STUDY - Technical - New Dacian's Medicine
Aphasia
and other Focal Disorders (6)
Translation Draft
I'll continue with the prefrontal network of attention and behavior.
Abulic syndrome appears to be associated with damage to the dorsolateral prefrontal cortex, and disinhibition, to damage to the medial or orbitofrontal prefrontal cortex. These syndromes occur almost exclusively through bilateral damage, most commonly in the case of head trauma, stroke, rupture of aneurysm, hydrocephalus or tumors (including metastases, glioblastoma and meningiomas of the olfactory or seam trench). Unilateral lesions limited to the prefrontal cortex may remain asymptomatic until the pathological process extends to the other side.
The urgent appearance of primitive developmental reflexes, such as grasping, gripping and sucking reflexes, are also signs of frontal lobe disease. However, these reflexes are particularly common in patients with extensive structural lesions, which extend into the premotor components of the frontal lobes or occur in the context of metabolic encephalopathy. The vast majority of patients with prefrontal lesions and behavioral syndromes of the frontal lobe do not exhibit these reflexes. Thus, the absence of sucking, gripping, grasping reflexes does not exclude a frontal lobe injury.
The damage to the prefrontal network affects reasoning, abstract thinking and the ability to formulate hypotheses and leads to a mental functioning related to stimuli, concrete and impulsive. Also, damage to this part of the brain alters a variety of attention-related functions, including ability to concentrate, verbal fluency, inhibition of immediate but inadequate responses, and mental flexibility.
The ability to count (which normally is 7 digits forward and 5 back) is low, the enumeration of the months of the year in reverse order (normally lasts less than 15 seconds) is slowed down, and the number of words beginning with "a," "f" or "s" that can be found in a minute (normal, 12 or more for a letter) is diminished even in nonaphasic patients. Typically, there is a gradual decrease in performance as the test progresses, for example, the patient is asked to count in reverse from 20 and will respond by counting with increasing pauses with each number "traveled", and may not even finish the count.
In the "act-sit" test (in which a patient must lift a finger when he hears a beat and remain calm when he hears two beats), the patient is characteristically unable to remain calm in response to the stimulus indicating "wait", mental flexibility (tested by the ability to move from one criterion to another in sorting objects) is low , distraction through irrelevant stimuli is increased and there is a pronounced tendency to persevere. Effective internal evaluation of acquired information, the ability to focus on a thought and the ability to move attention flexibly from one thought or stimulus to another are altered.
These attention deficits lead to the development of "working memory" disorders. Work memory capacity refers to the amount of information that can be kept active (consciously usable) at any given time. Working memory disorder interferes with the ability to maintain a coherent flow of thoughts and causes confusion, especially in special situations that require simultaneous evaluation of multiple variables.
Attention deficit alters the recording and recovery of new information and causes secondary memory deficits. These memory difficulties can be differentiated from those in amnesiac states by demonstrating that they improve when the attention needed to perform this test decreases.
Working memory (also called short-term memory) is a function of attention based on the active, temporary retention of information. It is closely related to the integrity of the prefrontal network and the ascending SRA. long-term memory, on the other hand, depends on stable (inactive) storage of information and is associated with the integrity of the limbic network.
The distinction between basic neural mechanisms is illustrated by the observation that severely amnesiac patients, who cannot remember events that occurred a few minutes before, may have an intact but not even superior working memory capacity, as the counting capacity test shows. Working memory is closely related to the integrity of the dorsolateral prefrontal cortex, while attention functions such as the ability to inhibit inappropriate responses (assessed on the "act-stay" test) depend primarily on the integrity of the medial or orbitofrontal prefrontal cortex.
The network approach posits that the same cognitive domain can be affected by damaging different parts of the brain as long as they belong to the same neural network. Consequently, lesions of the caudate nucleus or dorsomedial talamic nucleus (structures that are considered subcortical components of the prefrontal network) also determine the clinical picture of frontal lobe syndrome.
This is one of the reasons why changes in mental state associated with degenerative diseases of the basal ganglia, such as Parkinson's disease or Huntington's disease, can take the form of frontal lobe syndrome. Due to widespread connections with other regions of the association cortex, an essential role of the prefrontal network is to function as an integrator or coordinator of other networks.
Bilateral multifocal lesions of the cerebral hemispheres, none of which are large enough to cause specific cognitive deficits, such as aphasia or neglect, can together interfere with the integrative and connecting function of the prefrontal cortex.
This is one reason why frontal lobe syndrome is the most common behavioral profile associated with a variety of bilateral multifocal brain disorders, such as metabolic encephalopathy, multiple sclerosis, vitamin B12 deficiency and others.
In fact, the vast majority of patients with clinical diagnosis of frontal lobe syndrome tend to show lesions that do not involve the prefrontal cortex, but the subcortical components of the prefrontal network or its connections to other parts of the brain. In order to avoid the paradoxical situation of diagnosing a "frontal lobe syndrome" in a patient who has no symptoms of disease of the frontal cortex, it is recommended to use the diagnostic term of prefrontal network syndrome, implying that the causative lesion can be located anywhere in this extensive network.
Patients with frontal lobe disease raise some problems of differential diagnosis, abulia and placidity can be misinterpreted as depression, and disinhibition as mania or pretence. Curative interventions may be delayed while a treatable tumour spreads/develops.
Let me type now on the care of patients with cognitive impairments. Some of the disorders described are so complex that not only the patient and family, but also the doctor cannot cope. It is important to establish a systematic clinical assessment to characterize the nature of the deficiency and to clearly explain it to the patient and the family.
These explanations may improve at least some of the anxieties, remove the mistaken impression that this deficit (e.g. social disinhibition or inability to recognise family members) is psychologically motivated and provide practical suggestions for everyday life.
Patients with simultagnosia, for example, should be advised to move back when they cannot find an object, so that a larger search area enters the field of their gaze. Doctors tend to give too much importance to the signs they manage to obtain through the clinical examination.
However, in some patients, anamnesis may be more important and may conflict with examination at the patient's bed. For example, patients with frontal lobe disease may be extremely irritable and abusive towards their spouse and at the same time behave flawlessly during a visit to the doctor.
Reactive depression is common in patients with high cortical dysfunction and should be treated. These patients may be sensitive to the usual doses of antidepressants or anxiolytics and require careful titration of doses. Brain injuries can cause a dissociation between emotional status and its expression, so a patient who appears to be cheerful on a superficial examination may suffer from a basic depression to be treated.
In many cases, agitation can be controlled by soothing words. In others, treatment with benzodiazepines or sedative antidepressants may be necessary. The use of neuroleptics for agitation control should be reserved only for refractory cases, as extrapyramidal side effects are common in patients with coexisting brain damage.
The evaluation of high cortical functions can be systematic, as can the rest of the neurological examination, but it also requires time and knowledge of specialized tests. Consultation with an experienced neuropsychologist can help in formulating diagnosis and treatment.
The accessibility of TC, MRI, positron emission tomography and single photon emission TC does not exclude the need for careful clinical evaluation, since the results and complex implications of these diagnostic procedures cannot be interpreted solely in the light of the results of the full clinical examination.
Spontaneous improvement of cognitive deficits due to acute neurological damage is common. The improvement is rapid in the first four weeks, but can continue up to 2 years, especially in young people with unique brain damage. The mechanisms of this recovery are not fully understood. Some of the initial deficits appear to be caused by remote dysfunction (diaschisis) in parts of the brain that are interconnected with the primary site of the lesion. Improvement in these patients may reflect, at least in part, a normalization of this remote dysfunction.
Other mechanisms that may involve functional reorganization in neurons that have survived around the lesion or compensatory use of analogous structures, for example, the right upper temporal gyrus in the recovery of Wernicke aphasia. Cognitive rehabilitation procedures have been used in the treatment of upper cortical deficits.
There are few controlled studies, but some demonstrate a benefit of rehabilitation in the recovery of hemispatial neglect and aphasia. In some cases, the recovery of cognitive deficits reflects the development of compensatory mechanisms. In others, recovery involves the reorganization of relevant neural networks. Some types of deficits may be easier to recover than others.
For example, patients with non-fluent aphasia benefit more from speech therapy than patients with fluent aphasia and comprehension deficits. In general, lesions that lead to disease denial (e.g. anosognosia) are associated with cognitive deficits that are more resistant to rehabilitation.
Recovery of upper cortical dysfunction is rarely complete. Periodic neuropsychological evaluation is necessary to quantify the evolution of improvement, to make specific recommendations for cognitive rehabilitation, changes in the family environment and to determine the time of return to school or work.
Yes, I'm done... From tomorrow we'll talk about memory loss and dementia...
I'll continue with the prefrontal network of attention and behavior.
Abulic syndrome appears to be associated with damage to the dorsolateral prefrontal cortex, and disinhibition, to damage to the medial or orbitofrontal prefrontal cortex. These syndromes occur almost exclusively through bilateral damage, most commonly in the case of head trauma, stroke, rupture of aneurysm, hydrocephalus or tumors (including metastases, glioblastoma and meningiomas of the olfactory or seam trench). Unilateral lesions limited to the prefrontal cortex may remain asymptomatic until the pathological process extends to the other side.
The urgent appearance of primitive developmental reflexes, such as grasping, gripping and sucking reflexes, are also signs of frontal lobe disease. However, these reflexes are particularly common in patients with extensive structural lesions, which extend into the premotor components of the frontal lobes or occur in the context of metabolic encephalopathy. The vast majority of patients with prefrontal lesions and behavioral syndromes of the frontal lobe do not exhibit these reflexes. Thus, the absence of sucking, gripping, grasping reflexes does not exclude a frontal lobe injury.
The damage to the prefrontal network affects reasoning, abstract thinking and the ability to formulate hypotheses and leads to a mental functioning related to stimuli, concrete and impulsive. Also, damage to this part of the brain alters a variety of attention-related functions, including ability to concentrate, verbal fluency, inhibition of immediate but inadequate responses, and mental flexibility.
The ability to count (which normally is 7 digits forward and 5 back) is low, the enumeration of the months of the year in reverse order (normally lasts less than 15 seconds) is slowed down, and the number of words beginning with "a," "f" or "s" that can be found in a minute (normal, 12 or more for a letter) is diminished even in nonaphasic patients. Typically, there is a gradual decrease in performance as the test progresses, for example, the patient is asked to count in reverse from 20 and will respond by counting with increasing pauses with each number "traveled", and may not even finish the count.
In the "act-sit" test (in which a patient must lift a finger when he hears a beat and remain calm when he hears two beats), the patient is characteristically unable to remain calm in response to the stimulus indicating "wait", mental flexibility (tested by the ability to move from one criterion to another in sorting objects) is low , distraction through irrelevant stimuli is increased and there is a pronounced tendency to persevere. Effective internal evaluation of acquired information, the ability to focus on a thought and the ability to move attention flexibly from one thought or stimulus to another are altered.
These attention deficits lead to the development of "working memory" disorders. Work memory capacity refers to the amount of information that can be kept active (consciously usable) at any given time. Working memory disorder interferes with the ability to maintain a coherent flow of thoughts and causes confusion, especially in special situations that require simultaneous evaluation of multiple variables.
Attention deficit alters the recording and recovery of new information and causes secondary memory deficits. These memory difficulties can be differentiated from those in amnesiac states by demonstrating that they improve when the attention needed to perform this test decreases.
Working memory (also called short-term memory) is a function of attention based on the active, temporary retention of information. It is closely related to the integrity of the prefrontal network and the ascending SRA. long-term memory, on the other hand, depends on stable (inactive) storage of information and is associated with the integrity of the limbic network.
The distinction between basic neural mechanisms is illustrated by the observation that severely amnesiac patients, who cannot remember events that occurred a few minutes before, may have an intact but not even superior working memory capacity, as the counting capacity test shows. Working memory is closely related to the integrity of the dorsolateral prefrontal cortex, while attention functions such as the ability to inhibit inappropriate responses (assessed on the "act-stay" test) depend primarily on the integrity of the medial or orbitofrontal prefrontal cortex.
The network approach posits that the same cognitive domain can be affected by damaging different parts of the brain as long as they belong to the same neural network. Consequently, lesions of the caudate nucleus or dorsomedial talamic nucleus (structures that are considered subcortical components of the prefrontal network) also determine the clinical picture of frontal lobe syndrome.
This is one of the reasons why changes in mental state associated with degenerative diseases of the basal ganglia, such as Parkinson's disease or Huntington's disease, can take the form of frontal lobe syndrome. Due to widespread connections with other regions of the association cortex, an essential role of the prefrontal network is to function as an integrator or coordinator of other networks.
Bilateral multifocal lesions of the cerebral hemispheres, none of which are large enough to cause specific cognitive deficits, such as aphasia or neglect, can together interfere with the integrative and connecting function of the prefrontal cortex.
This is one reason why frontal lobe syndrome is the most common behavioral profile associated with a variety of bilateral multifocal brain disorders, such as metabolic encephalopathy, multiple sclerosis, vitamin B12 deficiency and others.
In fact, the vast majority of patients with clinical diagnosis of frontal lobe syndrome tend to show lesions that do not involve the prefrontal cortex, but the subcortical components of the prefrontal network or its connections to other parts of the brain. In order to avoid the paradoxical situation of diagnosing a "frontal lobe syndrome" in a patient who has no symptoms of disease of the frontal cortex, it is recommended to use the diagnostic term of prefrontal network syndrome, implying that the causative lesion can be located anywhere in this extensive network.
Patients with frontal lobe disease raise some problems of differential diagnosis, abulia and placidity can be misinterpreted as depression, and disinhibition as mania or pretence. Curative interventions may be delayed while a treatable tumour spreads/develops.
Let me type now on the care of patients with cognitive impairments. Some of the disorders described are so complex that not only the patient and family, but also the doctor cannot cope. It is important to establish a systematic clinical assessment to characterize the nature of the deficiency and to clearly explain it to the patient and the family.
These explanations may improve at least some of the anxieties, remove the mistaken impression that this deficit (e.g. social disinhibition or inability to recognise family members) is psychologically motivated and provide practical suggestions for everyday life.
Patients with simultagnosia, for example, should be advised to move back when they cannot find an object, so that a larger search area enters the field of their gaze. Doctors tend to give too much importance to the signs they manage to obtain through the clinical examination.
However, in some patients, anamnesis may be more important and may conflict with examination at the patient's bed. For example, patients with frontal lobe disease may be extremely irritable and abusive towards their spouse and at the same time behave flawlessly during a visit to the doctor.
Reactive depression is common in patients with high cortical dysfunction and should be treated. These patients may be sensitive to the usual doses of antidepressants or anxiolytics and require careful titration of doses. Brain injuries can cause a dissociation between emotional status and its expression, so a patient who appears to be cheerful on a superficial examination may suffer from a basic depression to be treated.
In many cases, agitation can be controlled by soothing words. In others, treatment with benzodiazepines or sedative antidepressants may be necessary. The use of neuroleptics for agitation control should be reserved only for refractory cases, as extrapyramidal side effects are common in patients with coexisting brain damage.
The evaluation of high cortical functions can be systematic, as can the rest of the neurological examination, but it also requires time and knowledge of specialized tests. Consultation with an experienced neuropsychologist can help in formulating diagnosis and treatment.
The accessibility of TC, MRI, positron emission tomography and single photon emission TC does not exclude the need for careful clinical evaluation, since the results and complex implications of these diagnostic procedures cannot be interpreted solely in the light of the results of the full clinical examination.
Spontaneous improvement of cognitive deficits due to acute neurological damage is common. The improvement is rapid in the first four weeks, but can continue up to 2 years, especially in young people with unique brain damage. The mechanisms of this recovery are not fully understood. Some of the initial deficits appear to be caused by remote dysfunction (diaschisis) in parts of the brain that are interconnected with the primary site of the lesion. Improvement in these patients may reflect, at least in part, a normalization of this remote dysfunction.
Other mechanisms that may involve functional reorganization in neurons that have survived around the lesion or compensatory use of analogous structures, for example, the right upper temporal gyrus in the recovery of Wernicke aphasia. Cognitive rehabilitation procedures have been used in the treatment of upper cortical deficits.
There are few controlled studies, but some demonstrate a benefit of rehabilitation in the recovery of hemispatial neglect and aphasia. In some cases, the recovery of cognitive deficits reflects the development of compensatory mechanisms. In others, recovery involves the reorganization of relevant neural networks. Some types of deficits may be easier to recover than others.
For example, patients with non-fluent aphasia benefit more from speech therapy than patients with fluent aphasia and comprehension deficits. In general, lesions that lead to disease denial (e.g. anosognosia) are associated with cognitive deficits that are more resistant to rehabilitation.
Recovery of upper cortical dysfunction is rarely complete. Periodic neuropsychological evaluation is necessary to quantify the evolution of improvement, to make specific recommendations for cognitive rehabilitation, changes in the family environment and to determine the time of return to school or work.
Yes, I'm done... From tomorrow we'll talk about memory loss and dementia...
One of the best, spornic,
blah, blah, blah...
Dorin, Merticaru