This video is available for licensing on our website. Click HERE!

The ability to understand language and produce speech is associated with several areas of the cerebral cortex. Basically, spoken language is first perceived in the auditory cortex, while written text, or sign language, is processed in the visual cortex. This information is then sent to the Wernicke’s area, in the temporal lobe, where it is matched against the person’s vocabulary stored in the memory. This is where meaning is assigned to words and language comprehension is achieved.  The signals are then transmitted via a bundle of nerve fibers, known as the arcuate fasciculus, to Broca’s area in the frontal lobe.  Broca’s area is responsible for production of speech. Output from Broca’s area goes to the motor cortex which controls muscle movements necessary for speech.

A language disorder caused by brain damage is called aphasia. Lesions in the Wernicke’s area cause sensory, or receptive, aphasia. Wernicke’s aphasics have trouble understanding language, whether it is spoken or written, but have NO motor problems. They can speak at a fluent pace but their speech is often INcoherent. It can be described as a strange mixture of words that may sound like complete sentences but makes no sense and has nothing to do with the subject of conversation.

Patients with lesions in the Broca’s area, on the other hand, CAN understand language, but have difficulties speaking. They talk slowly, searching for words, forming INcomplete sentences with poor syntax, but usually manage to say important words to get their message across.

In the early days, research of language pathways was based mainly on studying patients who had a specific language deficit that could be associated with a specific brain damage. Nowadays, advanced brain imaging techniques allow mapping, in real time, the areas of the brain that are activated when a person carries on a specific task. Thanks to these techniques, a THIRD area is found to be essential for language comprehension: the inferior parietal lobule. This lobule is not only connected to both Wernicke’s and Broca’s, but also to the auditory, visual, and somatosensory cortical areas. The inferior parietal lobule is therefore perfectly wired to perform a multimodal, complex synthesis of information; it can process and connect different word elements such as the sound of the word with the look and feel of the object.

The languages centers are usually located in ONLY ONE hemisphere – the “dominant” hemisphere of the brain, which is the LEFT side in RIGHT-handed people. The corresponding areas in the right hemisphere are responsible for the emotional aspect of language. Lesions in the right hemisphere do NOT affect speech comprehension or formation but result in emotionless speech and inability to understand the emotion behind the speech such as sarcasm or a joke.  The right hemisphere may also develop to take over the MAIN language functions if the left side is damaged in early childhood. This phenomenon is known as neuroplasticity.

This video is available for licensing on our website. Click HERE!

The autonomic nervous system, or ANS, is the part of the nervous system that regulates activities of internal organs. The ANS is largely AUTONOMOUS, acting independently of the body’s consciousness and voluntary control. It has two main divisions: sympathetic, SNS, and parasympathetic, PSNS.

In situations that require alertness and energy, such as facing danger or doing physical activities, the ANS activates its sympathetic division to mobilize the body for action. This division increases cardiac output, accelerates respiratory rate, releases stored energy, and dilates pupils. At the same time, it also inhibits body processes that are less important in emergencies, such as digestion and urination.

On the other hand, during ordinary situations, the parasympathetic division conserves and restores. It slows heartbeats, decreases respiratory rate, stimulates digestion, removes waste and stores energy.

The sympathetic division is therefore known as the “fight or flight” response, while the parasympathetic division is associated with the “rest and digest” state.

Despite having opposite effects on the same organ, the SNS and PSNS are NOT mutually exclusive. In most organs, both systems are simultaneously active, producing a background rate of activity called the “autonomic tone” – a balance between sympathetic and parasympathetic inputs. This balance SHIFTS, one way or the other, in response to the body’s changing needs.

Some organs, however, receive inputs from ONLY ONE system. For example, the smooth muscles of blood vessels only receive sympathetic fibers, which keep them partially constricted and thus maintaining normal blood pressure. An increase in sympathetic firing rate causes further constriction and increases blood pressure, while a decrease in firing rate dilates blood vessels, lowering blood pressure.

The autonomic nerve pathways, from the control centers in the central nervous system to the target organs, are composed of 2 neurons, which meet and synapse in an autonomic ganglion. Accordingly, these neurons are called preganglionic and postganglionic.

In the SNS, the preganglionic neurons arise from the thoracic and lumbar regions of the spinal cord; their fibers exit by way of spinal nerves to the nearby sympathetic chain of ganglia. Once in the chain, preganglionic fibers may follow any of 3 routes: some fibers synapse immediately with postganglionic neurons; some travel up or down the chain before synapsing; some pass through the chain without synapsing – this third group continues as splanchnic nerves to nearby collateral ganglia for synapsing instead. From the ganglia, LONG postganglionic fibers run all the way to target organs. The SNS has a high degree of neuronal DIVERGENCE: one preganglionic fiber can synapse with up to 20 postganglionic neurons. Thus, effects of the SNS tend to be WIDESPREAD.

In the PSNS, the preganglionic neurons arise from the brainstem and sacral region of the spinal cord. Preganglionic fibers exit the brainstem via several cranial nerves and exit the spinal cord via spinal nerves before forming the pelvic splanchnic nerves. Parasympathetic ganglia are located near or within target organs, so postganglionic fibers are relatively short. The degree of neuronal divergence in the PSNS is much lower than that of the SNS. Thus, the PSNS produces more SPECIFIC, LOCALIZED responses compared to the SNS.

This video is available for licensing on our website. Click HERE!

As undesirable as it might seem, PAIN is actually a very important defense mechanism. It WARNS the body about potential or actual injuries or diseases, so that protective actions can be taken. Basically, noxious signals send impulses to the spinal cord, which relays the information to the brain. The brain interprets the information as pain, localizes it, and sends back instructions for the body to react.

Pain sensation is mediated by pain receptors, or nociceptors, which are present in the skin, superficial tissues and virtually all organs, except for the brain. These receptors are essentially the nerve endings of so-called “first-order neurons” in the pain pathway. The axons of these neurons can be myelinated, A type, or, unmyelinated, C type. Myelinated A fibers conduct at FAST speeds and are responsible for the initial SHARP pain perceived at the time of injury. Unmyelinated C fibers conduct at SLOWER speeds and are responsible for a longer-lasting, dull, diffusing pain.

First-order neurons travel by way of spinal nerves to the spinal cord, where they synapse with second-order neurons in the dorsal horn. These second-order neurons cross over to the OTHER side of the cord, before ascending to the brain. This is how information of pain on the left side of the body is transmitted to the right side of the brain, and vice versa.

There are two major pathways that carry pain signals from the spinal cord to the brain:

– The spinothalamic tract: second-order neurons travel up within the spinothalamic tract to the thalamus where they synapse with third-order neurons; third-order neurons then project to their designated locations in the somatosensory cortex. This pathway is involved in LOCALIZATION of pain.

– The spinoreticular tract: second-order neurons ascend to the reticular formation of the brainstem, before running up to the thalamus, hypothalamus, and the cortex. This tract is responsible for the EMOTIONAL aspect of pain.

Pain signals from the face follow a DIFFERENT route to the thalamus. First-order neurons travel mainly via the trigeminal nerve to the brainstem, where they synapse with second-order neurons, which ascend to the thalamus.

Pain from the skin, muscles and joints is called SOMATIC pain, while pain from INTERNAL organs is known as VISCERAL pain. Visceral pain is often perceived at a DIFFERENT location in a phenomenon known as REFERRED pain. For example, pain from a heart attack may be felt in the left shoulder, arm or back, rather than in the chest, where the heart is located. This happens because of the CONVERGENCE of pain pathways at the spinal cord level. In this example, spinal segments T1 to T5 receive pain signals from the heart as well as the shoulders and arms, and the brain canNOT tell them apart. Because the superficial tissues have MORE pain receptors and are MORE often injured, it’s common for the brain to make an assumption that the pain comes from the shoulder or arm instead of the heart.

This video is available for licensing on our website. Click HERE!

Parkinson’s disease, or PD, is a neurodegenerative disorder in which DOPAMINE-producing neurons of a brain structure called the SUBSTANTIA NIGRA, are damaged and die over time, leading to a number of MOTOR problems and mental disabilities.

The substantia nigra is part of the basal ganglia, whose major function is to INHIBIT UNwanted motor activities. When a person intends to make a movement, this inhibition is removed by the action of dopamine. As dopaminergic neurons are progressively lost in PD patients, LOW levels of dopamine make it HARDER to INITIATE voluntary movements.

The events leading to neuronal cell death are poorly understood but the presence of so-called “Lewy bodies” in the neurons before they die may offer a clue and is currently the subject of intensive research.

Symptoms develop slowly over time; most prominent are MOTOR problems which include hand tremors, slow movements, limb rigidity and problems with gait and balance. These motor symptoms are collectively known as “PARKINSONISM”. However, parkinsonism may also be caused by a variety of other factors, which must be excluded before a person can be diagnosed with PD. Other motor-related problems may include slurred speech and reduced facial expressions. In later stages, non-motor symptoms such as mood and behavioral changes, cognitive impairment and sleep disturbances… may be observed.

The cause of Parkinson’s remains largely unknown but is likely to involve both genetic and environmental factors.

There is no cure for PD but current treatments are effective in managing motor symptoms:

First-line treatment involves medications which aim to INcrease dopamine levels in the brain. Major classes of medication include:

– Levodopa, a precursor of dopamine: levodopa can cross the blood brain barrier and is converted into dopamine inside the brain. Levodopa is the most effective of all medications but because it also produces dopamine elsewhere in the body, its side effects may become serious in the long-term. For this reason, levodopa is always administered together with some other drugs that inhibit its action OUTSIDE the brain.

– Dopamine agonists: substances that bind to dopamine receptors and mimic the action of dopamine.

– Another class of drugs includes INHIBITORS of enzymes that break down dopamine.

For people who do NOT respond to medications, surgery may be recommended. The most commonly performed procedure, deep brain stimulation, involves the implantation of a device called a neurostimulator, which sends electrical impulses to specific parts of the brain. By doing so, the device controls brain activities to relieve symptoms.

This video is available for licensing on our website. Click HERE!

Huntington’s disease, or HD, is an INHERITED neurodegenerative disorder in which brain cells are damaged and die over time, leading to progressive loss of mental and physical abilities.
The disease is caused by an ABnormal version of the gene huntingtin, or HTT. The normal HTT gene has a stretch of 10 to 35 repeats of C-A-G nucleotide triplets, which encode for the amino acid glutamine. In people with HD, the HTT gene has MORE than 36 CAG repeats. The ABnormally LONG stretch of poly-glutamine ALTERS the structure of HTT protein, causing fragmentation and aggregation, forming a MIS-folded protein that is TOXIC to nerve cells. The resulting neuronal cell death is most prominent in the basal ganglia of the brain, especially in the striatum. Because the striatum’s function in motor control is to INHIBIT unwanted movements, its degeneration results in UNcontrollable dance-like movements, known as Huntington’s CHOREA, characteristic of the disease.
A person has 2 copies of the HTT gene but ONE ABnormal copy is sufficient to cause the disease. Children of an affected parent have a 50% chance of receiving the abnormal copy, hence a 50/50 chance of inheriting the disease. This pattern of inheritance is known as autosomal dominant.
The onset and progression of the disease depends on the number of CAG repeats – the greater the number of repeats, the earlier the age of onset and the faster the progression.
The high degree of sequence repetition also INcreases the likelihood of INaccurate DNA replication. Repeating sequences may form loops which cause the DNA polymerase to add more repeats as it replicates the DNA. This means a phenotypically-NORMAL father with 30-35 repeats MAY give his child a 40-repeats gene that would produce the disease. As the size of the polyglutamine stretch INcreases from generation to generation, the onset of symptoms gets earlier with each generation. This phenomenon is known as genetic ANTICIPATION.
An average person with a 40-50 CAG repeats in the HTT gene usually develops symptoms in their 40s. People with more than 60 repeats may start to show signs of the disease in their childhood. The first signs are SUBTLE mental and cognitive disturbances that may go unnoticed. As the disease progresses, chorea becomes prominent, followed by motor speech disorders, rigidity, swallowing difficulty, dysphagia, personality changes, memory loss, and other cognitive and psychiatric impairments.
Diagnosis is by genetic testing. Genetic counseling is available for people with family history of HD.
Life expectancy in HD is generally around 10 to 20 years following the onset of symptoms. Most life-threatening complications result from problems in muscle coordination, of which pulmonary aspiration is the most common cause of death. Currently there is no cure for Huntington’s disease, but treatments can relieve symptoms and improve quality of life.

This video is available for licensing on our website. Click HERE!

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.

This video is available for licensing on our website. Click HERE!

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.