Neuroscience is the scientific study of the nervous system.[1] Traditionally, neuroscience has been seen as a branch of biology. However, it is currently an interdisciplinary science that collaborates with other fields such as chemistry, cognitive science, computer science, engineering, linguistics, mathematics, medicine (including neurology), genetics, and allied disciplines including philosophy, physics, and psychology. It also exerts influence on other fields, such as neuroeducation,[2]neuroethics, and neurolaw. The term neurobiology is usually used interchangeably with the term neuroscience, although the former refers specifically to the biology of the nervous system, whereas the latter refers to the entire science of the nervous system.

The scope of neuroscience has broadened to include different approaches used to study the molecular, cellular, developmental, structural, functional, evolutionary, computational, and medical aspects of the nervous system. The techniques used by neuroscientists have also expanded enormously, from molecular and cellular studies of individual nerve cells to imaging of sensory and motor tasks in the brain. Recent theoretical advances in neuroscience have also been aided by the study of neural networks.

As a result of the increasing number of scientists who study the nervous system, several prominent neuroscience organizations have been formed to provide a forum to all neuroscientists and educators. For example, the International Brain Research Organization was founded in 1960,[3] the International Society for Neurochemistry in 1963,[4] the European Brain and Behaviour Society in 1968,[5] and the Society for Neuroscience in 1969.[6]

The study of the nervous system dates back to ancient Egypt. Evidence of trepanation, the surgical practice of either drilling or scraping a hole into the skull with the purpose of curing headaches or mental disorders or relieving cranial pressure, being performed on patients dates back to Neolithic times and has been found in various cultures throughout the world. Manuscripts dating back to 1700BC indicated that the Egyptians had some knowledge about symptoms of brain damage.[7]

Early views on the function of the brain regarded it to be a "cranial stuffing" of sorts. In Egypt, from the late Middle Kingdom onwards, the brain was regularly removed in preparation for mummification. It was believed at the time that the heart was the seat of intelligence. According to Herodotus, the first step of mummification was to "take a crooked piece of iron, and with it draw out the brain through the nostrils, thus getting rid of a portion, while the skull is cleared of the rest by rinsing with drugs."[8]

The view that the heart was the source of consciousness was not challenged until the time of the Greek physician Hippocrates. He believed that the brain was not only involved with sensationsince most specialized organs (e.g.,eyes, ears, tongue) are located in the head near the brainbut was also the seat of intelligence. Plato also speculated that the brain was the seat of the rational part of the soul.[9]Aristotle, however, believed the heart was the center of intelligence and that the brain regulated the amount of heat from the heart.[10] This view was generally accepted until the Roman physician Galen, a follower of Hippocrates and physician to Roman gladiators, observed that his patients lost their mental faculties when they had sustained damage to their brains.

Abulcasis, Averroes, Avenzoar, and Maimonides, active in the Medieval Muslim world, described a number of medical problems related to the brain. In Renaissance Europe, Vesalius (15141564), Ren Descartes (15961650), and Thomas Willis (16211675) also made several contributions to neuroscience.

Studies of the brain became more sophisticated after the invention of the microscope and the development of a staining procedure by Camillo Golgi during the late 1890s. The procedure used a silver chromate salt to reveal the intricate structures of individual neurons. His technique was used by Santiago Ramn y Cajal and led to the formation of the neuron doctrine, the hypothesis that the functional unit of the brain is the neuron.[11] Golgi and Ramn y Cajal shared the Nobel Prize in Physiology or Medicine in 1906 for their extensive observations, descriptions, and categorizations of neurons throughout the brain. While Luigi Galvani's pioneering work in the late 1700s had set the stage for studying the electrical excitability of muscles and neurons, it was in the late 19th century that Emil du Bois-Reymond, Johannes Peter Mller, and Hermann von Helmholtz demonstrated that the electrical excitation of neurons predictably affected the electrical states of adjacent neurons,[citation needed] and Richard Caton found electrical phenomena in the cerebral hemispheres of rabbits and monkeys.

In parallel with this research, work with brain-damaged patients by Paul Broca suggested that certain regions of the brain were responsible for certain functions. At the time, Broca's findings were seen as a confirmation of Franz Joseph Gall's theory that language was localized and that certain psychological functions were localized in specific areas of the cerebral cortex.[12][13] The localization of function hypothesis was supported by observations of epileptic patients conducted by John Hughlings Jackson, who correctly inferred the organization of the motor cortex by watching the progression of seizures through the body. Carl Wernicke further developed the theory of the specialization of specific brain structures in language comprehension and production. Modern research through neuroimaging techniques, still uses the Brodmann cerebral cytoarchitectonic map (referring to study of cell structure) anatomical definitions from this era in continuing to show that distinct areas of the cortex are activated in the execution of specific tasks.[14]

During the 20th century, neuroscience began to be recognized as a distinct academic discipline in its own right, rather than as studies of the nervous system within other disciplines. Eric Kandel and collaborators have cited David Rioch, Francis O. Schmitt, and Stephen Kuffler as having played critical roles in establishing the field.[15] Rioch originated the integration of basic anatomical and physiological research with clinical psychiatry at the Walter Reed Army Institute of Research, starting in the 1950s. During the same period, Schmitt established a neuroscience research program within the Biology Department at the Massachusetts Institute of Technology, bringing together biology, chemistry, physics, and mathematics. Kuffler started the Department of Neuroscience at Harvard Medical School in 1966, the first such freestanding department.

In 1952, Alan Lloyd Hodgkin and Andrew Huxley presented a mathematical model for transmission of electrical signals in neurons of the giant axon of a squid, action potentials, and how they are initiated and propagated, known as the HodgkinHuxley model. In 19612, Richard FitzHugh and J. Nagumo simplified HodgkinHuxley, in what is called the FitzHughNagumo model. In 1962, Bernard Katz modeled neurotransmission across the space between neurons known as synapses. Beginning in 1966, Eric Kandel and collaborators examined biochemical changes in neurons associated with learning and memory storage in Aplysia. In 1981 Catherine Morris and Harold Lecar combined these models in the MorrisLecar model.

The scientific study of the nervous system has increased significantly during the second half of the twentieth century, principally due to advances in molecular biology, electrophysiology, and computational neuroscience. This has allowed neuroscientists to study the nervous system in all its aspects: how it is structured, how it works, how it develops, how it malfunctions, and how it can be changed. For example, it has become possible to understand, in much detail, the complex processes occurring within a single neuron. Neurons are cells specialized for communication. They are able to communicate with neurons and other cell types through specialized junctions called synapses, at which electrical or electrochemical signals can be transmitted from one cell to another. Many neurons extrude long thin filaments of protoplasm called axons, which may extend to distant parts of the body and are capable of rapidly carrying electrical signals, influencing the activity of other neurons, muscles, or glands at their termination points. A nervous system emerges from the assemblage of neurons that are connected to each other.

In vertebrates, the nervous system can be split into two parts, the central nervous system (brain and spinal cord), and the peripheral nervous system. In many species including all vertebrates the nervous system is the most complex organ system in the body, with most of the complexity residing in the brain. The human brain alone contains around one hundred billion neurons and one hundred trillion synapses; it consists of thousands of distinguishable substructures, connected to each other in synaptic networks whose intricacies have only begun to be unraveled. The majority of the approximately 2025,000 genes belonging to the human genome are expressed specifically in the brain. Due to the plasticity of the human brain, the structure of its synapses and their resulting functions change throughout life.[16] Thus the challenge of making sense of all this complexity is formidable.

The study of the nervous system can be done at multiple levels, ranging from the molecular and cellular levels to the systems and cognitive levels. At the molecular level, the basic questions addressed in molecular neuroscience include the mechanisms by which neurons express and respond to molecular signals and how axons form complex connectivity patterns. At this level, tools from molecular biology and genetics are used to understand how neurons develop and how genetic changes affect biological functions. The morphology, molecular identity, and physiological characteristics of neurons and how they relate to different types of behavior are also of considerable interest.

The fundamental questions addressed in cellular neuroscience include the mechanisms of how neurons process signals physiologically and electrochemically. These questions include how signals are processed by neurites thin extensions from a neuronal cell body, consisting of dendrites (specialized to receive synaptic inputs from other neurons) and axons (specialized to conduct nerve impulses called action potentials) and somas (the cell bodies of the neurons containing the nucleus), and how neurotransmitters and electrical signals are used to process information in a neuron. Another major area of neuroscience is directed at investigations of the development of the nervous system. These questions include the patterning and regionalization of the nervous system, neural stem cells, differentiation of neurons and glia, neuronal migration, axonal and dendritic development, trophic interactions, and synapse formation.

At the systems level, the questions addressed in systems neuroscience include how neural circuits are formed and used anatomically and physiologically to produce functions such as reflexes, multisensory integration, motor coordination, circadian rhythms, emotional responses, learning, and memory. In other words, they address how these neural circuits function and the mechanisms through which behaviors are generated. For example, systems level analysis addresses questions concerning specific sensory and motor modalities: how does vision work? How do songbirds learn new songs and bats localize with ultrasound? How does the somatosensory system process tactile information? The related fields of neuroethology and neuropsychology address the question of how neural substrates underlie specific animal and human behaviors. Neuroendocrinology and psychoneuroimmunology examine interactions between the nervous system and the endocrine and immune systems, respectively. Despite many advancements, the way networks of neurons produce complex cognitions and behaviors is still poorly understood.

At the cognitive level, cognitive neuroscience addresses the questions of how psychological functions are produced by neural circuitry. The emergence of powerful new measurement techniques such as neuroimaging (e.g., fMRI, PET, SPECT), electrophysiology, and human genetic analysis combined with sophisticated experimental techniques from cognitive psychology allows neuroscientists and psychologists to address abstract questions such as how human cognition and emotion are mapped to specific neural substrates.

Neuroscience is also allied with the social and behavioral sciences as well as nascent interdisciplinary fields such as neuroeconomics, decision theory, and social neuroscience to address complex questions about interactions of the brain with its environment.

Ultimately neuroscientists would like to understand every aspect of the nervous system, including how it works, how it develops, how it malfunctions, and how it can be altered or repaired. The specific topics that form the main foci of research change over time, driven by an ever-expanding base of knowledge and the availability of increasingly sophisticated technical methods. Over the long term, improvements in technology have been the primary drivers of progress. Developments in electron microscopy, computers, electronics, functional brain imaging, and most recently genetics and genomics, have all been major drivers of progress.

Most studies in neurology have too few test subjects to be scientifically sure. Those insufficient size studies are the basis for all domain-specific diagnoses in neuropsychiatry, since the few large enough studies there are always find individuals with the brain changes thought to be associated with a mental condition but without any of the symptoms. The only diagnoses that can be validated through large enough brain studies are those on serious brain damages and neurodegenerative diseases that destroy most of the brain.[17][18]

Neurology, psychiatry, neurosurgery, psychosurgery, anesthesiology and pain medicine, neuropathology, neuroradiology, ophthalmology, otolaryngology, clinical neurophysiology, addiction medicine, and sleep medicine are some medical specialties that specifically address the diseases of the nervous system. These terms also refer to clinical disciplines involving diagnosis and treatment of these diseases. Neurology works with diseases of the central and peripheral nervous systems, such as amyotrophic lateral sclerosis (ALS) and stroke, and their medical treatment. Psychiatry focuses on affective, behavioral, cognitive, and perceptual disorders. Anesthesiology focuses on perception of pain, and pharmacologic alteration of consciousness. Neuropathology focuses upon the classification and underlying pathogenic mechanisms of central and peripheral nervous system and muscle diseases, with an emphasis on morphologic, microscopic, and chemically observable alterations. Neurosurgery and psychosurgery work primarily with surgical treatment of diseases of the central and peripheral nervous systems. The boundaries between these specialties have been blurring recently as they are all influenced by basic research in neuroscience. Brain imaging also enables objective, biological insights into mental illness, which can lead to faster diagnosis, more accurate prognosis, and help assess patient progress over time.[19]

Integrative neuroscience makes connections across these specialized areas of focus.

Modern neuroscience education and research activities can be very roughly categorized into the following major branches, based on the subject and scale of the system in examination as well as distinct experimental or curricular approaches. Individual neuroscientists, however, often work on questions that span several distinct subfields.

The largest professional neuroscience organization is the Society for Neuroscience (SFN), which is based in the United States but includes many members from other countries. Since its founding in 1969 the SFN has grown steadily: as of 2010 it recorded 40,290 members from 83 different countries.[22] Annual meetings, held each year in a different American city, draw attendance from researchers, postdoctoral fellows, graduate students, and undergraduates, as well as educational institutions, funding agencies, publishers, and hundreds of businesses that supply products used in research.

Other major organizations devoted to neuroscience include the International Brain Research Organization (IBRO), which holds its meetings in a country from a different part of the world each year, and the Federation of European Neuroscience Societies (FENS), which holds a meeting in a different European city every two years. FENS comprises a set of 32 national-level organizations, including the British Neuroscience Association, the German Neuroscience Society (Neurowissenschaftliche Gesellschaft), and the French Socit des Neurosciences. The first National Honor Society in Neuroscience, Nu Rho Psi, was founded in 2006.

In 2013, the BRAIN Initiative was announced in the US.

In addition to conducting traditional research in laboratory settings, neuroscientists have also been involved in the promotion of awareness and knowledge about the nervous system among the general public and government officials. Such promotions have been done by both individual neuroscientists and large organizations. For example, individual neuroscientists have promoted neuroscience education among young students by organizing the International Brain Bee, which is an academic competition for high school or secondary school students worldwide.[23] In the United States, large organizations such as the Society for Neuroscience have promoted neuroscience education by developing a primer called Brain Facts,[24] collaborating with public school teachers to develop Neuroscience Core Concepts for K-12 teachers and students,[25] and cosponsoring a campaign with the Dana Foundation called Brain Awareness Week to increase public awareness about the progress and benefits of brain research.[26] In Canada, the CIHR Canadian National Brain Bee is held annually at McMaster University.[27]

Finally, neuroscientists have also collaborated with other education experts to study and refine educational techniques to optimize learning among students, an emerging field called educational neuroscience.[28] Federal agencies in the United States, such as the National Institute of Health (NIH)[29] and National Science Foundation (NSF),[30] have also funded research that pertains to best practices in teaching and learning of neuroscience concepts.

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Neuroscience - Wikipedia, the free encyclopedia

Neurology - Anatomy and physiology - Dincephalon and Ventricular System
These videos are designed for medical students studying for the USMLE step 1 . I took step 1 when i was in 5th grade , my step 1 score : 241 , i did these videos while i was in 6th grade ,...

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Brian Belnap, D.O. Andrew Michael Blumenfeld, M.D. Thomas Chippendale, M.D Emeritus Bilal Choudry, M.D. Benjamin Frishberg, M.D. Michael Lobatz, M.D. Amy Nielsen, D.O. Irene Oh, M.D. Remia Paduga, M.D. Jay Rosen, Ph.D Jay Rosenberg, M.D Mark Sadoff, M.D. Gregory Sahagian, M.D. Jack Schim, M.D. Lesly Giselle Aguilar Tabora, M.D. Anchi Wang, M.D. Chunyang Tracy Wang, M.D., M.S. Michael Zupancic, M.D. Peter Heinen, P.A. Kathleen Hermanson, P.A. Stephanie Huang, P.A. Andrew Inocelda, P.A. Alicia Son, P.A. Megan Strowd, P.A. Melissa Mortin, N.P. Phyllis Taylor, N.P Brian Belnap, D.O.

Dr Belnap is accepting new patients. Please call 760-631-3000.

Dr. Belnap is a double board certified specialist in the fields of Pain Management and Rehabilitation Medicine. He completed his undergraduate training at Brigham Young University in Provo, UT and medical school at Midwestern University in Glendale, AZ. He then completed his residency in Physical Medicine and Rehabilitation at Walter Reed Army Medical Center in Washington DC followed by a fellowship in Pain Management at UC Davis Medical Center in Sacramento, California. He served as Chief Resident towards the end of his residency and upon completion of the program was selected as Chief of the Inpatient Rehabilitation Service at Walter Reed Army Medical Center. He was then chosen by the Surgeon General of the Army to relocate west with the task to help establish a highly specialized combat casualty rehabilitation center at Naval Medical Center San Diego. He became the first Medical Director of this center and upon separation from the military was awarded the Meritorious Service Medal which is equivalent to the Bronze Star for combat service.

Dr. Belnap has expertise in providing treatment for a wide array of conditions including sports injuries, spine & joint disorders, complex polytraumatic injuries, amputations and neurologic disorders. He has been a contributing author in peer reviewed journal articles and medical textbook chapters in his specialty. He has also given numerous presentations at national and local conferences throughout his career. He is a native of Southern California and enjoys basketball, volleyball, surfing, volunteering in his church & community and spending time with his wife and four children.

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Dr. Blumenfeld is accepting new patients. Please call 760-631-3000.

Dr. Blumenfeld is director of the Headache Center of Southern California. As director, he has encouraged the development of a center addressing the multi-faceted needs of headache sufferers. These needs include acute care, educational programs and other specialty services. This comprehensive approach treats the whole person in a highly individualized manner and addresses the growing demand for one-stop treatment services.

Dr. Blumenfeld grew up in South Africa and graduated from St. Andrews College, South Africa, with a first class pass and distinction in mathematics. He attended the University of the Witwatersrand, Johannesburg, South Africa Medical School and completed a neurology residency at Johannesburg Hospital. In 1986 he moved to the United States and completed a neurology residency at the University of Massachusetts Medical School. Following this, he completed an EEG and EMG fellowship, also at University of Massachusetts Medical School.

He served as staff neurologist at Kaiser Permanente, San Diego from 1990 to 2004. As Chief of Neurology Service at Kaiser from 1999-2004, his unit was named a Neurotoxin Center of Excellence by Thomas Jefferson University and Jefferson Medical College. The Neurotoxin Centers of Excellence recognize excellence in neurologists and other physicians who specialize in headache management.

Dr Blumenfeld is a member of the American Academy of Neurology and the American Headache Society. He has published widely and has been an active researcher in headaches.

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HI Ianna- some sources report that TOO MUCH calcium taken at the same TIME- can interfere w/ magnesium absorption. They compete for absorption and calcium usually wins. Slow- mag the kind i take, does have a LITTLE calcium in it-- but not enough to interfere and enough ratio to help them work together. it is recommended to take calcium and magnesium at different times if you are to take more calcium in a day. I take my calcium supplement at a different time. for people with a deficiency, definately need to take their magnesium separately or in a combo ratio like Slow-mag. below is some literature from the web on the subject (different views on the absorption issue): (remember, regular blood serum tests will be innacurate- it does not show a deficiency or low "intracellular" amounts)

Magnesium

Type

Mineral

Source

Wheat germ, wheat bran, brewer's yeast, nuts whole grains, brown rice, green leafy vegetables, honey, fish, fruits, figs, almonds, beans, pistachio nuts, sunflower seeds.

Dosage

300-1600mg daily.

Discussion

Magnesium is needed for healthy nerve and muscle tissue. It is responsible for more biochemical reactions in the body than any other mineral. It acts with calcium and phosphorus to ensure proper metabolism and with potassium to modify sodium levels. Magnesium is needed by every cell for synthesis of protein, utilization of fats and carbohydrates, and production of energy. It is used with B6 in many enzyme systems and to produce energy. * Magnesium is lost with excess sugar and caffeine intake. * Alcohol and sodium deplete magnesium. * Too much calcium blocks magnesium absorption/utilization. * Saturated fat blocks magnesium absorption and utilization. * Magnesium consumption decreases as we age. * 1 soda drink contains about 30mg of phosphate. Every mg of phosphate eliminates 1mg of magnesium from your body. Magnesium glycinate is magnesium chelated with glycine, which is a great carrier for magnesium. Its low molecular weight gives higher absorption and it does not require stomach acid to be absorbed. A magnesium deficiency is associated with low levels of calcium and potassium. Excessive amounts of magnesium can prevent calcium from being absorbed so some doctors recommend taking calcium and magnesium at different times. Other sources say that calcium and magnesium are absorbed differently and do not interfere with each other. Magnesium and B6 work together. B6 assures proper magnesium in red blood cells and magnesium activates dozens of B6 enzymes. You cannot metabolize C, D, phosphorus, sodium, and potassium without sufficient magnesium.

Deficiency Symptoms

It is thought that 20-80% of the population of the United States is deficient in magnesium. It is implicated in ischemic heart disease, angina, cardiac arrhythmia, hypertension, osteoporosis, diabetes, stroke, vascular-spasm and diabetes-caused vision problems. Magnesium is used with B6 in many enzyme systems and to produce energy. Many B6 deficiency symptoms are the same as magnesium - convulsions, tremors, kidney stones, and insomnia. Magnesium Deficiency Symptoms: * Tremors, muscle twitches and cramps, muscle weakness and pain * Palpitations, breathlessness * Insomnia, sensitivity to loud noises * Migraine or tension headaches * Nervousness, irritability * Mental and physical fatigue * Fearfulness, confusion, disorientation, poor concentration * Psychiatric disturbances, depression, schizophrenia, autism * Glandular disturbances * Poor circulation, constriction of blood vessels, high blood pressure, high LDL * Calcium deposits * Heart disease, chest pain * Poor complexion * Menopause-associated insomnia, infertility, premature birth * Abdominal pain, constipation * Feeling like your skin is crawling

Caution

* Magnesium should be used cautiously by patients with an impaired kidney function. * Taking over 3000mg may have laxative effect. * Taking over 5000mg may cause nausea, calcium/phosphorus imbalance. * If you get muscle cramps that you didn't have before taking magnesium, you may need less magnesium or more calcium. * The correct ratio of calcium to magnesium must be maintained. Generally, it is 2 times as much calcium as magnesium. For example, take 200mg calcium with 100mg magnesium. Women need a higher magnesium percentage, often equal to that of calcium. For example 200mg calcium/200mg of magnesium.

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Muscle Twitches All OVER - Neurology - MedHelp

Meet Dr. Leon Epstein, Head of the Division of Neurology at Lurie Children #39;s
Dr. Leon Epstein is the head of the Division of Neurology at Ann Robert H. Lurie Children #39;s Hospital of Chicago. The division is ranked #4 in the nation by US News World Report. His special...

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April Fools Day at Florida Child Neurology
April 1 was a fun day at Florida Child Neurology. Several employees stayed late the night before and set up all kinds of fun pranks and practical jokes for their coworkers. From changing their...

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Neurology (Original Mix)
Neurology Original Mix Innovix Copyright Control Released on: 2011-03-21 Unknown: Martin Modestov Auto-generated by YouTube.

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Prof Andrea E. Cavanna Consultant in Behavioural Neurology
Prof Andrea E. Cavanna Consultant in Behavioural Neurology The Brain and Behaviour Conference Thursday 12th March 2015 Stoke on Trent Moat House, UK.

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Clinical neurology for final 2

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Clinical neurology for final 1

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What is Functional Neurology?
Neural FX.

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Download Stroke Recovery with Cellular Therapies Current Clinical Neurology PDF
Download Link : http://bit.ly/1GTTsXG Login to the website and feel free to download the PDF. Please register first if you don #39;t have an account.

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Neurology - Anatomy and physiology - Cerebellum and Basal Ganglia
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First Coast Neurology - Orange Park
First Coast Neurology is located in Orange Park, FL. For more information, please visit http://www.firstcoastneurology.com.

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Vlog Doctors (Neurology) Office Part 1
I #39;m at the Pain Doctor and I wanted to share.

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Neurology 101
A quick, simplified explanation of what actually happens in your brain to perform any sort of voluntary movement.

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Neurologist in Phoenix

At Foothills Neurology, we understand that seeing a neurologist in Phoenix, or any type of specialist,can make some people feel anxious. Our staff and providers are dedicated to putting you at ease throughout the entire process. From scheduling the visit to understanding your diagnosis and treatment, Foothills Neurology practices compassionate, open communication. That open communications includesyour primary care physician and any other providers who are coordinating your care, all the while keeping you firmly in the center of the loop.

WithFoothills Neurology, your story matters. We start by listening to you. Taking in all the relevant medical history as well as your personal input, we begin the diagnosis process. Each highly experienced neurologists and provider stays current on the developments and changes in our field of neurology. You will find our diagnostics are among the most advanced available. Finding the source of aconcern and treating our patients with the best care possible is what we do. That is why each neurologist at Foothills Neurology isat the top of the listoftrusted neurologists in Phoenix.

Accurate treatment begins with strong diagnostic tools. Theneurologists in Phoenix at Foothills Neurology has both the diagnostics and the specialized treatment necessary to provideexcellent neurology care.

The Foothills Neurology staff consists of a full range of dedicated providers ready to assist your neurological care. Our top neurologist and neurology care providers work as a team to offer patients some of the most comprehensive carein the Phoenix area. As experts in neurological disorders, we treat each individual with the compassion and excellent care we would offer our own family. We take time to get to know you as a person, not just a diagnosis.

We understandthe anxiety of having a neurological condition can, at times, feel worsethan the condition itself. That is why our dedicated team is hear to support you. We take as much time as you need to discuss your condition as well as understand the possibilities and the treatment plan. We are happy to answer your questions and ease your fears by replacing them with genuine support and understanding.

Our commitment is toenhance yourquality of life. Our patients are in good hands with ourstrong team of specialists, neurologists and other providers devoted to your health.

Schedule an appointment with a Phoenix neurologist at our conveniently located office off the I-10 Maricopa Freeway and East Chandler Boulevard.

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Neurologist Phoenix | Foothills Neurology

Aphasia is a combination of a speech and language disorder caused by damage to the brain that affects about one million individuals within the US.[1][2][3] Most often caused by a cerebral vascular accident (CVA), which is also known as a stroke, aphasia can cause impairments in speech and language modalities. To be diagnosed with aphasia, a person's speech or language must be significantly impaired in one (or several) of the four communication modalities following acquired brain injury or have significant decline over a short time period (progressive aphasia). The four communication modalities are auditory comprehension, verbal expression, reading and writing, and functional communication.

The difficulties of people with aphasia can range from occasional trouble finding words to losing the ability to speak, read, or write; intelligence, however, is unaffected.[1] Aphasia also affects visual language such as sign language.[2] In contrast, the use of formulaic expressions in everyday communication is often preserved.[4] One prevalent deficit in the aphasias is anomia, which is a deficit in word finding ability.[5]

The term "aphasia" implies that one or more communication modalities have been damaged and are therefore functioning incorrectly. Aphasia does not refer to damage to the brain that results in motor or sensory deficits, as it is not related to speech (which is the verbal aspect of communicating) but rather the individuals language. An individual's "language" is the socially shared set of rules as well as the thought processes that go behind verbalized speech. It is not a result of a more peripheral motor or sensory difficulty, such as paralysis affecting the speech muscles or a general hearing impairment.

Aphasia is from Greek a- ("without") + phsis (, "speech"). The word aphasia comes from the word aphasia, in Ancient Greek, which means[6] "speechlessness",[7] derived from aphatos, "speechless"[8] from - a-, "not, un" and phemi, "I speak".

Aphasia is most often caused by stroke, but any disease or damage to the parts of the brain that control language can cause aphasia. Some of these can include brain tumors, traumatic brain injury, and progressive neurological disorders.[10] In rare cases, aphasia may also result from herpesviral encephalitis.[11] The herpes simplex virus affects the frontal and temporal lobes, subcortical structures, and the hippocampal tissue, which can trigger aphasia.[12] In acute disorders, such as head injury or stroke, aphasia usually develops quickly. When caused by brain tumor, infection, or dementia, it develops more slowly.[1][13][14]

There are two types of strokes: ischemic stroke and hemorrhagic stroke. An ischemic stroke happens when a persons artery which supplies blood to different areas of the brain becomes blocked with a blood clot. This type of stroke happens 80% of the time. The blood clot may form in the blood vessel which is called a thrombus or the blood clot can travel from somewhere else in the blood system that is called an embolus. A hemorrhagic stroke occurs when a blood vessel in the brain ruptures or bursts. Overall, people experience bleeding inside or around brain tissue. This type of stroke happens 20% of the time and is very serious. The most common cause of hemorrhagic stroke is an aneurysm.

Although all of the diseases listed above are potential causes, aphasia will generally only result when there is substantial damage to the left hemisphere (responsible for language function) of the brain, either the cortex (outer layer) and/or the underlying white matter.

Substantial damage to tissue anywhere within the region shown in blue on the figure below can potentially result in aphasia.[15] Aphasia can also sometimes be caused by damage to subcortical structures deep within the left hemisphere, including the thalamus, the internal and external capsules, and the caudate nucleus of the basal ganglia.[16][17] The area and extent of brain damage or atrophy will determine the type of aphasia and its symptoms.[1][13] A very small number of people can experience aphasia after damage to the right hemisphere only. It has been suggested that these individuals may have had an unusual brain organization prior to their illness or injury, with perhaps greater overall reliance on the right hemisphere for language skills than in the general population.[18][19]

Primary Progressive Aphasia (PPA), while its name can be misleading, is actually a form of dementia that has some symptoms closely related to several forms of aphasia. It is characterized by a gradual loss in language functioning while other cognitive domains are mostly preserved, such as memory and personality. PPA usually initiates with sudden word-finding difficulties in an individual and progresses to a reduced ability to formulate grammatically correct sentences (syntax) and impaired comprehension. The etiology of PPA is not due to a stroke, traumatic brain injury (TBI), or infectious disease; it is still uncertain what initiates the onset of PPA in those affected by it.[20]

Finally, certain chronic neurological disorders, such as epilepsy or migraine, can also include transient aphasia as a prodromal or episodic symptom.[21] Aphasia is also listed as a rare side-effect of the fentanyl patch, an opioid used to control chronic pain.[22][23]

Aphasia is best thought of as a collection of different disorders, rather than a single problem. Each individual with aphasia will present with their own particular combination of language strengths and weaknesses. Consequently, it is a major challenge just to document the various difficulties that can occur in different people, let alone decide how they might best be treated. Most classifications of the aphasias tend to divide the various symptoms into broad classes. A common approach is to distinguish between the fluent aphasias (where speech remains fluent, but content may be lacking, and the person may have difficulties understanding others), and the nonfluent aphasias (where speech is very halting and effortful, and may consist of just one or two words at a time).

However, no such broad-based grouping has proven fully adequate. There is a huge variation among patients within the same broad grouping, and aphasias can be highly selective. For instance, patients with naming deficits (anomic aphasia) might show an inability only for naming buildings, or people, or colors.[24]

It is important to note that there are typical difficulties with speech and language that come with normal aging as well. As we age language can become more difficult to process resulting in slowing of verbal comprehension, reading abilities and more likely word finding difficulties. With each of these though, unlike some aphasias, functionality within daily life remains intact.[25]

Localizationist approaches aim to classify the aphasias according to their major presenting characteristics and the regions of the brain that most probably gave rise to them.[26][27] Inspired by the early work of nineteenth century neurologists Paul Broca and Carl Wernicke, these approaches identify two major subtypes of aphasia and several more minor subtypes:

Recent classification schemes adopting this approach, such as the "Boston-Neoclassical Model" [26] also group these classical aphasia subtypes into two larger classes: the nonfluent aphasias (which encompasses Broca's aphasia and transcortical motor aphasia) and the fluent aphasias (which encompasses Wernicke's aphasia, conduction aphasia and transcortical sensory aphasia). These schemes also identify several further aphasia subtypes, including: Anomic aphasia, which is characterized by a selective difficulty finding the names for things; and Global aphasia where both expression and comprehension of speech are severely compromised.

Many localizationist approaches also recognize the existence of additional, more "pure" forms of language disorder that may affect only a single language skill.[29] For example, in Pure alexia, a person may be able to write but not read, and in Pure word deafness, they may be able to produce speech and to read, but not understand speech when it is spoken to them.

Although localizationist approaches provide a useful way of classifying the different patterns of language difficulty into broad groups, one problem is that a sizeable number of individuals do not fit neatly into one category or another.[30][31] Another problem is that the categories, particularly the major ones such as Broca's and Wernicke's aphasia, still remain quite broad. Consequently, even amongst individuals who meet the criteria for classification into a subtype, there can be enormous variability in the types of difficulties they experience.

Instead of categorizing every individual into a specific subtype, cognitive neuropsychological approaches aim to identify the key language skills or "modules" that are not functioning properly in each individual. A person could potentially have difficulty with just one module, or with a number of modules. This type of approach requires a framework or theory as to what skills/modules are needed to perform different kinds of language tasks. For example, the model of Max Coltheart identifies a module that recognizes phonemes as they are spoken, which is essential for any task involving recognition of words. Similarly, there is a module that stores phonemes that the person is planning to produce in speech, and this module is critical for any task involving the production of long words or long strings of speech. Once a theoretical framework has been established, the functioning of each module can then be assessed using a specific test or set of tests. In the clinical setting, use of this model usually involves conducting a battery of assessments,[32][33] each of which tests one or a number of these modules. Once a diagnosis is reached as to the skills/modules where the most significant impairment lies, therapy can proceed to treat these skills.

In practice, the cognitive neuropsychological approach can be unwieldy due to the wide variety of skills that can potentially be tested. Also, it is perhaps best suited to milder cases of aphasia: If the person has little expressive or receptive language ability, sometimes test performance can be difficult to interpret. In practice, clinicians will often use a blend of assessment approaches, which include broad subtyping based on a localizationist framework, and some finer exploration of specific language skills based on the cognitive neuropsychological framework.

Primary progressive aphasia (PPA) is a focal dementia that can be associated with progressive illnesses or dementia, such as frontotemporal dementia / Pick Complex Motor neuron disease, Progressive supranuclear palsy, and Alzheimer's disease, which is the gradual process of progressively losing the ability to think. Gradual loss of language function occurs in the context of relatively well-preserved memory, visual processing, and personality until the advanced stages. Symptoms usually begin with word-finding problems (naming) and progress to impaired grammar (syntax) and comprehension (sentence processing and semantics). People suffering from PPA may have difficulties comprehending what others are saying. They can also have difficulty trying to find the right words to make a sentence.[34][35][36] There are three classifications of Primary Progressive Aphasia: Progressive nonfluent aphasia (PNFA), Semantic Dementia (SD), and Logopenic progressive aphasia (LPA)[36][37]

Progressive Jargon Aphasia is a fluent or receptive aphasia in which the patient's speech is incomprehensible, but appears to make sense to them. Speech is fluent and effortless with intact syntax and grammar, but the patient has problems with the selection of nouns. Either they will replace the desired word with another that sounds or looks like the original one or has some other connection or they will replace it with sounds. As such, patients with jargon aphasia often use neologisms, and may perseverate if they try to replace the words they cannot find with sounds. Substitutions commonly involve picking another (actual) word starting with the same sound (e.g., clocktower - colander), picking another semantically related to the first (e.g., letter - scroll), or picking one phonetically similar to the intended one (e.g., lane - late).

There have been many instances showing that there is a form of aphasia among deaf individuals. Sign language is, after all, a form of communication that has been shown to use the same areas of the brain as verbal forms of communication. Mirror neurons become activated when an animal is acting in a particular way or watching another individual act in the same manner. These mirror neurons are important in giving an individual the ability to mimic movements of hands. Broca's area of speech production has been shown to contain several of these mirror neurons resulting in significant similarities of brain activity between sign language and vocal speech communication. Facial communication is a significant portion of how animals interact with each other. Humans use facial movements to create, what other humans perceive, to be faces of emotions. While combining these facial movements with speech, a more full form of language is created which enables the species to interact with a much more complex and detailed form of communication. Sign language also uses these facial movements and emotions along with the primary hand movement way of communicating. These facial movement forms of communication come from the same areas of the brain. When dealing with damages to certain areas of the brain, vocal forms of communication are in jeopardy of severe forms of aphasia. Since these same areas of the brain are being used for sign language, these same, at least very similar, forms of aphasia can show in the Deaf community. Individuals can show a form of Wernicke's aphasia with sign language and they show deficits in their abilities in being able to produce any form of expressions. Broca's aphasia shows up in some patients, as well. These individuals find tremendous difficulty in being able to actually sign the linguistic concepts they are trying to express.[38]

People with aphasia may experience any of the following behaviors due to an acquired brain injury, although some of these symptoms may be due to related or concomitant problems such as dysarthria or apraxia and not primarily due to aphasia. Aphasia symptoms can vary based on the location of damage in the brain. Signs and symptoms may or may not be present in individuals with aphasia and may vary in severity and level of disruption to communication.[39] Often those with aphasia will try to hide their inability to name objects by using words like thing. So when asked to name a pencil they may say it is a thing used to write.[40]

Given the previously stated signs and symptoms the following behaviors are often seen in people with aphasia as a result of attempted compensation for incurred speech and language deficits:

Acute aphasias

The following table summarizes some major characteristics of different acute aphasias:

Subcortical aphasias

Most acute aphasia patients can recover some or most skills by working with a speech-language pathologist. This rehabilitation can take two or more years and is most effective when begun quickly. After the onset of Aphasia, there is approximately a six-month period of spontaneous recovery. During this time, the brain is attempting to recover and repair the damaged neurons. Therapy for Aphasia during this time facilitates an even greater level of recovery than if no intervention was given at this time.[44] Improvement varies widely, depending on the aphasia's cause, type, and severity. Recovery also depends on the patient's age, health, motivation, handedness, and educational level.[13]

There is no one treatment proven to be effective for all types of aphasias. The reason that there is no universal treatment for aphasia is because of the nature of the disorder and the various ways it is presented, as explained in the above sections. Aphasia is rarely exhibited identically, implying that treatment needs to be catered specifically to the individual. Studies have shown that, although there is no consistency on treatment methodology in literature, there is a strong indication that treatment in general has positive outcomes.[45] Therapy for aphasia ranges from increasing functional communication to improving speech accuracy, depending on the person's severity, needs and support of family and friends.[46] Group therapy allows individuals to work on their pragmatic and communication skills with other individuals with aphasia, which are skills that may not often be addressed in individual one-on-one therapy sessions. It can also help increase confidence and social skills in a comfortable setting.[47]

A multi-disciplinary team, including doctors (often a physician is involved, but more likely a clinical neuropsychologist will head the treatment team), physiotherapist, occupational therapist, speech-language pathologist, and social worker, works together in treating aphasia. For the most part, treatment relies heavily on repetition and aims to address language performance by working on task-specific skills. The primary goal is to help the individual and those closest to them adjust to changes and limitations in communication.[45]

Treatment techniques mostly fall under two approaches:

Several treatment techniques include the following:

Melodic Intonation Therapy is used to treat non-fluent aphasia and has proved to be effective in some cases.[52] However, there is still no evidence from randomized controlled trials confirming the efficacy of MIT in chronic aphasia. MIT is used to help people with aphasia vocalize themselves through speech song which is then transferred as a spoken word. Good candidates for this therapy include left hemisphere stroke patients, non-fluent aphasias such as Broca's, good auditory comprehension, poor repetition and articulation, and good emotional stability and memory.[53] It has been hypothesized that MIT is effective because prosody and singing both rely on areas of the right hemisphere; it may be these right-hemisphere areas that are recruited for natural speech production after intensive training.[54] An alternative explanation is that the efficacy of MIT depends on neural circuits involved in the processing of rhythmicity and formulaic expressions (examples taken from the MIT manual: I am fine, how are you? or thank you); while rhythmic features associated with melodic intonation may engage primarily left-hemisphere subcortical areas of the brain, the use of formulaic expressions is known to be supported by right-hemisphere cortical and bilateral subcortical neural networks.[4][55]

More recently, computer technology has been incorporated into treatment options. A key indication for good prognosis is treatment intensity. A minimum of twothree hours per week has been specified to produce positive results.[56] The main advantage of using computers is that it can greatly increase intensity of therapy. These programs consist of a large variety of exercises and can be done at home in addition to face-to-face treatment with a therapist. However, since aphasia presents differently among individuals, these programs must be dynamic and flexible in order to adapt to the variability in impairments. Another barrier is the capability of computer programs to imitate normal speech and keep up with the speed of regular conversation. Therefore, computer technology seems to be limited in a communicative setting, however is effective in producing improvements in communication training.[56]

The intensity of aphasia therapy is determined by the length of each session, total hours of therapy per week, and total weeks of therapy provided. There is no consensus about what intense aphasia therapy entails, or how intense therapy should be to yield the best outcomes. Overall, treatment is considered more intense when total therapy hours per week are increased, and on average, research suggests more intense therapy leads to better outcomes. For example, one study found that patients who were treated for 8.8 hours a week for 11.2 weeks progressed more than patients who were treated 2 hours a week for 22.9 weeks.[57] Results of another study corroborate these findings. The researchers found that patients who received intensive therapy of 100 treatment hours over 62 weeks scored higher on language measures than the control group who received less intensive therapy.[58] Therefore, although there is a general consensus that intense treatment encourages more improvement, there is not a straightforward definition of intense treatment.

Intensity of treatment should be individualized based on the recency of stroke, therapy goals, and other patient-specific characteristics such as age, size of lesion, overall health status, and motivation.[59][60] Each individual reacts differently to treatment intensity and is able to tolerate treatment at different times post-stroke.[61] Some patients cannot tolerate therapy directly after a stroke due to confusion or exhaustion, but may tolerate therapy better later. Intensity of treatment after a stroke should be dependent on the patients motivation, stamina, and tolerance for therapy.[61] Level of intensity also depends on therapy goals; for certain goals non-intensive therapy is more beneficial. For example, non-intensive therapy has been found to be more effective than intensive therapy when targeting naming accuracy in patients with anomia.[60] This is because more time in between sessions allows for rehearsal and reinforces long term learning.[60]

Intensity of therapy is also dependent on the recency of stroke. Patients react differently to intense treatment in the acute phase (03 months post stroke), sub-acute phase (36 months post stroke), or chronic phase (6+ months post stroke). Intensive therapy has been found to be effective for patients with nonfluent and fluent chronic aphasia, but less effective for patients with acute aphasia.[59][62] Patients with sub-acute aphasia also respond well to intensive therapy of 100 hours over 62 weeks. This suggests patients in the sub-acute phase can improve greatly in language and functional communication measures with intensive therapy compared to regular therapy.[58] Research suggests that intense treatment is most beneficial in the sub-acute or chronic phase, rather than directly post stroke.[58][59][62] More research needs to be done to examine the optimal time for providing intense therapy to all aphasic patients.[59]

Intensive therapy can be alternatively characterized by the magnitude of the demands placed on a client within a session. Under this definition, intensive therapy includes a few specific techniques such as Constraint Induced Aphasia Therapy (CIAT) and Speech Intensive Rehabilitation Intervention (SP-I-R-IT). CIAT places high demands on the patient by restricting use of the strongest areas of the patients brain and requiring the weakest areas to work harder. Typical CIAT therapy sessions are intense and last for about 3 hours.[63] One study found that when given intensive CIAT therapy, participant performance in verbal communication in everyday life significantly improved. Each participant in the study also showed improvement on at least one subtest within the Aachen Aphasia Test; which assesses language performance and comprehension in aphasia patients. These results suggest that intensive CIAT therapy is effective in patients with moderate, fluent aphasias in the chronic stage of recovery.[62] SP-I-R-IT focuses heavily on speech production strategies and intervention. SPIRIT therapy has been found to be effective; patients participating in intensive SPIRIT therapy improved performance on standardized measures by 15% after 50 weeks of therapy.[58]

Overall, intensity of aphasia treatment is an area that requires more research. Current research suggests that intense treatment is effective, although the definition of intense is variable. Most importantly, intensity of treatment should be determined on a case by case basis and should depend upon recency of stroke and the patients stamina, tolerance for therapy, motivation, overall health status, and treatment goals.

There are several outcomes that contribute to a patient's overall outcomes once diagnosed with aphasia including: neuroplasticity, age, overall health status, and patient motivation. Neuroplasticity is the brain's capability of change in response to the environment. Neuroplaticity underlies normal processes such as: typical development, learning & maintaining performance while aging, and the brain's response to a severe injury.[64] Positive outcomes are most prominent when neuroplasticity is maximized for the aphasic patient, and is predicted by the patient's response to the other stated outcomes.[65] The patient's age directly impacts the neuroplasticity the brain can allow, the younger the patient is, the greater plasticity is.[64] Overall health status also greatly impacts outcomes in aphasic patients. If a patient has no underlying health problems, and is young, then they have better outcomes than someone who is older, has severe health issues (such as: obesity, heart disease, cancer, high blood pressure, etc.) in conjunction with aphasia.[65] However, the most important factor affecting the outcomes of a patient with aphasia is a patient's motivation. In order to be successful, regardless of the contributing outcomes, the patient must be highly motivated in order to make the most efficient outcomes. If the patient is not motivated to make positive outcomes in their life after being diagnosed with any type of aphasia, their prognosis to make great improvements is much less than someone who is highly motivated to make positive changes in their life.[64][65] All of these outcomes contribute to success in Wernicke's, Broca's, Global, and Conduction aphasia, and are detailed below:

Wernicke's Aphasia:

Wernickes is considered a more severe form of aphasia, and is more commonly seen in older populations. Wernickes aphasia has shown a high recovery rate and frequent evolution to other forms of aphasia. Though some cases of Wernickes aphasia has shown greater improvements than more mild forms of aphasia, people with Wernickes aphasia may not reach as high of a level of speech abilities as those with mild forms of aphasia.[66]

Broca's Aphasia:

(Brocas and Anomic):

The term, Anomic Aphasia, usually refers to patients whose only prevalent symptom is impaired word retrieval in speech and writing.[67] Typically, the spontaneous speech of a person with anomic aphasia is fluent and grammatically correct but contains many word retrieval failures. These failures lead to unusual pauses, talking around the intended word, or substituting the intended word for a different word.[67] Anomic aphasia is the mildest form of aphasia, indicating a likely possibility for better recovery.[68] Patients with Brocas aphasia may also have difficulty with word retrieval, or anomia. In addition, patients with Brocas aphasia comprehend spoken and written language better than they can speak or write. These patients self-monitor, are aware of their communicative impairments, and frequently try to repeat or attempt repairs.[67] The preceding factors discussed correlate with a good prognosis for patients with Brocas aphasia. Many patients with an acute onset of Brocas aphasia, eventually progress to milder forms of aphasia, such as conduction or anomic.[69]

Therapy for Expressive Aphasia (nonfluent) is beneficial, even for patients with severe nonfluent aphasia. A study conducted by Marangolo and co-workers (2013) administered conversational therapy to patients with severe nonfluent aphasia. The results of the study demonstrated a significant increase in the patients expressive language. The authors suggested that an intensive conversational therapy program should be considered for patients with moderately severe nonfluent aphasia in order to enhance the patient's quality of life and improve their language expression.[70] In addition, although Anomic Aphasia is seen to be less severe than other aphasias, therapy is still imperative to help decrease the patients word finding deficits. A research study conducted by Harnish and co-workers (2014), provided intense treatment to patients with anomic aphasia. Results of the study concluded significant increases in the participants expressive language. These results suggest that an intensive intervention program for patients with anomic aphasia provides a surprisingly quick expressive language increase. Specifically, these patients relearned to correctly produce the problematic words after one to three hours of speech-language therapy.[71]

Global Aphasia:

Global aphasia is considered a severe impairment in many language aspects since it impacts expressive and receptive language, reading, and writing.[72] Despite these many deficits, there is evidence that has shown individuals benefited from speech language therapy.[73] Even though each case is different, it has been noted that individuals with global aphasia had greater improvements during the second six months following the stroke when compared to the first 6 months.[74] Intense and frequent speech-language therapy had been shown to be more effective, with the addition of daily homework.[73] Improvement has also been shown when the individual was attentive, motivated, and information was presented in multiple ways.[75]

In one study, 23 individuals that had previously received speech-language therapy, but had been dismissed because further recovery was not expected, participated in intense speech-language therapy.[73] Results showed significant improvements in oral and written noun and sentence production, naming actions, and daily communication.[73]

Even though individuals with global aphasia will not become competent speakers, listeners, writers, or readers, goals can be created to improve the individuals quality of life.[67] Collins (1991) suggests therapy targeting attainable goals that will have the greatest impact on an individuals daily life, such as getting reliable yes/no answers or providing the patient gestures. Individuals with global aphasia usually respond well to treatment that includes personally relevant information, which is also important to consider for therapy.[67]

Conduction Aphasia:

Conduction and transcortical aphasias are caused by damage to the white matter tracts. These aphasias spare the cortex of the language centers, but instead create a disconnection between them.

Conduction aphasia is caused by damage to the arcuate fasciculus. The arcuate fasciculus is a white matter tract that connects Brocas and Wernickes areas. Patients with conduction aphasia typically have good language comprehension, but poor speech repetition and mild difficulty with word retrieval and speech production. Patients with conduction aphasia are typically aware of their errors.[67] The awareness of errors and the milder nature of conduction aphasia compared to other types contributes to a positive outcome. Additionally, a case study completed on a 54-year-old man with a large infarct in the arcuate fasciculus indicated that severe conduction aphasia can be successfully treated. Despite his global deficits, he made a full recovery after 30 months.[76]

Transcortical aphasias include transcortical motor aphasia, transcortical sensory aphasia, and mixed transcortical aphasia. Patients with transcortical motor aphasia typically have intact comprehension and awareness of their errors, but poor word finding and speech production. Patients with transcortical sensory and mixed transcortical aphasia have poor comprehension and unawareness of their errors.[67] Despite poor comprehension and more severe deficits in some transcortical aphasias, small studies have indicated that full recovery is possible for all types of transcortical aphasia.[77] Due to the limited research on outcomes for the specific subtypes of these aphasias, it is more important to focus on the other factors and severity of deficits in order to predict a reasonable outcome.

The first recorded case of aphasia is from an Egyptian papyrus, the Edwin Smith Papyrus, which details speech problems in a person with a traumatic brain injury to the temporal lobe.[78] During the second half of the 19th century, Aphasia was a major focus for scientists and philosophers who were working in the beginning stages in the field of psychology.[2]

This section primarily repeats material that should be found in the page Stroke. Please add additional material or remove this section.

Please consider turning this section into a table.

150,074 people suffered a lethal stroke in the US in 2004. It is the third largest cause of death globally, ranking behind cardiovascular disease and all forms of cancer. Stroke is a leading cause of serious, long-term disability in the United States. About 5,800,000 stroke survivors are alive in the US today; 2,300,000 are males and 3,400,000 are females. Studies show that about 780,000 people suffer a new or recurrent stroke each year. About 600,000 of these are first attacks and 180,000 are recurrent attacks. In 2004, females accounted for 60.8 percent of stroke deaths. From 1994 to 2004 the death rate from stroke declined 24.2 percent, and the actual number of stroke deaths declined 6.8 percent.[citation needed]

Like the previous section, this section repeats material that should be found in the page Stroke. Please merge or delete this section.

Following are some precautions that should be taken to avoid aphasia, by decreasing the risk of stroke, the main cause of aphasia:

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