john2mulligan's Blog

The Role of MRI and Nuclear Medicine in Epilepsy Patients

Introduction

I decided to do my blog this week on epilepsy due to the fact that a close friend of mine suffers from severe epilepsy and he went for surgery this week to remove the whole of his right temporal lobe, which I found astonishing. I also did not have that much knowledge on epilepsy and what procedures were followed for patients that suffered with this incredible condition. By studying this topic in more depth will be of great benefit in the future when I am a practising radiographer as many patients with this condition present themselves to the clinic so by knowing this information I will then know how to deal with these patients.

What is Epilepsy?

Epilepsy is a neurological disorder characterised by repeated and abnormal firing of neurones leading to episodes of unpredictable seizures (Cenedella, 2008). A seizure is caused by a sudden peak of excess electrical activity in the brain, causing a temporary disruption in the normal signals and communication passing between brain cells. This disruption results in the brain’s messages becoming halted or mixed up. The brain is responsible for the body to function in a normal way, so what you experience during a seizure will depend on where in your brain the epileptic activity begins and how widely and rapidly it spreads. The seizure manifests itself as a disturbance of consciousness, behaviour, emotion, motor function, or sensation. For this reason, there are many different types of seizure and each person will experience epilepsy in a way that is unique to them. (Epilepsy Action, 2012)epilepsy                                                                                                                                                                                 (Epilepsy Foundation, 2010)

Epilepsy has a prevalence of 4 – 8 cases/1,000 population, with the highest incidence in infants and elderly people where the highest incidence occurs in the first two decades, and then falls over next few but increases again in late life owing mainly to cerebrovascular diseases. Greater than 60% of patients achieve long-term remission, usually within 5 years of diagnosis where there is an increase in premature death – sudden death, trauma, suicide, pneumonia & status epilepticus.  (Walker, 2007)

Seizures are classed as focal (partial) seizure, or generalised seizure.  Partial seizures are characterised by abnormal neuronal discharge which initiates within a local region in the brain with the potential of influencing the function of other neighbouring neurones – leading to further complications. Generalised seizures on the other hand, start at a focal point and spread throughout the brain (Gregory & Holmes, 2004).  The classification of seizures are explained below in figure 1.

Classification: By clinical pattern of seizures

(a) Generalised: Absence(petit mal)

Myoclonic

Tonic

Tonic -clonic (grand mal)

( b) Partial: Simple (no impairment of  consciousness)

Complex (impairment of consciousness)

(c)  Absence seizures: Patient becomes still and starring and looks pale

Eye lids may twitch

No recollection of the event

Attack lasts a few seconds during which the patient is unresponsive

(D) Generalised tonic-clonic : Warning- vague

Tonic phase- body becomes rigid before patient falls

(often with a cry).biting the tongue and with urinary incontinence

Clonic phase- a generalised convulsion with rhythmic jerking of muscles and frothing at the mouth.e                                                                                                                                                                                                                                            (Rang, 2011)

(E)Partial (focal seizures): Aura, example strange smell, tingling in a limb

Motor (jacksonian)

Jerking movement begins in the angle of the mouth or in the hand, spreading to to involve the limbs on the side opposite the epileptic

Patient remains conscious

Feeling of unreality, often deja-vu, associated with vertigo or absence attacks.

rang                                                                                                                                                                                                                                    (Rang, 2011)

clinical

brodie                                                                                                                                                                                                 (Brodie et al, 2009)

Simple partial seizures present with rhythmic or semi-rhythmic clonic activity in the face, arm or leg. Seizures of generalised epilepsy are tonic-clonic, absent seizure, myoclonic, or atonic; they are associated with the following clinical features: loss of consciousness, muscles rigidity, convulsions, confusion and “auras” (Smith et al, 2003a; Damjanov, 2012; NICE, 2004). According to NICE CG 139  the “auras”  associated with epilepsy include: changes in the way things look, smell, feel, taste or sound, an intense feeling that events have happened before (déjà vu), a tingling sensation or ‘pins and needles’, in the arms and legs, and twitching on one side of your body. (NICE, 2004). It is the most common neurological condition in the UK, and is usually presented at childhood although diagnosis later in life is also possible. (NICE, 2004). Epilepsy is diagnosed as two seizures of unknown origin, within 24 hours. (Cavazos et al, 2011).There is a 1% risk of developing epilepsy up to the age of 20 years.  According to Smith et al 2003, 2% or more of the population experience seizure during their lifetime.

The cause of epilepsy is idiopathic, however it is thought that there may be a genetic link and it may also be provoked by head injury leading to loss of consciousness or blackout. (Smith et al, 2003a).  Ms SS slipped on ice and banged her head, this could have provoked an epileptic event hence epilepsy is a high possibility in this patient.

Tests to be carried out to diagnose epilepsy

-Patient Questioning

-Look for evidence of tongue biting

-Cognitive Tests

-EEG

-MRI

-CT Scan

-Provocation Technique

The Glasgow Coma Scale is a key clinical indicator used in practice to assess severity of falls; it assesses level of consciousness, pupil reaction, and includes neurological and radiological investigation (Adina et al, 2010)

EPILEPSY Investigations (NICE, 2012).

 

– Detailed patient history

  • The      patient’s medical history, including any family history of seizures,      associated medical conditions and current medications. Some important      questions you will be asked include:

–          At what age did the seizures begin?

–          What circumstances surrounded your first seizure?

–          What factors seem to bring on the seizures?

–          What do you feel before, during, and after the seizures?

–          How long do the seizures last?

–          Have you been treated for epilepsy before?

–          What medications were prescribed and in what dosages?

–          Was the treatment effective?

-An eye witness (where possible)

  • Others      who have often seen you before, during, and after seizures, such as family      and close friends, should be present to provide details of your seizures      if they involve loss of consciousness.

-Prospective recording of events (i.e.: video or written)

  • A complete physical      and neurological exam of muscle strength, reflexes,eyesight, hearing, and      ability to detect various sensations are tested so your doctors can better      understand the cause of your seizures

-EEG (inform patient and carer this is to check neuronal activity and to determine type of seizure)

-Provocation technique (i.e. photo stimulation, hyperventilation) – warn patient/carer this action can provoke seizure

ecgeeg                                                                                                                                                                                                                                                 (Walker, 2007)

-MRI (for neuro-imaging or to identify any structural abnormalities)

-CT (for underlying gross pathology if MRI is not available or contraindicated – sedation prior to MRI is not preferred)

-Referral to a tertiary epilepsy specialist

– Tongue biting and lip cyanosis (pale blue lips) are key clinical features often associated with tonic-clonic (convulsion) seizure. A bite to the side of the tongue is indicative of patients with convulsive epileptic seizures and bites to the cheek are considered non-epileptic seizures. Lip smacking is observed prior to a generalised seizure and during a complex partial seizure. Tongue Biting especially if it is lateral is associated with tonic-clonic seizures. (Selim et al, 1995) (Oliva et al, 2008).

Blood tests to measure red and white blood cell counts, blood sugar, blood calcium, and electrolyte levels; and to evaluate liver and kidney function. Blood tests help rule out the presence of other illnesses.

Other tests, as needed, including magnetic resonance spectroscopy (MRS), positron emission tomography (PET) and single photon emission computed tomography (SPECT)

Management

  • Choice of antiepileptic guided by seizure type, epilepsy syndrome, co-medication and comorbidity,
  • lifestyle & patient/carer preferences
  • Monotherapy preferred
  • If initial treatment unsuccessful, try monotherapy with an alternative first line or a second line drug

introduce second drug titrating up slowly over weeks until effective then withdraw first drug slowl

  • If second drug unhelpful, taper off either one before starting another

–          Combination only if monotherapy not seizure-free

–          Note: people my choose not to treat at all after discussion of risks and benefits

  • Around 60% seizure-free with first or second drug; 40% refractory – may need 2 antiepileptic drugs
  • Highlight the Expert Patients Programme to patients who wish to manage their condition more effectively: http://www.expertpatients.co.uk/
  • Children / young adult non responders – refer for consideration of the use of a ketogenic diet

(NICE, 2004)

Clobazam Gabapentin Primidone Valproate
Clonazepam Pregabalin Phenytoin Vigabatrin
Carbamazepine Lacosamide Retigabine Zonisamide
Eslicarbazepine Lamotrigine Rufinamide Fosphenytoin
Oxcarbazepine Levetiracetam Tiagabine
Ethosuximide Phenobarbital Topiramate
  • Older (e.g. carbamazepine, phenytoin, valproate) vs newer (e.g. pregabalin, lamotrigine,
  • vigabatrin) – no more effective
  • Fosphenytoin pro-drug of phenytoin – iv infusion
  • Lorazepam, midazolam, and diazepam may be used in status epilepticus
  • Some drugs need to prescribe by brand – e.g carbamazepine – may vary in bioavailability. In all cases consider consistent supply of the same manufacturer’s preparation to avoid reduced effect or excessive side effects.

(BNF, 2011a; NICE, 2004)

Side effects

Common side effects include:

  • Somnolence
  • Headache
  • Dizziness

(BNF, 2011a)

Rare but serious side effects:

  • Carbamazepine – blood, hepatic and skin disorders
  • Phenytoin – blood and skin disorders, (rarely gingival hyperplasia and hirsutism)
  • Lamotrigine – serious skin reactions and blood disorders
  • Topiramate – ↑ IOP (intraocular pressure)
  • Sodium valproate – hepatic, blood, pancreatitis
  • Vigabatrin – visual field defects

(BNF, 2011a)

 

Interactions

Most frequent with enzyme-inducing antiepileptics –phenobarbital, primidone, phenytoin,

carbamazepine, oxcarbazepine, topiramate

Examples include:

  • Anticoagulants,
  • Antibiotics,
  • Antidepressants,
  • Antipsychotics,
  • Oestrogens & progestogens

(BNF, 2011b)

Monitoring

  • Therapeutic Drug Monitoring available for phenytoin (most useful), valproate, carbamazepine, oxcarbazepine, phenobarbitone & ethosuximide etc
  • Do not measure routinely, only if control suboptimal, compliance in doubt or toxicity
  • Remember to tailor dose to patient, not to blood concentration
  • Phenytoin – small increase in dose can result in a large increase in blood level (non-linear pharmacokinetics)
  • Vigabatrin, gabapentin, lamotrigine, sodium valproate and primidone of little utility
  • Insufficient data on topiramate, pregabalin, tiagabine, levetiracetam

 

Withdrawing antiepileptics

  • Abrupt cessation may precipitate status epilepticus (medical emergency)
  • Withdraw slowly over at least 2-3 months (benzodiazepines & barbiturates – 6 months)
  • Risk of seizure highest in first 6 months – DVLA advice
  • If on >1 AED, withdraw one at a time
  • If seizures recur, reverse last dose reduction
  • Must be seizure-free for at least 2 years

Contraception in epilepsy

  • Hepatic enzyme-inducing drugs increase metabolism of oestrogen and progestogen
  • Avoid Progestogen Only Pill or implant
  • If using Combined Oral Contraceptive, oestrogen ≥ 50mcg
  • If using depot – 10 week interval (not 12)
  • Use additional barrier methods
  • Emergency Hormonal Contraception – 1.5mg and 750mcg 12 hrs apart

 

Pregnancy in epilepsy

  • Most seizures do not adversely affect foetus (unless fall and sustain an injury); generalised tonic-clonic seizure – foetus at relatively higher risk of harm, but still very low risk
  • Benefit of treatment versus risk to foetus – risk of teratogenicity ↑ if > one antiepileptic – should discuss with patient about risks of drugs causing malformations /neurodevelopmental impairments
  • Folic acid 5 mg 3 months prior to conception to end of first trimester; Folate antagonists – prevent neural tube defects – give higher folic acid dose
  • Some antiepileptic levels can ↓, esp. in second and third trimester breakthrough seizures
  • Enzyme-inducing antiepileptic can cause haemorrhagic disease of newborn
  • Breastfeeding generally recommended: but current SPC / BNF guidance should be checked before prescribing

Social issues

  • Driving
  • Employment: e.g. pilots, heights, dangerous machinery
  • Safety issues: e.g. microwaves, baths
  • Leisure activities/travel: aim for normal life – sleep deprivation/excess alcohol provoke seizure?
  • Long-distance travel, time zones – tiredness etc

 

 

 

Imaging for Epilepsy:

pet

(Studhome, 2012)

In patients with epilepsy most imaging discovers an area of focal abnormality. The most type of imaging adapted is either MRI or more recently the use of PET and
SPECT imaging. When using MR imaging, assessment is done by taking thin slice coronal views for the assessment of the hippocampus in patients that suffer
temporal lobe seizures. When assessing patients with the use of PET imaging the viewing of the patients metabolic functions and changes in the temporal lobe
with the use of flurodeoxyglucose. With this process it is noted that a decrease in regional cerebral metabolism is observed in 55-80% of patients. With
hypometabolic areas seen using PET, these are usually larger than the area with the seizure present that otherwise maybe carried out by use of electrical connectivity or by the use of MRI or CT for structural defects.

spect                                                                                                                                                                                                                                            (Studhome, 2012)

Another common assessment practice is the use of SPECT imaging. This technique involves the assessment of cerebral blood flow. This is usually a common assessment as the changes in blood flow is invective of the changes of metabolism, when doing this findings are similar to that of a PET scan. (la Fougere et al, 2009)

spect 2                                                                                                                                                                                                                            (Manford, 2012)

After doing this blog I feel I have a better uderstanding about this condition and how it may be managed. I have not seen this process in practice while on placement, this is mainly due to the fact that the hospital I was plaeced did not specialise in neurological disorders. Hopefully while on my next placement I will become more involved and be spending more time working in conjunction with MRI and Nuclear Medicine and thus when I see such patients have a better understanding of the true extent of the condition they live with on a daily basis.

Background reading

Clinical focus articles and lifelong learning questions on Epilepsy. Clinical Pharmacist, March

2010; 2 (3).

Parsons LM, Angus-Leppan H. Epilepsy management. Medicine 2008; 36: 579-85

National Prescribing Centre (NPC). Epilepsy http://www.npc.nhs.uk/therapeutics/cns/

 

 

 

 

References:

  1. Epilepsy Action. (2012). What is Epilepsy. Available: http://www.epilepsy.org.uk/info/what-is-epilepsy. Last accessed 16th November.

 

  1. Epilepsy Foundation . (2010). Seizure Syndromes. Available:http://www.epilepsyheartland.org/Current/about%20epilepsy/types.php. Last accessed 16th November.
  1. Walker, R (2007). Clinical Pharmacy and Therapeutics. 4th ed. London: Churchill Livingstone. p447-454.
  1. Rang, P (2011). Rang & Dale’s Pharmacology. 7th ed. London: Churchill Livingstone. p575-578.
  1. Martin J. Brodie, Steven C. Schachter,Patrick Kwan. (2009) Fast Facts: Epilepsy [online]. 4th ed. ed. GB: Health Press.
  1. BNF 61, a (2011) Section 4.8.1, page 280, 282, & 580.
  1. BNF 61, b (2011) Section 4.8.1
  1. Studhome, C. (2012). MRI SPECT Imaging. Available: http://www.colin

studholme.net/research/ipag/mrdspect/mrspect3.html. Last accessed 23rd November.

  1. Manford, M. (2012). Epilepsy Imaging. Available:

http://coacs.com/bespoke_software/portfolio_pages/nse.htm. Last accessed 23rd November

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