Seizures and Epilepsy Flashcards
Intracranial causes of LOC
- trauma e.g. haematoma (extradural, subdural, intracerebral)
- tumour
- epilepsy
- hydrocephalus
- SAH
- intracerebral haematoma
- stroke + shift
- brainstem infarction or haemorrhage
- meningitis/encephalitis
- abscess
Extracranial causes of LOC
- electrolyte imbalances
- DKA/hypoglycaemia
- lactic acidosis
- hypo/hyperthremia
- hepatic failure
- hypercapnia
- hypoxia
- any endocrine disturbance
- anaemia
- blood loss
- vasovagal attack
- valvular disease
- MI
- arrhtyhmia
- hypotensive drugs
- sedatives
- opiates
- alcohol
- CO poisoning
Features of history that help identify a cause for LOC
Trauma prior to admission Previous head injury - chronic subdural Sudden collapse - SAH or stroke Limb twitching, incontinence - epilepsy/postictal state Gradual development of symptoms - mass lesion, metabolic or infective cause Previous illness - diabetes - epilepsy - psychiatric illness (overdose) - alcoholism or drug abuse (drug toxicity) - viral infection (encephalits) - malignancy (mets)
Definition of seizures and epilepsy
A seizure or epileptic attack is the consequence of a paroxysmal uncontrolled discharge of neurons within the central nervous system
- clinical manifestations range from a major motor convulsion to a brief period of lack of awareness
Classifcations of types of seizures
1) partial (focal, localisation related) seizure
- A: simple, partial complex seizures with preserved conciseness
- B: complex partial seizure accompanied by any degree of impaired conscious level
- C: partial seizures evolving to tonic/clonic convulsion
2) generalised seizures (convulsive or non-convulsive)
- A: absences
- B: myoclonic seizures
- C: clonic seizures
- D: tonic seizures
- E: tonic/clonic seizures
- F: atonic seizures
3) unclassified seizures - if insufficient information
Investigations for patients with loss of conciousness
Bloods - FBC, TFTs, U&Es, LFTs, CK, prolocatin, calcium
Blood cultures
Drug screen
VBG
Blood glucose - hypo/hyperglycaemia
Urine dipstick - glucose or infective causes
ECG and 24-hour ECG - cardiac arrhythmia
CT head - trauma or suspected rasied ICP
- LP and CSF examination if negative (meningitis)
Echo - cardiomyopathy
EEG - may reveal a focal or generalised disturbance (epilepsy)
CT/MRI
- structural brain lesions
- indicated in late onset, partial seizures and abnormal clinical signs
Medical management long-term epilepsy
Idiopathic generalised epilepsy
- 1st line: sodium valporate or lamotrigine
- 2nd line: topiramate, levetiracetam or carbamazepine
Partial/focal epilespy
- 1st line: lamotrigine or carbamazepine
- 2nd line: sodium valporate, phenobarbitone or levetiracetam
Absence seizures
- 1st line: sodium valporate or ethosuximide
- 2nd line: lamotrigine
What should you be wary of when prescribing anti-epileptics
Teratogenicity
- risk highest with sodium valporate and polytherapy
- lamotrigine and carbamazepine considered safe
Interactions
- many anti-epileptics induce liver enzymes to increase the metabolism of other drugs (OCP, warfarin and other anti-epileptics) e.g. carbamazepine, phenytoin, phenobarbitone
- valporate inhibits liver enzymes
Blood levels
- useful in phenytoin due to the difficult pharmacokinetics
- in case of toxicity
What are the main adverse effects with the main anti-epileptics
Lamotrigine - rash (SJS risk) drowsiness
Carbamazepine - rash, drowsiness, ataxia, diploplia, hyponatraemia and thrombocytopenia
Sodium valporate - abdominal pain, hair loss, weight gain, tremor and thrombocytopenia
Phenytoin - gum hypertrophy, acne, ataxia, diploplia, skin thickening and neuropathy
Phenobarbitone - sedation, behavioural changes and withdrawal seizures
Gabapentin/pregabalin - drowsiness, ataxia and weight gain
Topiramate - drowsiness, weight loss, renal stones and parasthesiae
Levetiracetam - irritability and weight loss
What are the possible surgical interventions for epilepsy?
Extra-temporal cortical resection Anterior temporal lobectomy Corpus callosal section Hemispherectomy/otomy Selective amygdalo-hippocampectomy Vagal nerve stimulation
What is status epilepticus
A succession of tonic/clonic convulsions, one after the other with a gap between each = serial epilepsy
When consciousness doesn’t return between attacks = status epilepticus
- may be life threatening with the development of pyrexia, deepening come and circulatory collapse
Causes of status epilepticus
Frontal lobe lesions Following head injury Reducing drug therapy - esp. phenobarbitone Alcohol or other sedation withdrawal Drug intoxications - TCA Infections Metabolic disturbances e.g. hyponatraemia Pregnancy
Management of status epilepticus
Pre-hospital
- diazepam rectally, or midazolam buccally (short term efficacy)
Early status
- lorazepam IV (beware of respiratory distress)
Established status
- phenytoin or phenobarbitone IV and cardiac monitoring
- status should be controlled and oral maintainance therapy resumed
Refractory status
- GA with propofol or thiopentone - bolus followed by continuous infusion
- administered under EEG control to induce and maintain a ‘burst suppression’ pattern
Considerations of seizures developing during pregnancy
Mostly idiopathic
- tumours and AVM may enlarge during pregnancy and produce such seizures
In late pregnancy seizures occur often in association with hypertension and proteinuria as eclampsia
- emergency, immediate delivery required
Post-partum
- consider cortical venous thrombus
Considerations of patients with established epilepsy during pregnancy
Risks of teratogenicity from anticonvulsants
- discuss with all women of childbearing age before they become pregnant
- avoid sodium valporate, phenytoin and polytherapy
Patients offered early, detailed scans
>90% of women deliver a normal child
Most drugs present in breast milk
- except carbamazepine and valporate
- lamotrigine not harmful to the infant
Interactions between contraceptives and anticonvulsants
Anticonvulsants reduce the efficacy of the progesterone only pill
Oestrogen containing drugs lower lamotrigine levels (may require an increased dose)
Elements of a seizure
Prodrome - may have a change in mood or behaviour
Aura - often from the temporal lobe
Post-ictal
- headache, confusion and myalgia/temporary weakness after a focal seizure in the motor cortex (Todd’s palsy)
- dysphasia following focal seizure in the temporal lobe
Causes of epilepsy
Idiopathic Structural - cortical scarring - developmental - space occupying lesion - hippocampal sclerosis - vascular malformations - including stroke and AVM Others - tuberous sclerosis - sarcoidosis - SLE - autoantibodies to voltage gated potassium channels
Pathology of epilepsy
Abnormal synchronised discharge of neurons (failed inhibitory mechanics)
- seizure threshold is the level of excitability at which neurons discharge at ( lower in epileptics - neurons are hyperexcitable)
- glutamate (excitory) and GABA (inhibitory) main neurotransmitters
What triggers can over excite neurons and cause an epilepsy attack
Sleep deprivation Alcohol Drug misuse Physical and mental exhaustion Flickering lights Infection/metabolic disturbances Uncommon - loud noises - hot bath - reading - strange shapes - strange smells and sounds
What should you ask about in a seizure history
Witness Tongue biting Slow recovery Incontinence 1st seizure - ask about previous funny turns/behaviour - deja vu/episodic fever
When would a patient be commenced on anticonvulsant medication
After a minimum of two fits - discussion with the patient/see how it affects their job and social life
- may want to risk no treatment
Gradually increase the dose until seizures are controlled, toxic effects occur, max dose is reached or drug interactions occur
What are the rules surrounding driving and epilepsy
After seizure, patient has to stop driving and inform the DVLA - doctor can report them if they refuse and continue to drive
Can’t drive if
- medication change <6 months
- seizure <12 months
- if the patient has nocturnal seizures, they can drive if they have had no daytime activity for >3 years
