STUDY - Technical - New Dacian's Medicine
Memory
loss and Dementia (3)
Translation Draft
Let's move on to differential diagnosis in case of memory loss and dementia.
Primary and metastatic CNS neoplasms usually produce focused neurological manifestations and seizures, and less often dementia. However, if the tumor develops in the temporal or frontal lobe, the initial manifestations may be memory loss and behavioral changes.
A rare paraneoplastic dementia syndrome associated with occult carcinoma (usually small cell lung cancer) has been called limbic encephalitis. Confusion, agitation, seizures, memory loss and dementia in association with sensory neuropathy occur in this syndrome. CRL usually has high cellularity and protein concentration. There is a loss of neurons and a perivascular lymphocytic infiltration into the hippocampus, amygdala and the frontal and cingulate cortex. Circulated nuclear antineuronal antibodies may be present. There is no specific treatment.
Hydrocephalus syndrome with normal pressure is frequently discussed, but difficult to diagnose. Clinically, triad memory loss, gait disorders and bladder incontinence is characteristic. Walking disorders are often the first symptom, and dementia is usually mild.
Imaging studies show that the lateral ventricles are enlarged, but cortical atrophy is minimal or non-existent. The lumbar puncture shows a normal or slightly increased opening pressure with normal CRL. The disease may be idiopathic or may be the result of subarachnoid meningitis due to rupture of an aneurysm or head trauma.
The pathogenic mechanism is probably an obstacle in the normal flow of CRL over convexity and delayed reabsorption in the nervous system, which leads to contraction and contortion of the white substance tracts in the radiated corona. The condition of some patients is improved by ventricular shaming, but in many cases the improvement does not occur. Differential diagnosis of the disease with BA is difficult to make.
A nonconvulsive epileptic condition can cause confusional syndrome, consciousness disorder and truncated speech. Psychiatric disease is often suspected, but the EEG demonstrates the existence of epileptic discharges.
If recurrent or persistent, the condition can be called partially complex epilepticus status. Cognitive disorder often occurs in response to anticonvulsant treatment. The causes can be small strokes or previous head trauma (some cases are idiopathic).
It is important to recognize systemic disease that indirectly affects the brain and causes chronic confusion or dementia. Such conditions are dysthyroid states (especially hypothyroidism), vasculitis and liver, kidney or lung diseases. Hepatic encephalopathy can start with irritability and confusion, and can evolve slowly with agitation, lethargy and coma.
CNS insulating angeitis (CNS granulomatous angeitis) occasionally produces chronic encephalopathy associated with confusion, disorientation and disturbance of consciousness. Headache is common, and strokes and cranial neuropathies may also occur. Brain imaging studies may be normal or nonspecifically abnormal. The CRL exam shows mild pleiocytosis or increased protein levels in half of the cases. Cerebral angiography frequently detects multifocal stenosis and narrowing of vessels.
A few patients only affected small vessels that do not appear at angiography. Angiographic images are not specific and can also be found in arteriosclerosis, infections or other causes of vascular disease. Brain or meninge biopsy reveals abnormal arteries, with the proliferation of endothelial cells and mononuclear cell infiltration. Antibodies and immune complexes are not present, most likely there is a cell-mediated inflammatory process. The prognosis is reserved, but some patients respond to treatment with glucocorticoids or chemotherapy.
Chronic metal poisoning can also cause a dementia syndrome. The key to diagnosis is the history of exposure at home, at work or even as a result of a medical intervention such as dialysis. Lead poisoning has extremely varied neurological manifestations.
Fatigue, depression and confusion may be associated with episodic abdominal pain and peripheral neuropathy. Grey lead deposits may occur in the gums. There is usually anaemia associated with basophilic punctuation of erythrocytes. The clinical picture resembles that of acute intermittent porphyria, including increased urinary levels of porphyria. Chronic lead poisoning has been found due to insufficiently smitted ceramic vessels. Treatment consists of the administration of chelating agents such as EDTA. Chronic mercury poisoning can cause dementia, peripheral neuropathy and fine tremors that can progress to intentional cerebellar tremor or choreoatetosis.
Confusion and memory loss in chronic arsenic poisoning are also associated with nausea, weight loss, peripheral neuropathy, skin pigmentation and peeling and white cross-sections of the nails (Mee lines). Chelator treatment is done with dimercaptol (BAL). Aluminum poisoning was best studied in the demential dialysis syndrome, when the water used for renal dialysis was contaminated with excessive amounts of aluminum.
This led to progressive encephalopathy associated with confusion, memory loss, agitation and, later, lethargy and stupor. Inability to speak and myoclonic contractions are common and are associated with generalized and severe EEG changes. The disease is often fatal. There were no specific anatomological elements, but the large aluminum content of the brain was discovered. This syndrome is avoided today by using deionized water for dialysis. Although the aluminum injection of experimental animals causes neurofibrillary degeneration, patients with dialysis dementia have neither neurofibrillary degeneration nor amyloid plaques and there was no direct association between aluminum and BA poisoning.
Repeated head trauma in professional boxers leads to dementia, often referred to as "boxer drunkenness" syndrome or pugilistic dementia. Symptoms are progressive and may start late in the boxer's career or even long after retirement. The severity of the syndrome correlates with the duration of the boxer's career and the total number of matches.
At the beginning of the disease there is a personality change associated with social instability and sometimes delirium paranoia. Later, memory loss progresses to total dementia, often associated with Parkinson's signs and intentional ataxia or tremor. At autopsy, the cerebral cortex may experience BA-like changes, although neurofibrillary degeneration is usually predominant over amyloid plaques (which are more commonly diffuse than neural). Loss of neurons in the substance nigra may also occur. Also, chronic subdural hematoma is occasionally associated with dementia, often in the context of cortical atrophy caused by diseases like BA or BH. In these cases, the evacuation of the subdural hematoma will not alter the underlying degenerative process.
Head injuries may also be associated with temporary amnesia. Memory disorder includes events that occurred before trauma (retrograde amnesia) and during the post-traumatic period (post-traumatic or anterograde amnesia).
Retrograde amnesia following severe head trauma can extend to hours or weeks before trauma, with long-term memory usually intact. As patients recover, the expansion of retrograde amnesia shrinks and may disappear. Often retrograde amnesia causes a permanent inability to invoke the minutes that preceded the head trauma, which implies alteration of immediate memory and the ability to record long-term memory.
The duration of post-traumatic amnesia generally corresponds to that of post-concussion confusion, but post-traumatic amnesia persists even in the presence of an immediate memory and a normal counting capacity. The duration of post-traumatic amnesia indicates the severity of the head trauma, the ability to learn new information being usually the last recovered deficit.
There are data on the recovery of retrograde amnesia that occurs months or years after the head trauma, the recovery is sometimes rushed by hypnosis, interview or amobarbital or electrical stimulation. The theory that explains this type of recovery involves restoring the lateral schemas of the neural arrays that serve memory.
Transitional global amnesia (AGT) is characterized by the sudden onset of anterograde memory loss and learning capacity, which usually occurs in people over 50 years of age. The onset of amnesia may occur in the context of emotional stimulation or physical exertion. During the attack the individual is vigil and communicative, the general perception seems intact and there is no other neurological sign or symptom. The patient can be diffused and asks repeatedly about present events.
The ability to acquire new information returns after a period of hours and the individual returns to normal, but has no memory of the period of the attack. Frequently no cause is found, but sometimes cerebrovascular diseases, epilepsy (in 7% of cases), migraines or cardiac arrhythmias are involved. The existence of a history of migraine in 14% of patients and cerebrovascular disease in 11% is relevant, but these diseases were not associated at that time with Episodes of GtA. Almost a quarter of patients have recurrent attacks but do not have an increased risk for a subsequent stroke. Rare cases of permanent memory loss have been reported after a sudden onset.
Psychogenic amnesia for important personal memories is common, although it is difficult to determine whether it occurs by deliberately avoiding unpleasant memories or by unconscious repression. Amnesia related to a particular event occurs especially after particularly unpleasant events such as the death of a particularly close person (especially if he has violent aspects, such as an accident), violent crimes, such as the murder of a close relative or a friend or after sexual abuse. It can also occur in severe alcohol or drug intoxication and sometimes in schizophrenia. More prolonged psychogenic amnesia occurs in states of flight, which also usually follow severe emotional stress.
Patients with a state of flight suffer a sudden loss of their own identity and can be found wandering away from home. Compared to organic amnesia, fleeing states are associated with amnesia for one's own identity and for events closely related to personal past. At the same time, memory for other recent events and the ability to learn and use new information are preserved. Episodes usually last for hours or days, sometimes weeks or months, during which time the patient takes a different identity. After recovery remains a residual amnesiac void of the runaway period.
Psychiatric diseases can mimic dementia. Individuals with severe depression may appear to be demented, a phenomenon called pseudodementia. Unlike cortical dementia, memory and language are usually intact when carefully tested in depressives. Patients may be confused and unable to perform routine activities. Vegetative symptoms such as insomnia, lack of energy, decreased appetite and concern about bladder function frequently occur.
The psychosocial doctor may provide obvious reasons for depression. patients respond to antidepressant treatment. Usually it is not difficult to differentiate dementia and schizophrenia, but sometimes establishing the diagnosis can cause problems (Kraepelin's original term for schizophrenia was "dementia praecox").
Schizophrenia usually sets in at a much younger age (second and third decade of life) than most diseases that cause dementia, memory is intact, and delirium and hallucinations in schizophrenia are much more complex and bizarre than those in dementia. Some chronic schizophrenics develop an unexplained, progressive dementia in old age that is not related to BA. Memory loss may be part of a conversion reaction.
In this situation, patients usually complain bitterly of memory loss, but carefully conducted cognitive tests either do not confirm the deficiency or demonstrate some unconscious or unusual cognitive abnormalities. Patient behaviour and "wrong" answers to questions often indicate both that they understand the question and that they know the right answer.
Let's move on to differential diagnosis in case of memory loss and dementia.
Primary and metastatic CNS neoplasms usually produce focused neurological manifestations and seizures, and less often dementia. However, if the tumor develops in the temporal or frontal lobe, the initial manifestations may be memory loss and behavioral changes.
A rare paraneoplastic dementia syndrome associated with occult carcinoma (usually small cell lung cancer) has been called limbic encephalitis. Confusion, agitation, seizures, memory loss and dementia in association with sensory neuropathy occur in this syndrome. CRL usually has high cellularity and protein concentration. There is a loss of neurons and a perivascular lymphocytic infiltration into the hippocampus, amygdala and the frontal and cingulate cortex. Circulated nuclear antineuronal antibodies may be present. There is no specific treatment.
Hydrocephalus syndrome with normal pressure is frequently discussed, but difficult to diagnose. Clinically, triad memory loss, gait disorders and bladder incontinence is characteristic. Walking disorders are often the first symptom, and dementia is usually mild.
Imaging studies show that the lateral ventricles are enlarged, but cortical atrophy is minimal or non-existent. The lumbar puncture shows a normal or slightly increased opening pressure with normal CRL. The disease may be idiopathic or may be the result of subarachnoid meningitis due to rupture of an aneurysm or head trauma.
The pathogenic mechanism is probably an obstacle in the normal flow of CRL over convexity and delayed reabsorption in the nervous system, which leads to contraction and contortion of the white substance tracts in the radiated corona. The condition of some patients is improved by ventricular shaming, but in many cases the improvement does not occur. Differential diagnosis of the disease with BA is difficult to make.
A nonconvulsive epileptic condition can cause confusional syndrome, consciousness disorder and truncated speech. Psychiatric disease is often suspected, but the EEG demonstrates the existence of epileptic discharges.
If recurrent or persistent, the condition can be called partially complex epilepticus status. Cognitive disorder often occurs in response to anticonvulsant treatment. The causes can be small strokes or previous head trauma (some cases are idiopathic).
It is important to recognize systemic disease that indirectly affects the brain and causes chronic confusion or dementia. Such conditions are dysthyroid states (especially hypothyroidism), vasculitis and liver, kidney or lung diseases. Hepatic encephalopathy can start with irritability and confusion, and can evolve slowly with agitation, lethargy and coma.
CNS insulating angeitis (CNS granulomatous angeitis) occasionally produces chronic encephalopathy associated with confusion, disorientation and disturbance of consciousness. Headache is common, and strokes and cranial neuropathies may also occur. Brain imaging studies may be normal or nonspecifically abnormal. The CRL exam shows mild pleiocytosis or increased protein levels in half of the cases. Cerebral angiography frequently detects multifocal stenosis and narrowing of vessels.
A few patients only affected small vessels that do not appear at angiography. Angiographic images are not specific and can also be found in arteriosclerosis, infections or other causes of vascular disease. Brain or meninge biopsy reveals abnormal arteries, with the proliferation of endothelial cells and mononuclear cell infiltration. Antibodies and immune complexes are not present, most likely there is a cell-mediated inflammatory process. The prognosis is reserved, but some patients respond to treatment with glucocorticoids or chemotherapy.
Chronic metal poisoning can also cause a dementia syndrome. The key to diagnosis is the history of exposure at home, at work or even as a result of a medical intervention such as dialysis. Lead poisoning has extremely varied neurological manifestations.
Fatigue, depression and confusion may be associated with episodic abdominal pain and peripheral neuropathy. Grey lead deposits may occur in the gums. There is usually anaemia associated with basophilic punctuation of erythrocytes. The clinical picture resembles that of acute intermittent porphyria, including increased urinary levels of porphyria. Chronic lead poisoning has been found due to insufficiently smitted ceramic vessels. Treatment consists of the administration of chelating agents such as EDTA. Chronic mercury poisoning can cause dementia, peripheral neuropathy and fine tremors that can progress to intentional cerebellar tremor or choreoatetosis.
Confusion and memory loss in chronic arsenic poisoning are also associated with nausea, weight loss, peripheral neuropathy, skin pigmentation and peeling and white cross-sections of the nails (Mee lines). Chelator treatment is done with dimercaptol (BAL). Aluminum poisoning was best studied in the demential dialysis syndrome, when the water used for renal dialysis was contaminated with excessive amounts of aluminum.
This led to progressive encephalopathy associated with confusion, memory loss, agitation and, later, lethargy and stupor. Inability to speak and myoclonic contractions are common and are associated with generalized and severe EEG changes. The disease is often fatal. There were no specific anatomological elements, but the large aluminum content of the brain was discovered. This syndrome is avoided today by using deionized water for dialysis. Although the aluminum injection of experimental animals causes neurofibrillary degeneration, patients with dialysis dementia have neither neurofibrillary degeneration nor amyloid plaques and there was no direct association between aluminum and BA poisoning.
Repeated head trauma in professional boxers leads to dementia, often referred to as "boxer drunkenness" syndrome or pugilistic dementia. Symptoms are progressive and may start late in the boxer's career or even long after retirement. The severity of the syndrome correlates with the duration of the boxer's career and the total number of matches.
At the beginning of the disease there is a personality change associated with social instability and sometimes delirium paranoia. Later, memory loss progresses to total dementia, often associated with Parkinson's signs and intentional ataxia or tremor. At autopsy, the cerebral cortex may experience BA-like changes, although neurofibrillary degeneration is usually predominant over amyloid plaques (which are more commonly diffuse than neural). Loss of neurons in the substance nigra may also occur. Also, chronic subdural hematoma is occasionally associated with dementia, often in the context of cortical atrophy caused by diseases like BA or BH. In these cases, the evacuation of the subdural hematoma will not alter the underlying degenerative process.
Head injuries may also be associated with temporary amnesia. Memory disorder includes events that occurred before trauma (retrograde amnesia) and during the post-traumatic period (post-traumatic or anterograde amnesia).
Retrograde amnesia following severe head trauma can extend to hours or weeks before trauma, with long-term memory usually intact. As patients recover, the expansion of retrograde amnesia shrinks and may disappear. Often retrograde amnesia causes a permanent inability to invoke the minutes that preceded the head trauma, which implies alteration of immediate memory and the ability to record long-term memory.
The duration of post-traumatic amnesia generally corresponds to that of post-concussion confusion, but post-traumatic amnesia persists even in the presence of an immediate memory and a normal counting capacity. The duration of post-traumatic amnesia indicates the severity of the head trauma, the ability to learn new information being usually the last recovered deficit.
There are data on the recovery of retrograde amnesia that occurs months or years after the head trauma, the recovery is sometimes rushed by hypnosis, interview or amobarbital or electrical stimulation. The theory that explains this type of recovery involves restoring the lateral schemas of the neural arrays that serve memory.
Transitional global amnesia (AGT) is characterized by the sudden onset of anterograde memory loss and learning capacity, which usually occurs in people over 50 years of age. The onset of amnesia may occur in the context of emotional stimulation or physical exertion. During the attack the individual is vigil and communicative, the general perception seems intact and there is no other neurological sign or symptom. The patient can be diffused and asks repeatedly about present events.
The ability to acquire new information returns after a period of hours and the individual returns to normal, but has no memory of the period of the attack. Frequently no cause is found, but sometimes cerebrovascular diseases, epilepsy (in 7% of cases), migraines or cardiac arrhythmias are involved. The existence of a history of migraine in 14% of patients and cerebrovascular disease in 11% is relevant, but these diseases were not associated at that time with Episodes of GtA. Almost a quarter of patients have recurrent attacks but do not have an increased risk for a subsequent stroke. Rare cases of permanent memory loss have been reported after a sudden onset.
Psychogenic amnesia for important personal memories is common, although it is difficult to determine whether it occurs by deliberately avoiding unpleasant memories or by unconscious repression. Amnesia related to a particular event occurs especially after particularly unpleasant events such as the death of a particularly close person (especially if he has violent aspects, such as an accident), violent crimes, such as the murder of a close relative or a friend or after sexual abuse. It can also occur in severe alcohol or drug intoxication and sometimes in schizophrenia. More prolonged psychogenic amnesia occurs in states of flight, which also usually follow severe emotional stress.
Patients with a state of flight suffer a sudden loss of their own identity and can be found wandering away from home. Compared to organic amnesia, fleeing states are associated with amnesia for one's own identity and for events closely related to personal past. At the same time, memory for other recent events and the ability to learn and use new information are preserved. Episodes usually last for hours or days, sometimes weeks or months, during which time the patient takes a different identity. After recovery remains a residual amnesiac void of the runaway period.
Psychiatric diseases can mimic dementia. Individuals with severe depression may appear to be demented, a phenomenon called pseudodementia. Unlike cortical dementia, memory and language are usually intact when carefully tested in depressives. Patients may be confused and unable to perform routine activities. Vegetative symptoms such as insomnia, lack of energy, decreased appetite and concern about bladder function frequently occur.
The psychosocial doctor may provide obvious reasons for depression. patients respond to antidepressant treatment. Usually it is not difficult to differentiate dementia and schizophrenia, but sometimes establishing the diagnosis can cause problems (Kraepelin's original term for schizophrenia was "dementia praecox").
Schizophrenia usually sets in at a much younger age (second and third decade of life) than most diseases that cause dementia, memory is intact, and delirium and hallucinations in schizophrenia are much more complex and bizarre than those in dementia. Some chronic schizophrenics develop an unexplained, progressive dementia in old age that is not related to BA. Memory loss may be part of a conversion reaction.
In this situation, patients usually complain bitterly of memory loss, but carefully conducted cognitive tests either do not confirm the deficiency or demonstrate some unconscious or unusual cognitive abnormalities. Patient behaviour and "wrong" answers to questions often indicate both that they understand the question and that they know the right answer.
Ready for today (actually
for yesterday).
Have a nice weekend and
prepare for the feast of Jesus' entry into Jerusalem, including
the feast of all the flowers in your life!
Dorin, Merticaru