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.

Dear Sir/Madam,

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

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

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

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

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

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

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

 
I hope I have answered some of your questions N.

Personal Regards,

Nitin Sethi, MD

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

http://www.healthcentral.com/alzheimers/c/84292/147499/neurologist

The blog remains free of any commercial interests. I had started it as a means of disseminating information about neurological diseases to the public at large. I am happy to report that after 4 years,  the goal of my blog and website (http://braindiseases.info) remains unchanged. There are no financial incentives and the two projects remain a solo effort on my part.

Thank you for your continued support.

Nitin Sethi, MD

Personal Regards,

Nitin Sethi, MD

Rash: can be associated with the use of a number of anticonvulsants. Phenytoin, lamotrigine, carabamazepine are the anticonvulsants commonly associated with rash. The rash may be mild or it may become quite fulminant leading to involvement of the mucous membranes (Steven Johnson Syndrome). The rash usually appears right at the onset (meaning a few days after the medication is started) but it may also appear at any point of time during the course of therapy. If rash is documented the usual advise is to stop the medication and consult your physician as soon as possible. Please remember though that sudden stoppage of anticonvulsant is not advisable since it may lead to a flurry of seizures. So it is your doctor who shall be the best person to make the decision: either stopping the medication cold turkey and substituting another anticonvulsant in its place  or slowing down the upward taper of the anticonvulsant and allowing the rash to subside.

Cognitive side-effects: a number of anticonvulsants can cause cognitive side-effects. Patients may complain of feeling dull (“I do not feel as sharp as usual” or “my mind is in a fog”). Some complain of difficulty concentrating and focusing while others have word finding difficulty (has been reported with the use of topiramate). Again if you experience any of these side-effects bring them to the attention of your doctor. At times lowering the dose of the anticonvulsant leads to resolution of these side-effects. At times taking the bulk of the anticonvulsant at night (larger dose at night and smaller dose in the morning) may be helpful since you can sleep off most of the side-effects.

Bone loss: many anticonvulsants lead to bone loss. The most commonly cited culprit drugs are phenytoin, carbamazepine and phenobarbital. Prolonged use of these anticonvulsants leads to bone loss and osteoporosis. That is the reason why your physician may advise you to supplement calcium and vitamin D. How much calcium and vitamin D to take on a daily basis though? The National Osteoporosis Foundation and National Institute of Health has given recommendations for daily calcium and vitamin D intake and most of the physicians refer to these.  Again your physician shall be the best person to determine how much calcium and vitamin D supplementation is required based on your age, the various medications you are taking and your risk of osteoporosis in the future. He may refer you for a bone densitometry test (commonly referred to as a DEXA scan).

Congenital malformations (major and minor): this applies to women of child bearing age who are exposed to/ taking anticonvulsants. Data from various pregnancy registries collected over many years has now informed us that anticonvulsant use by a woman during pregnancy may at times lead to major or minor malformations (cleft lip, cleft palate, congenital heart disease, spina bifida and so forth) in the baby. The risk though varies with some anticonvulsants “safer” than others.  No anticonvulsant though is completely free of this risk and again it is your doctor who shall be the best person to advise you about this.  The choice of an anticonvulsant in a woman of child bearing age is made after due consideration of the above risk. Folic acid supplementation before and during pregnancy may help to mitigate some of this risk to some extent.  So it is imperative that all women of child bearing age who are on anticonvulsants (and are contemplating pregnancy) should have a discussion about the risk of congenital malformations with their doctors.

Mood changes: anticonvulsants can lead to mood changes. Studies have shown that some are more likely to do so than others. Patients may complain of low mood, caregivers may notice that the patient is more agitated, snappy or restless. Some patients may become depressed. Hence the FDA has issued a warning on anticonvulsants and the risk of suicide and suicidal thoughts. Again your physician shall be the best person to decide which anticonvulsant is appropriate for you.

Apart from the above mentioned side-effects, each anticonvulsant has side-effects which are unique to it.  So it is important that you read the package insert and tell your doctor about any other medical conditions that you may have. Also mention other medications that you taking so that your doctor can determine and tell you about important drug-drug interactions.

I hope this information helps some of the readers of my blog.

Nitin Sethi, MD

The information provided in this blog should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. A licensed medical professional should be consulted for diagnosis and treatment of any and all medical conditions. Call 911 if you have a medical emergency.

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Nitin Sethi, MD

So what is trigeminal neuralgia and how does the patient present? As the name suggests trigeminal neuralgia is basically pain in the distribution of the trigeminal nerve. The trigeminal nerve is a cranial nerve which supplies the skin of the face (so when I touch you on the forehead or on your cheek, you are able to appreciate that touch basically on account of the trigeminal nerve). Every nerve starts from somewhere and ends somewhere. In the case of the trigeminal nerve, the nerve originates in the brain (brainstem area) and then courses inside the brain/skull for a while before it exits out and supplies the skin of the face. The nerve also has a motor branch which innervates the muscles of mastication (which help in chweing function). Now if the nerve is compressed/pinched somewhere along its course (usually occurs near the origin of the nerve in the brainstem), it gives rise to a particularly painful and distressing condition which is called trigeminal neuralgia.

Patients with trigeminal neuralgia present with pain. The pain has been described as shooting, stabbing, brief electrical shock like sensations that radiate down into the face. Usually the history is typical. The pain is triggered by touching the face as what happens when the patient attempts to shave or brush his teeth. Sometimes even a gust of wind may trigger the paroxysm of pain. The pain does not respond to conventional pain killers such as ibuprofen (Advil or Motrin) and even stronger pain killers such as codeine and this results in a visit to a doctor.

Frequently the diagnosis may be delayed and the patient may initially consult a dentist since it is wrongly assumed that the pain is dental pain. Patients have undergone root canal and tooth extraction only to realise that the pain was not dental to begin with.

So what causes trigeminal neuralgia? Well the cause usually varies with age. Idiopathic trigeminal neuralgia usually occurs in the older age group. In these patients a MRI of the brain may reveal no gross abnormality (aka there is no obvious tumor found). The thinking behind idiopathic trigeminal neuralgia is that the nerve gets pinched by a tortuous blood vessel. As we grow old our blood vessels (including those inside the brain) become tortuous and thickened. A tortuous artery may press on the delicate trigeminal nerve in the brainstem giving rise to the pain of trigeminal neuralgia. When trigeminal neuralgia occurs in a young person other things need to be ruled out. Is there a tumor in the brainstem pressing on the nerve? Does the patient have multiple sclerosis (a young lady presenting with trigeminal neuralgia is the typical example. In such patients the multiple sclerosis lesion/ plaque is the culprit and presses on the nerve near its origin).

So now lets talk about management. There are two aspects to this. Firstly the cause of trigeminal neuralgia needs to be determined. Your doctor shall order a MRI scan of the brain with and without contrast with close attention at the trigeminal nerve. The idea is to find the culprit blood vessel which is pressing on the nerve and to rule out other lesions such as multiple sclerosis plaque or a small brainstem tumor. Simultaneously the pain has to be addressed. The pain does not respond to conventional pain killers but may respond to medications which are effective for neuropathic pain such as carbamazepine (Tegretol), oxcarbazepine (Trileptal), gabapentin (Neurontin). Other medications which may work include baclofen and amitriptyline (Elavil). My personal experience has been that the pain responds to carbamazepine but high doses are frequently needed. If pain relief is inadequate, I add low dose baclofen.

If the pain subsides well and good. At times I shall only keep the patient under observation and do nothing more (this of course applies to patients who have idiopathic trigeminal neuralgia).  If there is a tumor that is pressing on the nerve then that of course needs to be addressed. If the cause is multiple sclerosis then multiple sclerosis needs to be addressed. There are other options available. Namely:

Surgery–the surgery is called microvascular decompression. As the name suggests the idea is to decompress the nerve. The neurosurgeon shall expose the nerve and identify the blood vessel pressing on it. The vessel is then lifted off the nerve thus decompressing the nerve and providing long lasting pain relief. The surgery is not simple. It requires the expertise of a neurosurgeon trained in this procedure. As the trigeminal nerve is hidden deep in the brain, it takes sometime to expose the nerve. Another procedure which is becoming more popular nowdays is radiosurgery. Several reports have documented the efficacy of Gamma Knife‚ stereotactic radiosurgery for trigeminal neuralgia. This though is available only in some centers around the country. Percutaneous procedures are also available. They bascially involve injecting the trigeminal nerve ganglion with chemicals such as glycerol. The idea is to kill the nerve and hence abolish the pain.

I hope some of you find this post helpful.

Nitin Sethi, MD