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For other uses, see Amnesia (disambiguation). "Amnesiac" redirects here. For the Radiohead album, see Amnesiac (album).
Amnesia
ICD-10
F04, R41.3
ICD-9
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
2 Causes 3 Types
o o
4.1 Acquisition of new declarative information 4.2 Acquisition of new non-declarative information
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]
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.
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]
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]
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]
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]
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
o o o o o
3.1 Precipitating events 3.2 Vascular hypotheses 3.3 Migraine 3.4 Epilepsy 3.5 Other putative associations
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.
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]
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.
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]
Amnesia
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]
o o
3.1 Top Philippine Medical Schools 3.2 List of APMC Accredited Philippine Medical Schools
o o
6 Medical practice 7 Notable Filipino doctors 8 See also 9 References 10 External links
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]
390
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555
89.37%
482
430
89.21%
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435
86.82%
337
289
85.75%
10
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368
83.06%
11
University of the East Ramon Magsaysay Memorial Medical Center (UERMMMC) 1294
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82.53%
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134
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81.34%
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80.16%
14
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78.57%
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17
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68.75%
Makati City
Pasig City
Zamboanga City
Ermita, Manila
Caloocan City
Valenzuela City
Intramuros, Manila
Mendiola, Manila
Name
Dean
Location
Espaa, Manila
Baguio City
Baguio City
Dagupan City
University of Northern-Philippines
Tuguegarao City
Angeles City
Dasmarias, Cavite
Bian, Laguna
Legazpi City
Iloilo City
Iloilo City
Bacolod City
Name
Dean
Location
Iloilo City
Cebu City
Cebu City
Dumaguete City
Cebu City
Mandaue City
Tacloban City
Palo, Leyte
Iligan City
Davao City
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]