<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Aphasia and can you explain it in depth? [/INST] Aphasia is an inability to comprehend or formulate language because of damage to specific brain regions. The major causes are stroke and head trauma; prevalence is hard to determine but aphasia due to stroke is estimated to be 0.1–0.4% in the Global North. Aphasia can also be the result of brain tumors, brain infections, or neurodegenerative diseases (such as dementias).To be diagnosed with aphasia, a persons speech or language must be significantly impaired in one (or more) of the four aspects of communication following acquired brain injury. Alternatively, in the case of progressive aphasia, it must have significantly declined over a short period of time. The four aspects of communication 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. Expressive language and receptive language can both be affected as well. Aphasia also affects visual language such as sign language. In contrast, the use of formulaic expressions in everyday communication is often preserved. For example, while a person with aphasia, particularly expressive aphasia (Brocas aphasia), may not be able to ask a loved one when their birthday is, they may still be able to sing "Happy Birthday". One prevalent deficit in the aphasias is anomia, which is a difficulty in finding the correct word.: 72 With aphasia, one or more modes of communication in the brain have been damaged and are therefore functioning incorrectly. Aphasia is not caused by damage to the brain that results in motor or sensory deficits, which produces abnormal speech; that is, aphasia is not related to the mechanics of speech but rather the individuals language cognition (although a person can have both problems, as an example, if they have a haemorrhage that damaged a large area of the brain). An individuals language is the socially shared set of rules, as well as the thought processes that go behind communication (as it affects both verbal and nonverbal language). 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.
Neurodevelopmental forms of auditory processing disorder are differentiable from aphasia in that aphasia is by definition caused by acquired brain injury, but acquired epileptic aphasia has been viewed as a form of APD.

Prevalence
Aphasia affects about two million people in the U.S. and 250,000 people in Great Britain. Nearly 180,000 people acquire the disorder every year in the U.S., 170,000 due to stroke. Any person of any age can develop aphasia, given that it is often caused by a traumatic injury. However, people who are middle aged and older are the most likely to acquire aphasia, as the other etiologies are more likely at older ages. For example, approximately 75% of all strokes occur in individuals over the age of 65. Strokes account for most documented cases of aphasia: 25% to 40% of people who survive a stroke develop aphasia as a result of damage to the language-processing regions of the brain.

Aphasia and dysphasia
Technically, dysphasia means impaired language and aphasia means lack of language. There have been calls to use the term aphasia regardless of severity. Reasons for doing so include dysphasia being easily confused with the swallowing disorder dysphagia, consumers and speech pathologists preferring the term aphasia, and many languages other than English using a word similar to aphasia. The term "aphasia" is more commonly used in North America, while "dysphasia" is more frequently used elsewhere.

Signs and symptoms
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. Often those with aphasia may have a difficulty with naming objects, so they might use words such as thing or point at the objects. When asked to name a pencil they may say it is a “thing used to write”.

Related behaviors
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:

Self-repairs: Further disruptions in fluent speech as a result of mis-attempts to repair erred speech production.
Struggle in non-fluent aphasias: A severe increase in expelled effort to speak after a life where talking and communicating was an ability that came so easily can cause visible frustration.
Preserved and automatic language: A behavior in which some language or language sequences that were used so frequently prior to onset are still produced with more ease than other language post onset.

Subcortical
Subcortical aphasias characteristics and symptoms depend upon the site and size of subcortical lesion. Possible sites of lesions include the thalamus, internal capsule, and basal ganglia.

Causes
Aphasia is most often caused by stroke, where about a quarter of patients who experience an acute stroke develop aphasia. However, 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. In rare cases, aphasia may also result from herpesviral encephalitis. The herpes simplex virus affects the frontal and temporal lobes, subcortical structures, and the hippocampal tissue, which can trigger aphasia. 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.Substantial damage to tissue anywhere within the region shown in blue (on the figure in the infobox above) can potentially result in aphasia. 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. The area and extent of brain damage or atrophy will determine the type of aphasia and its symptoms. 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.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.Epilepsy can also include transient aphasia as a prodromal or episodic symptom. Aphasia is also listed as a rare side-effect of the fentanyl patch, an opioid used to control chronic pain.

Classification
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 wide variation among people even within the same broad grouping, and aphasias can be highly selective. For instance, people with naming deficits (anomic aphasia) might show an inability only for naming buildings, or people, or colors.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 a 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.: 7

Boston classification
Individuals with receptive aphasia (Wernickes aphasia), also referred to as fluent aphasia, may speak in long sentences that have no meaning, add unnecessary words, and even create new "words" (neologisms). For example, someone with receptive aphasia may say, "delicious taco", meaning "The dog needs to go out so I will take him for a walk". They have poor auditory and reading comprehension, and fluent, but nonsensical, oral and written expression. Individuals with receptive aphasia usually have great difficulty understanding the speech of both themselves and others and are, therefore, often unaware of their mistakes. Receptive language deficits usually arise from lesions in the posterior portion of the left hemisphere at or near Wernickes area.: 71  It is often the result of trauma to the temporal region of the brain, specifically damage to Wernickes area. Trauma can be the result from an array of problems, however it is most commonly seen as a result of stroke
Individuals with expressive aphasia (Brocas aphasia) frequently speak short, meaningful phrases that are produced with great effort. It is thus characterized as a nonfluent aphasia. Affected people often omit small words such as "is", "and", and "the". For example, a person with expressive aphasia may say, "walk dog", which could mean "I will take the dog for a walk", "you take the dog for a walk" or even "the dog walked out of the yard." Individuals with expressive aphasia are able to understand the speech of others to varying degrees. Because of this, they are often aware of their difficulties and can become easily frustrated by their speaking problems. While Brocas aphasia may appear to be solely an issue with language production, evidence suggests that it may be rooted in an inability to process syntactical information. Individuals with expressive aphasia may have a speech automatism (also called recurring or recurrent utterance). These speech automatisms can be repeated lexical speech automatisms; e.g., modalisations (I cant..., I cant...), expletives/swearwords, numbers (one two, one two) or non-lexical utterances made up of repeated, legal but meaningless, consonant-vowel syllables (e.g.., /tan tan/, /bi bi/). In severe cases, the individual may be able to utter only the same speech automatism each time they attempt speech.
Individuals with anomic aphasia have difficulty with naming. People with this aphasia may have difficulties naming certain words, linked by their grammatical type (e.g., difficulty naming verbs and not nouns) or by their semantic category (e.g., difficulty naming words relating to photography but nothing else) or a more general naming difficulty. People tend to produce grammatic, yet empty, speech. Auditory comprehension tends to be preserved. Anomic aphasia is the aphasial presentation of tumors in the language zone; it is the aphasial presentation of Alzheimers disease. Anomic aphasia is the mildest form of aphasia, indicating a likely possibility for better recovery.
Individuals with transcortical sensory aphasia, in principle the most general and potentially among the most complex forms of aphasia, may have similar deficits as in receptive aphasia, but their repetition ability may remain intact.
Global aphasia is considered a severe impairment in many language aspects since it impacts expressive and receptive language, reading, and writing. Despite these many deficits, there is evidence that has shown individuals benefited from speech language therapy. 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. Individuals with global aphasia usually respond well to treatment that includes personally relevant information, which is also important to consider for therapy.
Individuals with conduction aphasia have deficits in the connections between the speech-comprehension and speech-production areas. This might be caused by damage to the arcuate fasciculus, the structure that transmits information between Wernickes area and Brocas area. Similar symptoms, however, can be present after damage to the insula or to the auditory cortex. Auditory comprehension is near normal, and oral expression is fluent with occasional paraphasic errors. Paraphasic errors include phonemic/literal or semantic/verbal. Repetition ability is poor. 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. People with conduction aphasia typically have good language comprehension, but poor speech repetition and mild difficulty with word retrieval and speech production. People with conduction aphasia are typically aware of their errors. Two forms of conduction aphasia have been described: reproduction conduction aphasia (repetition of a single relatively unfamiliar multisyllabic word) and repetition conduction aphasia (repetition of unconnected short familiar words.
Transcortical aphasias include transcortical motor aphasia, transcortical sensory aphasia, and mixed transcortical aphasia. People with transcortical motor aphasia typically have intact comprehension and awareness of their errors, but poor word finding and speech production. People with transcortical sensory and mixed transcortical aphasia have poor comprehension and unawareness of their errors. 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.

Classical-localizationist approaches
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. 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:

Expressive aphasia (also known as "motor aphasia" or "Brocas aphasia"), which is characterized by halted, fragmented, effortful speech, but well-preserved comprehension relative to expression. Damage is typically in the anterior portion of the left hemisphere, most notably Brocas area. Individuals with Brocas aphasia often have right-sided weakness or paralysis of the arm and leg, because the left frontal lobe is also important for body movement, particularly on the right side.
Receptive aphasia (also known as "sensory aphasia" or "Wernickes aphasia"), which is characterized by fluent speech, but marked difficulties understanding words and sentences. Although fluent, the speech may lack in key substantive words (nouns, verbs, adjectives), and may contain incorrect words or even nonsense words. This subtype has been associated with damage to the posterior left temporal cortex, most notably Wernickes area. These individuals usually have no body weakness, because their brain injury is not near the parts of the brain that control movement.
Conduction aphasia, where speech remains fluent, and comprehension is preserved, but the person may have disproportionate difficulty repeating words or sentences. Damage typically involves the arcuate fasciculus and the left parietal region.
Transcortical motor aphasia and transcortical sensory aphasia, which are similar to Brocas and Wernickes aphasia respectively, but the ability to repeat words and sentences is disproportionately preserved.Recent classification schemes adopting this approach, such as the Boston-Neoclassical Model, also group these classical aphasia subtypes into two larger classes: the nonfluent aphasias (which encompasses Brocas aphasia and transcortical motor aphasia) and the fluent aphasias (which encompasses Wernickes 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. 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.

Cognitive neuropsychological approaches
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. Another problem is that the categories, particularly the major ones such as Brocas and Wernickes aphasia, still remain quite broad. Consequently, even amongst those 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, 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.

Progressive aphasias
Primary progressive aphasia (PPA) is a neurodegenerative focal dementia that can be associated with progressive illnesses or dementia, such as frontotemporal dementia / Pick Complex Motor neuron disease, Progressive supranuclear palsy, and Alzheimers 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). The loss of language before the loss of memory differentiates PPA from typical dementias. People with PPA may have difficulties comprehending what others are saying. They can also have difficulty trying to find the right words to make a sentence. There are three classifications of Primary Progressive Aphasia : Progressive nonfluent aphasia (PNFA), Semantic Dementia (SD), and Logopenic progressive aphasia (LPA).Progressive Jargon Aphasia is a fluent or receptive aphasia in which the persons speech is incomprehensible, but appears to make sense to them. Speech is fluent and effortless with intact syntax and grammar, but the person 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, people 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).

Deaf aphasia
There have been many instances showing that there is a form of aphasia among deaf individuals. Sign languages are, after all, forms of language that have been shown to use the same areas of the brain as verbal forms of language. 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. Brocas 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 Wernickes aphasia with sign language and they show deficits in their abilities in being able to produce any form of expressions. Brocas aphasia shows up in some people, as well. These individuals find tremendous difficulty in being able to actually sign the linguistic concepts they are trying to express.

Severity
The severity of the type of aphasia varies depending on the size of the stroke. However, there is much variance between how often one type of severity occurs in certain types of aphasia. For instance, any type of aphasia can range from mild to profound. Regardless of the severity of aphasia, people can make improvements due to spontaneous recovery and treatment in the acute stages of recovery. Additionally, while most studies propose that the greatest outcomes occur in people with severe aphasia when treatment is provided in the acute stages of recovery, Robey (1998) also found that those with severe aphasia are capable of making strong language gains in the chronic stage of recovery as well. This finding implies that persons with aphasia have the potential to have functional outcomes regardless of how severe their aphasia may be. While there is no distinct pattern of the outcomes of aphasia based on severity alone, global aphasia typically makes functional language gains, but may be gradual since global aphasia affects many language areas.

Cognitive deficits in aphasia
While aphasia has traditionally been described in terms of language deficits, there is increasing evidence that many people with aphasia commonly experience co-occurring non-linguistic cognitive deficits in areas such as attention, memory, executive functions and learning. By some accounts, cognitive deficits, such as attention and working memory constitute the underlying cause of language impairment in people with aphasia. Others suggest that cognitive deficits often co-occur but are comparable to cognitive deficits in stroke patients without aphasia and reflect general brain dysfunction following injury. The degree to which deficits in attention and other cognitive domains underlie language deficits in aphasia is still unclear.In particular, people with aphasia often demonstrate short-term and working memory deficits. These deficits can occur in both the verbal domain as well as the visuospatial domain. Furthermore, these deficits are often associated with performance on language specific tasks such as naming, lexical processing, and sentence comprehension, and discourse production. Other studies have found that most, but not all people with aphasia demonstrate performance deficits on tasks of attention, and their performance on these tasks correlate with language performance and cognitive ability in other domains. Even patients with mild aphasia, who score near the ceiling on tests of language often demonstrate slower response times and interference effects in non-verbal attention abilities.In addition to deficits in short-term memory, working memory, and attention, people with aphasia can also demonstrate deficits in executive function. For instance, people with aphasia may demonstrate deficits in initiation, planning, self-monitoring, and cognitive flexibility. Other studies have found that people with aphasia demonstrate reduced speed and efficiency during completion executive function assessments.Regardless of their role in the underlying nature of aphasia, cognitive deficits have a clear role in the study and rehabilitation of aphasia. For instance, the severity of cognitive deficits in people with aphasia has been associated with lower quality of life, even more so than the severity of language deficits. Furthermore, cognitive deficits may influence the learning process of rehabilitation and language treatment outcomes in aphasia. Non-linguistic cognitive deficits have also been the target of interventions directed at improving language ability, though outcomes are not definitive. While some studies have demonstrated language improvement secondary to cognitively-focused treatment, others have found little evidence that the treatment of cognitive deficits in people with aphasia has an influence on language outcomes.One important caveat in the measurement and treatment of cognitive deficits in people with aphasia is the degree to which assessments of cognition rely on language abilities for successful performance. Most studies have attempted to circumvent this challenge by utilizing non-verbal cognitive assessments to evaluate cognitive ability in people with aphasia. However, the degree to which these tasks are truly non-verbal and not mediated by language in unclear. For instance, Wall et al. found that language and non-linguistic performance was related, except when non-linguistic performance was measured by real life cognitive tasks.

Prevention of aphasia
Aphasia is largely caused by unavoidable instances. However, some precautions can be taken to decrease risk for experiencing one of the two major causes of aphasia: stroke and traumatic brain injury (TBI). To decrease the probability of having an ischemic or hemorrhagic stroke, one should take the following precautions:

Exercising regularly
Eating a healthy diet, avoiding cholesterol in particular
Keeping alcohol consumption low and avoiding tobacco use
Controlling blood pressure
Going to the emergency room immediately if you begin to experience unilateral extremity (especially leg) swelling, warmth, redness, and/or tenderness as these are symptoms of a deep vein thrombosis which can lead to a strokeTo prevent aphasia due to traumatic injury, one should take precautionary measures when engaging in dangerous activities such as:

Wearing a helmet when operating a bicycle, motor cycle, ATV, or any other moving vehicle that could potentially be involved in an accident
Wearing a seatbelt when driving or riding in a car
Wearing proper protective gear when playing contact sports, especially American football, rugby, and hockey, or refraining from such activities
Minimizing anticoagulant use (including aspirin) if at all possible as they increase the risk of hemorrhage after a head injuryAdditionally, one should always seek medical attention after sustaining head trauma due to a fall or accident. The sooner that one receives medical attention for a traumatic brain injury, the less likely one is to experience long-term or severe effects.

Management
When addressing Wernickes aphasia, according to Bakheit et al. (2007), the lack of awareness of the language impairments, a common characteristic of Wernickes aphasia, may affect the rate and extent of therapy outcomes. Robey (1998) determined that at least 2 hours of treatment per week is recommended for making significant language gains. Spontaneous recovery may cause some language gains, but without speech-language therapy, the outcomes can be half as strong as those with therapy.When addressing Brocas aphasia, better outcomes occur when the person participates in therapy, and treatment is more effective than no treatment for people in the acute period. Two or more hours of therapy per week in acute and post-acute stages produced the greatest results. High-intensity therapy was most effective, and low-intensity therapy was almost equivalent to no therapy.People with global aphasia are sometimes referred to as having irreversible aphasic syndrome, often making limited gains in auditory comprehension, and recovering no functional language modality with therapy. With this said, people with global aphasia may retain gestural communication skills that may enable success when communicating with conversational partners within familiar conditions. Process-oriented treatment options are limited, and people may not become competent language users as readers, listeners, writers, or speakers no matter how extensive therapy is. However, peoples daily routines and quality of life can be enhanced with reasonable and modest goals. After the first month, there is limited to no healing to language abilities of most people. There is a grim prognosis leaving 83% who were globally aphasic after the first month they will remain globally aphasic at the first year. Some people are so severely impaired that their existing process-oriented treatment approaches offer no signs of progress, and therefore cannot justify the cost of therapy.Perhaps due to the relative rareness of conduction aphasia, few studies have specifically studied the effectiveness of therapy for people with this type of aphasia. From the studies performed, results showed that therapy can help to improve specific language outcomes. One intervention that has had positive results is auditory repetition training. Kohn et al. (1990) reported that drilled auditory repetition training related to improvements in spontaneous speech, Francis et al. (2003) reported improvements in sentence comprehension, and Kalinyak-Fliszar et al. (2011) reported improvements in auditory-visual short-term memory.Most acute cases of aphasia recover some or most skills by working with a speech-language pathologist. Recovery and improvement can continue for years after the stroke. 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. Improvement varies widely, depending on the aphasias cause, type, and severity. Recovery also depends on the persons age, health, motivation, handedness, and educational level.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. Therapy for aphasia ranges from increasing functional communication to improving speech accuracy, depending on the persons severity, needs and support of family and friends. 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.: 97 Evidence does not support the use of transcranial direct current stimulation (tDCS) for improving aphasia after stroke. Moderate quality evidence does indicate naming performance improvements for nouns but not verbs using tDCSSpecific treatment techniques include the following:

Copy and recall therapy (CART) –  repetition and recall of targeted words within therapy may strengthen orthographic representations and improve single word reading, writing, and naming
Visual communication therapy (VIC) –  the use of index cards with symbols to represent various components of speech
Visual action therapy (VAT) –  typically treats individuals with global aphasia to train the use of hand gestures for specific items
Functional communication treatment (FCT) –  focuses on improving activities specific to functional tasks, social interaction, and self-expression
Promoting aphasics communicative effectiveness (PACE) –  a means of encouraging normal interaction between people with aphasia and clinicians. In this kind of therapy, the focus is on pragmatic communication rather than treatment itself. People are asked to communicate a given message to their therapists by means of drawing, making hand gestures or even pointing to an object
Melodic intonation therapy (MIT) –  aims to use the intact melodic/prosodic processing skills of the right hemisphere to help cue retrieval of words and expressive language: 93
Other –  i.e. drawing as a way of communicating, trained conversation partnersSemantic feature analysis (SFA) – a type of aphasia treatment that targets word-finding deficits. It is based on the theory that neural connections can be strengthened by using related words and phrases that are similar to the target word, to eventually activate the target word in the brain. SFA can be implemented in multiple forms such as verbally, written, using picture cards, etc. The SLP provides prompting questions to the individual with aphasia in order for the person to name the picture provided. Studies show that SFA is an effective intervention for improving confrontational naming.Melodic intonation therapy is used to treat non-fluent aphasia and has proved to be effective in some cases. 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 people who have had left hemisphere strokes, non-fluent aphasias such as Brocas, good auditory comprehension, poor repetition and articulation, and good emotional stability and memory. 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.Systematic reviews support the effectiveness and importance of partner training. According to the National Institute on Deafness and Other Communication Disorders (NIDCD), involving family with the treatment of an aphasic loved one is ideal for all involved, because while it will no doubt assist in their recovery, it will also make it easier for members of the family to learn how best to communicate with them.When a persons speech is insufficient, different kinds of augmentative and alternative communication could be considered such as alphabet boards, pictorial communication books, specialized software for computers or apps for tablets or smartphones.

Intensity of treatment
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. A 2016 Cochrane review of speech and language therapy for people with aphasia found that treatments that are higher intensity, higher dose or over a long duration of time led to significantly better functional communication but people were more likely to drop out of high intensity treatment (up to 15 hours per week).Intensity of therapy is also dependent on the recency of stroke. People with aphasia react differently to intense treatment in the acute phase (0–3 months post stroke), sub-acute phase (3–6 months post stroke), or chronic phase (6+ months post stroke). Intensive therapy has been found to be effective for people with nonfluent and fluent chronic aphasia, but less effective for people with acute aphasia. People with sub-acute aphasia also respond well to intensive therapy of 100 hours over 62 weeks. This suggests people in the sub-acute phase can improve greatly in language and functional communication measures with intensive therapy compared to regular therapy.

Individualized service delivery
Intensity of treatment should be individualized based on the recency of stroke, therapy goals, and other specific characteristics such as age, size of lesion, overall health status, and motivation. Each individual reacts differently to treatment intensity and is able to tolerate treatment at different times post-stroke. Intensity of treatment after a stroke should be dependent on the persons motivation, stamina, and tolerance for therapy.

Outcomes
If the symptoms of aphasia last longer than two or three months after a stroke, a complete recovery is unlikely. However, it is important to note that some people continue to improve over a period of years and even decades. Improvement is a slow process that usually involves both helping the individual and family understand the nature of aphasia and learning compensatory strategies for communicating.After a traumatic brain injury (TBI) or cerebrovascular accident (CVA), the brain undergoes several healing and re-organization processes, which may result in improved language function. This is referred to as spontaneous recovery. Spontaneous recovery is the natural recovery the brain makes without treatment, and the brain begins to reorganize and change in order to recover. There are several factors that contribute to a persons chance of recovery caused by stroke, including stroke size and location. Age, sex, and education have not been found to be very predictive. There is also research pointing to damage in the left hemisphere healing more effectively than the right.Specific to aphasia, spontaneous recovery varies among affected people and may not look the same in everyone, making it difficult to predict recovery.Though some cases of Wernickes aphasia have shown greater improvements than more mild forms of aphasia, people with Wernickes aphasia may not reach as high a level of speech abilities as those with mild forms of aphasia.

History
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.During the second half of the 19th century, aphasia was a major focus for scientists and philosophers who were working in the beginning stages of the field of psychology.
In medical research, speechlessness was described as an incorrect prognosis, and there was no assumption that underlying language complications existed. Broca and his colleagues were some of the first to write about aphasia, but Wernicke was the first credited to have written extensively about aphasia being a disorder that contained comprehension difficulties. Despite claims of who reported on aphasia first, it was F.J. Gall that gave the first full description of aphasia after studying wounds to the brain, as well as his observation of speech difficulties resulting from vascular lesions. A recent book on the entire history of aphasia is available (Reference: Tesak, J. & Code, C. (2008) Milestones in the History of Aphasia: Theories and Protagonists. Hove, East Sussex: Psychology Press).

Etymology
Aphasia is from Greek a- ("without", negative prefix) + phásis (φάσις, "speech").
The word aphasia comes from the word ἀφασία aphasia, in Ancient Greek, which means "speechlessness", derived from ἄφατος aphatos, "speechless" from ἀ- a-, "not, un" and φημί phemi, "I speak".

Neuroimaging Methods
Magnetic resonance imaging (MRI) and functional magnetic resonance imaging (fMRI) are the most common neuroimaging tools used in identifying aphasia and studying the extent of damage in the loss of language abilities. This is done by doing MRI scans and locating the extent of lesions or damage within brain tissue, particularly within areas of the left frontal and temporal regions- where a lot of language related areas lie. In fMRI studies a language related task is often completed and then the BOLD image is analyzed. If there are lower than normal BOLD responses that indicate a lessening of blood flow to the affected area and can show quantitatively that the cognitive task is not being completed.
There are limitations to the use of fMRI in aphasic patients particularly. Because a high percentage of aphasic patients develop it because of stroke there can be infarcts present which is the total loss of blood flow. This can be due to the thinning of blood vessels or the complete blockage of it. This is important in fMRI as it relies on the BOLD response (the oxygen levels of the blood vessels), and this can create a false hyporesponse upon fMRI study. Due to the limitations of fMRI such as a lower spatial resolution, it can show that some areas of the brain are not active during a task when they in reality are. Additionally, with stroke being the cause of many cases of aphasia the extent of damage to brain tissue can be difficult to quantify therefore the effects of stroke brain damage on the functionality of the patient can vary.
Neural Substrates of Aphasia Subtypes
MRI is often used to predict or confirm the subtype of aphasia present. Researchers compared 3 subtypes of aphasia- nonfluent-variant primary progressive aphasia (nfPPA), logopenic-variant primary progressive aphasia (lvPPA), and semantic-variant primary progressive aphasia (svPPA), with primary progressive aphasia (PPA) and Alzheimer’s disease. This was done by analyzing the MRIs of patients with each of the subsets of PPA.  Images which compare subtypes of aphasia as well as for finding the extent of lesions are generated by overlapping images of different participants brains (if applicable) and isolating areas of lesions or damage using third party software such as MRIcron. MRI has also been used to study the relationship between the type of aphasia developed and the age of the person with aphasia. It was found that patients with fluent aphasia are on average older than people with non-fluent aphasia. It was also found that among patients with lesions confined to the anterior portion of the brain an unexpected portion of them presented with fluent aphasia and were remarkably older than those with non-fluent aphasia. This effect was not found when the posterior portion of the brain was studied.Associated Conditions
In a study on the features associated with different disease trajectories in Alzheimers disease (AD)-related primary progressive aphasia (PPA), it was found that metabolic patterns via PET SPM analysis can help predict progression of total loss of speech and functional autonomy in AD and PPA patients. This was done by comparing an MRI or CT image of the brain and presence of a radioactive biomarker with normal levels in patients without Alzheimer’s Disease. Apraxia is another disorder often correlated with aphasia. This is due to a subset of apraxia which affects speech. Specifically, this subset affects the movement of muscles associated with speech production, apraxia and aphasia are often correlated due to the proximity of neural substrates associated with each of the disorders. Researchers concluded that there were 2 areas of lesion overlap between patients with apraxia and aphasia, the anterior temporal lobe and the left inferior parietal lobe.Treatment and Neuroimaging
Evidence for positive treatment outcomes can also be quantified using neuroimaging tools. The use of fMRI and an automatic classifier can help predict language recovery outcomes in stroke patients with 86% accuracy when coupled with age and language test scores. The stimuli tested were sentences both correct and incorrect and the subject had to press a button whenever the sentence was incorrect. The fMRI data collected focused on responses in regions of interest identified by healthy subjects.   Recovery from aphasia can also be quantified using diffusion tensor imaging. The accurate fasciculus (AF) connects the right and left superior temporal lobe, premotor regions/posterior inferior frontal gyrus </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Thigh and can you explain it in depth? [/INST] In human anatomy, the thigh is the area between the hip (pelvis) and the knee. Anatomically, it is part of the lower limb.The single bone in the thigh is called the femur. This bone is very thick and strong (due to the high proportion of bone tissue), and forms a ball and socket joint at the hip, and a modified hinge joint at the knee.

Structure
Bones
The femur is the only bone in the thigh and serves as an attachment site for all muscles in the thigh. The head of the femur articulates with the acetabulum in the pelvic bone forming the hip joint, while the distal part of the femur articulates with the tibia and patella forming the knee </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Rheumatism and can you explain it in depth? [/INST] Rheumatism or rheumatic disorders are conditions causing chronic, often intermittent pain affecting the joints or connective tissue. Rheumatism does not designate any specific disorder, but covers at least 200 different conditions, including arthritis and  "non-articular rheumatism", also known as "regional pain syndrome" or "soft tissue rheumatism". There is a close overlap between the term soft tissue disorder and rheumatism. Sometimes the term "soft tissue rheumatic disorders" is used to describe these conditions.The term "Rheumatic Diseases" is used in MeSH to refer to connective tissue disorders. The branch of medicine devoted to the diagnosis and therapy of rheumatism is called rheumatology.

Types
Many rheumatic disorders of chronic, intermittent pain (including joint pain, neck pain or back pain) have historically been caused by infectious diseases. Their etiology was unknown until the 20th century and not treatable. Postinfectious arthritis, also known as reactive arthritis, and rheumatic fever are other examples.
In the United States, major rheumatic disorders are divided into 10 major categories based on the nomenclature and classification proposed by the American College of Rheumatology (ACR) in 1983.
Diffuse connective tissue diseases
Rheumatoid arthritis
Juvenile arthritis
Systemic lupus erythematosus
Sjögren syndrome
Scleroderma
Polymyositis
Dermatomyositis
Behçets disease
Relapsing polychondritis
Arthritis associated with spondylitis (i.e. spondarthritis)
Ankylosing spondylitis
Reactive arthritis
Psoriatic arthritis
Osteoarthritis (i.e. osteoarthrosis, degenerative joint disease)
Rheumatic syndromes associated with infectious agents (direct and indirect or reactive)
Metabolic and endocrine diseases associated with rheumatic states
Gout, pseudogout
Neoplasms
Neurovascular disorders
Bone and cartilage disorders
Extraarticular disorders
Bursitis/Tendinitis of the shoulder, wrist, biceps, leg, knee cap (patella), ankle, hip, and Achilles tendon
Capsulitis
Miscellaneous disorders associated with articular manifestations
Palindromic rheumatism is thought to be a form of rheumatoid arthritis.

Diagnosis
Blood and urine tests will measure levels of creatinine and uric acid to determine kidney function, an elevation of the ESR and CRP is possible. After a purine-restricted diet, another urine test will help determine whether the body is producing too much uric acid or the body isnt excreting enough uric acid </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Bandemia and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Peritoneal cavity and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Polyphagia and can you explain it in depth? [/INST] Polyphagia or hyperphagia is an abnormally strong, incessant sensation of hunger or desire to eat often leading to overeating. In contrast to an increase in appetite following exercise, polyphagia does not subside after eating and often leads to rapid intake of excessive quantities of food </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Arteriovenous fistula and can you explain it in depth? [/INST] An arteriovenous fistula is an abnormal connection or passageway between an artery and a vein. It may be congenital, surgically created for hemodialysis treatments, or acquired due to pathologic process, such as trauma or erosion of an arterial aneurysm.

Clinical features
Pathological
Hereditary hemorrhagic telangiectasia is a condition where there is direct connection between arterioles and venules without intervening capillary beds, at the mucocutaneous region and internal bodily organs. Those who are affected by this conditions usually do not experience any symptoms. Difficulty in breathing is the most common symptom for those who experience symptoms.Just like berry aneurysm, a cerebral arteriovenous malformation can rupture causing subarachnoid hemorrhage.

Causes
The cause of this condition include
Congenital (developmental defect)
Rupture of arterial aneurysm into an adjacent vein
Penetrating injuries
Inflammatory necrosis of adjacent vessels
Complication of catheter insertion rarely causes arteriovenous fistula. It is usually caused by brachial artery puncture because brachial artery is located between two brachial veins.Surgically created Cimino fistula is used as a vascular access for hemodialysis. Blood must be aspirated from the body of the patient, and since arteries are not easy to reach compared to the veins, blood may be aspirated from veins. The problem is that the walls of the veins are thin compared to those of the arteries. The AV fistula is the solution for this problem because, after 4–6 weeks, the walls of the veins become thicker due to the high arterial pressure. Thus, this vein can now tolerate needles during hemodialysis sessions.

Mechanism
When an arteriovenous fistula is formed involving a major artery like the abdominal aorta, it can lead to a large decrease in peripheral resistance </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Smear and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Avalanche and can you explain it in depth? [/INST] An avalanche  is a rapid flow of snow down a slope, such as a hill or mountain.Avalanches can be set off spontaneously, by such factors as increased precipitation or snowpack weakening, or by external means such as humans, animals, and earthquakes. Primarily composed of flowing snow and air, large avalanches have the capability to capture and move ice, rocks, and trees.
Avalanches occur in two general forms, or combinations thereof: slab avalanches made of tightly packed snow, triggered by a collapse of an underlying weak snow layer, and loose snow avalanches made of looser snow. After being set off, avalanches usually accelerate rapidly and grow in mass and volume as they capture more snow. If an avalanche moves fast enough, some of the snow may mix with the air, forming a powder snow avalanche.
Though they appear to share similarities, avalanches are distinct from slush flows, mudslides, rock slides, and serac collapses. They are also different from large scale movements of ice.
Avalanches can happen in any mountain range that has an enduring snowpack. They are most frequent in winter or spring, but may occur at any time of year. In mountainous areas, avalanches are among the most serious natural hazards to life and property, so great efforts are made in avalanche control.
There are many classification systems for the different forms of avalanches, which vary according to their users needs. Avalanches can be described by their size, destructive potential, initiation mechanism, composition, and dynamics.

Formation
Most avalanches occur spontaneously during storms under increased load due to snowfall and/or erosion. The second largest cause of natural avalanches is metamorphic changes in the snowpack such as melting due to solar radiation. Other natural causes include rain, earthquakes, rockfall and icefall. Artificial triggers of avalanches include skiers, snowmobiles, and controlled explosive work. Contrary to popular belief, avalanches are not triggered by loud sound; the pressure from sound is orders of magnitude too small to trigger an avalanche.Avalanche initiation can start at a point with only a small amount of snow moving initially; this is typical of wet snow avalanches or avalanches in dry unconsolidated snow. However, if the snow has sintered into a stiff slab overlying a weak layer then fractures can propagate very rapidly, so that a large volume of snow, that may be thousands of cubic metres, can start moving almost simultaneously.
A snowpack will fail when the load exceeds the strength. The load is straightforward; it is the weight of the snow. However, the strength of the snowpack is much more difficult to determine and is extremely heterogeneous. It varies in detail with properties of the snow grains, size, density, morphology, temperature, water content; and the properties of the bonds between the grains. These properties may all metamorphose in time according to the local humidity, water vapour flux, temperature and heat flux. The top of the snowpack is also extensively influenced by incoming radiation and the local air flow. One of the aims of avalanche research is to develop and validate computer models that can describe the evolution of the seasonal snowpack over time. A complicating factor is the complex interaction of terrain and weather, which causes significant spatial and temporal variability of the depths, crystal forms, and layering of the seasonal snowpack.

Slab avalanches
Slab avalanches form frequently in snow that has been deposited, or redeposited by wind. They have the characteristic appearance of a block (slab) of snow cut out from its surroundings by fractures. Elements of slab avalanches include the following: a crown fracture at the top of the start zone, flank fractures on the sides of the start zones, and a fracture at the bottom called the stauchwall. The crown and flank fractures are vertical walls in the snow delineating the snow that was entrained in the avalanche from the snow that remained on the slope. Slabs can vary in thickness from a few centimetres to three metres. Slab avalanches account for around 90% of avalanche-related fatalities in backcountry users.

Powder snow avalanches
The largest avalanches form turbulent suspension currents known as powder snow avalanches or mixed avalanches, a kind of gravity current. These consist of a powder cloud, which overlies a dense avalanche. They can form from any type of snow or initiation mechanism, but usually occur with fresh dry powder. They can exceed speeds of 300 km/h (190 mph), and masses of 10,000,000 tonnes; their flows can travel long distances along flat valley bottoms and even uphill for short distances.

Wet snow avalanches
In contrast to powder snow avalanches, wet snow avalanches are a low velocity suspension of snow and water, with the flow confined to the track surface (McClung, first edition 1999, page 108). The low speed of travel is due to the friction between the sliding surface of the track and the water saturated flow. Despite the low speed of travel (≈10–40 km/h), wet snow avalanches are capable of generating powerful destructive forces, due to the large mass and density. The body of the flow of a wet snow avalanche can plough through soft snow, and can scour boulders, earth, trees, and other vegetation; leaving exposed and often scored ground in the avalanche track. Wet snow avalanches can be initiated from either loose snow releases, or slab releases, and only occur in snowpacks that are water saturated and isothermally equilibrated to the melting point of water. The isothermal characteristic of wet snow avalanches has led to the secondary term of isothermal slides found in the literature (for example in Daffern, 1999, page 93). At temperate latitudes wet snow avalanches are frequently associated with climatic avalanche cycles at the end of the winter season, when there is significant daytime warming.

Ice avalanche
An ice avalanche occurs when a large piece of ice, such as from a serac or calving glacier, falls onto ice (such as the Khumbu Icefall), triggering a movement of broken ice chunks. The resulting movement is more analogous to a rockfall or a landslide than a snow avalanche. They are typically very difficult to predict and almost impossible to mitigate.

Avalanche pathway
As an avalanche moves down a slope it follows a certain pathway that is dependent on the slopes degree of steepness and the volume of snow/ice involved in the mass movement. The origin of an avalanche is called the Starting Point and typically occurs on a 30–45 degree slope. The body of the pathway is called the Track of the avalanche and usually occurs on a 20–30 degree slope. When the avalanche loses its momentum and eventually stops it reaches the Runout Zone. This usually occurs when the slope has reached a steepness that is less than 20 degrees. These degrees are not consistently true due to the fact that each avalanche is unique depending on the stability of the snowpack that it was derived from as well as the environmental or human influences that triggered the mass movement.

Injuries and deaths
People caught in avalanches can die from suffocation, trauma, or hypothermia.
From "1950 - 1951 to 2020 - 2021" there were 1,169 people who died in avalanches in the United states.  For the 11-year period ending April 2006 445 people died in avalanches throughout North America. On average, 28 people die in avalanches every winter in the United States.In 2001 it was reported that globally an average of 150 people die each year from avalanches. Three of the deadliest recorded avalanches have killed over a thousand people each.

Terrain, snowpack, weather
Doug Fesler and Jill Fredston developed a conceptual model of the three primary elements of avalanches: terrain, weather, and snowpack. Terrain describes the places where avalanches occur, weather describes the meteorological conditions that create the snowpack, and snowpack describes the structural characteristics of snow that make avalanche formation possible.

Terrain
Avalanche formation requires a slope shallow enough for snow to accumulate but steep enough for the snow to accelerate once set in motion by the combination of mechanical failure (of the snowpack) and gravity. The angle of the slope that can hold snow, called the angle of repose, depends on a variety of factors such as crystal form and moisture content. Some forms of drier and colder snow will only stick to shallower slopes, while wet and warm snow can bond to very steep surfaces. In particular, in coastal mountains, such as the Cordillera del Paine region of Patagonia, deep snowpacks collect on vertical and even overhanging rock faces. The slope angle that can allow moving snow to accelerate depends on a variety of factors such as the snows shear strength (which is itself dependent upon crystal form) and the configuration of layers and inter-layer interfaces.
The snowpack on slopes with sunny exposures is strongly influenced by sunshine. Diurnal cycles of thawing and refreezing can stabilize the snowpack by promoting settlement. Strong freeze-thaw cycles result in the formation of surface crusts during the night and of unstable surface snow during the day. Slopes in the lee of a ridge or of another wind obstacle accumulate more snow and are more likely to include pockets of deep snow, wind slabs, and cornices, all of which, when disturbed, may result in avalanche formation. Conversely, the snowpack on a windward slope is often much shallower than on a lee slope.

Avalanches and avalanche paths share common elements: a start zone where the avalanche originates, a track along which the avalanche flows, and a runout zone where the avalanche comes to rest. The debris deposit is the accumulated mass of the avalanched snow once it has come to rest in the run-out zone. For the image at left, many small avalanches form in this avalanche path every year, but most of these avalanches do not run the full vertical or horizontal length of the path. The frequency with which avalanches form in a given area is known as the return period.
The start zone of an avalanche must be steep enough to allow snow to accelerate once set in motion, additionally convex slopes are less stable than concave slopes, because of the disparity between the tensile strength of snow layers and their compressive strength. The composition and structure of the ground surface beneath the snowpack influences the stability of the snowpack, either being a source of strength or weakness. Avalanches are unlikely to form in very thick forests, but boulders and sparsely distributed vegetation can create weak areas deep within the snowpack through the formation of strong temperature gradients. Full-depth avalanches (avalanches that sweep a slope virtually clean of snow cover) are more common on slopes with smooth ground, such as grass or rock slabs.
Generally speaking, avalanches follow drainages down-slope, frequently sharing drainage features with summertime watersheds. At and below tree line, avalanche paths through drainages are well defined by vegetation boundaries called trim lines, which occur where avalanches have removed trees and prevented regrowth of large vegetation. Engineered drainages, such as the avalanche dam on Mount Stephen in Kicking Horse Pass, have been constructed to protect people and property by redirecting the flow of avalanches. Deep debris deposits from avalanches will collect in catchments at the terminus of a run out, such as gullies and river beds.
Slopes flatter than 25 degrees or steeper than 60 degrees typically have a lower incidence of avalanches. Human-triggered avalanches have the greatest incidence when the snows angle of repose is between 35 and 45 degrees; the critical angle, the angle at which human-triggered avalanches are most frequent, is 38 degrees. When the incidence of human triggered avalanches is normalized by the rates of recreational use, however, hazard increases uniformly with slope angle, and no significant difference in hazard for a given exposure direction can be found.  The rule of thumb is: A slope that is flat enough to hold snow but steep enough to ski has the potential to generate an avalanche, regardless of the angle.

Snowpack structure and characteristics
The snowpack is composed of ground-parallel layers that accumulate over the winter. Each layer contains ice grains that are representative of the distinct meteorological conditions during which the snow formed and was deposited. Once deposited, a snow layer continues to evolve under the influence of the meteorological conditions that prevail after deposition.
For an avalanche to occur, it is necessary that a snowpack have a weak layer (or instability) below a slab of cohesive snow. In practice the formal mechanical and structural factors related to snowpack instability are not directly observable outside of laboratories, thus the more easily observed properties of the snow layers (e.g. penetration resistance, grain size, grain type, temperature) are used as index measurements of the mechanical properties of the snow (e.g. tensile strength, friction coefficients, shear strength, and ductile strength). This results in two principal sources of uncertainty in determining snowpack stability based on snow structure: First, both the factors influencing snow stability and the specific characteristics of the snowpack vary widely within small areas and time scales, resulting in significant difficulty extrapolating point observations of snow layers across different scales of space and time. Second, the relationship between readily observable snowpack characteristics and the snowpacks critical mechanical properties has not been completely developed.
While the deterministic relationship between snowpack characteristics and snowpack stability is still a matter of ongoing scientific study, there is a growing empirical understanding of the snow composition and deposition characteristics that influence the likelihood of an avalanche. Observation and experience has shown that newly fallen snow requires time to bond with the snow layers beneath it, especially if the new snow falls during very cold and dry conditions. If ambient air temperatures are cold enough, shallow snow above or around boulders, plants, and other discontinuities in the slope, weakens from rapid crystal growth that occurs in the presence of a critical temperature gradient. Large, angular snow crystals are indicators of weak snow, because such crystals have fewer bonds per unit volume than small, rounded crystals that pack tightly together. Consolidated snow is less likely to slough than loose powdery layers or wet isothermal snow; however, consolidated snow is a necessary condition for the occurrence of slab avalanches, and persistent instabilities within the snowpack can hide below well-consolidated surface layers. Uncertainty associated with the empirical understanding of the factors influencing snow stability leads most professional avalanche workers to recommend conservative use of avalanche terrain relative to current snowpack instability.

Weather
Avalanches only occur in a standing diksnowpack. Typically winter seasons at high latitudes, high altitudes, or both have weather that is sufficiently unsettled and cold enough for precipitated snow to accumulate into a seasonal snowpack. Continentality, through its potentiating influence on the meteorological extremes experienced by snowpacks, is an important factor in the evolution of instabilities, and consequential occurrence of avalanches faster stabilization of the snowpack after storm cycles. The evolution of the snowpack is critically sensitive to small variations within the narrow range of meteorological conditions that allow for the accumulation of snow into a snowpack. Among the critical factors controlling snowpack evolution are: heating by the sun, radiational cooling, vertical temperature gradients in standing snow, snowfall amounts, and snow types. Generally, mild winter weather will promote the settlement and stabilization of the snowpack; conversely, very cold, windy, or hot weather will weaken the snowpack.
At temperatures close to the freezing point of water, or during times of moderate solar radiation, a gentle freeze-thaw cycle will take place. The melting and refreezing of water in the snow strengthens the snowpack during the freezing phase and weakens it during the thawing phase. A rapid rise in temperature, to a point significantly above the freezing point of water, may cause avalanche formation at any time of year.
Persistent cold temperatures can either prevent new snow from stabilizing or destabilize the existing snowpack. Cold air temperatures on the snow surface produce a temperature gradient in the snow, because the ground temperature at the base of the snowpack is usually around 0 °C, and the ambient air temperature can be much colder. When a temperature gradient greater than 10 °C change per vertical meter of snow is sustained for more than a day, angular crystals called depth hoar or facets begin forming in the snowpack because of rapid moisture transport along the temperature gradient. These angular crystals, which bond poorly to one another and the surrounding snow, often become a persistent weakness in the snowpack. When a slab lying on top of a persistent weakness is loaded by a force greater than the strength of the slab and persistent weak layer, the persistent weak layer can fail and generate an avalanche.
Any wind stronger than a light breeze can contribute to a rapid accumulation of snow on sheltered slopes downwind. Wind slabs form quickly and, if present, weaker snow below the slab may not have time to adjust to the new load. Even on a clear day, wind can quickly load a slope with snow by blowing snow from one place to another. Top-loading occurs when wind deposits snow from the top of a slope; cross-loading occurs when wind deposits snow parallel to the slope. When a wind blows over the top of a mountain, the leeward, or downwind, side of the mountain experiences top-loading, from the top to the bottom of that lee slope. When the wind blows across a ridge that leads up the mountain, the leeward side of the ridge is subject to cross-loading. Cross-loaded wind-slabs are usually difficult to identify visually.
Snowstorms and rainstorms are important contributors to avalanche danger. Heavy snowfall will cause instability in the existing snowpack, both because of the additional weight and because the new snow has insufficient time to bond to underlying snow layers. Rain has a similar effect. In the short-term, rain causes instability because, like a heavy snowfall, it imposes an additional load on the snowpack; and, once rainwater seeps down through the snow, it acts as a lubricant, reducing the natural friction between snow layers that holds the snowpack together. Most avalanches happen during or soon after a storm.
Daytime exposure to sunlight will rapidly destabilize the upper layers of the snowpack if the sunlight is strong enough to melt the snow, thereby reducing its hardness. During clear nights, the snowpack can re-freeze when ambient air temperatures fall below freezing, through the process of long-wave radiative cooling, or both. Radiative heat loss occurs when the night air is significantly cooler than the snowpack, and the heat stored in the snow is re-radiated into the atmosphere.

Dynamics
When a slab avalanche forms, the slab disintegrates into increasingly smaller fragments as the snow travels downhill. If the fragments become small enough the outer layer of the avalanche, called a saltation layer, takes on the characteristics of a fluid. When sufficiently fine particles are present they can become airborne and, given a sufficient quantity of airborne snow, this portion of the avalanche can become separated from the bulk of the avalanche and travel a greater distance as a powder snow avalanche. Scientific studies using radar, following the 1999 Galtür avalanche disaster, confirmed the hypothesis that a saltation layer forms between the surface and the airborne components of an avalanche, which can also separate from the bulk of the avalanche.Driving an avalanche is the component of the avalanches weight parallel to the slope; as the avalanche progresses any unstable snow in its path will tend to become incorporated, so increasing the overall weight. This force will increase as the steepness of the slope increases, and diminish as the slope flattens. Resisting this are a number of components that are thought to interact with each other: the friction between the avalanche and the surface beneath; friction between the air and snow within the fluid; fluid-dynamic drag at the leading edge of the avalanche; shear resistance between the avalanche and the air through which it is passing, and shear resistance between the fragments within the avalanche itself. An avalanche will continue to accelerate until the resistance exceeds the forward force.

Modelling
Attempts to model avalanche behaviour date from the early 20th century, notably the work of Professor Lagotala in preparation for the 1924 Winter Olympics in Chamonix. His method was developed by A. Voellmy and popularised following the publication in 1955 of his Ueber die Zerstoerungskraft von Lawinen (On the Destructive Force of Avalanches).Voellmy used a simple empirical formula, treating an avalanche as a sliding block of snow moving with a drag force that was proportional to the square of the speed of its flow:

            Pref

        =

            1
            2

          ρ

            v

              2

    {\displaystyle {\textrm {Pref}}={\frac {1}{2}}\,{\rho }\,{v^{2}}\,\!}
  He and others subsequently derived other formulae that take other factors into account, with the Voellmy-Salm-Gubler and the Perla-Cheng-McClung models becoming most widely used as simple tools to model flowing (as opposed to powder snow) avalanches.Since the 1990s many more sophisticated models have been developed. In Europe much of the recent work was carried out as part of the SATSIE (Avalanche Studies and Model Validation in Europe) research project supported by the European Commission which produced the leading-edge MN2L model, now in use with the Service Restauration des Terrains en Montagne (Mountain Rescue Service) in France, and D2FRAM (Dynamical Two-Flow-Regime Avalanche Model), which was still undergoing validation as of 2007. Other known models are the SAMOS-AT avalanche simulation software and the RAMMS software.

Human involvement
Prevention
Preventative measures are employed in areas where avalanches pose a significant threat to people, such as ski resorts, mountain towns, roads, and railways. There are several ways to prevent avalanches and lessen their power and develop preventative measures to reduce the likelihood and size of avalanches by disrupting the structure of the snowpack, while passive measures reinforce and stabilize the snowpack in situ. The simplest active measure is repeatedly traveling on a snowpack as snow accumulates; this can be by means of boot-packing, ski-cutting, or machine grooming. Explosives are used extensively to prevent avalanches, by triggering smaller avalanches that break down instabilities in the snowpack, and removing overburden that can result in larger avalanches. Explosive charges are delivered by a number of methods including hand-tossed charges, helicopter-dropped bombs, Gazex concussion lines, and ballistic projectiles launched by air cannons and artillery. Passive preventive systems such as snow fences and light walls can be used to direct the placement of snow. Snow builds up around the fence, especially the side that faces the prevailing winds. Downwind of the fence, snow build-up is lessened. This is caused by the loss of snow at the fence that would have been deposited and the pickup of the snow that is already there by the wind, which was depleted of snow at the fence. When there is a sufficient density of trees, they can greatly reduce the strength of avalanches. They hold snow in place and when there is an avalanche, the impact of the snow against the trees slows it down. Trees can either be planted or they can be conserved, such as in the building of a ski resort, to reduce the strength of avalanches.
In turn, socio-environmental changes can influence the occurrence of damaging avalanches: some studies linking changes in land-use/land-cover patterns and the evolution of snow avalanche damage in mid latitude mountains show the importance of the role played by vegetation cover, that is at the root of the increase of damage  when the protective forest is deforested (because of demographic growth, intensive grazing and industrial or legal causes), and at the root of the decrease of damage because of the transformation of a traditional land-management system based on overexploitation into a system based on land marginalization and reforestation, something that has happened mainly since the mid-20th century in mountain environments of developed countries

Mitigation
In many areas, regular avalanche tracks can be identified and precautions can be taken to minimize damage, such as the prevention of development in these areas. To mitigate the effect of avalanches the construction of artificial barriers can be very effective in reducing avalanche damage. There are several types: One kind of barrier (snow net) uses a net strung between poles that are anchored by guy wires in addition to their foundations. These barriers are similar to those used for rockslides. Another type of barrier is a rigid fence-like structure (snow fence) and may be constructed of steel, wood or pre-stressed concrete. They usually have gaps between the beams and are built perpendicular to the slope, with reinforcing beams on the downhill side. Rigid barriers are often considered unsightly, especially when many rows must be built. They are also expensive and vulnerable to damage from falling rocks in the warmer months. In addition to industrially manufactured barriers, landscaped barriers, called avalanche dams stop or deflect avalanches with their weight and strength. These barriers are made out of concrete, rocks, or earth. They are usually placed right above the structure, road, or railway that they are trying to protect, although they can also be used to channel avalanches into other barriers. Occasionally, earth mounds are placed in the avalanches path to slow it down. Finally, along transportation corridors, large shelters, called snow sheds, can be built directly in the slide path of an avalanche to protect traffic from avalanches.

Early warning systems
Warning systems can detect avalanches which develop slowly, such as ice avalanches caused by icefalls from glaciers. Interferometric radars, high-resolution cameras, or motion sensors can monitor instable areas over a long term, lasting from days to years. Experts interpret the recorded data and are able to recognize upcoming ruptures in order to initiate appropriate measures. Such systems (e.g. the monitoring of the Weissmies glacier in Switzerland) can recognize events several days in advance.

Alarm systems
Modern radar technology enables the monitoring of large areas and the localization of avalanches at any weather condition, by day and by night. Complex alarm systems are able to detect avalanches within a short time in order to close (e.g. roads and rails) or evacuate (e.g. construction sites) endangered areas. An example of such a system is installed on the only access road of Zermatt in Switzerland. Two radars monitor the slope of a mountain above the road. The system automatically closes the road by activating several barriers and traffic lights within seconds such that no people are harmed.

Survival, rescue, and recovery
Avalanche accidents are broadly differentiated into 2 categories: accidents in recreational settings, and accidents in residential, industrial, and transportation settings. This distinction is motivated by the observed difference in the causes of avalanche accidents in the two settings. In the recreational setting most accidents are caused by the people involved in the avalanche. In a 1996 study, Jamieson et al. (pages 7–20) found that 83% of all avalanches in the recreational setting were caused by those who were involved in the accident. In contrast, all of the accidents in the residential, industrial, and transportation settings were due to spontaneous natural avalanches. Because of the difference in the causes of avalanche accidents, and the activities pursued in the two settings, avalanche and disaster management professionals have developed two related preparedness, rescue, and recovery strategies for each of the settings.

Notable avalanches
Two avalanches occurred in March 1910 in the Cascade and Selkirk Mountain ranges; On 1 March the Wellington avalanche killed 96 in Washington state, United States. Three days later 62 railroad workers were killed in the Rogers Pass avalanche in British Columbia, Canada.
During World War I, an estimated 40,000 to 80,000 soldiers died as a result of avalanches during the mountain campaign in the Alps at the Austrian-Italian front, many of which were caused by artillery fire. Some 10,000 men, from both sides, lost their lives in avalanches in December 1916.In the northern hemisphere winter of 1950–1951 approximately 649 avalanches were recorded in a three-month period throughout the Alps in Austria, France, Switzerland, Italy and Germany. This series of avalanches killed around 265 people and was termed the Winter of Terror.
A mountain climbing camp on Lenin Peak, in what is now Kyrgyzstan, was wiped out in 1990 when an earthquake triggered a large avalanche that overran the camp. Forty-three climbers were killed.In 1993, the Bayburt Üzengili avalanche killed 60 individuals in Üzengili in the province of Bayburt, Turkey.
A large avalanche in Montroc, France, in 1999, 300,000 cubic metres of snow slid on a 30° slope, achieving a speed in the region of  100 km/h (62 mph). It killed 12 people in their chalets under 100,000 tons of snow, 5 meters (16 feet) deep. The mayor of Chamonix was convicted of second-degree murder for not evacuating the area, but received a suspended sentence.The small Austrian village of Galtür was hit by the Galtür avalanche in 1999. The village was thought to be in a safe zone but the avalanche was exceptionally large and flowed into the village. Thirty-one people died.
On 1 December 2000, the Glory Bowl Avalanche formed on Mt. Glory which is located within the Teton Mountain Range in Wyoming, United States. Joel Roof was snowboarding recreationally in this backcountry, bowl-shaped run and triggered the avalanche. He was carried nearly 2,000 feet to the base of the mountain and was not successfully rescued.

Classification
European avalanche risk
In Europe, the avalanche risk is widely rated on the following scale, which was adopted in April 1993 to replace the earlier non-standard national schemes. Descriptions were last updated in May 2003 to enhance uniformity.In France, most avalanche deaths occur at risk levels 3 and 4. In Switzerland most occur at levels 2 and 3. It is thought that this may be due to national differences of interpretation when assessing the risks.
[1] Stability:

Generally described in more detail in the avalanche bulletin (regarding the altitude, aspect, type of terrain etc.)[2] additional load:

heavy: two or more skiers or boarders without spacing between them, a single hiker or climber, a grooming machine, avalanche blasting
light: a single skier or snowboarder smoothly linking turns and without falling, a group of skiers or snowboarders with a minimum 10 m gap between each person, a single person on snowshoesGradient:

gentle slopes: with an incline below about 30°
steep slopes: with an incline over 30°
very steep slopes: with an incline over 35°
extremely steep slopes: extreme in terms of the incline (over 40°), the terrain profile, proximity of the ridge, smoothness of underlying ground

European avalanche size table
Avalanche size:

North American Avalanche Danger Scale
In the United States and Canada, the following avalanche danger scale is used. Descriptors vary depending on country.

Avalanche Problems
There are nine different types of avalanche problems:
Storm slab
Wind slab
Wet slab avalanches
Persistent slab
Deep persistent slab
Loose dry avalanches
Loose wet avalanches
Glide avalanches
Cornice fall

Canadian classification for avalanche size
The Canadian classification for avalanche size is based upon the consequences of the avalanche. Half sizes are commonly used.

United States classification for avalanche size
The size of avalanches are classified using two scales; size relative to destructive force or D-scale and size relative to the avalanche path or R-scale. Both size scales range from 1 to 5 with the D size scale half sizes can be used.

Rutschblock Test
Slab avalanche hazard analysis can be done using the Rutschblock Test. A 2 m wide block of snow is isolated from the rest of the slope and progressively loaded. The result is a rating of slope stability on a seven step scale.
(Rutsch means slide in German).

Avalanches and climate change
Avalanche formation and frequency is highly affected by weather patterns and the local climate. Snowpack layers will form differently depending on whether snow is falling in very cold or very warm conditions, and very dry or very humid conditions.  Thus, climate change may affect when, where, and how often avalanches occur, and may also change the type of avalanches that are occurring.

Impacts on avalanche type and frequency
Overall, a rising seasonal snow line and a decrease in the number of days with snow cover are predicted. Climate change-caused temperature increases and changes in precipitation patterns will likely differ between the different mountain regions, and the impacts of these changes on avalanches will change at different elevations. In the long term, avalanche frequency at lower elevations is expected to decline corresponding to a decrease in snow cover and depth, and a short-term increase in the number of wet avalanches are predicted.Precipitation is expected to increase, meaning more snow or rain depending on the elevation. Higher elevations predicted to remain above the seasonal snow line will likely see an increase in avalanche activity due to the increases in precipitation during the winter season. Storm precipitation intensity is also expected to increase, which is likely to lead to more days with enough snowfall to cause the snowpack to become unstable. Moderate and high elevations may see an increase in volatile swings from one weather extreme to the other. Predictions also show an increase in the number of rain on snow events, and wet avalanche cycles occurring earlier in the spring during the remainder of this century.

Impacts on burial survival rate
The warm, wet snowpacks that are likely to increase in frequency due to climate change may also make avalanche burials more deadly. Warm snow has a higher moisture content and is therefore denser than colder snow. Denser avalanche debris decreases the ability for a buried person to breath and the amount of time they have before they run out of oxygen. This increases the likelihood of death by asphyxia in the event of a burial. Additionally, the predicted thinner snowpacks may increase the frequency of injuries due to trauma, such as a buried skier striking a rock or tree.

Avalanches on the planet Mars
See also
Related flows
Avalanche disasters
1999 Galtür avalanche
Montroc
2012 Gayari Sector avalanche

References
Bibliography
McClung, David. Snow Avalanches as a Non-critical, Punctuated Equilibrium System: Chapter 24 in Nonlinear Dynamics in Geosciences, A.A. Tsonsis and J.B. Elsner (Eds.), Springer, 2007
Daffern, Tony: Avalanche Safety for Skiers, Climbers and Snowboarders, Rocky Mountain Books, 1999, ISBN 0-921102-72-0
Billman, John: Mike Elggren on Surviving an Avalanche </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Sacroiliitis and can you explain it in depth? [/INST] Sacroiliitis is inflammation within the sacroiliac joint. It is a feature of spondyloarthropathies, such as axial spondyloarthritis (including ankylosing spondylitis), psoriatic arthritis, reactive arthritis or arthritis related to inflammatory bowel diseases, including ulcerative colitis or Crohns disease. It is also the most common presentation of arthritis from brucellosis.

Symptoms and signs
People suffering from sacroiliitis can often experience symptoms in a number of different ways, however it is commonly related to the amount of pressure that is put onto the sacroiliac joint. Sacroiliitis pain is typically axial, meaning that the location of the condition is also where the pain is occurring. Symptoms commonly include prolonged, inflammatory pain in the lower back region, hips or buttocks.However, in more severe cases, pain can become more radicular and manifest itself in seemingly unrelated areas of the body including the legs, groin and feet.Symptoms are typically aggravated by:
Transitioning from sitting to standing
Walking or standing for extended periods of time
Running
Climbing stairs
Taking long strides
Rolling over in bed
Bearing more weight on one leg

Cause
Sacroiliitis is a condition caused by inflammation within the sacroiliac joint. This joint is located where the base of the spine, known as the sacrum, and the pelvis, known as the ilium, intersect. "Itis" is a Latin term denoting inflammation.Since sacroiliitis can describe any type of inflammation found within the sacroiliac joint, there can be a number of issues that cause it. These include:
Degenerative arthritis, or osteoarthritis of the spine, can cause degeneration within the sacroiliac joints and lead to inflammation and joint pain.
Any form of spondyloarthropathies, which includes ankylosing spondylitis, psoriatic arthritis, reactive arthritis or arthritis related to inflammatory bowel diseases, including ulcerative colitis or Crohns disease.
Pregnancy can cause inflammation as a result of the widening and stretching of the sacroiliac joints to prepare for childbirth. Additionally, the added weight carried during childbearing can put an extra amount of stress on the SI joints, leading to abnormal wear.
Traumatic injury such as a fall or car crash that affects the lower back, hips, buttocks or legs.

Though rare, infection within the sacroiliac joints or another part of the body, such as a urinary tract infection, can cause inflammation.

Diagnosis
Sacroiliitis can be somewhat difficult to diagnose because the symptoms it manifests can also be caused by other, more common, conditions. If a physician suspects sacroiliitis, they will typically begin their diagnosis by performing a physical exam </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Cerebral atherosclerosis and can you explain it in depth? [/INST] Cerebral atherosclerosis is a type of atherosclerosis where build-up of plaque in the blood vessels of the brain occurs. Some of the main components of the plaques are connective tissue, extracellular matrix, including collagen, proteoglycans, fibronectin, and elastic fibers; crystalline cholesterol, cholesteryl esters, and phospholipids; cells such as monocyte derived macrophages, T-lymphocytes, and smooth muscle cells.  The plaque that builds up can lead to further complications such as stroke, as the plaque disrupts blood flow within the intracranial arterioles.  This causes the downstream sections of the brain that would normally be supplied by the blocked artery to suffer from ischemia. Diagnosis of the disease is normally done through imaging technology such as angiograms or magnetic resonance imaging. The risk of cerebral atherosclerosis and its associated diseases appears to increase with increasing age;  however there are numerous factors that can be controlled in attempt to lessen risk.

Diagnosis
Diagnostic methods include:

AngiogramDue to positive remodeling the plaque build-up shown on angiogram may appear further downstream on the x-ray where the luminal diameter would look normal even though there is severe narrowing at the real site. Because angiograms require x-rays to be visualized the number of times an individual can have it done over a year is limited by the guidelines for the amount of radiation they can be exposed to in a one-year period.

Magnetic resonance imaging (MRI)Magnetic resonance imaging has the ability to quantify the plaque anatomy and composition. This allows physicians to determine certain characteristics of the plaque such as how likely it is to break away from the wall and become an embolus. MRI does not use ionizing radiation, so the number of times that it is used on a single person is not a concern; however since it uses strong magnetic fields those who have metal implants cannot use this technique.
Computed tomography (CT)In the context of imaging cerebral atherosclerosis, multidirectional computed tomography (MDCT) is often superior to regular CT scans, because it can provide a higher spatial resolution and it has a shorter acquisition time. MDCT uses x-rays to obtain the image; however it can identify the composition of the plaque. Thus it can be determined whether the plaque is calcified plaque and lipid-rich plaque, so the inherent risks can be determined. Subjects are exposed to a substantial amount of radiation with this procedure, so their use is limited.

Treatment
Asymptomatic individuals with intracranial stenosis are typically told to take over the counter platelet inhibitors like aspirin whereas those with symptomatic presentation are prescribed anti-coagulation medications.  For asymptomatic persons the idea is to stop the buildup of plaque from continuing. They are not experiencing symptoms; however if more build up occurs it is likely they will. For symptomatic individuals it is necessary to try and reduce the amount of stenosis </s>