Salt and stroke: what is the connection?

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                                                    Salt and stroke: what is the connection?

            Nitin K Sethi, MD

I recently read an editorial written by Norman Campbell and David Spence on “Stroke prevention and sodium restriction” in the Canadian Journal of Neurological Sciences in which they talk about the effect of dietary sodium restriction on the incidence of stroke. As we all know stroke prevention is a much more cost effective strategy as compared to treatment of acute stroke. Unfortunately more attention is being paid to treatment and management issues surrounding acute stroke and precious little to the prevention of stroke. I strongly feel that for every 1 lecture which a neurologist gives about treatment of acute stroke, he should give 10 lectures about the prevention of stroke.

Restriction of dietary sodium or rather salt in the diet is one such cost-effective strategy to prevent strokes.  Increased salt in the diet raises the blood pressure and blood pressure is the number one risk factor for strokes.  The authors make a strong point for government legislation to cut down the amount of salt added to processed foods or that eaten in restaurants. As they rightly say advise to patients to reduce salt intake is by itself relatively ineffective because sodium (salt) sources are ubiquitous and not apparent to the consumer. You may not add any salt to your diet when you cook at home but salt is added to nearly every food item at the time of processing. It is only by government legislation and action that salt content of food items can be lowered. Low salt content shall help in lowering blood pressures and thus prevent cardiovascular and cerebrovascular events (heart attacks and brain attacks!!!)

So watch the salt in your diet everyone. Remember a stroke prevented is a brain saved!!!

Analgesic overuse headache

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Analgesic overuse headache

Nitin K Sethi, MD

Assistant Professor of Neurology

New York-Presbyterian Hospital

Weill Cornell Medical Center

New York, NY 10065

 

Recently I saw a patient in the hospital who had complaint of constant severe daily headaches. She was a 34-year-old otherwise healthy African American woman who first developed headaches at the age of 15. At that time she used to get throbbing hemicranial (one half of the head) headaches which were accompanied by nausea. At times she used to throw up if the headache was particularly bad. During the headache episode she complained of light sensitivity (bright lights bothered her, we refer to this as photophobia) perferring to lie in a quiet dark room. Sleep usually aborted her headache attack. She was correctly diagnosed as suffering from common migraine (this is migraine which is not associated with aura) and treated with Inderal (propanolol-a beta blocker). Later she started using Imitrex (a triptan) whenever she had an acute migraine attack. Around the age of 18, she developed pelvic inflammatory disease for which she started using ibuprofen.

At the time of her current presentation, she said her headache character had changed. Now instead of having episodic migraine attacks, she had a headache “all the time”. She was taking 4-6 pills of ibuprofen a day and 8 to 10 Imitrex pills a month.

This brings us to the topic under discussion “analgesic overuse headaches” also at times referred to as “medication overuse headaches”. Research has shown that about 1% of the general population experiences medication overuse headache and the condition is thought to occur due to an interaction between a therapeutic agent (in this case an analgesic) used excessively by a suspectible patient.

The overuse of anti-migraine drugs and analgesics gives rise to a mixed picture of migraine-type and tension-type headaches that occur at least 15 days a month. Patients start taking more and more analgesics to treat the headache and this sets up a vicious cycle of headache-analgesic-headache-analgesic.

Chronic daily headaches due to overuse of analgesics are particularly difficut to treat.  Analgesics are discontinued (some patients of course have worsening of their headache during this time). To keep headaches under check during this time (when the analgesics have been discontinued), the doctor may prescribe a low dose tricyclic antidepressant such as Elavil (amitriptyline). The headache usually resolves or reverts to its previous pattern within two months after discontinuation of the drug (analgesic).

Syncope: making sense of its various causes

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Recently I was consulted on two patients who presented to the hospital after a syncopal episode. As syncope is relatively common, I thought that is what I should discuss in my next post.

So what is syncope? Well simply put a syncopal episode is nothing other than a fainting episode. It is characterized by momentary/ temporary loss of consciousness and posture. Patients may refer to it as I “fainted” or “passed out”.  Whenever a patient presents to the hospital after a syncopal episode we take pains to find out what led to the syncope.

So what are the different causes of syncope?  Syncope can come either from the heart or from the brain. Let me explain this further. If for some reason the heart suddenly malfunctions and stops pumping blood to the brain, you will pass out (lose consciousness). This is referred to as cardiogenic syncope. Among the various causes of cardiogenic syncope are included disorders of cardiac rhythm such as atrial and ventricular arrhythmias. Heart blocks and of course an acute myocardical infarction (heart attack) may present as a syncopal episode with the patient collapsing and passing out.

Syncope though can also come from the brain and this is referred to as neurogenic syncope or at times as neurocardiogenic syncope. This neurally mediated syncope is also at times referred to as vasovagal or vasodepressor syncope. Let me explain what vasovagal syncope is with a classical example. Lets assume you are walking on the street. A car hits a cyclist right in front of you. You rush to help the poor man. As you come near, you see him bleeding profusely, his skull cracked open. You go pale, the blood drains from your face and you pass out. There you just had a vasovagal syncopal episode. Why you may ask did you pass out?

Vasovagal syncopal episodes classically occur in the upright position meaning either you are sitting upright or standing (they usually do not occur when you are reclining). The episode is usually preceded by an unpleasant or painful episode such as the sight of blood, a medical procedure, an intense emotionally disturbing argument or news (sudden extreme emotions), standing in the hot sun or a hot shower for a long time especially if you are hungry and dehydrated at the same time.

Other less common triggers may include a bout of violent coughing (cough syncope), urination (micturition syncope) and abdominal straining as during defecation.

Usually prior to the onset of the syncope (prior to passing out), patients feel dizzy and light headed. They may complain of blurring of vision and feel as if they are about to faint. If at this stage the person sits down, they usually do not pass out or lose consciousness. This is referred to as pre-syncope (A syncopal episode was about to occur but since the patient sat down it was aborted midway).

During a vasovagal synope episode there is transient loss of the baroreflexes (this is the autonomic nervous system which helps to maintain our blood pressure). Pooling of blood occurs in the dependent calf muscles and there is lack of blood flow to the brain resulting in the patient passing out. Hence one of the simple things to do when a person has a vasovagal syncopal episode is to make them lie down flat on the ground on their back and to lift the legs above the plane of the heart. As the blood rushes back to the brain, the person quickly comes around and may look a little dazed wondering what happened.

As seizures too are associated with loss of consciousness, one always has to differentiate whether a patient had a seizure Vs a syncopal episode. As you can imagine it is important to make this differentiation as the two conditions are treated in very different ways. So how does one differentiate a seizure from a syncopal episode?

A seizure can occur with the patient in any position: sitting, standing or lying down. Syncope usually occurs in the erect posture.

Seizures are usually not preceded by the prodrome seen in syncope. Patients before they pass out in a syncopal episode complain of feeling light-headed, dizzy, room spinning and blurring of vision. Seizure patients on the other hand may give history of their aura prior to the seizure. Common auras include smelling of burning rubber, metallic taste in their mouth or a funny rising sensation in their tummy.

Patients who have a seizure and fall usually hit and hurt themselves. They fall hard and may come to the hospital with craniofacial injuries like broken teeth. Syncopal patients on the other hand do not fall hard, they rather ease themselves to the ground.

Some but not all seizures are associated with tongue biting and loss of bladder and bowel control (patient may pee on themselves and wet their pants). Most syncopal episodes are not associated with tongue biting or loss of bladder control.

Patients after a seizure are usually confused and disoriented, they may fall asleep. We call this a post-ictal state. Syncopal patients as they come out of their syncope are not confused. They know where their are and may be embrassed by the fact they fainted.

In my next post I shall discuss the diagnostic work-up and management of syncope.

Nitin Sethi, MD

The dead donar rule and how it applies to organ donation after cardiac death

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The dead donar rule and how it applies to organ donation after cardiac death

 

Nitin. K. Sethi, MD

 

The August 14th issue of the New England Journal of Medicine has a series of perspectives on organ transplantation after cardiac death and how it conflicts ethically with the dead donar rule. It is a fascinating and at the same time complex ethical problem and that prompted me to write this post.

The dead donar rule simply states that a patient must be declared dead before any of the vital organs can be removed for organ transplantation. Death can be defined in two ways. Either it is the irreversible cessation of cardiorespiratory function or simply put when your heart stops you die!!!. Mind you the important word here is irreversible. Death can also be defined as the irreversible cessation of brain function, this is the concept of brain death, a concept now well accepted by caregivers and doctors alike. (See my earlier post on brain death at http://braindiseases.info). In the case of brain death, the patient’s heart may be beating, respiration supported by a ventilator but the brain is so badly damaged that there is no chance of a meaningful neurological recovery.

That all makes sense till now. Ethical problems arise when the dead donar rule is applied to organ donation after cardiac death especially with respect to cardiac transplantation after cardiac death. Hmm getting confused? Let me explain with the help of an example.

Let us take the example of an infant who is overwhelmly sick, the family wants to donate organs including the heart. Studies have shown that the human heart does not auto-resuscitate (meaning start on its own) after 5-10 minutes of cardiac arrest. It does not auto-resuscitate but can be resuscitated by doctors by giving drugs like atropine or by giving electric shocks to it. The infant’s heart stops, the doctors wait for 5 minutes, at times 2 minutes sometimes even less to document that it does not auto-resuscitate (the longer the heart is not beating and not getting blood, it starts to get damaged). The heart is then taken out and transplanted into another infant’s chest cavity. The doctors then resuscitate the heart and restart it in the transplanted infant.

All good you may say but how can you declare the first infant dead on the basis of irreversible loss of cardiac function when that very heart has been transplanted and has successfully functioned in the infant who received it. The dead donar rule gets violated, the first infant was never really dead if the loss of cardiac function was reversible.

As you can imagine opinions are sharply divided on this subject. Some feel that the dead donar rule is violated, while others try to justify it by saying that a heart cannot be legally restarted if resuscitation has been refused by the family in case of infants and minors, so its loss of function meets the defination of irreversibility as commented so eloquently by Drs Truog and Miller in their New England Journal of Medicine article.

I would encourage my readers to read more about this topic in the New England Journal of Medicine or online and I welcome their comments.

If we live long enough, will we all be demented?

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If we live long enough, will we all be demented?

NK Sethi, MD

Assistant Professor of Neurology

NYP-Weill Cornell Medical Center

New York, NY 1021

Recently in the journal “Neurology” there was published an editorial by Dr. David Hogan titled ” if we live long enough will we all be demented?”. This is an interesting editorial which touches on the issue of cognitive decline with aging and is based on data from the 90+ study.  This study looked at the prevalence of all cause dementia in the oldest old that is people above the age of 90 residing in Orange County, California.  According to the study the prevalence of Alzheimer’s dementia and all cause dementia increases with aging with the prevalence doubling every 5 years for women but not men aged 90 and above.

If this data is accurate, it will have important consequences on health care costs in light of the expected growth in the numbers of the oldest old. We know that women outlive men so the lack of an age associated increase of dementia in the oldest old men may very well be on account of the shorter life expectancy of men as compared to women.

This study and the accompanying editorial raise some other important questions. If a significant majority of us are going to become demented especially if we are fortunate to live past 90, should not we all be striving to improve our memory, nourish and nuture our brains so as to stack the odds in our favor. Regular indulgence in neurobics (read my previous posts on neurobics at http://braindiseases.info) may be well advised. Doing crossword puzzles, learning a new language, a new motor skill, a musical instrument, eating brain healthy foods (read post on brain foods at http://braindiseases.info) and doing brain friendly activities like yoga as well as meditation may all help to prevent the onset of dementia. At the very least it cannot hurt and the sooner we start the better may be the odds in our favor. This may hold especially true for women given their expected longer life expectancy.

Maybe then some of us will be able to escape the ravage of dementia and live productive lifes past 90.

Meningitis or encephalitis?

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Let us discuss viral encephalitis in this post. First what do we mean when we say a patient has encephalitis and how does encephalitis differ from meningitis.

Meningitis is inflammation of the meninges of the brain. The meninges are the thin layers which cover the brain and include from inwards outwards pia mater, arachnoid mater and dura mater. When they get inflammed usually due to an infectious etiology a patient develops meningitis. There are numerous causes of meningits and they can be classified as bacterial causes (common bacteria which cause meningits include Haemophilus Influenzae type B, Nesseria meningitidis, Streptococcus pneumoniae, Listeria), viral causes (most of the viruses which cause meningitis are seasonal viruses and usually it is hard to isolate them. We do not try too hard to find out the particular virus causing the meningits as viral meningitis is usually self limited and has a good outcome with most patients recovering completely), fungal causes, parasitic causes and so on. So how does meningits present clinically? Patients usually have complaint of fever, headache and stiff neck. They feel tired and listless and may also have nausea and vomiting. Patients who have meningitis are bothered by bright light (we call this photophobia and hence they prefer to lie in a quiet dark room), loud sounds are also bothersome (we call this phonophobia). When we assess such patients clinically we look for tell-tale signs of meningitis: namely we check for neck stiffness (neck stiffness in a febrile patient is quite sensitive for meningitis). Patients with meningitis at least initially in their disease course are awake and alert and do not present with seizures (remember it is the meninges which are involved not the brain itself at least initally). Later on if the meningitis remains untreated patients become stuporous and comatosed. Bacterial meningitis as compared to viral meningitis is more fulminant and if untreated can prove fatal (bacterial meningitis patients usually look more “sick” as compared to those with viral meningitis). Once the diagnosis of meningitis is entertained we usually admit these patients to the hospital (some patients with viral meningitis may be managed on an outpatient basis if close supervision can be ensured). A CT scan is usually done next followed by a spinal tap to get some cerebrospinal fluid. This fluid is then sent for various tests. The diagnosis is confirmed if the spinal fluid shows inflammatory cells. On the basis of tests on the spinal fluid we can determine whether the patient has bacterial, viral, fungal or tubercular meningitis (each type has its own spinal fluid characteristic. Moreover we examine the fluid under the microscope and further culture it to isolate the organism). As you can imagine, it takes time for some of these tests to come back, so patients may be empirically started on antibiotics pending CSF culture results. Once the CSF results come back, the antibiotics can be changed depending upon which organism is isolated from the CSF.

So then what is encephalitis and how does it differ from meningitis. Encephalitis simply put is inflammation of the brain itself (not the meninges). Usually the term is used in connection with a viral etiology. The common causes of encephalitis include viruses like herpes simplex, cytomegalovirus, West Nile, flaviviruses to name a few and the common encephalitis are: herpes simplex encephalitis, Japanese encephalitis, Eastern Equine and Western Equine encephalitis, California encephalitis and tick-borne and arthropod borne encephalitis (such as Lyme encephalitis). Since in encephalitis the brain parenchyma is involved, these patients may present with depressed level of consciousness, altered personality, abnormal behavior and seizures. Usually in encephalitis the brain MRI is abnormal and gives us a hint to the extent of brain parenchymal involvement. The spinal fluid may show inflammatory cells (some patients have a component of meningitis along with their encephalitis: MENINGOENCEPHALITIS). Doctors may also order other tests like EEG to rule out seizures. The treatment of encephalitis varies. In the case of herpes encephalitis we use anti-viral drugs like acyclovir. In other encephalitis the treatment is more supportive. Some patients recover (those detected and treated in time), others are left behind with devastating neurological sequelae

 

Nitin Sethi, MD

Multiple consultations versus medical shopping

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                             Multiple consultations versus medical shopping

NK Sethi, MD

Assistant Professor of Neurology

NYP-Weill Cornell Medical Center

New York, NY 10021

I recently read an article in New York Times titled “The story behind Kennedy’s Surgery” by Lawrence K. Altman in which he discusses the decision making process which led to Senator Kennedy undergoing brain surgery for his malignant brain tumor at Duke University. As per the article a few days after Senator Kennedy learned he had a malignant brain tumor in the left parietal lobe, he invited a group of national experts to discuss his case.  These experts were leaders in their field and came from different academic centers of excellence. I assume they included neurosurgeons, neurooncologists and other specialists in radiotherapy and oncology. Senator Kennedy’s case was discussed and the best plan of therapy decided on “by all”. While it is easy for a man of Senator Kennedy’s stature (he is the chairman of the Senate’s health committee) to summon all these experts, can a common man achieve this level of care.

Well yes and no and this brings me to what I wanted to discuss, the benefits of multiple consultations versus the risks of medical shopping. While most of us do not have the ability to assemble experts across multiple specialities under one roof to discuss our case, we all can and should seek a second opinion when confronted by a vexing medical issue. This is especially true when either the diagnosis itself is in doubt or when there are multiple approaches to treatment like for example in Senator Kennedy’s case where the issue was whether the tumor should be operated and surgically excised versus should he opt for radiation and chemotherapy. In a case like that I would surely recommend getting a second opinion and multiple consultations if need be, one from a neurosurgeon, another from a neurooncologist and a third from a specialist in radiation oncology.

There though is a fine line between seeking multiple consultations versus ending up medical/ doctor shopping. How should one go about getting these multiple consultations? One way would be to let your doctor act as the “middleman”. Go via him and not try to bypass him. Most physicians do not mind if their patients request a second opinion especially when confronted with a difficult case.Yes to an extent it is a blow to our ego that our opinion is been questioned but in the end most physicians do not mind. Your physician shall make sure you navigate the maze of second opinions successfully and gain the most out of it. From referring you to the right person to making sure you carry all your relevant medical information when you go and seek the second opinion. He or she may also in the end help you decide on the best course of action. Else it is easy to fall into the trap of medical/ doctor shopping. Looking around till you find a doctor who tells you what you want to hear!!!

Seizures due to hypoglycemia (low blood sugar)

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Seizures in the setting of hypoglycemia are well described. The brain needs sugar to function and when the blood sugar falls “too low”, one of the things that can happen is that the patient may have a seizure (this is usually a generalized convulsion-a tonic-clonic or Grand Mal seizure). There is no one level of blood sugar below which one has a seizure (rather the level varies from person to person). Let me explain that with an example. Lets assume you are a diabetic and you take your insulin shot but for once forget to take a meal (maybe you are a hard working executive on the run). You have a convulsion while at work and are taken to the nearest ER. There your blood sugar at the time of presentation is recorded to be 60 mg/dl. There might be another similar patient whose blood sugar falls to 52mg/dl yet he does not have a convulsion. So there is no set limit below which the brain shall have a seizure but speaking in broader terms usually the brain does not tolerate blood sugar below 60mg/dl and below 40 mg/dl most patients shall be symptomatic (either have a convulsion or be confused and obtunded. The term used for this constellation of neurological signs and symptoms as a result of hypoglycemia is NEUROHYPOGLYCEMIA).

The good news though is that seizures due to hypoglycemia are readily treatable. In the ER we load the patient with glucose (usually this is given via an intravenous drip as the patient is obtunded and confused and cannot accept anything from the mouth). The blood sugar quickly rises and the seizures stop. Patients who suffer from hypoglycemic seizures do not need to be on an anti-epileptic drug. These patients do not have epilepsy. If their blood sugar does not fall down again, they will not have another seizure.

Rather a meticulous search should be conducted to find out the cause of hypoglycemia:

-is the patient a diabetic who took too much insulin by mistake?

 -did he miss his meal but took his insulin?

-is there any other cause of hypoglycemia such an insulin secreting tumor?

-is the patient septic?

Hypoglycemic seizures are most commonly seen in diabetics. This emphasizes the importance of good glycemic control in this vulnerable population.

Nitin Sethi, MD

Warning signs of an impending stroke

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I want to lay stress on the warning signs of a stroke. We all need to be aware of these as a stroke can strike anyone anywhere and with stroke time is brain. The sooner the stroke is recognized and help is sought the better is the outcome.

So let us get to the heart of the topic. The following are some of the warning signs of an impending stroke/ stroke in evolution:

1) Sudden onset of speech difficulty. Either unable to speak or unable to comprehend speech (the patient can speak but cannot understand, so whatever he speaks makes no sense. We call this jargon speech). At times the problem with language can be more subtle: unable to name things (we call this nominal aphasia or anomia), the speech is slurred (we call this dysarthia).

2) Sudden onset of weakness in one arm or leg usually of the same side. For example weakness in right arm and right leg or in the left arm and left leg. This weakness may be prominent and the patient may not be able to move the arm and leg at all or it may be more subtle.

3) Sudden onset of numbness in one arm or leg usually of the same side. Numbness is hard to define and patients may use words like “weakness”, “tightness”, “dead feeling” or “my one side feels as if I slept on it”.

4) Sudden onset of facial weakness. One side of the face usually starts to sag, the smile is crooked when the patient attempts to smile and the patient may drool from the angle of the mouth.

5) Sudden onset of gait problems: the patient is unsteady and falls when attempting to walk. The balance is off. Patient is clumpsy and appears “drunk”.

6) Sudden onset of visual problems: patient may have an episode of transient loss of vision in one eye ( I felt as if a curtain decended in front of my eye). We call this transient monocular blindness and this is a TIA (transient ischemic attack). Patients may also complain of a field cut (unable to see one part of the visual field).

7) Acute loss of hearing in one ear especially in the elderly (this is a rare sign of a stroke).

Nitin Sethi, MD

Alcoholic neuropathy

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Continuing with the posts on the neurological manifestations of alcoholism, I shall cover the topic of alcoholic neuropathy here. Simply put alcohol is a neurotoxin especially when it is consumed in excess. People who consume large amounts of alcohol on a chronic (daily) basis frequently develop neuropathy. It does not depend upon the kind of alcohol consumed (top of the shelf Scotch whisky Vs a cheap rum) rather it depends upon the amount and frequency of use. Patients develop a predominantly sensory neuropathy and have complaints of pain, burning, tingling, pins and needle sensation in the feet and sometimes in the finger tips. Rarely if the neuropathy is severe patients may also develop peripheral weakness (motor symptoms).

Alcoholic neuropathy is also thought to be not entirely due to alcohol, rather it is a nutritional neuropathy and occurs due to lack of essential nutrients and vitamins in the marginal diets of alcoholics. It is uncertain whether the neuropathy would develop in an alcoholic who supplements his diet with essential nutrients and vitamins. Alcoholic neuropathy is more commonly seen in patients who have other neuropathic conditions like diabetes. In this subgroup of patients, alcohol acts as an additional neurotoxin and makes the neuropathy worse. The same principle applies to cancer patients been treated with neurotoxic chemotherapy medications or an HIV patient been treated with neurotoxic antiretroviral medications.

Thus the message is simple.

Drink alcohol in moderation applies to all of us.

People who have diabetes should avoid alcohol if possible or if that is not possible consume as little.

Patients been treated with neurotoxic medications should also avoid alcohol.

Supplement your diet with at least one to two tablets of a good multivitamin every day.

Alcoholic neuropathy is treated much the same as any other neuropathy (see my post on diabetic neuropathy http://braindiseases.info)

Nitin Sethi, MD