Author: braindiseases

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

Depression superimposed on dementia–two hits to the brain!!!

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Depression superimposed on dementia–two hits to the brain!!!

Nitin K Sethi, MD

Assistant Professor of Neurology

New York-Presbyterian Hospital

Weill Cornell Medical Center

New York, NY

In recent years the link between depression and dementia has been closely looked at.  Many questions await a definitive answer-

—do attacks of major depression predispose to dementia later in life?  (or put in more simpler terms, does depression hurt the brain and kills  neurons leading to cerebral atrophy and dementia?)

—is depression more common in patients with primary dementia such as Alzheimer’s dementia?

—is depression frequently missed or misdiagnosed in  patients with primary dementia ?

—do patients with dementia have depression which is more refractory to medical treatment?

—does depression accelerate the rate of cognitive decline in patients with dementia?

I recently saw a patient who was referred to me to evaluate for dementia. She was 74-years old and her past medical history was significant for hypertension for which she was on anti-hypertensive medications. When the patient saw her primary medical doctor she had volunteered the information that she was having some problems with her memory. She at times forgot the names of her loved ones, one time she had got lost while heading from home to the hospital. Her home aide further added that she had noticed that the patient frequently misplaced objects and then could not recall what she had done with them. At times she forgot to add an essential ingredient to a dish she was preparing. Recent neuropsychological examination was suggestive of a primary dementia.

As I spoke to the patient, I found her to be quite high functioning. She made eye-contact, gave a succulent history and most importantly had insight into what was plaguing her namely her problems with memory. As the interview went on I learnt that she had been depressed for a while. Though she was on anti-depressants, the recent loss of close family members had made her more depressed. She suffered from a loss of appetite and few things in life gave her pleasure.

So where do we go from here? What is the optimum treatment for someone who might have an underlying primary dementia such as Alzhemier’s disease but also has superimposed incompletely treated depression. Most doctors would agree that her depression needs to be treated more agggressively but the questions which arose in my mind were the following:

–should I treat her for dementia now or reassess her after treating her depression more aggressively?

–is the ongoing chronic depression actually predisposing her to memory problems and maybe even dementia?

–what came first—depression or dementia?

–who is the bigger culprit here–depression or dementia?

All questions for whom we still do not have good answers.  The brain can take a hit here and there but depression-dementia is a deadly combo–likely a death blow to the delicate brain. Maybe one day we shall be able to win the battle against these two scourges.

Multiple sclerosis: making the diagnosis

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So let us start from where we left off. Just how do we (doctors) go about making (confirming) the diagnosis of MS.

MRI scan: Well one of the test most commonly requested (infact done in nearly every patient) is a MRI scan of the brain and at times of the cervical spinal cord. What are we looking for you may ask? Well multiple sclerosis on the MRI is characterized by plaques (lesions) which are disseminated in space and in time. What does that mean? In a typical patient of MS, the MRI scan shall show evidence of disease activity which is scattered around in different parts of the brain. Meaning there are MS lesions seen in different parts of the brain white matter (typically MS is a white matter disease though recent research indicates involvement of the grey matter too). So for example a typical MRI scan shall show plaques scattered  in the white matter of the frontal lobe, parietal, temporal lobe, cerebellum and so forth. Moreover the MRI scan shall indicate that these plaques are of different age (which indicates that the disease has been present for sometime now). Remember what I said –relapsing and remitting MS. Sometimes to help secure the diagnosis, your doctor shall also order a MRI scan of the spine most commonly cervical spine. The intention is the same and that is to see evidence of dissemination of the disease process in the brain and spinal cord.

Spinal tap: a lumbar puncture is usually carried out. Does every patient need a spinal tap to help secure the diagnosis of MS? No. Remember the diagnosis of MS can be made clinically in some patients. In patients where the characteristic history is not forthcoming and in whom the MRI scan does not prove helpful (does not evidence of dissemination of disease process in space and time), a spinal tap may be warranted.  The spinal fluid of MS patients is analyzed for certain proteins which suggest evidence of disease process. These include myelin basic protein (MBP), oligoclonal bands (OCBs) and IgG index.

Other tests: these tests may be requested in special circumstances (usually when the diagnosis remains elusive inspite of MRI scans and spinal tap).

1) Visual evoked potential (VEP), brainstem auditory evoked potential (BAEP) and somatosensory evoked potentials (SSEP):  these tests usually involve testing the integrity of different pathways in the brain. VEP tests the visual pathway from the eye to the occipital (visual) cortex, BAEP–tests the brainstem auditory pathways while SSEP check for the integrity of the white matter tracts carrying somatosensory information (vibration, joint sense and position sense) from the periphery (arm or leg) to the somatosensory cortex.  MS lesions involving any of these pathways cause a delay in the rate of conduction of nerve impulse and provide ancillary evidence of involvement of white matter tracts of the brain by a demyelinating disease process.

I hope these two posts help you all in understanding how the diagnosis of MS is made.

 

Nitin Sethi, MD

Brain disease weblog update and future directions

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I apologize that I have not posted any new information on my blog for the past few months. Have no good excuse apart from the fact that work has kept me really busy. Thank you for all your questions. I have caught up with my answers and hopefully you shall find them informative.

It is time to get the blog up and running again. So I shall pick it up from where I left off and discuss MS in my next post.

 

Personal Regards,

Nitin Sethi, MD

Multiple Sclerosis–making the diagnosis

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I still continue to get many questions from the readers of my blog regarding multiple sclerosis (MS). A significant majority of them write to me because they are concerned they may have MS either because of white matter lesions found on a MRI scan of the brain or because they are plagued by various non-specific signs and symptoms. Though I have written about this before, I thought this shall be a good time to go over how the diagnosis of MS is made. What are the symptoms that raise the suspicion for MS, what are the clinical signs on examination that suggest MS and finally what are the tests that may help to confirm the diagnosis.

Before I dwell deeper into this topic, please remember: THE DIAGNOSIS OF MS IS A CLINICAL ONE. Meaning that it can be made on the basis of a history and clinical examination itself. No tests are needed in such a situation to confirm the diagnosis.  Of course as it is often in medicine–it is always not that easy.

So let us begin—

Clinical history: Are there any points in the clinical history of the patient that suggest the diagnosis of MS? Patients with MS may give a history of neurological symptoms and signs (remember signs are elicted on clinical examination-meaning when the doctor examines you) that wax and wane (relapsing and remitting MS). A patient may present with acute loss of vision in one eye along with pain in the eye  (I am talking about optic neuritis). As the doctor dwells deeper into the history, the patient volunteers that a couple of years ago he had a similar problem in the other eye which had resolved on its own and he had not been investigated further. Hmmm–now we have history of 2 attacks separated in time. As a neurologist this makes me think of MS as a possible diagnosis. The problem with MS though is that it may present with non-specific signs or symptoms or rather it may present with signs and symptoms that localize to different parts of the central nervous system (CNS). By CNS I mean the brain and the spinal cord. So for example patients may present with numbness on weakness on one side of the body (this localizes to the contralateral motor or sensory cortex), problems with the bladder (incontinence–this usually localizes to the spinal cord), problems with balance and coordination (their gait is off and they may have a prominent tremor in their limbs–this localizes to the cerebellum or the brain stem), double vision (this localizes to the cranial nerves which control the movement of the eyes). Virtually any part of the central nervous system can be involved–hence the presentation is at times non-specific. BUT WHAT HELPS US AS DOCTORS IS WHEN WE GET HISTORY WHICH SUGGESTS A DISEASE DISSEMINATED IN SPACE AND IN TIME. Meaning a disease process which is involving different parts of the central nervous system and which has shown evidence of multiple attacks separated by time. REMEMBER MS IS NOT A MONOPHASIC ILLNESS (it relapses and remits!!!)

Clinical examination: So what are the clinical examination findings which make me as a neurologist think of MS in  a patient. There are certain neurological signs which have been said to be pathogonomic of MS (meaning the presence of these signs virtually seals the diagnosis of MS). These include certain eye signs. Bilateral internuclear opthalmoplegia (INO) (who said neurology was easy!!!) is one such sign. This is an eye-sign in which the patient’s eyes do not move as directed by the examiner. One eye fails to adduct (that is move inwards) while the other eye  abducts (moves outwards) but the abducting eye shows a nystagmus (shaky side to side movement). Other eye signs such as an afferent pupillary defect (this is elicted by shining a penlight into the eye) also raise suspicion for MS. What we as neurologists look for though is this–we look for signs that suggest the disease is disseminated in the CNS. REMEMBER WHAT I TOLD YOU ABOUT MS. IT IS A DISEASE WHICH IS DISSEMINATED IN TIME AND SPACE.

Tests: so when a diagnosis of MS cannot be made on the basis of history and examination alone, we as doctors have to fall back on tests to rule in or rule out the diagnosis. No test seals the diagnosis of MS by itself. They just help to add to our certainity. I shall discuss the various tests namely –imaging studies such as MRI scan of the brain and spinal cord., evoked potential studies such as visual evoked potential (VEP), somatosensory evoked potential (SSEP), brain stem auditory evoked potential (BAEP), spinal fluid (CSF) examination in the next post.

 

Nitin Sethi, MD

Post traumatic epilepsy or seizures after head trauma

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Post Traumatic Epilepsy

Nitin K Sethi, MD

Assistant Professor of Neurology

New York-Presbyterian Hospital

Weill Cornell Medical Center

New York, NY 10065

 

In this post I shall discuss the entity called post traumatic epilepsy/ post traumatic seizure disorder.  Epilepsy is a condition characterized by two or more seizures in a person’s lifetime. Broadly speaking epilepsy can be of two kinds:

1. Primary Epilepsy

2. Secondary Epilepsy

Patients who have primary epilepsy have seizures usually due to an underlying genetic predisposition. They do not have a secondary cause for their seizures and neuroimaging is usually normal.  On the other hands patients who have secondary epilepsy usually have seizures secondary to something (example secondary to brain tumor, secondary to an abscess in the brain, after a stroke and so forth). Under this category of secondary epilepsies is included post traumatic epilepsy (as the name suggests patients have seizures secondary to brain trauma).

Let me explain with the aid of an example.  Let us assume our patient (we shall call him Philip) is a 27-year-old healthy male with no significant medical or surgical history. Bikes are his passion especially Harleys.  Have you seen the ones they show on American Chopper. But we are digressing from our story line. Philip loves to ride them fast. A bright sunny Sunday morning finds him zipping down FDR drive at 80 mph.  With a bike under me, I felt like a real man. And then disaster strikes. Philip’s bike gets clipped by a speeding SUV. Philip is flung from the bike and hits the ground hard. Did I mention he was not wearing a helmet at this time. He is rushed to the nearest hospital. A lacerated spleen, couple of broken ribs and a fractured collar bone. Not too bad you might say. He shall live to ride another day. But all is not so rosy. Philip does not regain consciousness and does not respond to verbal commands.  A quick CT scan yields the answer. Philip has suffered extensive bleeding in the brain (neuro trauma). He is admitted to the neurological ICU. Recovery is painfully slow and after a months stay in the hospital, Philip is discharged to a sub-acute rehab facility. Alls well that ends well? Not quite done yet, I am afraid. Six months after his motorbike accident, Philip is again rushed back to the hospital after a witnessed tonic clonic convulsion. He is evaluated by a neurologist (like me) and a diagnosis of post traumatic epilepsy is made.

So what exactly is post traumatic epilepsy? As the name suggests epilepsy develops after head injury. Seizures can occur anytime after head injury. If they occur immediately after head injury it is referred to as immediate post traumatic epilepsy (also called impact seizures, as seizures occur at the time of impact to head).  If seizures occur within the first month after head injury it is referred to as early post traumatic epilepsy. Patients may have their first seizure as long as 18 months after head trauma. This is referred to as late post traumatic epilepsy.

Patients develop post traumatic epilepsy as a result of scarring of brain tissue.  They usually have convulsions. The treatment of post traumatic epilepsy is essentially the same as that of any other type of epilepsy. Once the seizure type is characterized, the right anti-epileptic drug is usually effective in controlling the seizures.

Braindisease Weblog

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I wanted to thank all my readers for their comments and suggestions.  I shall try to improve this blog further. Bear with me though, it is a solo endeavor. Most of the posts are written on the run and so if my grammer or spelling is off, please excuse me.

Personal Regards,

Nitin Sethi, MD

Disclaimer

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Please do read my disclaimer. The purpose of my blog is purely educational and to disseminate information about neurological and neurosurgical diseases and condition. It is not meant to diagnose yourself over the Internet.

The information provided in this blog should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. A licensed medical professional should be consulted for diagnosis and treatment of any and all medical conditions. Call 911 if you have a medical emergency.

Links to other sites are provided for information only — they do not constitute my endorsements of those  sites.

 Any duplication or distribution of the information contained herein is strictly prohibited.

 

 

Nitin Sethi, MD

Incidentally discovered aneurysms in the brain-what to do about them?

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Incidentally discovered aneurysms in the brain-what to do about them?

 

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 my office. She had undergone a MRI scan for headache. The MRI scan revealed a 4 mm aneurysm in the left middle cerebral artery with a 2 mm neck. I reassured her that the aneurysm was not the cause of her headache and that she more than likely had migraine headaches when she asked me the million dollar question which I had been expecting all along.

Dr. Sethi, but what to do about the aneurysm? Can it rupture? Do I need surgery to take care of it she asked me? I answered her questions according to the best scientific evidence I had at my disposal. That patient visit though got me thinking about how many patients face the same dilemma. That is the purpose of this post. When aneurysms are discovered incidentally in the brain, what needs to be done?

In keeping with my style of writing, I shall keep this simple. Simply put when an aneurysm is discovered in the brain, there are 2 avenues open to us.

 

Avenue 1. DO NOTHING (otherwise called the WAIT AND WATCH policy). The aneurysm may never rupture in the patient’s lifetime so why touch it. The wait and watch policy works best for aneurysms which are small in size (less that 5 mm in size, some books say aneurysms less that 7 mm in size may be safety observed). Small sized aneurysms in hard to reach areas of the brain can be justifiably observed. What do I mean by hard to reach areas of the brain? Let me explain with the aid of an example. Let us assume Kim our fictitious patient has a 3 mm aneurysm in the cavernous portion of the left internal carotid artery. This is the portion of the internal carotid artery that traverses the cavernous sinus. Now this area is difficult to reach “safely” by the neurosurgeon. The risks of surgery are tangible and may outweigh the potential benefits (remember as the aneurysm is small in size the risk of rupture is low). Better to wait and watch rather than go about chasing this aneurysm.

I said WAIT AND WATCH not WAIT AND FORGET. Meaning the patient should be advised to remain in follow up. The aneurysm should be followed by serial MRI scans done at intervals varying from 6 months to 1 year. Initially the follow up is more frequent, once we have documented that the aneurysm is not increasing in size, the scans can be repeated less frequently. If the aneurysm starts increasing in size then a more “active” course can be pursued. If the patient is hypertensive, good blood pressure control should be the goal as risk of aneurysm growth and rupture increases if blood pressure remains elevated.

 

Avenue 2. PURSUE AN ACTIVE STRATERGY. Simply put it means “taking care” of the aneurysm surgically either via open craniotomy or via an endovascular approach. Let me explain this. Let us assume Kim has a 10 mm sized aneurysm is the right middle cerebral artery territory. We can approach this aneurysm in 2 ways. First is via an open craniotomy, meaning that open up the skull (we call this a craniotomy), visualize the aneurysm and then secure it with a clip or a band. Once the aneurysm is clipped it cannot rupture as it is excluded from the circulation. PROBLEM SOLVED!!!

 

Second approach is via an endovascular route. No craniotomy is required. The endovascular surgeon or the interventional neuroradiologist threads a catheter via the femoral artery in the groin and reaches the aneurysm in the brain. Once there he coils it (coils of platinum coated with a thrombogenic material are deployed inside the aneurysm). Over time the aneurysm clots and seals itself from the circulation. PROBLEM SOLVED!!!

 

Broadly speaking endovascular coiling is superior to open craniotomy (at least in some respects). As no craniotomy is required hospital stay is shorter and post-operative recovery quicker. The endovascular surgeon can reach areas where the neurosurgeon may fear to tread. Certain aneurysm though are not amenable to coiling (example those with a broad neck as the coils fall out). Also once an aneurysm is coiled it takes time before it gets completely thrombosed, surgery on the other hand takes care of the problem then and there.

A Doctor’s Point of View on the Doctor Patient Relationship

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I recently did an interview on the doctor patient relationship. Here I reproduce just a small part of it.

You can read the whole interview on Multiple Sclerosis Central.com by clicking on the following link.

http://www.healthcentral.com/multiple-sclerosis/c/73302/70302/patient

I have asked Doctor Nitin Sethi to contribute to this discussion through an interview about this very topic of the doctor-patient relationship.  Doctor Sethi will discuss this relationship from a doctor’s point of view and in part two of this series we will examine the same relationship from a patient’s perspective.  The patient will be me.   I do encourage you to offer your viewpoints through the form of comments to these articles.

 

I introduce to you:  Nitin K Sethi, MD who is the Assistant Professor of Neurology at New York-Presbyterian Hospital of Weill Cornell Medical Center located in New York City.

 

What do you feel are some of the personal qualities which are important for a doctor to develop rapport and trust with patients?

 

A lot has been written about doctor patient relationship and what qualities define it. Nowadays in medical school itself there is a thrust not just to produce smart doctors but also to produce more humane doctors. A study had shown that student doctors (medical students) have the highest levels of empathy. As they go through their long training (residency and at times fellowship), this empathy progressively decreases. One may argue that “experienced” doctors become less humane. I do not buy that argument. I feel the empathy gets replaced by knowledge. You know what you are dealing with and you understand disease pathology better. This might make a doctor sound aloof and like a “machine”.  He is very good at what he does but he is cold and aloof.

 

My patients frequently tell me that they left their previous doctor because he would not hear them out or he was not caring enough. They rarely say I left him because he was incompetent. I want to make this point to answer your question. Some of the smartest doctors I know (people I would go to if I had a neurological problem) do not have the greatest bedside manners. They are not most suave. But as a patient I would rather go to a competent doctor than to one who says all the right things in the right way but is not the smartest light.