Nawgan is back after a brief hiatus. The last post focused on caloric intake and increased risk for dementia and the entry generated some great comments from Nawgan readers. At some point in the near future we’ll revisit those comments and in the process I will review in greater depth the research literature that currently exists regarding caloric restriction and animal models of Alzheimer’s disease. However, until then I’ve been asked by a Nawgan reader to discuss a condition called arachnoid cysts – and that is what we’ll do in this post.
I’ll start with my standard caveat – I am not a physician (an no I don’t play one on TV). My review of the literature on arachnoid cysts is based on my experience as a clinical neuropsychologist and my own research and training regarding brain anatomy, medical diseases, and cognitive function.
The question that was presented to me is whether or not arachnoid cysts can negatively impact thinking skills. The answer to that question is “yes” but these symptoms do not appear for quite some time, if at all, and they typically improve with treatment.
Arachnoid cysts are collections of fluid underneath one of the thin membranes that surround the brain. The cysts are believed to be congenital, meaning that they began to develop during the very early stages of fetal brain development. If the cyst expands in size (e.g., through continued increase in fluid accumulation within the cyst) it is possible that the cyst will push/compress the normal brain tissue surrounding the cyst. Such cysts more commonly occur in males and they more commonly occur on the left side of the brain rather than the right (but just about any variation is possible).
The compression of the surrounding brain tissue may compromise cognitive function and the nature of the symptoms (e.g., memory impairment, difficulties with processing speed or spatial skills) depends on where the cyst is located, the size of the cyst, and consequently what surrounding brain tissue is affected. In a common scenario, a large left-sided cyst could result in difficulties with brain functions normally governed by the right hemisphere. This may sound counterintuitive but the effect is explained by a principle first described in the 1970s called the “crowding principle”. This theory suggests that anatomical changes to one hemisphere (e.g., left hemisphere cyst) will result in a shift of left hemisphere skills (e.g., language) to the right hemisphere. As a result of the shift, normal functions governed by the right hemisphere (e.g., spatial skills) are reduced because of crowding due to integration of left hemisphere functions.
Despite the negative description noted above, a few important positive issues should be noted regarding arachnoid cysts. First, not all cysts will expand and result in cognitive or emotional difficulties. Second, surgical treatment of the cyst has been shown to restore cognitive abilities suggesting that the effects of the cyst on brain function are reversible! Third, in several reported cases, changes in cognitive function associated with arachnoid cysts were only evident with very detailed cognitive assessments – in other words, basic cognitive abilities and daily function were largely unaffected.
So in summary, arachnoid cysts can impair thinking skills, but there are a number of factors that determine the degree and the nature of these effects and most importantly treatment can help restore cognitive abilities.
The Nawgan blog will be published on a flexible but fairly regular schedule. I will certainly post a blog every few weeks if not more frequently. C
Contact me at rpaul.nawgan@gmail.com to request a topic for review in the Nawgan blog. It is important to note that the Nawgan blog is not intended to replace professional care. Individuals with questions and concerns about their health are strongly encouraged to seek input from their medical provider.
Sincerely,
Dr. Rob Paul, ABPP/ABCN
Board Certified Clinical Neuropsychologist
Posted by Dr. Rob Paul, ABPP/ABCN
Tuesday, March 24, 2009
Tuesday, March 10, 2009
The neuropsychology of calories and dementia
Caloric intake and optimum cognitive function may seem like two unrelated concepts. In fact I imagine that the great philosopher Decartes would have argued against any relationship between calories and mental health. However, there is substantial research that demonstrates the two are very much related suggesting that Decartes' Mind-Body Dualism theory was not very accurate.
High caloric intake and more specifically, retention of calories in the form of a high body-mass index and/or obesity, has at least two links to brain function. The first is fairly obvious in that individuals who are overweight are at increased risk for developing diabetes and sleep apnea. Both of these conditions are risk factors for stroke and stroke is a major cause of cognitive decline associated with age. Individuals that maintain their weight within recommended guidelines are less likely to develop cognitive difficulties from either diabetes-related stroke or apnea. As an aside, individuals with apnea typically report cognitive difficulties associated with fatigue and these improve with treatment (e.g., CPAP, BiPAP) but when left untreated, but many individuals do not adhere to treatment and uncontrolled apnea remains a risk factor for stroke.
High caloric intake is also linked to an increased risk for developing Alzheimer's disease (e.g., Luchsinger et al., 2002). This is just one representative study, but to highlight - this study reported that individuals with the highest caloric intake exhibited a significantly increased risk for AD compared to individuals with the lowest caloric intake, and this was further magnified among individuals with genetic risk factors for cognitive impairment. These studies are supported by others showing that obesity and diabetes increase the risk of developing AD by more than 4-fold. Further, animal studies have demonstrated that restriction of calories results in reduced brain abnormalities that are know signatures of AD pathology. Animals maintained on a strict caloric diet are much less likely to develop brain features associated with AD than animals on a high caloric diet.
In studies that I have been involved in with investigators at Kent State University, obesity is related to reduced brain volume among otherwise healthy adults. Further, our studies showed that obesity is associated with poorer performances on tests of executive function and memory among otherwise healthy adults. Importantly, these studies were not conducted on individuals with dementia!
The exact mechanisms of these relationships require further investigation but there is no question that the mind and body are linked. Healthy brains require healthy bodies! Also, since risk factors like apnea and type 2 diabetes can be controlled (if not eliminated) by reducing caloric intake to achieve an optimal BMI, individuals can directly influence their risk of developing cognitive difficulties and dementia by regulating their caloric intake. This by no means is a call for unhealthy caloric restriction, but just a reminder that moderation is the key to both physical and mental health and the two are highly integrated.
The Nawgan blog will be published on a flexible but fairly regular schedule. I will certainly post a blog every few weeks if not more frequently.
Contact me at rpaul.nawgan@gmail.com to request a topic for review in the Nawgan blog. It is important to note that the Nawgan blog is not intended to replace professional care. Individuals with questions and concerns about their health are strongly encouraged to seek input from their medical provider.
Sincerely,
Dr. Rob Paul, ABPP/ABCN
Certified Clinical Neuropsychologist
High caloric intake and more specifically, retention of calories in the form of a high body-mass index and/or obesity, has at least two links to brain function. The first is fairly obvious in that individuals who are overweight are at increased risk for developing diabetes and sleep apnea. Both of these conditions are risk factors for stroke and stroke is a major cause of cognitive decline associated with age. Individuals that maintain their weight within recommended guidelines are less likely to develop cognitive difficulties from either diabetes-related stroke or apnea. As an aside, individuals with apnea typically report cognitive difficulties associated with fatigue and these improve with treatment (e.g., CPAP, BiPAP) but when left untreated, but many individuals do not adhere to treatment and uncontrolled apnea remains a risk factor for stroke.
High caloric intake is also linked to an increased risk for developing Alzheimer's disease (e.g., Luchsinger et al., 2002). This is just one representative study, but to highlight - this study reported that individuals with the highest caloric intake exhibited a significantly increased risk for AD compared to individuals with the lowest caloric intake, and this was further magnified among individuals with genetic risk factors for cognitive impairment. These studies are supported by others showing that obesity and diabetes increase the risk of developing AD by more than 4-fold. Further, animal studies have demonstrated that restriction of calories results in reduced brain abnormalities that are know signatures of AD pathology. Animals maintained on a strict caloric diet are much less likely to develop brain features associated with AD than animals on a high caloric diet.
In studies that I have been involved in with investigators at Kent State University, obesity is related to reduced brain volume among otherwise healthy adults. Further, our studies showed that obesity is associated with poorer performances on tests of executive function and memory among otherwise healthy adults. Importantly, these studies were not conducted on individuals with dementia!
The exact mechanisms of these relationships require further investigation but there is no question that the mind and body are linked. Healthy brains require healthy bodies! Also, since risk factors like apnea and type 2 diabetes can be controlled (if not eliminated) by reducing caloric intake to achieve an optimal BMI, individuals can directly influence their risk of developing cognitive difficulties and dementia by regulating their caloric intake. This by no means is a call for unhealthy caloric restriction, but just a reminder that moderation is the key to both physical and mental health and the two are highly integrated.
The Nawgan blog will be published on a flexible but fairly regular schedule. I will certainly post a blog every few weeks if not more frequently.
Contact me at rpaul.nawgan@gmail.com to request a topic for review in the Nawgan blog. It is important to note that the Nawgan blog is not intended to replace professional care. Individuals with questions and concerns about their health are strongly encouraged to seek input from their medical provider.
Sincerely,
Dr. Rob Paul, ABPP/ABCN
Certified Clinical Neuropsychologist
Monday, March 2, 2009
HIV dementia in the developing world
Greetings,
Apologies for the delay in posting but I do have a good excuse. I just returned from a week in Thailand and Cambodia, where I am involved in two research projects. Last Monday at about the time I normally would have written my post, I was in Cambodia trying my very best to keep my eyes open.
Now that I'm back, I figure a quick recap of my trip, and more importantly, the purpose of my trip seems like a reasonable approach for this blog.
If I remember correctly I have mentioned in past posts that my research program is directed at understanding the role of specific structures and systems deep within in the brain in terms of thinking skills. Two conditions that I study to investigate these deep brain regions include HIV and small vessel stroke associated with age. Both of these conditions have a propensity to attack the clusters of cells and pathways deep inside the brain.
My research lab is currently funded by the National Institutes of Health to study both conditions but this trip to Thailand and Cambodia was specifically devoted to HIV.
Most individuals may not be aware, but HIV gets inside of the brain within two weeks of the initial infection (regardless of the method of infection). Once inside the brain, the virus kicks off an inflammatory response (because the body recognizes the virus should not be there) and this inflammatory response is toxic to brain cells, especially the brain cells that are deep within the brain (i.e., the focus of my research program). As a result, studies regarding HIV brain involvement can teach us a great deal about how to best care for HIV patients (e.g., we now know that cognitive abilities are important predictors of accurate medication adherence and poor adherence results in treatment failure) as well as how viruses such as HIV interfere with the brain.
Interestingly, HIV does not exist in a single genetic form, but rather the virus exists in multiple forms that are spread through the world in specific geographic locations. In North America, the genetic strain is referred to as clade B but worldwide other clades are far more prevalent.
Previous research has suggested that the different genetic strains interfere with the brain in different ways, and that some forms such as clade C which is common in Asia are less likely to interfere with brain function than clade B. My colleagues and I tested this theory in Chennai, India where clade C is the most common strain of the virus. In contrast to the clinical lore, we identified important and significant impairments among patients infected with clade C on cognitive tests.
In Thailand and Cambodia we are also looking for similarities and differences in how the virus affects brain function. In Thailand, the most common clade is a combination of strains A and E and we have been collecting data in Bangkok for several years now under the direction of Dr. Victor Valcour. Preliminary data look very similar to the results obtained from India - i.e., the brain is vulnerable regardless of clade type. In Cambodia we also are investigating the impact of treatment delays on brain development among children infected with HIV. At present we have no information about the long-term consequences of HIV and different treatment regimens of the virus among children in these settings.
These studies are critical because HIV is now recognized as the most common cause of dementia among young adults worldwide. Unless we get a handle on this disease and the impact of the virus on the brain, HIV may very well become the most common cause of dementia worldwide for all ages.
Remember - The Nawgan blog is now updated weekly on Monday evenings (CST).
Contact me at rpaul.nawgan@gmail.com to request a topic for review in the Nawgan blog.
It is important to note that the Nawgan blog is not intended to replace professional care.Individuals with questions and concerns about their health are strongly encouraged to seek input from their medical provider.
Sincerely,Dr. Rob Paul, ABPP/ABCN
Certified Clinical Neuropsychologist
Apologies for the delay in posting but I do have a good excuse. I just returned from a week in Thailand and Cambodia, where I am involved in two research projects. Last Monday at about the time I normally would have written my post, I was in Cambodia trying my very best to keep my eyes open.
Now that I'm back, I figure a quick recap of my trip, and more importantly, the purpose of my trip seems like a reasonable approach for this blog.
If I remember correctly I have mentioned in past posts that my research program is directed at understanding the role of specific structures and systems deep within in the brain in terms of thinking skills. Two conditions that I study to investigate these deep brain regions include HIV and small vessel stroke associated with age. Both of these conditions have a propensity to attack the clusters of cells and pathways deep inside the brain.
My research lab is currently funded by the National Institutes of Health to study both conditions but this trip to Thailand and Cambodia was specifically devoted to HIV.
Most individuals may not be aware, but HIV gets inside of the brain within two weeks of the initial infection (regardless of the method of infection). Once inside the brain, the virus kicks off an inflammatory response (because the body recognizes the virus should not be there) and this inflammatory response is toxic to brain cells, especially the brain cells that are deep within the brain (i.e., the focus of my research program). As a result, studies regarding HIV brain involvement can teach us a great deal about how to best care for HIV patients (e.g., we now know that cognitive abilities are important predictors of accurate medication adherence and poor adherence results in treatment failure) as well as how viruses such as HIV interfere with the brain.
Interestingly, HIV does not exist in a single genetic form, but rather the virus exists in multiple forms that are spread through the world in specific geographic locations. In North America, the genetic strain is referred to as clade B but worldwide other clades are far more prevalent.
Previous research has suggested that the different genetic strains interfere with the brain in different ways, and that some forms such as clade C which is common in Asia are less likely to interfere with brain function than clade B. My colleagues and I tested this theory in Chennai, India where clade C is the most common strain of the virus. In contrast to the clinical lore, we identified important and significant impairments among patients infected with clade C on cognitive tests.
In Thailand and Cambodia we are also looking for similarities and differences in how the virus affects brain function. In Thailand, the most common clade is a combination of strains A and E and we have been collecting data in Bangkok for several years now under the direction of Dr. Victor Valcour. Preliminary data look very similar to the results obtained from India - i.e., the brain is vulnerable regardless of clade type. In Cambodia we also are investigating the impact of treatment delays on brain development among children infected with HIV. At present we have no information about the long-term consequences of HIV and different treatment regimens of the virus among children in these settings.
These studies are critical because HIV is now recognized as the most common cause of dementia among young adults worldwide. Unless we get a handle on this disease and the impact of the virus on the brain, HIV may very well become the most common cause of dementia worldwide for all ages.
Remember - The Nawgan blog is now updated weekly on Monday evenings (CST).
Contact me at rpaul.nawgan@gmail.com to request a topic for review in the Nawgan blog.
It is important to note that the Nawgan blog is not intended to replace professional care.Individuals with questions and concerns about their health are strongly encouraged to seek input from their medical provider.
Sincerely,Dr. Rob Paul, ABPP/ABCN
Certified Clinical Neuropsychologist
Monday, February 16, 2009
Does ginkgo biloba protect against Alzheimer's disease?
Greetings readers.
Before getting into the thick of this blog entry, it is important that I inform you that I, like other clinicians, have financial interests associated with the outcomes from pharmaceutical trials for new medications and health supplements such as the focus of the current blog (ginkgo). When those conflicts exist, I will always do my best to simply report the science as it stands and not introduce my bias. Nevertheless, it is always wise to read "conflicted" blogs with an additional degree of caution. Since I have a particular personal interest in supplements for the brain, you should read this blog with an extra dose of caution (but I will still do my best to just report the science).
With that lengthy disclaimer behind us, I'd like to review the recent results of the GEM study that was published in the Journal of the American Medical Association in 2008 (DeKosky et al.). The GEM study is described as the largest and most scientifically rigorous evaluation of ginkgo for the prevention of Alzheimer's disease.
The study evaluated 2,587 older adults (over 75 years of age) with normal cognition and 482 individuals with mild cognitive impairment (recall this refers to mild impairments without evidence of significant impairment in daily living skills). Individuals were randomly assigned to receive either 120mg of ginkgo extract two times per day (240mg per day) versus placebo.
Individuals underwent extensive cognitive and physical evaluations and they were followed for approximately 6 years from the start of the trial.
After nearly 6 years of 240mg per day of ginkgo supplement or placebo, the two groups were compared for frequency of newly diagnosed dementia and potential side effects. According to the results described by the authors, there was no difference in the number of individuals that developed Alzheimer's disease or other forms of dementia between the two treatment conditions (i.e., those that received ginkgo versus individuals that received placebo).
The authors did report an unexpected finding in that individuals that had a history of cardiovascular disease and who took the ginkgo supplement were more likely to be diagnosed with Alzheimer's disease at the follow-up visit nearly 6 years later. The authors described this finding as "puzzling" and warned that the result should be interpreted with caution because there is no known reason why ginkgo would increase the risk of dementia among individuals with cardiovascular disease. Fortunately, the side effect profiles were pretty similar between the two treatment groups. As noted by the authors, twice as many individuals that received ginkgo experienced hemmorhagic strokes in the brain compared to individuals that received placebo BUT the total number of cases was low for both conditions (16 vs 8 respectively) considering the number of total participants enrolled in the study.
The authors warned that the effects of ginkgo (positive or negative) may require more time than the 6 years studied in the present investigation. In conclusion the authors of the study stated that "based on the results of this trial, ginkgo biloba cannot be recommended for the purpose of preventing dementia".
Remember - The Nawgan blog is updated weekly on Monday evenings (CST).
Contact me at rpaul.nawgan@gmail.com to request a topic for review in the Nawgan blog.
It is important to note that the Nawgan blog is not intended to replace professional care.Individuals with questions and concerns about their health are strongly encouraged to seek input from their medical provider.
Sincerely,Dr. Rob Paul, ABPP/ABCN
Certified Clinical Neuropsychologist
Before getting into the thick of this blog entry, it is important that I inform you that I, like other clinicians, have financial interests associated with the outcomes from pharmaceutical trials for new medications and health supplements such as the focus of the current blog (ginkgo). When those conflicts exist, I will always do my best to simply report the science as it stands and not introduce my bias. Nevertheless, it is always wise to read "conflicted" blogs with an additional degree of caution. Since I have a particular personal interest in supplements for the brain, you should read this blog with an extra dose of caution (but I will still do my best to just report the science).
With that lengthy disclaimer behind us, I'd like to review the recent results of the GEM study that was published in the Journal of the American Medical Association in 2008 (DeKosky et al.). The GEM study is described as the largest and most scientifically rigorous evaluation of ginkgo for the prevention of Alzheimer's disease.
The study evaluated 2,587 older adults (over 75 years of age) with normal cognition and 482 individuals with mild cognitive impairment (recall this refers to mild impairments without evidence of significant impairment in daily living skills). Individuals were randomly assigned to receive either 120mg of ginkgo extract two times per day (240mg per day) versus placebo.
Individuals underwent extensive cognitive and physical evaluations and they were followed for approximately 6 years from the start of the trial.
After nearly 6 years of 240mg per day of ginkgo supplement or placebo, the two groups were compared for frequency of newly diagnosed dementia and potential side effects. According to the results described by the authors, there was no difference in the number of individuals that developed Alzheimer's disease or other forms of dementia between the two treatment conditions (i.e., those that received ginkgo versus individuals that received placebo).
The authors did report an unexpected finding in that individuals that had a history of cardiovascular disease and who took the ginkgo supplement were more likely to be diagnosed with Alzheimer's disease at the follow-up visit nearly 6 years later. The authors described this finding as "puzzling" and warned that the result should be interpreted with caution because there is no known reason why ginkgo would increase the risk of dementia among individuals with cardiovascular disease. Fortunately, the side effect profiles were pretty similar between the two treatment groups. As noted by the authors, twice as many individuals that received ginkgo experienced hemmorhagic strokes in the brain compared to individuals that received placebo BUT the total number of cases was low for both conditions (16 vs 8 respectively) considering the number of total participants enrolled in the study.
The authors warned that the effects of ginkgo (positive or negative) may require more time than the 6 years studied in the present investigation. In conclusion the authors of the study stated that "based on the results of this trial, ginkgo biloba cannot be recommended for the purpose of preventing dementia".
Remember - The Nawgan blog is updated weekly on Monday evenings (CST).
Contact me at rpaul.nawgan@gmail.com to request a topic for review in the Nawgan blog.
It is important to note that the Nawgan blog is not intended to replace professional care.Individuals with questions and concerns about their health are strongly encouraged to seek input from their medical provider.
Sincerely,Dr. Rob Paul, ABPP/ABCN
Certified Clinical Neuropsychologist
Monday, February 9, 2009
How does mood impact cognition?
Welcome readers.
My initial plan for this post was to review the outcomes from the largest study of ginkgo biloba on cognitive outcomes in older adults (known as the GEM study). However, a Nawgan reader posted a comment associated with the previous blog that is important and interesting and I want to spend time during this post to address the comment.
Specifically, a Nawgan reader commented they had read that as many as 50% of individuals that are referred for neuropsychological evaluations are eventually referred for psychological treatment for depression, anxiety, or some other mental health concern. The reader asked if behavioral symptoms (e.g., memory problems, attention problems, etc) can be caused by something other than structural or functional abnormalities of the nervous system.
This is a really important question, and one that I often spend some time discussing with patients in my clinic. The answer is "Yes" - and as examples depression and anxiety are two very common causes of poor cognitive performance. A number of research studies have demonstrated that cognitive performance suffers when feelings of depression and anxiety increase. In mild cases, the changes in cognitive performance may be limited to the area of attention. When the brain is utilizing resources to address mental health concerns such as depression or anxiety, fewer brain resources are available to attend to complex information. The old adage that we only use "10% of our brain" is 100% inaccurate. We don't have an infinite ability to process information and therefore, it becomes more complicated to focus, filter irrelevant information, and quickly process complex data when we are simultaneously struggling with depression, anxiety or other mental health concern.
In more severe cases of mood disorders, cognitive function may be impaired beyond the area of attention. For example, memory, speed of processing, and motor speed can also be disrupted. Fortunately, all of these areas of function can improve with treatment of the underlying mood symptoms.
It is also worth noting that many other factors can influence neuropsychological performance including fatigue, sleepiness, infection (such as a urinary tract infection), and even boredom! In order to perform well on neuropsychological tests, patients have to give their best effort, otherwise it is not possible to really test the health of the brain systems responsible for attention, memory, language and the other cognitive systems.
Thanks for question regarding non-neurological contributions to neuropsychological performance! We'll check out the GEM study next week unless we have a chance to answer another comment from a reader.
Remember - The Nawgan blog is now updated weekly on Monday evenings (CST).
Contact me at rpaul.nawgan@gmail.com to request a topic for review in the Nawgan blog.
It is important to note that the Nawgan blog is not intended to replace professional care.Individuals with questions and concerns about their health are strongly encouraged to seek input from their medical provider.
Sincerely,
Dr. Rob Paul, ABPP/ABCN
Certified Clinical Neuropsychologist
My initial plan for this post was to review the outcomes from the largest study of ginkgo biloba on cognitive outcomes in older adults (known as the GEM study). However, a Nawgan reader posted a comment associated with the previous blog that is important and interesting and I want to spend time during this post to address the comment.
Specifically, a Nawgan reader commented they had read that as many as 50% of individuals that are referred for neuropsychological evaluations are eventually referred for psychological treatment for depression, anxiety, or some other mental health concern. The reader asked if behavioral symptoms (e.g., memory problems, attention problems, etc) can be caused by something other than structural or functional abnormalities of the nervous system.
This is a really important question, and one that I often spend some time discussing with patients in my clinic. The answer is "Yes" - and as examples depression and anxiety are two very common causes of poor cognitive performance. A number of research studies have demonstrated that cognitive performance suffers when feelings of depression and anxiety increase. In mild cases, the changes in cognitive performance may be limited to the area of attention. When the brain is utilizing resources to address mental health concerns such as depression or anxiety, fewer brain resources are available to attend to complex information. The old adage that we only use "10% of our brain" is 100% inaccurate. We don't have an infinite ability to process information and therefore, it becomes more complicated to focus, filter irrelevant information, and quickly process complex data when we are simultaneously struggling with depression, anxiety or other mental health concern.
In more severe cases of mood disorders, cognitive function may be impaired beyond the area of attention. For example, memory, speed of processing, and motor speed can also be disrupted. Fortunately, all of these areas of function can improve with treatment of the underlying mood symptoms.
It is also worth noting that many other factors can influence neuropsychological performance including fatigue, sleepiness, infection (such as a urinary tract infection), and even boredom! In order to perform well on neuropsychological tests, patients have to give their best effort, otherwise it is not possible to really test the health of the brain systems responsible for attention, memory, language and the other cognitive systems.
Thanks for question regarding non-neurological contributions to neuropsychological performance! We'll check out the GEM study next week unless we have a chance to answer another comment from a reader.
Remember - The Nawgan blog is now updated weekly on Monday evenings (CST).
Contact me at rpaul.nawgan@gmail.com to request a topic for review in the Nawgan blog.
It is important to note that the Nawgan blog is not intended to replace professional care.Individuals with questions and concerns about their health are strongly encouraged to seek input from their medical provider.
Sincerely,
Dr. Rob Paul, ABPP/ABCN
Certified Clinical Neuropsychologist
Monday, February 2, 2009
NPH vs. Alzheimer's disease
The previous post discussed the symptoms of Lewy Body disease, including the common cognitive difficulties often expressed by individuals diagnosed with this condition. At the end of the post I mentioned that I would discuss yet another condition referred to as normal pressure hydrocephalus (NPH). I will get to NPH in this post, but before I do I want be sure to follow-up on an important point raised by Nawgan reader Pem from the last post and it is related to many topics that we discuss in this blog - i.e., the definition of dementia.
Dementia typically is defined as acquired (i.e., not from early development) cognitive impairment of significant severity to significantly interfere with activities of daily living. This is effectively the same definition described by Pem, in that the cognitive changes interfere with a person's ability to continue to do what they were doing. Most often the complicated tasks of doing are lost first (managing finances, medications, driving, etc), while the more basic activities are maintained much longer (e.g., bathing, dressing, eating, etc). The diagnosis of dementia for a given patient depends on the degree to which the ADLs are significantly interrupted. Please let me know via a comment or email if I have muddied the water more or if more information would be helpful. I know of some clinicians that are quick to apply the diagnosis based on minimal ADL disruption and others that are more conservative.
Another condition that can cause dementia or at least result in significant cognitive impairment is a condition called NPH. NPH occurs most commonly among older adults (over age 60) and the process develops slowly over time. The condition is caused by reduced drainage of the fluid inside large cavities in the brain known as ventricles. With poor drainage the fluid in the ventricles builds up and eventually causes the ventricles to enlarge to accommodate the expanding volume of fluid. As the ventricles expand they impinge on the surrounding brain tissue resulting in a variety of symptoms. Without question a neurologist or other physician is the appropriate person to make the diagnosis (not a neuropsychologist), but a neuropsychologist is often involved in identifying the changes in cognition that may occur.
Individuals with NPH may have a change in their walking balance and they may have difficulty with urinary incontinence or urinary frequency. However, many other conditions can result in changes these symptoms, so again, a physician is the appropriate individual to render a diagnosis.
In terms of cognition, individuals with NPH typically have difficulties with executive functions (planning, organization, cognitive flexibility) and processing speed. Memory might also be affected, but the pattern of memory difficulties is different from Alzheimer's disease. In Alzheimer's disease, retention of new information is most impaired, whereas in NPH, retention may be pretty normal but the learning of new information is reduced. In addition, while language (e.g., naming items) is significantly affected in Alzheimer's disease, similar problems are not common in NPH. In terms of neuropsychological profiles, the two conditions can be differentiated with good accuracy. When combined with the symptoms described above and evidence of enlarged ventricles on MRI and minimal overall reduction in brain size, the diagnosis is well defined. Interestingly, the symptoms may improve some for individuals after beginning treatment.
In the absence of any suggestions for topics from Nawgan readers, the next post will review the GEM study. GEM is an acronym for The Gingko Evaluation of Memory Study - a large study of ginkgo biloba for the prevention of Alzheimer' s disease. The results may surprise you.
Remember - The Nawgan blog is now updated weekly on Monday evenings (CST).
Contact me at rpaul.nawgan@gmail.com to request a topic for review in the Nawgan blog.
It is important to note that the Nawgan blog is not intended to replace professional care.
Individuals with questions and concerns about their health are strongly encouraged to seek input from their medical provider.
Sincerely,
Dr. Rob Paul, ABPP/ABCN
Certified Clinical Neuropsychologist
Dementia typically is defined as acquired (i.e., not from early development) cognitive impairment of significant severity to significantly interfere with activities of daily living. This is effectively the same definition described by Pem, in that the cognitive changes interfere with a person's ability to continue to do what they were doing. Most often the complicated tasks of doing are lost first (managing finances, medications, driving, etc), while the more basic activities are maintained much longer (e.g., bathing, dressing, eating, etc). The diagnosis of dementia for a given patient depends on the degree to which the ADLs are significantly interrupted. Please let me know via a comment or email if I have muddied the water more or if more information would be helpful. I know of some clinicians that are quick to apply the diagnosis based on minimal ADL disruption and others that are more conservative.
Another condition that can cause dementia or at least result in significant cognitive impairment is a condition called NPH. NPH occurs most commonly among older adults (over age 60) and the process develops slowly over time. The condition is caused by reduced drainage of the fluid inside large cavities in the brain known as ventricles. With poor drainage the fluid in the ventricles builds up and eventually causes the ventricles to enlarge to accommodate the expanding volume of fluid. As the ventricles expand they impinge on the surrounding brain tissue resulting in a variety of symptoms. Without question a neurologist or other physician is the appropriate person to make the diagnosis (not a neuropsychologist), but a neuropsychologist is often involved in identifying the changes in cognition that may occur.
Individuals with NPH may have a change in their walking balance and they may have difficulty with urinary incontinence or urinary frequency. However, many other conditions can result in changes these symptoms, so again, a physician is the appropriate individual to render a diagnosis.
In terms of cognition, individuals with NPH typically have difficulties with executive functions (planning, organization, cognitive flexibility) and processing speed. Memory might also be affected, but the pattern of memory difficulties is different from Alzheimer's disease. In Alzheimer's disease, retention of new information is most impaired, whereas in NPH, retention may be pretty normal but the learning of new information is reduced. In addition, while language (e.g., naming items) is significantly affected in Alzheimer's disease, similar problems are not common in NPH. In terms of neuropsychological profiles, the two conditions can be differentiated with good accuracy. When combined with the symptoms described above and evidence of enlarged ventricles on MRI and minimal overall reduction in brain size, the diagnosis is well defined. Interestingly, the symptoms may improve some for individuals after beginning treatment.
In the absence of any suggestions for topics from Nawgan readers, the next post will review the GEM study. GEM is an acronym for The Gingko Evaluation of Memory Study - a large study of ginkgo biloba for the prevention of Alzheimer' s disease. The results may surprise you.
Remember - The Nawgan blog is now updated weekly on Monday evenings (CST).
Contact me at rpaul.nawgan@gmail.com to request a topic for review in the Nawgan blog.
It is important to note that the Nawgan blog is not intended to replace professional care.
Individuals with questions and concerns about their health are strongly encouraged to seek input from their medical provider.
Sincerely,
Dr. Rob Paul, ABPP/ABCN
Certified Clinical Neuropsychologist
Tuesday, January 27, 2009
Is Alzheimer's disease the only form of dementia?
Apologies for the late post - I've just returned from Washington DC where I was reviewing grant applications for the National Institutes of Health. I'm back, despite the winter storm, and finally getting to the post.
In the last post we discussed mild traumatic brain injury and introduced the idea that the vast majority of individuals who suffer a mild traumatic brain injury will recovery fully (they will resume employment, return to school, etc). However, we also discussed the unfortunate reality that individuals who suffer a severe brain injury may experience significant cognitive impairment, and for some of these individuals they may meet clinical criteria for dementia. So a quick answer to the question in the title is "No" - Alzheimer' s disease is not the only form of dementia.
Since dementia is usually defined as severe cognitive impairment that interferes with daily living skills, any condition (including brain injury) can result in dementia. In North America Alzheimer's disease is the most common cause of dementia and this is particularly true among older individuals. As we've mentioned in past posts, vascular disease is also a common contributor to cognitive impairment as people reach advanced age.
Another cause of dementia associated with advanced age that we have not mentioned includes Lewy Body disease. Lewy body disease is characterized by a unique form of abnormal changes in brain structure that develop for unknown reasons. Clinically, individuals with Lewy Body disease present with many of the same features as Parkinson's disease. Specifically, their body may appear rigid and stiff, and they may exhibit a slow walking speed, or tremor in the hands or other parts of the body. A neurologist is best trained to identify these symptoms and ensure that the cause of the motor symptoms is not due to Parkinson's disease or other form of what is called Parkinsonism.
In addition to the motor symptoms of Lewy Body disease noted above, patients also experience vivid visual hallucinations (seeing things that do not exist) and fluctuation in the severity of their symptoms. Both of these differ from Alzheimer's disease in important ways. Visual hallucinations certainly can occur in Alzheimer's disease, but usually they develop late in the course of the disease (moderate and severe stages), whereas they are present early in the course of Lewy Body disease. In addition, significant fluctuations in symptoms is not a common feature of Alzheimer's disease but it is very common in Lewy Body disease. Sometimes families will describe their loved one with Lewy Body disease as appearing pretty normal on some days and very confused on other days. When levels of confusion change rapidly in Alzheimer's disease, the cause is often due to changes in the immediate environment (new residency, or some social event, change in medications, etc).
Lewy Body disease cannot be cured, but the symptoms can be managed by a neurologist. For more detailed information about Lewy Body disease, readers are referred to: http://www.mayoclinic.com/health/lewy-body-dementia/DS00795
In the next post we will review yet another cause of dementia - normal pressure hydrocephalus.
Lewy Body disease is a more common cause of dementia among older individuals than what was previously appreciated.
Remember - The Nawgan blog is now updated weekly on Monday evenings (CST).
Contact me at rpaul.nawgan@gmail.com to request a topic for review in the Nawgan blog.
It is important to note that the Nawgan blog is not intended to replace professional care.
Individuals with questions and concerns about their health are strongly encouraged to seek input from their medical provider.
Sincerely,
Dr. Rob Paul, ABPP/ABCN
Certified Clinical Neuropsychologist
In the last post we discussed mild traumatic brain injury and introduced the idea that the vast majority of individuals who suffer a mild traumatic brain injury will recovery fully (they will resume employment, return to school, etc). However, we also discussed the unfortunate reality that individuals who suffer a severe brain injury may experience significant cognitive impairment, and for some of these individuals they may meet clinical criteria for dementia. So a quick answer to the question in the title is "No" - Alzheimer' s disease is not the only form of dementia.
Since dementia is usually defined as severe cognitive impairment that interferes with daily living skills, any condition (including brain injury) can result in dementia. In North America Alzheimer's disease is the most common cause of dementia and this is particularly true among older individuals. As we've mentioned in past posts, vascular disease is also a common contributor to cognitive impairment as people reach advanced age.
Another cause of dementia associated with advanced age that we have not mentioned includes Lewy Body disease. Lewy body disease is characterized by a unique form of abnormal changes in brain structure that develop for unknown reasons. Clinically, individuals with Lewy Body disease present with many of the same features as Parkinson's disease. Specifically, their body may appear rigid and stiff, and they may exhibit a slow walking speed, or tremor in the hands or other parts of the body. A neurologist is best trained to identify these symptoms and ensure that the cause of the motor symptoms is not due to Parkinson's disease or other form of what is called Parkinsonism.
In addition to the motor symptoms of Lewy Body disease noted above, patients also experience vivid visual hallucinations (seeing things that do not exist) and fluctuation in the severity of their symptoms. Both of these differ from Alzheimer's disease in important ways. Visual hallucinations certainly can occur in Alzheimer's disease, but usually they develop late in the course of the disease (moderate and severe stages), whereas they are present early in the course of Lewy Body disease. In addition, significant fluctuations in symptoms is not a common feature of Alzheimer's disease but it is very common in Lewy Body disease. Sometimes families will describe their loved one with Lewy Body disease as appearing pretty normal on some days and very confused on other days. When levels of confusion change rapidly in Alzheimer's disease, the cause is often due to changes in the immediate environment (new residency, or some social event, change in medications, etc).
Lewy Body disease cannot be cured, but the symptoms can be managed by a neurologist. For more detailed information about Lewy Body disease, readers are referred to: http://www.mayoclinic.com/health/lewy-body-dementia/DS00795
In the next post we will review yet another cause of dementia - normal pressure hydrocephalus.
Lewy Body disease is a more common cause of dementia among older individuals than what was previously appreciated.
Remember - The Nawgan blog is now updated weekly on Monday evenings (CST).
Contact me at rpaul.nawgan@gmail.com to request a topic for review in the Nawgan blog.
It is important to note that the Nawgan blog is not intended to replace professional care.
Individuals with questions and concerns about their health are strongly encouraged to seek input from their medical provider.
Sincerely,
Dr. Rob Paul, ABPP/ABCN
Certified Clinical Neuropsychologist
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