Amnesia

From Wikipedia, the free encyclopedia

For other uses, see Amnesia (disambiguation). "Amnesiac" redirects here. For the Radiohead album, see Amnesiac (album).

Amnesia

Classification and external resources

ICD-10

F04, R41.3

ICD-9

294.0, 780.9, 780.93

MedlinePlus

003257

MeSH

D000647

Amnesia (from Greek "a" meaning "without", "" memory) is a deficit in memory caused by brain damage, disease, or psychological trauma.[1] Amnesia can also be caused temporarily by the use of various sedatives and hypnotic drugs. Essentially, amnesia is loss of memory. The memory can be either wholly or partially lost due to the extent of damage that was caused.[2] There are two main types of amnesia: retrograde amnesia and anterograde amnesia. Retrograde amnesia is the inability to retrieve information that was acquired before a particular date, usually the date of an accident or operation.[3] In some cases the memory loss can extend back decades, while in others the person may lose only a few months of memory. Anterograde amnesia is the inability to transfer new information from the short-term store into the long-term store. People with this type of amnesia cannot remember things for long periods of time. These two types are not mutually exclusive. Both can occur within a patient at one time. Case studies, such as that of patient R.B., show that both types of amnesia can occur simultaneously. Case studies also show that amnesia is typically associated with damage to the medial temporal lobe. In addition, specific areas of the hippocampus (the CA1 region) are involved with memory. Research has also shown that when areas of the diencephalon are damaged, amnesia can occur. In people suffering with amnesia the ability to recall immediate information is still retained,[4][full citation needed] and they may still be able to form new memories. However, a severe reduction in the ability to learn new material and retrieve old information can be observed. Patients can learn new procedural knowledge. In addition, priming (both perceptual and conceptual) can assist amnesiacs in the learning of fresh non-declarative knowledge.[1] Amnesic patients also retain substantial intellectual, linguistic, and social skill despite profound impairments in the ability to recall specific information encountered in prior learning episodes.[5][6][7]
Contents
[hide]

1 Discovery

1.1 Important case studies

2 Causes 3 Types

1.1.1 Henry Molaison 1.1.2 Patient R.B.

4 Acquisition of new memories

o o

4.1 Acquisition of new declarative information 4.2 Acquisition of new non-declarative information

5 Treatment 6 See also 7 References

Discovery [edit]
French psychologist Theodule-Armand Ribot was among the first scientists to study amnesia. He proposed Ribot's Law which states that there is a time gradient in retrograde amnesia. The law follows a logical progression of memory-loss due to disease. First, a patient loses the recent memories, then personal memories, and finally intellectual memories. He implied that the most recent memories were lost first.[8]

Important case studies [edit]

Case studies played a large role in the discovery of amnesia and the parts of the brain that were affected. The studies gave important insight into how amnesia affects the brain. The studies also gave scientists the resources into improving their knowledge about amnesia and insight into a cure or prevention. There are two extremely important case studies: Henry Molaison and R.B.

Henry Molaison [edit]

Henry Molaison, formerly known as H.M., changed the way people thought of memory. He was a patient who suffered from severe epilepsy. Physicians were unable to control his seizures with drugs, so they tried a new approach involving brain surgery. Doctors removed his medial temporal lobe bilaterally by doing a temporal lobectomy. His epilepsy did improve, but Molaison lost the ability to form new long-term memories (anterograde amnesia). He exhibited normal short-term memory ability. If he was given a list of words, he would forget them in about a minute's time. In fact, he would forget that he was even given a list in the first place. He was able to learn things through his implicit memory. The psychologists would ask him to draw something on a piece of paper, but to look at the paper using a mirror. Though he could never remember ever doing that task, he would improve after doing it over and over again. This showed the psychologists that he was learning and remembering things unconsciously.[9] Studies were completed consistently throughout Molaisons lifetime to discover more about amnesia.[1] Researchers did a 14-year follow-up study on Molaison. They studied him for a period of two weeks to learn more about his amnesia. After 14 years, Molaison still could not recall things that have happened since his surgery. However, he can still remember things that happened prior to the operation. Researchers also found that, when asked, Molaison could answer

questions about national or international events, but he could not remember his own personal memories. [10] This case study provided important insight to the areas of the brain that are affected in anterograde amnesia, as well as how amnesia works.

Patient R.B. [edit]

After an ischemic episode (reduction of blood to the brain) that was caused from a heart bypass surgery, R.B. lost his memory. Unlike Molaison, R.B. developed both anterograde and retrograde amnesia. His lesions were restricted to the hippocampus. It wasnt until after his death that researchers had the chance to examine his brain. They found that his lesions were restricted to the CA1 portion of the hippocampus. This case study led to important research involving the role of the hippocampus and the function of memory.[11]

Causes [edit]
There are three generalized categories in which amnesia could be acquired by a person. The three categories are head trauma (example: head injuries), traumatic events (example: seeing something devastating to the mind), or physical deficiencies (example: atrophy of the hippocampus). The majority of amnesia and related memory issues derive from the first two categories as these are more common and the third could be considered a sub category of the first.

Head trauma is a very broad range as it deals with any kind of injury or active action toward the brain which might cause amnesia. Retrograde and Anterograde amnesia are more often seen from events like this, an exact example of a cause of the two would be electroshock therapy, which would cause both briefly for the receiving patient.

Traumatic events are more subjective. What is traumatic is dependent on what the person finds to be traumatic. Regardless, a traumatic event is an event where something so distressing occurs that the mind chooses to forget rather than deal with the stress. A common example of amnesia that is caused by traumatic events is dissociative amnesia, which occurs when the person forgets an event that has deeply disturbed them.[12] An example would be forgetting what happened to your friends after you see them harmed in a gruesome fashion.

Physical deficiencies are different from head trauma as physical lean more toward passive physical issues. The difference would be having surgery that removes part of your brain, this would be active and thus head trauma, while the surgery caused the surrounding areas to atrophy, which is passive. Henry Molaison is a great example of physical deficiencies as parts of his brain began to atrophy after his surgery.[1]

Amongst specific causes of amnesia are the following:

Electroconvulsive therapy in which seizures are electrically induced in patients for therapeutic effect can have acute effects including both retrograde and anterograde amnesia.[13]

Alcohol can both cause blackouts[14] and have deleterious effects on memory formation.[15]

Types [edit]

Anterograde amnesia refers to the inability to create new memories due to brain damage, while long-term memories from before the event remain intact. The brain damage can be caused by the effects of long-term alcoholism, severe malnutrition, stroke, head trauma, surgery, Wernicke-Korsakoff Syndrome, cerebrovascular events, anoxia or other trauma.[16] The two brain regions related with this condition are medial temporal lobe and medial diencephalon. Anterograde amnesia can't be treated with pharmacological methods due to neuronal loss.[17] However, treatment exists in educating patients to define

their daily routines and after several steps they begin to benefit from their procedural memory. Likewise, social and emotional support is critical to improving quality of life for anterograde amnesia sufferers. [17]

Retrograde amnesia refers to inability to recall memories before onset of amnesia. One may be able to encode new memories after the incident. Retrograde is usually caused by head trauma or brain damage to parts of the brain besides the hippocampus. The hippocampus is responsible for encoding new memory. Episodic memory is more likely to be affected than semantic memory. The damage is usually caused by head trauma, cerebrovascular accident, stroke, tumor, hypoxia, encephalitis, or chronic alcoholism. People suffering from retrograde amnesia are more likely to remember general knowledge rather than specifics. Recent memories are less likely to be recovered, but older memories will be easier to recall due to strengthening over time.[18] Retrograde amnesia is usually temporary and can be treated by exposing them to memories from the loss.[19] Another type of consolidation (process by which memories become stable in the brain) occurs over much longer periods of time/days, weeks, months and years and likely involves transfer of information from the hippocampus to more permanent storage site in the cortex. The operation of this longer-term consolidation process is seen in the retrograde amnesia of patients with hippocampal damage who can recall memories from childhood relatively normally, but are impaired when recalling experiences that occurred just a few years prior to the time they became amnesic. (Kirwan et al.,2008)

Post-traumatic amnesia is generally due to a head injury (example: a fall, a knock on the head). Traumatic amnesia is often transient, but may be permanent or either anterograde, retrograde, or mixed type. The extent of the period covered by the amnesia is related to the degree of injury and may give an indication of the prognosis for recovery of other functions. Mild trauma, such as a car accident that results in no more than mild whiplash, might cause the occupant of a car to have no memory of the moments just before the accident due to a brief interruption in the short/long-term memory transfer mechanism. The sufferer may also lose knowledge of who people are. Having longer periods of amnesia or consciousness after an injury may be an indication that recovery from remaining concussion symptoms will take much longer.[20]

Dissociative amnesia results from a psychological cause as opposed to direct damage to the brain caused by head injury, physical trauma or disease, which is known as organic amnesia. Dissociative amnesia can include:

Repressed memory refers to the inability to recall information, usually about stressful or traumatic events in persons' lives, such as a violent attack or disaster. The memory is stored in long-term memory, but access to it is impaired because of psychological defense mechanisms. Persons retain the capacity to learn new information and there may be some later partial or complete recovery of memory. Formerly known as "Psychogenic Amnesia".

Dissociative fugue (formerly psychogenic fugue) is also known as fugue state. It is caused by psychological trauma and is usually temporary, unresolved and therefore may return. An individual with dissociative fugue disorder is unaware or confused about his or her identity and will travel in journeys away from familiar surroundings to discover or create new identities.[21]The Merck Manual defines it as " one or more episodes of amnesia in which patients cannot recall some or all of their past and either lose their identity or form a new identity. The episodes, called fugues, result from trauma or stress. Dissociative fugue often manifests as sudden, unexpected, purposeful travel away from home."[22] While popular in fiction, it is extremely rare.

Post-hypnotic amnesia occurs when events during hypnosis are forgotten, or where past memories are unable to be recalled. The failure to remember those events is induced by suggestions made during the hypnosis.[23]

Lacunar amnesia is the loss of memory about one specific event.

Childhood amnesia (also known as infantile amnesia) is the common inability to remember events from one's own childhood. Sigmund Freud notoriously attributed this to sexual repression, while modern scientific approaches generally attribute it to aspects of brain development or developmental psychology, including language development. Researchers have found that implicit memories cannot be recalled and are hardily described. Remembering how to play the piano is a common example of implicit memory. Explicit memories, on the other hand, can be recalled and described in words. Remembering the first day that you met your piano teacher is an example of explicit memories. [24]

Transient global amnesia is a well-described medical and clinical phenomenon. This form of amnesia is distinct in that abnormalities in the hippocampus can sometimes be visualized using a special form of magnetic resonance imaging of the brain known as diffusion-weighted imaging (DWI). Symptoms typically last for less than a day and there is often no clear precipitating factor or any other neurological deficits. The cause of this syndrome is not clear. The hypothesis of the syndrome includes transient reduced blood flow, possible seizure or an atypical type of migraine. Patients are typically amnestic of events more than a few minutes in the past, though immediate recall is usually preserved.

Source amnesia is the inability to remember where, when or how previously learned information has been acquired, while retaining the factual knowledge.[25] Source amnesia is both part of ordinary forgetting and can be a memory disorder caused by different factors.[26] People suffering from source amnesia can also get confused about the content of what is remembered. This confusion has been loosely termed memory distrust syndrome. Individuals who suffer from this syndrome distrust their memory and may be motivated to rely on external (non-self) sources.[26]

Korsakoff's syndrome can result from long-term alcoholism or malnutrition. It is caused by brain damage due to a vitamin B1 deficiency and will be progressive if alcohol intake and nutrition pattern are not modified. Other neurological problems are likely to be present in combination with this type of Amnesia. Korsakoff's syndrome is also known to be connected with confabulation. It should be noted that the person's short-term memory may appear to be normal, however the person may have a difficult time attempting to recall a past story, or with unrelated words, as well as complicated patterns. [27]

Drug-induced amnesia is intentionally caused by injection of an amnesiac drug to help a patient forget surgery or medical procedures, particularly those not performed under full anesthesia, or likely to be particularly traumatic. Such drugs are also referred to as "premedicants." Most commonly a 2'-halogenated benzodiazepine such as midazolam or flunitrazepam is the drug of choice, although other strongly amnestic drugs such as propofol or scopolamine may also be used for this application. Memories of the short time-frame in which the procedure was performed are permanently lost or at least substantially reduced, but once the drug wears off, memory is no longer affected.

Prosopamnesia is the inability to recognize or remember faces, even in the presence of intact facial recognition capabilities. Both acquired and inborn cases have been documented.

Situation-Specific amnesia can arise in a variety of circumstances (e.g., committing an offence, child sexual abuse) resulting in PTSD. It has been claimed that it involves a narrowing of consciousness with attention focused on central perceptual details and/or that the emotional or traumatic events are processed differently from ordinary memories.

Transient epileptic amnesia is a rare and unrecognized form of temporal lobe epilepsy, which is typically an episodic isolated memory loss. It has been recognized as a treatment-responsive syndrome congenial to anti-epileptic drugs.[28]

Acquisition of new memories [edit]

Patients with amnesia can learn new information, particularly non-declarative knowledge. However, some patients with dense anterograde amnesia do not remember the episodes during which they learned or observed the information previously.

Acquisition of new declarative information [edit]

Some patients with anterograde amnesia can still acquire some semantic information, even though it might be more difficult and might remain rather unrelated to more general knowledge. H.M. could accurately draw a floor plan of the home in which he lived after surgery, even though he had not lived there in years. The reason patients couldnt form new episodic memories is likely because the CA1 region of the hippocampus was lesioned, and thus th e hippocampus couldnt make connections to the cortex. After an ischemic episode following surgery, an MRI of patient R.B. showed his hippocampus to be intact except for a specific lesion restricted to the CA1 pyramidal cells.[1]

Acquisition of new non-declarative information [edit]

Some retrograde and anterograde amnesics are capable of non-declarative memory, including implicit learning and procedural learning. For example, some patients show improvement on the pseudorandom sequences experiment as healthy people do. Therefore, procedural learning can proceed independently of the brain system required for episodic memory. According to fMRI studies, the acquisition of procedural memories activates the basal ganglia, the premotor cortex and the supplementary motor area, regions which are not normally associated with the formation of episodic memories. This type of dissociation between declarative and procedural memory can also be found in patients with diencephalic amnesia such as Korsakoffs syndrome. Another example is that some patients, such as K.C. and H.M, who have medial temporal damage and anterograde amnesia, still have perceptual priming. Those patients did well in the word fragment completion test. [1]

Treatment [edit]
Many forms of amnesia fix themselves without being treated.[29] However, there are a few ways to cope with memory loss if that is not the case. One of these ways is cognitive or occupational therapy. In therapy, amnesiacs will develop the memory skills they have and try to regain some they have lost by finding which techniques help retrieve memories or create new retrieval paths.[30]This may also include strategies for organizing information to remember it more easily and for improving understanding of lengthy conversation.[31] Another coping mechanism is taking advantage of technological assistance, such as a personal digital device to keep track of day-to-day tasks. Reminders can be set up for appointments, when to take medications, birthdays and other important events. Many pictures can also be stored to help amnesiacs remember names of friends, family and co-workers.[30] Notebooks, wall calendars, pill reminders and photographs of people and places are low-tech memory aids that can help as well.[31] While there are no medications available to treat amnesia, underlying medical conditions can be treated to improve memory. Such conditions include but are not limited to low thyroid function, liver or kidney disease, stroke, depression, bipolar disorder and blood clots in the brain.[32] WernickeKorsakoff syndrome involves a lack of thiamin and replacing this vitamin by consuming thiamin-rich foods such as whole-grain cereals, legumes (beans and lentils), nuts, lean pork, and yeast.[29] Treating alcoholism and preventing alcohol and illicit drug use can prevent further damage, but in most cases will not recover lost memory.[31] Although improvements occur when patients receive certain treatments, there is still no actual cure remedy for amnesia so far. To what extent the patient recovers and how long the amnesia will continue depends on the type and severity of the lesion. [33]

Transient global amnesia

From Wikipedia, the free encyclopedia

Transient global amnesia

Classification and external resources

ICD-10

G45.4

ICD-9

437.7

DiseasesDB

13251

eMedicine

neuro/380

MeSH

D020236

Transient global amnesia (TGA) is a syndrome in clinical neurology whose key defining characteristic is a temporary but almost total disruption of short-term memory with a range of problems accessing older memories. A person in a state of TGA exhibits no other signs of impaired cognitive functioning but recalls only the last few moments of consciousness plus deeply encoded facts of the individuals past, such as his or her own name.[1][2]
Contents
[hide]

1 Symptoms

1.1 Progression of a TGA event

2 Differential diagnosis 3 Causes

o o o o o

3.1 Precipitating events 3.2 Vascular hypotheses 3.3 Migraine 3.4 Epilepsy 3.5 Other putative associations

4 Prognosis 5 Epidemiology 6 See also 7 Movie Reference 8 References 9 External links

Symptoms [edit]
A person having an attack of TGA has almost no capacity to establish new memories, but generally appears otherwise mentally alert and lucid, possessing full knowledge of self-identity and identity of close family, and maintaining intact perceptual skills and a wide repertoire of complex learned behavior. The individual simply cannot recall anything that happened outside the last few minutes, while memory for more temporally distant events may or may not be largely intact.[1][2] The degree of amnesia is profound, and, in the interval during which the individual is aware of his or her condition, is often accompanied by anxiety.[3] The diagnostic criteria for TGA, as defined for purposes of clinical research, include: [2]

The attack was witnessed by a capable observer and reported as being a definite loss of recent memory (anterograde amnesia).

There was an absence of clouding of consciousness or other cognitive impairment other than amnesia. There were no focal neurological signs or deficits during or after the attack. There were no features of epilepsy, or active epilepsy in the past two years, and the patient did not have any recent head injury.

The attack resolved within 24 hours.

Progression of a TGA event [edit]

This onset of TGA is generally fairly rapid, and its duration varies but generally lasts between 2 to 8 hours.[2] A person experiencing TGA typically has memory only of the past few minutes or less, and cannot retain new information beyond that period of time. One of its bizarre features is perseverance, in which the victim of an attack faithfully and methodically repeats statements or questions, complete with profoundly identical intonation and gestures "as if a fragment of a sound track is being repeatedly rerun."[4] This is found in almost all TGA attacks and is sometimes considered a defining characteristic of the condition.[2][5][6] The individual experiencing TGA retains social skills and older significant memories, almost always including knowing his or her own identity and the identity of family members, and the ability to perform various complex learned tasks including driving and other learned behavior; one individual "was able to continue putting together the alternator of his car."[2] Though outwardly appearing normal, a person in TGA is disoriented in time and space, perhaps knowing neither the year nor where he or she resides. Although confusion is sometimes reported, others consider this an imprecise observation, [6] but an elevated emotional state (compared to patients experiencing Transient Ischemic Attack, or TIA) is common.[7] In a large survey, 11% of individuals in a TGA state were described as exhibiting "emotionalism" and 14% "fear of dying".[8] The attack lessens over a period of hours, with older memories returning first, and the repetitive fugue slowly lengthening so that the victim retains short-term memory for longer periods. While seemingly back to normal within 24 hours, there are subtle effects on memory that can persist longer.[9][10] In the majority of cases there are no long-term effects other than a complete lack of recall for this period of the attack and an hour or two before its onset.[2][11] There is emerging evidence for observable impairments in a minority of cases weeks or even years following a TGA attack.[9][12][13] There is also evidence that the victim is aware that something is not quite right, even though they can't pinpoint it. The person suffering from the attack may vocalize signs that 'they just lost their memory', or that they believed they had a stroke, although they aren't aware of the other signs that they are displaying. The main sign of this condition is the repetitive actions of something that is not usually repeated.[citation needed]

Differential diagnosis [edit]

A differential diagnosis should include:[14]

Thrombosis of the basilar artery Cardioembolic stroke Complex partial seizures Frontal lobe epilepsy Lacunar syndromes Migraine variants Posterior cerebral artery stroke Syncope and related paroxysmal spells Temporal lobe epilepsy

If the event lasts less than one hour, transient epileptic amnesia (TEA) might be implicated.[2][15] If the condition lasts longer than 24 hours, it is not considered TGA by definition. A diagnostic investigation would then probably focus on some form of undetected ischemic attack or cranial bleed.[11][16]

Causes [edit]
The underlying cause of TGA remains enigmatic. The leading hypotheses are some form of epileptic event, a problem with blood circulation around, to or from the brain, or some kind of migraine-like phenomenon.[7][17][18][19] The differences are sufficiently meaningful that transient amnesia may be considered a heterogeneous clinical syndrome [2] with multiple etiologies, corresponding mechanisms, and differing prognoses.[8] Another widely disputed cause of TGA is excessive contact with bleach products.[citation needed]

Precipitating events [edit]

TGA attacks are associated with some form of precipitating event in at least one-third of cases.[20] In females, this event is more often of a strong emotional character; in males, it is more often related to some physical exertion. [8] The most commonly cited precipitating events include vigorous exercise (including sexual intercourse), swimming in cold water or enduring other temperature changes, and emotionally traumatic or stressful events.[2] There are reports of TGA-like conditions following certain medical procedures and disease states.[18] There is a slight (2%) familial incidence.[2] If the definition of a precipitating event is widened to include events days or weeks earlier, and to take in emotionally stressful burdens such as money worries, attending a funeral or exhaustion due to overwork or unusual childcare responsibilities, a large majority, over 80%, of TGA attacks are said to correlate with precipitating events.[8] The role of psychological co-factors has been addressed by some research. It is the case that people in a state of TGA exhibit measurably elevated levels of anxiety and/or depression.[3]Emotional instability may leave some people vulnerable to stressful triggers and thus be associated with TGA.[8] Individuals who have experienced TGA, compared with similar people with TIA, are more likely to have some kind of emotional problem (such as depression or phobias) in their personal or family history [21] or to have experienced some kind of phobic or emotionally challenging precipitating event.[22]

Vascular hypotheses [edit]

Cerebral ischemia is a frequently disputed possible cause, at least for some segment of the TGA population, and until the 1990s it was generally thought that TGA was a variant of transient ischemic attack (TIA) secondary to some form of cerebrovascular disease.[7][19] Those who argue against a vascular cause point to evidence that those experiencing TGA are no more likely than the general population to have subsequent cerebral vascular disease.[7] In fact, "in comparison with TIA patients, TGA patients had a significantly lower risk of combined stroke, myocardial infarct, and death."[21] Other vascular origins remain a possibility, however, according to research of jugular vein valve insufficiency in patients with TGA. In these cases, mostly men, TGA has followed vigorous exertion. One current hypothesis is that TGA may be due to venous congestion of the brain,[23] leading to ischemia of structures involved with memory, such as the hippocampus.[24] It has been shown that performing a Valsalva maneuver (involving ""bearing down"" and increasing breath pressure against a closed glottis, which occurs frequently during exertion) may be related to retrograde flow of blood in the jugular vein, and therefore, presumably, cerebral blood circulation, in patients with TGA.[23][25][26][27]

Migraine [edit]
A history of migraine is a statistically significant risk factor identified in the medical literature.[7][8] "When comparing TGA patients with normal control subjects the only factor significantly associated with an increased risk for TGA was migraine." [19] 14% of people with TGA had a history of migraine in one study,[20] and approximately a third of the participants in another clinical study reported such a history.[2] However, migraine does not appear to occur simultaneously with TGA nor serve as a precipitating event. Headache frequently occurs during TGA, as does nausea, both symptoms often associated with migraine, but it appears that these do not indicate migraine in patients during a TGA event. The connection remains conceptual, and muddied further by a lack of consensus about the definition of migraine itself, and by the differences in age, gender, and psychological characteristics of migraine sufferers when compared to those variables in the TGA cohort.[8]

Epilepsy [edit]
Amnesia is often a symptom in epilepsy, and for that reason people with known epilepsy are disqualified from most studies of TGA. In a study where strict criteria were applied to TGA diagnosis, no epileptic features were seen in EEGs of over 100 patients with TGA.[8] However, despite the fact that EEG readings are usually normal during a TGA attack, and other usual symptoms of epilepsy are not observed with TGA [19] it has been speculated that some initial epileptic attacks present as TGA.[2] The observation that 7% of people who experience TGA will develop epilepsy calls into question whether those case are, in fact, TGA or transient epileptic amnesia (TEA).[7] TEA attacks tend to be short (under one hour) and tend to recur, so that a person who has experienced both repeated attacks of temporary amnesia resembling TGA and if those events lasted less than one hour is very likely to develop epilepsy.[2] There is additional speculation that atypical cases of TEA in the form of nonconvulsive status epilepticus may present with duration similar to TGA.[28] This may constitute a distinct subgroup of TGA. TEA, as opposed to "pure" TGA, is also characterized by "two unusual forms of memory deficit : (i) accelerated long-term forgetting (ALF): the excessively rapid loss of newly acquired memories over a period of days or weeks and (ii) remote autobiographical memory loss: a loss of memories for salient, personally experienced events of the past few decades."[5] Whether an amnestic event is TGA or TEA thus presents a diagnostic challenge,[18] especially in light of the recently published descriptions of possible long-term cognitive deficits with (presumably correctly diagnosed) TGA.

Other putative associations [edit]

There have been assertions of a possible link between TGA and the use of statins (a class of drug used in treating cholesterol).[29][30]

Prognosis [edit]
The prognosis of "pure" TGA is very good. It does not affect mortality or morbidity[14] and unlike earlier understanding of the condition, TGA is not a risk factor for stroke or ischemic disease.[7]Rates of recurrence are variously reported, with one systematic calculation suggesting the rate is under 6% per year.[21] TGA is universally felt to be a benign condition which requires no further treatment other than reassurance to the patient and their family. [11] "The most important part of management after diagnosis is looking after the psychological needs of the patient and his or her relatives. Seeing a once competent and healthy partner, sibling or parent become incapable of remembering what was said only a minute ago is very distressing, and hence it is often the relatives who will require reassurance." [31] TGA may have multiple etiologies and prognoses.[8] Atypical presentations may masquerade as epilepsy[7] and be more properly considered TEA. In addition to such probable TEA cases, some people experiencing amnestic events diverging from the diagnostic criteria articulated above may have a less benign prognosis than those with "pure" TGA. [2] Recently, moreover, both imaging and neurocognitive testing studies question whether TGA is as benign as has been thought. MRI scans of the brain in one study showed that among people who had experienced TGA, all had cavities in the hippocampus, and these cavities were far more numerous, larger, and more suggestive of pathological damage than in either healthy controls or a large control group of people with tumor or stroke.[12] Verbal and cognitive impairments have been observed days after TGA attacks, of such severity that the researchers estimated the effects would be unlikely to resolve within a short time frame.[13] A large neurocognitive study of patients more than a year after their attacks has shown persistent effects consistent with amnestic mild cognitive impairment (MCI-a) in a third of the people who had experienced TGA.[32] In another study, "selective cognitive dysfunctions after the clinical recovery" were observed, suggesting a prefrontal impairment. [10] These dysfunctions may not be in memory per se but in retrieval, in which speed of access is part of the problem among people who have had TGA and experience ongoing memory problems.[9]

Epidemiology [edit]
The estimated annual incidence of TGA varies from a minimum of 2.9 cases per 100,000 population (in Spain) and 5.2 per 100,000 (in USA),[14] but among people aged over 50, the rate of TGA incidence is reported to range from approximately 23 per 100,000 (in a US population) to 32 per 100,000 (in a population in Scandinavia).[20][33] TGA is most common in people between age 56 and 75,[8] with the average age of a person experiencing TGA being approximately 62.[7]

See also [edit]

Amnesia

Movie Reference [edit]

The Tamil movie Naduvula Konjam Pakkatha Kaanom depicts an individual suffering from a condition which appears similar to TGA.

Medical education in the Philippines

From Wikipedia, the free encyclopedia

Medical education in the Philippines is principally offered and developed by accredited and government recognized medical schools in the country. The Philippine medical schools are graduate schools offering the Doctor of Medicine (M.D.) degree. The M.D. is a fouryear professional degree program which qualifies the degree holder to take the licensure exam for medical doctors in the Philippines.
Contents
[hide]

1 Admission to medical schools 2 Professional medical degree 3 Philippine medical schools

o o

3.1 Top Philippine Medical Schools 3.2 List of APMC Accredited Philippine Medical Schools

4 Physicians' licensure examinations 5 Advanced medical studies

o o

5.1 Graduate medical programs 5.2 Medical specialization

6 Medical practice 7 Notable Filipino doctors 8 See also 9 References 10 External links

Admission to medical schools [edit]

Before applying to any medical school, a candidate must earn a bachelor's degree with credits in certain required subjects. The most common pre-medical degrees include biology, psychology,medical technology, pharmacy, nursing, and physical therapy.[1] In addition, a candidate must take and pass the National Medical Admission Test (NMAT), the national entrance exam for all medical schools in the Philippines.[1]

Professional medical degree [edit]

The Doctor of Medicine (M.D.) is a four-year professional degree program dealing with medical theories, practices, technologies, and problem solving. The completion of the degree program with one-year postgraduate internship qualifies a candidate to take the licensure exam for medical doctors in the Philippines.[1]

Philippine medical schools [edit]

Medical schools in the country are regulated by the Commission on Higher Education (CHED) of the Philippines, and accredited by the Association of Philippine Medical Colleges.[1]

Top Philippine Medical Schools [edit]

The Board of Medicine has released a list of the outstanding colleges of medicine in the Philippines with percentage passing above the national average (62.71%) based on the Physician Licensure Examinations from 2007-2012. They were recognized in the oath-taking of the new physicians held at the PICC Plenary Hall in Pasay City on September 15, 2012. [2][3][4]
Rank Name Number of Examinees Passed Passing Percentage

Cebu Institute of Medicine (CIM)

390

388

99.48%

University of the Philippines College of Medicine (UPCM)

962

948

98.54%

University of Santo Tomas Faculty of Medicine and Surgery (UST-FMS)

2355

2269

96.34%

Pamantasan ng Lungsod ng Maynila College of Medicine (PLM-CM)

701

658

93.86%

Mindanao State University College of Medicine (MSU-COM)

276

254

92.02%

West Visayas State University College of Medicine (WVSU-COM)

621

555

89.37%

Saint Luke's College of Medicine (SLCM)

482

430

89.21%

Saint Louis University (Baguio) School of Medicine (SLU-SoM)

501

435

86.82%

Xavier University School of Medicine

337

289

85.75%

10

Cebu Doctors' University College of Medicine (CDU-CM)

443

368

83.06%

11

University of the East Ramon Magsaysay Memorial Medical Center (UERMMMC) 1294

1068

82.53%

12

Cagayan State University College of Medicine and Surgery

134

109

81.34%

13

Far Eastern University Nicanor Reyes Medical Foundation (FEU-NRMF)

1558

1249

80.16%

14

Ateneo de Zamboanga University School of Medicine (AdZU-SOM)

154

121

78.57%

15

Davao Medical School Foundation, Inc. College of Medicine

508

393

77.36%

16

University of St. La Salle College of Medicine (USLS-CM)

141

107

75.88%

17

De La Salle Health Sciences Institute

1197

823

68.75%

List of APMC Accredited Philippine Medical Schools [edit]

There are 38 APMC member schools and colleges as of 2009.[5]
Name Dean Location

AMA College of Medicine

Esperanza C. Lansang, M.D.

Makati City

Ateneo de Manila University School of Medicine & Public Health

Dean Alfredo Bengzon, M.D.

Pasig City

Ateneo de Zamboanga University School of Medicine

Fortunato L. Cristobal, M.D.

Zamboanga City

Emilio Aguinaldo College

Asuncion Abaya-Morido, M.D.

Ermita, Manila

Far Eastern University Dr. Nicanor Reyes Medical Foundation

Remedios T. Habacon, M.D.

Fairview, Quezon City

University of Perpetual Help Rizal Jonelta Foundation School of Medicine

Aretas P. Singson-Alday, M.D.

Las Pias City

Manila Central University-Filemon D. Tanchoco Sr. Medical Foundation

Elvira M. Abreu, M.D.

Caloocan City

Our Lady of Fatima University

Reynaldo A. Olazo, M.D.

Valenzuela City

Pamantasan ng Lungsod ng Manila

Rose Anna R. Banal, M.D.

Intramuros, Manila

San Beda College of Medicine

Ferdinand Francis L. Cid, M.D.

Mendiola, Manila

St. Luke's College of Medicine William H. Quasha Memorial

Brigido L. Carandang, Jr., M.D.

Sta. Ignacia St., Quezon City

Name

Dean

Location

UERM Memorial Medical Center

Alfaretta Luisa T. Reyes, M.D.

Aurora Blvd., Quezon City

University of Santo Tomas Faculty of Medicine & Surgery

Maria Graciela G. Gonzaga, M.D.

Espaa, Manila

University of the Philippines-Manila

Agnes Mejia, M.D.

Pedro Gil, Manila

Baguio Central University

Ma. Ana P. Custodio, M.D.

Baguio City

Saint Louis University

John Anthony A. Domantay, M.D.

Baguio City

Lyceum-Northwestern University Dr. Francisco Q. Duque Medical Foundation

Felipe H. Rodriguez, M.D.

Dagupan City

University of Northern-Philippines

Larguita P. Reotutar, M.D.

Vigan, Ilocos Sur

Virgen Milagrosa University Foundation

Estrella S. Valerio, M.D.

San Carlos City

Cagayan State University

Pablo M. Afidchao, M.D.

Tuguegarao City

Angeles University Foundation School of Medicine

Evelyn B. Yumiaco, M.D.

Angeles City

De La Salle Health Sciences Institute

Dina C. Gonzales, M.D.

Dasmarias, Cavite

University of Perpetual Help - Dr. Jose G. Tamayo Medical University

Winnie P. Siao, M.D.

Bian, Laguna

Bicol Christian College of Medicine

Sonia G. Rosario, M.D.

Legazpi City

Central Philippines University

Glenn A. M. Catedral, M.D.

Iloilo City

Iloilo Doctors College of Medicine

Ludovico Jurao, M.D.

Iloilo City

University of Saint. La Salle

Carmelo C. Canto, M.D.

Bacolod City

Name

Dean

Location

West Visayas State University

Joselito F. Villaruz, M.D.

Iloilo City

Cebu Doctors University

Enrico B. Gruet, M.D.

Cebu City

Cebu Institute of Medicine

Thelma L. Fernandez, M.D.

Cebu City

Silliman University Medical School

Jonathan C. Amante, M.D.

Dumaguete City

Southwestern University Matias H. Aznar Memorial College of Medicine, Inc.

Peter S. Aznar, M.D.

Cebu City

Gullas College of Medicine University of the Visayas

Leonardo Raymund C. Cimafranca, M.D.

Mandaue City

Remedios Trinidad Romualdez Medical School Foundation

Jesus G. Reyes, M.D.

Tacloban City

University of the Philippines School of Health Sciences

Jusie Lydia Siega-Sur, M.D.

Palo, Leyte

Mindanao State University College of Medicine

Cristina D. Achacoso, M.D.

Iligan City

Xavier University-Dr. Jose P. Rizal School of Medicine Ateneo de Cagayan

Ruth S. Beltran, M.D.

Cagayan De Oro City

Davao Medical School of Medicine

Petronilo A. Basa, M.D.

Davao City

Physicians' licensure examinations [edit]

The licensure exams for physicians (board exam for doctors) are administered by the Philippine Board of Medicine, a professional regulatory body under the general control and supervision of the Professional Regulation Commission (PRC) of the Philippines.[1]

Advanced medical studies [edit]

After graduation from medical school and passing the board exam for doctors, a Filipino doctor is labelled as a general medical practitioner. He may seek further training by way of graduate programs in medicine (i.e., Master of Public Health, Master of Health Services Administration, etc.), or by way of medical specialization.[1]

Graduate medical programs [edit]

Graduate programs are offered in some medical schools in the country and abroad. Candidates usually attend lectures and practical exercises in an academic environment and in laboratory settings. The program may require the presentation and defense of a graduate-level thesis, an independent research project, or supervised professional practice as a final graduation requirement. The entire academic program may last from one year to five years, depending on the requirements of the curriculum; the demands of the institution; and the academic load, availability, and dedication of the individual student. [1]

Medical specialization [edit]

Medical specialization usually takes three to six years of residency training in accredited hospitals and clinics, and the taking of diplomate board examinations conducted by a board of medical specialists in a particular field (i.e., Philippine Board of Psychiatry, Philippine Board of Pediatrics, Philippine Board of Cardiology, Philippine Board of Pulmonology, Philippine Academy of Family Physicians Board of Examiners etc.).[1]

Medical practice [edit]

Medical practice in the Philippines is developed, monitored, and regulated by the Philippine Medical Association (PMA), the largest organization of medical doctors in the country. Other medical and health societies co-exist to pursue more specific interests in the medical field (i.e. Philippine Academy of Family Physicians, Philippine Dermatological Society, Philippine Cancer Society, Philippine Pediatric Society, Philippine Association for the Study of Overweight and Obesity, etc.).[6] The Department of Health, a cabinet-level department under the Office of the President of the Philippines, exercises general monitoring supervisory powers over medical practitioners and allied health personnel in the Philippines.[7]

Notable Filipino doctors [edit]

Jos Rizal - the National Hero of the Philippines Mariano Ponce - Filipino propagandist, was managing editor of La Solidaridad Juan Flavier - former Health Secretary and Senator of the Philippines Manuel Dayrit - former Health Secretary and Officer of the World Health Organization Ramon Gustilo - Orthopedic surgeon; responsible for the commonly used Gustilo open fracture classification.[8] Senen Reyes - the first and only Filipino Cosmonaut-Doctor[9] Fe del Mundo - First Filipino woman and female medical student to enter the Harvard Medical School. A pioneer of Pediatrics in the Philippines.[10]