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 disease of the brain: what do we know about it? Should I worry?

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I frequently get asked about white matter disease of the brain. It is commonly reported when MRI scans are carried out causing concern to patients and family alike. So in this blog post that is the topic we shall discuss.

Just what is white matter disease of the brain? As you all may be aware of in very simple terms the brain is made of grey matter (comprising the cell bodies of the neurons) and white matter (fiber tracts). Think of white matter disease as changes seen in the white matter of different parts (lobes) of the brain visualized on a MRI scan of the brain. Either the white matter appears scarred or atrophic. If the white matter is examined under the microscope, degenerative (ischemic) changes are visualized in the small blood vessels hence the term ischemic microvascular small vessel disease is sometimes used. A point to remember here is that these white matter changes visualized on the brain MRI can be seen in many different diseases of the brain-diseases as diverse as leukodystrophies, nutritional deficiencies, toxic drug exposures, vascular dementia and multiple sclerosis (MS). So the radiologist’s report invariably lists all these differential diagnoses and when patients read their MRI report they get worried. Many write in to me asking me if they have MS.

White matter changes on brain MRI need to be correlated with the patient’s history and examination findings and that is where I as a neurologist step into the picture. Let me explain with a few examples:

1. A 29-year-old woman with history of acute loss of vision in one eye (optic neuritis) . MRI brain shows white matter lesions in a characteristic distribution (perpendicular to the long axis of the lateral ventricles). In this case multiple sclerosis is high up in the differential.

2. A 29-year-old woman with history of episodic headaches which are usually unilateral, throbbing in quality and accompanied by nausea and photophobia (brights lights bother her during the headache episode). MRI brain shows a few non-specific white matter lesions scattered in the brain. In this case the most likely diagnosis is migraine headaches.

3. A 75-year-old woman with complaints of memory impairment. MRI brain shows white matter lesions scattered diffusely in the frontal and temporal lobes. In this case vascular dementia is the diagnosis which comes to mind.

Should white matter disease of the brain be treated: if the white matter disease of the brain represents ischemic white matter disease it may be prudent to address vascular risk factors such as better control of hypertension and diabetes, lowering the cholesterol and advising the patient to stop smoking. There is now increasing evidence that white matter disease may cause cognitive impairment and may coexist with other causes of memory impairment such as Alzheimer’s disease in the same patient. On the other hand if the white matter lesions are demyelinating lesions of MS, then treatment is aggressive treatment of MS. If they are due to migraine then usually no treatment is warranted.

In children the cause of white matter disease of the brain is different. Various leukoencephalopathies, metabolic, hereditary and degenerative diseases are in the differential and have to be screened for and ruled out systematically.

I hope this small post helps to answer some of my readers concerns.

 
Nitin K Sethi, MD

Dementia-it comes in many forms

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As a neurologist I frequently see patients who complain of memory impairment and forgetfulness. Some consult me primarily for this problem; many others who have come to consult me for some other problem such as headaches voice this concern during the course of their patient interview. All are concerned that they may have dementia. So in this post I shall discuss dementia. In keeping with the style of writing on this blog, I shall keep it simple and free of excessive medical jargon.

So what is dementia?

Broadly speaking dementia may be defined as a disorder in which a person experiences problems in multiple cognitive domains. So for example a patient who has moderate Alzheimer’s dementia shall experience problems with memory (cannot recall old information and may not be able to make new memories), speech (speech is sparse, vocabulary is markedly decreased), may experience problems with calculation, concentration, executive functioning (such as planning for the future), balancing his check book and learned tasks (such as tying his shoelaces, driving a car, using a spoon to eat, brushing his teeth). Family and friends may notice a change in personality (patient might becomes disinhibited, aggressive, argumentative or quieter and mute) and behavior (disruption of sleep wake cycles, night time wandering and so forth). A point to note here is that the motor and sensory parts of the brain remain largely intact so the patient is not weak if formal strength testing is carried out. The disease predominantly affects the higher mental functions—that is the functions which separate us from animals and make us so unique as a species—aka our ability to think, to calculate, to remember, to speak and our individual personality and behavior.

How does dementia present in the early stages?

The onset of dementia is usually subtle. In the early stages of the disease, the patient appears “normal”. Social graces are maintained. Appearance remains well groomed and if you meet such a person casually at a party you shall not mind anything miss. The patient also remains independent in all activities of daily living (ADLs) for example he can brush his own teeth, wear his clothes without any help, drive or take a bath. They may also be able to maintain/keep their jobs. This stage has been referred to minimal cognitive impairment or MCI for short. Further on from here things become trickier. A person may remain in MCI stage and not progress further or progress very very slowly. We still do not know the reason for this. Why some patients remain in MCI stage and do nor progress further. Others may advance on to frank dementia. Why this occurs in some patients rather abruptly and quickly as compared to others is still not known. As the patient advances from moderate to severe dementia he becomes progressively more and more dependent on care givers for ADLs.  In the late/final stages of dementia, the patient is bed bound, mute, totally dependent on care givers, stiff and incontinent of both urine and feces.  Death usually occurs due to superimposed infection such as pneumonia, sepsis or a urinary tract infection.

Are there different types of dementia?

There are indeed many different types of dementia: Alzheimer’s dementia, frontotemporal dementia (Pick’s disease), diffuse Lewy body dementia, dementia of Parkinson’s disease, vascular dementia and so forth. A dementia like clinical picture may also result from certain infectious diseases such as AIDS dementia complex also called HIV encephalopathy and mad cow disease. Vitamin B12 deficiency, hypothyroidism, chronic alcoholism, syphilis are other conditions which may cause a picture indistinguishable from primary dementias such as Alzheimer’s disease. It is important that these be looked for and ruled out since they are treatable causes of memory impairment.  If depression is present, it should be identified in a timely fashion, treated and then the patient should be reassessed.

A point to note here is that all the above mentioned conditions present clinically in much the same fashion. It is indeed quite difficult if not impossible to make a definitive diagnosis such based on history and examination findings as clinical features overlap.  Ancillary tests such as MRI brain, PET and SPECT scans may help to narrow the differential diagnosis. In the near future we remain confident that we shall be able to diagnose the different types of dementia more accurately and more importantly early on in the disease course.

How is dementia diagnosed?

 

The diagnosis of dementia till today remains predominantly clinical. By that I mean that the diagnosis is made after taking a thorough history and after considering the examination findings. In my personal experience I have found a good neuropsychological evaluation conducted by an experienced neuropsychologist as particularly helpful.  MRI brain, PET and SPECT scans are helpful and may help narrow the differential diagnosis and in ruling out other conditions which may mimic dementia. A EEG study is useful and helps to collaborate the examination findings. There is a tremendous thrust to identify biomarkers for dementias such as Alzheimer’s disease both in the blood and the cerebrospinal fluid (CSF). In the same vein, MRI biomarkers are also getting close inspection and may be ready for clinical use in the near future.

How is dementia treated?

Primary dementias such as Alzheimer’s disease, frontotemporal dementia and dementia of Lewy body are progressive neurodegenerative conditions. At present we have no cure but there are drugs available which may slow down the rate of cognitive decline and ensure better quality of life both for the patient and the family members who care for them. None though is a magic wand and none work once the dementia is moderate to severely advanced. Research continues at a feverish pace and I remain confident of a breakthrough in my lifetime.

Can dementia be prevented?

Or rather can I take any steps now so that I do not get dementia in my later years? Many drugs, herbal and other supplements have been looked at, tested but none have shown a consistent benefit. High dose vitamin E supplementation did not work. Gingko does not work. This is what I advice my patients:

If they have vascular risk factors such as hypertension, diabetes mellitus or high cholesterol, these should be aggressively controlled.

Do not smoke and if you do—stop.

If you do have vascular risk factors, speak to your doctor about taking a tablet of baby aspirin daily. Follow his advice.

Exercise, exercise, exercise. There is ever more research that exercise is neuroprotective.

If you are big on supplements, I advice taking Vitamin B12 500 micrograms once or twice daily and fish oils (omega 3 fatty acids). Again speak to your doctor before you take any supplements.

Attacks of major depression “hurt” the brain. So depression should be identified and treated.

Nitin K Sethi, MD

I have infrequent seizures: to treat or not to treat? -that is the question

braindiseases1 Comment

A great question from a concerned sister. My reply follows.

 

Hi Dr Sethi,

Thank you for your very informative site. My brother was recently diagnised with complex partial epilepsy. His seizures (that he is aware of at least) are very few and far between, on average one every two to six months. He says he knows in advance when the sezures are beginning as he starts with loss of vision slowly in one eye and then the other and then his hands go numb.

He feels that the side effects of the medication interfere with his busy schedule and active lifestyle and has opted not to take any medication due to the long periods between seizures. Is this advisable? If his condition is left untreated could it progress or cause any irreversible problems?

Thank you,
K

 

 

Dear K,
you have asked a very valid question and one that I have confronted personally at many times as a neurologist and epileptologist. If seizures are few and far inbetween do they warrant to be treated? There is no consensus on this. Let me explain in my usual simple way.

Argument in favor of not treating them:

1. At times patient’s get an aura and know their seizure is coming and feel they can take precautions such as sitting down if they are standing or pull over to the side of the road if they happen to be behind the wheel of a car when the aura starts. So the patient feels that since he has only infrequent seizures and that too accompanied by a reliable aura, why take an anticonvulsant medication.

2. Moreover every anticonvulsant has its own side-effect profile. Frequently the side-effects are unpleasant and so if possible the patient would like to avoid taking the medication on a regular basis.

3. Anticonvulsants have to be taken on a daily basis, some medicines have a twice daily or three times a day dosing. This interferes with their lifestyle.

4. If the seizures are few and far inbetween (like for example a patient who suffers one seizure every year), does it make sense to take a medicine on a daily basis (at times with unpleasant side-effects)?

 

 

Arguments in favor of treating these infrequent seizures:

1. One of the biggest problems with seizures is their unpredictable nature. A seizure can occur anytime, sometimes out of the blue when the patient least expects it. Moreover one does not want to have a seizure at the wrong place and the wrong time like for example when one is driving or when one is waiting by the side of the rail track or when one is swimming. Seizures can be associated with falls and injuries. Hence it makes sense to treat the seizures and aim for good seizure control no matter how infrequent the seizures may be. Many patients feel more confident when they know they are on an effective anticonvulsant and shall not have a seizure out of the blue.

2. In majority of the countries there are laws with respect to driving if you suffer from epilepsy. A patient may not like to risk loss of his driving privileges and independence if a seizure was to occur. He would rather take an anticonvulsant on a daily basis no matter how infrequent his seizures.

So you can see there are good arguments on both sides. Your brother’s doctor shall be the best person to turn to for advice.

Personal Regards,

Nitin K Sethi, MD

Seizure disorder/ epilepsy: making the diagnosis. The role of an EEG.

braindiseases2 Comments

 

A question and an answer.

R

Hello Everyone, I am glad to meet you. I am new here.

I noticed that a lot of you are having seizures, as well as your diabetes. Seizures are a complication of diabetes. I am going to give you a link:

I also have epilepsy, diabetes and Alzheimer’s. When I was diagnosed with diabetes, I stuck to my diet. My seizures are under control now.

When you have hypoglyclemia, you can have seizures, coma and death. The same is true of hyperglycemia..When your blood glucose goes to low, you need to have a small snack. i never let my BG goes below 90 or higher than 140.

Take care of your diabetes diet and you should not have any problems.

The reason your hypoglycemia seizure does not show up on the EEG, is because it is a Diabetic Seizure. Only epileptic seizures will show up on an EEG.

Your Friend, R

 

 

 

 

Dear R,

Thank you for writing in. I am glad you are taking such good control of your blood sugar. You say only an epileptic seizure shall show up on an EEG and not a diabetic seizure–that is not quite true. A seizure is a seizure and if you happen to have one while the EEG is running, it shall be recorded on the EEG.

What you are mentioning R is what we neurologists refer to as interictal epileptiform discharges. Think of them as abnormal blips which show up on the EEG when the EEG study is done inbetween the seizures (inbetween means the patient has an EEG study when he or she is not having a seizure at that very moment). Patients who have underlying epilepsy may show interical epileptiform discharges. On the other hand those who have seizures provoked by metabolic factors (low blood sugar–hypoglycemia, low sodium–hyponatremia, low calcium or magnesium) or toxic factors (excessive intake of alcohol or use of a recreational drug such as cocaine) usually do not show interictal epileptiform features and the EEG is frequently reported as normal.

Here I want to emphasize a point. The diagnosis of a seizure disorder/ epilepsy is not made simply based on an abnormal EEG. Put in another way, a normal EEG does not rule out or rule in epilepsy. Many epileptics may have normal EEGs even when the test is repeated many times. Conversely there are people who have abnormal EEGs but no epilepsy. Hence the diagnosis of a seizure disorder (epilepsy) is made based on a thorough history of the patient event (convulsion): what led to the event, what happened during the event, the clinical semiology of the event, whether there were any provoking factors and so forth. The past medical history is explored (any history of significant head trauma, any history of meningitis or encephalitis). The medications the patient was taking at that time are reviewed. Even the birth history is reviewed–was the patient born full term, were there any complications during child birth such as lack of oxygen.

 

 

Nitin Sethi, MD

 

Disclaimer

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Please read my disclaimer posted here and on my website http://braindiseases.info. The information presented on this blog is for information and educational purposes only. It is not a substitute to an actual visit to your physician. Also your physician is the best person to answer all your queries.

I again urge all of you who post on this blog to post under a fake name and fake email id. Medical information should always remain private.

 

Nitin Sethi, MD

Seizures associated with alcohol intake: to abstain or not to abstain that is the question

braindiseases

A reader of my blog wrote in to me. As has been the trend, I try to answer each and every question though lately I have to admit I have fallen back in this quest mostly due to constraint of time. I promise to be more timely in my replies going forward.

 

Here is his question. My answer to it follows:

 

HI, I was 21 when I had a seizure, following a weekend long music festival and drinking heavily and consuming amphetamines. Had about 5 or 6 following this up to the age of 25, mostly following drinking heavily and sometimes consuming amphetamines and/or diazepam. Have not taken any illegal substances since and now in my 30′s. Still drink regularly. No seizures and spent a few years taking a very low dose-100/200mg of epilim chrono(sodium valporate). Have not taken medication for 4 yrs approx. A junior doctor told me(while the consultant had left the room to fetch something) that he had studied this for his theses and it was very common for young adult males to “develop” seizures but assured me I would grow out of it, which appears so far(touch wood) to be true. Is there any truth in this? Is my case prob related to drink/illegal substance misuse?

 

S

 

 

Brain diseases reply:

 

Dear S,

Thank you for writing in to me at www.braindiseases.wordpress.com. I shall answer your question to me in a unique way. Here we go.

 

As a neurologist with interest in epilepsy I frequently encounter patients with history similar to yours. After a night of heavy drinking (usually different types of alcohol are consumed over a short course of time), at times along with other illicit drugs such as cocaine, amphetamines and more commonly prescription drugs such as Xanax and Valium (diazepam), lo and behold the person is witnessed to have a generalized convulsion soon there after (either that night itself or early next morning). The first encounter these patients have with the health care system is in the ER to which they present or are brought to by the EMS for evaluation. Now imagine that you are a physician in the ER and evaluate such a patient in the middle of the night. You are pressed for time. What shall be your assessment and plan? You shall order a few basic blood tests and a CT scan of the brain. CT scan comes back normal and the basic labs are normal too. Most of the times these patients are discharged from the ER after starting them on an anticonvulsant  (sodium valproate, phenytoin (Dilantin) and levetiracetam (Keppra) are the most commonly chosen drugs) with advice to follow up with a neurologist like me.

 

Now you may think that this “case” is closed but that is a fallacy.

 

Many questions remain unanswered:

 

  1. Was the seizure indeed induced by alcohol and the combination of illicit drugs? How sure are we of this fact? :  if this is indeed a seizure induced by alcohol and illicit drug use then surely the patient does not need an anticonvulsant drug. If he stops drinking/binging and stops illicit drug use he shall not have any more seizures.
  2. How long should the anticonvulsant medication continue?
  3. Can he drink a “little” amount or is alcohol completely off the bargaining table? Does he have to abstain for life?
  4. Who was the actual culprit—alcohol alone Vs alcohol in excess Vs alcohol and illicit drug combination Vs illicit drug by itself?
  5. Does the patient have an underlying seizure disorder (tendency to have seizure/ underlying epilepsy) and that alcohol/illicit drug combo was just the fuse. Such a patient of course shall warrant treatment with an anticonvulsant. Again more questions: which anticonvulsant and for how long? Does he need to be treated for life? If he takes an anticonvulsant can he again start drinking?

 

There is no one right answer to the above questions. No one size fits all model here. The answer to each has to be personalized to the patient at hand. Fortunately to answer the above questions as a neurologist I do not need expensive tests. All I need to do is to spend time with the patient and get a thorough history. In some cases I may order an electroencephalogram (EEG).

 

The rest is easy. Hope you found my answers insightful.

 

Nitin Sethi, MD

Post Traumatic Epilepsy: when head trauma leaves behind a seizure disorder

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Recently I have seen a few patients with post traumatic epilepsy and hence I decided it might be appropriate to talk about the same in more depth.

Before we begin though I want to wish all the readers of my blog from around the world a very Happy and Healthy New Year 2012. May it bring you not just a healthy brain but also a healthy mind.

Ok now to the topic at hand. Just what do neurologists and neurosurgeons mean when they say you have post traumatic epilepsy? As the name suggests post traumatic epilepsy (PTE) refers to epilepsy/seizures starting after a patient sustains head trauma. Let me explain with an example. Let us assume John is involved in an motor vehicle accident. While driving down the FDR drive late one night he falls asleep behind the wheel of his car. The roads are icy! John’s car spins out of control, jumps the curb and hits an embankment.  John who is not wearing a seat belt gets thrown out of the car striking his head first on the windscreen and then on the unyielding asphalt concrete. A passerby witnesses the accident and calls 911. EMS are on the screen within minutes but John is not moving. His neck is stabilized in a hard collar and he is rushed to the nearest hospital. Glasgow coma scale  (GCS) on arrival is documented to be 5. John is not responding to verbal commands and is rushed to the CT scanner for a stat head CT. CTscan shows all is not well. John has sustained significant head trauma. He has a fracture of the right temporal bone and an underlying epidural hematoma. There are bilateral frontotemporal contusions which are increasing in size. In addition there is diffuse subarachnoid hemorrhage. The epidural hematoma is evacuated that night itself by the neurosurgeon on call. It is decided that at present the frontal lobe contusions be closely observed. John is transferred to the neurological ICU where he is further stabilized. A close watch is kept on the intracranial pressure.

Fast forward 3 weeks.

After a rocky course in the neurological ICU, John makes a remarkable recovery taking the extent of his head injury into consideration. He is discharged from the hospital to a rehab facility skilled in traumatic brain injuries (TBI). In the rehab facility John makes a slow but steady progress. It is 12 noon and John as usual is working with his physical therapist. He suddenly stops what he is doing. Utters a loud guttural sound, falls down to the floor with his eyes rolled up. The therapist notes that he stiffens up for a few seconds and then starts to shake while frothing at the mouth. The whole seizure lasts for about 2 minutes and then subsides on its own. Post seizure John is confused and disoriented but slowly returns to his baseline in about 40 minutes. An appointment is made for John to see Dr. Feelgood a neurologist in the nearby community hospital.

Dr. Feelgood takes a detailed history and then examines John. You have post traumatic epilepsy John, he says and recommends that John consider starting anticonvulsant therapy without further delay.

The scenario I describe above is unfortunately not uncommon in patients who sustain significant head trauma. In fact head trauma is one of the leading causes of epilepsy in men and women below the age of 40 around the world. The human brain is well protected by an extremely rigid skull and so the trauma has to be significant to cause brain damage and resulting PTE.

MINOR BUMPS AND BRUISES TO THE HEAD DO NOT LEAD TO POST TRAUMATIC EPILEPSY. Post traumatic epilepsy is thus very rarely reported after closed head injuries aka concussions such as those sustained on the sport fields(please read my post about concussions either here or on my website http://braindiseases.info). On the other hand PTE is particularly common after penetrating head injuries such as gun shot wounds to the head or when the skull bone is fractured (especially depressed skull fracture where the bone fragment presses on the underlying brain) or when there is significant intracranial bleeding (remember what John’s CT scan showed: blood in the epidural space and hemorrhage into both the frontal and temporal lobes).

Seizures can occur at any time after a significant head injury. The patient may start having seizures immediately after sustaining the head injury. This is called early post traumatic epilepsy and at times this has a more favorable prognosis. After the blood in the brain goes away and the swelling/pressure in the brain subsides, the seizures may also stop spontaneously. Hence these patients may not need to remain on an anticonvulsant medication for a long time. Seizures though have been reported as far out as 5 years after the head injury. This is called late post traumatic epilepsy and these patients usually need to take anticonvulsant medication for a prolonged duration, at times even lifelong.

Depending on the extent of head trauma, seizures may be easy or hard to control in these brain trauma patients. They are usually prescribed anticonvulsant therapy and seizure control is then closely monitored. If seizures persist then a second or third anticonvulsant may be indicated.

Dr. Feelgood started John on a seizure medication by the name of levetiracetam. He advised John to follow up with him after 3 months. On the 3 month follow up visit, John walked into Dr. Feelgood’s office unaided and with a broad smile on his face.

I feel good, Dr Feelgood he said.

Transverse myelitis: a question and an answer

braindiseases1 Comment

A question from one of my readers. My reply to it follows.

 

 

Dear Sir/Madam,

I am under a Neurologist’s care at present. A few weeks back I had tingling, numbness, stiffness in my right wrist, within days/hours this spread from my hand to my neck all the way down the right side of my body. CAT scan and xray clear. MRI scan shows an abnormality within the upper part of the cervical spine consistent with demyelination. Also shows a single small focus of abnormal signal in the left frontal region. He feels it possible I may have an isolated episode of tranverse myelitis. I also have an odd sensation when I put my chin on my chest, I have felt this for approx 6 months plus, it feels like an elastic band stretching, not painful just an odd feeling. The symptoms have not got better 3 weeks on and now I feel the same tingling in my left fingers the same as this started in the right side. I have been given MEDRONE today (19/12/11) 100mg and told to take 5 tablets all in one go so I have 500mg dose. Not sure I like the feeling that comes with these tablets and thats spacing them out, don’t think I could take them all together. Any feed back would be greatfully appreciated. I’m 41 years old, fit and healthy usually, work hard, mum of 2. Just had an early diagnosis of menopause. Many thanks. Kind regards. N

 

 

Dear N,
thank you for writing in to me. From your history it seems you were diagnosed with transverse myelitis. Transverse myelitis (TM) as the name suggests is an inflammatory process of the spinal cord and usually involves the cervical or thoracic spinal cord. MRI of the cervical spine further helps to characterize it: complete TM Vs incomplete TM.

 

There can be many causes of TM: inflammatory/demyelinating (multiple sclerosis among other diseases), infectious causes, paraneoplastic, postvaccinal (drugs and other toxic causes) and autoimmune/collagen vascular diseases. Sometimes inspite of an extensive work-up no cause can be determined. This is termed idiopathic TM.

 
Based on the site and extent of the lesion, the symptoms vary. If the patient has a complete TM high up in the cervical cord (like around C5-C6): there is usually involvement of both arms and legs (quadriparesis). The bladder and bowel function may also be affected. If the lesion is small and eccentrically placed in the cervical cord (incomplete TM), the symptoms may not be so symmetrical and the patient may present with numbness and weakness in one arm and leg. If the lesion is below C6-C7, usually the arms are spared and only the legs are involved.

 
You say you experience an odd sensation when you put your chin to your chest. What you are experiencing is called the Lhermitte’s sign (LS). It is an electric/shock like sensation which runs down the back and into the limbs and is elicited by bending the head forward. This occurs because the nerve tracts (dorsal columns which carry sensations such as joint sense, vibration sense and position sense) running down the cervical spine are damaged. LS is a nonspecific sign and can be seen in many diseases which involve the dorsal columns. Transverse myelitis is one such disease process and hence this sign can be elicited in some patients.

 
Once a patient is diagnosed with TM, an extensive evaluation is carried out to determine the cause of TM. The diseases some of which I have mentioned before are looked for and meticulously excluded. MRI of the brain and other tests to rule out multiple sclerosis may be carried out (as it seems were done in your case) to secure the diagnosis–is the TM because of some underlying disease and if so what is the disease or is the TM truly idiopathic?

 
Treatment of TM depends upon the cause of TM. Like for example if the TM is due to a demyelinating disease such as multiple sclerosis, the treatment involves treatment of MS with immunomodulating drugs. If the cause is infectious, then the underlying infection is treated. If the patient has idiopathic TM and in some cases of inflammatory MS, then based on the time of your clinical presentation, your doctor may decide to treat you with high dose steroids (usually 500-1000mg of methylprednisolone is given once a day for 3 to 5 days). This helps to hasten recovery.

 
I hope I have answered some of your questions N.

Personal Regards,

Nitin Sethi, MD

 

Types of seizures: a question and an answer

braindiseases1 Comment

One of the readers of my blog sent me this question.  Thank you for the same. My answer follows.

 

QUESTION

I experienced something a few days ago. Without any warning as I was getting out of my chair, I hit the floor hard. I woke up after a few seconds and I was in a cold sweat, shaking and confused. I tried to get up, but, I couldn’t move for another few seconds. I am under a Neurologist’s care and he suspects complex partial seizures due to an abnormality on an EEG, but, he is not too sure. I went to the ER and everything seemed normal. I had another episode a few days later, the same thing, except this time I was just walking from one room to another and it happened. I have no idea what this could be. I have been accused of “spacing out” and I have callouses on my left finger knuckles. I never realized I was rubbing my fingers enough to get callouses. Is this seizure or just passing out? So confused!!

ANSWER

Dear so confused,

thank you for writing in. The episodes do sound suspicious for seizures though as my post indicates there is a broad differential of sudden unexplained loss of consciousness. Broadly speaking there can be three types of seizures:

1. Generalized seizures: as the name suggests in primary generalized seizures, the seizure starts off from the entire brain at the same time. So for example if you were to suffer a generalized seizure while the EEG is running, the EEG will show abrupt onset of epileptiform activity from the entire brain (both the hemispheres). Primary generalized tonic clonic seizures (at times referred to as grand mal seizures) are quite dramatic. If the person is standing when the seizure strikes, he shall suffer loss of body tone and fall down. Patients usually strike the ground hard and may suffer craniofacial injury as a result. There is complete loss of consciousness (so the patient shall be amnestic for the seizure). There is an initial tonic phase where in the body stiffens. This is soon followed by a clonic phase where in rhythmic inphase jerks of the limbs are observed. The patient may suffer a tongue bite or may suffer loss of bladder control during the ictus. The seizure itself lasts for about a minute or two and is followed by a more prolonged post ictal phase during which the patient has stopped shaking but is somnolent and difficult to arouse. The past ictal phase may last for about an hour with slow recovery to complete consciousness and a return to baseline. Of note the staring spells seen in children (also called Absence Epilepsy) is a type of generalized epilepsy.

2. Focal seizures/ partial seizures: as the name suggests these are seizures which arise from a focal area in the brain. Focal seizures are not accompanied by a complete loss of consciousness. Rather there is impairment in the level of consciousness/ awareness. Let me explain further. Let us assume that you are right handed. In people who are right handed, the left hemisphere is the dominant hemisphere and in the left temporal lobe is the speech center. Let us assume you suffer a focal seizure arising from the left temporal lobe. There shall be a sudden arrest in your behavior and you may stop speaking (since the left temporal lobe is now misfiring). If I speak to you at this time, you shall not reply back to me and you may not recall that I had spoken to you later. That said unlike a generalized seizure, you do not fall down and do not convulsive. Patients do display some non purposeful movements such as lip smacking and picking at the clothes. This is referred to an automatisms.  Prior to the onset of the seizure, patients may report an aura. The typical auras which are reported including an unpleasant smell (burning rubber), rising sensation in the tummy, a spinning sensation, unpleasant taste, psychic phenomena such as fear and so forth. This type of seizure is what we doctors refer to as a complex partial seizure (complex because awareness is impaired).

3. Focal seizure with secondary generalization: I think this is simple to understand now. The seizure starts off as a focal seizure but then spreads and crosses over to the other side of the brain and very soon (in a matter of milliseconds) the entire brain is showing the epileptiform activity. So initially you have a behavioral arrest and cannot speak but then very soon your entire body tenses up and you start convulsing.

There are other types of seizures some of which occur in the pediatric age group. At present I shall not dwell on them.

I hope I have been able to explain seizures to you in very simple terms. Follow up with your doctor. My very best to you.

Personal Regards,

Nitin Sethi, MD