astrocytes also absorb potassium ions released by neurons at synapses. This helps to regulate potassium concentrations in the extracellular space. Abnormal accumulation of extracellular potassium is known to result in epileptic neuronal activity.
Another function of astrocytes is to form scar tissues to replace damaged tissues.
Recently, it has been shown that astrocytes can also communicate electrically with neurons and modify the signals they send and receive. In a manner similar to neurons, astrocytes can release transmitters, called gliotransmitters, upon stimulation. These open up a possibility that astrocytes maybe much more involved in the communication functions of the brain than we currently believe.

Clinical implication
From a clinical viewpoint, neurons have little capacity for renewal and therefore rarely form tumors. On the contrary, glial cells are capable of dividing throughout life and are the primary source of brain tumors.

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Alzheimer’s disease. What do we know? With animation.

The videos on this page can be downloaded upon purchase of a license on Alila medical Media website. Click here!


Alzheimer’s disease, or AD, is a very common neurodegenerative disorder in which brain cells are progressively damaged and die, leading to loss of memory, thinking skills and eventually all other brain functions.

A brain consists of billions of neurons, or nerve cells, which communicate via chemical messages, or neurotransmitters. This communication occurs in a space between neurons, called a synapse. Neuron communication is essential to all brain activities.

An Alzheimer’s brain is characterized by presence of abnormal plaques and tangles.

Plaques are clumps of a peptide known as beta-amyloid. Beta-amyloid derives from a larger membrane protein normally present on the surface of nerve cells. These clumps are toxic to nerve cells and may block cell-to-cell signaling at synapses. They are also believed to trigger inflammation responses that bring further damage to the brain tissue.

Tangles are formations of a protein named tau. Tau protein’s major function is to stabilize axonal microtubules – the tubular structures that run along axons of neurons and are responsible for intracellular transport. In AD patients, tau molecules are mis-folded and clump into tangles. As a result, the microtubules are disintegrated and cellular transport is impaired.

As the toxic deposits of plaques and tangles increase, neurons stop functioning, lose connections with each other, and die.

The damage initially takes place in the hippocampus, the part of the brain that is essential in forming memories. That is why short-term memory loss is usually one of the first symptoms of Alzheimer’s. Plaques and tangles tend to spread through the cortex in a predictable pattern as the disease progresses. New symptoms appear accordingly and in an order that corresponds to different stages of the disease. At the final stage, the brain shrinks dramatically and nearly all its functions are affected.

Most people with Alzheimer’s show first symptoms after the age of 65, while the process of neuron destruction has probably started many years earlier. For this form of late-onset AD, the cause remains largely unknown, but a combination of environmental and genetic factors is  likely. Notably, a certain form of a lipoprotein named Apolipoprotein E is shown to increase susceptibility to the disease.

For a small subset of AD cases known as Familial Alzheimer’s Disease, genetic factors have been identified. This rare form of AD is linked to a mutation in one of several genes involved in beta-amyloid production. For this group, the disease strikes earlier in life, commonly between 50 and 65 years of age, but can be earlier.

Currently there is no cure for Alzheimer’s. Treatments aim to slow down the process of destruction and relieve symptoms to improve quality of life for patients and caregivers.

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Mecanismo de la Adicción a las Drogas en el Cerebro

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La adicción es un desorden neurológico que afecta al sistema de recompensa en el cerebro. En una persona sana, el sistema de recompensa refuerza comportamientos importantes que son esenciales para la supervivencia tales como comer, beber, el comportamiento sexual e interacción social. Por ejemplo, el sistema de recompensa asegura que busques comida cuando tienes hambre, porque sabes que después de comer te sentirás bien. En otras palabras, hace la actividad de comer placentera y memorable, por lo que querrás hacerlo una y otra vez cada vez que sientas hambre. Las drogas de abuso se apropian de este sistema, tornando las necesidades naturales de la persona en necesidad de drogas.

El cerebro consiste en billones de neuronas, o células nerviosas, que se comunican a través de mensajeros químicos, o neurotransmisores. Cuando una neurona es estimulada lo suficiente, un impulso eléctrico llamado potencial de acción es generado y viaja por el axón a la terminal nerviosa. Aquí, desencadena la liberación de un neurotransmisor en la hendidura sináptica – un espacio entre neuronas. El neurotransmisor luego se une a un receptor en una neurona vecina, generando una señal en ella, transmitiendo así la información a esa neurona.

Las principales vías de recompensa involucran la transmisión del neurotransmisor DOPAMINA del área tegmental ventral – el ATV – del mesencéfalo al sistema límbico y la corteza frontal. Participar en actividades agradables genera potenciales de acción en neuronas productoras de dopamina del ATV. Esto causa liberación de dopamina desde las neuronas en el espacio sináptico. Luego esta se une y estimula el receptor de dopamina en la neurona receptora. Se cree que esta estimulación por dopamina produce los sentimientos placenteros o efecto de recompensa. Las moléculas de dopamina después son removidas del espacio sináptico y transportadas de nuevo hacia la neurona transmisora por una proteína especial llamada transportador de dopamina.

La mayoría de las drogas de abuso INCREMENTAN el nivel de dopamina en la vía de recompensa. Algunas drogas como el alcohol, la heroína y nicotina indirectamente excitan a las neuronas productoras de dopamina en el ATV de modo que estas generan más potenciales de acción. La cocaína actúa en la terminal nerviosa. Se une al transportador de dopamina y bloquea la recaptación de dopamina. La metanfetamina – un psicoestimulante – actúa de forma similar a la cocaína en el bloqueo de la remoción de dopamina. Además, esta puede entrar en la neurona, en las vesículas que contienen dopamina donde desencadena la liberación de dopamina incluso en ausencia de potenciales de acción.

Diferentes drogas actúan de forma diferente pero el resultado común es que la dopamina se acumule en la sinapsis en una cantidad mucho MAYOR de lo normal. Esto causa una estimulación continua, tal vez sobreestimulación de las neuronas receptoras y es responsable de una euforia prolongada e intensa que experimentan los usuarios de drogas. Exposiciones repetitivas a oleadas de dopamina causadas por drogas eventualmente desensibilizan el sistema de recompensa. El sistema ya no es sensible a los estímulos cotidianos; La única cosa que es gratificante es la droga. Así es como las drogas cambian las prioridades en la vida de la persona. Después de un tiempo, incluso la droga pierde su habilidad para recompensar y dosis más altas son necesarias para lograr el efecto gratificante. Esto finalmente conduce a una sobredosis.

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Arteriovenous Malformation (AVM) and Embolization Treatment

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An arteriovenous malformation or an AVM is an abnormal formation of blood vessels connecting arteries and veins, BYPASSING the capillary system. The blood vessels of an AVM are commonly dilated and weakened due to high blood pressure and an AMV may bleed. Bleeding from an AVM may cause damage to surrounding brain tissue and result in a hemorrhagic stroke.
An AVM can develop anywhere in the body but occurs most often in the brain or spine. AVMs are mostly congenital but not hereditary. They are believed to form during embryonic or fetal development.
AVM embolization is an endovascular treatment aimed to block blood flow in to an AVM and therefore reduce the risks of AVM bleeding.
In this procedure, a catheter is inserted through the femoral artery at the groin and threaded all the way to the brain AVM. The catheter is used to inject a special glue into the AVM. The glue hardens when it comes into contact with the blood and seals off the AVM from the blood flow.
AVM blood vessels do not supply normal brain tissue and therefore their blockage will not have any consequences on the patient.
AVM embolization is rarely successful on its own. It is useful, however, in conjunction with other procedures such as surgery or radiation. Performing AVM embolization PRIOR to surgical removal helps to reduce significantly the risk of AVM bleeding during surgery.

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Flow Diversion for Treatment of Cerebral Aneurysm


Below is a narrated animation of Flow diversion. Click here to license this video and other similar images/videos on Alila Medical Media website.

Flow diversion is a newer endovascular technique used to treat brain aneurysms. The procedure involves placing a flow-diverting device – a specially designed metal mesh tube – in the blood vessel adjacent to the aneurysm to divert blood flow AWAY from the aneurysm.

In this procedure, a catheter guided by a wire is inserted through the femoral artery at the groin and threaded all the way to the affected brain artery. The guide-wire is removed. A micro-catheter carrying the flow-diverting device is introduced inside the initial catheter and is navigated PAST the aneurysm opening, without entering it. The device is then deployed across the neck of the aneurysm.

The tube slows and eventually stops blood flow into the aneurysm, which, over time, is believed to shrink and disappear.

Flow diversion is particularly useful for treatment of large or wide-neck aneurysms where coiling may be difficult to perform. It is also more suitable for treating un-ruptured aneurysms due to the fact that the device and the catheter system do NOT need to enter the aneurysm itself. This significantly reduces the risk of the aneurysm rupturing during the procedure.

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Endovascular Coiling for Treatment of Cerebral Aneurysm

Below is a narrated animation of Endovascular coiling. Click here to license this video and other similar images/videos on Alila Medical Media website.


Endovascular coiling or endovascular embolization is a minimally invasive technique performed to treat brain aneurysms. The goal of the treatment is to block blood flow into the aneurysm and therefore reduce the risk of aneurysm rupturing.

In this procedure, a catheter guided by a wire is inserted through the femoral artery at the groin and threaded all the way to the affected brain artery. The guide wire is removed. A micro-catheter carrying a soft platinum coil is introduced inside the initial catheter and is navigated into the aneurysm opening. The coil is then deployed into the aneurysm sac. A small electrical current is passed to detach the coil from the catheter. It may take several coils to fill the aneurysm. The coils induce blood clotting inside the aneurysm and seal it off from the artery.

In some cases, when the neck of the aneurysm is too wide, a stent may be used to keep the coils within the aneurysm sac. Stent-assisted coiling involves permanently placing a stent in the artery prior to coiling. The stent acts as a scaffold inside the artery to help holding the coils in place.

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Mechanism of Drug Addiction in the Brain

Below is a narrated animation of drug addiction mechanism. Click here to license this video on Alila Medical Media website.


The Brain Reward Pathway

Addiction is a neurological disorder that affects the reward system in the brain. In a healthy person, the reward system reinforces important behaviors that are essential for survival such as eating, drinking, sex, and social interaction. For example, the reward system ensures that you reach for food when you are hungry, because you know that after eating you will feel good. In other words, it makes the activity of eating pleasurable and memorable, so you would want to do it again and again whenever you feel hungry. Drugs of abuse hijack this system, turning the person’s natural needs into drug needs.
The brain consists of billions of neurons, or nerve cells, which communicate via chemical messages, or neurotransmitters. When a neuron is sufficiently stimulated, an electrical impulse called an action potential is generated and travels down the axon to the nerve terminal. Here, it triggers the release of a neurotransmitter 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.
Motor neuron with Schwann cell and synapse, labeled.
Fig. 1: Structure of a neuron, with details of myelin and synapse. Click on image to see it on Alila Medical Media website where the image is also available for licensing.

 

 

 

 

 
The major reward pathways involve transmission of the neurotransmitter dopamine from the ventral tegmental area – the VTA – of the midbrain to the limbic system and the frontal cortex. Engaging in enjoyable activities generates action potentials in dopamine-producing neurons of the VTA. This causes dopamine release from the neurons into the synaptic space. Dopamine then binds to and stimulates dopamine-receptor on the receiving neuron. This stimulation by dopamine is believed to produce the pleasurable feelings or rewarding effect. Dopamine molecules are then removed from the synaptic space and transported back in to the transmitting neuron by a special protein called dopamine-transporter.
Dopamine pathways.

Fig. 2: The dopaminergic pathways. Click on image to see it on Alila Medical Media website where the image is also available for licensing.

Mechanism of Drug Addiction in the Brain

Most drugs of abuse increase the level of dopamine in the reward pathway. Some drugs such as alcohol, heroin, and nicotine indirectly excite the dopamine-producing neurons in the VTA so that they generate more action potentials. Cocaine acts at the nerve terminal. It binds to dopamine-transporter and blocks the re-uptake of dopamine. Methamphetamine – a psychostimulant – acts similarly to cocaine in blocking dopamine removal. In addition, it can enter the neuron, into the dopamine-containing vesicles where it triggers dopamine release even in the absence of action potentials.
Action of methamphetamine on dopaminergic synapse.
Fig. 3: Methamphetamine action on dopamine synapse. Click on image to see it on Alila Medical Media website where the image is also available for licensing.

 

 

 

 

Different drugs act different way but the common outcome is that dopamine builds-up in the synapse to a much greater amount than normal. This causes a continuous stimulation, maybe over-stimulation of receiving neurons and is responsible for prolonged and intense euphoria experienced by drug users. Repeated exposure to dopamine surges caused by drugs eventually de-sensitizes the reward system. The system is no longer responsive to everyday stimuli; the only thing that is rewarding is the drug. That is how drugs change the person’s life priority. After some time, even the drug loses its ability to reward and higher doses are required to achieve the rewarding effect. This ultimately leads to drug overdose.

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