White matter lesions, migraine and memory problems: a question and an answer

One of the readers of my blog wrote in with a question about white matter lesions on brain MRI. Her question and my response to it follows.


I was recently referred to a neurologist by my primary care physician for treatment of my migraines. While migraines have a been a part of my life, they have been occuring with greater frequency of late (10+ per month). To rule out any other cause of my migraines, the doctor ordered an MRI. The MRI revealed 20+ white matter lesions throughout my brain (various locations, various sizes). The neuro was at a loss as to why I had so many. I did inform him that approx 15 years ago I had unilateral ect, and asked if perhaps this had caused it? I also let him know that I was experiencing significant memory issues (forgetting short term and long term memories, and even blanking on spelling my own last name for a minute or two). I asked him if ect could be responsible? The neuro has since followed up with me and has stated that ect could NOT be responsible for the lesions, and was not likely to be responsible for my recent, memory issues. I have been tested for MS, lyme, infection, etc. – all negative. I do not suffer from depression or take any other medications which would cause memory issues. Any thoughts? What else could cause these lesions? Is these any research at all into lesions and ect? I am trying to get into Neuropsych testing to determine the extent of my memory loss. The migraines are now currently being sufficiently controlled with Imitrex.


Thank you for writing in to me M.  White matter lesions are commonly documented on brain MRI done for various reasons (in your case as a work up of migraines). The differential diagnosis of white matter lesions is broad and varies based on the age of the patient. In “most” adult patients especially those with risk factors for microvascular disease such as diabetes mellitus, essential hypertension (high blood pressure), dyslipidemia (high cholesterol), current or past heavy smokers these white matter lesions respresent small vessel disease (also referred to as microvascular ischemic small vessel disease). Meaning that the small blood vessels in the brain are showing signs of ischemia (lack of blood flow). So when I see extensive microvascular (small vessel) disease on a patient’s MRI scan of the brain what I worry about is the possibility of a stroke in the future. As a neurologist, I then try to identify his stroke risk factors and attempt to modify them. If he has high blood pressure and is not an on anti-hypertensive medication–start an appropriate anti-hypertensive, if he is already taking a blood pressure medication but the blood pressure is still not well controlled then I may need to increase the dose of his medication and/or change it. As per the new Joint National Commission guidelines broadly speaking the lower the blood pressure the better it is (earlier a blood pressure of 140/80 mm Hg was accepted as ” normal”, now we aim for level of 120/70 mm Hg). If the patient’s blood sugar is high (fasting blood sugar greater than 107mg/dl), I would investigate him for diabetes mellitus. For this blood sugar is tested in a fasting state and after meal (post prandial). There are normal values and if the patient’s blood sugar exceeds these normal values, then he has diabetes mellitus. Diabetes mellitus can be controlled by a combination of dietary modification, exercise, oral hypoglycemic medications (pills) and/or insulin injections. If the lipid profile is deranged (high total cholesterol, high low density lipoprotein, high triglycerides and low high density lipoprotein), then again dietary modifications, exercise and lipid lowering medications (statin group of medications such as Lipitor are one example) are recommended.

Now what do white matter lesions represent when they are seen in a young person (like for example in a  young lady 25 years of age)?  The main differential and what concerns most patients and physicians alike is whether this could represent multiple sclerosis. I have written about this before and again want to emphasize that the diagnosis of multiple sclerosis is a clinical one and not based solely on the MRI scan of the brain. The MRI scan always has to be interpreted after taking the history and examination findings into consideration. Also the white matter lesions of ischemic small vessel disease are different from the white matter lesions (plaques) of multiple sclerosis. In multiple sclerosis the lesions have a characteristic appearance and distribution in the brain.

White matter lesions can also be seen in many other infectious (Lyme disease is a good example) and inflammatory conditions (sarcoidosis, connective tissue diseases which cause vasculitis in the brain). Most of these diseases can be identified with the help of a good history and some basic tests.

White matter lesions are also commonly seen in people who suffer from migraines (more commonly seen in women migraine sufferers). Why do white matter lesions occur in migraine patients. While there are many theories of migraine pathophysiology, migraine is a vascular headache and hence the blood vessels are again involved.

Do white matter lesions cause memory problems. Now that is a tough question to answer. When I see extensive white matter disease in a brain MRI, it tells me about the health of the brain and the blood vessels. If a person has extensive white matter disease, the same pathology shall be seen in the blood vessels of the heart. So they are prone to both heart disease and brain disease (stroke, transient ischemic attacks). While Alzhemier’s disease is the most common primary dementia, vascular dementia is exceedingly common too. What is vascular dementia? As the name suggests, it is dementia (memory impairment, problems in multiple cognitive domains) caused due to multiple small strokes in the brain or rather strokes in a strategic location. These strokes occur over a period of time and may be clinically silent (meaning that the patient may not even realise that he has suffered a stroke). The small strokes over a period of time though add up and cause vascular dementia.

I hope this helps in answering some of your questions M. My advise to you is to follow up with your primary care physician and the neurologist. They shall help guide your work-up further.

Personal Regards,

Nitin Sethi, MD

Depression superimposed on dementia–two hits to the brain!!!

Depression superimposed on dementia–two hits to the brain!!!

Nitin K Sethi, MD

Assistant Professor of Neurology

New York-Presbyterian Hospital

Weill Cornell Medical Center

New York, NY

In recent years the link between depression and dementia has been closely looked at.  Many questions await a definitive answer-

do attacks of major depression predispose to dementia later in life?  (or put in more simpler terms, does depression hurt the brain and kills  neurons leading to cerebral atrophy and dementia?)

is depression more common in patients with primary dementia such as Alzheimer’s dementia?

is depression frequently missed or misdiagnosed in  patients with primary dementia ?

do patients with dementia have depression which is more refractory to medical treatment?

does depression accelerate the rate of cognitive decline in patients with dementia?

I recently saw a patient who was referred to me to evaluate for dementia. She was 74-years old and her past medical history was significant for hypertension for which she was on anti-hypertensive medications. When the patient saw her primary medical doctor she had volunteered the information that she was having some problems with her memory. She at times forgot the names of her loved ones, one time she had got lost while heading from home to the hospital. Her home aide further added that she had noticed that the patient frequently misplaced objects and then could not recall what she had done with them. At times she forgot to add an essential ingredient to a dish she was preparing. Recent neuropsychological examination was suggestive of a primary dementia.

As I spoke to the patient, I found her to be quite high functioning. She made eye-contact, gave a succulent history and most importantly had insight into what was plaguing her namely her problems with memory. As the interview went on I learnt that she had been depressed for a while. Though she was on anti-depressants, the recent loss of close family members had made her more depressed. She suffered from a loss of appetite and few things in life gave her pleasure.

So where do we go from here? What is the optimum treatment for someone who might have an underlying primary dementia such as Alzhemier’s disease but also has superimposed incompletely treated depression. Most doctors would agree that her depression needs to be treated more agggressively but the questions which arose in my mind were the following:

–should I treat her for dementia now or reassess her after treating her depression more aggressively?

–is the ongoing chronic depression actually predisposing her to memory problems and maybe even dementia?

–what came first—depression or dementia?

–who is the bigger culprit here–depression or dementia?

All questions for whom we still do not have good answers.  The brain can take a hit here and there but depression-dementia is a deadly combo–likely a death blow to the delicate brain. Maybe one day we shall be able to win the battle against these two scourges.

Behavioral problems in dementia, how common are they and is there any help for it?

Behavioral problems in dementia, how common are they and is there any help for it?

Nitin K Sethi, MD


I recently saw a 75-year-old patient in my office which has prompted me to write this post. His wife brought him in  for memory problems. As I took the history, I realised that it was not memory problems per se that was bothering her, it was his change in behavior. Recently he had become aggressive, at times verbally and physically abusive to her. True he had some memory difficulties which were apparent in the history. He had lost his way once and got confused when he could not recall the names of his grandchildren at a family get together. But as I took his history and asked him questions, I found him to have a good fund of general knowledge. He was aware of recent events like the election of President Obama and the war between Israel and Hamas. He was physically active and liked to cycle around the neighbourhood. But it was his change in behavior which was causing a strain in his relationship with his wife and she was having a difficult time taking care of him and administering all his medications.

The patient above obviously has dementia settling in. One can argue about the type of dementia (is it Alzheimer’s or some other type of dementia such as fronto-temporal dementia? You can read more about the same on my website http://braindiseases.info). But what I wanted to stress in this post was the prevalence of behavioral problems in dementia. Behavioral problems are common in all forms of dementia and are a frequent cause of caregiver stress and burnout.  Patients with dementia may present witha multitude of behavioral issues. They may either become too aggressive and hard to control (verbally and physically abusive they may lash out at loved ones when they attempt to nurse them) or they may become aphathic with loss of motivation and drive. Caregivers may complain that they are listless, just sit in one place thoughout the day and do not attempt any new task on their own.

I want to stress that caregivers need to understand that these behavioral problems are a part and parcel of the dementia complex. Lot of people just associate dementia with memory problems, little realising that the disorder is more pervasive. Thankfully now there are many drugs which can control some of these behavioral issues, thus making life easier for caregivers. These range from antidepressants to antipsychotic drugs apart from cognitive and behavioral therapy.

My advise to my readers is this.  If any of you has a loved one with dementia, learn to recognize behavioral problems early on. Bring them to the attention of the doctor since many of them can be effectively treated.


Not quite dementia? red flags to watch out for

Not quite dementia?  red flags to watch out for

Nitin K Sethi, MD

Assistant Professor of Neurology

New York-Presbyterian Hospital

Weill Cornell Medical Center

New York, NY 10065

I get many patients who tell me during their office visit that they are worried they may be getting dementia. The thought of Alzheimer’s disease with its progressive neurocognitive decline and memory loss is a frightening thought indeed and patients are justifiably worried.

SO LETS GET DOWN TO THE BASICS. What are the red flags/ warning sings that you indeed do have Alzheimer’s dementia starting off?

Patients who have Alzheimer’s dementia are usually not aware that they have a memory problem. In the initial stages of the disease, social graces are maintained. These early patients may be able to hold down a job, socialize with friends and no one is aware that they have a memory problem.  Small problems may be starting off though. Losing keys, misplacing things, having problems with numbers, having problems balancing the cheque books and in counting change, forgetting names etc. As you can imagine these are not “major issues” and may not be noticed by the patient or family initially.

So usually when a patient hinself comes to me and tells me, he feels he may be getting demented, I approach it with a healthy dose of skepticism. Most of the times these patients do not have dementia, rather they may be depressed. Depression at times can lead to dementia like symptoms with loss of energy and drive and feelings of self-doubt. It is hence sometimes referred to as pseudo-dementia. You treat their depression and the patient feels much better and the memory problems resolve.

But when the patient is brought to my attention by a family member with complaints of memory problems, getting lost in the neighbourhood, change in personality, becoming indifferent to his personal appearance and grooming, apathy and lost of interest in activities previously enjoyed, in such patients the possibility of dementia crosses my mind.

One must remember that in dementias like Alzheimer’s disease (there are many different types of dementia), the problem is not just with memory. Dementias like Alzheimer’s disease affect a range of neuro-cognitive abilities. Thes patients have problems with language (we call this aphasia–there are many different kinds of aphasia), calculation, ability to sustain attention, ability of abstract thinking, of planning for the future (what I shall do next week) and in executitive functioning. They also suffer from what we call apraxias. Let me explain what apraxia is. Lets assume I can button and unbutton my shirt. Now this is a learned act, which I learned as a small child. Now suppose I get demented. Even though I am not weak (meaning the strength in my arms is intact), I forget how to button and unbutton my shirt. This loss of ability to carry out learned tasks despite intact motor/ muscle strength is called apraxia. Patients who have Alzheimer’s dementia forget how to tie their shoes laces, how to drive a car, how to eat with a spoon and so on. Hence in a way they become totally dependent on care-givers for all activities of daily living. Memory loss is just a component of a much bigger problem. Even when it comes to memory, they have problems in short term memory (what they ate for breakfast, who is the current President elect, whom did he defeat in the elections etc),  long term memory (what is your name, your wife’s name, your child’s name, where you were born, what date) may remain intact in the initial stages of the disease.

 So watch out for the red flags, not everything is dementia!!!

Ginkgo biloba for memory-a dream that did not materalize

Just a quick post about Ginkgo biloba. Some of my patients use Ginkgo biloba extract as a supplement to enhance memory and prevent neurodegenerative conditions like Alzhemier’s dementia. The data that it is indeed effective has always been inconclusive. I always feel that if  a drug is truly effective for a condition then we seldom need studies to prove it. It is only when the evidence is insufficient to suport a recommendation that studies are needed. Many of these are funded by the drug manufacturer (large pharmaceutical companies).

Recently results were made available from a big study looking at whether Ginkgo biloba extract actually aided in preventing Alzheimer’s dementia. The study found that Ginkgo biloba did not prevent or delay dementia or Alzhemier’s disease. In simple words, the study showed that it does not work. Further there is some data to show that it may actually be dangerous to take this extract as it increases the risk of hemorrhagic strokes (bleeding in the brain).

My advise to my readers would be to avoid taking this supplement till we have more conclusive data on its effectiveness. Especially avoid taking supratherapeutic doses (large doses).


Nitin Sethi, MD

Deficiency of vitamin B12 causes cerebral atrophy

                               Deficiency of vitamin B12 causes cerebral atrophy

                                                    Nitin .K. Sethi, MD

                                            Assistant Professor of Neurology

                                            New York-Presbyterian Hospital

                                              Weill Cornell Medical Center

                                                New York, NY 10065

I am big on vitamins both when it comes to taking it myself and recommending it to my patients. So my interest was naturally piqued when I read an article in the journal Neurology titled ” Vitamin B12  status and rate of brain volume loss in community-dwelling elderly” by Vogiatzoglou et al. The authors investigated the relationship between markers of Vitamin B12 status and brain volume loss in an elderly population. They concluded that low levels of vitamin B12 may contribute to brain volume loss (cerebral atrophy) and may be one of the causes of subsequent cognitive impairment in this population. So how do we interpret this data?

Can vitamin B12 intake prevent the onset of dementia.?

 If so how much of this vitamin should one take?

And at what age should one start taking this?

Questions for which we still do not have good answers. As I see it, vitamin B12 is pretty innocuous (side-effects are few if any) and thus can be safely taken by the majority of people. Moreover it is cheap (as unlike some other vitamins and anti-oxidants in the market eg coenzyme Q10). Dementia is a devastating neurodegenerative condition for which at present there is no cure. If vitamin B12 intake prevents cerebral atrophy then it may be worthwhile recommending it to my patients.

The elderly are a vulnerable population group. Many times their diet is marginal and thus they are prone to having nutritional (vitamin) deficiencies.  Other vulnerable groups include alcoholics (people who drink heavily, usually have marginal diets and thus are prone to vitamin deficiencies), people who have conditions which prevent the body from absorbing vitamin B12 example pernicious anemia, those who have had bowel surgery, Crohn’s diseases, ulcerative colitis etc.

Vitamin B12 is present in meat including fish, poultry, eggs, milk, and milk products. It is important for neuronal function and also helps to maintain healthy red blood cells. So deficiency is more commonly seen in vegetarians especially those who do not have even milk or milk products. It is this group whom I feel shall surely benefit from vitamin B12 dietary supplementation.

At what age should one start taking Vitamin B12 is difficult to answer. Vitamin B12 is stored in the liver and so a person who eats a healthy diet should have ample reserves of this vitamin and does not need supplementation. I usually check the vitamin B12 status of my patients especially those who are elderly or suffering from a chronic medical condition. This can be done by a simple blood test. If they are deficient, I prescribe vitamin B12 (vitamin B12 comes in tablet form. In patients who have very low stores, we sometimes give them a shot of vitamin B12 intramuscularly).

As for the rest of us (“healthy” and not too old) what should we do? One way would be to take a tablet of multivitamin a day. Most good multivitamin combinations do have B12 in them. That is what I do!!!

” the mind is a wonderful thing and a healthy mind is truly beautiful”

Normal pressure hydrocephalus (NPH)

Normal pressure hydrocephalus (NPH) is another potentially reversible cause of “dementia” or rather memory problems in the elderly. NPH is characterized by the triad of gait disturbance, urinary incontinence and memory problems. The dementia in NPH is of the subcortical type meaning that it is mostly characterized by psychomotor retardation (patients are slow to respond), unlike cortical dementias like Alzheimers disease they do not have language deficits (aphasia), inability to do learned things (apraxia) or agnosia.

The etiology of NPH is still not fully elucidated but it is thought to involve some obstruction to the normal flow of the cerebrospinal fluid (CSF). This obstruction may be due to previous history of meningitis or CNS trauma. When you image these patients with either a CT scan or a MRI scan, one finds the ventricles are dilated (large enlarged ventricles) but there is not much corresponding cortical (brain0 atrophy. This is against what is found in cortical dementias like Alzheimers disease where apart from the ventricles been dilated and enlarged, the brain also is shrunken (atrophy).

So in which patients should the diagnosis of NPH be entertained? Mostly these are patients who are elderly and who have had a subacute onset of memory problems accompanied by difficulty in walking (patients who have NPH have a characteristic gait (they walk slowly and stiffly, we call their gait as magnetic gait). They may or may not have urinary incontinence (the entire triad may not be present in all the patients). Neurologists entertain the diagnosis of NPH if they see a patient with the above symptoms and if the imaging is characteristic.

To confirm the diagnosis though requires further testing. Normally what we do is a therapeutic as well as diagnostic spinal tap. What does that mean you may ask?

Well we bring the patient into the hospital and do a spinal tap. Before the tap is done the patient is examined to determine the memory deficits. A timed walking test is carried out ( we make the patient walk a fixed distance and measure the time taken to do so ). Then a good amount of spinal fluid is removed about 20-30 cc. The pressure of the spinal fluid is measured at that time and in a typical patient of NPH it should be normal (hence the name normal pressure hydrocephalus). Once the spinal fluid has been removed the patient is again tested. Has the memory improved. We make the patient walk the same distance as before. If now the walk is much faster and steadier, then we document a positive reponse to large volume CSF removal. Our diagnosis of NPH is now strengthened and there has also been a therapeutic response to the procedure ( remember I told you the test is both diagnostic and therapeutic).

Before I usually subject the patient to a surgical option for more definitive treatment, I usually like to repeat the above test at least two more times. If there is a consistent positive response to large volume CSF removal, then I feel confident in going ahead and asking the neurosurgeon to place a shunt.  What is a shunt? Well a shunt is a device which as the name suggests shunts the spinal fluid from the brain into the peritoneal cavitiy (the gut). It has a valve which can be set to open at a particular pressure. So whenever the CSF pressure rises above that pressure, the valve shall open and the extra spinal fluid shall be shunted from the brain into the gut.

Simple device but does have its own risk of complications. Shunts can get infected, they can get dislodged from the brain and start migrating, they may get obstructed and have to be replaced etc. Hence before I advise putting any sort of hardware into the brain, I try to be as sure as possible that my patient indeed does have NPH and not a cortical dementia like Alzheimers or Parkinsons disease (as these do not respond to shunt placement).

It is Friday the 20th, I am off home on my vacation but shall be keeping the blog active. Please do contact me if you have any questions or want me to discuss something particular.

Personal Regards,

Nitin Sethi, MD

Successful aging and living with adversity

                             Successful aging and living with adversity

Nitin K Sethi, MD


        Comprehensive Epilepsy Center, Department of Neurology, NYP-Weill Cornell Medical Center, New York, NY (U.S.A.)

Address for Correspondence:

NK Sethi, MD

Comprehensive Epilepsy Center

Department of Neurology

NYP-Weill Cornell Medical Center

525 East 68th Street, York Avenue

New York, NY 10021

Fax: 212-746-8984

Email: sethinitinmd@hotmail.com

I read a very fascinating article recently in the Journal of Neurology Neurosurgery and Psychiatry about successful aging in adversity. We all want to age successfully . Successful aging though is just not about escaping illness as the authors (Livingston et.al) point out but also of having a positive attitude towards one’s life despite poor health. In their study they interviewed patients with dementia to find out how they view their aging. To my pleasant surprise they found that many people with dementia feel that they are aging successfully and rate their quality of life as good. This may be against what their caregivers feel. I should add these were people with mild to moderate and not severe dementia.

So how can we age successfully both in health and disease? Well if you are healthy, good then the odds are with you. Your quality of life is good, you have no physical or mental impairments due to disease and if you maintain a positive attitude and avoid depression and anxiety successful aging can be readily achieved. Exercise regulary, keep your mind occupied (read books, watch television, read the newspaper), maintain good and healthy social interactions (surround yourself with family and friends, date if you are single) and hey you are on your way to aging successfully.

But what if you are sick?  Is successful aging possible in adversity. YES as the study points out. It is very much so. What is needed is good mental health and social relationships. Have a positive frame of mind. The study points out that an individual’s underlying resilience plays a big role in successful aging and even though the disease may progress as time goes by, the individual shall still continue to feel he is aging well. Again the importance of mental health is stressed. Avoiding depression and anxiety is the key to successful aging in the face of adversity. The importance of social relationships and support of family and friends cannot be stressed more.

Well there you have it, maybe a small piece to the puzzle of successful aging and at least to some of us in the face of adversity.


Tip of the tongue and “senior moments”: the truths behind dementia

Tip of the tongue and “senior moments”: the truths behind dementia

Nitin K Sethi, MD


        Comprehensive Epilepsy Center, Department of Neurology, NYP-Weill Cornell Medical Center, New York, NY (U.S.A.)


Address for Correspondence:

NK Sethi, MD

Comprehensive Epilepsy Center

Department of Neurology

NYP-Weill Cornell Medical Center

525 East 68th Street, York Avenue

New York, NY 10021

Fax: 212-746-8984

Email: sethinitinmd@hotmail.com

I read an interesting article in the Wall Street Journal by Melinda Beck titled ” The science behind senior moments”. In it she talks about “senior moments”-episodes where-in you are temporarily unable to recall a name, forget a number (like the telephone number of a close friend or a relative) or enter a room and forget what you were supposed to do. Just what do these “senior moments” represent-are they just signs of normal aging process or are they a warning sign of impending dementia?

Let me give you an example. Let us assume you are watching a movie starring Cary Grant. You see Cary Grant on the screen, you know who he is but for the life of you, you cannot recall his name. we call this the “tip of the tongue” syndrome. You have the name on the tip of your tongue but are unable to get it out. We all have older family members and friends. We notice that at times they are more forgetful. They forget their keys, forget names: are these “senior moments” or are they signs of dementia? Is there anything called senile dementia? (that is dementia occuring due to old age itself, not due to a neurodegenerative condition like Alzheimer’s disease).

Before we discuss this further, we should try to understand how memories are formed and stored in the brain. In simple terms we first register and encode memory, then this is stored and finally it is retrieved. What do i mean by this? Well the first thing which occurs is registration and encoding. For one to retain memory, one must first register what one is trying to remember. Let me explain this with an example. Lets assume you are reading a book. At the same time you are watching the TV and talking to your friend on the phone (that is you are multi-tasking). Now if I ask you to recall what you just read, it is possible that you shall not be able to do so well. Why? This is because your attention was divided and hence you never really registered what you were reading in the first place. If you did not register, you did not commit it to your memory and hence you cannot recall it. So first lession is that when you are trying to memorize something, make sure you pay attention.

Then comes consolidation and storage of memory, the process by which the brain stores the memory. Memory is usually stored in the temporal lobes and the hippocampus. This is a complex process and a lot is still not known how exactly are these memory programs laid down in the brain. Consolidation and storage of memory ensures that the memories become more permanent. There is some data to suggest that consolidation and storage of memory occurs at night while we are asleep. Maybe there is some truth to grandma’s saying of getting a good night sleep before a big examination.

Finally is the process of retrieval. This is the process by which we are able to recall an old memory. One can have a problem at any step of this memory process. Patient’s with Alzheimer’s dementia usually have a problem with both consolidation and retreival. Someone who is intoxicated but does not have Alzhemier’s dementia like an alcoholic shall have problems with encoding as he is delirious.

Now that we know how memory is formed, I want to stress that the tip of the tongue syndrome occurs in many healthy people. Why does it occur? Why is there a temporary memory block which then clears by itself and we are able to remember everything? No one quite knows the answers to these questions.

Senior moments though (especially if they are occuring in the senior population above the age of 65) deserve a more closer look. Is the problem episodic (comes and goes) or is it constant (always present)? Is is static and stable or is it progressive? Does it involve just one domain of memory (like names) or is it more widespread involving multiple domains (not just names but things like forgetting how to drive a car, problems with calculations and abstract thinking etc).

If the above are present, then it is not senior moments and is more likely to be dementia. Some neurologists doubt if something like senile dementia actually exists. We all have met some elderly people with razor sharp memory.

That in essence is the truth behind senior moments and the tip of the tongue syndrome.



In this section we shall discuss a little about dementia. Just what do we mean when we say a person has dementia?

Dementia is a disorder in which a person has cognitive impairments in multiple domains. Meaning a patient with dementia has problems with memory ( forgets things), language ( speech gets sparse and content/ vocabulary decreases), calculation (person loses the ability to calculate: subtract, multiply etc), and abstract thinking. Depending upon what part of the brain gets affected, a patient with dementia may have personality changes and problems with executive functions like planning and other goal directed actions. They may also experience what we neurologists refer to as apraxias. Apraxia is an inability to do a learned act (example you can tie your shoe laces, it is an act you learnt as a small child. Now assume you get demented, you lose the ability to tie your shoes laces even though you are not weak and have full strength in your arms and legs). Patients with dementia may exhibit various kinds of apraxias, as the disease evolves they become dependent on care-givers for nearly all activities of daily living: cannot drive, cannot tie their shoe laces, cannot feed themselves or take a shower on their own.

There are many different types of dementia. These differ from each other in the cognitive domains affected and in the way they present clinically.

Classification of dementias:


1) Alzheimer’s dementia

2) Fronto-temporal dementia also referred to as Pick’s disease

3) Multi-infarct dementia also called vascular dementia

4) Dementia associated with Parkinson’s disease also called Parkinson’s disease dementia

5) Diffuse Lewy Body dementia

6) Primary Progressive Aphasia

7) AIDS dementia complex or HIV encephalopathy

8) Dementias associated with infections like syphilis

9) Reversible dementias like that due to hypothyroidism, deficiency of vitamin B12, thiamine (vitamin B1), hydrocephalus (normal pressure hydrocephalus)

10) Conditions which can mimic dementia example depression (pseudodementia)


Let us now discuss a few of these disorders. I shall start with the most common cause of dementia in the elderly namely Alzheimer’s dementia.


Alzheimer’s dementia: AD is the most common primary dementia seen in the elderly age-group. The onset of AD may be very subtle and frequently the care-givers or the patient cannot tell when did the disease first start. By the time the patients come to medical attention, the dementia is usually quite prominent. A point to note here, patients with dementia usually do not seek help by themselves. They do not feel anything is wrong with them, are not bothered by the lack of memory or their forgetfulness. It is their relatives and friends who first notice something is amiss. They notice that the patient keeps forgetting simple things, may get lost in their own neighbourhood ( for example the patient may not know what street he lives on and get lost while driving), other things like going to the grocery store and forgetting why one went there in the first place and having problems with names etc may be noticed.

Suprisingly in the earlier stages of the disease patients maintain their social graces pretty well. They may interact pretty gracefully in a social setting like a party or at work and if you are inter-acting with them casually you may never realise that they are having memory problems.

Diagnosing Alzheimer’s dementia: the diagnosis of Alzheimer’s disease is mostly clinical and a neurologist would be able to make the diagnosis clinically with a reasonable level of accuracy. Your doctor may order some tests like an MRI study of the brain and some blood tests to measure the thyroid hormone levels in your body, vitamin B12 level and also to rule out diseases which can mimic Alzheimer’s disease in its presentation such as syphilis. Nowdays more advanced imaging tests are been used to diagnose Alzheimer’s disease at an earlier stage of minimal cognitive impairment (MCI), these include PET (positron emission tomography) scan, SPECT (single photon emission computed tomography) scan and fMRI (functional MRI) scans. These facilities should be available in the big neurological centers.


Managament of Alzheimer’s Dementia: Alzheimer’s dementia is as of now incurable. However there are medications which can slow the progression of this neurodegenerative disease and improve the cognitive abilities of the patients. These drugs belong to a class of drug called cholinesterase inhibitors.  They inhibit the cholinesterase enzyme from breaking down acetylcholine, so increasing both the level and duration of action of the neurotransmitter  acetylcholine. Commonly prescribed drugs include: donepezil (Aricept), rivastigmine (Excelon), tacrine (tetrahydro aminoacridine) and galantamine. A few years ago, a new drug called memantine (Nemanda) was introduced into the market. This has a different mechanism of action as compared to the cholinesterase inhibitors. It is a NMDA receptor antagonist. Treatment with cholinesterase inhibitors does not alter the natural history of Alzheimer’s dementia. Patients though do get a few more months and possibly a few more years of relatively preserved cognitive abilities. Caregiver burden is reduced and patients may remain independent in some activities of daily living. Certain other medications and nutritional supplements have been advocated for Alzheimer’s disease patients with no proven efficacy. These include supplements like Ginkgo biloba and supratherapeutic doses of Vitamin E.

In the more advanced stages of the disease, patient’s become mute, akinetic (do not move spontaneously), they are incontinent, cannot feed themselves and become totally dependent on caregivers. Caregiver burn out is quite common and patients may be placed in nursing homes. In this advanced stage urinary tract infections (UTI), respiratory tract infections (pneumonias) and bed sores (decubitus ulcers) are common causes of morbidity and mortality. These advanced Alzheimer’s disease patients need good nursing care.


Let us talk a little about other neurodegenerative dementias. Fronto-temporal dementia also called Pick’s disease resembles Alzheimer’s disease except that these patients have early and more prominent frontal lobe involvement. Thus early on in the disease course, these patients have executive dysfunction (problems with planning things, thinking about future plans and how to go about making them happen). They also have prominent personality changes (may become angry, argumentative and suspicious) and also disinhibited (say whatever comes to mind, act inappropiately in social gatherings eg may start masturbating or touch themselves inappropiately).  The cholinesterase inhibitors used to treat Alzhemier’s dementia may also be tried in patient’s with fronto-temporal dementia (Pick’s disease). The name fronto-temporal dementia comes from the fact that these patients have prominent atrophy (decrease in mass or bulk or size) of the frontal and temporal poles/lobes.

Dementia of Lewy Bodies: is another type of dementia in which patient’s typically exhibit fluctuating symptoms. Visual hallucinations is a prominent component of this type of dementia. Patient’s respond poorly if medications like Haldol (haloperidol) are used to control their behavior. Atypical antipsychotics like Seroquel (quetiapine) are better drugs to control behavioral problems in these patients like agitation and aggression.

Dementia of Parkinson’s disease: Patient’s who have Parkinson disease may also develop dementia (memory problems) later on in their disease course. I shall discuss this further under Parkinson’s disease.

Depression or pseudodementia: Patients who have major depression may also look as if they are demented. These patients have anhedonia (no interest in any pleasurable activity like watching TV, getting a cup of coffee, watching a movie with friends). They just sit still, may not eat if not asked too and look akinetic. These depressed patient’s superfically may resemble dementia patients and hence depression is also referred to as pseudodementia. Once you treat their depression, they improve and all their “memory problems” go away.

Demented patients may have superimposed depression and vice versa hence a thorough search should be made to rule out depression in a patient with dementia as it is readily treatable.

I shall discuss depression under a separate heading. There are caretaker support groups for people who have loved ones suffering from dementia. They offer advice and help in preventing caretaker burnout.



A self realised man is one who controls his mind

Lord Krishna in the Bhagavad Gita