Waking up to epilepsy

The University of Exeter Medical School’s Waking up to Epilepsy event took place in  2016; in this review of the day, Dr Bill Vennells gives us an overview of what took place at the event; including knowledge sharing between attendees and presentations.

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Awake! For morning in the bowl of night

Has cast the stone that puts the stars to flight.

The Rubaiyat of Omar Khayyam

Waking up to epilepsy

We do wake up to the topic before coming on a course, at first a rather dim awareness that one could know more about the subject.  We draw on stored memories and knowledge.

There were eighty of us in the lecture theatre, nine GPs. We started with a run through the causes and types of epilepsy, generalised or focal, different anatomical sites.

A video from the 80s: German medical students squat, hyperventilate, and then stand up to induce epileptiform seizures in a significant percentage of them. We noted it was a sign of the times that we probably could not expect modern medical students to do anything like this, even while the Daily Mail complains about “political correctness gone mad.”

Non epileptic attacks

Videos of epilepsy and nonepileptic attack disorder demonstrated quite violent movements and sounds which were a bit alarming but also educational. We were invited to consider the fundamental question of whether the patient is “present” or not.

It turned out on a show of hands that 50 per cent of the audience had suffered from another cause of loss of consciousness: syncope. An ignoble episode from my past when I found myself face down on a toilet cistern flashed through my mind: micturition syncope.

Syncope is sub-classified: reflex (situational), orthostatic (volume depletion /autonomic), cardiac, structural (cardiac valve disorders / cardiomyopathy/ pulmonary embolism), or miscellaneous (hypoglycaemia/ pseudosyncope).

Some very practical nuggets of information included the fact that a cut tongue favours epilepsy rather than syncope. Counter-intuitively incontinence of urine can occur quite commonly in both. You do not see cyanosis in vasovagal syncope but you do in syncope associated with arrhythmia. The importance of ECG monitoring in suspected syncope with arrhythmia was emphasised. There is a particular condition where bradycardia can occur during seizures.  A pacemaker should be considered if the heart is beating so slowly that it causes any distress.

A “syncope or seizure” game broke up the presentation.

Captain Barbossa

We apparently share with the pirate Captain Barbossa the spirit behind: “the (Pirate) Code is really what you might call Guidelines”. It appears that if NICE suggest scanning then we do so.  However when scanning may not really be necessary we can rather disingenuously interpret the code and justify a scan to assuage our anxiety.  Not exactly the same motives as Captain Barbossa however.

The presentation on scanning was quite technical, giving an insight into what goes on behind the scenes before reports are generated. The images themselves were interesting, and the concepts of hypertrophic dysplasia and focal cortical dysplasia were worth considering, not being phrases that we often used in our applied fields.

The coffee break was welcome, having assimilated a lot of information. The multi-disciplinary quality of the day now came into its own, our name badges proclaim our respective roles.

Knowledge sharing

I talked to someone from the Royal London Hospital, where I did my training.  He was a volunteer who spent time with patients after their consultations. They often had not understood everything, had misconceptions and anxieties.

I also talked to a pure scientist whose work involved manipulating the chromosomes of fish to induce convulsions, then investigating the effects of anti-epileptic drugs.  Apparently fish are a bit more ethically acceptable then mice and yet do you have metabolism in common with us. I suppose there’s an equation of maximising animal welfare versus benefit to patients, a whole other area of debate.

Refreshed, we return to a presentation by Epilepsy Nurses.  They are a valuable resource in short supply who have a very significant clinical and decision-making, as well as supportive and educational, role.

Patients’ experiences

The nurses’ presentation included patients’ experience, the important issues of transport, IT access of information, and finding one’s way around the benefits’ system. A patient in the audience expressed how crucial the nurses’ contribution had been to her. I felt more patient input would have added value to the day.

The keynote speakers took us back to first principles, starting with my A-level physics, and reminding me of medical school subjects. The knowledge was still there, having been applied in different ways over the years. It is good to be reminded that there is a logical basis for our pragmatic work. It helps the thinking process to go back to these principles.

We covered the basis of wave theory and neurological synapses. The EEG tracing it is not like an ECG – it picks up patterns of oscillations detected on the surface of the scalp from within. Different regions of the brain share information. Similar patterns of oscillation demonstrate areas of the brain that communicate with each other. The thalamocortical system is involved in generalised convulsions, which nevertheless start from a focal point, the focal seizures OFTEN start in the hippocampus.

Brain networks

We were introduced to brain networks: in effect wiring diagrams of brain connections, some being long range connections.

The functional MRI scan also measures activity of networks as do other scanning methods. There are correlations between signals from different brain regions.

A mathematical equation can reproduce the tendency to seizures, a hyper-excitable focus producing a seizure pattern on mathematical modelling, either at foci of the equation or by modifying connections between them. Humbling, to see an aspect of our experience reduced to a quite simple equation.

EEG patterns also obey the rules of graph theory, another mathematical concept. First degree relatives of sufferers show similar patterns. Patterns can predict epilepsy, in silico diagnostics, a possible prognostic tool.

A welcome lunch break, excellent catering, the support to the day was well organised. I found myself in the queue with the patient who had expressed appreciation of the Nurses’s role, and heard about the impact on her life. She appreciated the GPs’ role, but found consultations had to be very focused and could have a sort of clipped, moving-on quality. This is useful learning too, necessary to hear.

Non Epileptic Attack Disorder

Non Epileptic Attack Disorder is associated with past traumas, learning difficulty, and social learning. Traumas are remembered at a muscular and emotional level. They occur because of four Ps:

  • Predisposing: perhaps a strong drive to succeed, plenty of that among us, it was suggested.
  • Precipitating trauma: physical and psychological disaster.
  • Perpetuating: pressing on regardless, for example.
  • Protecting: the other side of the equation, supportive social networks. When things go wrong they can be disrupted though, and isolation aggravates the situation. A friend in need is a friend indeed.

There followed a presentation on EEGs, alpha – fastest, beta, theta and delta – slowest rhythms.

Brain maps are coloured representations of rhythms and are more attractive to those of us who are put off by the conventional wavy lines, but sadly are not so practically useful.

There are quite specific clinical implications and uses apart from the type of epilepsy. The elderly patient who is a bit confused with a preponderance of delta waves is probably hypoxic and needs oxygen. The EEG is a biomarker for types of epilepsy. However it is not very specific: 0.5 per cent of normal adults have ictal changes that falsely suggest epilepsy, nor is it very sensitive: the EEG can be quite normal in a person who suffers epilepsy.

More nuggets of information. A dyscognitive seizure state exists where a patient can obey simple commands and speak. Infantile spasms are a variety of seizure occurring at three – six months of age, that delay a child’s development, as does childhood absences, even though the latter are otherwise benign.

We saw a video of a childhood breath-holding attack, to contrast with epileptic seizures.

Medication

A neuropsychiatrist took us from the earliest antiepileptic drug – bromide, from the time of Queen Victoria – to the present panoply of dozens of medications. Barbiturates were also one of the earlier treatments.

This certainly makes sense to me. When I was training as a student you could probably memorise all the anti-convulsant medications. Nowadays that is quite impossible. They literally range from A to Z in the alphabet. From Acetozolamide to Zonisamide. Many are also mood stabilisers, particularly type 2 bipolar disorder where episodes of depression are more prominent. Broadly they fall into two groups, the Gamma Amino Benzoic Acid (GABA) AGONISTS and the anti-glutamatergic drugs.

Dostoevsky suffered epilepsy, and described a state of calm, serene knowledge that can precede convulsions in some, a type of aura. He also suffered a gambling addiction, which is associated with epilepsy, described in his novel, The Gambler.

Depression is also associated with epilepsy. Just as in non-epileptic patients, if antidepressants are used they should continue for at least six months after a first episode, and twelve months after a second one.

We were told of a distressing condition, forced normalisation. In this situation when convulsions are controlled, psychosis occurs, so a choice between uncontrolled fits or psychosis has to be made.

I was really surprised to learn that the earliest versions of the drink Seven-Up contained the mood stabiliser Lithium.

Channel blockers

The concept of channel blockers, gated channels between the inside and outside of cells was presented to us. Sodium, calcium, and potassium atoms all go through these different channels. The concept of physically blocking a channel at a microscopic level is quite remarkable to reflect on. Nature has a way of countering what we do. Drugs that block these channels are opposed at microscopic level, and so become less effective after a while.

NICE guidance recommends treatment for more than one convulsion, or after one convulsion with an abnormal EEG, abnormal imaging, if the patient is at increased risk of convulsions or if there is neurological deficit after a fit.

It seems monotherapy is the best policy, increasing the dosage to the maximum. If the patient is not fit free then a second drug is to be added. The first drug can then be tapered off if this is possible without convulsions occurring

If there are no fits for two years and there is a normal MRI scan, then treatment can be tapered off.

We were reminded that carbamazepine and sodium valproate can reduce serum sodium levels.

Cytochrome 250 enzymes break down and eliminate medications after they’ve done their work. Anticonvulsants really speed up that process, so the liver gobbles up and chucks out anticoagulants, antibiotics and oral contraceptives. We need to be aware of increased dosing and monitoring in these situations, as I suspect the General Medical Council has explained to more than one doctor. I’d rather hear it from Exeter University. In the opposite direction, painkillers and the universal panacea alcohol decrease the fit threshold, another nugget of knowledge to keep the patients and ourselves out of harm’s way. Sodium valproate in particular is associated with neural tube defects, the higher five mg dose of folic acid is necessary in pregnant women or those planning a child, and the issue should be raised with all couples of child-bearing age.

Epilepsy savvy

The “Wake Up to” Exeter teaching is wide-ranging. There were light-hearted apologies for the presentation on syncope, as that this is not actually epilepsy. However I really value the fact that the presentations covered general medicine, psychiatry and pharmacology. That is certainly of value for those of us in primary care. Taking us through to the present state of knowledge from first principles is also very useful. We are now epilepsy-savvy. We go out armed with a better understanding in the world of diagnosis and treatment, paraphrasing Omar Khayyam:

“Awake my little ones and fill the cup

E’re life’s liquor in it’s cup be dry.”

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