Author: braindiseases

I am a qualified neurologist with sub specialization in the fields of epilepsy, clinical neurophysiology, sleep medicine and traumatic brain injury.

A neurologist reflects…..

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Nitin Sethi, MD

Assistant Professor of Neurology

New York Presbyterian Hospital

Weill Cornell Medical Center

New York, NY 10065

 

Saturday morning finds me in my favorite  coffee shop in the West Village reflecting on the week that went by.  It was a long week, even by my standards and I am happy to have the time to sit down and reflect on it. The week also saw me confronted with a moral and ethical delimma. Electroencephalogram (EEG) (this is a test to look at the brain waves) monitoring was requested for prognostication purposes on a patient in the intensive care unit. Patient had suffered multiple strokes and was on a mechanical ventilator. The purpose of getting the EEG was to get an idea of the extent of his cerebral dysfunction. His EEG showed some slowing of brain waves but otherwise surprisingly looked “good” given the extent of pathology in the brain and the fact that he was comatosed.

His wife tearfully was considering termination of care. Patient had a living will, in which he had clearly made his wishes apparent that he did not wish to live in a state where he was dependent on others, bed-bound and unable to participate in activities of daily living. Objectively as a doctor I knew he was not brain dead, my neurological examination told me that. I did know that his chances of a meaningful neurological recovery were very poor and likely he was heading to a persistent vegetative state (read more about PVS on my website http://braindiseases.info).

His wife had justifiably struggled to come to the decision of termination of care of her beloved husband. Next day when she finally made her decision to terminate care, the patient was noted to wince to pain as she walked into his room…..

There started the moral and ethical delimma for everyone, his wife as well as us doctors. Can we ever prognosticate sufficiently about the extent of someone’s neurological recovery? Can we ever be 100% sure about the extent of someone’s neurological recovery especially if we are attempting to make that decision soon after the neurological insult. Various neurological papers have attempted to answer this vexing question. We do have some leads. We know that a patient who loses brainstem reflexes such as pupillary light reflex (shine a light into the pupils and the pupils constrict) shall have a universally poor outcome. Tests like MRI brain, EEG and evoked potentials further help us in prognostication.

But what does meaningful neurological recovery  mean to the patient, his family and to us doctors? To us doctors it means being independent in activities of daily living, a patient conscious and alert and productive member of society. We have scales to help us grade this recovery. But meaningful neurological recovery might have a completely different meaning for the patient and his family. For his wife, the very fact that her husband is alive, someone she can reach out and touch may mean the world. True along with that shall come the burdens of caregiving.

Now what about the patient? True our patient made a living will, a will made when he was fully alert and in control of his senses. He made his choices known. But did he plan for a situation like this?  He is critically ill and the doctors are not certain what his chances for a meaningful neurological recovery are. Would he have liked to have his life sustanied if the answer was not black or white but a shade of grey?

The more I reflect on this, the more I realise that life is never simple and there are seldom easy answers. The struggle continues…..

Pinched nerve-a question and an answer

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One of the readers of my blog raised a great question. Her question and my answer follows.

Merely me

Thanks for this information. I have never experienced that before fortunately. I have heard that some folks who have MS may think that they have a pinched nerve at first.

Dear Merely me,

                               thank you for writing in. You raise an important point. Multiple sclerosis rarely may present with signs and symptoms of radiculopathy. This usually occurs when a MS plaque (MS demyelinating lesion) occurs at the root entry zone of a nerve. Let me explain that in more common language. If a plaque of MS happens to be where a nerve is starting off, it shall cause demyelination and present with signs and symptoms mimicking radiculopathy.

This though is not a common way with which MS presents and hence MS is not the first diagnosis which comes to a doctor’s mind when a patient presents with radiculopathy.

 

Personal Regards,

Nitin Sethi, MD

I have a pinched nerve-now what do I do?

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I get a lot of patients who say thay have a pinched nerve either in their backs or in their necks. They are invariably on pain-killers and some of them even have had surgery for their pinched nerves. As there is a lot of confusion and misperception in the minds of patients when it comes to “pinched nerves” I thought this might be a good time to discuss this topic.

So what exactly is a “pinched nerve”? When patients say they have a pinched nerve, they are referring to what we as neurologists call “radiculopathy”. Let me try to explain this in simple terms. The nerves that supply the muscles of the arms and legs come out from the spinal cord. These nerves exit as small nerve rootlets (radicles) from inbetween the bones that make the vertebral column (spine). At times these nerve rootlets (radicles) may be compressed (pinched) by either a bony spur of the vertebral column or a disk might herniate out and compress the nerve rootlet. This compression of the nerve (radicle) leads to pain which characteristically radiates down along the length of the nerve. So for example if you have a pinched nerve in the neck, the pain shall radiate down your arm and if you have a pinched nerve in the back, the pain shall radiate down your leg. This is what is called RADICULOPATHY.

The pain of radiculopathy can be excrutiating causing much discomfort and distress. In the acute stage, patient may find it so painful that they cannot move. They complain of “current” running down their arm or leg.

So how do we treat a pinched nerve? Well in the acute stage (when the nerve is inflammed), bed-rest is prescribed. This may vary anywhere from 3 days to a week. The acute pain of a radiculopathy is treated with painkillers–these may range from simple analgesics like Tylenol to anti-inflammatory drugs like Motrin, Advil and even corticosteroids for a short duration. Other medications used include medications effective against neuropathic pain such as gabapentin (Neurontin) and carbamazepine (Tegretol).

Recent studies have shown than most radiculopathies shall settle down over time with the above conservative measures. At times a disectomy is carried out (removal of the herniated disk) for pain relief. Epidural steroid injections may provide temporary relief.

BUT AS I STATED EARLIER MOST RADICULOPATHIES (PINCHED NERVES) SHALL SETTLE  DOWN WITH CONSERVATIVE MANAGEMENT.

Nitin Sethi, MD

Bell’s palsy–a patient’s story

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Just received this from an unknown reader. Just goes to show how the onset of Bell’s palsy might be subtle and patient’s frequently think they may be having a stroke.

Personal Regards,

Nitin Sethi, MD

 

 

A patient’s story follows…..

 

well i am on my first full day and my storie goes like this.
starting yesterday at about 7:30 am I started to learn a new appreciation for life. It all started on Saturday night I felt a sinus headache coming on and later a pain in the left side of my neck & ear. I then proceeded to get a few Excedrin and a cup of hot coffee. I had a great time at a Halloween party that night woke up on Sunday felt fine other than a little sinus pressure. So I proceeded to take some Tylenol multi symptom sinus medicine which I rarely take because I hate man made drugs! Went to bed woke up Monday and felt some pressure in my left side of my face, had some breakfast, kissed the wife and kids goodbye and was off to my hour drive down to West Palm Beach. Got to work and felt a little sleepy, I ended up sleeping for like the first hour at work. Then sally called me up to the front office for something and when I got there she said “what is wrong with your face” of course I laughed and said “nothing more than normal why is it killing you LOL” she said
no your left eye looks weird and your face looks swollen . Well to cut it shout I was having a severe allergic reaction to the Tylenol multi-symptom medicine. So I called the doc and they said to take some Benadryl, so I did. Shortly after I noticed I started to have a numbing in my left side of my face. I could not close my left eye by its self and when I took a drink of water it streamed down the left side of my face. I went to the mirror to find that the left side of my face was droopy and is seemed to be paralyzed. I was freaking out by now of course thinking I was having a stroke. I went to the doctor and found out that between a pinched nerve in my neck that was a result of a dislocating rib under my shoulder blade and a Sinus infection I had damaged my 7th cranial nerve resulting in a condition called Bell’s palsy.

Chronic traumatic encephalopathy/ boxers encephalopathy/ dementia pugilistica

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Chronic traumatic encephalopathy

 

Nitin K Sethi, MD

Assistant Professor of Neurology

New York-Presbyterian Hospital

Weill Cornell Medical Center

New York, NY

I recently read an article dealing with chronic traumatic encephalopathy (CTE) and the pledge by some professional football players to donate their brains for the study of CTE. As everything to do with brain health fascinates me, I decided this might be a good time to share my thoughts about CTE with my readers.

So what exactly is CTE? In simple terms it means encephalopathy (brain damage) caused by chronic trauma. Professional athletes especially those playing contact sports like American football, rugby, boxing and wrestling are prone to repeated head trauma. Have any of you ever watched a UFC fight? They are brutal, though as a spectator, I have to admit I love them and find them quite entertaining. Matt Hughes is my hero and I marvel at his strength and skills. But this entertainment comes at a price, at least for the athlete involved. A boxer during his professional career gets hit on his head countless times. Even though he may never get knocked out (have a concussion), the repeated blows to the head do take a toll. Studies have shown these players get small microbleeds in the deeper parts of the brain such as the basal ganglia. Over years this microdamage to the brain accumulates and these players complain of memory and other cognitive problems. They may further develop symptoms suggestive of Parkinsonism and Alzheimer’s disease. They have headache and also complain of balance problems (this was labeled in the past as “punch-drunk syndrome“). The dementia seen in patients with CTE has histopathological features similar to those seen in Alzheimer’s dementia (hence the term “dementia pugilistica“).

So how do you prevent yourself from CTE?  Simple, avoid contact sports especially if you are not doing it for professional reasons. Concussions do hurt the brain and contrary to common belief may cause permanent structural damage to the brain. If you suffer a concussion while playing in school or college do not return to play till you feel completely better and have a doctor’s clearence (read my post on concussions and return to play decision at http://braindiseases.info). Give your brain time to heal and drink alcohol in moderation (remember alcohol is a neurotoxin and too much is bad for the brain). If like me you indulge in contact sports like boxing, always always do wear protective head gear when you fight.

“YOUR BRAIN IS YOUR BEST FRIEND, DO NOT HURT HIM FOR WHOMSOEVER OR WHATSOEVER”

 

Paging Dr. Google

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Paging Dr. Google

 

 

Nitin K Sethi, MD

Assistant Professor of Neurology

New York-Presbyterian Hospital

Weill Cornell Medical Center

New York, NY

 

I get quite a few patients who prior to coming to see me for a neurological consultation have already googled their disease or at least the disease they think they have. Many of the readers of my blog too, it seems spend a significant amount of their time searching the internet for information about their medical condition. Paging Dr. Google to come to the rescue can have its pros and cons. Lets start with the pros.

 

 

Dr. Google obviously is well informed, a vast sea of knowledge, thousands and thousands of pages of health related information is available at the click of a mouse. He is quick, rarely moody (unless you have a slow connection) and moreover cheap. One can spend hours with him, for even esoteric neurological conditions he has an answer, he sees patients 24/7 and even does house calls (though a café is at times his favorite de novo office). The internet already has and continues to revolutionize medicine and how health information is disseminated. When I did my internal medicine residency in India in the late 1990’s, the internet was still not available. I remember spending long hours in the National Medical Library in New Delhi pulling up articles I needed to research my thesis. The work was tedious, back breaking (big volumes of dust covered journals to be pulled off the shelves) and painstakingly slow. Even though I was a medical resident, I found it difficult to find relevant articles and information. A lay person had it even tougher. There were a few books available which touched on general medical conditions like how to take care of your diabetes and blood pressure. For anything else, you needed to pay a visit to your neighborhood doctor or to a specialist in a tertiary hospital.

 

Then along came Dr. Google. Smart and tech savvy. A few search words and up pops the answer, pages and pages of it too. For doctors, the internet has being a blessing. We can now share and assess each other’s work so much easily. When confronted with a difficult case, sitting in my office in New York City, with a click of the mouse I can find out if any of my colleagues have seen something similar. How did they treat this vexing neurological problem foxing me, what were their results and is there anything new on the treatment horizon? No more going to the medical library and trying to search through the journals. All the journals are available on the internet and Dr. Google makes my life easier by listing out which article appeared in which journal. In fact recently someone raised a relevant point, are the days of the medical library numbered? For the patient too, Dr. Google is a blessing. There are many good patient oriented websites which come up when Dr. Google is called upon for an opinion. Patients can learn more about their disease and this information gives them confidence and a hence of actively doing something to help themselves. Apart from health and disease related websites, Dr. Google also churns up blogs and various foundations providing much needed information to patients and caregivers alike. But does Dr. Google have any chinks in his armor?

 

Yes, he does. He can be wrong just like any of us mortal doctors. If you feed him the wrong history, he shall make a wrong diagnosis. Patient’s frequently search Dr. Google with key words. If the key words themselves are wrong, the diagnosis shall be flawed from the start. Here in lies Dr. Google’s weakness or rather our weakness. Dr. Google may diagnose you with amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative condition with no cure currently because your history to him included key words like muscle twitches and weakness. It is only after a visit to your mortal neurologist that a correct diagnosis of benign fasciculations is made.

 

So the moral of the story is that Dr. Google is indeed a physician extraordinary but he is no substitute to an actual visit to your physician. You may read about the disease you feel you have but always, always do consult your physician because unlike Dr. Google he has the advantage of sitting down in front of you, taking a thorough history and conducting a clinical examination.  Dr. Google’s services are most helpful when he is paged with the right information in hand.

 

 

Multiple Sclerosis-a question and an answer

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 One of readers emailed me this question. My response to it follows.

Riddler on October 17, 2008 said: Edit Link

Hello Dr,

I am a 28 asian/indian female. I was brought up in India for large part of my file.
I had symptoms of blind spots in my vision sometime back. The condition persisted for 2 days before I scheduled an appointment with my opthamalogist. He suspected that I have optic nueritis and advised me for a MRI. Now the lab technician says that I have a few lesions in my brain and asked me to consult a nuerologist. I have a pending appointment. My eye became completely normal in about 10 days from onset. By googling I found that it might be a case of MS.

Is it always the case optic nueritis + MRI lesions = MS? Is there anything else I should be looking at? I’ve had problems of vitamin deficiencies in the past. I have had some tongue rashes, gastro problems. Nothing serious but minor issues though.

Thanks,
Riddler

Dear Riddler,

                                      patients who have optic neuritis usually do not complain of blind spots, rather they have acute/sudden loss of vision (usually in one eye, though in a condition called neuromyelitis optica they may have optic neuritis in both eyes). This condition may be painful (complaint of pain in the eye). Not all patients who have optic neuritis have multiple sclerosis. There can be many other causes of optic neuritis namely other infectious and inflammatory conditions. Patients who present with optic neuritis and are in the right age group (eg a woman in her 20s or 30s presenting with optic neuritis), need to be worked up for multiple sclerosis. Usually we order a MRI brain, to see if there is evidence of multiple sclerosis (read my posts on white matter lesions in the MRI brain of MS patients at http://braindiseases.info). As I have stated repeatedly, not all white matter lesions on the MRI represent multiple sclerosis.

In answer to your question, yes some vitamin deficiencies can cause blind spots and lesions in the brain. My advise to you would be to see a neurologist, the diagnosis of optic neuritis can be confirmed with the aid of certain tests like visual evoked potentials (VEP). Then the MRI can be interpreted in the right context.

Personal Regards,

Nitin Sethi, MD

Tremor: a question and an answer

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Another of my readers emailed me this question. My response to it follows:

Jeff Street
on October 16, 2008 said:

I’ve been having tremors over the past 4 months in my hands, feet and legs, and lips. They are more prominent (especially in my hands) after exercise. My physician did blood work and it indicated I was “mildly” hyperthyroid (slightly low TSH, normal T3/T4). He blames the tremors on this condition. He has prescribed propranolol 20mg BID for the tremors, but wants to wait and see if the thyroid might correct itself before putting me on Methimazole (due to its side effects). My symptoms seem rather profound for a “mild” case of hyperthyroidism. Do you have any further suggestions or input?

Dear Jeff,
thank you writing in. As I stated in my earlier post on tremors (you can read my post at my website  http://braindiseases.info ) tremors can be of various kinds. The kind of tremors you are describing when your hands are outstretched (but you also have them in your feet and lips) are likely not due to a neurological condition per-se. We all have a subtle tremor in our hands, this is called physiological tremor. If you make people hold their hands out in front of you, you shall be able to notice it is you pay close attention. Now suppose this person goes and drinks 6 cups of large Starbucks coffee and you again make him or her stretch their arms in front of you, the tremor shall be more prominent. This is called enchanced physiological tremor. As the name says, these tremors are physiological and not pathological (we all have them, some more prominently than others).
There are certain medical conditions which may cause tremors or make the physiological tremor more prominent. One such condition is hyperthyroidism. Patients who have hyperthyroidism do have tremors of their hands and also of their tongue (if you make them stick their tongue out, you shall be able to notice the tremor). Some medicines and drugs of abuse also cause tremors. Patients who drink alcohol heavily are tremulous, especially if they stop drinking suddenly.

Not all tremors need to be treated. We only treat a tremor if it becomes disabling for a patient or causes social embrassement. Propanolol (a beta blocker drug used as an anti-hypertensive medication) does have a role in treating postural tremors. Your doctor may like to slowly taper the dose up and see if it gives you any relief. I cannot comment if hyperthyroidism indeed is the cause of your tremor. As you can see from what I wrote above there can be protean causes of tremor some neurological (neurodegenerative in etiology like Parkinsos’s disease), other more benign (Benign Essential Tremor) and toxic/ metabolic causes of tremors (hyperthyroidism, drug induced tremors etc).
My advise to you would be to follow your doctors instructions and see if the propanolol gives you benefit. As I stated earlier, he has started you on a low dose and may taper it up over a period of time. If this tremor does not subside, then you may need a neurological work-up to try to determine the etiology of the tremor.
Please feel free to write in again.

Personal Regards,
Nitin Sethi, MD

Syncope-a question and an answer

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Laura one of my readers had an interesting query. I am publishing her question here as I feel, it may help others who are experiencing the same problem. My answer to her query follows.

Laura Frankiewicz on October 6, 2008 said: Edit Link

Dear Dr. Sethi,
I seem to have been having vasovagul syncope for at least 6 years or so. I feel that they started when I began menopause (I am now 56 and haven’t had a period for over a year. I almost always have a prodomal senation and have never actually passed out. My last episode happened yesterday at the theatre. Let me begin by saying that I take altace for high blood pressure and hychlorathyizide as a diuretic so I may have been dehydrated but I had just drunk quite a bit of water. What I am wondering instead if the lightling could have affected me. The lobby of the theatre has very dim and strange lighting that I find very disturbing. We got there early so I sat under the lighting for almost an hour. Then when we were seated, the area was fairly small and cramped. I had my legs crossed but fairly soon broke out into a sweat and began getting intestinal cramps. The feeling that I had to move my bowels became extreme and I got up to go to the bathroom but by then I was pretty woozy and weak. I managed to get to the usher but had to lie down. After a few minutes they helped me up and I laid down with my Legs elevated. I stayed in this position for only a few minutes while they got my information and I convinced the theatre staff not to call the paramedics. They helped me to the bathroom where upon I was able to evacuate and felt much better. I also drank some more water. I was ultimately re-seated on the ground floor and was able to finish watching the performance. But I have had close calls in this same theatre. It is close and crowded but I always wear sleeveless clothes so as not to overheat. I am not a nervois or panicky person. Most of my syncope episodes have been in warm places; after eating soup, having a pedicure with my feet in warm water. I can always avert the actual fainting. I have never lost consciousness. I guess what I am wondering is if lighting can have a neurological impact that would cause vasovagul syncope. I have had a number of stress tests, the last being last year, a nuclear echocardiagram; all clear. I do not think this is related to my heart but now I am wondering if I should consult with a neurologist. I would appreciate your advice. Also, very often the prodomal sensation includes a strong urge to move my bowels. Has this sensation been reported by others with syncope?
Thank you,
Laura Frankiewicz

  • 4 braindiseases on October 7, 2008 said: Edit Link

    Dear Laura,
    thank you for writing in. It does seem you have being having what we refer to as pre-syncopal episodes (meaning a syncope like episode but not quite syncope, since you do not pass out and lose consciousness). Moreover your history suggests you feel these episodes coming-feeling dizzy, light headed, about to faint type feeling and breaking out into a sweat.
    Various factors might precipitate a syncopal episode. In the case of vasovagal syncope these might include strong emotional experiences like for example seeing blood for the first time. Strong visceral sensations may also bring on an episode. Micturition syncope has been reported in elderly men (they pass out when they get up at night to void urine). Patients have been reported to pass out as they sit on the toilet seat and exert pressure.
    It is likely that something along the same mechanism might be operative in your case. Dehydration and been in a closed crammped theatre may have further contributed to the problem. Whenever a patient presents to the hospital with syncope, we have to determine whether the cause is the heart or the brain (cardiogenic versus neurogenic/ vasovagal). Also at times it is hard to differentiate seizures from syncope.
    My advise to you would be to consult a neurologist (ask your PMD to refer you to one). I am sure they would be able to get to the bottom of your problem. Feel free to write in again.
    Personal Regards,
    Nitin Sethi, MD

    • Thrombolysis for stroke- sooner the better!!!

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    Thrombolysis for stroke- sooner the better!!!

    Nitin K.Sethi, MD

    A new study on treatment of stroke was published this week in the New England Journal of Medicine (NEJM). The study concerns thrombolytic therapy for stroke and since I feel very strongly about stroke prevention and treatment, I thought I would share the relevant details with my readers. The study “Thrombolysis with Alteplase 3 to 4.5 hours after acute ischemic stroke” and the accompanying editorial by Dr. Lyden appears in the Sep 25th issue of NEJM.

    Ischemic stroke (stroke due to lack of blood flow to the brain) can be devastating leaving survivors with neurological deficits (paralysed on one half of the body, unable to walk or talk). When a patient lands up in the ER with an acute ischemic stroke (I like to refer to it as “brain attack” kind of similar to “heart attack”  which patients and family members find easier to understand), as doctors we try hard to salvage the brain tissue at risk of “death”. One of the main drugs in our armament in this fight is a drug called tPA (Tissue plasminogen activator). tPA acts like a clot buster (the drug lyses/ bursts the clot in the brain and helps to reestablish blood flow).

    Let me try to explain this in a more simple way. A blood clot breaks from the heart and travels up to the brain, there it lodges in a small blood vessel of the brain preventing blood flow distally (beyond the clot). Patient presents with left arm and leg weakness to the hospital. The brain tissue supplied by the blocked blood vessel now gets no blood and starts to die. “A STROKE IN EVOLUTION” . If blood flow is not reestablished soon, the brain tissue suffers irreversible necrosis and death. This patient is given tPA, the drug lyses/ bursts the clot and helps to reestablish blood flow. The patient who was weak on one side starts moving his arm and leg again.

    It is not as simple as I made it out to be above. Patients have to meet strict inclusion criteria before tPA can be administered. Also the drug has a window period and has to be given intravenously within 3 hours of the stroke starting. 3 HOURS THAT IS THE GOLDEN PERIOD. Patients presenting to the ER after 3 hours are usually denied tPA for 2 main reasons-one the tissue which was at risk for stroke is now irreversibly destroyed and thus cannot be salvaged and second the risk for intracranial hemorrhage (bleeding inside the brain) is high. 

    The study reported in NEJM extends this window period (golden period) from 3 to now 4 and half hours. You can now understang why this study is generating so much interests among doctors and neurologists in particular. Patients presenting to the hospital upto 4 and half hours after an ischemic stroke can be given tPA provided they meet the other inclusion criteria (and none of the exclusion criteria).

    But as Dr. Lyden in his editorial rightly points out, this should not be taken to mean that now you have more time to wait before going to the hospital to seek help (or for us doctors as more time to wait before we decide to administer tPA). When it comes to stroke, TIME IS BRAIN. The more you wait, the more brain tissue is lost, the more brain cells die, the more disability the patient is left behind with.

    It is extremely important that the public learn to recognize the early warning signs of stroke and seek help as soon as possible. You can read more about the early warning signs of stroke either on my blog here or on my website http://braindiseases.info.