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Synesthesia is a phenomenon in which stimulation of a certain sensation leads to a simultaneous activation of another unrelated sensory pathway. For example, some synesthetes see colors when they hear sounds, while others can taste distinct flavors when they hear unrelated words. Remarkably, this involves not only the five senses, but also cognitive and mental experiences such as pattern recognition, spatial orientation or even emotions. Some forms of synesthesia involve more than two senses or experiences at a time.
In theory, there can be as many types of synesthesia as there are possible combinations of sensory or perceptual experiences, but some forms are much more common than others. These include: grapheme-to-color synesthesia, where individual letters and numbers are seen with a specific color; sound-to-color, or chromesthesia, where sounds produce colors; and spatial sequence synesthesia where elements of a sequence, such as days in a week, are assigned a specific location in a 3D arrangement around the person. It’s not uncommon for a person to experience more than one form.
Once thought to be rare, synesthesia is now estimated to be very common. The numbers are far from accurate, however, perhaps because most synesthetes have their experiences since a very young age and do not realize that anything is “unusual” until much later in life, at which point many tend to keep it a secret for fear of being different or diagnosed with mental illness. With today’s better understanding of the phenomenon, synesthetes are more likely to come forward sharing their experience. Despite being referred to as a neurological condition by some neurologists, synesthesia is not a disease; it is not associated with cognitive or mental disabilities. In fact synesthetes generally perform better in memory tests than an average person and tend to be more creative. They have built-in capabilities that are to their advantage: seeing colors when hearing musical notes can help achieve perfect pitch; automatically arranging items in space aids with memory; and having numbers color-coded can help quickly spot differences and patterns. Most synesthetes perceive their experiences as a gift rather than a handicap. Many tend to have inclination for creative, artistic professions.
A “true” synesthetic experience is automatic, involuntary and consistent over time. These experiences are the only way a synesthete perceives the world: a sound, or a letter, always gives the same color, every time without fail; and if they hear a new sound they never heard before, or see a new character they never seen before, a color will be automatically assigned to it.
Some drugs may produce synesthetic-like effects but these are not real synesthetic experience because they do not last.
Genetic make-up seems to have a role in predisposition to synesthesia as it tends to run in family, but family members can have different forms of synesthesia.
Mechanism of synesthesia is still poorly understood, but there is evidence that the cross-talk between various sensory pathways accounts for the experience. For example, with the help of brain imaging techniques, the brain V4 region responsible for color recognition can be seen activated when a sound-to-color synesthete is presented with auditory stimuli. Synesthetes also seem to have more grey matter in the implicated brain areas, as well as more white matter connecting them.
There is a theory that we are all born synesthetic, with all the connections between senses, but lose them, together with synesthetic ability, as our brain matures, while synesthetes retain it. This may explains why most people still have some degree of synesthesia as adults.

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Synaptic pruning is the process of synapse removal that takes place naturally, as part of brain maturation. A human brain starts its development in early embryonic stage and reaches the maximum number of synaptic connections sometime in early childhood, at which point it is about double of what is normally present in an adult brain. This is when the elimination of excess neuronal synapses, known as synaptic pruning, begins. The process removes roughly half of all synapses, and occurs mainly during adolescence, but may continue well into young adulthood. By getting rid of unnecessary connections, synaptic pruning helps to refine neural circuits and increase network efficiency.

Computational models suggest that learning performance is optimal when synaptic connections are first over-generated and then pruned. An analogy is the task of writing an essay: the easiest way is to put all possible ideas into a longer-than-needed first draft, then trim it to keep only the essential points to create an effective final message.

Synaptic pruning is activity-driven, and follows the “use it or lose it” rule – synapses that are rarely used are eliminated, while frequently used synapses are protected from removal.  In fact, it has been shown that activation of the glutamate receptor NMDA, a marker associated with long-term memory retention and learning, is the major protective factor for a synapse. Thus, active synapses are selectively stabilized, while superfluous synapses are eliminated.

While the mechanism underlying synaptic pruning is, in most part, still a mystery, recent studies have implicated the brain’s supportive cells, known as glial cells, or glia. Specifically, two types of glia – astrocytes and microglia – are responsible for identifying and removing unnecessary neural connections. A number of signaling molecules are involved in control of glial cell movement, target recognition and ingestion.

Given the important role of synaptic pruning in sculpturing and refining the brain’s neural circuits, it is plausible that aberrant synaptic pruning is associated with a number of neurological disorders such as schizophrenia, autism and epilepsy. Too much pruning results in shortage of connections and is thought to underlie schizophrenia. The first occurrence of schizophrenia symptoms, typically in late adolescence or early adulthood, coincides with the time when synaptic pruning is most prominent.

Too little pruning, on the other hand, leaves the brain with too many redundant connections, which can be confusing, inefficient and may limit learning potential. Excessive synapses are observed in autism spectrum disorders, and epilepsy.

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Neuroplasticity is the ability of the brain to change, or rewire, throughout a person’s life. It is the basis of learning and brain repair after injuries.

The brain consists of billions of neurons. Neurons communicate with each other through a space between them, called a synapse. This communication is made possible by chemical messages, or neurotransmitters. Basically, the pre-synaptic neuron releases a neurotransmitter, which binds to, and activates a receptor on the post-synaptic neuron. 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, as well as neurons themselves, can change over time, and this phenomenon is called neural plasticity, or neuroplasticity. Neuroplasticity is activity-driven and follows the “use it or lose it” rule: frequently used synapses are strengthened, while rarely used connections are weakened or eliminated; new activities generate new connections.

Changes in synaptic strength can be temporary or long-lasting depending on the intensity and reoccurrence of the signal the synapse receives. Neurons can temporarily enhance their connections by releasing more neurotransmitter, activating a new receptor, or modifying an existing receptor. This is the basis of short-term memory. Long-term memory retention requires strong or sustained activities that produce structural changes, such as growth of new dendritic spines and synaptic connections, or even formation of new neurons. Structural neuroplasticity may also result in enlargement of the cortical area associated with the increased activity, and shrinkage of areas that receive less or no activity. For example, in right-handed people, the hand motor region on the left side of the brain, which controls the right hand, is larger than the other side.

Neuroplastic changes can also be functional, meaning neurons may adopt a new function when they are sufficiently stimulated. This is how the brain survives injuries, such as strokes. Healthy brain tissues can take over the functions of the damaged area during post-stroke rehabilitation. Some stimuli, such as stress or physical exercise, can cause certain neurons to switch from one neurotransmitter to another, often converting them from excitatory to inhibitory or vice versa. This neurotransmitter switching is thought to be the basis of behavioral changes induced by such stimuli.

An intriguing example of neural plasticity is the phenomenon of phantom limb sensation, in which patients who have lost a limb through amputation can still feel the limb. For example, patients may feel that their lost arm is being touched when their face is touched.  Because incoming sensory signals from the arms and face project to neighboring regions in the somatosensory cortex, it is plausible that sensory inputs from the face spill over to the now inactive arm region that no longer receives any inputs, tricking the brain’s higher centers into interpreting that the sensation comes from the absent arm.

The plasticity of the brain is not limited by age, but is much more remarkable in children as their young brain is still developing. Neuroplasticity is essential for normal brain development, it helps create functional brain circuits and is the basis of learning. This is why acquiring a new skill, such as speaking a language or playing a musical instrument, is much easier in childhood than in adulthood. But changes brought about by neural plasticity can also be negative/maladaptive and have unfortunate consequences especially if happen in childhood. Childhood traumas are more likely to have long-lasting effects into a person’s life.

Neuroplastic changes happen all the time, but their magnitude depends on the amount of activity the brain receives. More practice leads to more learning. Keeping the brain busy is the way to keep it healthy and effective.

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Concussion is a MILD traumatic brain injury that affects normal brain functions. It occurs as a result of a forceful blow, either DIRECT or INdirect to the head. An example of an INdirect blow is a whiplash-type injury that causes the brain to SHAKE quickly back and forth inside the skull. In a direct blow, injury may develop on the side of contact with the force, or on the OPPOSITE side of the head. Concussion may be caused by falls, contact sports, motor vehicle accidents, or physical abuse. Brain injury can occur with translational, rotational or angular movements of the head. Rotational and/or angular forces cause the brain to TWIST against the BRAINSTEM – the thin stalk that connects the brain to the spinal cord, and damage the structures within. Because the brainstem controls many VITAL bodily functions, including consciousness, rotational and angular injuries usually result in LOSS of consciousness and are often more serious.
Concussion is a FUNCTIONAL injury, rather than structural. A concussed brain usually looks NORMAL on a brain-imaging test. The damage occurs at a MICROSCOPIC level and generally affects a LARGE area of the brain. The mechanical impact exerted by the blow sends shock waves that diffuse through the brain tissues, STRETCHING and possibly SHEARING membranes of neurons, especially along the long axons that are responsible for transmitting signals from one neuron to another. The events that take place during and after concussion are complex and not fully understood, but likely to involve IONIC IMbalances and ENERGY CRISIS due to REDUCED blood flow. Ionic disturbances, such as ABnormal potassium EFflux and calcium INflux, INTERFERE with action potential dynamics, DISRUPTING normal communication between neurons. Reduced blood supply IMPAIRS cellular functions and makes the brain MORE vulnerable to further damage.
Children and teens are at GREATER risks for brain injury because their brain is STILL DEVELOPING and therefore more susceptible to insults. Axons in young brains are not FULLY myelinated, EASIER to get damaged and take LONGER to recover. Brain development may also STOP for some time after sustaining a concussion.
Signs and symptoms of concussion can be SUBTLE and may NOT appear immediately. It is common for the first signs to show up after 20 minutes to hours from the time of impact. COMMON symptoms include headache, drowsiness, dizziness, sensitivity to light, loss of memory, difficulty concentrating and feeling slowed down. Patients should be observed for at least 48h for worsening signs such as loss of consciousness, INcreasing headache, REPEATED vomiting, slurred speech, confusion, unusual behaviors, seizures, and limb weakness or numbness. Any of these would require emergency care.
Concussion usually revolves on its own, with PROPER physical and cognitive REST. The majority of people fully recover after a couple of weeks but some may take longer. During recovery the brain is MUCH more vulnerable to further insults and any activities that may potentially cause another impact SHOULD be avoided. A REPEATED injury while the brain is recovering may exacerbate symptoms, result in PERMANENT brain damage, and can be fatal.

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Causes of progressive dementias: Alzheimer’s disease, vascular dementia, Lewy body dementia and frontotemporal dementia. Also includes less common causes and reversible dementias.
Dementia is a general term for a DECLINE in memory and other cognitive abilities. It is NOT a disease on its own but rather a group of symptoms caused by an UNDERLYING condition. Most dementias WORSEN over time and are irreversible, but some types can be reversed with treatment. While the incidence of dementia increases with age, it is NOT a normal part of aging.
The most common cause of dementia, responsible for more than 50% of all cases, is Alzheimer’s disease. In this condition, abnormal toxic deposits of proteins, known as PLAQUES and TANGLES, cause the death of neurons. The damage initially takes place in the hippocampus, the part of the brain that is essential in forming memories. Short-term memory loss is usually one of the earliest symptoms. Most patients show first signs of mental decline after the age of 65, but for a small subset of cases, the disease runs in FAMILIES and strikes EARLIER in life.
Second to Alzheimer’s is VASCULAR dementia, a condition in which POOR blood supply to the brain IMPAIRES normal function of neurons. Symptoms may appear SUDDENLY after a stroke; in a STEP-wise fashion after a series of mini-strokes; or GRADUALLY as a result of age-related vascular wear-and-tear, or any conditions that DAMAGE or NARROW blood vessels over time, such as high blood pressure, high cholesterol, and diabetes. Incidence of vascular dementia increases with age and cardiovascular risk factors.
In the third place is LEWY BODY dementia. Lewy bodies refer to abnormal protein clumps typically found in neurons of these patients. The earliest, and also most PROMINENT feature of this type, is a SLEEP BEHAVIOR disorder in which patients physically, sometimes violently, ACT OUT their dreams. Other early symptoms may include visual hallucinations. Memory loss may NOT be noticeable until LATER stages. Dementia caused by advanced Parkinson’s disease belongs to this group.
FRONTOTEMPORAL dementia is another common type of progressive dementia. This group is characterized by neuronal cell death in the FRONTAL and TEMPORAL lobes of the brain – the areas associated with behaviors and language. Common signs and symptoms include changes in behaviors, apathy, blunting of emotions, and language deficits. A significant portion of this type has a STRONG GENETIC component and tends to occur EARLY, in the MIDDLE-AGE population.
More than one type of the above-mentioned dementias may CO-exist in ONE patient.
Less common causes of dementia include Huntington’s disease, Creutzfeldt-Jakob disease, and traumatic brain injuries.
Dementia may also develop as a result of endocrine or metabolic problems, such as thyroid disorders and vitamin deficiencies; or infections such as Lyme disease and neurosyphilis. For these types, symptoms can be reversed with treatment of the underlying condition.

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Vascular dementia (also known as Vascular Cognitive Impairment) refers to a group of conditions in which IMPAIRED blood supply to the brain causes neuronal DYSfunction, leading to loss of memory and other cognitive abilities. It is the second most common type of dementia, after Alzheimer’s – a neurodegenerative disease.
Vascular dementia may develop following a stroke, or a series of mini-strokes. A stroke can be ischemic or hemorrhagic. An ischemic stroke happens when a blood clot BLOCKS an artery, interrupting blood flow. Blood clots may form locally, on top of cholesterol plaques as these rupture; or, travel to the brain from the heart, in a condition known as atrial fibrillation, where the heart does not pump properly, blood stagnates and coagulates. Hemorrhagic stroke, on the other hand, occurs when an artery leaks or ruptures. This can result from high blood pressures, overuse of blood-thinners/anticoagulant drugs, or abnormal formations of blood vessels such as aneurysms. 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.
Dementia symptoms may appear SUDDENLY following a SINGLE LARGE stroke, or develop in a STEPWISE fashion as a result of multiple, sometimes unnoticeable, small strokes. Symptoms VARY from person to person depending on the part of the brain that is affected, and may include: problems with memory or thinking skills, confusion, mood changes, speech disorders, impaired balance and movement. The way the symptoms appear can be used to differentiate stroke-related dementia from Alzheimer’s disease, which usually develops GRADUALLY, with specific symptoms appearing in a largely typical order.
But vascular dementia may also progress silently in a CONTINUOUS manner, as a result of age-related vascular wear-and-tear, or any conditions that DAMAGE or NARROW blood vessels over time, such as high blood pressure, high cholesterol, diabetes and amyloid deposit. These factors often affect SMALLER blood vessels deep inside the white matter of the brain, causing small blockages and microbleeds that often go unnoticed to the patients. This is known as “cerebral small vessel disease” and is the most common cause of vascular dementia in older adults.
Another cause of vascular dementia is HYPOperfusion of the entire brain. This may result from heart failures, hypotension, or carotid artery occlusion.
There is no cure for vascular dementia but prevention by controlling vascular risk factors, such as high blood pressures, can be effective. Life style changes such as healthy diets, quitting smoking, and physical exercise have been proven to be beneficial. Treatment is by managing the underlying conditions.