STUDY - Technical - New Dacian's Medicine
Aphasia
and other Focal Disorders (5)
Translation Draft
The time has come to discuss the limbic network of memory, specifically amnesia.
The central limbic and paralimbic areas, the anterior and medial talamic nucleus, the medial and basal parts of the striated nucleus and the hypothalamus together constitute a large network known as the limbic system. The behavioral affiliations of this network are the coordination of emotion, motivation, vegetative tone and endocrine functions.
An additional area of specialization of the limbic network, with the greatest clinical importance, is that of declarative (conscious) memory for events and experience. Damage to limbic network components can cause global and severe long-term memory disorders. This type of memory alteration is called an amnesiac state.
In the absence of deficits in motivation, attention, language and visual function, the clinical diagnosis of a global and persistent amnesiac state implies the existence of a primary alteration in the core of the long-term memory mechanism and is always associated with bilateral lesions in the limbic network.
Memory disorder in the amnesiac state is multimodal and includes retrograde and anterograde components. Retrograde amnesia refers to the inability to evoke events that occurred before the installation of the amnesiac state. Relatively recent events are more vulnerable in retrograde amnesia than more distant ones.
This phenomenon is called Ribot's gradient and explains why the patient with severe retrograde amnesia rarely forgets the events of childhood. A patient who comes to the emergency room complaining that he can't remember what it's called, but can evoke events that day, is almost certainly not suffering from a neurological cause of memory disorder.
The second and most important component of the amnesiac state is anterograde amnesia, which consists of the inability to store, retain and evoke recent information. Patients with amnesiac conditions are vigilant and motivated, but cannot remember what they ate a few minutes ago or details of an important event experienced a few hours ago.
Also, in acute states may appear the tendency to fill memory gaps with incorrect, fabricated and often implausible information. This phenomenon is called confabulation. Patients with amnesiac syndrome forget that they forget and tend to deny the existence of a memory problem when asked.
The amnesiac patient is almost always disoriented, especially over time. The correct temporal orientation and correct evocation of new information exclude a major amnesiac state. Memory can be tested with a list of four or five words, read aloud by the examiner five times, or until the patient can immediately repeat the entire list without breaks.
In the next stage of testing the patient is allowed to focus on words without being distracted and repeat them in thought for one minute before being asked to remember them. The exact fulfilment of this requirement indicates that the patient is motivated and careful enough to retain the words for at least one minute. The last phase of testing involves a retention for a period of 5 to 10 minutes, during which the patient performs other tasks. Proper evocation at the end of this interval requires encoding, retention, and recovery.
Amnesiac patients fail to pass this last stage of the test and may even forget that they have been given a list of words to memorize. Accurate recognition of words through multiple attempts in a patient who cannot conjure them indicates a less severe memory disorder, which particularly affects the stage of memory recovery.
Many neurological diseases can cause an amnesiac state. These include tumors (of the sphenoidal wing, posterior calos body, thalamus or medial temporal lobe), infarctions (in the territories of the anterior or posterior cerebral artery), head trauma, herpes simplex encephalitis, Wernicke-Korsakoff encephalopathy, neoplastic limbic encephalitis and degenerative dementia, such as Alzheimer's disease or Pick.
A common denominator of these diseases is that it bilaterally affects one or more components of the limbic network. Occasionally, unilateral lesions located on the left may cause an amnesiac state, but the memory disorder tends to be transient.
Depending on the nature and extent of the underlying neurological disease, the patient may also experience visual field changes, limitations of eye movements or cerebellar symptoms. In many patients there are no associated neurological manifestations, occasionally differential diagnosis with psychiatric diseases is necessary. In this case, amnesia may remain undetected and lead to incorrect approach to patients with head trauma or encephalitis with herpes simplex.
Transitional global amnesia is a characteristic syndrome, usually found at the second age. Patients suddenly become disoriented and ask repeatedly who they are, where they are, what they are doing. the syndrome is characterized by anterograde amnesia (inability to retain new information) and retrograde amnesia for relatively recent events that occurred before onset.
The syndrome usually improves in 24-48 hours and is followed by a reminder of the period affected by retrograde amnesia, although memory loss persists for events that occurred during the attack. Recurrences occur in about 20% of patients.
They were postulated as causes of transient global amnesia migraines, temporal seizures and transient ischemic attacks in the territory of the posterior cerebral artery (Pecheron's artery). Although the limbic network reflects the location of the lesion that causes amnesiac states, it is almost certain that memories are not stored here. They are stored in a widely dispersed form in the association cortex.
The role assigned to the limbic network is to link these scattered fragments into coherent events and experiences that can be consciously evoked. Damage to the limbic system does not necessarily destroy memories, but interferes with their conscious (declarative) memory in a coherent form. Individual fragments of information remain preserved despite limbic lesions and can support what is called latent memory (default). For example, amnesiac patients may acquire new motor or perception skills, even if they are not aware of the experiences that have allowed them to acquire these skills.
It's the turn of the prefrontal network of attention and behavior. About a third of the human brain cortex is located in the frontal lobes. frontal lobes may be subdivided into motor-premotor, dorsolateral, prefrontal medial and orbitofrontal components.
The terms frontal lobe syndrome and prefrontal cortex refer only to the last three of the four components. These are the parts of the cerebral cortex that exhibit the greatest philogenic expansion in primates and especially humans.
The dorsolateral, prefrontal medial and orbitofrontal areas and the subcortical structures with which they are connected (e.g. the head of the caudate nucleus and the dorsomedial thalamic nucleus) together form a large prefrontal network that coordinates extremely complex aspects of cognitive function and human behavior.
The orbitofrontal cortex is a place of convergence of signals in the association, paralimbic and limbic cortex and constitutes an area of intersection of prefrontal and limbic networks. Corresponding to this anatomical organization, the prefrontal network plays an important role in behavior, which requires an integration of thoughts with emotions and motivation.
There is no simple wording that includes the various functional affiliates of the prefrontal network. Its integrity seems to be important for simultaneous (conscious) awareness of context, options, consequences, relevance and perspectives so as to allow the formulation of actions, decisions and adaptive implications.
Damage to this part of the brain alters mental flexibility, judgment, the ability to anticipate and inhibit incorrect responses. Behaviours altered by damage to the prefrontal cortex are commonly referred to as "executive functions".
Even the largest bilateral prefrontal lesions can leave intact all basic sensory, motor and cognitive functions, while causing isolated but dramatic alterations in personality and behavior. Associated disorders can occur only in real-life situations, when the behavior is under minimal external control and may not be apparent in the structured environment of the medical office.
Therefore, the doctor must be prepared to diagnose a disease of the frontal lobe based only on anamnestic information, even if in the office the examination of the mental state is normal. The most common clinical manifestations of alteration of the prefrontal network take the form of two relatively distinct syndromes.
In frontal abulic syndrome, the patient manifests a loss of initiative, creativity and curiosity and displays a total apathy and emotional passivity. In frontal disinhibition syndrome, the patient becomes socially uninhibited and shows a severe alteration of judgment, discernment and provision.
The contrast between normal intellectual functions and the total lack of common sense, even rudimentary, is shocking. Despite maintaining all essential functions of memory, the patient cannot learn from experience and continues to behave inappropriately without seeming to feel emotional pain, guilt or regret when this kind of behavior has repeatedly disastrous consequences.
Testing the judgment, asking the patient what they would do if they discovered the outbreak of fire in a theater or what they would do if they found a closed envelope addressed on the street, is not very informative because the patient can correctly answer these questions and yet react wrong in a more complex situation of real life.
I'll continue tomorrow when I hope to finish postings about aphasia and other focal disorders.
The time has come to discuss the limbic network of memory, specifically amnesia.
The central limbic and paralimbic areas, the anterior and medial talamic nucleus, the medial and basal parts of the striated nucleus and the hypothalamus together constitute a large network known as the limbic system. The behavioral affiliations of this network are the coordination of emotion, motivation, vegetative tone and endocrine functions.
An additional area of specialization of the limbic network, with the greatest clinical importance, is that of declarative (conscious) memory for events and experience. Damage to limbic network components can cause global and severe long-term memory disorders. This type of memory alteration is called an amnesiac state.
In the absence of deficits in motivation, attention, language and visual function, the clinical diagnosis of a global and persistent amnesiac state implies the existence of a primary alteration in the core of the long-term memory mechanism and is always associated with bilateral lesions in the limbic network.
Memory disorder in the amnesiac state is multimodal and includes retrograde and anterograde components. Retrograde amnesia refers to the inability to evoke events that occurred before the installation of the amnesiac state. Relatively recent events are more vulnerable in retrograde amnesia than more distant ones.
This phenomenon is called Ribot's gradient and explains why the patient with severe retrograde amnesia rarely forgets the events of childhood. A patient who comes to the emergency room complaining that he can't remember what it's called, but can evoke events that day, is almost certainly not suffering from a neurological cause of memory disorder.
The second and most important component of the amnesiac state is anterograde amnesia, which consists of the inability to store, retain and evoke recent information. Patients with amnesiac conditions are vigilant and motivated, but cannot remember what they ate a few minutes ago or details of an important event experienced a few hours ago.
Also, in acute states may appear the tendency to fill memory gaps with incorrect, fabricated and often implausible information. This phenomenon is called confabulation. Patients with amnesiac syndrome forget that they forget and tend to deny the existence of a memory problem when asked.
The amnesiac patient is almost always disoriented, especially over time. The correct temporal orientation and correct evocation of new information exclude a major amnesiac state. Memory can be tested with a list of four or five words, read aloud by the examiner five times, or until the patient can immediately repeat the entire list without breaks.
In the next stage of testing the patient is allowed to focus on words without being distracted and repeat them in thought for one minute before being asked to remember them. The exact fulfilment of this requirement indicates that the patient is motivated and careful enough to retain the words for at least one minute. The last phase of testing involves a retention for a period of 5 to 10 minutes, during which the patient performs other tasks. Proper evocation at the end of this interval requires encoding, retention, and recovery.
Amnesiac patients fail to pass this last stage of the test and may even forget that they have been given a list of words to memorize. Accurate recognition of words through multiple attempts in a patient who cannot conjure them indicates a less severe memory disorder, which particularly affects the stage of memory recovery.
Many neurological diseases can cause an amnesiac state. These include tumors (of the sphenoidal wing, posterior calos body, thalamus or medial temporal lobe), infarctions (in the territories of the anterior or posterior cerebral artery), head trauma, herpes simplex encephalitis, Wernicke-Korsakoff encephalopathy, neoplastic limbic encephalitis and degenerative dementia, such as Alzheimer's disease or Pick.
A common denominator of these diseases is that it bilaterally affects one or more components of the limbic network. Occasionally, unilateral lesions located on the left may cause an amnesiac state, but the memory disorder tends to be transient.
Depending on the nature and extent of the underlying neurological disease, the patient may also experience visual field changes, limitations of eye movements or cerebellar symptoms. In many patients there are no associated neurological manifestations, occasionally differential diagnosis with psychiatric diseases is necessary. In this case, amnesia may remain undetected and lead to incorrect approach to patients with head trauma or encephalitis with herpes simplex.
Transitional global amnesia is a characteristic syndrome, usually found at the second age. Patients suddenly become disoriented and ask repeatedly who they are, where they are, what they are doing. the syndrome is characterized by anterograde amnesia (inability to retain new information) and retrograde amnesia for relatively recent events that occurred before onset.
The syndrome usually improves in 24-48 hours and is followed by a reminder of the period affected by retrograde amnesia, although memory loss persists for events that occurred during the attack. Recurrences occur in about 20% of patients.
They were postulated as causes of transient global amnesia migraines, temporal seizures and transient ischemic attacks in the territory of the posterior cerebral artery (Pecheron's artery). Although the limbic network reflects the location of the lesion that causes amnesiac states, it is almost certain that memories are not stored here. They are stored in a widely dispersed form in the association cortex.
The role assigned to the limbic network is to link these scattered fragments into coherent events and experiences that can be consciously evoked. Damage to the limbic system does not necessarily destroy memories, but interferes with their conscious (declarative) memory in a coherent form. Individual fragments of information remain preserved despite limbic lesions and can support what is called latent memory (default). For example, amnesiac patients may acquire new motor or perception skills, even if they are not aware of the experiences that have allowed them to acquire these skills.
It's the turn of the prefrontal network of attention and behavior. About a third of the human brain cortex is located in the frontal lobes. frontal lobes may be subdivided into motor-premotor, dorsolateral, prefrontal medial and orbitofrontal components.
The terms frontal lobe syndrome and prefrontal cortex refer only to the last three of the four components. These are the parts of the cerebral cortex that exhibit the greatest philogenic expansion in primates and especially humans.
The dorsolateral, prefrontal medial and orbitofrontal areas and the subcortical structures with which they are connected (e.g. the head of the caudate nucleus and the dorsomedial thalamic nucleus) together form a large prefrontal network that coordinates extremely complex aspects of cognitive function and human behavior.
The orbitofrontal cortex is a place of convergence of signals in the association, paralimbic and limbic cortex and constitutes an area of intersection of prefrontal and limbic networks. Corresponding to this anatomical organization, the prefrontal network plays an important role in behavior, which requires an integration of thoughts with emotions and motivation.
There is no simple wording that includes the various functional affiliates of the prefrontal network. Its integrity seems to be important for simultaneous (conscious) awareness of context, options, consequences, relevance and perspectives so as to allow the formulation of actions, decisions and adaptive implications.
Damage to this part of the brain alters mental flexibility, judgment, the ability to anticipate and inhibit incorrect responses. Behaviours altered by damage to the prefrontal cortex are commonly referred to as "executive functions".
Even the largest bilateral prefrontal lesions can leave intact all basic sensory, motor and cognitive functions, while causing isolated but dramatic alterations in personality and behavior. Associated disorders can occur only in real-life situations, when the behavior is under minimal external control and may not be apparent in the structured environment of the medical office.
Therefore, the doctor must be prepared to diagnose a disease of the frontal lobe based only on anamnestic information, even if in the office the examination of the mental state is normal. The most common clinical manifestations of alteration of the prefrontal network take the form of two relatively distinct syndromes.
In frontal abulic syndrome, the patient manifests a loss of initiative, creativity and curiosity and displays a total apathy and emotional passivity. In frontal disinhibition syndrome, the patient becomes socially uninhibited and shows a severe alteration of judgment, discernment and provision.
The contrast between normal intellectual functions and the total lack of common sense, even rudimentary, is shocking. Despite maintaining all essential functions of memory, the patient cannot learn from experience and continues to behave inappropriately without seeming to feel emotional pain, guilt or regret when this kind of behavior has repeatedly disastrous consequences.
Testing the judgment, asking the patient what they would do if they discovered the outbreak of fire in a theater or what they would do if they found a closed envelope addressed on the street, is not very informative because the patient can correctly answer these questions and yet react wrong in a more complex situation of real life.
I'll continue tomorrow when I hope to finish postings about aphasia and other focal disorders.
A week full of
achievements, trust, love and gratitude.
Dorin, Merticaru