Author: braindiseases

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

Narcolepsy Vs idiopathic hypersomnia-do we need to care?

braindiseases15 Comments

Two half days a week I see patients in the sleep center. One of the reasons patients come to see me is for excessive daytime sleepiness (EDS). Patients may voice the above complaint in different ways. Some say [Dr. Sethi my biggest problem is that I feel sleepy during most of the day. I find it hard to concentrate at work or my mind feels “dull”]. Others may say they find it difficult to wake up in the morning in time for work or college. The history may be more worrisome: the patient may have fallen asleep while driving. So how does one differentiate between the various causes of EDS? In this post I shall touch on these very topics.

The various causes of EDS can be broadly listed as follows:

1. Untreated sleep disordered breathing: Obstructive sleep apnea (OSA), Central sleep apnea (CSA), Mixed sleep apnea (MSA).

2. Poor sleep hygiene

3. Circadian rhythm disorder: Delayed sleep phase syndrome (DSPS), Shift work disorder

4. Narcolepsy: primary and secondary

5. Idiopathic hypersomnia.

6. Medical disorders causing poor sleep at night.

Narcolepsy: is characterized by excessive sleepiness. It may or may not be associated with cataplexy. Cataplexy in simple terms refers to loss of muscle tone. Let me explain with the aid of an example. Let us assume a narcoleptic patient hears a joke. He starts laughing and suddenly experiences loss of muscle tone and finds himself on the ground. This sudden loss of muscle tone is referred to as cataplexy. Another example of cataplexy is a runner who collapses when the starter gun goes off. Narcolepsy is usually accompanied with sleep paralysis and vivid hallucinations which are reported either at onset of sleep or when the patient is about to wake up (that is around sleep-wake transitions). A point to note is that if the patient has cataplexy then the diagnosis of narcolepsy is easy to make. It is narcolepsy without cataplexy that is tough to diagnosis. A caveat to remember here is that not “everything” is cataplexy-so weakness in the knees if you have been laughing hard does not constitute cataplexy. Narcolepsy occurs due to the loss of hypocretin neurons in the lateral hypothalamus. So secondary narcolepsy may also occur if these neurons are damaged by a hypothalamic stroke or a hypothalamic tumor or by a infectious/ inflammatory process (limbic encephalitis). The clinical presentation of secondary narcolepsy though is different: example the history is of excessive sleepiness after a stroke or a tumor.

The diagnosis of narcolepsy is made on the basis of an overnight polysomnography (sleep study) which is done to rule out sleep disordered breathing (sleep apnea). One needs to make sure that the patient does not have untreated sleep apnea before the EDS can be attrbuted to narcolepsy. The patient also undergoes a test called multiple sleep latency test (MSLT). During the MSLT the mean sleep latency is calculated. In narcoleptics the mean sleep latency is usually less than 5 minutes and they also have sleep onset REMs (meaning they enter REM sleep as soon as they fal asleep). This is against what is seen in idiopathic hypersomnia which too has a short sleep latency but there is no sleep onset REMs.

The treatment of narcolepsy and idiopathic hypersomnia is virtually identical. The patient is usually prescribed stimulants such as Adderall, modafinil (Provigil) or Nuvigil.

In my next post I shall elaborate on this further.

Nitin Sethi, MD

White matter lesions in the brain: a question and an answer

braindiseases9 Comments

One of the readers of my blog asked a very interesting question. I am reproducing her question here. My response to it follows. I hope you shall find it helpful.

Personal Regards,

Nitin Sethi, MD

I am 45 now when I was 25 I was diagnosed as have a pituitary adenoma that caused no active symptoms. Over the years my PCP would follow up with MRI’s and visual field tests. An MRI performed in 03 showed some non specific periventricular high signal white matter changes on the left. Recently in Oct 2010 another MRI was repeated for follow up purposes only. This time it showed several tiny areas of subcortical white matter high signal changes are identified in the right parietal region as well. Pituitary was normal. I am 125 lbs, caucasian femal and I have no neurological symptoms, high blood pressure or diabetes an occasional headache that I get is so mild and I usually pass if off for being tired. My question is what can I do (if anything) to stop these changes from occurring. Does calcium have an effect on this, alcohol consumption (8 to 10 per week) or can cognitive games, etc? Thank you for any input. Best Regards D

 
  
braindiseases Dear D,
thank you for writing in. You ask a very good question. Like I explained in my post not all white matter lesions represent MS plaques. The majority of these white matter lesions are what we refer to as ischemic small vessel disease. As the name suggests the pathology lies in the small vessels in the brain. Ischemic white matter disease is more commonly seen as we age. Also patients who have vascular risk factors are more likely to show white matter disease. The common modifiable risk factors are: essential hypertension, diabetes mellitus, dyslipidemia (increased total cholesterol, increased low density lipoprotein and triglycerides and decreased high density lipoprotein), smoking, excessive alcohol intake, obesity and sedentary lifestyle. Some people are hypercoagulable and thus are more prone to strokes and heart disease. Patients who suffer from chronic migraines (especially women) also frequently have “excessive” white matter disease.
Now the million dollar question is whether this white matter disease is harmful to the brain. Does it affect the patient cognitively? There are indeed studies that show that excessive white matter disease may make the person prone to cognitive problems later on in life. This is called vascular dementia. My advise to you would be this:
If you have any of the above vascular risk factors, I would attempt to modify them. Good control of blood pressure is paramount. Earlier a blood pressure of 130/80 or 140/80 was considered acceptable. Nowdays the teaching is “lower the better”. Hence the new guidelines recommend lowering the blood pressure down to 120/70 mm Hg. In the same vein the guidelines with respect to acceptable cholesterol, triglycerides (TG) and low density lipoprotein (LDL) have become more stringent and again the teaching nowdays is “the lower the better”. If you smoke, quit completely as no amount of smoking is good for your heart or the brain. I would advise you to eat a healthy diet rich in vegetables, fruits and nuts. Exercise on a regular basis (cardiovascular exercise such as jogging or brisk walking has been found to be the most beneficial). I usually recommend my patients to take 1-2 tablets of a good multivitamin per day (one that has all the B group of vitamins). Studies have shown that vitamin B12 plays an important role in cognition and so I usually recommend it to most of my elderly patients especially those who are vegetarians and have a marginal diet. I find my patients frequently deficient in Vitamin D (vitamin D is made in the skin from sunlight and so caucasians living in the temperate areas are frequently vitamin D deficient) and so I supplement it. The amount of vitamin D needed on a daily basis varies according to your sex and age and you should consult your primary care physician to determine how much you should take. I usually give my patients around 400 international units of vitamin D per day.
I am a big believer in cognitive games (the fancy word for this now is Neurobics). You can read more about these in my neurobic post here or on my website http://braindiseases.info.
I hope I have addressed your concerns adequately.

Personal Regards,
Nitin Sethi, MD

Not all tremors represent Parkinson’s disease

braindiseases5 Comments

Patients frequently come to see me for evaluation of their tremor.  Invariably the history is that the tremor was first brought to their attention by a close friend or a family member. The patient is worried that he/she has Parkinson’s disease and hence seek a neurologist’ s attention. Rarely are they bothered by the tremor per-se. By that I mean the tremor is usually not disabling and does not impair their quality of life at least initially. So do all tremors represent Parkinson’s disease? Are there any benign tremors? Which tremors warrant medical attention? These are some of the issues I plan to dwell on in this blog post. I hope some of my readers shall find the information useful.

So what exactly is a tremor. Well neurologically a tremor is characterized by rhythmic oscillatory and involuntary movement across a joint. I used the work involuntary because tremors at times can be voluntary. Voluntary tremor is usually psychogenic (meaning it has a psychological basis to it). We shall not discuss psychogenic/voluntary tremors in this post though. Suffice to say that a doctor shall be able to identify psychogenic tremor based on the history and examination findings alone.

So what do I look for when a patient with tremor comes to me seeking an explanation. Well the age of the patient is the first clue to the etiology of the tremor. Idiopathic Parkinson’s disease usually starts off in the sixth to seventh decade of life. Familial Parkinson’s disease can start at a younger age but usually the tremor is not so prominent nor is it the initial manifestation. There can be many causes of tremor in the “young”.  Various medical conditions some more common such as hyperthyroidism, hepatic and renal diseases and some more exotic such as Wilson’s disease (due to a problem with copper metabolism in the body)come to mind.  At times the answer is more innocuous and the tremor is either due to stress or excessive intake of coffee and other caffeine containing drinks. In that case all that is needed is reassurance. One other disease that needs to be kept in mind is multiple sclerosis though usually more findings are documented in exam (meaning that the tremor is not see in isolation). One should never forget to ask patients about the use of prescription, over the counter and illicit drugs. Many drugs such as sodium valproate (commonly used to treat seizures and at times bipolar disorder), bronchodilators (drugs used to treat asthma, reactive airway disease and chronic obstructive airway disease) cause a coarse postural and kinetic tremor as a side-effect. Once the drug is stopped the tremor abates.

Another common entity frequently confused with Parkinson’s disease is what is called essential tremor or also sometimes referred to as benign essential tremor. Patients who have essential tremor are usually in the same age group as patients with idiopathic Parkinson’s disease and hence the confusion and concern arises. Essential tremor has the following characteristics: it is usually a postural tremor (meaning that the tremor is most prominent when the hands are kept out and maintained at a posture such as having them stretched out in front of you. Remember the classical tremor of Parkinson’s disease is a resting tremor. Meaning the tremor is most prominent when the hands are at rest like for example resting on the patient’s lap and the patient’s attention is diverted). Essential tremor is a faster and finer tremor as compared to the tremor of Parkinson’s disease which is a slower (2-5 Hz) and of higher amplitude. A point to note here is that tremors are frequently classified based on their frequency, amplitude and position (rest Vs postural Vs kinetic).  Patients who have essential tremor frequently in addition to the hand tremor also may have a head tremor (the head shakes either from side to side [no-no tremor] or up and down [yes-yes tremor]). They may also have a tremor in their speech (voice tremor). On further questioning some of them may admit to having the tremor run in their family (meaning their father and grandfather also had a similar tremor). They may have also noted that when they drink alcohol the tremor becomes less prominent.  Infact some patients start drinking excessively for this very reason! Essential tremor usually progresses very very slowly (if at all) and may never become problematic and disabling in the patient’s lifetime.  Hence it does not need to be treated unless it is socially disabling (“Doctor Sethi I cannot drink a glass of wine without spilling it over my dress!” “Dr Sethi  I am so embrassed when my hands shake in a business meeting!”). Essential tremor is not accompanied by the other signs and symptoms which accompany Parkinson’s disease such as gait problems, freezing, stiffness, rigidity and mask like facies.

So not all tremors represent Parkinson’s disease. A quick visit to your “local” neurologist shall give you an answer to what kind of tremor you have.

When a headache is a pain! About primary and secondary headaches

braindiseases1 Comment

When a headache is a pain! About primary and secondary headaches

Nitin K. Sethi, MD

Assistant Professor of Neurology

New York-Presbyterian Hospital

Weill Cornell Medical Center

New York, NY 10065

 

 

Headaches are a very common reason that patients consult a neurologist like me.  The intensity of the headache, its character and duration are some of the factors which determine if and when patients seek medical attention. So in this post I shall go over the different types of headaches and list their main differentiating features.

Broadly speaking we can divide headaches into primary and secondary headaches. Primary headaches are those headaches for which there is no structural/ secondary cause.  For example a migraine headache is an example of a primary headache. The migraine may be severe and frequently disabling but if you scan (CT or MRI) the patient’s brain no underlying structural lesion like a tumor is found. Secondary headaches as the name implies are secondary to a another cause. For example headache due to a large brain tumor or headache due to an infection (meningitis) represent secondary headaches.

Types of primary headaches:

1)      Migraine: common migraine and classical migraine

2)      Tension type headache

3)      Cluster headache

Types of secondary headaches:

1)      Headache secondary to a brain tumor or other masses (space occupying lesions) in the brain

2)      Headache secondary to an infectious and inflammatory process in the brain (example headache associated with meningitis)

Headaches can be a cause of concern and distress. Patients frequently worry that may have a brain tumor. So let us go over some of the signs and symptoms which suggest that the headache is due to a secondary cause . These are the signs and symptoms which should make you seek urgent medical attention:

  1. Sudden onset of severe headache. When asked patients rate their headache as the “worse headache of their lives”. I shall be concerned if I encounter such as patient in the ER, more so if the patient tells me that they have never had a  headache in their life before. When accompanied with other signs such as nuchal (neck) rigidity and depressed sensorium (level of alertness), the question of subarachnoid hemorrhage (SAH) comes to mind. A common cause of non-traumatic SAH is the rupture of an aneurysm or arteriovenous malformation (AVH) in the brain. SAH is associated with high morbidity and mortality especially if the patient presents to medical attention late.

Caveat: Not all “worse headaches of my life” are due to SAH due to rupture of an intracranial aneurysm. Many times (especially if there is a past history of migraine headaches) these patients are suffering from a particularly debilitating/ severe attack of migraine. Thunderclap/ explosive headaches have also been reported at the time of coitus. They are referred to as post coital or orgasmic headache.

  1. Headaches in extreme of ages:  headaches which occur in the extreme of ages (such as in a young child or after middle age especially if there is no past history of headaches) deserve a more closer look. Signs such as neck stiffness or depressed level of sensorium may be masked or difficult to elicit in these age groups. As a neurologist my threshold of investigating these patients with tests such as MRI of the brain and more invasive tests such as spinal tap (lumbar puncture) is lower.

Caveat: small children frequently cannot express headache (meaning they cannot tell you that they are bothered by headache).  Primary headaches such as migraine may be missed in children as a result. The child may be agitated and parents may think he is acting up. So a high index of suspicion has to maintained by the physician to timely identify migraines in small children. Also it is well known that migraine is not “typical” in the pediatric age group. Various migraine variants have been identified in children such as abdominal migraine (the child complains of episodic abdominal pain), cyclical vomiting and so forth.

  1. Onset of headache in middle age (especially if there is no prior history of headaches): when a middle aged patient comes to me and says he is bothered by headaches for the past 3-4 months, never had headaches when he was in his teens, I pay close attention to him. A thorough neurological examination shall frequently tell me if there is anything “brewing” inside the brain aka does he have a mass lesion/ tumor? As a neurologist I have several tools to help me in this endeavor. I can look for signs of asymmetry: weakness/ numbness on one side of the body, problems with coordination on one side of the body, is the gait steady, are the reflexes symmetrical and so forth. I can further look into his eyes with an ophthalmoscope to see if there is increased pressure inside the brain (remember the eyes are the window into the brain).  Based on my exam, I may or may not order a MRI scan or CT scan to confirm my suspicion.
  2. Headaches associated with fever: are always a cause of concern. Various disease processes such as meningitis (bacterial, viral or fungal), brain abscesses and so forth come into the differential. Patients are admitted into the hospital and further management depends upon the underlying etiology.
  3. Recent onset of headache in an immunocompromised patient: recent onset of headache in a patient who is immunocompromised (example a HIV positive patient or a patient who is receiving chemotherapy for cancer) always warrant a thorough work-up. Such patients are frequently found to have a secondary cause for their headaches. So again my threshold for imaging such patients is low.  My threshold for doing a spinal tap in these patients is also low (provided I am confident that the pressure in the brain is normal).
  4. Headache/ temporal pain  in a patient past 65: temporal arteritis (Giant cell arteritis) is a disease entity which is seen in the elderly and is due to inflammation of the temporal arteries. Patients may not complain of headache per-se. When you examine them you find they have tenderness over the temporal arteries and the artery may feel beaded and thickened.  It is imperative that temporal arteritis be identified in a timely fashion and treated otherwise the patient may suffer loss of vision.

In the next post I shall talk about the primary headaches.

A question from a father and some answers for seizures due to hypoglycemia

braindiseases6 Comments

A father from the Netherlands recently wrote to me about his son. I thank him for his question.  He asked me a few very specific questions. I am reproducing them here as I feel it shall aid other people. My response to his questions follows. Names have been removed to maintain privacy.

QUESTION:

My son is diabetic type 1, since his 5th year. And he had several seizures in the last 5 years. Mostly once a year, every time he had a hypoglycaemia.
The last time he had a epileptic seizure, with a fracture of thoracic vertebra 2. I have made a MRI scan of the brains, but everything seems normal.
Are there other investigations necessary to be sure it is an epileptic insult due to hypoglycaemia, instead of real epilepsy

HK

ANSWER:

Dear HK,

                                  thank you for writing in to me. If I get you right you are saying that all of your son’s seizures have occured in the setting of hypoglycemia. Do you by any change recall what was his blood sugar during these ictal episodes. For a seizure to occur due to hypoglycemia, the blood sugar has to usually fall down to an extremely low level (we call this neurohypoglycemia). As you are aware the brain needs sugar for energy and its metabolism so when blood sugar falls down to the range of 60 mg/dl or less, that is when a seizure occurs. The seizure in the setting of hypoglycemia is usually a generalized convulsion. That said I and many other physicians have seen patients presenting to the ER with focal findings suggestive of a stroke only to find them completely reverse once the blood sugar was corrected.

I do have a few practical suggestions for you:

–have a home blood glucose meter and check your son’s blood sugar at various times during the day such as in the early morning when he wakes up (fasting blood sugar), prior and after lunch (post prandial blood sugar) and finally before he heads to bed during the night.  Do this for about 2 weeks and keep a record of the values in a notebook. This shall prove to be tremendously helpful to you as a parent and his physician to see how his blood sugar fluctuates during the day. Are there times when his blood sugar falls down/ bottoms out unexpectedly.

–a seizure due to hypoglycemia is rapidly reversible and in fact can be aborted with intravenous dextrose solution. Now it may be hard to administer intravenous dextrose at home.

–another very important point which comes to mind is why is he having so frequent hypoglycemic episodes. This shall require a thorough review by his endocrinologist. His insulin dose may need to be adjusted and/or he may warrant frequent small meals during the day to prevent his sugar from suddenly dropping.

–now to your final question: does your son actually have underlying epilepsy per-se. The answer to that depends upon this:

                -has he ever had a seizure in the setting of normal glucose level?

                -an EEG study shall be extremely useful. If the electroencephalogram shows inter-ictal epileptiform activity then likely your son does suffer from epilepsy. Remember in patients with seizures due to hypoglycemia per-se, the EEG between the seizures should be normal.

                -a routine EEG (30 minutes study) can fail to reveal an answer. In that case a long term EEG monitoring study (24-72 hours either in the hospital or in an outpatient setting) may aid in characterization of his typical events.

-as you may have guessed right, patients with seizures due to hypoglycemia per se do not need to be on anti-convulsant therapy. In these patients what we need to ensure that they do not become hypoglycemic. No hypoglycemia means no seizures.  On the other hand if your son does have underlying epilepsy, he shall warrant anti-convulsant therapy.

                -also a neuroimaging study (ideally MRI of the brain) may he helpful to rule out any intracerebral structural cause of seizure.

I hope you find this information helpful. Please feel free to contact me again.

Personal Regards,

Nitin Sethi, MD

Bumps to the head: minor concussion and post concussive symptoms

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Recently I have seen a few patients in my office with minor concussions. They all pressented with post concussive symptoms and hence that shall be the focus of my post on this gorgeous June day.  So what is a concussion and what is a “minor” concussion? Concussion is usually a closed head injury with temporary loss of brain function or rather loss of consciousness. By closed head injury, I mean that nothing penetrated the brain. Example of a penetrating head injury shall be a gun shot wound to the head.  Do not get me wrong here-obviously a penetrating head injury shall likely result in loss of consciousness and temporary or permanent loss of some brain function.

That said the word concussion is more commonly used for closed head injuries. Let me give you a few prime examples of concussion.  I am a big fan of boxing and the UFC. Anyone who watches these sports has seen a concussion. Boxer A walks into a stiff jab thrown by Boxer B. Down he goes and is out for the count. The ringside doctor jumps into the ring to examine him. Flips his eyes open and flashes a light into both of them.  After a momentary loss of consciousness, our fallen boxer comes to. Open his eyes but has a dazed look. He is able to answer the ringside doctors questions (show me two fingers with your left hand). He struggles to his feet but his legs are wobbly.  The referee consults the doctor and decides to halt the fight.  So what happened to our boxer? He just sustained a concussion.

Concussions can be graded into mild, moderate and severe. This is quite arbitrary. If the loss of consciousness is more than half an hour the concussion is graded as severe. Minor concussions, which shall be the focus of our talk henceforth, are usually associated with either no or momentary loss of consciousness.  Let me give you a few examples of minor concussions. Walking into a door, bumping your head against a low lying ceiling or a car door are all examples of minor closed head injury with or without concussion.  Majority of patients walk away from such an injury and never seek any medical attention because they experience no ill-effects. A few though  are not so lucky and post the head injury are plagued by headache (post concussive headache), problems with memory and concentration (especially when they are multi-tasking) and a myriad of other complaints such as subjectively feeling off balance, difficulty with sleeping and mood changes such as irritability. All these symptoms after a closed head injury/ concussion are included under the umbrella of post concussive symptoms.

In my next post, I  shall discuss post concussive syndrome and its treatment.

Nitin Sethi, MD

When hospitals fail

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My residency in neurology was in Saint Vincent’s Hospital and Medical Centers, New York, NY. Recently Saint Vincent’s or Vinney’s as we affectionately called it closed its doors. A sad day indeed for a lot of doctors who worked there.

Death of a hospital

 

Nitin K. Sethi, MD

Former Chief Resident in Neurology

Saint Vincent’s Hospital and Medical Center

New York, NY 10011

 

 

April 30th dawned just like any other April day. As the sun rose along the eastern seaboard, Manhattan came to life with its golden rays. A healthy glow permeated all around. But not all its residents were blessed with this good health. Saint Vincent was sick, terminally sick with multi organ failure. Its corridors once bustling with doctors and nurses in scrubs lay deserted. Its ER once full of patients was eerily quiet. Its intensive care units once a melody of ventilator hums and telemetry monitor beeps were quiet as if a great orchestra had played its last composition. Its cafeteria once full of hungry overworked residents had served its last meal. The end had come slowly but now the writing was on the wall. Terminally ill with no hope of a meaningful recovery they said as they went by. The hospital which had once given the gift of life to so many now itself lay on its death bed. Where critically ill patients once received life saving infusions of antibiotics found itself deserted in its final battle for survival. Saint Vincent found no one to turn to, no one to hold its hand and no one to administer CPR (cardiopulmonary resuscitation). It thought it was too big to fail but no one stepped forward to bail it out. Saint Vincent died on April 30th.

Pseudoseizures

braindiseases2 Comments

Psychogenic seizures/ Non-epileptic events

Nitin K. Sethi, MD

Assistant Professor of Neurology

New York-Presbyterian Hospital

Weill Cornell Medical Center

New York, NY 10065

 Non-epileptic events

Non-epileptic events are paroxysmal episodes that resemble and are often misdiagnosed as epileptic seizures. Non-epileptic events can be further of two kinds

Psychogenic non-epileptic seizures (PNES)

Non epileptic but not psychogenic (“physiologic”) event

Non-epileptic but not psychogenic (physiologic) events: examples include

  • Tremors
  • Myoclonus which is not cortical (segmental/ spinal)
  • Dystonia
  • Dyskinesias
  • Parasomnias: sleep walking, nocturnal panic attacks, nightmares, sleep terrors
  • Syncope
  • Complicated migraine
  • Transient ischemic attacks
  • Cataplexy
  • Startle induced phenomena

 Psychogenic non-epileptic events

Multiple terminology: pseudoseizures, nonepileptic seizures, nonepileptic events, and psychogenic non-epileptic seizures.

 By definition PNES are psychogenic (psychological) in origin.

Can be

  • a form of conversion disorder or more broadly somatoform disorder—these are involuntary 
  • a form of malingering or factitious disorder—these are voluntary

 

Frequency/ sex ratio and age of onset

  • Up to one in five patients with apparently medical intractable epilepsy referred to epilepsy centres.
  • Incidence and prevalence varies in different countries: likely on account of differences in social and cultural norms.
  • More frequent in women as compared to men.
  • Typical age of onset is young adulthood

 

 Making the diagnosis

Misdiagnosis is common!!!

Patients present with history of uncontrolled seizures/ typical events inspite of

multiple inpatient admissions

multiple physicians

multiple anti-epileptic drugs (AEDs)

multiple tests

Making the diagnosis

  • Good history forms the backbone
  • History of typical event
  • From patient
  • From family/ caregiver/bystander

Points to consider:

Does the event occur out of sleep or do the events always occur during daytime when people are around

Specific triggers that are unusual for epilepsy: events are clearly precipitated by emotional stress (“I become angry and then shake”)

Circumstances in which attacks occur: around an audience (family, social events)

Details of the typical event: motor movements characteristics that are inconsistent with epileptic seizures: side-to-side shaking of the head, bilateral asynchronous trashing movements which are out of phase, weeping, verbalization and arching of the back (pelvic thrusting), eyes are closed and cannot be pried open.

History of other coexisting psychogenic conditions: fibromyalgia, chronic fatigue syndrome, IBS.

Good psychosocial history: depression, bipolar disorder, personality disorders (hysterical personality), family dynamics.

History of sexual abuse is specially important.

 Making the diagnosis

 

 VIDEO-EEG study is the gold standard

  • Helps to make an electroclinical correlation: capture a typical event on the video and interpret the electrographic correlate.
  • No change in the background EEG during the clinical event.
  • Clinical event is inconsistent with known seizure semiology: event starts-stops-then starts again, awareness is preserved in spite of bilateral motor convulsive activity.

 If Video-EEG facility is unavailable: routine EEG, ambulatory EEG, extended EEG—with suggestibility—lower yield

Imaging studies may or may not be normal: correlate the MRI/ CT with the history

Blood tests: prolactin (increased for about 30 minutes after a generalized convulsion)—impractical, hence not too useful.

 Treatment

Not easy!!!

patients frequently do not accept their diagnosis (” I am not crazy” ” I shall see another doctor”)

hence the way one delivers/explains the diagnosis to patients and their families is an art: some physicians are blunt, others are more vague or mask their words

Patients may or may not be agreeable to seeing a psychiatrist

  • Assure continuity of care
  • Be supportive
  • Be non confrontational

 

Other issues:

can AEDs be tapered off?

Does the patient have co-existing true seizures?

So your doctor may get other professionals involved: social workers, psychiatrists

Outcomes!!!

 

 

  • Not all patients become “seizure”/spell free—many in fact do not
  • Males become spell free more than females
  • If they have a previous psychiatric diagnosis or some motive like disability/ unresolved marital stress—they shall not become spell free
  • Events may become less dramatic—less hospitalizations or visits to the doctor
  • They may be lost to follow up and find another doctor

Pseudoseizures: a question and an answer

braindiseasesLeave a comment
2010/04/15 at 3:17am

Hello,
I’m writing because I am feeling desperate. I have been in therapy for 10 years, only five of which I have been treated for pseudo seizures. I am on anti-depressants, which usually make my life quite manageable. My seizures, depression, and anxiety are incredibly exacerbated before my period, often leaving me unable to work, go to school, or function in society. I feel I have tried everything. Are there any doctors, therapists, or other groups doing research on this problem? If the seizures don’t originate in the brain, where the heck are they coming from? How can our brain waves be calm while our bodies are seizing? If therapy doesn’t seem to be solving the problem, what then?

Also, how common is this problem? I am so embarrased by it, I feel like I should be able to control it and it is my fault that I can’t. I feel so alone. Are there any others out there like me?
Thanks,
Ms. Psuedo Seizure.

|
Dear Ms. Pseudoseizure,
thank you for writing in to me. I have to admit your name (Ms. Pseudo seizure herself) grabbed my attention. Your struggle with this condition and your plea for help is heartrending. What follows is a detailed description of pseudoseizures. I hope this shall help answer some of your questions. My very best to you.Personal Regards,
Nitin Sethi, MD

Privacy concerns

braindiseases1 Comment

To the readers of my blog.  I had started this blog to disseminate information about neurological and neurosurgical conditions. Information which was written in a simple easy to understand language (aka free of medical jargon). Over the past 2 years, the readers of my blog started writing in to me with specific questions regarding their own health or that of a loved one.

While I attempt to answer these requests responsibly (please remember the Internet is no place to diagnose your condition and nothing quite replaces a face to face visit with your physician), what concerns me is that some of you are writing in and putting your MRI reports and medical record information in the email. Privacy concerns are paramount and hence I request you to refrain from doing this.  Also in your email, please remove any information which might identify you.

Things on the Internet stay for ever and can be misused. So a humble request, protect your private information!!!