Author: braindiseases

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

White matter lesions on MRI–a question and some answers

braindiseases105 Comments

I thank one of my readers Sandy for writing in.  Sandy asks some important questions. As a lot of you may be dealing with some of the same issues as her, I am reproducing her question here. My answers to her query follow.

Again thank you Sandy for writing in.

Sandy

Dear Dr.

In june I experienced some very unusual headaches that felt think electrical shocks throughout my head. One night I experienced the worst headache of my life in my forehead only. It lasted all night and in the morning it was better; however I experienced dizziness and if I bent over a swell of pain would radiate through my head. A week later I experienced an eye problem and was told that it was uveitis. Because uveitis can be caused by a virus or autoimmune problem, I immediately began testing for an autoimmune problem. During this testing I continued to experiece overall nerve pain in by head (forehead, temple, back of head) as well as neck pain, should nerve pain through fingers, neck, ankels), joint & chest pain. The only positive test result showed a high ANA test of 1:640 but all other blood tests(c-reactive protein, RF, Sed Rad, SM etc..) were normal. I also had an MRI and the radiologist noted several tiny foci white matter in the frontal lobe area. He indicated that it is may or may not be of clinical significane but could be small vessel ischemia disease or possible dymlienation. I wonder if there is a correlation to the several headache I had in my forehead with the MRI results. My neurologist initially said I had occpital headaches and is normally caused by a pinched nerve; but after receiving this MRI, I don’t think he has it right. I feel the headaches and vision problems along with the other symtoms correlate together. Should I be concerned about this MRI. I don’t feel that this is MS because I’m not having muscular/walking issues; but greatly concerned that if these headaches continue, cognitive problems could occur. Your opinion would be greatly appreciated.

From MRI white matter lesions: does it represent MS?, 2008/09/26 at 2:24 PM

 

Dear Sandy,

                      thank you for writing in. Your case history is intriguing, since I do not have all the details my assessment is severly limited.  I can though tell you that white matter lesions are commonly seen when patients undergo a MRI study of the brain. Some of the times these white matter lesions (also referred to as white matter hyperintensities (WMH), this is because they appear as bright white spots on the MRI) are incidental findings and may have nothing to do with the reason the MRI was done in the first place. Let me explain. Lets assume you come to see me since you have being lately experiencing headaches. I order an MRI because I want to rule out a brain tumor. MRI result comes back. There is no brain tumor but incidentally note is made of several scattered white matter hyperintense lesions. Likely in the case I describe above, the WMHs are incidental findings and not the cause of the patient’s severe headaches.

So what do these white matter lesions represent? Many diseases can cause white matter lesions in the brain MRI.  One of the diseases usually mentioned in MRI reports is multiple sclerosis. Patients rightly get scared that they may have MS. While multiple sclerosis is characterized by white matter lesions (we call them plaques in the case of MS) which are scattered in the brain, I want to re-emphasize that not all white matter lesions represent MS (see my website for more details http://braindiseases.info). In the case of MS, the plaques are scattered in the brain in a particular way. Moreover if you do not have any signs or symptoms of MS (your examination is normal), more than likely the white matter lesions do not represent MS. The diagnosis of MS is clinical, at times supplemented by tests like MRI brain, CSF/ spinal fluid examination and evoked potentials.

A lot of work has been done to determine the significance of white matter lesions. The thinking now is that they represent ischemia (lack of blood flow) in the small blood vessels of the brain. Hence they are also at times referred to as ischemic small vessel disease. Hence these lesions are more commonly seen in the MRI of patients who have cerebrovascular risk factors like hypertension, diabetes and high cholesterol as well those that smoke. Their incidence increases as we age (meaning you are more likely to see them on the MRI of someone who is 60 and above rather than someone who is in his 20’s).

They have been reported in the MRI of patients who suffer for migraine. The reason they are more commonly seen in migraine patients is again not fully elucidated but the thinking is that migraine is due to vascular causes and hence WMHs are more common in these patients.

While I cannot comment of your case in particular, you have a positive ANA though rest of the autoimmune markers are negative and your ESR is low. I would rule out the usual suspects, vasculitis though remains in the differential and it would be reasonable to make sure you do not have any underlying vasculitic etiology.

Your last question is important. Though there is no direct correlation between the extent of WMHs in the brain and the development of cognitive decline, as I stated earlier they become more common as we age. People who have extensive white matter disease in their MRI frequently do exhibit cognitive deficts when carefully tested for. Whether this represents a form of vascular dementia is not clear.

I would advise you to follow with your PMD and neurologist. They would be the best people to guide further diagnostic workup and treatment.

Personal Regards,

Nitin Sethi, MD

Absence seizures–a few questions and some answers

braindiseases2 Comments

One of my readers wrote to me today asking me a question about Absence seizures. She is a teacher and is concerned about a student in her care. I always feel teachers pick up Absence seizures far more frequently than parents. One of the reasons for this is that they spend so much time with the children (today most parents work and have limited time to spend with children). Teachers also are astute observers of children behavior and usually have a pretty good feel if something is wrong.

Here is what Ms. Lynn says, my answers to her query follow:

 

Ms J Lynn

Hi Dr Sethi,
I am a teacher and I have a student who is exhibiting these types of behaviors:
staring episodes, often says he can’t remember something we just talked about 30 seconds prior, he said recently that he feels like his “brain just wouldn’t work sometimes,” he has frequent meltdowns, easily agitated (but not aggressive), social (but very sensitive and easily hurt or offended), seems to have a low threshold for frustration and emotions escalate quickly, and he seems to overly react in situations when he feels physically hurt (if a ball hits him on any part of his body he is very upset, needs time to calm and he complains of feeling lots of pain).
Could all of these symptoms be related to some type of seizure activity?
Thank you for you help.

Dear Ms. Lynn,

                               thank you for writing in. Clinically seizures in children frequently look different from seizures in adults. In the case of Absence seizures, all the child may do would be to stare (hence the name staring spells), there are no gross convulsive movements seen (the child does not shake or have jerks of his arms and legs). During the time the child is having a seizure (staring), his brain is malfunctioning and hence the child is unable to recall things said or spoken to him during that time. Children may have hundreds of these small Absence seizures during the course of a day and hence you can imagine what follows. These children start slipping in their grades as compared to their peers.

I have to add here though, that not all staring spells in children turn out to be Absence seizures. As you are well aware there can be many behavioral and developmental problems in children which at times may mimic seizures (children who have Attention Deficit Disorder too do not do well in school etc).

I would advise you to report your observations to his parents. The child can be assessed by a pediatrician and further investigations if needed can then be carried out.

I sincerely appreciate your concern for your student. Teachers lay the foundation of our society. I am what I am today because of the hard work of my teachers and my parents.

Personal Regards,

Nitin Sethi, MD

When do we say seizures are refractory to medicines?

braindiseases3 Comments

                                 When do we say seizures are refractory to medicines?

                                                        Nitin.K.Sethi, MD

Assistant Professor of Neurology

New York-Presbyterian Hospital

Weill Cornell Medical Center

New York, NY 10065

 

Yesterday I saw a patient with medically refractory epilepsy in my office. As I took pains to explain to the family about refractory seizures, I realised that understanding the same can be difficult for a lay person. So in this post I shall talk about refractory seizures.

So what do I mean if I say a patient has medically refractory epilepsy or medically refractory seizure disorder? In simple words all I am saying is that the patient has a seizure disorder which has not shown an adequate response to anti-seizure medicines.

In most patients with epilepsy/ seizure disorder, adequate seizure control can be obtained by just one seizure medicine. By adequate control I mean no more seizures. No more seizures, the side-effects of the anti-seizure medication used are tolerable (if none that is the best): the patient is happy and I am happy. While good control of seizures can be obtained in the majority of patients, there are a few in whom the seizures are harder to control. You use one seizure medicine but the seizures still persist, you stop the first and use a second-still seizures, you try a third-same story. You start using 2 or more drugs together (at the same time) to try control the seizures. This is referred to as polytherapy or polypharmacy.  You can imagine what happens next. The patient is on 3 and at times more drugs, more side-effects, more drug-drug interaction and at times still poor seizure control. The patient feels miserable and I am not happy too. Such a patient has medically intractable epilepsy, seizures are refractory to medications.

So what can be done for a patient who has medically refractory epilepsy? Can we offer them something to control their seizures. I am happy to say yes. Patients with medically refractory epilepsy should be ideally seen in specialized epilepsy centers (comprehensive epilepsy centers).  These centers offer expertise: patients can be enrolled in trials of experimental drugs, other options like neurostimulation (vagus nerve stimulator) and finally epilepsy surgery can be explored (see my post on epilepsy surgery at http://braindiseases.info) .

The tremor of Parkinson’s disease

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                                                     The tremor of Parkinson’s disease

Nitin. K. Sethi, MD

Assistant Professor of Neurology

New York-Presbyterian

Weill Cornell Medical Center

New York, NY 10065

Since many of the readers of my blog and website (http://braindiseases.info) have written in asking about tremor, I thought in this post I shall describe the tremor seen in Parkinson’s disease in detail. The classical tremor described in Parkinson’s disease is a resting tremor which has a frequency of about 2-5 Hz. Let me explain in more simple terms what I mean by that.

The tremor in Parkinson’s disease is present at rest and not when the hands/ limbs are in motion (when the patient’s hands are placed on a table and are completely at rest, the tremor comes out. Now if you ask the patient to hold the hands in front of themselves or to perform some action like picking up a glass of water and bring it to their lips, the tremor becomes less prominent and may not be noticable. Hence it is called a RESTING TREMOR). Another way to observe the resting tremor is to see the patient walk. When we walk, our arms are held by the side of the body and are completely at rest, if a person has a resting tremor it is clearly visible.

The tremor in Parkinson’s disease has a frequency of about 2-5Hz ( meaning that the tremor is not very fast). It also has a large amplitude (meaning that it is not fine rather it is a gross tremor and can be well appreciated by the naked eye from a distance).

The tremor of Parkinson’s disease disappears/ stops when the patient falls asleep (most of the tremors abate on sleeping and hence this quality does not aid in differentiating the tremor of Parkinson’s disease from other tremors).

The classical tremor of Parkinson’s disease is a pill-rolling tremor (meaning the tremor consists of flexion and extension of the fingers in connection with adduction and abduction of the thumb. Imagine yourself rolling a pill, that is how the tremor looks like!!!)

Most importantly the tremor in Parkinson’s disease is accompanied by other signs of Parkinson’s disease such as rigidity (the tone of the muscles of the limbs is increased), bradykinesia (slowness in the execution of movement) and a disturbance of gait and posture (the gait is slow, stooped forward-we call this a festinating gait and their posture is off so patients are more prone to falls). That said and done signs of Parkinson’s disease may appear at different times and not all at once. At times the first/ earliest manifestation of Parkinson’s disease is the presence of an asymmetrical resting tremor (meaning the tremor usually appears asymmetrically/ only in one hand).

 

Few Multiple Sclerosis questions and their answers

braindiseases46 Comments

Nitin K Sethi, MD

Assistant Professor of Neurology

NYP-Weill Cornell Medical Center

New York, NY 10065

One of my readers Lisa asked me some very specific MS questions. Since I feel these questions shall be on many MS patients minds I am reproducing them here. Here are the questions followed by my answers. Thank you Lisa!!!

  1. Lisa on September 17, 2008 said:

Hi, I have enjoyed reading the information you posted. I have a few questions of my own:

At this point, I have an MRI with 8 lesions, one possibly of which is tumefactive MS, a postive LP for oligoclonal bands, and my neurologist has diagnosed me with “clinically isolated syndrome”…not full blown MS at this point, but still wants to begin treatment.

1. Is tumefactive MS considered more fatal or harder to treat than “regular” MS?

2. How many oligoclonal bands are needed for a low amount? High amount? My report states greater than 3 bands. Why is there not a specific number given?

3. I have been given the choice between Rebif and Copaxone. Which is the better treatment?

  1. 7 braindiseases on September 18, 2008 said:

Dear Lisa,
thank you for writing in. You ask some very specific questions and that is what I shall attempt to answer. I am not sure why your doctor has stil labelled you as a clinically isolated syndrome (likely it is because you have had only one clinical attack suggestive of MS). Your MRI though does show dissemination of the disease in space (you can read more about the clinical diagnosis of MS on my website http://braindiseases.info) and you have more than 3 oligoclonal bands in your CSF. Now to answer your first question. Some patients have large sized demyelinating plaques (lesions) on their MRI. This is commonly referred to as tumefactive MS (because on the MRI, the lesion is large and resembles a tumor more which it has to be differentiated). There is some data to suggest that MS patients with tumefactive disease have a more aggressive disease course. Though I have to add that this data is not robust.
Oligoclonal bands are frequently present in the CSF of MS patients. Here I have to add that oligoclonal bands can be seen in many other conditions other than MS hence one has to make sure that they are present only in the CSF and not in the blood (In MS these bands are produced intrathecally meaning present only in CSF but not in blood). One study suggested that low or absent number of oligoclonal bands in the cerebrospinal fluid at the time of diagnosis predicts a better prognosis. However quantification of oligoclonal bands in the CSF remains an insensitive prognostic indicator and hence should not be used to influence decisions regarding treatment.
Now to your third question. There is some evidence to suggest that higher dose interferon (Betaseron/ Rebif) are more effective as compared to lower dose interferon. The interferons as well as Copaxone are recommened for initial treatment of relapsing remitting MS. Most of the times it is the patient’s lifestyle, easy of administration and side-effect profile which determines the choice between them.
I hope that helps you out and feel free to write again. I wish you the best.


Personal Regards,
Nitin Sethi, MD

Deficiency of vitamin B12 causes cerebral atrophy

braindiseases10 Comments

                               Deficiency of vitamin B12 causes cerebral atrophy

                                                    Nitin .K. Sethi, MD

                                            Assistant Professor of Neurology

                                            New York-Presbyterian Hospital

                                              Weill Cornell Medical Center

                                                New York, NY 10065

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

Can vitamin B12 intake prevent the onset of dementia.?

 If so how much of this vitamin should one take?

And at what age should one start taking this?

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

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

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

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

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

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

Concussion during sports and return to play decisions

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                                      Concussion during sports and return to play decisions

Nitin K Sethi, MD

Assistant Professor of Neurology

New York-Presbyterian Hospital

Weill Cornell Medical Center

New York, NY 10065

I recently read an article in the Archives of Neurology ( Vol 65, Sep 2008) by Dr. Lester Mayers about return to play (RTP) criteria after athletic concussion. As concussions are relatively common sport related injuries (especially in contact sports like football, rugby and boxing) I thought it would be a good idea to review some of the salient points of the article in this forum.

Concussion is a common type of traumatic brain injury and has been referred to by other names such as mild traumatic brain injury, mild head injury and minor head trauma. No good defination for concussion exists though it is frequently described as head injury with transient loss of brain function (usually a short period of loss of consciousness occurs).

Let me explain with the help of an example. I love to box (true one of the few neurologist who actually likes boxing). Lets assume I am going a couple of rounds in the ring with another guy.  A southpaw with a mean right hand. First round here we go!!!. I got my right and left combinations going. Hmmm feeling good and then it happens. I walk into his right. BOOOOOM!!! My knees give in and I hit the canvas. I see stars shining and birds twittering. The referee is asking me “Are you okay? Are you okay?” I look dazed and then slowly come around and answer I am fine. I am helped out of the ring, the fight is over!!! THERE I JUST HAD MY FIRST CONCUSSION!!!

Can I return to play/ box after a 10 mins break?

 Or rather should I return to play after a break?

Is it safe?

 Am I okay?

All these questions are addressed by Dr. Mayers in his review. Traditionally return to play decisions are made by the field side by the team physician or in the case of boxing by the doctor at the ringside. This is usually a clinical judgement with doctors relying on the documentation of resolution of symptoms at rest and during exertion to provide an estimate of the appropiate time for the athletes to resume practice and play (return to play).

A stepwise process was outlined by the Canadian Academy of Sports Medicine:

Step 1: no activity, no play and complete rest till asymptomatic and with a normal neurological examination–if your clear this then Step 2: light aerobic exercise permitted, no resistance training–if you clear this then Step 3: can return to sports specific training and resistance training—if patient remains asymptomatic then can be cleared for Step 4: non-contact training can begin–if patient remains asymptomatic then he is cleared for Step 5: full contact training —if he still remains asymptomatic then he is cleared for Step 6-full play!!! (As you can imagine these criteria are for professional atheletes but also apply for others)

As you can see there are steps to be followed before return to play can be allowed. If you fail one step you go back to the previous step and remain there till you feel better and are ready to proceed further.

Why is this important? Studies have shown that even simple concussions cause cerebral dysfunction (reflecting damage to the brain at the celluar level) and that it takes a minimum of 4 weeks for the brain to revert back to normal. If RTP occurs earlier, the athlete is at risk for a recurrent concussion and further brain damage. Even death can occur (we have all heard of boxers who die during or shortly after a bout).

Learning points from Dr. Mayers review:

1) Concussions are common.

2) Concussions can be serious and even fatal.

3) Concussions lead to cerebral dysfunction and damage to the brain at the cellular level.

4) Return to play decision should be made by a doctor skilled in this task.  A postconcussion RTP interval of at least 4 weeks is imperative (Dr. Mayers takes pain to point out that even more time may be needed to permit complete brain healing and recovery).

My advise to you:

1) Treat a concussion with respect and see a doctor if you suffer one.

2) You may feel you are okay but you are not. The brain takes time to heal completely from a concussion.

3) Do not return to play. See a doctor and get his advise. Let him decide what the return to play interval should be.

Falls in neurodegenerative conditions: what can be done?

braindiseases1 Comment

               Nitin K Sethi, MD

Assistant Professor of Neurology

New York-Presbyterian Hospital

Weill Cornell Medical Center

New York, NY 10065

FALLS ARE COMMON IN THE ELDERLY!!!

Falls are common in neurodegenerative conditions so that is what I shall discuss in this post. Patients with diseases like Alzheimer’s dementia, fronto-temporal dementia (Pick’s disease), multi-infarct dementia (vascular dementia), Parkinson’s disease, multiple sclerosis, Progressive Supranuclear Palsy and some post stroke patients are all prone to falls either early or sometime in their disease course.

FALLS CAUSE MORBIDITY AND MORTALITY!!!

Falls are an important cause of morbidity and mortality in this vulnerable population. Imagine a-85-year old man with Alzheimer’s dementia. Even though he has cognitive deficits (decreased memory and problems with other cognitive skills like calculation, abstract thinking and language) he is still relatively mobile. Every day he takes a 30 min walk in his immediate neighbourhood. One day while walking, he trips over and falls when his foot gets caught in a crack in the side-walk. He is unable to get up by himself . Help only reaches him after an hour when his family comes looking for him. He is rushed to the nearest hospital where an X-ray reveals fracture of the hip and the pelvis. Surgical management is indicated for fracture stabilization.  He is admitted to the hospital and the hospital course gets complicated by development of pressure sores (bed sores), deep venous thrombosis (blood clots in the veins of the legs) and pulmonary embolism (blood clot in the lung vasculature).  All these are directly related to his forced immobilization due to hip and pelvic fractures. He gets progressively more disoriented during his prolonged hospital stay though survives and makes a slow recovery and is discharged to a sub-acute facility.

FALLS HURT AND CAUSE INJURIES!!!

Falls may lead to various injuries:

1) Fractures of the hips, long bones: tibia, fibula, femur, neck of femur, radius, ulna

2) Neurotrauma: head injuries: subdural and epidural hematomas, sub arachnoid hemorrhage, intracranial hemorrhage (bleeding into the brain)

3) Craniofacial injuries: injuries to the face, eyes, the orbit

4) Fractures of the ribs

5) Back injuries

THE STATISTICS ARE SCARY!!!!

The incidence of hip fracture increases as the population ages. One in five persons dies in the first year after sustaining a hip fracture, and of those who survive past one year many have significant functional limitation. Of those who survive one year after hip fracture, only 40 percent can perform all routine activities of daily living and only 54 percent can walk without an aid.

WHY DO THE ELDERLY FALL???

Why are falls common in the elderly and more so in the elderly population with a neurodegenerative condition? The causes are many:

1) Poor eye-sight (as we age cataracts and other retinal degenerative conditions become common contributing to poor eye-sight). They have poor depth perception and visual contrast sensitivity.

2) decreased acuity of hearing

3) concomitant neuropathy (many of the elderly population may have a condition like diabetes giving rise to a concomitant peripheral neuropathy. Persons with a sensory motor polyneuropathy are not able to sense the ground and thus their righting reflex is off). RIGHTING REFLEX: various reflexes that tend to bring the body into normal position in space and resist forces acting to displace it out of normal position.

4) Neurological conditions like Parkinson’s disease and Alzheimer’s dementia impair these postural reflexes/ righting reflexes making patients even more prone to falls and resultant injuries.

5) The elderly are on multiple medications like  benzodiazepines, anticonvulsants, sedatives and  antihypertensives which may contribute to the falls. 

6) Risk of osteoporosis and osteopenia increases as we age: when the elderly fall they are more likely to hurt themselves or fracture their bones.

7) Other concomitant medical conditions like diabetes, kidney problems, thyroid problems, blood pressure problems and cardiac problems may contribute to the falls.

WHAT CAN BE DONE?

The big question is how to prevent falls in the elderly. A number of interventions may help.

1) Treat the neurodegenerative/ underlying condition contributing to the falls. Gait and postural reflexes of patients with Parkinson’s disease improve when they are treated with medications like Levodopa-carbidopa and dopamine agonist. The response though varies, their tremor may improve though their gait may still remain off.

Good control of blood sugar in a diabetic patient helps and may halt the progression of the neuropathy.

Alzheimer’s disease patients also gain some benefit in their gait and mobility when they are treated with medications like Aricept.

2) Correct visual/ eye problems: timely cataract surgery, corrective lenses and glasses all help in improving stability and confidence of the elderly patient.

3) Hearing aids may be of help in those who have hearing loss.

4) Restriction of outdoor activities may be advisable in a patient who is at high risk of falls. If that is not acceptable, these activities should be carried out under direct supervision. Keep a walking partner etc.

5) Correct mechanical/ musculoskeletal gait problems such as ingrown toe nail, back and hip pain, foot drop etc.

6) Regular exercise is helpful. By keeping muscles supple and maintaining their tone it ensures that righting reflexes are not lost.

7) Physical therapy may be immensely helpful in some patients (laying emphasis on gait retraining).

8) Use of assist devices like canes (single point, four point), walker is helpful.

9) Fall proof the home and immediate patient surroundings: remove anything which may cause injury if the patient falls-this includes sharp objects, tables with sharp edges, loose carpets.

have fall prevention devices at the top of stairs.

have a bed whose sides can be put at night (just like in the hospital).

have an alarm or some other call device set-up at home so that help can be summoned.

Last but not least” MOST FALLS OCCUR TO AND FROM THE BED TO THE BATHROOM AT NIGHT, SO LEAVE THE BATHROOM LIGHT ON AT NIGHT!!!”

 

Irritable bowel syndrome (IBS) what has the brain to do with it?

braindiseases1 Comment

Nitin K Sethi, MD

Assistant Professor of Neurology

New York-Presbyterian Hospital

Weill Cornell Medical Center

New York, NY 10065

The New York Times always has some good articles in its health section which I enjoy reading.  One such article which I read recently was titled ” Let the mind help tame an irritable bowel” by Jane E. Brody. I think everyone who suffers from IBS should read this well written piece. Ms. Brody discusses  the role played by the brain in IBS by highlighting the intimate connection between the gut and the brain. 

When we talk about the nervous system most people are only familiar with the central nervous system (CNS) (brain and spinal cord) and the peripheral nervous system (PNS) (peripheral nerves which control the movements of the limbs and help to transmit sensation like pain, temperature and touch from the periphery back to the brain). In addition to the CNS and the PNS, there is another nervous system which plays an equally important role. This is referred to as the autonomic nervous system (ANS). The ANS is the system which helps to maintain functions like sweating, blood pressure, erectile function and functioning of the smooth muscles of the gut among numerous other functions. This system is essentially involuntary meaning not under our voluntary control.

The brain and the gut are intimately connected and this has being referred to as the brain-gut axis. The small and large bowel are richly innervated with nerve fibres transmitting information to and from the brain. The secretory functions of the gut are controlled by the brain though neurotransmittors like serotonin and hormones such as gastrin, somatostatin, secretin, cholecystokinin and neuropeptides. Thus in essence the gut is under the control of the supercomputer aka ” BRAIN”.

People who have IBS have symptoms of bloating, flatulence, diarrhoea, abdominal pain and constipation. They usually fall into two broad categories: 1)in which diarrhoea symptoms predominate 2) in whom constipation symptoms predominate. When these people seek medical help a work up is initiated to determine the etiology. As doctors we want to rule other diseases which may mimic the presentation of IBS. It is specially important to rule out tumors of the gut (colon cancer etc ) hence in some patients a colonoscopy may be ordered. It is also important to rule out inflammatory bowel diseases (IBD) such as Ulcerative Colitis and Crohn’s disease.

If after work-up nothing “organic/ structural” is found, the diagnosis of IBS is entertained. No one yet knows what causes IBS, why some people have it and others don’t. One of the theories is that in people who have IBS either the nerves or the smooth muscles of the gut are extra-sensitive. They respond differently (as compared to people who do not have IBS). Another theory is that the nerves and smooth muscles perse are fine, it is the brain which processes the signals it gets from the gut differently.

As Ms. Brody rightly points out in her article (www.nytimes.com) this does not mean IBS is a psychosomatic condition. For a long time these patients were misunderstood and tagged as being too emotional, “it is all in your mind meaning psychological” and “there is nothing wrong with you”  labels. Now we know this is not true though we still do not know what the underlying problem is.  We do know that IBS symptomatology is exacerbated by emotional upsets meaning symptoms worsen at the times of stress.  Large meals, change in diet, eating a diet rich in wheat, barley or milk products, drinking too much coffee and tea or an overindulgence in alcohol can lead to a flare up of symptoms.

So if the brain plays such a big role in the symptomatology of IBS, can we harness the power of the brain/mind to control this disease? IBS should be the ideal disease to demonstrate the power of mind-body medicine. Well yes and no. To some extent therapies like hypnosis, meditation, yoga and massage help. Controlling your response to stress is also helpful (how you deal with stressful situations, knowing which triggers to avoid-stress at work, at home, in a relationship etc). A very important role is played by dietary modifications-knowing your triggers and knowing which foods to eat and how much and which to avoid.

Medicines are there, unfortunately they do not abate the underlying disease though they certainly help in controlling the symptoms. If you have diarrhoea predominant IBS, your doctor may prescribe an anti-diarrhoeal agent along with probiotics (once infective causes of diarrhoea have been ruled out by stool cultures). Constipation predominant IBS patients may be helped by increasing the fiber in their diet or by the judicious use of laxatives.

A combination of the above therapies (mind-body medicine and allopathic drugs) works best. After all that is what is referred to as holistic medicine.