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Nitin K Sethi, MD

1. How many concussions are needed and how severe they need to be for CTE to develop? Is there a limit beyond which the brain loses its capacity to compensate for chronic trauma and signs and symptoms of CTE appear? If so what is this limit? Can it be defined? If a player stops playing before this limit is reached would CTE be aborted?

2. Once CTE develops can it be reversed?

3. Is there a way to protect the brain from developing CTE apart from changing the way the games are played. Changing the rules of the game (such as avoiding head butts during football, heading the ball in soccer, direct blows to the head in MMA, wearing safety gear/helmets) shall certainly help but are there other neuroprotective strategies such as medicines (antioxidants, anti-inflammatory drugs) which can be given to prevent the onset and progression of CTE?

As you can see there are many questions for which we still lack good answers. Making the games we play safer certainly sounds a logical principle and hence the thrust to identify concussions in a timely fashion on the playing field and rest the player till complete recovery is documented. Neurologists, neurosurgeons and other physicians skilled in neurosciences by virtue of their training are better equipped to identify concussions and thus there is a growing call to have them by the side of the playing field in every professional and now even college level game. Biomakers and imaging markers to identify CTE in the living brain are also been explored.

Till more is known about CTE and more importantly on how to prevent and reverse it, making the games we love and play safer should be the goal.

Nitin K Sethi, MD

Recently the above titled article was published in The New York Times dated January 20^th 2013. Holly, a domestic cat after getting lost on a family excursion was able to trek back to about a mile away from her family home, a distance of nearly 200 miles. Just how was this domestic animal able to achieve this remarkable feat of navigation ignited some healthy discussion among cat biologists. Wild animals navigate using visual, smell and magnetic cues. Domestic animals such as cats and dogs on the other hand are able to navigate successfully only in the immediate vicinity of their homes. It seems domestication and evolution resulted in loss of navigation qualities which their still wild ancestors (feral cats, big cats and wolves) possess. Take your dog and drop him off in a suburb of Washington DC and it is highly unlikely he shall show up at your apartment door in New York. This got me thinking on how the current generation of homo sapiens navigate. Take any self respecting New Yorker (no self respecting New Yorker will ask another New Yorker for directions) and ask him to find his way to Greenwich Street from say Charles Street and I bet you that only a few shall find their way in a timely fashion. Heck we even use GPS technology to navigate our way in the city we live in. Gone are the days when we navigated using the stars in the sky. We risk losing whatever remaining navigation skills we still possess thanks to the Google maps app on our smart phones. Maybe Holly the cat is a dying breed among cat explorers not just yet willing to let go of the traits of her ancestors.

Nitin K. Sethi, MD

New York-Presbyterian Hospital

WeillCornellMedicalCenter

525 East, 68^th Street

New York, NY10065

I decided that my first post in the New Year 2013 should be on strokes and more importantly on how to recognize a stroke in a timely fashion and how to prevent it. After all a stroke prevented is a brain saved.

So let us begin without delay. Keeping things simple the best way to describe a stroke is to compare it to a heart attack. A heart attack occurs when one of the main arteries of the heart suddenly gets blocked. The sudden lack of blood flow leads to ischemia of the heart (basically the part of the heart supplied by that blood vessel does not get blood/oxygen and if the blocked artery is not opened/ recanalized in time irreversible death of cardiac muscle/tissue occurs). Something similar happens during a stroke and hence sometimes strokes are referred to as brain attacks. A blood vessel in the brain either gets blocked (ischemic stroke) or ruptures (hemorrhagic stroke) and if not opened in time the part of the brain supplied by that blood vessel perishes. The signs and symptoms of the stroke depend upon which part of the brain is involved.

Warning signs of a stroke:

1. Sudden onset of weakness  in the arm and leg on one side of the body (for example abrupt onset of motor weakness in the right arm and leg usually indicates ischemia/lack of blood flow or hemorrhage involving the left side of the brain). That said strokes may be more subtle or unusual in their presentation–weakness in only one arm or one leg, weakness in one arm and contralateral face and so forth.

2. Sudden onset of numbness (loss of sensation but no marked weakness) on one side of the body. Again presentation may be more unusual–abrupt onset of numbness one side of face or just in one arm.

3. Sudden onset of vision problems–double vision or loss of vision in one eye or loss of vision in one half/part of visual field.

4. Sudden onset of difficulty walking or balance–unable to walk in a straight line, dizziness (not all dizziness is stroke though).

5. Sudden onset of speech difficulty–either unable to speak (words are mumbled, not clear, language difficulty), unable to comprehend speech.

6. Sudden onset of complete loss of hearing in one ear (rare form of stroke).

7. Sudden onset of a combination of the above symptoms-usually this is the case.

One of the major problems with stroke is that frequently the symptoms and signs are very subtle and may be ignored by the patient and his family/friends. By the time the patient seeks medical attention, the stroke is already completed (remember when it comes to stroke–TIME IS BRAIN) and the damage is already done. In the case of a heart attack the signs are hard to ignore–sudden onset of squeezing chest pain along with sweating and a sinking sensation. Patients are forced to go to the hospital and seek attention. On the other hand the brain is far more quieter when it suffers a brain attack–no pain, no sweating just quiet suffering of the ischemia.

So what to do when you or someone close to you is suffering a stroke? The most important thing is not to delay seeking attention. You can only be helped if you reach the hospital in a timely fashion ideally within the first hour to 90 minutes of the stroke.  So seek attention at once. It is better to reach the hospital and be told that you misread your symptoms and did not suffer a stroke rather than reach late when nothing can be done to help you apart from supportive care.

So let us start the New Year 2013 by preventing strokes. Remember your brain is your best friend. Protect him, nourish him, take care of him.

Nitin K Sethi, MD

Nitin K Sethi

Department of Neurology, New York-Presbyterian Hospital, Weill Cornell Medical Center, New York, NY (U.S.A.)

Address for correspondence:

Nitin K. Sethi, MD

ComprehensiveEpilepsyCenter

New York-Presbyterian Hospital

WeillCornellMedicalCenter

525 East, 68^th Street

New York, NY10065

Tel: + 212-746-2346

Fax: + 212-746-8845

The problem

Head injuries frequently occur while playing contact sports such as boxing, ice-hockey, American football, mixed martial arts (MMA) and even soccer. In sports such as boxing and MMA the goal is to knock out your opponent by causing a concussion. The perils of boxing are thus well recognized by the medical community especially by neurologists.  Boxer’s encephalopathy, punch-drunk syndrome and dementia pugilistica are terms used to describe the neurodegenerative changes seen in professional boxers as well as athletes in other contact sports who suffer repeated concussions during their professional careers. There is now increasing evidence that repeated concussions sustained by a boxer or an athlete in his or her professional career predisposes them to memory problems later on in life (says in their 40’s and 50’s) and Alzheimer’s disease (dementia) like pathological changes are visible in the brain on histopathology. These athletes are also plagued by neuropsychiatric disorders such as anxiety and depression in their later years. Parkinsonian features (problems with gait and balance) may appear later in life due to damage to the deep grey nuclei of the brain.

My own love for boxing

With this increased awareness about the perils of repeated concussions there is a thrust to make these sports safer. But can boxing, MMA and American football be made safer? It is ironic that I was personally drawn to boxing near about the time I started my neurology residency in Saint Vincent’s Hospital and Medical Center in New York.  Prior to that I knew little if anything about this sport. I had just joined a new gym and happened to walk into a boxing class. I was standing outside peeping in when Tyrone the boxing coach yelled out at me across the room. The first class is free come in he said. There and then my love for boxing was born. Since that fateful day 7 years ago, I have grown to love this sport. I have been boxing on and off since then, yes at times I spar usually with boxers who I know won’t throw a wild punch. For one to really understand this sport and the men and women behind it, one needs to spend time in a boxing gym. New York can boast of some world famous boxing gyms such as Gleason’s gym, I call Mendez boxing on 26^th Street and 6^th Avenue home. There I am known simply as doc. I see the passion and discipline in the men and women who train there especially the ones who are fighting on the amateur and professional circuits. Most of them are in the age range of 16-25. During my time at Mendez I have had the opportunity to closely observe how these men and women train and I tell you it is grueling. Most start with jumping rope for about 10-15 minutes. Then shadow boxing, a few rounds on the heavy bag and pad work. Then come the sparring sessions which can be highly entertaining to watch.  Most boxers end their work-out by going a few rounds on the speed bag. I can honestly say that boxing has changed me for the better; both in mind and in body. So I recently applied and got accepted to be a panel physician for the New York Athletic (boxing) Commission. I feel this shall accord be a unique opportunity to closely observe professional boxing from a neurologist’s point of view.

Making boxing and football safer

So how can we make boxing and other contact sports safer? Some say the best way is to change the rules that govern these sports. In the case of American football one option would be to limit aggressive and hard tackles that encourage helmet to helmet collisions. There has been a healthy debate on this subject. Some have advised better quality helmets the kind worn by soldiers in the battlefield to prevent traumatic brain injury (TBI). The new military helmets (advanced combat helmets) are especially designed to prevent TBI following an improvised explosive device detonation though it is still debatable whether the helmets actually do achieve this objective. The players helmets can be further fitted with a sensor which records the force of impact. This data can then be readily accessed by a physician on the sideline and a timely decision can be made to either pull a player out of play or allow him to continue after a concussion. We certainly have the technology to do this at present but do we know how to analyze the data? Like for example how much should the concussive force be to warrant pulling a player out of a critical game? Some advocate that the rules be amended more drastically such as a complete ban on head to head collisions be enforced. Players should be taught to tackle leading with their shoulder and not using their head as a battering ram. Or that helmets be taken away completely so that players and coaches are forced to switch to “safer” tactics. The main problem with some of these rather novel ideas is that you risk changing the very nature of the sport and driving away the fans. Coming back to boxing you all would agree that most of us go to a boxing match to see a hard knockout. Any Iron Mike fan shall testify to that! Boxing would not be boxing if the rules were amended so that blows to the head were not allowed and professional boxers were forced to wear protective head gear.  So when it comes to boxing and MMA a more “practical” solution would be to enhance our ability to detect concussions in a more comprehensive and timely fashion. But this itself is no easy task. Anyone can identify a concussion when the boxer is knocked out and suffers prolonged loss of consciousness (>5 minutes). Over and out! However it is the minor/subtle concussions which are harder to detect. At present this is what happens. A boxer goes down and a ring side physician like me jumps into the ring to assess him. Are you Okay? Do you want to go on? Raise your gloves for me. Track my finger with your eyes. If he is able to answer my questions and follow my commands, I clear him to fight further. Studies though show that many concussions are missed if examined in this rudimentary fashion. Grossly the boxer looks fine but he is not. There are a few well documented cases where in the boxer has gone on to fight after sustaining a concussion and even win the fight only to be found dead in his bed the next day (second impact syndrome). So is there any better way to identify concussions in a timely fashion?

The Kind Devick test (www.kingdevicktest.com) has been found to be quite sensitive in identifying concussions. It basically involves the testee reading a set of numbers off a card. The number of errors and time taken to accomplish this task is recorded and can be used to assess if a concussion has occurred. This test can be administered to boxers and other athletes prior to the fight or game and these scores serve as the baseline scores. If the boxer gets hit during the fight or a football player suffers a concussion on the field, the test can be administered on the sidelines and a decision to either pull the player/boxer or to let him continue can be made. The Kind Devick test has some inherent advantages. It is easy to administer by anyone (not just a physician), the test can be administered through hand held cards or on the Ipad, quick to administer (this is very helpful when it comes to boxing since the decision to stop or continue the fight has to be made in a matter of minutes), finally it can be administered ringside or on the sidelines.

Other ways to make boxing, American football and MMA safer include yearly neuropsychological testing of all participants to identify deficits in memory, cognition and other neuropsychiatric morbidities such as anxiety and depression. Serial  MRI scans of the brain should be carried out during the athletes career and a physician trained in the neurosciences such as a neurologist or neurosurgeon should be present ringside in all professional and amateur fights/ games (I agree this is not a very practical solution).

Final thoughts

Finally knowledge is power and all athletes, their coaches, parents of children who indulge in contact sports should be made aware of the perils of repeated concussions, how to identify and avoid them. Working together we can certainly making boxing and American football safer.

A not so uncommon cause of headache is when the pressure inside the skull suddenly drops.  Think of the brain as a ball floating in a bucket of CSF. The ball (brain) feels nice and happy when it is bobbing up and down in a full bucket of CSF. Now someone drills a small hole at the bottom of the bucket so that the CSF slowly starts leaking out.  As the amount of CSF in the bucket decreases and CSF pressure falls the brain is no longer bobbing. It sinks down as the CSF decreases and this puts pressure on the nerves which are at the base of the skull. So what happens next? Well the brain complains of a headache.  This in a simple way is what is called low CSF pressure headache.

Low CSF pressure headache has some defining characteristics. The headache is positional–meaning it is worse when the person is standing or sitting upright and abates when he lies down. Unlike migraines patients do not complain of throbbing unilateral headache accompanied by sensitivity to bright lights and loud sounds. Low CSF pressure headache is usually holocranial (whole head), dull, aching and like I said earlier positional. The positional component to the headache is its defining characteristic.

There can be many causes that lead to low CSF pressure headache. A common iatrogenic cause is a spinal tap (also called lumbar puncture). Let me give you a classical example. Let us assume you suffer from migraines  (though you may not be aware of it since it was never formally diagnosed by a doctor). One day you suffer a particularly severe and disabling headache episode (in the past you only had “minor” headaches). You end up going to the ER where the doctor orders a lumbar puncture to be carried out. Now you may ask why did the ER physician order a spinal tap in the first place. What was he looking for? Well the two most common conditions the ER physician wants to rule out is infection (meningitis) and subarachnoid hemorrhage (please see my post–thunderclap headache). So the lumbar puncture (spinal tap) is carried out by inserting the spinal tap needle into the lower part of the back. The needle pierces the dura and CSF starts flowing out. The sample is collected and sent to the lab. Soon enough the results are available and the ER physician comes back to update you. Good news the spinal fluid was clean. You do not have infection nor do you have subarachnoid hemorrhage. You just have a bad migraine attack. You are given pain medications for your headache and sent home.

You are relieved that it is nothing too serious. Next day however when you wake up you are bothered by a holocranial headache. Over the course of the next few days you realize that when you lie down the headache becomes better. It is worse when you are standing or sitting. After suffering through this for a few days two things may happen. The low CSF pressure headache may abate on its own and you are back to your good health or the low CSF pressure headache may persist and prompt a visit to your local neurologist.

The diagnosis is usually straight forward in someone who has the classical history which I have documented above. There are other less common causes of low CSF headache but I shall not dwell into that now.  No special investigations are needed. The neurologist advice is rest and drink plenty of fluids (water, caffeine, juices and so forth). I at times advice my patients to sleep on their tummy for a few nights.  The rationale of this advice–the CSF is leaking out of the small hole in the dura made by the spinal needle. The hole shall close on its own in a few days time. The CSF lost shall be replenished and the headache shall abate. Most of the times this advice works well. At times we prescribe the patient a pain killer containing Tylenol (acetaminophen) and caffeine.

In a few patients inspite of the above conservative treatment the headache persists. In these select patients a blood patch is extremely helpful. What is an epidural blood patch you may ask? Well we take about 10 cc of the patient’s own blood and inject into the epidural space (usually near the site where the original lumbar puncture was carried out). The blood clots and seals off the small opening in the dura. No more CSF leak and no more headache.

That is all about low CSF pressure headache for now folks. Now I too must lie down and enjoy my vacation in India. Miss my parents so it is always nice to be back home.

Nitin K Sethi, MD

Nitin K Sethi

 Department of Neurology, New York-Presbyterian Hospital, Weill Cornell Medical Center, New York, NY (U.S.A.)

Address for correspondence:

Nitin K. Sethi, MD

Comprehensive Epilepsy Center

New York-Presbyterian Hospital

Weill Cornell Medical Center

525 East, 68^th Street

New York, NY 10065

Neurophilia can be loosely defined as the love of or fascination for neurology. Now you may think this is a new recently described exotic neurological syndrome but dwell into the ancient eastern Hindu and Buddhist philosophies and you shall quickly realize that the disorder is as ancient as these civilizations themselves ¹. The workings of the brain and of the mind fascinated these first neurophilia inflicted philosophers and they spent an inordinate amount of time trying to decipher its secrets. Techniques to control the mind through meditation and introspection were described and perfected over the years. One can imagine these neurophiles wondering how this roughly 1400 gram lump of wrinkled tissue with no moving parts, no joints or valves could function as the motherboard for all other body systems as well as serve as the seat of the mind, thoughts, senses; in fact the very essence of the individual. As we slowly unlock the secrets of the living brain with the aid of sophisticated imaging techniques, the prevalence of neurophilia has increased exponentially. One would not be wrong to label it currently as a pandemic. Identification of this disorder is relatively easy (Table 1)

Table 1. Five signs that you may have neurophilia (in no particular order of importance)

Once inflicted with neurophilia the “disease” course is highly variable. In some it merely manifests with a curiosity to know more about the workings of the brain, yet in others (like us neurologists, neurosurgeons and neuroscientists) it becomes a lifelong obsession to know everything about the brain both in disease as well as in health. My own passion for neurology was kindled at a young age by my neurophilia inflicted neurologist father. Little did I realize that exposure at a tender age would result in such a passion for the study of the brain. Yes it is true and I admit it proudly-I have a bad case of neurophilia. Watch out people it is contagious!

References

1. Fuller GN. Neurophilia: a fascination for neurology–a new syndrome. Pract Neurol. 2012; 12:276-8.

I frequently wondered what set these neurologists apart from others. It could not be the medical school or the residency program they graduated from. Few were from Ivy League colleges and a seldom few were known outside the corridors of the institution they served in. On the other hand a good number of the ‘good’ neurologists made it to the New York’s best doctors list time and time again. Was it their depth of knowledge? Many of the ‘good’ neurologists would quote articles and studies with ease but still came up short at the patient’s bedside. It had to be Factor E (excellence factor) coded by the M (master) gene. Only a chosen few had it.

Now when I am on the other side of the fence teaching residents and fellows in training, I still at times wonder whether master clinicians are born de novo (with copious amounts of Factor E) or whether a chosen few good neurologists become master neurologists and the rest remain good. A lot has been written about improving residency training. The goal is to produce competent neurologists at the end of the training process but can good residents be trained to become master clinicians? Is Factor E teachable and transferable? Does training under the wings of these masters automatically ensure transfer of gene M to the trainee¹? The field of neurology glitters with examples of master clinicians who taught, mentored and inspired their residents and fellows to become master clinicians themselves. A closer look at these attending teacher-resident trainee relationships is worthy of our attention. The patient’s bedside is your laboratory is the central tenant that master clinicians teach their students encouraging them to spend time at the patient’s bedside hearing their stories with rapt attention for a small detail in the patient’s history may very well be the key which unlocks the whole puzzle². Sherlock Holmes the master sleuth once told his prodigy Dr. Watson “you see but you do not observe”. Blessed with astute powers of observation and an analytical mind master clinicians similarly teach their students that the eyes do not see what the mind does not know. James Parkinson, a master clinician in his own right, in his short monograph titled “The Shaking Palsy” described 6 patients in total, three of whom he simply observed walking on the city streets. Much of the description of the longitudinal course of the illness we now know as Parkinson’s disease was derived from his observations of a single case only. Master clinicians report just not their successes but also their failures. Always remembering and learning from their failures constantly striving to become better they inspire trainees to follow in their footsteps. Knowing all too well that medicine never was nor shall ever be an exact science, they encourage their trainees not to hesitate to think out of the box when confronted with a vexing case. “When you have eliminated the impossible, whatever remains, however improbable, must be the truth” another quote attributed to Sherlock Holmes is well worth remembering. Last but not the least these lone stars of neurology teach their trainees the importance of treating patients with respect and dignity reminding them ever so gently that our patients remain our best teachers.

“He who studies medicine without books sails an uncharted sea, but he who studies medicine without patients does not go to sea at all.”

(William Osler-Canadian physician 1849-1919)

References

1. Johnston A. Training under the wing of many masters. Pract Neurol. 2012 Jun; 12(3):144-6.
2. Caplan LR. Fisher’s Rules. Arch Neurol. 1982 Jul; 39(7):389-90.

Nitin K Sethi, MD

Just what is white matter disease of the brain? As you all may be aware of in very simple terms the brain is made of grey matter (comprising the cell bodies of the neurons) and white matter (fiber tracts). Think of white matter disease as changes seen in the white matter of different parts (lobes) of the brain visualized on a MRI scan of the brain. Either the white matter appears scarred or atrophic. If the white matter is examined under the microscope, degenerative (ischemic) changes are visualized in the small blood vessels hence the term ischemic microvascular small vessel disease is sometimes used. A point to remember here is that these white matter changes visualized on the brain MRI can be seen in many different diseases of the brain-diseases as diverse as leukodystrophies, nutritional deficiencies, toxic drug exposures, vascular dementia and multiple sclerosis (MS). So the radiologist’s report invariably lists all these differential diagnoses and when patients read their MRI report they get worried. Many write in to me asking me if they have MS.

White matter changes on brain MRI need to be correlated with the patient’s history and examination findings and that is where I as a neurologist step into the picture. Let me explain with a few examples:

1. A 29-year-old woman with history of acute loss of vision in one eye (optic neuritis) . MRI brain shows white matter lesions in a characteristic distribution (perpendicular to the long axis of the lateral ventricles). In this case multiple sclerosis is high up in the differential.

2. A 29-year-old woman with history of episodic headaches which are usually unilateral, throbbing in quality and accompanied by nausea and photophobia (brights lights bother her during the headache episode). MRI brain shows a few non-specific white matter lesions scattered in the brain. In this case the most likely diagnosis is migraine headaches.

3. A 75-year-old woman with complaints of memory impairment. MRI brain shows white matter lesions scattered diffusely in the frontal and temporal lobes. In this case vascular dementia is the diagnosis which comes to mind.

Should white matter disease of the brain be treated: if the white matter disease of the brain represents ischemic white matter disease it may be prudent to address vascular risk factors such as better control of hypertension and diabetes, lowering the cholesterol and advising the patient to stop smoking. There is now increasing evidence that white matter disease may cause cognitive impairment and may coexist with other causes of memory impairment such as Alzheimer’s disease in the same patient. On the other hand if the white matter lesions are demyelinating lesions of MS, then treatment is aggressive treatment of MS. If they are due to migraine then usually no treatment is warranted.

In children the cause of white matter disease of the brain is different. Various leukoencephalopathies, metabolic, hereditary and degenerative diseases are in the differential and have to be screened for and ruled out systematically.

I hope this small post helps to answer some of my readers concerns.

 
Nitin K Sethi, MD

As a neurologist I frequently see patients who complain of memory impairment and forgetfulness. Some consult me primarily for this problem; many others who have come to consult me for some other problem such as headaches voice this concern during the course of their patient interview. All are concerned that they may have dementia. So in this post I shall discuss dementia. In keeping with the style of writing on this blog, I shall keep it simple and free of excessive medical jargon.

So what is dementia?

Broadly speaking dementia may be defined as a disorder in which a person experiences problems in multiple cognitive domains. So for example a patient who has moderate Alzheimer’s dementia shall experience problems with memory (cannot recall old information and may not be able to make new memories), speech (speech is sparse, vocabulary is markedly decreased), may experience problems with calculation, concentration, executive functioning (such as planning for the future), balancing his check book and learned tasks (such as tying his shoelaces, driving a car, using a spoon to eat, brushing his teeth). Family and friends may notice a change in personality (patient might becomes disinhibited, aggressive, argumentative or quieter and mute) and behavior (disruption of sleep wake cycles, night time wandering and so forth). A point to note here is that the motor and sensory parts of the brain remain largely intact so the patient is not weak if formal strength testing is carried out. The disease predominantly affects the higher mental functions—that is the functions which separate us from animals and make us so unique as a species—aka our ability to think, to calculate, to remember, to speak and our individual personality and behavior.

How does dementia present in the early stages?

The onset of dementia is usually subtle. In the early stages of the disease, the patient appears “normal”. Social graces are maintained. Appearance remains well groomed and if you meet such a person casually at a party you shall not mind anything miss. The patient also remains independent in all activities of daily living (ADLs) for example he can brush his own teeth, wear his clothes without any help, drive or take a bath. They may also be able to maintain/keep their jobs. This stage has been referred to minimal cognitive impairment or MCI for short. Further on from here things become trickier. A person may remain in MCI stage and not progress further or progress very very slowly. We still do not know the reason for this. Why some patients remain in MCI stage and do nor progress further. Others may advance on to frank dementia. Why this occurs in some patients rather abruptly and quickly as compared to others is still not known. As the patient advances from moderate to severe dementia he becomes progressively more and more dependent on care givers for ADLs.  In the late/final stages of dementia, the patient is bed bound, mute, totally dependent on care givers, stiff and incontinent of both urine and feces.  Death usually occurs due to superimposed infection such as pneumonia, sepsis or a urinary tract infection.

Are there different types of dementia?

There are indeed many different types of dementia: Alzheimer’s dementia, frontotemporal dementia (Pick’s disease), diffuse Lewy body dementia, dementia of Parkinson’s disease, vascular dementia and so forth. A dementia like clinical picture may also result from certain infectious diseases such as AIDS dementia complex also called HIV encephalopathy and mad cow disease. Vitamin B12 deficiency, hypothyroidism, chronic alcoholism, syphilis are other conditions which may cause a picture indistinguishable from primary dementias such as Alzheimer’s disease. It is important that these be looked for and ruled out since they are treatable causes of memory impairment.  If depression is present, it should be identified in a timely fashion, treated and then the patient should be reassessed.

A point to note here is that all the above mentioned conditions present clinically in much the same fashion. It is indeed quite difficult if not impossible to make a definitive diagnosis such based on history and examination findings as clinical features overlap.  Ancillary tests such as MRI brain, PET and SPECT scans may help to narrow the differential diagnosis. In the near future we remain confident that we shall be able to diagnose the different types of dementia more accurately and more importantly early on in the disease course.

How is dementia diagnosed?

The diagnosis of dementia till today remains predominantly clinical. By that I mean that the diagnosis is made after taking a thorough history and after considering the examination findings. In my personal experience I have found a good neuropsychological evaluation conducted by an experienced neuropsychologist as particularly helpful.  MRI brain, PET and SPECT scans are helpful and may help narrow the differential diagnosis and in ruling out other conditions which may mimic dementia. A EEG study is useful and helps to collaborate the examination findings. There is a tremendous thrust to identify biomarkers for dementias such as Alzheimer’s disease both in the blood and the cerebrospinal fluid (CSF). In the same vein, MRI biomarkers are also getting close inspection and may be ready for clinical use in the near future.

How is dementia treated?

Primary dementias such as Alzheimer’s disease, frontotemporal dementia and dementia of Lewy body are progressive neurodegenerative conditions. At present we have no cure but there are drugs available which may slow down the rate of cognitive decline and ensure better quality of life both for the patient and the family members who care for them. None though is a magic wand and none work once the dementia is moderate to severely advanced. Research continues at a feverish pace and I remain confident of a breakthrough in my lifetime.

Can dementia be prevented?

Or rather can I take any steps now so that I do not get dementia in my later years? Many drugs, herbal and other supplements have been looked at, tested but none have shown a consistent benefit. High dose vitamin E supplementation did not work. Gingko does not work. This is what I advice my patients:

If they have vascular risk factors such as hypertension, diabetes mellitus or high cholesterol, these should be aggressively controlled.

Do not smoke and if you do—stop.

If you do have vascular risk factors, speak to your doctor about taking a tablet of baby aspirin daily. Follow his advice.

Exercise, exercise, exercise. There is ever more research that exercise is neuroprotective.

If you are big on supplements, I advice taking Vitamin B12 500 micrograms once or twice daily and fish oils (omega 3 fatty acids). Again speak to your doctor before you take any supplements.

Attacks of major depression “hurt” the brain. So depression should be identified and treated.

Nitin K Sethi, MD