There are many different types of genetic tests available to doctors treating epilepsy. Some of them are easy, low-cost tests that are less likely to find the cause of seizures. Some are much more expensive but are much more likely to get answers. When doing genetic tests, most epilepsy doctors start with the lower-cost tests first. If these do not find an answer, they often will order more expensive tests until an answer is found. We do not know if this is the best approach.

READ MORE

https://n.neurology.org/content/92/5/e523

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INTRODUCTION

Epilepsy is considered “resolved” for:

• People who have a type of epilepsy that the patient is expected to “outgrow”—and the patient is significantly older than the age that further seizures would be expected; or
• People who have remained seizure-free for the last 10 years, with no seizure medications for the last 5 years.

The term for a person who had epilepsy in the past and is no longer considered to have epilepsy is: “resolved epilepsy”. The ILAE used the word “resolved” rather than “in remission” or “cured” in order to send a clearer meaning. For example, “cured” indicates that the patient has no increased risk for seizures. Although patients who have, for example, gone > 10 years seizure free may have a very low risk for seizure activity, their risk may still be somewhat higher than the general population. It was thought that the word “resolved” conveyed a more precise description.

PATIENT STORY #1

A 22 year-old man has had three seizures in his life- at age 9, 10 and 14 years of age. Seizures consisted of facial twitching just prior to falling asleep. EEG at age 9 years showed spikes in a pattern consistent with Benign Epilepsy with Centrotemporal Spikes (BECTs). BECTs is an epilepsy syndrome that patients are expected to outgrow. At age 16 years he was tapered off his seizures medications. He has had no further seizures.

This patient would be considered to have his epilepsy resolved. This is because he is currently older than the age that seizures would be expected, given his type of epilepsy. He would be considered to have “outgrown” his epilepsy. Or, in the new terminology: his epilepsy is resolved.

PATIENT STORY #2

48 year-old male with the first seizure of his life at age 13 years. The initial seizure was a generalized tonic-clonic seizure. EEG was normal. No history of sleep deprivation or other triggers for seizures. No etiology was identified. He had a second generalized tonic-clonic seizure at age 14 years. He was started on a seizure medication. Because he had no further seizures, the seizure medication was tapered to off at age 17 years. He has had no further seizures.

This 48 year-old is currently a nurse working at a local hospital. He was recently filling out paperwork – he was asked if he had epilepsy. He wanted to be truthful. He decided to ask a Minnesota Epilepsy Group epileptologist if he had epilepsy or not. He really did not think he had epilepsy, since his last seizure was so many decades ago.

Our 48 year-old is exactly correct! His epilepsy is resolved. Based on the criteria above: he has remained seizure-free for the last 10 years, with no seizure medications for much greater than 5 years. As a matter of fact, his epilepsy was resolved a long time ago!

CONCLUSIONS

Patients who have not had seizures for many years may wonder if they still have epilepsy. The ILAE has provided the following criteria for epilepsy being resolved:

• People who have a type of epilepsy that the patient is expected to “outgrow”—and the patient is significantly older than the age that further seizures would be expected; or
• People who have remained seizure-free for the last 10 years, with no seizure medications for the last 5 years.

We are learning more and more about the natural history of seizures in people with epilepsy. In the past (before 1990), there was little data on what happens to patients with epilepsy over the course of their lives. The good news is that data in recent years suggests that a sizable percentage of patients will have long periods of seizure freedom off seizure medications. Further research is needed to better understand which individual patients will have their epilepsy resolve. Also, wouldn’t it be great if medications (used for a short time) or other treatments could be developed to substantially increase the percentage of patients with resolved epilepsy?

REFERENCES

Fisher RS. A practical clinical definition of epilepsy. Epilepsia 2014;55:475-482.
Kwan P, Sander JW. The natural history of epilepsy: an epidemiological view. J Neurol Neurosurg Psychiatry 2004;75:1376-1381.

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The purpose of this article is to highlight a recent study which reviews the literature in tremendous detail in order to answer the following questions:

1) Does marijuana improve seizure control?
2) Is marijuana safe?

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3639568/pdf/i1535-7511-13-2-81.pdf

STUDY DESIGN
The authors did a very extensive review of the literature- in order to identify all papers that performed randomized control trials assessing marijuana in the treatment of epilepsy.

RESULTS
The study found: ” four randomized reports which included a total of 48 patients, each of which used cannabidiol as the treatment agent. (Cannabidiol is an important extract of marijuana). One report was an abstract, and another was a letter to the editor. Anti-epileptic drugs were continued in all. Details of randomisation were not included in any study. There was no investigation of whether control and treatment groups were the same or different. All the reports were low quality. ”

As far as seizure control, little information is provided: One study reported two of four treated patients becoming seizure free for 3 months. The other studies either reported no benefit, or the effect was not clearly stated.

CONCLUSIONS
“No reliable conclusions can be drawn at present regarding the efficacy of cannabinoids as a treatment for epilepsy. The dose of 200 to 300 mg daily of cannabidiol was safely administered to small numbers of patients, for generally short periods of time, and so the safety of long term cannabidiol treatment cannot be reliably assessed.”

Thus, at this time, there is a lack of scientific evidence to recommend marijuana for the treatment of epilepsy. To quote the American Epilepsy Society:

“The lack of information does not mean that marijuana is ineffective for epilepsy. It merely means that we do not know if marijuana is a safe and efficacious treatment for epilepsy. Healthcare professionals, patients, and caregivers are reminded that use of marijuana for epilepsy may not be advisable due to lack of information on safety and efficacy, and that, despite some states legalizing the use of medical marijuana, it is against Federal Law to possess or use marijuana.  In addition, little is known about the long term effects of using marijuana in infants and children, and chronic exposure during adolescence has been shown to have lasting negative effects on cognition and mood.  Such safety concerns coupled with a lack of evidence of efficacy in controlled studies result in a risk/benefit ratio that does not support use of marijuana for treatment of seizures at this time. The American Epilepsy Society is supportive of well-designed research to determine the safety and efficacy of marijuana in the treatment of epilepsy.”

https://www.aesnet.org/press-room/consensus-statements/marijuana-and-epilepsy

Please send in your comments on this important topic! Thank you!

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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.

The post Migraine and Epilepsy appeared first on Minnesota Epilepsy Group.

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/

The post Surgery For Epilepsy May Improve Intellectual Function In Children appeared first on Minnesota Epilepsy Group.

• Long-term use of certain seizure medications can result in thinning of a person’s bones.
• Reduced bone density results in osteopenia (mild bone density loss) or osteoporosis (severe bone density loss).
• Osteoporosis can be very problematic for quality of life!
• Low bone density predisposes people to bone fractures. 
• People with epilepsy are at higher risk for falls and other accidents that can cause bone breaks.
• DEXA scan is an excellent way to determine a patient’s bone density- in order to diagnose if there is a problem with thinning of the bones.
• Building healthy bones (treatments are tailored to the individual):
  • Exercise
  • Vitamin D
  • Calcium
  • Prescribed medication to build bone strength (biphosphonate therapy)

INTRODUCTION

It has been known for decades that antiepileptic drugs (AEDs) are associated with bone density loss. Reduced bone density results in osteopenia (mild bone density loss) or osteoporosis (severe bone density loss). Low bone density predisposes people to fractures. Fractures usually involve the hip, spine or forearm. Bone health has recently become a hot-topic in the epilepsy community because much more is now known about the devastating impact of bone loss on quality of life. In the general population, approximately 40% of women and 13% of men older than 50 years will develop a fracture associated with reduced bone density. Patients with hip fractures far too commonly go from independent living to requiring nursing home placement. In selected populations, of those who develop a hip fracture, 20-30% will die within one year. The dramatic effect that osteoporosis has on quality of life has been a wake-up call for better diagnosis and treatment of this disorder.

This article reviews bone health issues pertinent to patients with epilepsy.

Bone Formation

Bone Mass Graph

A brief review on bone formation will help the reader understand important issues in this article. The most critical time for bone development occurs early in life. Bone density builds during childhood and peaks at approximately age 20 years. Between 20 and 40 years of age, bones remain at a fairly constant level of strength. After age 40, bone density gradually declines. As people reach older age, bones that are weakened by declining bone density may become easily broken with even minor falls.

Factors that are important in developing good bone strength include adequate calcium, vitamin D and exercise.

BONE HEALTH ISSUES

AEDs and bone loss

Long-term use of AEDs has been clearly associated with the development of osteopenia and osteoporosis. The use of more than one AED increases the risk. It is not clear how long it will take to develop bone density problems in patients taking AEDs. Once a patient has been on an AED for approximately 5 years, physicians may consider testing bone density. Certain AEDs have clear studies indicating an association with osteoporosis. These AEDs include phenytoin (= Dilantin), carbamazepine (=Tegretol, Carbatrol), valproic acid (= Depakote) and phenobarbital. The newer AEDs have not been as clearly shown to be associated with bone density loss, but fewer studies are available.

The question “How do AEDs cause osteoporosis?”  is currently a very active area of research. One possibility is by reducing vitamin D. Vitamin D is important for the normal absorption of calcium. If vitamin D is deficient, then calcium is not absorbed normally. Low calcium results in weak bones. Certain AEDs (phenytoin (= Dilantin), carbamazepine (=Tegretol, Carbatrol) and Phenobarbital) increase the metabolic rate of the liver. This increased metabolic rate causes a reduction in vitamin D. Although low vitamin D may be an important cause of osteoporosis in patients taking AEDs, other reasons are also hypothesized. The current thinking is that reduced vitamin D does not explain all cases of osteoporosis, so other mechanisms must be important.

Adequate bone formation early in life is critical for strong bones later in life. AEDs have the potential to prevent bones from reaching a normal peak density by age 20 years. If patients do not have strong bones by early adulthood, then the gradual decline over the years may result in low bone density at a relatively early age. Some patients can develop osteoporosis as young adults or even earlier! Also, AEDs started in adulthood can accelerate the loss of bone strength. Again, this can set a patient up for weakened bones.

Mobility/exercise:

Bones get stronger with hard work! The forceful pounding of the pavement, jumping, running and lifting the weight of their owner leads to good strong bones.  If patients are having limitations in mobility, then bones may have difficulty reaching their full strength. For example, patients who are in a wheelchair or have significant weakness in their arms and/or legs may not be able to adequately exercise to achieve normal bone density. Some people may have chronic diseases or other reasons that prevent them from being adequately mobile. Such patients are at higher risk for developing osteoporosis.

Exercise has been demonstrated to be beneficial for bone density. For example, women who performed weight-bearing exercise for 30 minutes every day had a 4% increase in spine bone density. In contrast, the controls (who did not exercise significantly) lost 3% of bone density. Thus, exercise is likely a good way to prevent and treat bone density loss.

Fractures:

Patients with epilepsy have 2-6 times the rate of breaking bones compared to the general population. There are multiple reasons for the increased risk of fracture in those with epilepsy. One reason is that patients with epilepsy are at increased risk for accidents. Patients with epilepsy may be at high risk for falling because of seizure activity. Seizures can result in some truly terrible accidents. Patients may not be able to brace a fall because of the seizure activity. The seizures may occur at very unfortunate times—in the shower, walking down stairs, while driving or up on a ladder. Also, patients are on medications which can make them walk in a very unsteady fashion. Patients know this issue well. Patients are often asked during a clinic appointment to walk with one foot in front of the other (like the police officer’s test!). Patients often have difficulty with this because of their AEDs. The poor balance can result in falls—especially if the patient is walking on an uneven surface, when it is dark or icy.

Another reason for the increased fractures in patients with epilepsy is the reduced bone density noted in this population. The weaker bones do not handle falls well—bones can break even with minor falls or injuries. To say this is frustrating is an understatement!

DIAGNOSIS

Bone density falls into one of three categories:

1. Normal
2. Osteopenia (mild bone density loss)
3. Osteoporosis (severe bone density loss)

The gold-standard test for testing bone density is the dual-energy x-ray aborptiometry scan. Do not try to remember this long term for this test. Just remember DEXA scan. The DEXA scan is a relatively easy test for a patient to go through. It will reliably diagnose problems with bone strength. There is a very strong correlation between reduced bone density (weak bones) and fractures.

It is not clear precisely when to obtain a bone density on an individual patient. It is often recommended that after 5 years of AED use, a bone density should be considered. Shorter time frames may be appropriate for certain high risk groups (such as elderly women and those who are wheelchair bound).

TREATMENT

Prevention

• Weight bearing exercise
• Do not smoke cigarettes
• Do not drink alcohol excessively
• Take vitamin D and calcium

Osteopenia (mild bone loss)

• Take calcium and vitamin D
• Depending on case, may consider changing AED—to reduce risk of developing osteoporosis (must be very cautious—do not want to risk serious seizures)

Osteoporosis (severe bone loss)

• Take calcium and vitamin D
• Depending on case, may consider changing AED—to reduce risk of developing osteoporosis (must be very cautious—do not want to risk serious seizures)
• Bisphosphonate therapy (= Fosamax, Actonel and Boniva)

CONCLUSIONS

Patients who have been taking seizure medications for several years need to be aware of the possibility of bone density loss. Bone density loss can be a major problem for quality of life—leading to possible osteoporosis. Health care providers and epilepsy patients need to: 1) discuss this issue in detail; 2) decide on whether or not testing for bone density is indicated; 3) use preventative measures to improve bone health (exercise, for example) and 4) if bone loss is a problem, then provide the optimal treatment. The real key is tailoring the prevention and treatment plan to the individual patient to obtain the best possible outcome!

REFERENCES

Sheth RD, Harden CL. Screening for bone health in epilepsy. Epilepsia 2007;48 (suppl):39-41.
Pack AM. The association between antiepileptic drugs and bone disease. Epilepsy Currents 2003;3:91-95.
Sheth RD. Bone health in epilepsy. Epilepsia 2002;43:1453-1454.

PHOTO CREDITS

Bone mass graph:  https://www2.kumc.edu/coa/images/Reynolds/bone-mass-graph.gif

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