Author Archives: Alila Medical Media

Cardiomyopathy, with animation

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Cardiomyopathy is a group of diseases that weaken the heart muscle – the myocardium, making it harder for the heart to pump blood. Cardiomyopathy reduces blood output, and may lead to heart failure. The condition may be inherited from a parent, or develop as a consequence of another disease or factor. Some patients do not experience any symptoms. When present, symptoms may include: shortness of breath, fatigue, rapid heartbeats, chest pain, swelling of lower limbs, dizziness and fainting. Progression of the disease varies greatly from person to person. In some people, symptoms may appear suddenly, and worsen quickly; while others see a gradual development over a long period of time.

There are 3 MAJOR types of cardiomyopathy:

  • Hypertrophic cardiomyopathy, or HCM, is the thickening of the heart muscle. Most commonly, this occurs in the inter-ventricular septum facing the left ventricle. The thickened septum obstructs blood flow to the aorta, a condition called “outflow tract obstruction” or “obstructive hypertrophic cardiomyopathy”.Thickening elsewhere in the heart muscle causes non-obstructive HCM. In both cases, cardiac output is reduced. While HCM can develop as a result of high blood pressure or aging, it is most commonly inherited as an autosomal dominant trait: children of an affected parent have a 50% chance of inheriting the disease. Multiple mutations have been identified in genes encoding for proteins of the heart muscle. Genetic screening is recommended as the disease may progress rapidly, from asymptomatic to heart failure and cardiac arrest. In fact, HCM is the major cause of sudden cardiac death among young a People who test positive for HCM are advised to avoid high-intensity activities.
  • Dilated cardiomyopathy, DCM, is the thinning of the myocardium and enlargement of a heart chamber, most commonly the left ventricle. DCM is usually acquired and the cause is unknown in most cases. Risk factors include high blood pressure; damage to the myocardium caused by previous heart attacks, alcohol or cocaine use, toxins or infections; and obesity or diabetes. While DCM may develop in anyone at any age, it is more common in men of middle age. Some DCM cases are inherited.
  • Restrictive cardiomyopathy, RCM, is when the heart muscle becomes rigid, lacking the elasticity required to properly fill and pump blood. RCM usually results from building-up of scar tissues or abnormal proteins, caused by a variety of conditions. RCM is more likely in older people.

Less common types of cardiomyopathy include: arrhythmogenic right ventricular dysplasia, a condition in which the right ventricle tissue is scarred, causing arrhythmias; and stress cardiomyopathy, or broken heart syndrome: a sudden temporary weakening of the heart muscle triggered by excessive emotional or physical stress.

Treatment varies depending on the type of cardiomyopathy, the underlying cause and severity of symptoms, and can range from life style changes, to medications and surgeries.

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Neuroplasticity, with animation

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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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How Birth Control Pills Work, with Animation

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Birth control pills are medication used to prevent pregnancy. They contain hormones that suppress ovulation. The most effective type is the combination pill which contains both estrogen and progestin – a synthetic form of progesterone. These 2 hormones interfere with the normal menstrual cycle to prevent ovulation.
The menstrual cycle refers to the monthly events that occur within a woman’s body in preparation for the possibility of pregnancy. Each month, an egg is released from an ovary in a process called ovulation. At the same time, the lining of the uterus thickens, ready for pregnancy. If fertilization does not take place, the lining of the uterus is shed in menstrual bleeding and the cycle starts over. The menstrual cycle is under control of multiple hormones secreted by the hypothalamus, pituitary gland, and ovaries. Basically, the hypothalamus produces gonadotropin-releasing hormone, GnRH; the pituitary secretes follicle-stimulating hormone, FSH, and luteinizing hormone, LH; while the ovaries produce estrogen and progesterone. These hormones are involved in a REGULATORY network that results in monthly cyclic changes responsible for ovulation and preparation for pregnancy.
The 2 hormones that are required for ovulation are: FSH, which starts the cycle by stimulating immature follicles to grow and produce a mature egg; and LH, which is responsible for the release of the egg from the ovary – the ovulation event itself. Two other hormones, estrogen and progesterone, are at high levels after ovulation, in the second half of the cycle. They suppress FSH and LH during this time, preventing the ovaries from releasing more eggs. If fertilization occurs, estrogen and progesterone levels REMAIN HIGH throughout pregnancy, providing a continuous suppression of ovulation. On the other hand, in the absence of pregnancy, their levels FALL, causing menstrual bleeding.
The levels of estrogen and progesterone in the combination pills mimic the hormonal state after ovulation, tricking the ovaries into thinking that ovulation has already occurred; FSH and LH are constantly suppressed, no egg is matured or released.
The pills are taken every day for three weeks, followed by one week of placebo pills containing no hormones. During the week of placebos, estrogen and progesterone levels fall, triggering a so-called withdrawal bleeding, or fake periods. The bleeding serves as a convenient indication that fertilization did not happen, but it is not required for birth control. In fact, there exist continuous-use contraceptive pills with less or no placebos, resulting in less or no menstrual periods. These pills are particularly beneficial for women who suffer from menstrual disorders such as excessive menstrual bleeding, painful menstruation and endometriosis.
For lactating women, or those who cannot tolerate estrogen, there are mini-pills that contain only progestin. These are not as effective as combination pills at preventing ovulation. Their effect relies more on the ability of progestin to promote secretion of a thick cervical mucus to obstruct sperm entry.

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Wolff-Parkinson-White Syndrome Pathophysiology, Pre-Excitation and AVRT, with Animation

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Wolff-Parkinson-White, or WPW, syndrome is a congenital heart disease characterized by presence of an ABnormal electrical CONNECTION between the atria and ventricles of the heart. WPW typical symptom is an abnormally FAST heart rate, or TACHYCARDIA.
In normal conduction, electrical signals are initiated in the SA node, and travel throughout the atria before they reach the AV node. The AV node is the GATEWAY to the ventricles. It DELAYS the passage of electrical impulses to the ventricles to ensure that the atria have ejected all the blood into the ventricles before the ventricles contract. This REFRACTORY property of the AV node is essential in LIMITING electrical activities that reach the ventricles. In situations where the ATRIAL rate is EXCESSIVELY high, such as during atrial fibrillation or atrial flutter, the AV node BLOCKS most of the impulses from passing to the ventricles, keeping the heart rate under control.
In WPW, there is an ADDITIONAL connection between the atria and the ventricles, called the ACCESSORY pathway, or bundle of Kent. This pathway is essentially a patch of conductive tissue that provides a SHORTCUT to the ventricles, BYPASSING the AV node. It allows PART of electrical impulses to arrive to the ventricles SOONER, causing a so-called “PRE-excitation”. This can be seen as a SHORTENED PR interval on an ECG. Because part of the ventricles depolarize EARLIER, ventricular depolarization develops in a more GRADUAL fashion and lasts LONGER, resulting in a SLURRING slow rise of the initial portion of the QRS complex, known as DELTA wave, and QRS prolongation.
To note, however, that the presence of an accessory pathway ALONE does NOT cause tachycardia. In fact, most people with a WPW pathway NEVER develop any symptoms. They are said to have a WPW PATTERN, as opposed to WPW SYNDROME in symptomatic patients.
There are 2 mechanisms by which tachycardia can happen in WPW:
– Most commonly, tachycardia develops when electrical impulses travel DOWN one pathway, either the normal or accessory, then BACK UP via the OTHER, creating a SELF-perpetuating LOOP, or a RE-ENTRANT circuit. The frequency of this loop determines heart rate and CAN be very fast, ranging from 150 to 250 beats per minute. This is known as Atrioventricular Re-entry Tachycardia, or AVRT. AVRT can be orthodromic or antidromic depending on the direction of the loop.
– Another scenario is when WPW patients ALSO suffer from Atrial Fibrillation. In this condition, the atria contract at a VERY HIGH rate but most of the electrical impulses do NOT make it through the AV node to the ventricles. This is where a WPW pathway can have a detrimental effect. It provides a BYPASS to let MORE impulses reach the ventricles, causing a FASTER heart rate that could potentially be fatal.
The severity of WPW tachycardia depends on how FAST the accessory pathway is able to conduct. This varies from person to person and can be evaluated in a procedure called Programmed Electrical Stimulation, in which the atria are stimulated to produce progressively HIGHER rates and the atrial-to-ventricular conduction ratio is monitored. Patients are at high risk of developing LETHAL tachycardia if their accessory pathway CONTINUES to conduct at 1-to-1 ratio with dangerously high atrial rates. High-risk patients are usually treated with catheter ablation to destroy the conductive tissue of the accessory pathway.

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Concussion: Pathophysiology, Causes, Signs and Symptoms, Treatment, with Animation

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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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Colon Cancer Pathology, Cause, Screening and Risk Factors, with Animation

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Colon cancer, commonly grouped together with colorectal cancer, is cancer of the large intestine – the final portion of the digestive tract. It is the most common of all gastrointestinal cancers.

Colon cancer usually starts from a small growth called a polyp. Polyps are very common, but most polyps do NOT become cancers. Polyps can be of various types, some of which are more likely to develop into malignant tumors than others.

Early-stage colon cancer generally produces NO symptoms. Advanced-stage symptoms VARY depending on the location of the tumor, and may include: changes in bowel habits that PERSIST for weeks; blood in stool; abdominal pain and discomfort; constant feeling that the bowel doesn’t empty completely; fatigue; and unexplained weight loss.

Early detection is the key to prevent colon cancer. Because a pre-cancerous polyp usually takes YEARS to develop into a malignant tumor, colon cancer can be effectively prevented with regular screening. There are 2 major types of screening tests:

– Stool-based tests: stool samples are examined for signs of cancer, such as blood and mutated DNA. These tests are NON-invasive but LESS effective and need to be done more often.

– Visual screening, such as colonoscopy, is more reliable and can be done every 5 or 10 years. Colonoscopy uses a long, flexible tube equipped with a camera and light, to view the entire colon. If polyps or abnormal structures are found, surgical tools are passed through the tube to remove polyps or take tissue samples for analysis. Typically, any polyps found in the colon are removed during colonoscopy and examined for pre-cancerous changes, known as dysplasia. If high-grade dysplasia is detected, a follow-up colonoscopy is required to monitor the condition.

Colorectal cancers are caused by mutations that increase the rate of cellular division. Some of these mutations can be INHERITED from parents. Examples of inherited colorectal cancers include:

– Familial adenomatous polyposis, or FAP: a condition caused by mutations in the APC gene. The APC protein acts as a tumor suppressor, keeping cells from growing and dividing too fast. Mutations in APC result in uncontrolled cell division, causing HUNDREDS of polyps to grow in the colon. FAP patients usually develop colon cancer by the age of 40.

– Lynch syndrome: another inherited condition caused by changes in genes that normally help repair DNA damages. A faulty DNA repair results in increased rate of mutations. Patients are at high risks of colorectal cancer as well as other types of cancers.

In most cases, however, the mutations that lead to cancer are ACQUIRED during a person’s life rather than being inherited. The early event is usually a mutation in the same APC gene that is responsible for FAP. While FAP is a rare condition, APC mutations are very common in sporadic colorectal cancers.

Apart from genetic predisposition, other risks factors for colon cancer include: aging, high-red meat and low-fiber diets, obesity, alcohol use, smoking, diabetes, and inflammatory intestinal conditions, such as ulcerative colitis and Crohn’s disease.

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High Cholesterol and Familial Hypercholesterolemia, with Animation

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Cholesterol is an essential component of all animal cells, but TOO MUCH cholesterol IN THE BLOOD is a high-risk factor for cardiovascular diseases such as heart attacks and strokes.
Cholesterol levels are measured in a blood test known as lipid panel or lipid profile. This test typically reports: total cholesterol; LOW-density lipoprotein, LDL, also known as “bad” cholesterol; HIGH-density lipoprotein, HDL, or “good” cholesterol; and triglycerides. A desirable profile includes LESS than 200mg/dL of TOTAL cholesterol, with LESS than 100mg/dL of LDL and MORE than 40mg/dL of HDL.
The body obtains cholesterol in 2 ways: from foods of animal origin, and its own endogenous production. Usually, cholesterol levels are kept in check by a negative feedback control. LOW levels of INTRACELLULAR cholesterol INDUCE its own production, while HIGH cholesterol levels INHIBIT it.
It is noteworthy, however, that this regulation applies to the concentration of cholesterol INSIDE the CELLS, NOT in the BLOOD. The HIGH prevalence of HIGH BLOOD cholesterol worldwide suggests that this control mechanism is NOT sufficient to maintain healthy cholesterol levels when challenged by a number of factors, including poor diet, lack of exercise, smoking, obesity, diabetes, and aging.
In addition, some people have an INHERITED condition called “familial hypercholesterolemia”, FH, that causes very HIGH levels of LDL, the “bad“ cholesterol, at a young age. Left untreated, patients are likely to have heart attacks in their 40s or 50s. LDL is basically a vehicle that transports cholesterol from the liver to peripheral cells so it can be used in the cell membrane. Peripheral cells TAKE UP LDL by endocytosis, using their LDL receptor, which binds to a protein ligand on LDL surface. Most cases of FH are caused by a MUTATION in the LDL receptor gene. A defective LDL receptor REDUCES LDL uptake, leaving MORE LDL in the circulation while the cells are DEFICIENT in cholesterol. LOW INTRAcellular cholesterol levels induce FURTHER production of endogenous cholesterol in the liver, eventually causing even HIGHER levels of circulating LDL. One copy of the mutated gene is enough to cause high cholesterol. The condition is therefore inherited in an autosomal DOMINANT manner. A parent with an altered gene has a 50% chance of passing it to a child. If both parents have FH, each child has a 50% chance of having FH, a 25% chance of NOT having FH, and a 25% chance of having TWO copies of the mutated gene, called HOMOZYGOUS FH. Without treatment, homozygous FH patients may have heart attacks in their 20s and may not survive past the age of 30.
Treatments for high cholesterol must start with life style changes such as healthy diets and physical exercise. On top of that, some people may require medications to lower cholesterol. These drugs INHIBIT cholesterol production, intestinal absorption, or reabsorption in the form of bile. Homozygous FH patients usually require more DRASTIC treatment measures which include a procedure called LDL APHERESIS. In this procedure, the blood is diverted through a FILTRATION device where LDL is REMOVED before the remaining plasma and blood cells are returned to the body. The procedure is repeated weekly or biweekly.

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Cervical Cancer, HPV and Pap Smear, with Animation

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Cervical cancer is cancer of the cervix, the lower part of the uterus that opens into the birth canal. It is one of the most common types of cancer in women worldwide, but also one of the most preventable, thanks to early detection with Pap tests.

The cervix has 2 major cell types: flat squamous cells lining the outer part, and column-shaped glandular cells covering the inside of the cervical canal. Both types can become cancerous but squamous cell carcinomas are MUCH more common. Cancer usually starts in the zone where the two cell types meet, known as the transformation zone.

Virtually all cervical cancers are caused by human papillomaviruses, or HPVs. There are over a hundred different types of HPV, some of which pose HIGHER risks than others.  About 70% of all cases are caused by just TWO types: HPV-16 and HPV-18. Two proteins produced by HPV, known as E6 and E7, INTERFERE with cell functions that normally PREVENT EXCESSIVE cell division. This causes the cells to grow in an UNcontrolled manner.

HPV is sexually transmitted and is VERY common, but in most women, HPV infections resolve on their own and do NOT cause cancers. Factors that may INcrease the risk of PERSISTENT HPV infections include WEAKENED immune system, other sexually transmitted diseases and smoking. Chances of developing cervical cancer also increase with having many children and LONG-term use of birth control pills.

Early-stage cervical cancer generally produces NO symptoms. Advanced-stage disease may cause ABnormal or IRregular vaginal bleeding, pelvic pain, or unusual vaginal discharge.

EARLY detection is the key to prevent cervical cancer. Cervical cancer screening may include pap tests ALONE, or in combination with HPV DNA tests.  In a pap test, cells are scraped from the cervix and examined for PRE-cancerous changes, known as cervical intraepithelial neoplasia, or cervical DYSPLASIA. These morphological changes can range from mild to severe. If the results are ABnormal, the test is repeated again after 6 months or a year to MONITOR the condition. Additional diagnostic tests may also be performed. In most cases, MILD dysplasia resolves on its own and a follow-up pap test is all that is required to confirm. In a small number of cases, these ABnormal cells may develop into cancer, but they usually take YEARS to do so, which allows plenty of time for treatment when detected early. In the US, a pap test is recommended every 3 years, from the age of 21, or every 5 years if combined with an HPV test.

Treatment options for cervical cancer include surgery, radiation, chemotherapy or a combination of these. Early-stage cervical cancer is typically treated with surgical removal of the uterus. This option is the most effective in preventing cancer from coming back and is usually preferred when patients do NOT need to maintain fertility.

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Psoriasis, Types, Symptoms, Causes, Pathology, Complication and Treatment, with Animation

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Psoriasis is a very common inflammatory skin condition affecting about 3% of the world population. It is a CHRONIC disease that evolves in the form of RECURRENT inflammatory flare-ups followed by periods of partial or complete remission. Psoriasis can begin at any age but often develops in young adulthood. The disease may LOOK contagious, but it is NOT.
The most common type, known as PLAQUE psoriasis, is characterized by the presence of red, raised, itchy and SCALY patches of skin. The plaques usually appear on the scalp, in front of the knees and behind the elbows.
Less common types include:
– Guttate psoriasis: lesions occur in the form of SMALL numerous spots over a large area of the body. This type primarily affects children and young adults.
– Inverse psoriasis: SMOOTH patches of inflamed skin that worsen with friction and sweating. These are usually found in between skin FOLDS.
– Pustular psoriasis: an uncommon form with pus-filled, NON-infectious blisters.
– Erythrodermic: a rare but SEVERE, potentially life-threatening form, with WIDEspread lesions all over the body.
Psoriasis has a strong GENETIC component, with multiple genes linked to the SUSCEPTIBILITY to the disease. Most of the identified genes are involved in the immune system, notably inflammatory pathways. In some families, psoriasis is an autosomal DOMINANT trait. Flare-ups can be trigged by a variety of factors, including infections, traumatic injuries, stress, smoking, alcohol use and certain medications. The FIRST lesion usually appears after an upper respiratory tract infection. The exact mechanism is not fully understood but likely to involve an OVERreaction of the body’s inflammatory response. Inflammation DILATES blood vessels, releasing chemicals, resulting in redness and itchiness. Large numbers of activated T-cells infiltrate the epidermis and INDUCE proliferation of skin cells. The cells divide and move up QUICKLY, in the matter of DAYS instead of weeks. This causes cells to build up rapidly on the surface of the skin and form SCALY patches.
Common complications include eye diseases, known as OCULAR psoriasis; and chronic joint inflammation in the fingers and toes, known as psoriatic arthritis. Psoriasis also associates with higher risks of cardiovascular diseases, obesity, diabetes, low self-esteem and depression.
Most people with MILD to moderate psoriasis can be treated effectively with TOPICAL agents. These creams and ointments have several effects: anti-inflammatory, slowing down skin cell growth, and reducing scaling and itching.
Severe psoriasis may benefit from additional treatment such as phototherapy – the use of natural or artificial UV light to SLOW skin cell proliferation and REDUCE inflammation. The exposure time should be controlled to avoid UNwanted skin damage and cancers.
SYSTEMIC treatment is considered when other methods fail. This type of treatment involves ORAL administration or INJECTION of drugs that REDUCE cell growth or SUPPRESS the immune system.

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Dementia, with animation

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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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