Concussions and the risk of post-traumatic epilepsy

Concussions and the risk of post-traumatic epilepsy

 

A concussion is a complex pathophysiological process affecting the brain, induced by traumatic biomechanical forces. Immediately following a concussion, an athlete is usually advised physical and cognitive rest till post-concussion symptoms abate. The athlete then enters a stepwise return to play protocol. Premature return to play risks a second concussion, second impact syndrome, exacerbation and persistence of post-concussive symptoms.

 

Sports and Epilepsy

Sport is important not only in normal healthy populations, but also in persons with medical illness, physical or mental disabilities. Active participation in sports is beneficial physically and psychologically. The main concern in sports for persons with epilepsy is safety.

 

Why are people with epilepsy restricted from some sports?

 

Rationale is that the occurrence of an untimely seizure during certain sporting event has the potential for causing substantial injury and bodily harm both to the patient with epilepsy as well as fellow athletes and even spectators.

 

Example: if a person with epilepsy has a generalized convulsion or a complex partial seizure while skydiving: he shall not be able to deploy his parachute and a fatal accident can occur.

 

:a person with epilepsy taking part in an automobile racing event suffers a seizure while making a bend at speeds in excess of 100mph

 

:a person with epilepsy suffers a seizure while taking part in a swimming meet.

 

:a person with epilepsy suffers a seizure while bicycling

 

:a person with epilepsy suffers a seizure while horseback riding

 

:a person with epilepsy suffers a seizure while skiing down a steep hill

 

:even things more mundane such as having a seizure while running on a treadmill, while playing tennis, while jogging outside have the potential to cause bodily harm to the patient and others.

 

 

Why are people with epilepsy restricted from some sports?

 

Rationale is that repeated injury to the head (concussions) during some sports could potentially exacerbate seizures.

Example: a person with epilepsy who is indulging in contact sports such as boxing, karate, kick-boxing, muay thai boxing, American football, ice-hockey, wrestling, judo

 

But are these restrictions and fears actually based on scientific evidence or are they unfounded? Which sports are safe and which are not? Could indulgence in some sports make seizures potentially worse Vs. could some sports actually be beneficial for people with epilepsy (physically and psychologically)? Can vigorous physical exercise provoke seizures?

 

 

Exercise and seizures

 

One reason that people with epilepsy have been traditionally restricted from certain sports is the fear both in the patient and the treating physician that exercise especially aerobic exercise may exacerbate seizures. Some studies have shown an increase in interictal discharges during or after exercise. Most frequently these patients have generalized epilepsies. At least some frontal lobe and temporal lobe seizures are clearly precipitated or at times solely occur during exercise suggests that these are a form of reflex epilepsies. A number of physiologic mechanism by which seizures may be provoked by exercise have been postulated. These include hyperventilation with resultant hypocarbia and alkalosis induced by exercise. Another possible mechanism which is postulated to cause exercise induced seizures is hypoglycemia. This usually causes seizures after exercise in diabetic patients. Other mechanisms which have been postulated for exercise triggered seizures include the physical and psychological stress of competitive sports and potential changes in anti-epileptic drug metabolism. Exercise is a complex behavior and involves not such the motor system and the motor cortex but also involves other domains such as attention, concentration, vigilance and presumably some limbic networks which mediate motivation, aggression and competitiveness. Hence it is possible that patients who have temporal or frontal lobe epilepsy may on rare occasions have seizures triggered by exercise.

 

There is some limited evidence that exercise may in fact be protective and have physical, physiological and psychological benefits in patients with epilepsy. Electroencephalographic studies have shown that inter-ictal epileptiform discharges either remain unchanged or may decrease during exercise so there is some hint that exercise may actually raise the seizure threshold. Regular exercise also influences neuronal and hippocampal plasticity by upregulation of neurotropic factors. There is further evidence to suggest that regular physical exercise can improve the quality of life, reduce anxiety and depression and improve seizure control in patients with chronic epilepsy.

 

 

 

 

 

 

 

 

What sports are off limits for people with epilepsy?

 

No sport is completely off limit for a patient with epilepsy. Key though is proper supervision to reduce the potential for injury. There are some sports such as skydiving, automobile racing, swimming in the open seas and horseback riding which should be avoided by patients with epilepsy. Other sports can be enjoyed by patients with epilepsy but one should remember that they all have the potential to result in bodily harm if seizures occur when the patient is not supervised or if he is not wearing protective head and body gear.

 

 

Concussion and seizures (post traumatic epilepsy): what is the link?

 

The link between concussion (closed head trauma) and seizures has been and continues to be closely looked at. The fear of concussions (minor head trauma) making seizures worse is the prime reason why people with epilepsy are discouraged from some sports such as tackle football, ice-hockey, boxing, mixed martial arts and wrestling. The human skull is quite resilient and the closed head trauma has to be significant for it to result in seizures. Usually a concussion which results in prolonged loss of consciousness (some authors say more than 30 minutes) is graded as a significant head trauma. Minor bumps and bruises to the head do not cause seizures, do not increase the risk of future seizures and more importantly do not make chronic epilepsy worse. Seizures may occur immediately following a severe closed head trauma. Immediate post traumatic seizures by definition occur within 24 hours of the injury. They have also been referred to as impact seizures. Early post traumatic epilepsy refers to seizures which occur about a week to 6 months after the injury. Seizures may occur as far out at 2 to 5 years after head trauma (late post traumatic epilepsy). Factors which increase the risk of post traumatic seizures/ epilepsy include severity of trauma, prolonged loss of consciousness (more than 24 hours), penetrating head injury, intra or extraaxial hemorrhage, depressed skull fracture and early post traumatic seizures.

Counseling patients

 

Patients with epilepsy should be encouraged to exercise and take part in sports. My personal feeling is that no sport should be off limits to them with the exception of maybe sky-diving, river rafting and boxing. The goal should be exercising and playing sports safely. Walking, running, cycling and yoga are great exercises which can be indulged in with little to no risks. I advise all my patients with epilepsy (especially those with poorly controlled epilepsy) to wear a Medic Alert bracelet or carry a card in their wallet. This is of immense help were a seizure to occur in the field (as for example when a patient is jogging or cycling and is not in the immediate vicinity of his or her home). Low risk recreational sports such as walking or running usually do not need a one is to one supervision if seizures are well controlled by history. Team sports such as volleyball, basketball, baseball and softball are popular sports which carry a low risk of injury. For cycling I advise my patients to wear a helmet and have their bikes fitted with lights and reflectors. I also advise them to keep off from the busy city streets. “you do not want to have a seizure at the wrong place and at the wrong time”. Swimming is a great way to keep fit and also to meet and make friends. I feel many patients with epilepsy are discouraged from swimming due to an irrational fear of caregivers and physicians of drowning. I advise my patients not to swim alone. Most of the city pools have life guards and a polite request to them to keep a watch out goes a long way in reassuring both the patient and the caregivers. Swimming in the open seas is more risky. I advise my patients to swim close to the beach under the watchful eyes of a life guard. Also having a buddy around helps, preferably someone strong enough to pull the patient out of the water if a seizure was to occur. The option of wearing a life jacket is under utilized.

 

Final thoughts (a patient’s perspective)

 

These are the thoughts of a young patient of mine:

 

“I have always been a very active person and love playing sports such as Tennis, Yoga, Running etc, and I always try to pursue my dreams and not let things get in the way, but being epileptic, it is sometime hard to not worry about things happening. Whenever I play sports I get hot easily (face turns purple) and in the back of my head I find myself always hoping that nothing happens that would cause me to have a seizure. I ran my first half marathon two years ago, and in the back of my head there is always the thought of something happening, so I started to motivate myself by saying “I can do this, you will be fine.” My father taught me when I was younger that I can choose to let it hold me back or make the most of life! Many people consider epilepsy a disability, but I try not to because I don’t let it hold me back.”

 

 

Nitin K Sethi, MD, MBBS, FAAN Assistant Professor of Neurology New York-Presbyterian Hospital Weill Cornell Medical Center

Devices in the treatment of epilepsy

Devices in the treatment of epilepsy

Nitin K Sethi, MD

A number of neurostimulation devices are now available for the treatment of medically refractory epilepsy. Medically refractory epilepsy is currently defined as the failure of the patient’s epilepsy to respond to the use of at least 2 frontline and appropriate anti-epileptic drugs (AEDs)) (some physicians use up to 3 drugs) used in a successive fashion.

Types of devices for the treatment of medically refractory epilepsy:

1. Vagus Nerve Stimulator (VNS)
2. Responsive Neurostimulator (RNS)
3. Deep brain stimulator (DBS)

Neurostimulation not a replacement for resective surgical options.

Vagus Nerve Stimulator (VNS): fundamental concepts

1. pacemaker like device to stimulate the Vagus (CN X) nerve.
2. manufactured by Cyberonics Inc, Houston, Tx
3. gained FDA approval in 1997 for the adjunctive treatment of patients over 12 years of age with medically intractable partial onset seizure disorder.
4. Approved in Europe in 1994.
5. simple device consisting of 2 electrodes, an externally programmable pulse generator and a battery pack.
6. the stimulating electrode is implanted around the midcervical portion of the left vagus nerve (composed of 80% afferent fibers) while the impulse generator along with the battery pack is implanted in a subcutaneous pocket in the left infraclavicular region.
7. left vagus nerve is the preferred site of stimulation due to the higher risks of cardiac arrhythmias with right vagus nerve stimulation as it innervates the sinoatrial node and thus influences heart rate and rhythm.
8. the pulse generator is programmed externally through the skin via a magnetic currently hand held wand.
9. different parameters of stimulation can be programmed such as current strength, pulse width, pulse train frequency, current on and off times as well as magnet current strength.
10. a magnet usually worn on the patient’s arm can provide on-demand stimulation.

Mechanism of action of VNS:

1. Not fully elucidated.
2. Vagus nerve has afferent inputs to multiple areas which may be involved in the generation or propagation of ictal activity: reticular formation, thalamus, cerebral cortex.
3. Electrical impulses via the left vagus nerve travel to the nucleus of tractus solitaries (NTS). From the NTS are outflow tracts to reticular formation and locus ceruleus (LC) increasing the release of norepinephrine and serotonin. VNS may thus increase the release of gamma amino butyric acid or inhibit the release of glutamate. Rats in which the LC is destroyed, VNS is no longer effective in controlling seizures.
4. Widespread cortical de-synchronization by the afferent volley of impulses leading to inhibition of recruitment of epileptic discharges may be another mechanism.
5. Alteration of cerebral blood flow (CBF) in specific areas of the brain-not widely accepted.
6. Peripheral stimulation of CN X may modify the epileptic network circuit in the brain by synaptic modulation.
7. Effects on the amygdala likely mediate the antidepressant effects and mood elevating effects of VNS.

Stimulation parameters which can be adjusted:

1. Output current (usual settings are between 1.5 and 2.25 mA)
2. Pulse width (usually between 250-500microsecs)
3. Frequency (usually between 20 to 30 Hz)
4. Time on (usually on for 30 secs)
5. Time off (usually off for 3 to 5 mins)
6. Magnet current (usually set at 0.25 mA above output current)
7. Fast cycling 7 secs on and 14 secs off.
8. Battery life depends upon stimulation settings

Generator models currently available:

1. 102 Pulse
2. 102 Pulse Duo
3. 103 Demipulse
4. 104 Demipulse Duo
5. 105 Aspire HC
6. 106 Aspire SR

Clinical efficacy of VNS:

1. Multiple studies establish the efficacy of VNS in patients with partial onset (focal) epilepsy both in children and adults.
2. Currently FDA approved for adjunctive therapy in reducing the frequency of seizures in adults and adolescents over 12 years of age with partial onset seizures that are refractory to antiepileptic medications.
3. Currently FDA approved for the adjunctive long-term treatment of chronic or recurrent depression for patients 18 years of age or older who are experiencing a major depressive episode and have not had an adequate response to four or more adequate antidepressant treatments.
4. Used at times for generalized epilepsy but efficacy not established-lack of good quality studies.
5. Case reports showing efficacy in Lennox-Gastaut syndrome (LGS).

Side-effects/ complications of VNS therapy:

1. infection at the generator implantation site.
2. dyspnea, coughing bouts, laryngeal spasms and choking as current is increased.
3. dysphagia, odynophagia as current is increased
4. hoarseness or change in voice
5. thermal injury to the Vagus nerve can occur but is not commonly reported
6. use with caution in patients with COPD and asthma.
7. VNS may worsen pre-existing obstructive sleep apnea (OSA) due to central and peripheral mechanisms by altering the tone of the upper airways mucles.
8. Recommendation is to turn off VNS prior to CPAP titration.

Contraindications of VNS therapy:

1. MRI is not an absolute contraindication.
2. MRI can be carried out-but recommendation is to turn the device off first.
3. Interrogate device both before and after MRI scan.
4. Avoid use of short-wave diathermy, microwave diathermy and devices which generate strong electric or magnetic fields in the vicinity of the VNS.

Responsive Neurostimulation Device (RNS): fundamental concepts

1. Pacemaker like device to stimulate the epileptogenic focus or foci in the brain.
2. manufactured by NeuroPace, Mountain View, California.
3. generator is implanted in a pocket drilled into the skull bone by the neurosurgeon.
4. cortical strip leads and NeuroPace depth leads are implanted onto or into the epileptogenic focus or foci determined by
5. remote monitor and wand used by patient to interrogate device, collect data and upload to the Internet for the physician.
6. programmer and wand used by physician to collect data and program the neurostimulator.
7. a magnet can be swiped over the device to trigger storage of ECoG and also to temporarily stop stimulation.
8. FDA approved as adjunctive therapy in individuals 18 years of age or older with partial onset seizures who have undergone diagnostic testing that localized no more than 2 epileptogenic foci, are refractory to two or more antiepileptic medications, and currently have frequent and disabling seizures (motor partial seizures, complex partial seizures and/or secondarily generalized seizures).
9. Unlike VNS which is an open-loop device, RNS is semi-closed. The device continuously records electrocorticogram (ECoG) and then based on an algorithm can be programmed to deliver brief pulses of electrical stimulation when it detects activity that could lead to a seizure.

Mechanism of action of RNS:

1. rationale for RNS is responsive stimulation of an epileptic focus/ foci in the brain
2. if stimulated in time and with current of appropriate intensity, evolving seizure shall get aborted
3. involves real time electrographic analysis and responsive and automatic delivery of stimulation

Stimulation parameters for RNS:

1. two different epileptogenic foci can be stimulated individually
2. wide range of stimulation settings/parameters that can be adjusted-from 40 to 1000 microseconds, 1 to 333 Hz, 0.5 to 12 mA

Clinical efficacy of RNS:

1. Results similar to other stimulation devices
2. At the end of 2 years, the median seizure reduction was 56%.

Side-effects/ complications of RNS therapy

1. Surgical complications during implantation of device-risk of hemorrhage, infection
2. Lead breakdown/disconnection
3. Replacement of generator requires another craniotomy
4. Patient needs close follow up for stimulation parameters adjustment hence not ideal for patients who live in rural areas or cannot come for regular follow ups.

Deep Brain Stimulator (DBS): fundamental concepts

1. Stimulation of the anterior nucleus of thalamus (ANT)
2. Electrodes implanted bilaterally in the ANT.
3. Stimulator and battery implanted under left clavicle.

Stimulation parameters for DBS:

1. high-frequency stimulation
2. 5 V, 145 pulses per sec, 90 microseconds, cycle time 1 minute on and 5 minutes off

Mechanism of action of DBS:

1. thalamus is a major relay station and thalamocortical networks are widely believed to be involved in seizure propogation by synchronization of ictal activity.
2. stimulation of ANT may cause desynchronization and thus inhibit seizure propogation.
3. in animal experiments low-frequency stimulation leads to EEG synchronization and high-frequency causes EEG desynchronization.

Clinical efficacy of DBS:

1. SANTE (stimulation of the anterior nucleus of thalamus for treatment of refractory epilepsy) study-results similar to other stimulation devices.
2. Fourteen patients were seizure-free for 6 months.

Side-effects/ complications of DBS therapy

1. Surgical complications during implantation of device-risk of hemorrhage, infection
2. Lead breakdown/disconnection
3. Replacement of generator requires another craniotomy
4. Patient needs close follow up for stimulation parameters adjustment hence not ideal for patients who live in rural areas or cannot come for regular follow ups.


References

1. Parakh M, Katewa V. Non-pharmacologic management of epilepsy. Indian J Pediatr. 2014 Oct;81(10):1073-80. doi: 10.1007/s12098-014-1519-z. Epub 2014 Jul 5.
2. Ulate-Campos A, Cean-Cabrera L, Petanas-Argemi J, García-Fructuoso G, Aparicio J, López-Sala A, Palacio-Navarro A, Mas MJ, Muchart J, Rebollo M, Sanmartí FX. Vagus nerve stimulator implantation for epilepsy in a paediatric hospital: outcomes and effect on quality of life. Neurologia. 2014 Jun 26. pii: S0213-4853(14)00122-4.
3. Terra VC, Amorim R, Silvado C, Oliveira AJ, Jorge CL, Faveret E, Ragazzo P, De Paola L. Vagus nerve stimulator in patients with epilepsy: indications and recommendations for use. Arq Neuropsiquiatr. 2013 Nov;71(11):902-6.
4. Meneses MS, Rocha SF, Simão C, Santos HN, Pereira C, Kowacs PA. Vagus nerve stimulation may be a sound therapeutic option in the treatment of refractory epilepsy. Arq Neuropsiquiatr. 2013 Jan;71(1):25-30.
5. Wang DD, Deans AE, Barkovich AJ, Tihan T, Barbaro NM, Garcia PA, Chang EF. Transmantle sign in focal cortical dysplasia: a unique radiological entity with excellent prognosis for seizure control. J Neurosurg. 2013 Feb;118(2):337-44.
6. Spatola M, Jeannet PY, Pollo C, Wider C, Labrum R, Rossetti AO. Effect of vagus nerve stimulation in an adult patient with Dravet syndrome: contribution to sudden unexpected death in epilepsy risk reduction?. Eur Neurol. 2013;69(2):119-21.
7. Aron M, Vlachos-Mayer H, Dorion D. Vocal cord adduction causing obstructive sleep apnea from vagal nerve stimulation: case report. J Pediatr. 2012 May;160(5):868-70.
8. Elliott RE, Morsi A, Kalhorn SP, Marcus J, Sellin J, Kang M, Silverberg A, Rivera E, Geller E, Carlson C, Devinsky O, Doyle WK. Vagus nerve stimulation in 436 consecutive patients with treatment-resistant epilepsy: long-term outcomes and predictors of response. Epilepsy Behav. 2011 Jan;20(1):57-63.
9. Ashton AK. Depressive relapse after vagal nerve stimulator explantation. Am J Psychiatry. 2010 Jun;167(6):719-20.
10. Air EL, Ghomri YM, Tyagi R, Grande AW, Crone K, Mangano FT. Management of vagal nerve stimulator infections: do they need to be removed? J Neurosurg Pediatr. 2009 Jan;3(1):73-8.
11. Bergey GK, Morrell MJ, Mizrahi EM, Goldman A, King-Stephens D, Nair D, Srinivasan S, Jobst B, Gross RE, Shields DC, Barkley G, Salanova V, Olejniczak P, Cole A, Cash SS, Noe K, Wharen R, Worrell G, Murro AM, Edwards J, Duchowny M, Spencer D, Smith M, Geller E, Gwinn R, Skidmore C, Eisenschenk S, Berg M, Heck C, Van Ness P, Fountain N, Rutecki P, Massey A, O’Donovan C, Labar D, Duckrow RB, Hirsch LJ, Courtney T, Sun FT, Seale CG. Long-term treatment with responsive brain stimulation in adults with refractory partial seizures. Neurology. 2015 Feb 24;84(8):810-7
12. Cox JH, Seri S, Cavanna AE. Clinical utility of implantable neurostimulation devices as adjunctive treatment of uncontrolled seizures. Neuropsychiatr Dis Treat. 2014 Nov 14;10:2191-200.
13. Morrell MJ. In response: The RNS System multicenter randomized double-blinded controlled trial of responsive cortical stimulation for adjunctive treatment of intractable partial epilepsy: knowledge and insights gained. Epilepsia. 2014 Sep;55(9):1470-1.
14. Heck CN, King-Stephens D, Massey AD, Nair DR, Jobst BC, Barkley GL, Salanova V, Cole AJ, Smith MC, Gwinn RP, Skidmore C, Van Ness PC, Bergey GK, Park YD, Miller I, Geller E, Rutecki PA, Zimmerman R, Spencer DC, Goldman A, Edwards JC, Leiphart JW, Wharen RE, Fessler J, Fountain NB, Worrell GA, Gross RE, Eisenschenk S, Duckrow RB, Hirsch LJ, Bazil C, O’Donovan CA, Sun FT, Courtney TA, Seale CG, Morrell MJ. Two-year seizure reduction in adults with medically intractable partial onset epilepsy treated with responsive neurostimulation: final results of the RNS System Pivotal trial. Epilepsia. 2014 Mar;55(3):432-41.
15. Salanova V, Witt T, Worth R, Henry TR, Gross RE, Nazzaro JM, Labar D, Sperling MR, Sharan A, Sandok E, Handforth A, Stern JM, Chung S, Henderson JM, French J, Baltuch G, Rosenfeld WE, Garcia P, Barbaro NM, Fountain NB, Elias WJ, Goodman RR, Pollard JR, Tröster AI, Irwin CP, Lambrecht K, Graves N, Fisher R; SANTE Study Group. Long-term efficacy and safety of thalamic stimulation for drug-resistant partial epilepsy. Neurology. 2015 Mar 10;84(10):1017-25.

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

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

 

Hi Dr Sethi,

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

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

Thank you,
K

 

 

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

Argument in favor of not treating them:

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

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

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

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

 

 

Arguments in favor of treating these infrequent seizures:

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

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

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

Personal Regards,

Nitin K Sethi, MD

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

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

 

Here is his question. My answer to it follows:

 

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

 

S

 

 

Brain diseases reply:

 

Dear S,

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

 

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

 

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

 

Many questions remain unanswered:

 

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

 

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

 

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

 

Nitin Sethi, MD

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

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

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

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

Fast forward 3 weeks.

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

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

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

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

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

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

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

I feel good, Dr Feelgood he said.

Types of seizures: a question and an answer

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

 

QUESTION

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

ANSWER

Dear so confused,

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

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

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

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

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

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

Personal Regards,

Nitin Sethi, MD

Alcohol and seizures: a few questions and their answers.

One of the readers of my blog asked me a few questions. His questions and my answers to them follow.

Hello Dr Sethi! To begin with, I’d like to thank you for clarifying and educate us about seizures.(esp. rum fits, alcohol withdrawal seizures and Dts seizures)

I have some questions:

1. How would I differentiate between epilepsy and alcoholic fits? Ignoring any test(EEG,CT), i mean based on the clinical manifestation?eg. duration of fits?the sequence of occurence (pattern of seizure)?etc…

2. how would i differentiate between epilepsy and the ‘fits’ that is seen in patients with hysteria (conversion disorder)?

3. is treatment necessary for alcohol fits? or just allow the patient to relax in the recovery position and let the fit go away?

4. how would you distinguish between: alcohol withdrawal syndrome and DT? is there any special cardinal symptom that will give me a clue that the patient is in DT.?

Thank you very much Dr Sethi. looking forward to hear from you.

Dr. Ronny Gooriah (doing Internship)

Dear Dr. Gooriah,
thank you for writing in to me. I am glad you found the information presented useful. Now without further delay, let me answer your questions.

1. If I understood your question you want to know how to differentiate between seizures caused by alcohol (alcohol fits) from seizures/epilepsy caused by other conditions. As you may be well aware of, epilepsy is a condition which predisposes the patient to multiple convulsions in his/her lifetime. There are numerous causes of epilepsy. Broadly speaking epilepsy can be idiopathic , symptomatic or cryptogenic. Seizures may also occur secondary to a medical condition which may or may not involve the brain like for example a brain tumor, head trauma, meningitis or encephalitis and in the setting of multiorgan failure such as sepsis, renal or hepatic failure. There is no absolute way of differentiating a seizure caused by alcohol (excessive use or sudden stoppage) from epilepsy (whether idiopathic, symptomatic or cryptogenic) specially early in the course of the disease. One needs to take a thorough history which should include a history of alcohol intake. How much? what kind? over what time frame were the drinks consumed? were drinks mixed? were recreational drugs taken along with the alcohol and so forth. Other history which may be helpful in determining if the patient has epilepsy include: a history of febrile convulsions, family history of seizures, history of meningitis or encephalitis, history of significant head trauma and if seizures have occured in settings where the patient was not abusing alcohol. The answer to all these questions and the results of tests such as EEG and neuroimaging (MRI brain) shall help in determining whether the patient has epilepsy per se or whether all his seizures can be attributed to alcohol.

2. Nonepileptic events (pseudoseizures) may occur as a manifestation of a somatoform or conversion disorder. These patients have events that look like seizures (sudden shaking of the body and the patient may appear to suffer loss of consciousness) but there is no EEG correlate to these events. Meaning that the EEG shows the patient is not having a seizure. Patients who exhibit nonepileptic events (some doctors refer to them as hysterical convulsions) usually fall in two categories. Either they are doing this for a secondary gain (seeking attention, disability or financial compensation aka they are malingering) or these events are really not under their conscious control (usually these patients are under severe mental stress or may have history of physical or sexual abuse). A trained eye (such as a neurologist) simply by looking at the clinical event shall at times be able to determine if it is a true seizure or a pseudoseizure/ hysterical convulsion. At times though the differentiation is indeed difficult (if solely based on the description of the event). A video-EEG in these cases is extremely helpful. As the name suggests the patient is attached to a EEG machine while under video surveillance. The idea is to capture a typical seizure on the camera and look at the EEG at the same time.

3. If the patient suffers a single alcohol related seizure, no treatment may be necessary apart from simple observation and making sure the patient does not hurt himself. On the other hand if the patient suffers a flurry of seizures one after the other, you may have to give medications to stop the seizures at least acutely. Whether such patients warrant long term anticonvulsant therapy is another issue and needs careful consideration.

4. Patients who are in DT or have impending DT usually have dysautonomia. They are frequently tachycardic or have irregular heart rate, their blood pressure may be high and have wide swings, they may have profuse sweating and are disoriented, confused and agitated (hence the word delirium). DT has a high mortality and hence these patients need close supervision and aggressive treatment usually in an intensive care setting.

I hope I have answered your questions to your satisfaction.

Personal Regards,

Nitin Sethi, MD