Acetylcholine also acts at various sites within the CNS, where it functions as a neurotransmitter and as a neuromodulator. It plays a role in various higher functioning processes like motivation, arousal, attention, learning, and memory, and is also involved in promoting REM sleep. Disrupted levels of acetylcholine, is believed to be one of the underlying pathophysiological mechanisms in cognitive disorders. Therefore, if you inhibit acetylcholine, you might cause further disruption of the underlying cognitive processes
Could the increase in ICP in the brain due to the enlarged ventricles in CSF pocketing , mask atrophy in some parts of the brain seeing as the tissue could be pushed together
Hello Luke. The condition in the presentation that I referred to, was called Normal Pressure Hydrocephalus aka NPH. This is a special condition which is characterized by a constellation of clinical findings referred to as the Wet (incontinence), Wacky (Dementia) & Wobbly (gait apraxia/bruns apraxia/lower half Parkinson's). This is a rapid form of dementia with early gait involvement, characterized by in increase in CSF production & decrease in CSF absorption. This creates features of hydrocephalus on neuro-imaging but it is not really hydrocephalus as the intracranial pressures are still normal when we perform manometry assessments. The csf then accumulates in the brain and ventricles creating pockets, hence the term DESH has been coined. There are numerous other diagnostic criteria that we look at for these patients, but that falls beyond the scope of 4th year level. If you do want the information I will be glad to share it with you. In patients with significant cerebral atrophy, you can get enlargement of the ventricles as well as subarachnoid spaces, this is referred to as ex-vacuole dilation If an unfortunate patient with significant cerebral atrophy do develop hydrocephalus, it will mask the atrophy by the cerebral swelling.
Dr. Kroon With regards to MCI-if we look at somebody with old age who has typical old age memory loss, do they then have MCI or is old age memory loss a Differential for MCI? Is dementia more of a symptom rather than a diseaseimpairment is a hallmark of neurodegenerative diseases rather than dementia?
Hello Carla, the best way to see neurodegenerative conditions are, rather, to view them as a continuum of cognitive impairment. None of it is normal or "old-age memory loss" as a differential. So on, one end of the spectrum, you have no cognitive abnormalities and on the other end of the spectrum you have Major Neurocognitive Disorder. So on this continuum of disorders (between a normal individual and MNCD) you can have the following: 1. you can a person with subjective cognitive loss, but objectively the neurobehavioral tests or screens like MMSE/MOCA are normal; eg, Einstein starts with a high baseline and then subjectively develops cogntivie problems - no test will pick the cognitive problems up at this stage. 2. you can have a person recorded cognitive deficits on the neurobehavioral tests or screens but doesn't influence his activities of daily living / social functioning status, this would be referred as Minor Neurocognitive Disorder. 3. Then you have a person with deficits on the neurobehavioral tests or screens as well as interference with ADL/social functioning status, and that would be classified as Major Neurocognitive Disorder. Each of these levels has its own differentials, depending on the diagnosis. eg Alzheimer's disease patients will start with point 1 - but will then eventually progress to point 3. Being in point one doesn't necessarily mean that you will end up in point 3 - there is a list of differentials for point 1 eg Vascular diseases, Hippocampal Sclerosis, Argyrophilic Grain Disease, and Primary Age-Related Tauopathy (these are beyond the scope for your level) so that means you might just stagnate at point 1. The risk of having something that will eventually cause progression is +/- 10% per year - which I mentioned in the presentation, this gets compounded by a multi-modal system. Vascular risk factors/lifestyle/diet etc. Therefore trying to make the diagnosis at point 1 will help you to calculate the risk of progression to point 3 in the future eg FTD, Alzheimer's, CBS etc etc. but will it necessarily help the patient? Irrespectively treatment at this stage (stage1 ) will be aimed to delay progression to stage 2/3 etc. and this will be aimed at minimizing risk factors; exercise etc. These risk factors, like I mentioned, compound this whole degenerative process, irrespective if you have amyloid/tau built up in the brain.
Dr., can you maybe explain why it is important to ask about anticholinergics when reviewing the medication list for mild cognitive impairment?
Acetylcholine also acts at various sites within the CNS, where it functions as a neurotransmitter and as a neuromodulator. It plays a role in various higher functioning processes like motivation, arousal, attention, learning, and memory, and is also involved in promoting REM sleep. Disrupted levels of acetylcholine, is believed to be one of the underlying pathophysiological mechanisms in cognitive disorders. Therefore, if you inhibit acetylcholine, you might cause further disruption of the underlying cognitive processes
Could the increase in ICP in the brain due to the enlarged ventricles in CSF pocketing , mask atrophy in some parts of the brain seeing as the tissue could be pushed together
Hello Luke. The condition in the presentation that I referred to, was called Normal Pressure Hydrocephalus aka NPH. This is a special condition which is characterized by a constellation of clinical findings referred to as the Wet (incontinence), Wacky (Dementia) & Wobbly (gait apraxia/bruns apraxia/lower half Parkinson's). This is a rapid form of dementia with early gait involvement, characterized by in increase in CSF production & decrease in CSF absorption. This creates features of hydrocephalus on neuro-imaging but it is not really hydrocephalus as the intracranial pressures are still normal when we perform manometry assessments. The csf then accumulates in the brain and ventricles creating pockets, hence the term DESH has been coined. There are numerous other diagnostic criteria that we look at for these patients, but that falls beyond the scope of 4th year level. If you do want the information I will be glad to share it with you.
In patients with significant cerebral atrophy, you can get enlargement of the ventricles as well as subarachnoid spaces, this is referred to as ex-vacuole dilation
If an unfortunate patient with significant cerebral atrophy do develop hydrocephalus, it will mask the atrophy by the cerebral swelling.
Dr. Kroon
With regards to MCI-if we look at somebody with old age who has typical old age memory loss, do they then have MCI or is old age memory loss a Differential for MCI?
Is dementia more of a symptom rather than a diseaseimpairment is a hallmark of neurodegenerative diseases rather than dementia?
Hello Carla, the best way to see neurodegenerative conditions are, rather, to view them as a continuum of cognitive impairment. None of it is normal or "old-age memory loss" as a differential. So on, one end of the spectrum, you have no cognitive abnormalities and on the other end of the spectrum you have Major Neurocognitive Disorder. So on this continuum of disorders (between a normal individual and MNCD) you can have the following:
1. you can a person with subjective cognitive loss, but objectively the neurobehavioral tests or screens like MMSE/MOCA are normal; eg, Einstein starts with a high baseline and then subjectively develops cogntivie problems - no test will pick the cognitive problems up at this stage.
2. you can have a person recorded cognitive deficits on the neurobehavioral tests or screens but doesn't influence his activities of daily living / social functioning status, this would be referred as Minor Neurocognitive Disorder.
3. Then you have a person with deficits on the neurobehavioral tests or screens as well as interference with ADL/social functioning status, and that would be classified as Major Neurocognitive Disorder.
Each of these levels has its own differentials, depending on the diagnosis. eg Alzheimer's disease patients will start with point 1 - but will then eventually progress to point 3.
Being in point one doesn't necessarily mean that you will end up in point 3 - there is a list of differentials for point 1 eg Vascular diseases, Hippocampal Sclerosis, Argyrophilic Grain Disease, and Primary Age-Related Tauopathy (these are beyond the scope for your level) so that means you might just stagnate at point 1. The risk of having something that will eventually cause progression is +/- 10% per year - which I mentioned in the presentation, this gets compounded by a multi-modal system. Vascular risk factors/lifestyle/diet etc.
Therefore trying to make the diagnosis at point 1 will help you to calculate the risk of progression to point 3 in the future eg FTD, Alzheimer's, CBS etc etc. but will it necessarily help the patient?
Irrespectively treatment at this stage (stage1 ) will be aimed to delay progression to stage 2/3 etc. and this will be aimed at minimizing risk factors; exercise etc. These risk factors, like I mentioned, compound this whole degenerative process, irrespective if you have amyloid/tau built up in the brain.