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Brain Disorders

Amnesia

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For other uses, see Amnesia (disambiguation).

Amnesia (from Greek Ἀμνησία) is a short term memory condition in which memory is disturbed. In simple terms it is the loss of memory. The causes of amnesia are organic or functional. Organic causes include damage to the brain, through trauma or disease, or use of certain (generally sedative) drugs. Functional causes are psychological factors, such as defense mechanisms. Hysterical post-traumatic amnesia is an example of this. Amnesia may also be spontaneous, in the case of transient global amnesia.[1] This global type of amnesia is more common in middle-aged to elderly people, particularly males, and usually lasts less than 24 hours.

Another effect of amnesia is the inability to imagine the future. A recent study published online in the Proceedings of the National Academy of Sciences shows that amnesiacs with damaged hippocampus cannot imagine the future.[2] This is because when a normal human being imagines the future, they use their past experiences to construct a possible scenario. For example, a person who would try to imagine what would happen at a party that would occur in the near future would use their past experience at parties to help construct the event.

Contents

Forms of Amnesia

  • In anterograde amnesia, new events contained in the immediate memory are not transferred to the permanent as long-term memory.
  • Retrograde amnesia is the distinct inability to recall some memory or memories of the past, beyond ordinary forgetfulness.

The terms are used to categorize patterns of symptoms, rather than to indicate a particular cause or etiology. Both categories of amnesia can occur together in the same patient, and commonly result from drug effects or damage to the brain regions most closely associated with episodic/declarative memory: the medial temporal lobes and especially the hippocampus.

An example of mixed retrograde and anterograde amnesia may be a motorcyclist unable to recall driving his motorbike prior to his head injury (retrograde amnesia), nor can he recall the hospital ward where he is told he had conversations with family over the next two days (anterograde amnesia).

The effects of amnesia can last long after the condition has passed; many sufferers claim that amnesia changes from a neurological condition to a psychological condition, whereby the patient loses confidence and faith in their own memory and accounts of past events.

Types and Causes of Amnesia

Post-traumatic amnesia is generally due to a head injury (e.g. a fall, a knock on the head). Traumatic amnesia is often transient, but may be permanent of 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, they may remember events, but will not remember faces of them.

  • 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 rape. 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. This contrasts with e.g. anterograde amnesia caused by amnestics such as benzodiazepines or alcohol, where an experience was prevented from being transferred from temporary to permanent memory storage: it will never be recovered, because it was never stored in the first place. 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. The Merck Manual defines it as "one or more episodes of amnesia in which the inability to recall some or all of one's past and either the loss of one's identity or the formation of a new identity occur with sudden, unexpected, purposeful travel away from home." [3] While popular in fiction, it is extremely rare.

·        Posthypnotic amnesia is where events during hypnosis are forgotten, or where past memories are unable to be recalled.

·        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 attributed this to sexual repression, while others have theorised that this may be due to language development or immature parts of the brain.

  • 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 nor any other neurological deficits. The cause of this syndrome is not clear, hypotheses include 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 a memory disorder in which someone can recall certain information, but they do not know where or how they obtained the information.
  • Blackout phenomenon can be caused by excessive short-term alcohol consumption, with the amnesia being of the anterograde type.
  • 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.
  • Drug-induced amnesia is intentionally caused by injection of an amnesiac drug to help a patient forget surgery or medical procedures, particularly those which are not performed under full anesthesia, or which are 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.

Amnesia in Fiction

Main article: List of appearances of amnesia in fiction

Amnesia is prevalent in many works of fiction. Global amnesia is a common motif in fiction despite being extraordinarily rare in reality. In movies and television, particularly sitcoms and soap operas, it is often depicted that a second hit to the head (similar to the first one) cures the amnesia. When one has amnesia in fiction, it is often followed by a melodramatic "Who am I? What am I? Where am I?", or sometimes, "[name of amnesiac]? Who's [name of amnesiac]? Amnesia has also been prominently used as a plot device in many video games to help explain why the main character (and in essence the player) knows very little about the world he is in. In reality, however, repeat concussions may cause cumulative deficits including cognitive problems, and in extremely rare cases may even cause deadly swelling of the brain associated with second-impact syndrome.

See also

References

  1. ^ eMedicine - Transient Global Amnesia : Article by Roy Sucholeiki
  2. ^ Patients with hippocampal amnesia cannot imagine new experiences, Proceedings of the National Academy of Sciences.
  3. ^ The Merck Manuals Online

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Brain Structures and their Functions

The nervous system is your body's decision and communication center. The central nervous system (CNS) is made of the brain and the spinal cord and the peripheral nervous system (PNS) is made of nerves. Together they control every part of your daily life, from breathing and blinking to helping you memorize facts for a test. Nerves reach from your brain to your face, ears, eyes, nose, and spinal cord... and from the spinal cord to the rest of your body. Sensory nerves gather information from the environment, send that info to the spinal cord, which then speed the message to the brain. The brain then makes sense of that message and fires off a response. Motor neurons deliver the instructions from the brain to the rest of your body. The spinal cord, made of a bundle of nerves running up and down the spine, is similar to a superhighway, speeding messages to and from the brain at every second.

The brain is made of three main parts: the forebrain, midbrain, and hindbrain. The forebrain consists of the cerebrum, thalamus, and hypothalamus (part of the limbic system). The midbrain consists of the tectum and tegmentum. The hindbrain is made of the cerebellum, pons and medulla. Often the midbrain, pons, and medulla are referred to together as the brainstem.

The Cerebrum: The cerebrum or cortex is the largest part of the human brain, associated with higher brain function such as thought and action. The cerebral cortex is divided into four sections, called "lobes": the frontal lobe, parietal lobe, occipital lobe, and temporal lobe. Here is a visual representation of the cortex:  

 

What do each of these lobes do?

  • Frontal Lobe- associated with reasoning, planning, parts of speech, movement, emotions, and problem solving
  • Parietal Lobe- associated with movement, orientation, recognition, perception of stimuli
  • Occipital Lobe- associated with visual processing
  • Temporal Lobe- associated with perception and recognition of auditory stimuli, memory, and speech

Note that the cerebral cortex is highly wrinkled. Essentially this makes the brain more efficient, because it can increase the surface area of the brain and the amount of neurons within it. We will discuss the relevance of the degree of cortical folding (or gyrencephalization) later. (Go here for more information about cortical folding)

A deep furrow divides the cerebrum into two halves, known as the left and right hemispheres. The two hemispheres look mostly symmetrical yet it has been shown that each side functions slightly different than the other. Sometimes the right hemisphere is associated with creativity and the left hemispheres is associated with logic abilities. The corpus callosum is a bundle of axons which connects these two hemispheres.

Nerve cells make up the gray surface of the cerebrum which is a little thicker than your thumb. White nerve fibers underneath carry signals between the nerve cells and other parts of the brain and body.

The neocortex occupies the bulk of the cerebrum. This is a six-layered structure of the cerebral cortex which is only found in mammals. It is thought that the neocortex is a recently evolved structure, and is associated with "higher" information processing by more fully evolved animals (such as humans, primates, dolphins, etc). For more information about the neocortex, click here.

The Cerebellum: The cerebellum, or "little brain", is similar to the cerebrum in that it has two hemispheres and has a highly folded surface or cortex. This structure is associated with regulation and coordination of movement, posture, and balance.

The cerebellum is assumed to be much older than the cerebrum, evolutionarily. What do I mean by this? In other words, animals which scientists assume to have evolved prior to humans, for example reptiles, do have developed cerebellums. However, reptiles do not have neocortex. Go here for more discussion of the neocortex or go to the following web site for a more detailed look at evolution of brain structures and intelligence: “Ask the Experts:” Evolution and Intelligence

Limbic System: The limbic system, often referred to as the “emotional brain,” is found buried within the cerebrum. Like the cerebellum, evolutionarily the structure is rather old.

This system contains the thalamus, hypothalamus, amygdala, and hippocampus. Here is a visual representation of this system, from a midsagittal view of the human brain:

Click on the words to learn what these structures do:

Brain Stem: Underneath the limbic system is the brain stem. This structure is responsible for basic vital life functions such as breathing, heartbeat, and blood pressure. Scientists say that this is the "simplest" part of human brains because animals' entire brains, such as reptiles (who appear early on the evolutionary scale) resemble our brain stem. Look at a good example of this here.

The brain stem is made of the midbrain, pons, and medulla. Click on the words to learn what these structures do:

Canadians open door to learning-disorder drug

CAROLYN ABRAHAM

From Tuesday's Globe and Mail

February 24, 2009 at 12:15 AM EST

An eight-year effort by Canadian scientists has connected a crucial brain protein with the power to learn, raising the possibility that learning disabilities could be corrected with a drug.

A Toronto research team discovered that this single protein, which helps brain cells talk to one another, results in learning impairments when it is missing or malfunctions. And in a remarkable one-two punch, the scientists have also found that a medication, now being tested in Alzheimer's patients, may fix the problem.

“Neurologists and neuroscientists have always tended to think that if the brain is abnormal at birth, nothing can be done to improve intellectual function, and that special education was virtually the only assistance available,” said senior investigator Roderick McInnes, a leading geneticist at the Hospital for Sick Children. “It is no longer a fantasy to think that drug treatment might, in the future, be available for such patients.”

It's estimated that roughly 10 per cent of the population suffers from a learning disability, although it is not known how many of those might carry a defective form of this protein, known as Neto1. Still, advocates for people with learning disabilities say the work is promising.

“It probably is the first indication that learning disabilities might be treatable [with medication],” said Barbara McElgunn, health policy adviser to the Learning Disabilities Association of Canada. “It sounds very positive and hopeful for kids with learning disabilities, even though, of course, this is in its early days.”

The work, published in the current issue of PLoS Biology, a peer-reviewed online scientific journal, does come with caveats. For one, the Toronto group conducted its studies with mice, and research is still under way to determine how faithfully the results will translate into humans.

As well, while the Alzheimer's drug in question has passed phase-one safety trials run by a U.S. biotech firm and has moved into larger phase-two trials to test its efficacy, it remains unknown when, or if, any researchers will try it in people with learning disabilities.

Dr. McInnes, who holds the Anne and Max Tanenbaum Chair in Molecular Medicine at the University of Toronto, said, “We're very concerned that every child and adult with a learning disability will want to take these drugs, when this is very early days [in the research].”

He said he would be particularly worried about trying such drugs on the developing brain of a child, since it could result in “disordered thinking or emotional disturbances, which can't be fully evaluated in an animal model.”

Still, the Toronto work is part of a growing body of evidence – most of it coming from animal studies – that, through the lifelong ability to make new brain cells and advances in genetics, it may be possible to reverse neuro-developmental disorders once thought beyond the reach of medicine.

Dr. McInnes, who specializes in genetic eye diseases, had been hunting genes involved in eye development in 2000 when he and his postdoctoral fellow David Ng came across the gene that makes Neto1. Eventually, research from his lab proved the protein to be very active in the brain – particularly in sending messages between cells in the hippocampus, the seahorse-shaped brain region heavily involved in memory and learning.

They discovered all sorts of species – from flies to people – carry versions of Neto1. “This suggests it has been strongly conserved [through evolution] and so it must be important,” Dr. McInnes explained.

To nail down precisely how Neto1 might affect behaviour, the researchers specially bred mice who were missing the gene that makes it. The “knock-out” mutants had no obvious physical or behavioural anomalies, but they did fare poorly on both electrophysiological measurements of brain activity and cognitive tests compared to normal, wild-type mice.

John Roder, at the Samuel Lunenfeld Research Institute at Mount Sinai Hospital found that mice missing Neto1 failed a water maze test in which they had to recall the location of a hidden safety platform. Normal mice swimming through the water maze were able to find the platform faster with each effort, but the Neto1 knock-out rodents got lost each time.

Michael Salter, head of the neuroscience and mental health program at Sick Kids and one of the research team leaders, found the knock-out mice were only able to generate electrical signals between brain cells at half the strength of normal mice.

The researchers conclude that mice missing the Neto1 gene have fewer so-called NMDA receptors on their brain cells. NMDA receptors, known to be crucial for forming memories and learning, are like windows into a brain cell that open and close, allowing electro-chemical signals to pass through.

They are different from AMPA receptors which are more involved in activities we do unconsciously, such as when “we talk, walk or breathe,” Dr. Salter said.

But AMPA receptors have to be activated and open first for an NMDA receptor to open. For this reason, Sinai's Dr. Roder wondered if new drugs known as ampakines might boost the learning abilities of the knock-out mice.

AMPA receptors usually fire open in flashes of a couple of milliseconds, but the drugs help them stay open longer and, in turn, researchers found this indirectly helped the fewer NMDA receptors in the mutant function better. With the drugs, the strength of their brain cell connections returned to normal and they performed cognitive tests as well as the wild mice. “The effects,” Dr. Salter said, “were almost immediate.”

“This is further evidence that as we come to know more about the molecular biology of the brain, the more hope there is that we can design therapies to correct cognitive disorders.”

 

 

 

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