Did you know that patients with epilepsy have a higher incidence of migraine headaches (and vice-versa!)? Patients are usually referred to our clinic for evaluation of their seizures. I will routinely ask patients about their headaches. If the patient has problematic headaches, treatment of the headaches may dramatically improve their quality of life.

It is not common, but sometimes an aura for a migraine can trigger a seizure. This shows the overlap in pathophysiology- between migraine and epilepsy.  The best thing for the patient is to treat the migraine and treat the seizure activity. Sometimes, one medication can treat both: “kill two birds with one stone!”

Some interesting/important points about migraine and epilepsy:

• Migraines can trigger seizures. Migraine triggered seizures are defined as seizures that occur within one hour of a migraine aura. The migraine aura is the warning that patients get before the headache gets severe- for example, patients may see flashing lights that slowly move across their visual fields. Patients may also have nausea that builds up over several minutes as their aura.
• Patient example: 28 year-old woman with a history of migraines and epilepsy for several years. The patient would note her migraine aura. This was a visual change—flashing lights that slowly moved from left to right across her visual field. The aura would become more intense over 10 minutes. Eventually, the symptoms could lead into a seizure (not always, but every few months)—patient would stare, lose contact, smack her lips and pick at her clothes. The seizure would last 60 seconds. She would then come out of the seizure. Although she would be mostly recovered, the patient would often be left with a headache. Headaches were often  a throbbing pain on one side of her head. Headaches were associated with nausea, light and sound would bother her. Headache would last for hours. Patient would often want to go lay down in a dark room.
• Migralepsy: this is the term for migraine-triggered seizure.
• Rates of migraine triggered seizures: In patients who have both epilepsy and migraine, migraine was noted to trigger seizures in 1.7-16% of patients.
• The prevalence of migraine in patients with epilepsy has been shown to be approximately 24%.
• Patients with epilepsy are 2.4 times more likely to be diagnosed with migraine (compared to the general population).
• 37%-51% of patients experience headaches after their seizures. These are called postictal headaches. These headaches can be as problematic as the seizures, for some patients.
• Mechanism of migraine and epilepsy:
  • Neurons are more active in both migraine and in epileptic seizures. A seizure, of course, is due to abnormal electrical activity coming from the brain. A migraine aura is due to  cortical spreading depression (CSD). CSD is a wave of electrical activity that slowly moves across the cerebral cortex. The abnormal electrical activity in a migraine aura moves more slowly than the typical spread of a seizure. One certainly can see how a migraine aura could trigger a seizure—the abnormal electricity of a migraine aura, in a patient with epilepsy, could trigger neuronal excitation and a seizure.
• Treatment can “kill two birds with one stone”.
  •  Certain medications can effectively treat both migraine headaches and epileptic seizures.
  • Such medications include topamax and depakote.
  • Possible reason that seizure medications work in migraine and epilepsy- similar mechanisms (both cause abnormal neuron excitation—see paragraph above).

REFERENCES

Forderreuther S, Henkel A, Noachtar S, Straube A. Headache associated with epileptic seizures: epidemiology and clinical characteristics. Headache 2002;42:649-55.

Haut SR, Fishman O, Lipton RB. Migraine, migralepsy and basilar migraine. In: Atlas of epilepsies. Edited by CP Panayiotopoulos.  Pp 629-637. Springer Verlag, London 2010.

Silberstein SD, Lipton RB, Haut S. Migraine. In: Epilepsy: A comprehensive textbook. Edited by Jerome Engel and Timothy Pedley. Pp 2733-2743. Lipppincott Williams & Wilkins, Philadelphia 2008.

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INTRODUCTION

A common question that we receive in clinic relates to the chance that a parent will “pass on” their epilepsy to their children. Also, if one child has epilepsy, will their brother or sister develop epilepsy? These are important questions. The answer is, of course, complicated. The answers to such questions must be tailored to the individual/family.

GENERAL FACTS ABOUT THE RISK OF DEVELOPING EPILEPSY:

• Remember: For the general population, the risk of developing epilepsy is approximately 1%. I always remind patients and families- even without a known family history of epilepsy or known genetic reason for epilepsy, any parent could have a child with epilepsy. Compare the 1% chance of epilepsy (for all people in the general population) to the higher risk groups described below.

• The risk of epilepsy is higher in the offspring of a mother with epilepsy compared to a father with epilepsy:
  • If mother has epilepsy, the risk of epilepsy in her children:
    • 2.9%-8.7%
  • If father has epilepsy, the risk of epilepsy in his children
    • 1.0%-3.6%

• If a parent has epilepsy, the risk of epilepsy in his or her daughter(s) is somewhat higher compared to the risk in son(s).

• If a parent develops epilepsy at a young age, the risk of epilepsy in his or her children is higher. An example may help clarify this: Let’s look at two fathers with epilepsy. Let’s compare the risk of these two fathers having a child with epilepsy. Father #1’s epilepsy began when he was 8 years old. Father #2’s epilepsy began at the age of 29 years of age. The father with the younger age of onset (Father #1) will have a higher risk of having a child/children with epilepsy
  • Parent with onset of epilepsy BEFORE the age of 20 years, risk of epilepsy in children:
    • 2.3%-6%
  • Parent with onset of epilepsy AFTERthe age of 20 years, risk of epilepsy in children
    • 1%-3.6%

• If a person has epilepsy, his or her sibling (brother or sister) is at higher risk of developing epilepsy. The younger the age of onset of epilepsy, the higher the risk that the sibling will develop epilepsy.
  • If  a patient develops epilepsy starting at age 0-9 years, the risk that the brother or sister will develop epilepsy:
    • 9.5%
  • If  a patient develops epilepsy starting at age 10-24 years, the risk that the brother or sister will develop epilepsy
    • 5.8%
  • If  a patient develops epilepsy starting after the age of 35 years, the risk that the brother or sister will develop epilepsy:
    • No increased risk

CHROMOSOME DISORDERS CONSISTENTLY ASSOCIATED WITH EPILEPSY

Some genetic neurologic conditions have seizures as a feature of their disorder. This may occur in all or nearly all patients with the genetic abnormality. It should be noted- these conditions are uncommon. Most patients with epilepsy do not have a specific chromosomal abnormality that the clinician can point to. The following is a list of two examples of chromosomal disorders in which patients typically develop seizures:

• Angelman Syndrome: Patients with this disorder have an abnormal chromosome 15. Patients have severe learning disabilities, tremor and poor coordination. The patient’s often have a happy appearance- they tend to smile and frequently laugh. Over 80% of patients will develop epilepsy.
• Ring Chromosome 20 Syndrome: Any person’s chromosomes can be looked at- with all the patients chromosomes laid out for analysis. The total number of chromosomes in a normal person is 46 chromosomes. The chromosomes can be laid out and a picture taken. If you have ever seen a chromosome picture, the chromosome looks like a little worm or a match stick. For patients with Ring Chromosome 20 Syndrome, chromosome 20 looks like a ring—instead of a straight stick, the chromosome has curled into a ring shape. This is abnormal. Patients with this disorder have poor concentration, impulsive behavior and sleep problems. Essentially all patients develop epilepsy at some point. Seizures usually occur out of sleep. Seizures are often associated with hallucinations.

COMPLEX  EPILEPSIES

Some patients, as noted in the above section, can have a single chromosome abnormality that can be clearly tested for and identified.  The single chromosome abnormality causes the neurologic disorder and epilepsy. This is (relatively!) straight forward. This is also relatively rare. A much more common scenario is that genetics plays a role in a patient developing epilepsy, but the cause and effect nature is not clearly understood and may be very complex. For example, some patients may have multiple genes that are abnormal, and it is the combination of these abnormalities that result in the epilepsy.

Let’s use mild head trauma as an example to help clarify some of these issues. Have you ever wondered why some people with mild head trauma develop epilepsy and some people do not? It is possible that there are people in the world who carry genes that predispose them to have seizures. But they may never develop epilepsy unless something happens to trigger the seizure activity. In our example, a person may have never developed epilepsy until he or she had the mild head trauma. Thus, it could be the combination of the genes and the mild head trauma that results in the epilepsy. If you could analyze 100 people who had the exact same mild head trauma, some of these patients may go on to develop epilepsy. The reason that some people develop epilepsy and some do not- may be related to differences in their genes!

(Please note: for many people, genetics may play only a minor role or no role whatsoever in their epilepsy. For example, people with head trauma may have no genetic predisposition to epilepsy. The trauma causes scarring in the brain and that is the whole cause of the epilepsy. The main point I want to make is that genetics may play a role in some patient’s epilepsy that may be surprising. The old thinking was that an injury to the brain like head trauma was the entire explanation for the cause of the epilepsy—and genetics had nothing to do with the seizures. The new thinking- genetics may play a role in some patients, even in cases of brain injury. This may be true even in adults.  As is often the case, the full story can be complicated!).

CONCLUSIONS

The information on genetics and epilepsy is progressing at a rapid pace. The research is absolutely fascinating!

If readers would like more information on this topic, let me know. For example, more information on the basics of genetics, DNA etc. Also, additional information on what genes to test for in patients with epilepsy may also be of interest.

References

Elmslie F. Genetic Counseling. In: Engel J, Pedley T, ed. Epilepsy: A comprehensive Textbook. Philadelphia: Lippincott Williams &Wilkins 2008: p. 211-215.

Goldman AM. Genes, seizures and epilepsy. Epilepsy.com

https://www.epilepsy.com/pdfs/Except_parent_art4.pdf

Zuberi S. Chromosome Disorders Associated with epileptic seizures. In: Panayiotopoulos CP, ed. Atlas of Epilepsies. London: Springer 2010: p. 121-127.

The post Facts on Genetics and Epilepsy appeared first on Minnesota Epilepsy Group.

• seizure control
• intellectual function  (measured by neuropsychological testing before and after surgery)

The study found that epilepsy surgery improved seizure control dramatically and many children were completely seizure-free.  Several studies have shown this and this was not unexpected.

Probably the most interesting finding in the study was that intellectual function appeared to improve after the surgery.  Isn’t that interesting- brain tissue was removed to control seizures.  Even with removing brain tissue, intellectual function improved!  IQ scores were noted to improve after greater than 6 years of follow-up.  Thus, the improvement was not noted immediately, but rather several years after the surgery.

The most important factor in improving IQ scores after surgery was stopping antiepileptic drugs.  I think this is important for patients and doctors to be aware of.  In our patient’s who have well controlled seizures after surgery, lowering or stopping medications certainly should be discussed thoroughly.

I thought pointing out the results of this study would be helpful for our readers.  This is further evidence that for those who are candidates for epilepsy surgery, the benefits may potentially outweigh the risks.  Thus, surgery is not just about improving seizure control.  Surgery may also lead to the added benefit of better intellectual function!

The entire article is available on-line (free!):

Skirrow C, et al. Long-term Intellectual Outcome After Temporal Lobe Surgery in Childhood. Neurology 2011;76:1330-1337.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3090063/pdf/znl1330.pdf

There is also a review of the article in Epilepsy Currents (free on-line!)

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3220420/

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Neuropace

Approximately 30% of patients with epilepsy continue to have seizures despite trying several antiepileptic drugs (AEDs). This 30% of patients is considered to have intractable epilepsy. Some of these patients can have surgery for their seizures- this is where a surgeon removes a piece of brain tissue to remove the seizure focus. This type of surgery can be very helpful—in some cases, > 70% of patients would be expected to be seizure free.

So, what about the patients who do not respond to seizure medications and also are not resective surgery candidates? What do they do? Such patients may be considered for a device to treat their seizures. A device for epilepsy is something that is placed into a patient by a surgeon. The device is programmed to perform a function that stops seizures.

Currently, there are three devices for epilepsy that are commonly discussed. Only one is FDA approved—this is the Vagus Nerve Stimulator. The other two (Deep Brain Stimulator and Neuropace) are not fully FDA approved. At this time, the Vagus Nerve Stimulator can be ordered by your clinicians. Deep Brain Stimulator and Neuropace are not fully FDA approved and are thus not available to the general public.

A brief description of each of these three devices may be of interest:

Vagus Nerve Stimulator (VNS):

• How it works: A battery is placed under the skin on the left side of the chest. A wire goes from this battery to the vagus nerve—this is a large nerve in the neck. Thus, the patient has two areas of surgery- 1) the skin on the left side of the chest and 2) the left side of the neck to attach wires to the vagus nerve. No brain surgery is done. The vagus nerve has connections to the brain—in a widespread manner. The battery produces electrical charge that is transmitted to the vagus nerve. This electrical stimulation is then transmitted to the brain. The device is often programmed to stimulate for 30 seconds and then be off for 5 minutes. This stimulation goes on like clockwork: 30 seconds on/5 minutes off. By stimulating the vagus nerve, which then stimulates the brain, the seizure potential is changed for the better- seizure control can be improved!

Deep Brain Stimulator:

• How it works: Small probes are placed deep in the brain. This requires surgery that involves going through the skull and brain tissue. The probes are programmed to delivery electricity to areas deep in the brain. By stimulating this area, the brain activity changes in a good way- seizure activity can be reduced. Like the Vagus Nerve Stimulator, the Deep Brain Stimulator is programmed to stimulate at a pre-programmed set time. For those who love neuroanatomy, the deep brain area is called the anterior nucleus of the thalamus.

Neuropace:

• How it works: Electrodes are placed on the surface of the brain. This involves brain surgery-a piece of skull is opened to place these electrodes. The electrodes are very sophisticated- they are attached to a computer system that allows the detection of seizure activity. Imagine this- the electrodes are placed directly over the part of the brain where seizures are coming from. When a patient has a seizure, the electrodes can detect this activity. The electrodes are then programmed to delivery electricity to the brain. The electricity from the electrodes zaps the brain—and the seizure activity is stopped!

The three devices described in this article can reduce the frequency and intensity of seizure activity, but they are not expected to stop seizures completely. Obviously, this is important for patients to know. For example, the devices are not expected to stop seizures to the point where patients can drive. Placing one of the above devices may help patients reduce seizure medications. This may help with side effects.  The devices would not be expected to produce the well known seizure medication side effects, such as feeling sleepy, dizzy, poor coordination (you know—feeling like you are drugged!).

Each device has its own side effects. When a patient has surgery, infection and stroke are always discussed. Fortunately, the procedures do have a very good safety records.

I will plan on going into more detail about these devices in a future article. I will review the risks and benefits in more detail.

Please comment, ask questions.

For more information:

• VNS
• Deep Brain Stimulator
• Neuropace

The post Devices for Epilepsy appeared first on Minnesota Epilepsy Group.

1-2% of the world’s population has epilepsy

9% of people will have at least one seizure in their lifetime

If you have a first seizure in your life, what is the chance you will have a second seizure in the next two years?

• If neurological exam, EEG and MRI brain are normal: 25%
• If  neurological exam, EEG and/or MRI are abnormal: may be > 40-50%

If you have had 2 or more seizures in your life, what is the chance that you will have more seizures?

• 70%

Percentage of patients with epilepsy who do NOT  have an identified reason for their seizures (unknown category):

• 50 %

If you have the first seizure in your life, what is the percent chance your seizures will be completely controlled?

• First seizure medication: 50%
• Second seizure medication: 10%
• Third seizure medication and combination therapy: 3%
• Total percentage of patients who continue to have seizures despite > 3 seizure medication trials: 30%

The typical seizure lasts 30-60 seconds.

30 minutes: This is the duration of essentially continuous seizure activity required to meet criteria for status epilepticus. Status epilepticus is prolonged seizure activity that can be severe and even life-threatening.

Approximately 50 million people have epilepsy, worldwide.

3/4 of people in developing countries do not get the treatment that they need.

Dates are numbers (of course!).  Here are some dates that are very important in the history of epilepsy:

• 11^th century BC: Approximate date that the oldest known medical reference to epilepsy was written. It was written on two clay tablets found separately in Turkey and Iraq. The translation provides a clear description of seizure activity.
• 400 BC: Date Hippocrates wrote The Sacred Disease. This medical text was the first to describe seizures as coming from the brain. It should be noted that there is some controversy as to whether or not Hippocrates was the author of this important text
• 1857: Potassium bromide is introduced to treat seizures. This is the first scientifically validated seizure medication
• 1886: Modern era of epilepsy surgery begins: Sir Victor Horsley successfully performs brain surgery on a patient with focal seizures due to a depressed skull fracture.
• 1929: First EEG was used to record human brain waves.

LATEST UPDATE: 6/6/2011

Seizures By The Numbers - Infographic

Seizures By The Numbers Infographic on Visual.ly

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For most patients, changing from brand to generic AEDs does not cause problems. This is because, again, the FDA mandates that the brand and generic AED be very close, in terms of their function and metabolism. The way the studies are usually done are to compare the generics to the brand. To clarify: assume we have generic medication A, generic medication B and generic medication C.  Currently, each of these medications are compared to the brand seizure medication- to make sure the metabolism of the drugs are very similar.

ILLUSTRATION 1: To illustrate how studies are usually done (FDA required):

GENERIC A compared to BRAND SEIZURE MED

GENERIC B compared to BRAND SEIZURE MED

GENERIC C compared to BRAND SEIZURE MED

A recent article (Krauss 2011) was published that compared the metabolism of different generic AEDs. Thus, they compared blood levels of generic medication A to generic medication B to generic medication C.

ILLUSTRATION 2: To illustrate how this study was done:

GENERIC A compared to GENERIC B compared to GENERIC C

Remember, usually the generic medications are compared to the brand, as required by the FDA (see Illustration 1, above). This study did something that the FDA does not require—it compared the metabolism of the different generic AEDs to one another (see Illustration 2, above). What they found was that for some patients, the differences between the various generic formulations was significant.

This study did not determine if the variability in blood levels caused problems- such as seizures. That will be left to another study. What the study suggests is that switching from one generic AED to another generic AED may result in significant increases or decreases in AED levels- for a small percentage of patients. It is thought that some patients may have seizure activity due to this fluctuation, although the percentage of patients is likely not high.

As our readers may well know, a pharmacy can switch from one generic AED to another. There can be more than 10 different generic AED manufacturers for a given seizure medication. A patient may be getting a peach colored pill that is shaped like a diamond one month, then the patient is switched to a white round pill. This may be due to changing the manufacturer. Thus, the study I describe in this article is important—it demonstrates that levels can fluctuate significantly in a small percentage of patients- when patients are switched from one generic AED to another.

The message of this article is NOT- stop taking generic seizure meds. Rather, the message is – understand that there may be some risk in changing from one generic AED to another. This is a risk that can be discussed between a patient and their clinician. It is important and complex!

For more information on the brand vs generic seizure medication debate, see our article on this website:

What to take: Brand vs generic seizure medications?

https://www.mnepilepsyhudson.org/education/featured-topics/what-to-take-brand-vs-generic-seizure-medications/

REFERENCES

The reference for the above described study:

Krauss GL, Caffo B, Chang YT, Hendrix CW, Chuang K. Assessing bioequivalence of generic antiepilepsy drugs. Ann Neurol 2011;70:221-228.

The article is reviewed in Epilepsy Currents.

Gidal BE. Generic antiepileptic drugs: How good is good enough? Epilepsy Currents 2012;12:32-34.

You can review the Epilepsy Currents article at:

https://www.aesnet.org/files/dmfile/epcu-12-1-32ClinicalCommentaryGidal.pdf

The post Switching From One Generic Seizure Medication To Another appeared first on Minnesota Epilepsy Group.

ARTICLE HIGHLIGHTS

• The North American Antiepileptic Drug Pregnancy Registry recently reported its important new findings (Hernandez-Diaz, 2012).
• The report compares the frequency of major malformations in the developing fetus in women taking an antiepileptic drug (AED) during their pregnancy. New and older AEDs are analyzed. Major malformations are serious medical problems that the fetus can develop during early development in the womb.
• What is really important about this study: it describes the risks/safety of using the newer AEDs during pregnancy.
• The study provides information about the relative risk/safety during pregnancy of 11 of the most commonly used AEDs. It looks at older AEDs, such as Dilantin and Depakote, and newer AED, such as Lamictal and Keppra. Prior to this study, there was not enough information available to say, with hardly any degree of confidence, which of the newer AEDs are the safest. This study describes a relatively large number of women exposed to AEDs during their pregnancies in order to compare the rates of problems with the fetal development- for both old and the new AEDs.
• The study indicates that some of the newer AEDs may be safer during pregnancy than some of the older AEDs. Some of the relatively safer new AEDs:
  • Lamictal (generic = lamotrigine)
  • Keppra (generic = levetiracetam)
• Depakote (generic= valproate) was associated with a 9.3% prevalence of major malformations- significantly higher than the relatively safer AEDs.
• Take a look at the Table below—it lists the 11 AEDs and each AED’s prevalence of major malformations. A very valuable Table for clinicians and patients!
• The website for the pregnancy registry:www.aedpregnancyregistry.org

INTRODUCTION

In 1963, one of the earliest reports describing a problem with fetal development in a woman taking an antiepileptic drug (AED) was published. The report described that the woman was taking mephenytoin, a medication similar to Dilantin, throughout her pregnancy. The child was found to have a low IQ, cleft palate, speech problems and a small head. Since that early report, it is clear that AEDs can be associated with an increased risk of medical problems with the developing fetus.

While seizure medications can cause problems for the developing baby, not taking seizure medications may result in more problems- a real double edged sword! Remember, intense seizures, especially generalized tonic-clonic seizures (= grand mal seizures) can result in serious problems for developing fetus. For most women with epilepsy, the safest strategy for their developing baby is to take a seizure medication.

In the old days, women with epilepsy were discouraged by some clinicians from going through a pregnancy—because of concerns about having a medically handicapped child. The latest data suggests that it is quite safe for the overwhelming number of women with epilepsy to consider pregnancy. Although the risk of having a medical problem may be higher than the general population, the increased risk may not be all that high and the majority of women with epilepsy can deliver healthy children. See the Table below for more details.

So, which AED should a woman take during her pregnancy? This is an extremely important question. The North American Antiepileptic Drug Pregnancy Registry recently reported its important new findings. These findings will be of great help in this important decision making process. The report compares the frequency of major malformations in the developing fetus in women taking an antiepileptic drug (AED) during their pregnancy. New and older AEDs are analyzed. Major malformations are serious medical problems that the fetus can develop during early development in the womb. Examples of major fetal malformations include cleft palate, spina-bifida and heart valve defects.

What is really important about this study: it compares the risk/safety of taking older and the newer AEDs during pregnancy. The study provides information for clinicians about the relative safety during pregnancy of 11 of the most commonly used AEDs. Prior to this study, there was not enough information available to say, with hardly any confidence, which of the newer AEDs is the safest. Past studies had too few women exposed to the newer AEDs to make conclusions. I am sure it makes sense-you need a large number of women exposed to an AED during their pregnancy to see what the problems are. You also need to compare women taking AEDs to controls (women going through their pregnancy not taking AEDs). This way, you can study what the problems are. That is why the North American Pregnancy Registry report is so important. This study describes a relatively large number of women exposed to AEDs during their pregnancies in order to compare the rates of problems with the fetal development- for both old and the new AEDs.

The study evaluated women from 1997 through 2011. 7,370 women were enrolled in the study. 4,899 women were taking only one seizure medication. The women taking only one AED are an important group—because they are only on one AED, it is easier to determine what problems are the result of the seizure medication. In contrast, if a woman is on three AEDs (Depakote, Dilantin and Keppra, for example), then it is harder to determine which AED is causing an identified problem. The study describes the rates of fetal malformations in women taking only one AED. These women are compared to controls (women not taking AEDs).

The following table summarizes some of the key findings (based on Table from North American Antiepileptic Drug Pregnancy Registry Spring 2012 newsletter). This is a great Table!:

www.aedpregnancyregistry.org

Take-away points:

• Lamictal and Keppra appear to be safer, compared to some of the older AEDs (Depakote and Phenobarbital).
• Depakote has a relatively higher rate of major malformations (9.3%). This does not mean that women should never take Depakote during pregnancy. Rather, other AEDs should be considered first, and Depakote should only be used if it is clearly needed for seizure control.
• Topamax (a newer AED) was associated with a higher risk of cleft lip.
• You may have noticed that Zonegran had no reported malformations. It should be noted, only 90 women were on Zonegran – this is too few patients to make a determination on the safety of Zonegran. More study is needed!
• Please note- in the controls (women not taking AEDs) , 1.1% of patients had malformations.

CONCLUSIONS

The results of this study will be helpful as the clinician and patient consider going through a pregnancy on an AED. We encourage women with epilepsy who are considering pregnancy to have a detailed discussion with their healthcare provider—to optimally plan the pregnancy. The results from the North American Antiepileptic Drug Pregnancy Registry are a great addition to the literature (see their newsletter:www.aedpregnancyregistry.org for more information). The results of other pregnancy registries are going to be reported in the near future—and will further add to our understanding of this complicated and important topic!

REFERENCES

Hernandez-Diaz S, Smith CR, Shen A, et al. Comparative safety of antiepileptic drugs during pregnancy. Neurology 2012;78:1692-1699.

Mullers-Kupper vM. Embryopathy during pregnancy caused by taking anticonvulsants. Acta Paeddopsychiatr 1963;30:401-405.

The North American Antiepileptic Drug Pregnancy Registry Spring Newsletter: www.aedpregnancyregistry.org

Yerby MS, Battino D, Montouris GD. General principles: teratogenicity of antiepileptic drugs. In: Engel J, Pedley T, ed. Epilepsy: a comprehensive textbook. Philadelphia: LWW; p. 1213-1224.

LATEST UPDATE: 5/23/2012

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ARTICLE HIGHLIGHTS

• Catamenial epilepsy is a condition in which seizures increase around the time of a woman’s period.
• The change in seizure frequency noted around the time of the period appears to be due to hormonal changes.
• Estrogen tends to increase seizure activity
• Progesterone tends to reduce seizure activity.
• As women go through the changes in their hormones during their lifetime, seizure frequency can also change. During perimenopause, there is a tendency for women to have an increase in seizure activity. During menopause, there is a trend towards improved seizure control. These patterns are noted more often in women with catamenial epilepsy.
• There are medication options currently available for the treatment of catamenial epilepsy.

INTRODUCTION

Women with epilepsy will often note an increase in their seizures around the time of their periods (Penovich, 2008). It is not unusual for the patient herself to bring this observation up to the doctor. The increase in seizure activity correlates with changes in hormones that occurs during the menstrual cycle. The worsening in seizure control can best be documented on a calendar: the patient’s periods can be charted along with the seizures. A clear clustering of seizures may be noted in close association with the periods. The medical term for an exacerbation of seizures around the menstrual cycle is catamenial epilepsy (Penovich 2008, Herzog 2008). I should stress-this is a common phenomenon! Approximately one-third of women with inadequately controlled seizures meet criteria for catamenial epilepsy (Herzog, 2008). The purpose of this article is to explore how hormones can change seizure activity in women with epilepsy.

EXAMPLE CASE

32 year-old woman with history of seizures since 13 years of age. Her typical seizures are described as follows: She has an aura- it is a rising sensation in her stomach. It is a combination of mild nausea and fear. This will last for a few seconds. She then loses contact. She stares and is unresponsive. She will pick at her clothes and grab at people or items that are in front of her. Seizures last for 30 seconds. Frequency of seizures was 3 per month.

The patient pointed out to her doctor that her seizures seemed to occur around the time of her period. The patient ended up keeping a careful calendar for 5 months- charting the days of her period and the days of her seizures. Just like clock-work, her seizures occurred over a 2 day span, consistently two days before her period started. She was diagnosed with catamenial epilepsy.

The patient was started on progesterone therapy. Progesterone was given 10 days before her period started and was then tapered to off four days into her period. Thus, she was on progesterone for 14 days and off progesterone for 14 days. The progesterone was allowed to build-up in her system before the increase in her seizures was expected (seizures were expected to increase 2 days before her period started).

The patient had an excellent response. Her seizure frequency was reduced by 60%.

ESTROGEN AND PROGESTERONE

Estrogen and progesterone are two important hormones that change during the course of a menstrual cycle as well as during a woman’s lifetime. During the approximately 28 day cycle, the fluctuations in estrogen and progesterone can be quite dramatic. For example, around ovulation (mid-cycle), estrogen level may be quite high. During puberty, perimenopause and menopause, there are major changes in the relative levels of estrogen and progesterone. There is robust research in both human and animal models which support the following basic concepts:

• Estrogen tends to increase seizures.
• Progesterone tends to reduce seizures.

It has been observed that when estrogen levels are high, seizure activity tends to cluster. In contrast, progesterone is being studied as a possible treatment for seizures (see below).

SEIZURES AND THE MENSTRUAL CYCLE

During the typical 28 day menstrual cycle, there are variations in the relative levels of estrogen and progesterone. At times, the levels of estrogen are much higher compared to the levels of progesterone. It is when estrogen is relatively high that seizure activity is most likely to occur. There are three times during the menstrual cycle that hormonally triggered seizures are most likely (Herzog, 2008):

1. Around the time of ovulation (between days 10 to 15 of menstrual cycle).
2. Around the time of the period (between three days before and three days after the period starts).
3. During second half of menstrual cycle (between days 18 of cycle through three days after period starts).

It is during these three times that women with catamenial epilepsy will notice an increase in their seizures.

LIFETIME CHANGES IN SEIZURES: FROM PUBERTY TO MENOPAUSE

A very common question we receive in clinic is: What will happen to my seizures when I hit menopause? Another common question is: Did puberty trigger my daughter’s seizures? These are great questions. Research to answer these questions is ongoing. There is information currently available to guide patients on these important issues.

Puberty

As everyone knows, puberty is a time of dramatic hormonal changes! The adolescent physical appearance, emotions and thinking are all undergoing remarkable changes. Mood changes can fluctuate in remarkable ways. Given all the hormonal activity, it is not surprising that some girls experience changes in their seizures during puberty. Certain types of epilepsy are more likely to start during puberty (for example, Juvenile Myoclonic Epilepsy).

Pregnancy

Of course- pregnancy includes remarkable changes in hormones! These changes have many important effects. Pregnancy in women with epilepsy is such an important topic, I will plan on writing a separate article on this topic. Keep on the look-out for the article!

Perimenopause/menopause

Perimenopause is the time in a woman’s life where her menstrual cycle is shifting- from regular cycles to toward permanent infertility. Perimenopause is characterized by erratic fluctuations in hormones.  Estrogen levels can often be quite high during this perimenopause period.  For some women with epilepsy, seizures can become much more frequent as they go through perimenopause.  This is thought to be due to the high levels of estrogen.

When women enter menopause, hormone levels are characterized by low and stable estrogen levels.  During menopause, women with epilepsy often have a reduction in the frequency of her seizures. Thus, women with epilepsy often will often have an increase in the frequency of seizures during perimenopause, and a reduction in seizures during menopause.  This pattern is more frequently noted in those women who have a history of catamenial epilepsy (Harden, 1999).

TREATMENT OF CATEMENIAL EPILEPSY

There are several treatment options for catemanial epilepsy. Some of the options include:

• Natural progesterone lozenges ( a hormone)
• Acetazolemide (a diuretic)
• Clobazam (a benzodiazepine, effects GABA receptor)
• Ganaxolone ( a steroid, effects GABA receptor)

Data on progesterone was presented at the most recent American Epilepsy Society Meeting (Herzog et al, December 2011). A randomized, double-blind, placebo controlled multicenter trial was described. Progesterone was noted to be an effective treatment for selected women with catamenial epilepsy. It appeared that the more frequent a patient’s seizures are around their periods, the better the response to progesterone.

A suggested treatment strategy is to give progesterone for 14 days of the menstrual cycle (Herzog 2008, Pennell 2009). Thus, the patient may be on progesterone for 14 days and then off for14 days. The progesterone is started several days before the period starts and before the seizures are expected to occur. This allows the progesterone to buildup in the body. The progesterone is then continued a few days into the period, and then tapered to off. It is hoped that the higher progesterone will stop the seizures!

Progesterone has side effects—sedation, mood changes, bloating, weight gain, breast tenderness and other side effects. These need to be considered—a thorough discussion between the patient and clinician is important. Also, natural progesterone appears to have better efficacy than synthetic progesterone. In order to obtain natural progesterone, ordering from a compounding pharmacy may be necessary.

Conclusions:

Hormones can play an important role in seizures in women with epilepsy.  Increasing levels of estrogen tends to increase seizures, while higher levels of progesterone tends to reduce seizures. Women who have an increase in their seizures related to their periods may be diagnosed with catamenial epilepsy. This is a surprisingly common condition, noted in one-third of woman with intractable epilepsy. In order to determine if a person has catamenial epilepsy, careful tracking of seizures and periods on a calendar is needed. Treatments that are relatively specific for hormone triggered seizures exist and appear to be effective. Clinicians can currently prescribe such treatments. Research is ongoing to develop better treatments for this important condition.

REFERENCES:

Harden CL, Pulver MC, Ravdin L, et al. The effect of menopause and perimenopause on the course of epilepsy. Epilepsia 1999;40:1402.

Herzog AG. Progesterone therapy in women with epilepsy: A 3-year follow-up . Neurology 1999;52:1917.

Herzog A. Catamenial epilepsy:Definition, prevalence, pathophysiology and treatment. Seizure 2008;17:151-159.

Herzog AG, Fowler JM, Massaro JM, et al. Progesterone therapy for women with epilepsy:results of the phase 3 NIH progesterone trial. Presented at the American Epilepsy Society Meeting, December 2012.

Pennell PB. Hormonal aspects of epilepsy. Neurol Clin 2009;27:1-25.

Penovich PE, Helmers S. Catamenial Epilepsy. International Review of Neurobiology 2008;83:79-90.

The post Hormones and Seizures in Women with Epilepsy appeared first on Minnesota Epilepsy Group.

ARTICLE HIGHLIGHTS

• Concussion is defined as trauma induced alteration in mental status (= not thinking right) that may or may not involve loss of consciousness.
• 1.6-3.8 million concussions per year occur in the United States.
• Those who experience a concussion with loss of consciousness are 6 times more likely to have another concussion (compared to controls).
• Chronic Traumatic Encephalopathy is a condition that occurs in some people who have had repeated concussions. It is not certain how frequent this condition occurs or how many concussions are needed. Patients with this condition are noted to have neurologic decline that is usually noted several  years or even decades after retiring from contact sports. The patients are noted to have decline in their memory, mood, and movements. Some develop a Parkinsons like syndrome. Some go on to develop severe dementia.
• Neuropsychological testing is considered a very useful tool to assess a patient with concussion.
• Protocols to have a baseline neuropsychological test (for example, at the beginning of the season) are being developed. If a patient has a concussion, the patient can have another neuropsychological test- and compare it to the baseline test.
• CT scan of the brain is the most commonly used imaging modality in patients with concussion. Other imaging possibilities: MRI, magnet source imaging, and fMRI.
• There is data to support that NFL players who have experienced repeated concussions during their careers can develop Chronic Traumatic Encephalopathy (CTE). However, the studies so far do not answer the most critical questions, including how much of a risk do NFL players face for serious memory problems in their retirement- specifically, what are the percentage of players who develop CTE?
• According to the latest research, there is not a clear relationship between repeatedly heading a soccer ball and having memory problems or other cognitive issues. This issue is still being studied.
• Players should not return to play after a head injury until all symptoms of the concussion have completely resolved.

INTRODUCTION

Concussion is a hot-topic. Reports on concussion are common in neurology journals, newspaper articles and news programs. Public interest in concussion has been sparked by such controversial issues as: 1) dementia has been noted to develop in retired NFL players who have experienced repeated concussions during their careers; and 2) questions about a possible link between repeatedly heading a soccer ball and memory problems. It should be noted that the frequency of dementia in NFL players is really not known (see below for details—I review the data). Also, the most recent research does not support the concept that heading a soccer ball causes cognitive problems (again- see below- I review the data). These news stories highlight the public’s concerns about head trauma, especially sports related concussions, on cognitive function.

The goal of this article is to describe the short-term and long-term impact of concussion. By summarizing key information on concussion, I hope to underscore how important it is to get expert advice when a patient has head injury- in order to provide the best possible outcome and to avoid potentially devastating long-term sequelae.

CLINICAL FEATURES

photo: xedos4

Concussion is defined as trauma induced alteration in mental status (= not thinking right) that may or may not involve loss of consciousness (Meehan, Pediatrics, 2009).  Sports and bicycle accidents account for the majority of concussions in 5- to 14-year-olds, whereas falls and motor vehicle accidents account for the majority of concussions in adults (Ropper, NEJM, 2007). Concussion is very common. An estimated 1.6-3.8 million sports- and recreation-related concussions occur in the United States each year. This is an estimate- since many concussions are not recognized or reported. In addition, players in collision sports such as American football may experience many hits to the head during the season that are not full concussions, but considered subconcussive impacts (impacts that do not cause symptoms that the player is aware of). For example, a lineman in football may experience 1400 impacts during a season (Stern, PM&R, 2011).

There is often amnesia with the head trauma. Anterograde amnesia (the inability to retain new information) and retrograde amnesia (inability to recall what happened before the head injury) are often seen. The more severe trauma is associated with longer periods of amnesia.

Did you know: Those who experience concussion with loss of consciousness are 6 times more likely to have another concussion, compared to those who have never lost consciousness (Delaney, Clin J Sport Med, 2000). The reason for this is complex- it could be that once an athlete has a concussion, the athlete’s brain may be more susceptible to injury. It could also be that patients who have concussions have more aggressive playing styles- resulting in increased risk for further head trauma.

The clinical course of a patient with a concussion has several possible outcomes.

• QUICK RECOVERY (< 7-10 days): The overwhelming majority of patients with concussion recover quickly and completely.
• POSTCONCUSSION SYNDROME: Some patients- weeks or months of headache, dizziness, irritability.
• SERIOUS NEUROLOGICAL DEFICITS: For example, bleeding in the brain. Uncommon.
• CHRONIC TRAUMATIC ENCEPHALOPATHY: Develops years or even decades after repeated concussions. Symptoms can include a serious decline in function- memory problems, depression, parkinsons like symptoms (tremor, slow walking) and even dementia. This is uncommon.

Most patients experience quick and complete recovery: After concussion, patients will often have mild symptoms, including headache, cognitive problems (concentration and memory complaints), dizziness, and/or fatigue for approximately 7-10 days. At this point, the overwhelming number of patients with concussion have completely recovered to baseline.

Postconcussion Syndrome: Some patients are noted to have these symptoms persist for several weeks or months. Such patients are diagnosed with Postconcussion Syndrome. The headaches can be described by the patient as very severe and essentially continuous. Concentration is one of the most prominent complaints. A mild degree of dizziness/poor balance is often described. In addition, depression and anxiety are often prominent. The symptoms will vary as to how long they persist. Although not the typical course, some patients can have these symptoms continue for > 1 year.

Serious neurological deficits: Head injury can be associated with serious neurological impairment. Intracranial hemorrhage (= bleeding in the brain) is a serious issue for some patients. Bleeding in the brain can lead to a build-up in pressure in the brain. This can cause the brain to shift. The patient may develop weakness on one side of the body, seizure activity and coma (among other symptoms). This can be a neurosurgical emergency-the surgeon may be called on to immediately open the skull and remove the blood and repair the damaged blood vessels. Because of the potential for serious neurological impairment, patients with significant concussions need a thorough evaluation.

An example of a very worrisome scenario: Person has significant head injury after falling off her bike and hitting her head- she is knocked unconscious for 5 minutes. She recovers, but has mild headache and is mildly unsteady. Two hours after the trauma, she experiences  a steadily increasingly severe headache, difficulty with speech, has right arm and leg weakness. This patient is found to have an epidural hematoma on the left side of her brain (a rapidly expanding mass of blood from a torn blood vessel). This requires emergency neurosurgery to remove the expanding blood and to repair the damage.

Chronic Traumatic Encephalopathy (CTE):

It has been observed that some people who have experienced repeated concussions in their life-time are at risk to develop neurological problems years or even decades after their last head trauma (Gavett, Clin Sports Med, 2011)(Stern, PM&R, 2011). For example, a hockey player who has had many concussions during his career may appear to be quite healthy for several years after he stops playing the sport. He may start to have memory problems developing in his early 50’s. Over the next 10 years, he may slowly decline in his function- developing slow movements and eventual dementia.

The early neurological problems for CTE include problems with memory, multitasking, organization, depression, and impulse control. The patient may have trouble taking care of their finances. Impulse control problems can lead to severe anger outbursts or illicit drug use. Depression is common. Some patients commit suicide. Late symptoms include worsening in memory function, language impairment and movement problems (similar to Parkinson’s Disease). Patients may develop dementia. Their walking may be stooped with a slow shuffling gait. The patient may be very slow to answer questions. The symptoms of CTE are usually slowly progressive over many years. Ultimately, the patient can be very limited with movements and can have severe dementia.

The link between repeated concussions and later neurological problems has been known for many years. In 1928, a group of boxers were noted to have a condition that included mental confusion and clumsy movements (Martland, JAMA, 1928). The symptoms appeared to be related to the repeated blows to the head the boxers had experienced in their careers. The term used to describe this constellation of symptoms was “punch drunk.”Over the years, more groups of boxers were described with this symptom spectrum. With further research, it was determined that activities other than boxing could produce the symptoms- this lead to the term CTE. Activities that have been associated with CTE include American football, soccer, wrestling and hockey, to name a few. In addition, victims of child abuse and patients with epilepsy have been described with CTE.

A consistent finding of CTE is a history of repeated head trauma. It has not yet been determined how many concussions or the severity of the concussions that are necessary to result in CTE. For example, it is not clear whether a few severe concussions are the most likely predisposing factor to develop CTE or whether a long history of many less severe blows to the head (such as experienced by a linemen in football) would lead to CTE. Also, it should be stressed, not all people who have repeated concussion develop CTE. It is possible that underlying genetic predisposition may lead to a higher likelihood for developing CTE. This is an important area of research!

The mechanism for developing CTE is not well understood. It has been hypothesized that stretching of neurons in the brain could lead to a cascade of events that ultimately leads to neuronal death. Pathology examination reveals that large regions of brain are shrunken- due to neurons shrinking or dying off. Microscopic examination reveals clumps of abnormal protein in various regions of the brain. These clumps of abnormal protein are called tau and are deposited in the brain in the form of neurofibrillary tangles, neuropil neurites and glial tangles. The abnormalities are prominent in the temporal lobes—which explains the problems with memory; and the frontal lobes- which explains the problems with organization and disinhibited behavior (Gavett, Clin Sports Med, 2011).

CTE is an important area of research. A better understanding of the following would be incredibly helpful: 1) what types of head trauma lead to CTE; 2) who is most likely to develop CTE; 3) how do we prevent the development of CTE in at risk people. Given that millions of athletes take part in contact sports and that large numbers of military personnel experience concussions, CTE represents an important public health issue (Stern, PM&R, 2011).

NEUROPSYCHOLOGICAL TESTING

photo: nattavut

Patients who have a concussion may experience cognitive impairment. Neuropsychological testing can be a very valuable tool to measure these impairments. Neuropsychological testing in patients with a recent concussion reveals cognitive deficits in the following areas (Putukian, PM&R, 2011):

• Memory
• Learning
• Attention
• Ability to process information
• Reaction time
• Problem solving

Neuropsychological testing can be administered and interpreted by a trained neuropsychologist. Comprehensive testing is very thorough- it can involve 6-8 hours of testing. Tests of memory (verbal and visual memory), problem solving, and attention are administered. Shorter examinations, including computerized testing, are alternatives. Currently, the optimal testing procedures are being studied.

A very interesting idea is to obtain baseline testing, especially in high risk individuals such as athletes in contact sports. A certain percentage of these athletes will have a concussion. Comparing the cognitive testing before the concussion (baseline test) to the testing after the concussion is an excellent way to determine what cognitive impairment is new.

For example, all players on a team could have neuropsychological testing at the beginning of the season- this is the baseline test. Then, any player who had a concussion would have undergo a repeat neuropsychological exam. The baseline test and the post – trauma test could then be compared. This would, of course, provide very good information on what problems in cognition were the results of the head trauma.

The above procedure (baseline testing at beginning of season/comparison testing if head trauma) has been done on sports teams already—and good information has been provided (Erlanger, J Athl Train, 2001). Currently, leaders in the field are discussing the optimal testing strategy. The concerns about the cognitive problems caused by concussion make optimal neuropsychological testing a high priority!

IMAGING

Not all patients with concussion undergo brain imaging. Patients with mild head trauma with rapid recovery may simply be observed. More severe trauma, especially with longer periods of loss of consciousness or in patients with neurological deficits (such as weakness on one side of the body, for example) may need a brain scan. The clinician evaluating the patient will make the decision. The following are some of the options for brain imaging:

• CT scan: CT scans are the most commonly used brain imaging procedure after concussion. CT provides a picture of the brain’s structure. CT scans are readily available to most emergency rooms. The scans can be done quickly- which is useful in a patient who is in significant pain. CT will identify the most critical abnormalities, including bone fractures and bleeding problems. Blood expanding in the brain is one of the most important reasons to do a brain scan after concussion. Expanding blood can be lethal if it is not surgically corrected.
• MRI: Provides a picture of the brain’s structure. The picture provided by MRI is superior to CT. Thus, MRI is used to identify more subtle brain lesions not identified with CT. MRI takes much longer than a CT to perform—that is one of the main reasons that CT is performed more often than MRI in the emergency room setting. MRIs are sometimes obtained on patients who are having cognitive problems for several days or weeks after the concussion.
• Magnet Source Imaging: This is a procedure which measures the brain’s electrical activity. Neurons in the brain produce electricity as part of their normal function. The scan will light-up when the area of the brain responsible for a function is in use. For example, if a patient is thinking of a word, the area of the brain for language will light-up. Pretty interesting! Subtle electrical abnormalities can be identified with Magnetic Source Imaging. It has been suggested that this procedure can help study: 1) the brain’s injury after concussion; and 2) to study the recovery of neuronal functional. Magnetic source imaging is currently being studied for its potential usefulness after concussion.
• Functional MRI: This is a procedure that provides information about the function of the brain. Similar to magnet source imaging, the functional mri scan will light-up when the area of the brain responsible for a given function is in use. Functional MRI measures blood flow. Similar to magnetic source imaging, this procedure is being studied for its potential usefulness after concussion.

NFL DATA

photo: freedigitalphotos

Studies on NFL players have raised concerns that repeated head trauma can lead to memory problems and even dementia (with some similarities to Alzheimer’s Disease), after the players have retired. It has been demonstrated that some players do develop dementia—see above discussion on Chronic Traumatic Encephalopathy (CTE). However, the percentage of NFL players that develop the memory problems/dementia is not clear.

Some information is provided by the “NFL’s brain bank.” This is also known as the Boston University Center for the Study of Traumatic Encephalopathy (BU CSTE). This brain bank is located at the Bedford VA Medical Center. This is the largest “brain bank” for CTE. This center has recently reported that 14 out of 15 NFL players that have so far been studied have been diagnosed with CTE.

14 out of 15- this sounds like an incredibly high number! Does this mean that 93% of NFL players are doomed to develop CTE? The answer is NO! Remember, these 15 brains had to be donated by the deceased player’s family for study at autopsy. This leads to a very important selection bias: families are much more likely to donate their loved one’s body to autopsy if they are concerned about CTE. Thus, there is likely an overrepresentation of CTE in “NFL’s brain bank.” Regardless, it does illustrate how repeated head trauma can produce serious and devastating long-term cognitive problems. It is extremely important to determine an accurate estimation of the frequency of CTE in athletes. This research is hopefully going to be accomplished- since there are so many important questions that need to be answered.

The 14^th NFL player (from above study) to be diagnosed with CTE was Dave Duerson. Dave Duerson played safety for 11 seasons with the Chicago Bears, NY Giants and Phoenix Cardinals. He committed suicide at age 50 years. Prior to his death, he noted problems with his memory, spelling, vision and emotional control. He expressed concerns to family and friends that he may have CTE. He left a suicide note that read: “Please, see that my brain is given to the NFL’s Brain Bank.” He committed suicide by shooting himself in the chest, presumably to preserve his brain for neuropathological examination (BU CSTE website).

In addition to the data from the brain bank, there has been other data suggesting that NFL players are at increased risk for cognitive problems after they have retired. For example, one study reported the results of a general health questionnaire completed by 2552 retired professional football players (Guskiewicz KM, Neurosurgery, 2005). A second questionnaire focusing on memory related questions was completed by 758 players. The study found that retired players with 3 or more concussions during their careers had a higher incidence (fivefold increase) of significant memory problems, compared to players without a history of concussion. The authors concluded that repeated concussions during a players’ career could have serious consequences on the player’s cognitive function later in life. It should be noted that this study has been criticized for methodological problems (Casson, Neurology Today, 2010).

In summary, there is data to support that NFL players who have experienced repeated concussions during their careers can develop CTE. However, the studies so far do not answer the most critical questions, including how much of a risk do NFL players face for serious memory problems in their retirement- specifically, what are the percentage of players who develop CTE? Well designed, long-term, prospective studies with large numbers of players are needed to answer the most critical questions. We are not there yet, but studies are being undertaken/designed to answer these questions.

HEADING SOCCER BALL DATA

photo: master isolated ima

The possibility that heading a soccer ball repeatedly may result in memory and other cognitive problems has been the focus of much intense media attention. This is understandable- can you imagine if simply heading a soccer ball over and over resulted in children and young adults not reaching their potential! This would be a serious problem, especially given the huge numbers of athletes heading the soccer ball across the entire world. The concerns about heading a soccer ball were raised in part after the death of Jeffrey Astle, a legendary soccer player known for his heading of the ball. He died at age 59 after several years of dementia (Spiotta A, Neurosurgery, 2012). He was found to have Chronic Traumatic Encephalopathy (CTE, see above for description).

In addition, during the 1980’s and 1990’s, multiple studies had reported a link between heading a soccer ball and cognitive problems. These studies, it should be noted, have been criticized for methodological limitations. They were also carried out at a time when the soccer ball was heavier—leather balls were used that would get very heavy, especially when wet. A major problem with these earlier studies was that there were limitations on clarifying which patients had full concussions. Consider how that would complicate these studies—if significant concussions are not controlled for, then how can you assess the milder effects of heading a soccer ball?

More recent studies have examined whether heading a soccer ball results in neurocognitive problems. These studies have not shown an association between heading a soccer ball and memory or other cognitive problems (Spiotta A, Neurosurgery, 2012).

Thus, at this time, there is not a clear relationship between repeatedly heading a soccer ball and having memory problems or other cognitive issues. This issue is still being studied. It is thought that good heading technique is important to reduce head injuries. Also, reducing player-to-player head contact and player-to-goal post collisions would also be important- it is these types of crashes that cause the symptomatic concussions—and severe concussions certainly can adversely impact cognition.

RETURN TO PLAY CONSIDERATIONS

photo:naypong

A big decision occurs every day in the world of sports- when a player has a concussion, when can they return to the game? A generally accepted management principle is that players should not return to play until all symptoms of the concussion have completely resolved (Meehan, Pediatrics, 2009). For most players, the dizziness, concentration problems and memory difficulties that were caused by the concussion will resolve in less than 7-10 days. For some players, longer periods of time will be required. In order to determine if a patient is recovered, a careful history and exam is needed. Also, neuropsychological testing can be performed. Ideally, the patient would have baseline neuropsychological data for comparison-before the concussion (for example, a baseline neuropsychological test obtained at the beginning of the season). It has been suggested that the patient not return to play until the neuropsychological testing is equal to baseline scores.

There is a condition known as “second impact syndrome.” This tragic condition was described in a 19 year-old college football player who returned to the game after a concussion, despite still having symptoms (Saunders, JAMA, 1984). He experienced some minor trauma during the remainder of the game, but not unusual contact. He walked off the field, collapsed and died. His brain had massive swelling. Although second impact syndrome is rare and controversial (some experts question if it is a real phenomena), the message is clear to most experts—conservative management of concussion is likely a good idea.

The days of having a significant concussion and then returning to the game with symptoms—for example feeling unsteady on the feet and having trouble thinking- are hopefully over. It used to be considered a sign of courage to return to the game with symptoms of a head injury. Now, such actions are strongly discouraged.

CONCLUSIONS

photo: salvatore vuono

Concussion is a common and important issue. Fortunately, most patients recover fully after a concussion. Some patients may not have full recovery, especially after relatively severe head trauma. Cognitive problems after concussion include headaches, concentration issues, memory problems and impaired mood (depression and irritability). Patients should not return to play until they have fully recovered from a concussion. Coaches, schools, players and families are becoming much more aware of the seriousness of head injury. Repeated concussion in sports such as boxing, football and hockey, can result in Chronic Traumatic Encephalopathy (CTE)- this usually develops several years after retiring from contact sports. CTE results in a decline in neurologic function that can be severe.

There are many important questions to be answered about concussion. For example: 1) What are the best ways to prevent concussion? 2) Are there people who are predisposed to get concussions? 3) What testing is most appropriate- before and after concussion?  4) What kind of trauma results in CTE? Research to answer these important questions is ongoing.

REFERENCES

BU CSTE website

https://www.bu.edu/cste/2011/05/03/nfl-player-dave-duerson-suffered-from-advanced-cte/

Casson IR. Do the facts really support an association between NFL players’ concussions, dementia and depression. Neurology Today 2010.

Delaney JS, Lacroix VJ, Leclerc S, Johnston KM. Concussions during the 1997 Canadian Football League season. Clin J Sport Med 2000;10:9-14.

Gavett BE, Stern RA, Mckee AC. Chronic traumatic encephalopathy: a potential late effect of sport-related concussive and subconcussive head trauma. Clin Sports Med 2011;30:1-10.

Martland HS. Punch drunk. JAMA 1928;91:1103-1107.

Meehand W, Bachur RG. Sport-related concussion. Pediatrics 2009;123:114-123.

Putukian M. Neuropsychological testing as it relates to recovery from sports-related concussion. PM&R 2011;3:S425-S432.

Ropper AH, Gorson KC. Concussion. N Engl J Med 2007;356:166-72.

Spiotta AM, Bartsch AJ, Benzel EC. Heading in soccer:dangerous play? Neurosurgery 2012;70:1-11.

Stern R, Riley DO, Daneshvar DH, et al. Long-term consequences of repetitive brain trauma: chronic traumatic encephalopathy. PM&R 2011;3:S460-S467.

Xedos4 (Sport photo)
https://www.freedigitalphotos.net/images/view_photog.php?photogid=1539

Nattavut’s (Numbers in brain photo)
https://www.freedigitalphotos.net/images/view_photog.php?photogid=1675

Football helmet photo

FreeDigitalPhotos.net

Master isolated image (figure and soccer ball)
https://www.freedigitalphotos.net/images/view_photog.php?photogid=1962

Naypong (whistle and ball photo)
https://www.freedigitalphotos.net/images/view_photog.php?photogid=2617

Salvatore Vuono (skier sign photo)
https://www.freedigitalphotos.net/images/view_photog.php?photogid=659

The post CONCUSSION: Short and Long-Term Impact appeared first on Minnesota Epilepsy Group.

Despite a proven track record, it is typically many years from the time the patient starts having seizures to the time they finally have epilepsy surgery. Studies suggest that patients are finally referred for epilepsy surgery after 20 years of seizure activity. There is mounting data that performing epilepsy surgery sooner rather later may be helpful. Surely, it does not take 20 years to see if 2 or 3 seizure medications are going to control the seizures! Please note- if a patient has not had his or her seizures controlled after trying 2 AEDs, the chances of having AEDs completely control the seizures is quite low. That is why epilepsy surgery is considered in those who have tried 2 AEDs.

Of course, epilepsy surgery has risks. Remember, the surgery involves having the surgeon remove a piece of the skull and removing a piece of brain tissue. This brain tissue is the area of the brain that the seizures were starting. By removing this abnormal tissue, the seizures can be controlled. Risks include stroke, infection or memory problems. With careful evaluation, these risks can be minimized.

A recent article has been published entitled “Early Surgical Therapy for Drug-Resistant Temporal Lobe Epilepsy.” (Engel, JAMA, 2012). The goal of the study was to compare: 1) epilepsy surgery to 2) continued AED therapy without epilepsy surgery. The study looked at the effect of surgery on seizure control and the effect on quality of life. The patients in the study had tried 2 AEDs and were still having seizures. The seizures had to be disabling for no more than 2 consecutive years. This is important—this is the “early” part of the study. Rather than waiting for many many years, the study sought to evaluate those who had seizures for only a short period of time (< 2 years).

A total of 38 patients (18 men and 20 women) with temporal lobe epilepsy were included in the study. 15 patients were randomized to the surgery group and 23 patients were randomized to the medical group (medical group – treated with AED only, did not have surgery). It should be noted, the surgery patients did continue their AEDs.

Results:

• Surgery group: 11 of 15 patients were seizure free.
• Medical group: 0 of 23 patients were seizure free. (P < 0.001)
• Quality of life scores were better in the surgery group, but the findings did not reach statistical significance (p=0.08).
• Surgery group adverse events: 1 patient had a postoperative stroke. Neurologic symptoms resolved.
• Medical group adverse events: 3 patients went into status epilepticus (prolonged and potentially dangerous seizure activity).

The authors concluded that early surgery is superior to AED treatment alone for controlling seizures in patients with temporal lobe epilepsy. This study clearly supports the idea that you should not wait years and years for surgery. If a patient is not responding to AEDs, then surgery should be considered sooner rather than later.

The study suggested that quality of life was also better in the surgery group, but the small number of patients resulted in a non-significant finding. It should be noted that the study was stopped early because it was a challenge to recruit patients that met the inclusion criteria. The actual study had a total of 38 patients—the goal was 200. Because of the small numbers, the results need to be interpreted with appropriate caution.

This study supports the recommendation of the American Academy of Neurology: if a patient’s seizures are not controlled by 2 AEDs, then evaluation for possible epilepsy surgery should be considered. This should happen sooner rather than later!

REFERENCES

Engel J, McDermott M, Wiebe S, et al. Early surgical therapy for drug-resistant temporal lobe epilepsy. JAMA 2012;307:922-930.

The post Surgery for Epilepsy Sooner Rather Than Later appeared first on Minnesota Epilepsy Group.