STUDY - Technical - New Dacian's Medicine
Memory
loss and Dementia (2)
Translation Draft
Let's get on with what we started yesterday!
Damage to relatively specific cortical-subcortical pathways can have significant effects on behavior. The prefrontal dorsolateral cortex has connections in the dorsolateral caudate nucleus, with globus pallidus and thalamus. Injury to these paths leads to a decrease in organizational and planning capacity, perseverance and reduced cognitive flexibility with impaired judgment.
The lateral orbital frontal cortex connects with the anteromedial caudate nucleus, the pallidus globus and the thalamus. Damage to these connections causes irritability, impulsivity and distraction. The anterior cingulate cortex is connected with the nucleus accumbens, globus pallidus and thalamus. Interrupting these connections causes apathy and impoverishment of speech or even akinetic mutism.
The strongest risk factor for dementia is aging. The prevalence of incapacitating memory loss increases with each decade over 50 years and is most commonly associated with microscopic ba changes at autopsy. Slow accumulation of mutations in neuronal mitochondria is thought to increase the prevalence of dementia with age. However, many people over the age of 100 have intact memory and no significant clinical signs of dementia. The assumption that dementia is an inevitable consequence of ageing remains controversial.
Let's move on to differential diagnosis. Dementia has many causes, the most "important" being represented by: alcoholism, BA and various poisonings (with drugs, drugs). The frequency of each disease depends on the age studied, the country of origin and perhaps on racial and ethnic variations. BA is the most common etiology of dementia in Western countries, accounting for more than half of dementia patients.
Vascular diseases are the second most common, representing 20 to 25% but are less common compared to BA in Asian countries. Dementia is associated with chronic alcoholism and Parkinson's disease (BP) are the following etiologies in order of frequency. Chronic poisoning, including those resulting from prescriptions, is an important, potentially curable cause of dementia. Other diseases are rare but important because many are reversible. The classification of diseases associated with dementia into two curable and incurable categories is a useful approach in the differential diagnosis of dementia.
Subtle, cumulative memory loss is a natural component of aging. This frustrating experience, often a source of jokes, is called "benign forgetting the elderly." Benign means that it is not so progressive or serious as to disturb the likely completed and productive daily activities, although the distinction between benign and severe memory loss may be difficult to make. Some people with benign memory loss progress to french dementia, usually caused by BA.
It is not clear why in some individuals the disease evolves and in others does not. In the past it was assumed that the cumulative loss of hippocampal neurons, as we age, could cause this forgetit, but recent quantitative neural determinations indicate that this "natural" loss of neurons may not occur.
Alzheimer's disease (BA) is a slow-progressing dementia syndrome associated with diffuse cortical atrophy and specific neuropathological elements (amyloid plaques and neurofibrillary degeneration). Although it is quite common in the elderly, BA remains a diagnosis of exclusion that can only be definitively confirmed by autopsy. The clinical diagnosis of BA, established by experienced neurologists is proven to be correct at autopsy in approximately 85 to 90% of cases.
Two major types of vascular dementia can be identified. The first, often called multi-infarct dementia, results from the accumulation of small strokes that cause incapacitating deficits in memory, behavior and other cognitive functions. Patients usually describe a history of unexpected, separate ischemic episodes with gradual deterioration of mental state.
On examination, focal neurological deficits, such as hemiparesis, babinski reflex unilaterally, aphasia or other visual field alterations, are common. The imaging examination of the brain shows multiple areas of strokes, which can be ischemic or hemorrhagic.
A second, more subtle and insidious type of vascular dementia, Binswanger disease, is a dementia syndrome associated with diffuse subcortical white fever, which commonly occurs in patients with chronic hypertension and/ or severe arteriosclerosis. Changes to the white substance are viewed most accurately by MRI. pathogenesis of Binswanger disease is unknown. Because BA and vascular dementia are common, sometimes patients may experience both pathological conditions.
Dementia usually accompanies chronic alcoholism. It may be the result of associated malnutrition, especially the insufficiency of B vitamins and, in particular, of thiamine. However, other aspects of chronic alcohol intake, which are not known, can cause lesions and cerebral dystrophy.
An idiopathic syndrome, with dementia and seizures, rarely encountered and accompanied by the degeneration of the calos body, was first reported by Italian male consumers of red wine (Marchiafava-Bignami disease).
Thiamine deficiency (vitamin B1) produces Wernicke encephalopathy. The patient is malnourished (frequently, but not necessarily alcoholic) and presents confusion, ataxia and diplopia by ophthalmoplegia (Charcot triad).
Thiamine deficiency causes damage to the thalamus, mammalian bodies, middle cerebellum, periventricular grey substance of the mesencephalus and peripheral nerves. Damage to the medial thalamic region correlates closely with memory loss. Prompt administration of parenteral thiamine may improve the disease if done in the first few days after the onset of symptomatology. However, prolonged, untreated thiamine deficiency leads to irreversible amnesiac syndrome (Korsakoff psychosis) or even death.
In Korsakoff syndrome, the patient cannot recall recent information, despite immediate memory, attention and normal level of consciousness. Memorization of recent events is severely impaired, while memory for information acquired before the onset of the disease is relatively intact. Patients are slightly confused, disoriented, unable to recall recent information for more than a short period of time. At first glance they can be volubile, funny, able to meet simple requirements and immediately follow orders. Confabulation is common, though not always present, and can lead to obviously erroneous elaborations and phrases. There is no specific treatment because thiamine deficiency previously produced irreversible damage in medial talamic sacs and mammalian children. The atrophy of the mammalian bodies can be viewed by high-resolution MRI.
Vitamin B12 deficiency, found in pernicious anemia, causes macrocytic amnesia and can also cause damage to the nervous system. Neurologically, it most commonly produces a medullary syndrome (myelopathy), affecting the posterior cords (loss of vibrating and proprioceptive sensitivity) and lateral corticospinal pathways (living tendinous reflexes and Babinski reflex present).
It can also cause damage to peripheral neurons, leading to loss of sensitivity with attenuated tendon reflexes. And damage to cerebral myelinized threads can cause dementia. The mechanism of neurological alteration is unclear, but it appears to be related to S-adenosylmethionine deficiency (necessary for methylation of myelin phospholipids), due to decreased methionine synthesis or accumulation of propionate and methylmalonate, which provideabnormal substrates for fatty acid synthesis in myelin.
Neurological signs of vitamin B12 deficiency are usually associated with macrocytic anaemia, but can sometimes occur in its absence. Treatment with vitamin B12 administered parenterally stops the progression of the disease if promptly instituted, but no recovery of advanced lesions of the nervous system is obtained.
Nicotinic acid deficiency (pelagra) is associated with tegumentary rash in areas exposed to sun, glossitis and angular stomatitis. Severe dietary deficiency of nicotinic acid and other B vitamins, such as pyridoxine, can lead to spastic paraparesis, peripheral neuropathy, fatigue, irritability and dementia. This syndrome has been found in prisoners of war and in concentration camps. A coarse indicator of malnutrition appears to be low serum phosphate levels, but isolated phosphate deficiency has not been shown to be a specific cause of dementia.
Approximately 20% of PATIENTS with BP eventually develop dementia. Some patients with BP and dementia have neural cytoplasmic inclusions (Lewy bodies) or BA-specific changes in the cerebral cortex, but others do not have specific, identifiable pathological brain damage.
Infections of the central nervous system (CNS) generally cause delirium and other acute neurological syndromes. However, some chronic CNS infections such as tuberculosis and cryptococosis can cause dementia. Between 20 and 30% of patients in advanced stages AIDS become demented.
The main manifestations are psychomotor retardation, apathy and memory disorders. These may be the result of opportunistic secondary infections, but they can also be directly caused by infection of CNS neurons with HIV, in this case there is multi-closted giant cell encephalitis and diffuse pallor of the white substance. Herpes simplex encephalitis has a predilection for the lower temporal lobes and may present with disorientation and subacute confusion, but much more common as acute syndrome than as chronic dementia. TC, MRI and EEC can detect the location of lesions in the temporal lobe.
CRL usually has lymphocytic pleiocytosis and an increased protein concentration. CNS syphilis was a common cause of dementia in the preantibiotic era, now rarely present, but can still be found in the population group with multiple sexual partners. Characteristic changes in CRL are pleiocytosis, increased protein concentration and the vDRL positive test.
Prionic diseases, such as Creutzfeldt-Jakob disease (BCJ), are very rare pathological conditions (1 person per million) that usually produce dementia. BCJ is usually rapidly progressive, associated with dementia, stiffness and myoclonia, causing death in less than 1 to 2 years. These clinical manifestations can also rarely be found in BA, with differential diagnosis usually based on the slow evolution of BA and abnormal, periodic ECG discharges, also found in BA, with differential diagnosis usually based on the slow evolution of BA and abnormal, periodic ECG discharges found in BCJ.
I have about two more posts before I'm done with my memory disorders and my demented description, so arm yourself with patience and curiosity!
Let's get on with what we started yesterday!
Damage to relatively specific cortical-subcortical pathways can have significant effects on behavior. The prefrontal dorsolateral cortex has connections in the dorsolateral caudate nucleus, with globus pallidus and thalamus. Injury to these paths leads to a decrease in organizational and planning capacity, perseverance and reduced cognitive flexibility with impaired judgment.
The lateral orbital frontal cortex connects with the anteromedial caudate nucleus, the pallidus globus and the thalamus. Damage to these connections causes irritability, impulsivity and distraction. The anterior cingulate cortex is connected with the nucleus accumbens, globus pallidus and thalamus. Interrupting these connections causes apathy and impoverishment of speech or even akinetic mutism.
The strongest risk factor for dementia is aging. The prevalence of incapacitating memory loss increases with each decade over 50 years and is most commonly associated with microscopic ba changes at autopsy. Slow accumulation of mutations in neuronal mitochondria is thought to increase the prevalence of dementia with age. However, many people over the age of 100 have intact memory and no significant clinical signs of dementia. The assumption that dementia is an inevitable consequence of ageing remains controversial.
Let's move on to differential diagnosis. Dementia has many causes, the most "important" being represented by: alcoholism, BA and various poisonings (with drugs, drugs). The frequency of each disease depends on the age studied, the country of origin and perhaps on racial and ethnic variations. BA is the most common etiology of dementia in Western countries, accounting for more than half of dementia patients.
Vascular diseases are the second most common, representing 20 to 25% but are less common compared to BA in Asian countries. Dementia is associated with chronic alcoholism and Parkinson's disease (BP) are the following etiologies in order of frequency. Chronic poisoning, including those resulting from prescriptions, is an important, potentially curable cause of dementia. Other diseases are rare but important because many are reversible. The classification of diseases associated with dementia into two curable and incurable categories is a useful approach in the differential diagnosis of dementia.
Subtle, cumulative memory loss is a natural component of aging. This frustrating experience, often a source of jokes, is called "benign forgetting the elderly." Benign means that it is not so progressive or serious as to disturb the likely completed and productive daily activities, although the distinction between benign and severe memory loss may be difficult to make. Some people with benign memory loss progress to french dementia, usually caused by BA.
It is not clear why in some individuals the disease evolves and in others does not. In the past it was assumed that the cumulative loss of hippocampal neurons, as we age, could cause this forgetit, but recent quantitative neural determinations indicate that this "natural" loss of neurons may not occur.
Alzheimer's disease (BA) is a slow-progressing dementia syndrome associated with diffuse cortical atrophy and specific neuropathological elements (amyloid plaques and neurofibrillary degeneration). Although it is quite common in the elderly, BA remains a diagnosis of exclusion that can only be definitively confirmed by autopsy. The clinical diagnosis of BA, established by experienced neurologists is proven to be correct at autopsy in approximately 85 to 90% of cases.
Two major types of vascular dementia can be identified. The first, often called multi-infarct dementia, results from the accumulation of small strokes that cause incapacitating deficits in memory, behavior and other cognitive functions. Patients usually describe a history of unexpected, separate ischemic episodes with gradual deterioration of mental state.
On examination, focal neurological deficits, such as hemiparesis, babinski reflex unilaterally, aphasia or other visual field alterations, are common. The imaging examination of the brain shows multiple areas of strokes, which can be ischemic or hemorrhagic.
A second, more subtle and insidious type of vascular dementia, Binswanger disease, is a dementia syndrome associated with diffuse subcortical white fever, which commonly occurs in patients with chronic hypertension and/ or severe arteriosclerosis. Changes to the white substance are viewed most accurately by MRI. pathogenesis of Binswanger disease is unknown. Because BA and vascular dementia are common, sometimes patients may experience both pathological conditions.
Dementia usually accompanies chronic alcoholism. It may be the result of associated malnutrition, especially the insufficiency of B vitamins and, in particular, of thiamine. However, other aspects of chronic alcohol intake, which are not known, can cause lesions and cerebral dystrophy.
An idiopathic syndrome, with dementia and seizures, rarely encountered and accompanied by the degeneration of the calos body, was first reported by Italian male consumers of red wine (Marchiafava-Bignami disease).
Thiamine deficiency (vitamin B1) produces Wernicke encephalopathy. The patient is malnourished (frequently, but not necessarily alcoholic) and presents confusion, ataxia and diplopia by ophthalmoplegia (Charcot triad).
Thiamine deficiency causes damage to the thalamus, mammalian bodies, middle cerebellum, periventricular grey substance of the mesencephalus and peripheral nerves. Damage to the medial thalamic region correlates closely with memory loss. Prompt administration of parenteral thiamine may improve the disease if done in the first few days after the onset of symptomatology. However, prolonged, untreated thiamine deficiency leads to irreversible amnesiac syndrome (Korsakoff psychosis) or even death.
In Korsakoff syndrome, the patient cannot recall recent information, despite immediate memory, attention and normal level of consciousness. Memorization of recent events is severely impaired, while memory for information acquired before the onset of the disease is relatively intact. Patients are slightly confused, disoriented, unable to recall recent information for more than a short period of time. At first glance they can be volubile, funny, able to meet simple requirements and immediately follow orders. Confabulation is common, though not always present, and can lead to obviously erroneous elaborations and phrases. There is no specific treatment because thiamine deficiency previously produced irreversible damage in medial talamic sacs and mammalian children. The atrophy of the mammalian bodies can be viewed by high-resolution MRI.
Vitamin B12 deficiency, found in pernicious anemia, causes macrocytic amnesia and can also cause damage to the nervous system. Neurologically, it most commonly produces a medullary syndrome (myelopathy), affecting the posterior cords (loss of vibrating and proprioceptive sensitivity) and lateral corticospinal pathways (living tendinous reflexes and Babinski reflex present).
It can also cause damage to peripheral neurons, leading to loss of sensitivity with attenuated tendon reflexes. And damage to cerebral myelinized threads can cause dementia. The mechanism of neurological alteration is unclear, but it appears to be related to S-adenosylmethionine deficiency (necessary for methylation of myelin phospholipids), due to decreased methionine synthesis or accumulation of propionate and methylmalonate, which provideabnormal substrates for fatty acid synthesis in myelin.
Neurological signs of vitamin B12 deficiency are usually associated with macrocytic anaemia, but can sometimes occur in its absence. Treatment with vitamin B12 administered parenterally stops the progression of the disease if promptly instituted, but no recovery of advanced lesions of the nervous system is obtained.
Nicotinic acid deficiency (pelagra) is associated with tegumentary rash in areas exposed to sun, glossitis and angular stomatitis. Severe dietary deficiency of nicotinic acid and other B vitamins, such as pyridoxine, can lead to spastic paraparesis, peripheral neuropathy, fatigue, irritability and dementia. This syndrome has been found in prisoners of war and in concentration camps. A coarse indicator of malnutrition appears to be low serum phosphate levels, but isolated phosphate deficiency has not been shown to be a specific cause of dementia.
Approximately 20% of PATIENTS with BP eventually develop dementia. Some patients with BP and dementia have neural cytoplasmic inclusions (Lewy bodies) or BA-specific changes in the cerebral cortex, but others do not have specific, identifiable pathological brain damage.
Infections of the central nervous system (CNS) generally cause delirium and other acute neurological syndromes. However, some chronic CNS infections such as tuberculosis and cryptococosis can cause dementia. Between 20 and 30% of patients in advanced stages AIDS become demented.
The main manifestations are psychomotor retardation, apathy and memory disorders. These may be the result of opportunistic secondary infections, but they can also be directly caused by infection of CNS neurons with HIV, in this case there is multi-closted giant cell encephalitis and diffuse pallor of the white substance. Herpes simplex encephalitis has a predilection for the lower temporal lobes and may present with disorientation and subacute confusion, but much more common as acute syndrome than as chronic dementia. TC, MRI and EEC can detect the location of lesions in the temporal lobe.
CRL usually has lymphocytic pleiocytosis and an increased protein concentration. CNS syphilis was a common cause of dementia in the preantibiotic era, now rarely present, but can still be found in the population group with multiple sexual partners. Characteristic changes in CRL are pleiocytosis, increased protein concentration and the vDRL positive test.
Prionic diseases, such as Creutzfeldt-Jakob disease (BCJ), are very rare pathological conditions (1 person per million) that usually produce dementia. BCJ is usually rapidly progressive, associated with dementia, stiffness and myoclonia, causing death in less than 1 to 2 years. These clinical manifestations can also rarely be found in BA, with differential diagnosis usually based on the slow evolution of BA and abnormal, periodic ECG discharges, also found in BA, with differential diagnosis usually based on the slow evolution of BA and abnormal, periodic ECG discharges found in BCJ.
I have about two more posts before I'm done with my memory disorders and my demented description, so arm yourself with patience and curiosity!
Have a good, sunny day,
full of the perception of life!
Dorin, Merticaru