Stroke prevention: tackling the basics

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Today I was having dinner when a friend asked me ” how can I reduce my risk of stroke?”. Briefly he explained to me that he had 2 heart attacks in the past. At that time he was found to have “slightly” high blood pressure and “bad” cholesterol. He said he was talking 2 medicines to lower his blood pressure and one to bring down his cholesterol. He could not provide me with further details and again I was suprised how little some of us know about our own medical condition. If I had asked him how his car was doing, I am sure he would have been able to furnish me a ton of detail. The mileage, the last oil change date, the date when the next oil change was due would have come rolling out.

Why do we neglect our own health? Is it just something we are not comfortable in talking about. Like a bad dream which one day when we wake up we shall not have to deal with any more. Some patients have inherent faith that God is watching out for them. This is particularly true in some cultures like for example in India, where some people feel that everything is God’s will. Hence they either detest taking medications or feel they do not need to take them. Some are lax with their follow up appointments. Other shall take the blood pressure and cholesterol lowering medications, only to self discontinue them when their blood pressure and cholesterol becomes ” normal”.

In any case, let me here tackle the basics in stroke prevention. Just straight talk, the kind you may not hear from many of your doctors.

1) IF YOU ARE A SMOKER THEN QUIT SMOKING. That is probably the single best thing you can do yourself to cut down your risk of a stroke as well as a heart attack. There is no excuse, like I have cut down from a pack a day to about 3 cigarettes a day. NO AMOUNT OF SMOKING IS HEALTHY. You should quit completely if you want to cut down your risks of a heart attack or a brain attack (stroke). Now I do understand it is difficult to quit but here I am talking straight and not beating around the bush.

2) Exercise: again a thing which you can do yourself to reduce your risks of a heart attack or a stroke. The exercise which is recommended is more the aerobics kind. The idea is to increase your heart rate and sustain it at this level for some time. Running or brisk walking all are beneficial. Now before you do embark on a exercise program, run it past your doctor to make sure that you are fit enough to exercise. You do not want to strain a weak heart and exercise ideally should be graded. YOU START SLOW AND BUILD UP AS YOUR BODY GETS USED TO IT.

3) Blood pressure: we have known for a while now that elevated blood pressure is one of the most important risk factors for strokes.  Recent studies have shown that the lower down you can get the blood pressure to, the more are the benefits. Earlier we used to advise our patients to aim for 130/80 mm Hg, now we say go for 120/70 mm Hg especially if you have other risk factors like stroke or previous history of coronary artery disease. There are many different medications that can be used to bring down the elevated blood pressure but some are recommended more because they have other added benefits apart from just lowering the blood pressure. Prominent among these is a group of medications called the ACE inhibitors. My advise to you shall be to get your blood pressure checked and than have your doctor decide which blood pressure medication shall be the best for you.

5) Bad cholesterol: bad cholesterol may run in your family that is it might be genetic in etiology. So not all bad cholesterol is your fault and due to the fact that your diet is bad.  In either case it is one of the major risk factors for strokes and heart attacks. When we measure the cholesterol in the blood ideally we should measure it in a fasting state (so the blood sample should be taken when you are fasting like in the morning before breakfast). We measure the total cholesterol level in the blood and then measure the differrnt fractions of cholesterol. Some as you know is what is called good cholesterol, this is called HDL or high density cholesterol. The other is bad cholesterol, the one which we want to be lower ideally. These include LDL or low density lipoprotein, triglycerides or TG and very low density lipoprotein (VLDL) among others. The goal is to raise the good cholesterol or HDL and lower the bad cholesterol like TG and LDL.

We aim for total cholesterol less than 200, LDL less than 100 (nowdays we are even more aggressive and may aim for it to be less than 70) and TG less than 200 too. These goals can be achieved by a combination of dietary modification, exercise and medications. Fish is rich in omega 3 fatty acids and raises your HDL or good cholesterol. So replace the red meat with more fish. There are a number of medications out there. The most commonly used class is called statins and they  help to raise your HDL and lower your LDL by a few points. However if your TGs are elevated, you may need a different class of drug.

My advise get your lipid profile done in a fasting state, then discuss the results with your doctor and have him help you decide whether you need just dietary modification or drugs too.

6) Control your blood sugar: if you are a diabetic this is very important because diabetes too is a risk factor for stroke. My advise get your blood sugar checked frequently both in the fasting and post prandial (after eating) state. The goal is fasting blood sugar less than 107 and post prandial less than 200 (in the case of post prandial it depends upon the time after eating when the sugar is measured). Your doctor may also check your Hemoglobin A1 C, the ideal goal for this is less than 7. Recent study in New England Journal of Medicine suggested that too aggressive lowering of hemoglobin A1C causes more harm than good (if you lower it less than 6) and may infact increase mortality. Hence again speak to your doctor and determine your goals.

7) Reduce your stress: mental stress is a killer and nothing is more important than your health. Do meditation and whatever else that works for you.

8) Drink alcohol in moderation: old saying too much of anything is bad and that includes the spirits!!!

 REMEMBER A STROKE PREVENTED IS A BRAIN SAVED!!!

Nitin Sethi, MD

Spinal cord lesions in MS

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Multiple sclerosis is a demyelinating disease of the central nervous system (demyelinating because the disease is characterized by the loss of the myelin sheath around the axons of the nerve cells). As I have stated in my previous posts on MS (see http://braindiseases.info for all the previous posts on MS), the disease is characterized by plaques which are disseminated in space and time.

Most of these plaques (demyelinating lesions of MS) are seen in the brain but a few patients have what is loosely called spinal MS or rather MS in which the plaques are more commonly seen in the spinal cord (remember the spinal cord is a part of the central nervous system). These patients with spinal MS present with slightly different clinical signs and symptoms. They may present with what is called transverse myelitis (this is an involvement of the spinal cord usually at the cervical or thoracic level). Transverse myelitis can be devastating because all the descending motor fibers from the brain and the ascending sensory tracks are packed in the small diameter of the spinal cord. So any involvement of the spinal cord has the potential to affect all these tracks. Depending upon the level of cord involvement patients may have either weakness of just the legs (paraparesis or paraplegia) or all the four limbs may be involved (quadriparesis or quadriplegia). Usually the bladder and bowel are involved too and patients may have complaints of urinary incontinence. Sexual dysfunction is also commonly reported (erectile dysfunction in males, see my previous post on it).

As the involvement of the brain is less, these patients are relatively well preserved cognitively and may not have prominent cerebellar findings.

Spinal involvement in MS is treated in much the same way as other forms of MS. Your doctor may use a course of intravenous corticosteroids if you present to the hospital with acute transverse myelitis. Immuno modulating drugs like interferons may later be prescribed.

Personal Regards,

Nitin Sethi, MD

Erectile dysfunction-some neurological causes

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I thought I would discuss some neurological causes of erectile dysfunction and decreased libido. There are many neurological diseases which are associated with erectile dysfunction and may also result in decreased libido. One of the most common is diabetic autonomic neuropathy. Diabetic patients especially those who have autonomic neuropathy (dysautonomia) frequently have erectile dyfunction. Supprisingly many do not volunteer this information, unless their doctor asks about it. They may complain of other symptoms of neuropathy like pain and numbess in their hands and feet but may not volunteer the history that they are having erectile dysfunction. Many patients do not realize that their erectile problems are a part and parcel of their uncontrolled diabetes.

Erectile problems and decrease libido is also frequently seen in patients who have multiple sclerosis. Fortunately this aspect of MS is now been given increasing recognition by doctors and a discussion is initiated with the patient at some stage of their treatment. Women with MS may have complaints of decreased vaginal lubrication, loss of vaginal muscle tone and diminished clitoral engorgement.
All this can lead to a decrease or loss of sex drive. Decreased or unpleasant genital sensations may lead to a diminished capacity for orgasm. Men with MS experience  erectile dysfunction and a decrease in or loss of ejaculatory force or frequency.

Erectile dysfunction and sexual difficulties are also a part and parcel of certain neurodegenerative conditions like multi system atrophy especially a syndrome called Shy Drager Syndrome in which autonomic failure is prominent. Parkinsons disease and patients with degenerative dementias may also have some of these problems. In these patients the cause is usually multifactorial.

Patients with epilepsy also frequently have sexual dysfunction. Again the causes are multifactorial but one important reversible cause is drug side-effects. Some anti-epileptic drugs and antidepressants frequently cause sexual dysfunction as a side-effect.

The good news is that sexual dysfunction is now more readily recognized as a part and parcel of certain neurological disorders. Neurologists are nowdays more adept in asking patients about it. It is important that patients volunteer information if they are experiencing sexual dysfunction as many of the causes are treatable. Drugs with sexual dysfunction as a side-effect can be stopped and replaced with other drugs. Also some of the symptoms can be ameriolated by using medications like sildenafil (Viagra).

Personal Regards,

Nitin Sethi, MD

Stroke rehabilitation

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I thought in this post I shall discuss a little about stroke rehabilitation. A stroke can be devastating and causes significant morbidity and mortality. Stroke survivors are frequently left behind with neurological deficits. Common deficits include: motor (weakness on one side of the body usually arm and leg), speech deficits (patients may be left with a significant disorder of language. We call this aphasia and patients may have either difficully in comprehending speech or in the fluency of speech. Their speech may be slow and halting. At times they also have what we refer to as nominal aphasia also called anomia. These patients experience difficulty in naming things, like for example if you show them a pen, they would not be able to tell you that it is a pen. They shall know what it is used for but cannot get the name out). Patients may be left behind with residual numbness on one side of the body and depending upon the location of the stroke they may experience difficulty with seeing one half of their visual field (we call this a field cut). Some stroke patients are disabled by ataxia or unsteady gait, others may have disabling cerebellar symptoms.

Stroke rehabilitation plays a big role in the care of stroke patients. Contrary to popular held views, rehabilitation starts right at the onset of stroke and not once the acute stroke is over and the patient is been discharged. Now most of the big hospitals in the United States have acute stroke units. One of the biggest tenants of these acute stroke units is that rehabilitation is started soon after the patient presents to the hospital with an acute stroke. Studies have shown that the human brain has the maximum ability to heal and repair itself acutely (upto 6 months to a year) after a stroke. As time goes on, the brain loses this plasticity and the neurological deficits become more or less fixed. Thus  rehabilitation in the acute stroke setting plays a vital role. Usually patients are evaluated by physical medicine doctors (rehab doctors) while they are still in the hospital with the acute stroke. An assessment is made of their deficits and depending upon that we decide which rehabilitation services are needed. Patients may get physical and occupational therapy in the hospital. They may also be seen by a speech and language therapist so that speech therapy can begin.

Nowdays there are many different modalities of rehablitation therapy which have been proven to be of benefit to patients with stroke. One of the popular ones is constraint induced movement therapy. In this the good arm of the patient is immobilized so that the patient is forced to use the weak arm. Melodic intonation therapy has recently gained popularity too. This therapy uses a style of singing called melodic intonation to stimulate activity in the right hemisphere of the brain in order to assist in speech production in patients who have aphasia.

Stroke rehabilitation does not end once the patient is discharged from the hospital. Most of these patients benefit from ongoing rehab (as I stated earlier this mostly occurs in the first 6-12 months). Patients may either be discharged to a rehab unit or a sub acute rehabilitation facility where these therapies can be carried out in a less hospital like atmosphere.

It is Saturday afternoon New York time. I though pen this from across the seven seas (I am on vacation!!). Hope some of you find this useful.

Personal Regards,

Nitin Sethi, MD

Normal pressure hydrocephalus (NPH)

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

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

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

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

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

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

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

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

Personal Regards,

Nitin Sethi, MD

Carpel Tunnel Syndrome (CTS)

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Let us talk here about carpel tunnel syndrome (CTS), a relatively common neurological condition involving a peripheral nerve namely the median nerve. The median nerve is a long nerve which originates from the brachial plexus and runs down the arm and forearm. As it cross from the forearm to the wrist, it goes into a tunnel formed by the transverse carpel ligaments. This tunnel is called the carpel tunnel.

CTS refers to the condition when the median nerve is pinched as it tranverses the carpel tunnel. Hence CTS is nothing other than a compressive neuropathy of the median nerve across the wrist (the site of compression of course is the carpel tunnel). So what do I mean when I say compressive neuropathy? Simple it means due to external pressure on the nerve, the nerve gets compressed. When the nerve is compressed there is interruption in the flow of signals across the nerve. This causes a neuropathy and presents clinically with neuropathic symptoms. So how does CTS present clinically?

–patients may have complain of numbness involving the area of the thumb and the first two fingers (index and middle).

–at times they may not complain of numbness per se, rather have burning, tingling, pins and needle sensation and at times frank pain in the same distribution. This is especially prominent at night and may keep them from falling asleep..

–if CTS is severe, patients may develop weakness and have difficulty in gripping things or making a fist. Severe CTS causes atrophy (weakness) of the mucles supplied by the median nerve.

Etiology of CTS:

So lets now discuss some of the causes of CTS. CTS occurs when the carpel tunnel gets narrowed and the median nerve starts getting pinched. There are many causes of CTS. One of the most common is job or occupation related. CTS is frequently seen in people whose job involves repetitive motion of the wrist-just as excessive typing (manual and/or the computer), washing clothes with your hands (wringing motion of the wrists as you try to squeeze the water out) are a few of the examples.  Other causes of CTS include:

1) Rheumatoid arthritis (especially if the arthritis involves the wrist).

2) Pregnancy: CTS is more common during pregnancy. The thinking is that during pregnancy, weight gain occurs and this somehow narrows the carpel tunnel.

3)Amyloidosis: patients who have amyloidosis are more prone to getting CTS.

4) Acromegaly: patients who have acromegaly ( due to excessive secretion of growth hormone from the pituitary gland) again are more prone to CTS.

5) CTS may occur after trauma or fractures involving the wrist joint.

Diagnosis and management of CTS:

The diagnosis of CTS is clinical. Your doctor shall be able to diagnose if you have CTS on the basis or your history and clinical examination. Usually no other testing is warranted. Unless there is a doubt in my mind, I do not order tests like nerve conduction studies or EMG (electromyogram or needle study). Nor is there a need to have a MRI scan of your neck. Your doctor may order one if there is doubt that the nerve is not pinched at the wrist rather higher up in the neck (this though should be detectable from the history and clinical examination).

Once the diagnosis of CTS is made, the treatment depends upon the cause. The patient is advised to avoid activities like typing (this may be difficult to avoid all together especially if it a part of your job). In any case either by modifying the way you position your hands or the amount of time you spend on the computer some benefit can be obtained. Initial treatment of CTS is usually conservative. Your doctor might advise some conventional pain medications like ibuprofen. Using wrist spints also helps and I advise my patients to wear them at night too while asleep. Patients are usually referred for physicial therapy so that they can learn better hand ergonomics. The role of injecting steroids into the carpel tunnel to lessen the inflammation is unclear. They likely do provide some relief though for a short time. Most patients recover with the above. In a few severe cases especially the ones which have weakness, surgery may be needed. The surgery usually involves cutting the carpel ligaments and making space so that the pressure on the median nerve is removed and that it can breathe.

I hope this helps some of you.

Personal Regards,

Nitin Sethi, MD

Mind-body interventions: applications in neurology

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A comprehensive review  on mind-body interventions and its application in various neurological disorders was recently published in Neurology. The authors Wahbeh, Elas and Oken searched Medline and PsychoInfo databases to identify clinical trials, reviews and published evidence on mind-body therapies and neurological diseases.

Meditation, relaxation, breathing exercises, yoga, tai-chi, qigong, hypnosis and biofeedback are some of the mind-body interventions that have been used in various neurological conditions like general pain, back and neck pain, carpel tunnel syndrome, headaches (migraine and tension), fibromyalgia, multiple sclerosis, epilepsy, neuromuscular diseases, stroke, falls with aging, Parkinson disease, stroke and attention deficit hyperactivity disorder (ADHD).

The authors do a good job in shifting through all the data to try to identify the effectiveness of mind-body interventions. As they point out in their discussion , many patients as many as 62% use complementary and alternative medicine therapies (CAM). Some with and many without the knowledge of their physicians. One of the reason why CAM therapies are popular is that they are relatively easy to implement, cheap (though many patients have to pay out of their pocket. Some insurance companies shall reimburse if you have a letter from your doctor) and more importantly as the authors point out it makes the patients feel empowered. They feel that they are in control of some of the decision making in their disease process and treatment. Moreover it gives a sense of general well being.

The authors righly point out that is difficult to scientifically judge whether these interventions are all effective. The reason for this is that many of the studies included small number of subjects and some of them did not have a control group. Moreover it is hard to blind these studies so as to avoid a placebo effect. Like suppose I want to study whether acupuncture is effective for lower back pain. One group I give acupuncture. Ideally I should have a control, a group which receives sham acupuncture so as to null the placebo effect. Now this is difficult to implement.

Th authors in their review conclude that there are several neurological conditions where the evidence in favor of mind-body therapies is quite strong such as migraine headaches. In other conditions the evidence is limited due to small clincial trials and inadequate control group.

It is reasonable to conclude that CAM therapies like yoga, tai-chi and qigong improve balance in the elderly and decrease the incidence of falls. Moreover they give a sense of well being and happiness. Meditation exercises whether it is mindfulness meditation, transcendental meditation or concentration meditation with the repetition of a word like Om or a mantra

“Hare Krishna Hare Krishna

Krishna Krishna Hare Hare 

Hare Rama Hare Rama

Rama Rama Hare Hare”

all help in relaxation and reducing stress. This may decrease blood pressure and reduce the incidence of strokes and heart attacks. Brain changes have been observes during meditation in EEG and imaging studies and there is evidence that these exercises have wide spread effects on the endocrine and immune systems as well neurotransmitters. Hatha yoga may help in improving mobility and balance and thus decreasing fall risk. As the authors point out righly Bikram yoga  which is carried out in very hot temperatures is likely not good for patients with MS, as it may worsen their weakness. This is called Uhthoff phenomena.

There is also some evidence to suggest benefits of these interventions in patients who have chronic lower back and neck pain, those with fibromyalgia, osteoarthritis as well as carpel tunnel syndrome (some studies suggest benefit while others do not).

My advise to patients who want to try out CAM therapies for various neurological conditions is to take their doctors into confidence. It is likely that some of these therapies when used along with allopathic medicines shall give added benefits and likely make you feel better. Like with any other therapy one must find a knowledgeable practitioner who knows what he or she is doing.

Then one can truly reap the benefits of these ancient therapies.

Personal Regards,

Nitin Sethi, MD

Incidental cerebral aneursym on brain imaging: what to do?

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At times an incidental cerebral aneurysm is found when neuroimaging is carried out. Let me explain this with an example. You go to your doctor as you have been having headaches or suppose you have a history of migraine, your doctor orders a MRI brain. A  cerebral aneurysm is found on brain imaging.

What to do now is the question?

Does the aneurysm warrant treatment?

If yes what treatment?

To answer the above questions it is essential to first understand the natural history of cerebral aneurysm. An aneurysm is a dilatation of a blood vessel. These dilatations may be congenital (meaning you are born with it) or they may develop later in life due to trauma or turbulent blood flow. Cerebral aneurysms can rupture. When they do rupture they cause bleeding into the brain. This bleeding occurs into the subarachnoid space and hence it is called subarachnoid hemorrhage (SAH). SAH has a high morbidity and mortality and hence it is essential that if an incidental aneurysm is found we should know what to do about it.

Well first the question is whether the aneursym is indeed the cause of the symptom for which the imaging was done in the first place. As I stated earlier, the aneurysm may be entirely unrelated to the headache and may just be an incidental finding.

If the aneursym is incidental then the question is what needs to be done about it. What is the risk that it would rupture and cause hemorrhage? How soon should it be taken care of? Fortunately we now have some answers to the above questions. Studies have shown that the risk of rupture is directly related to the size of the aneurysm. Aneurysms which are small in size, less than 7 mm have a lower risk of rupture as compared to those above 10 mm in size. Hence a small aneurysm may be watched. Your doctor may opt to do nothing apart from recommending that the MRI scan be repeated after 6 months to 1 year. If there is interval increase in size of the aneurysm, then definitive treatment options can be pursued.

For aneuryms which are larger than 10 mm, it is important that they be treated on an urgent basis as the risk of rupture is high. There are different modalities to treat the aneurysm. One may either opt for endovascular coiling (here the skull is not opened, instead the aneurysm is approached via the endovascular route and then thrombogenic coils are placed into the aneurysm. The idea is to thrombose the aneurysm over time and hence to obliterate it). The other more invasive approach is to do a formal surgery, the skull is opened up, the aneurysm is located by the neurosurgeon and then a clip or band is placed across its neck to obliterate it.

Which option should be employed depends upon the aneurysm characteristics. Aneurysms which have a broad neck are difficult to coil, those which are in surgically inaccessible locations are more easy to coil endovascularly.

Hope this helps some of my readers. It is a beautiful Sunday afternoon here in New York City. Time to go for a run.

Personal Regards,

Nitin Sethi, MD

Brain death

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Today I was called to conduct a brain death evaluation on a patient in the medical intensive care unit. As I spoke with the family I again realised how alien  this concept of death is. How very hard it is for the family to comprehend what brain death means.

” Doctor Sethi his heart is beating, the machine (ventilator) is moving his chest, how can he be dead?”

So what exactly is brain death?  The old dictionary defination of death is relatively simple to understand and comprehend by the lay person. Death is the cessation of cardiorespiratory function. When your heart stops you die. Everyone understands this. But as medicine advanced in the 1960’s we reached the stage when we were able to sustain and keep patients alive with advanced cardiorespiratory support. We had ventilators now which did the work of breathing and good medicines to sustain the blood pressure. It was at this time that the need was felt to have an alternative defination of death. The reason was that there were many patients who were on ventilators and their heart was strong, but who had suffered so much damage to the brain that their chance of a meaningful neurological recovery was zero.

Also at this time transplant medicine was kicking off and there was need for organs for transplantation. A brain dead patient usually is a good candidate for organ harvesting because the heart is still perfusing organs like kidneys etc. That is when a new defination of death was born: brain death.

So what exactly is brain death? Well like I said earlier a brain dead patient is one whose brain has suffered irreversible damage and there is zero chance of a neurological recovery. The heart may be beating on its own and the respiration may be aided by a ventilator but the brain is no more. Usually these are patients who have suffered head trauma or a major bleed or stroke in the brain such as a massive subarachnoid hemorrhage.

So how is the diagnosis of brain death made? Well first and foremost the diagnosis of brain death is a clinical diagnosis and you do not need any confirmatory tests unless there is doubt or because the clinical examination is hampered by something. The doctor who usually does the clinical examination testing is one trained in neurosciences either a neurologist or a neurosurgeon. What we usually test for is the integrity of the brain stem (the lower part of the brain which controls the vital functions of the heart and respiration). We do this by checking the brain stem reflexes, are they intact or not?

Do the pupils react to light or they fixed and dilated?

Does the patient have a corneal reflex?

Do they have spontaneous respiration when we disconnect them from the ventilator? This is an important test called apnea test.

Do they gag when we try to suction them?

Do they have an oculocephalic reflex?

Do their eyes move when we put cold water into their ears (this is a test called cold caloric testing)?

We go over the entire chart to make sure that the patient is not on any medication (sedatives) or has any other condition that might explain his current examination. We make sure that the patient is not hypothermic.

If all the above conditions are met then the patient meets the criteria for brain death. I want to add the criteria for brain death vary from country to country and the protocol may vary from one hospital to another. In some countries four doctor are needed to make a diagnosis or brain death. One of them has to be a neurologist or neurosurgeon, the other a doctor who is not involved in the active care of the patient, the third is the doctor involved in the care of the patient and the fourth is usually the medical superintendent of the hospital (like I said the criteria vary from country to country).

The criteria also vary with regards to the time of observation between two examinations of brain death. In some countries the examination has to repeated to confirm there is no change in the findings after 6 hours and in others this time is 12 to 24 hours.

Need for confirmatory testing: as I stated at the onset, brain death is a clinical diagnosis and no confirmatory testing is required. In situations where we cannot do some of the tests like the apnea test or the diagnosis is in doubt or the family requests it, confirmatory testing may be done. The most common test done is an EEG (this EEG is done under specific criteria and should show no activity above 2 microvolts). Other confirmatory tests include angiogram, transcranial doppler or a radioisotope scan.

Once the diagnosis of brain death is confimed the patient can be disconnected from the ventilator legally (the law gives the doctor permission to do that). Of course we try to make the family understand and be part of the final decision of removing from the ventilator.

IF YOU ARE BRAIN DEAD, YOU ARE DEAD. YOU CANNOT DIE TWICE, ONCE WHEN YOUR HEART STOPS AND ONCE WHEN YOUR BRAIN STOPS.

I hope I have made some sense of this technical topic for my readers

Personal Regards,

Nitin Sethi, MD

 

Fibromyalgia and other chronic pain syndromes

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Hmm since fibromyalgia is in the news nowdays, maybe it is a good time to talk about it on the braindiseases weblog. I did my internal medicine residency before I did neurology and I remember reading about fibromyalgia in Harrison’s Principles and Practices of Internal Medicine (this book is called the bible of internal medicine, a book every good internal medicine doctor should know well). Fibromyalgia occupied half a page and was right at the end of the section a kind of neglected disease. Many doctors (and I include myself in that group) do not consider that the disease actually exists.

We all have patients in our practice who carry the diagnosis of fibromyalgia, they have constant complain of pain in different areas of the body. When they first present to a doctor a work-up is carried out to determine the etiology of this constant pain. However inspite of multiple tests including but not limited to blood tests, imaging studies and sometimes even invasive studies no cause can be found. All the inflammatory markers in the blood come back negative (these include tests like ESR). These patients frequently have other diagnosis which fall into the category of psychosomatic disorders like IBS (irritable bowel syndrome) and chronic fatigue syndrome. Some of them may carry psychiatric diagnosis like depression or somatisation disorder. Thus fibromyalgia has been in the past a kind of waste-basket diagnosis given to patients with unexplained complaint of chronic pain referrable to different parts of the body. Since we did not truly believe that the disease exists, we did not have any good treatments for it. Doctors either treated these patients with anti-depressants or pain killers. This caused some unintended problems with some patients becoming dependent on pain killers like vicodin.

So do we know anything more of fibromyalgia now than in the 90’s?

Do we understand its pathophysiology better today?

Does the disease actually exists?

Fibromyalgia is currently diagnosed as per the criteria laid out by the American College of Rheumatology (ACR).

FIBROMYALGIA CRITERIA

A. Widespread pain must be present for at least 3 months. This pain must appear in all of the following locations:

  • Both sides of the body
  • Above and below the waist
  • Along the length of the spine

B. Pain in at least 11 of 18 specific areas called tender points on the body. The pain experienced when pressing on a tender point is very localized and intensely painful (not just tender). Tender points are located in the following areas:

  • The left or right side of the back of the neck, directly below the hairline
  • The left or right side of the front of the neck, above the collar bone (clavicle)
  • The left or right side of the chest, right below the collar bone
  • The left or right side of the upper back, near where the neck and shoulder join
  • The left or right side of the spine in the upper back between the shoulder blades (scapula)
  • The inside of either arm, where it bends at the elbow
  • The left or right side of the lower back, right below the waist
  • Either side of the buttocks below the hip bones
  • Either knee cap

Other long-term symptoms that may indicate fibromyalgia include:

  • Morning stiffness
  • Fatigue
  • Sleep disturbance
  • Numbness or tingling in the hands and feet
  • Headache

We nowdays think that these patients have an altered perception of pain and other visceral as well as somatic sensations. Let me explain this with a crude example. Suppose you have inflammation in your left shoulder joint, your brain shall get sensation from the sensory receptors located in the periphery of the joint.  The sensation shall travel to the sensory cortex of the brain (the part of the brain dealing with sensation) and you shall experience pain as a result. It is believed that fibromyalgia patients have altered pain perception in their brain, they either feel the pain too much or that it persists for longer than it is supposed to (crudely put maybe their brain is more pain sensitive). Some recent work involving functional MRI and other imaging studies does give some scientific evidence to suggest this.

Whatever the etiopathogenesis behind this disorder (if in fact the disorder does exist in the first place) now there are new drugs in the market been touted (and FDA approved) for the treatment of fibromyalgias. One of them is pregabalin marketed under the name of Lyrica. My personal experience using this drug in patients with fibromyalgia is very limited. If you or any of your loved ones is diagnosed with fibromyalgia, I would advise you to see a doctor with interest and experience in this disorder so that you can get benefits of newer treatment modalities.

Personal Regards,

Nitin Sethi, MD