epilepsy Flashcards

1
Q

definition

A

recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of brain, manifests as seizures

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2
Q

prodrome define

A
  • Not part of seizure
  • change in mood or behaviour - may precede the attack by some hrs - days.
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3
Q

aura- define

A
  • Part of seizure- patient aware
  • Partial (focal) seizure
  • Experienced as “Strange feelings”:
    • epigastric rising - strange feeling in the gut
    • déjà/jamais vu
    • strange smells or flashing lights
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4
Q

post ictal period define

A

headache, confusion, myalgia, sore tongue

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5
Q

todds paralysis -define

A
  • temporary weakness if focal seizure is in the motor cortex
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6
Q

dysphasia

A

focal seizure in temporal lobe

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7
Q

epidemiology

A
  • Common presentation: childhood/adolescence
  • Prevalence:
  • active epilepsy in ~1%
  • one or two seizures: 3-5% population
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8
Q

conditions associated with epilepsy

A

Epilepsy most commonly occurs in isolation although certain conditions have an association with epilepsy:

  1. cerebral palsy: around 30% have epilepsy
  2. tuberous sclerosis
  3. mitochondrial diseases
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9
Q

other causes of seizures

A

Febrile convulsions

  • typically occur in children between the ages of 6 months and 5 years
  • around 3% of children will have at least one febrile convulsion
  • usually occur early in a viral infection as the temperature rises rapidly
  • seizures are typically brief and generalised tonic/tonic-clonic in nature

Alcohol withdrawal seizures

  • occur in patients with a history of alcohol excess who suddenly stop drinking, for example following admission to hospital
  • chronic alcohol consumption enhances GABA mediated inhibition in the CNS (similar to benzodiazepines) and inhibits NMDA-type glutamate receptors.Alcohol withdrawal is thought to be lead to the opposite (decreased inhibitory GABA and increased NMDA glutamate transmission)
  • the peak incidence of seizures is at around 36 hours following cessation of drinking
  • patients are often given benzodiazepines following cessation of drinking to reduce the risk

Psychogenic non-epileptic seizures

  • previously termed pseudoseizures, this term describes patients who present with epileptic-like seizures but do not have characteristic electrical discharges
  • patients may have a history of mental health problems or a personality disorder
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10
Q

classification of seizures

A
  1. Where seizures begin in the brain
  2. Level of awareness during a seizure (important as can affect safety during seizure)
  3. Other features of seizures
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11
Q

define ‘focal’ seizure

A

Focal seizures

  • previously termed partial seizures
  • these start in a specific area, on one side of the brain
  • the level of awareness can vary in focal seizures. The terms focal aware (previously termed ‘simple partial’), focal impaired awareness (previously termed ‘complex partial’) and awareness unknown are used to further describe focal seizures
  • further to this, focal seizures can be classified as being motor (e.g. Jacksonian march), non-motor (e.g. déjà vu, jamais vu; ) or having other features such as aura
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12
Q

define generalised seizures

A

Generalised

  • these engage or involve networks on both sides of the brain at the onset
  • consciousness lost immediately. The level of awareness in the above classification is therefore not needed, as all patients lose consciousness
  • generalised seizures can be further subdivided into motor (e.g. tonic-clonic) and non-motor (e.g. absence)

specific types include:

→ tonic-clonic (grand mal)

→ tonic

→ clonic

→ typical absence (petit mal)

→ myoclonic: brief, rapid muscle jerks

→ atonic

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13
Q

what does ‘unknown onset’ mean

A

this termed is reserved for when the origin of the seizure is unknown

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14
Q

define term ‘focal to bilateral seizures’

A
  • starts on one side of the brain in a specific area before spreading to both lobes
  • previously termed secondary generalized seizures
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15
Q

special forms of epilepsy recognized in children

A

Syndrome

Notes

Infantile spasms (West’s syndrome)

Brief spasms beginning in first few months of life

    1. Flexion of head, trunk, limbs → extension of arms (Salaam attack); last 1-2 secs, repeat up to 50 times
    1. Progressive mental handicap
    1. EEG: hypsarrhythmia
  • usually 2nd to serious neurological abnormality (e.g. TS, encephalitis, birth asphyxia) or may be cryptogenic
  • poor prognosis

Lennox-Gastaut syndrome

May be extension of infantile spasms (50% have hx)

  • onset 1-5 yrs
  • atypical absences, falls, jerks
  • 90% moderate-severe mental handicap
  • EEG: slow spike
  • ketogenic diet may help

Benign rolandic epilepsy

  • paraesthesia (e.g. unilateral face), usually on waking up

Juvenile myoclonic epilepsy (Janz syndrome)

Typical onset in the teens, more common in girls

    1. Infrequent generalized seizures, often in morning
    1. Daytime absences
    1. Sudden, shock like myoclonic seizure
  • usually good response to sodium valproate
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16
Q

aetiology of seizures

A
  • 2/3 are idiopathic (often familial)

  • Structural:
  • Head injury = cortical scarring – yrs post-head injury
  • Developmentalantenatal and prenatal factors
    • Intrauterine infections such as rubella and toxoplasmosis
    • Maternal drug abuse
    • perinatal trauma and anoxia = brain injury
  • Space-occupying lesion - intracranial tumours = sudden onset seizures
  • Stroke
  • Hippocampal sclerosis: post febrile convulsion
  • Vascular malformations
  • Non-epileptic cause of seizures:
  • Withdrawal: EtOH, opiates, benzodiazepine
  • Metabolic:
    • Acute hypoxia:respiratory or cardiac arrest 2O to anoxic encephalopathy
    • Glucose: ↑↓
    • Electrolyte disturbance: ↑↓ Na, ↓Ca, ↓Mg
    • Failure: uraemia, hepatic failure, porphyria
    • Chronic encephalopathy: grey matter damage
  • Trauma: head trauma, haemorrhage, ↑ICP
  • Infection:
    • meningitis, encephalitis, cycticerosis (parasitic tissue infection – tapeworm),HIV
    • Febrile convulsions: high fever secondary to non-cerebral infections (> six months and < six years)
  • Systemic disease: polyarteritisnordosa, SLE, sarcoidosis, tuberous sclerosis
  • Drugs: tricyclics, cocaine, tramadol, theophylline
  • Pregnancy: Eclampsia

Pseudoseizure: psychogenic seizures

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17
Q

pathophysiology

A
  • Genetics: autosomal dominant inheritance –channelopathiesin voltage-gated or ligand gated ion channels

- Neurotransmitters: abnormalities in excitatory neurotransmitter glutamate and the inhibitory neurotransmitter GABA

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18
Q

s/s

A

As well as the seizure activity described above patients who have had generalised seizures may

  1. bite their tongue
  2. experience incontinence of urine

Asking about such features can be useful way of detecting epileptic seizures when taking a history from a patient who presents with a ‘blackout’ or ‘collapse’.

Following a seizure patients typically have a postictal phase where they feel drowsy and tired for around 15 minutes.

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19
Q

Investigations

A

Following their first seizure patients generally have both an electroencephalogram (EEG) and neuroimaging (usually a MRI).

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20
Q

Management

A

Most neurologists now start antiepileptics following a second epileptic seizure.

As a general rule:

  • sodium valproate is used first-line for patients with generalised seizures
  • carbamazepine is used first-line for patients with partial seizures

Antiepileptics are one of the few drugs where it is recommended that we prescribe by brand, rather than generically, due to the risk of slightly different bioavailability resulting in a lowered seizure threshold.

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21
Q

drug mx of epilepsy

A

Epilepsy: treatment

Most neurologists now start antiepileptics following a second epileptic seizure. NICE guidelines suggest starting antiepileptics after the first seizure if any of the following are present:

  • the patient has a neurological deficit
  • brain imaging shows a structural abnormality
  • the EEG shows unequivocal epileptic activity
  • the patient or their family or carers consider the risk of having a further seizure unacceptable

Sodium valproate is considered the first line treatment for patients with generalised seizures with carbamazepine used for partial seizures

Generalised tonic-clonic seizures

sodium valproate

second line: lamotrigine, carbamazepine

Absence seizures* (Petit mal)

sodium valproate or ethosuximide

sodium valproate particularly effective if co-existent tonic-clonic seizures in primary generalised epilepsy

Myoclonic seizures

sodium valproate

second line: clonazepam, lamotrigine

Focal** seizures

carbamazepine or lamotrigine

second line: levetiracetam, oxcarbazepine or sodium valproate

*carbamazepine may actually exacerbate absence seizure

** the preferred term for partial seizures

22
Q

which group of people must you be careful of when

A

It is useful when thinking about the management of epilepsy to consider certain groups of patients:

patients who drive: generally patients cannot drive for 6 months following a seizure. For patients with established epilepsy they must be fit free for 12 months before being able to drive

patients taking other medications: antiepileptics can induce/inhibit the P450 system resulting in varied metabolism of other medications, for example warfarin

women wishing to get pregnant: antiepileptics are generally teratogenic, particularly sodium valproate. It is important that women take advice from a neurologist prior to becoming pregnant, to ensure they are on the most suitable antiepileptic medication. Breast feeding is generally considered safe for mothers taking antiepileptics with the possible exception of the barbiturates

women taking contraception: both the effect of the contraceptive on the effectiveness of the anti-epileptic medication and the effect of the anti-epileptic on the effectiveness of the contraceptive need to be considered

23
Q

common medications used in epilepsy

A

Sodium valproate:

MOA: Increases GABA activityFirst-line for generalised seizures

  • increased appetite and weight gain
  • alopecia: regrowth may be curly
  • P450 enzyme inhibitor
  • ataxia
  • tremor
  • hepatitis
  • pancreatitis
  • thrombocytopaenia
  • teratogenic (neural tube defects)

Carbamazepine

MOA: Binds to sodium channels increasing their refractory periodFirst-line for partial seizures

  • P450 enzyme inducer
  • dizziness and ataxia
  • drowsiness
  • leucopenia and agranulocytosis
  • syndrome of inappropriate ADH secretion
  • visual disturbances (especially diplopia)

Lamotrigine

MOA:Sodium channel blockerUsed second-line for a variety of generalised and partial seizures

  • Stevens-Johnson syndrome

Phenytoin

MOA: Binds to sodium channels increasing their refractory periodNo longer used first-line due to side-effect profile

  • P450 enzyme inducer
  • dizziness and ataxia
  • drowsiness
  • gingival hyperplasia, hirsutism, coarsening of facial features
  • megaloblastic anaemia
  • peripheral neuropathy
  • enhanced vitamin D metabolism causing osteomalacia
  • lymphadenopathy
24
Q

acute mx of seizures

A

Acute management of seizures

Most seizures terminate spontaneously.

When seizures don’t terminate after 5-10 minutes then it is often appropriate to administer medication to terminate the seizure.

Patients are often prescribed these so family members may administer them in this eventuality, often termed ‘rescue medication’.

Benzodiazepines such as diazepam are typically used are may be administered rectally or intranasally/under the tongue.

If a patient continues to fit despite such measures then they are termed to have status epilepticus.

This is a medical emergency requiring hospital treatment.

Management options include further benzodiazepine medication, infusions of antiepileptics or even the use of general anaesthetic agents.

25
Q

partial seizures= define

A

Partial seizures have clinical features that are referable to a part of one hemisphere.

These can be divided into simple and complex subgroups, depending upon consciousness being maintained during the episode.

26
Q

SIMPLE partial seizure

A

In a simple partial seizure the awareness is preserved. The EEG shows unilateral paroxysmal activity during the attack.

Some examples of patterns of simple partial epileptic seizures:

  • motor - causes contralateral movement of the face and limbs. Often movement begins at the angle of the finger and then spreads progressively to the arm, trunk, and then leg and foot - termed Jacksonian epilepsy.
  • versive - seizures arising in the contralateral frontal lobe, affecting the frontal eye field, and causing turning of eyes to the contralateral side.
  • visual - occipital foci may cause crude visual images, for example, balls of light.
  • temporal foci - associated with olfactory hallucinations, for example, burning rubber and feelings of unreality. Autonomic activity, for example, flushing, and sexual sensations may occur.
27
Q

complex partial seizure

A

A complex partial seizure is a partial seizure in which consciousness is impaired.

  • 5As
  • Aura
  • Autonomic: change in skin colour, temperature, palps
  • Awareness lost: motor arrest, motionless stare
  • Automatisms: lip-smacking, fumbling, chewing, swallowing
  • Amnesia: post-ictal confusion (seizure in temporal lobe)

There is often a period of confusion, aimless wandering, fearfulness, incoherent speech or other inappropriate behaviour which can be misconstrued as a psychological disorder. The attack may be heralded by the patient being aware of a curious taste or smell. During the remainder of the attack, lip-smacking and swallowing are not uncommon.

28
Q

seizures- generalised partial

A

Simple or complex partial seizures may progress to generalised seizures with loss of consciousness and often with convulsive motor activity.

Additionally, many patients with focal seizures have generalised seizure without an obvious focal component and which are difficult to distinguish from primary generalised seizures.

Clues to a focal origin to the seizure include:

  • presence of an aura or observation of any focal feature, e.g. twitching of one extremity, aphasia, tonic eye deviation
  • presence of a post-ictal - post-seizure - focal neurologic deficit - Todd’s paralysis
29
Q

benign rolandic epilepsy of childhood

A
  • Rolandic epilepsy typically occurs in children aged seven to ten, but may start as young as three years of age, and is twice as common in boys
  • speech dyspraxia and language impairments are frequent comorbidities predating the onset of seizures. There is a six times higher odds of dyslexia, which should be anticipated at diagnosis and during routine follow-up
  • there is often a family history of speech and language disorders
  • seizure remission is universal by the age of 15 although a small but elevated risk of epilepsy in adult life remains and the risk of migraine is also increased
30
Q

general seizures- define + types

A

Generalised epileptic seizures have no features that are referable to only one hemisphere.

  • simultaneous onset of electrical discharge throughout cortex w/o localising features to one hemisphere

Types include:

  • absences (petit mal)
  • tonic-clonic (grand mal)
  • myoclonic jerk
  • tonic
  • atonic
  • akinetic
31
Q

[TONIC-CLONIC] grand mal seizures

  • DEFINE + S/S
A

A classic epileptic seizure is a stereotyped event, where there are tonic and clonic phases.

TONIC PHASE:

  • In a classic epileptic seizure, the first phase is tonic.
  • get LOC and pt falls to the ground.
  • The phase lasts 10 to 30 seconds during which the legs become extended and the arms abducted, flexed at the elbows and wrists.

CLONIC PHASE:

  • In a classic epileptic seizure, immediately following the tonic phase there is a clonic phase, during which there is clonic jerking of the muscles.
  • Incontinence of urine, dribbling from the mouth and tongue-biting are characteristic.
  • This usually lasts 1 to 5 minutes.
  • The movements are initially rapid and then become slower.

COMA PHASE:

  • ollowing the tonic-clonic phases of a classic epileptic seizure there is a phase which can be described as coma.
  • During this phase the patient is deeply unconscious, with complete muscular flaccidity.
  • Also there is absence of corneal and tendon reflexes, and extensor plantar responses.
  • This state may last up to several hours.
  • On awakening, the patient may have a headache and be dazed.
32
Q

petit mal [absence] seizures- define + s/s

A
  • Absence seizures or Petit mal is a form of primary generalised epilepsy that is seen mostly in children.
  • Patients with absences in childhood may not suffer them as an adult. However, a proportion of patients may go on to develop primary generalized seizures.
  • The EEG shows a characteristic 3 cycle per second spike and wave activity, which may be stimulated by hyperventilation.

s/s:

  • ABrupt onset and offset
  • Short: <10s
  • Eyes: glazed, blank-stare
  • Normal: intelligence, examination, brain-scan
  • Clonus or automatisms may occur
  • EEG: 3Hz spike and wave
  • Stimulated by hyperventilation and photics
33
Q

mx of childhood-onset typical absence epilepsy

A

management of childhood-onset typical absence epilepsy

The most effective treatments are:

  • sodium valproate - may also control the tonic-clonic and myoclonic seizures in the syndrome
  • ethosuximide - may control the myoclonic seizures; however will not control tonic-clonic seizures
  • lamotrigine - may control all seizure types

Note that phenytoin, carbamazepine and vigabatrin may exacerbate absences, especially if associated with myoclonus, and so should be avoided

NICE also states that ethosuximide, lamotrigine or sodium valproate are the first line treatments for childhood absence epilepsy (3).

Lamotrigine or sodium valproate are first-line treatments for juvenile absence epilepsy

34
Q

myoclonic epilepsy

A
  • Juvenile myoclonic epilepsy (JME) has an age of onset of 6-22 (peak 10-16 years).
  • It accounts for 4-12 % of childhood epilepsy.
  • The defining seizure is myoclonic. Generally the seizure occurs in the first hour after waking. These seizures occur as sudden jerks which commonly involve the arms and/or trunk but may effect any muscle.
  • Epileptogeneic photosensitivity occurs in at least half of patients with JME.

s/s:

Teenagers may suffer myoclonic jerks, usually in the arms, within one hour of awakening.

After a few years there may be the onset of generalised seizures.

A variant of this form of epilepsy is akinetic attacks where the patient suddenly loses body tone and falls to the floor.

35
Q

management and prognosis of juvenile myoclonic epilepsy

A

Treatments, available include:

  • sodium valproate - controls all the seizure types in about 90% of children with juvenile myoclonic epilepsy
  • lamotrigine - this treatment also appears effective. This treatment option may be preferable in adolescent girls, in whom menstrual irregularities, transient hair loss, and weight gain may troublesome side effects of sodium valproate therapy

Spontaneous remission before puberty occurs in fewer than 20% of children with juvenile myoclonic epilepsy. Also drug withdrawal is often unsuccessful even after 2 or more years of seizure-freedom, with at least 70% of patients relapsing. Often lifelong treatment will be required to ensure seizure-freedom.

NICE state that lamotrigine or sodium valproate are the first-line drugs for this condition

36
Q

infantile spasms- define + s/s + mx

A

Infantile spasms, or West syndrome, is a type of childhood epilepsy which typically presents in the first 4 to 8 months of life and is more common in male infants. They are often associated with a serious underlying condition and carry a poor prognosis

Features

  • characteristic ‘salaam’ attacks: flexion of the head, trunk and arms followed by extension of the arms
  • this lasts only 1-2 seconds but may be repeated up to 50 times
  • progressive mental handicap

Investigation

  • the EEG shows hypsarrhythmia in two-thirds of infants
  • CT demonstrates diffuse or localised brain disease in 70% (e.g. tuberous sclerosis)

Management

  • poor prognosis
  • vigabatrin is now considered first-line therapy
  • ACTH is also used
37
Q

atonic [akinetic] seizures

A
  • Sudden loss of muscle tone → fall
  • No LOC
38
Q

febrile convulsions

A

Febrile convulsions are seizures provoked by fever in otherwise normal children.

They typically occur between the ages of 6 months and 5 years and are seen in 3% of children

Clinical features

  • usually occur early in a viral infection as the temperature rises rapidly
  • seizures are usually brief, lasting less than 5 minutes
  • are most commonly tonic-clonic

Types of febrile convulsion:

Simple

Complex

Febrile status epilepticus

< 15 minutes

15 - 30 minutes

> 30 minutes

Generalised seizure

Focal seizure

Typically no recurrence within 24 hours

May have repeat seizures within 24 hours

Should be complete recovery within an hour

Management following a seizure

  • children who have had a first seizure OR any features of a complex seizure should be admitted to paediatrics

Prognosis

  • the overall risk of further febrile convulsion = 1 in 3. However, this varies widely depending on risk factors for further seizure. These include: age of onset < 18 months, fever < 39ºC, shorter duration of fever before seizure and a family history of febrile convulsions
  • if recurrences, try teaching parents how to use rectal diazepam or buccal midazolam. Parents should be advised to phone for an ambulance if the seizure lasts > 5 minutes
  • regular antipyretics have not been shown to reduce the chance of a febrile seizure occurring

Link to epilepsy

  • risk factors for developing epilepsy include a family history of epilepsy, having complex febrile seizures and a background of neurodevelopmental disorder
  • children with no risk factors have 2.5% risk of developing epilepsy
  • if children have all 3 features the risk of developing epilepsy is much higher (e.g. 50%)
39
Q

localising features of seizures [seen in partial seizures]

A

Localising Features

  • Temporal
  • Automatisms:
    • Oral: lip smacking, chewing, swallowing
    • Manual: fumbling, fiddling, grabbing
    • Movements of complex actions: singing, kissing, driving a car and violent acts
  • Abdominal rising sensation or pain: n/v
  • Dysphasia: ictal or post-ictal
  • Deja/jamias vu:memory phenomena
  • Emotional disturbance: terror, panic, anger, elation and derealisation – hippocampal involvement
  • Tastes, smells and auditory Hallucination: involvement uncus and auditory cortex
  • Delusional behaviour
  • Frontal
  • Motor features:
    • posturing
    • movement of head and eyes
    • peddling of legs
    • motor arrest
    • Jacksonian march (spreading (face to thumb) focal seizure/retained awareness)
    • Todd’s palsy
  • Parietal
  • Sensory disturbance: (contralateral) tingling, numbness, pain
  • Occipital

Visual phenomena: spots, lines, flashes

40
Q

Qs to ask during clinical assessment

A

Three questions to consider:

  • Are these really seizures?
  • detailed description/witness
  • suggestive features: tongue biting and slow recovery(not twitching - seen in reflex anoxia convulsions due to syncope)
  • What type of seizures is its -partial or generalised?
  • Onset is key
    • Focal features: partial
    • Rapid onset: generalised

Any triggers?EtOH, stress, fevers, sounds, lights, contrasting patterns, reading/writing

41
Q

ix

A

the suggested necessary investigations for a first seizure are:

  1. clinical examination
  2. assessment of seizure semiology
  3. routine laboratory tests (depending on clinical circumstances)
  4. cerebrospinal fluid (if encephalitis or subarachnoid haemorrhage is suspected and drug screening (depending on clinical circumstances)
  5. early standard electroencephalography, if possible within 24 hours
  6. sleep deprived electroencephalography within 1 week
  7. high resolution magnetic resonance imaging, if possible

~~~~~~~~~~~~~~~

  • Diagnosis – Clinical Hx:Don’t diagnose epilepsy from a single seizure

There is no single test which can diagnose epilepsy (1). Investigations that can be helpful in epilepsy are:

  • EEG -
    • should be carried out only to support a diagnosis of epilepsy when the clinical history suggests that the seizure is likely to be epileptic in origin. The EEG should not be used in isolation to make a diagnosis of epilepsy.
  • CT and MRI- may be necessary in those suspected of having focal neurological deficit
    • neuroimaging should be used to identify structural abnormalities that cause certain epilepsies.
    • MRI should be the imaging investigation of choice in individuals with epilepsy. It is particularly important in patients
      • who develop epilepsy before the age of 2 years or in adulthood
      • who have any suggestion of a focal onset on history, examination or EEG (unless clear evidence of benign focal epilepsy)
      • in whom seizures continue in spite of first-line medication.
    • CT is used when MRI is not available or contraindicated to identify underlying gross pathology or for children and young people in whom a general anaesthetic or sedation would be required for MRI but not CT
    • neuroimaging should not be routinely requested when a diagnosis of idiopathic generalized epilepsy has been made.
  • other investigation which should be considered to identify potential causes and/or to identify any significant co-morbidity include
    • in adults - appropriate blood tests (plasma electrolytes, glucose, calcium)
    • in children and young people - blood and urine biochemistry
    • measurement of serum prolactin is not recommended for the diagnosis of epilepsy
  • Basic bloods: FBC, U+Es, glucose
    • pO2 and pH ↓, creatine phosphokinase (CPK) or creatine kinase↑, ↑ serum Prolactin 10 min after fit (relative to baseline) – raised in generalized seizures

  • a 12-lead ECG
    • should be performed in adults with suspected epilepsy
    • should be considered in children in cases of diagnostic uncertainty
42
Q

general mx

A
  • Advice: against driving, operating heavy machinery, swimming SE of drugs
  • DVLA: contact DVLA - avoid driving until seizure-free for >1yr
  • MDT: epilepsy specialist nurse, neurologist, GP

- Patient centred: involve patient in all decisions

43
Q
A
44
Q

ddx

A

Differentials of convulsive seizures:

  • Syncope - vasovagal attacks, arrhythmias, carotid sinus hypersensitivity, postural hypotension
  • prodrome: pallor, nausea, sweating
  • hypoxia: reflex anoxia seizure
  • Doesn’toccurs when lying flat
  • Floppy during syncope and rigid during seizure
  • Arrhythmias = palpitations
  • Associations: urinary incontinence, unilateral limb jerking
  • Non-epileptic attack disorder (pseudo- or psychogenic) seizures:
  • common: women
  • PMH: psychiatric Hx
  • pupils/BP/HR/pO2/pH – unchanged - Clinical features during an epileptic attack that support the diagnosis of a seizure include pupil dilatation, raised blood pressure and heart rate, extensor plantar responses, and central and peripheral cyanosis
  • EEG: no seizure, no postictal
  • TIA: transient loss of consciousness
  • Migraine
  • Metabolic abnormalities:
  • Hypoglycaemia

↓ Na+

45
Q

epilepsy: pregnancy and breast feeding

A
  • In Women / Pregnancy
  • Avoid valproate: take lamotrigine (or CBZ) – teratogenicity
  • 5mg folic acid daily if child-bearing age
  • pre-conception counselling
  • breastfeeding: AED present in breast milk (except valproate and carbamazepine)
  • CBZ and PHE are enzyme inducers and ↓ the effectiveness of the OCP

~~~~~~

The risks of uncontrolled epilepsy during pregnancy generally outweigh the risks of medication to the fetus. All women thinking about becoming pregnant should be advised to take folic acid 5mg per day well before pregnancy to minimise the risk of neural tube defects. Around 1-2% of newborns born to non-epileptic mothers have congenital defects. This rises to 3-4% if the mother takes antiepileptic medication.

Other points

  • aim for monotherapy
  • there is no indication to monitor antiepileptic drug levels
  • sodium valproate: associated with neural tube defects
  • carbamazepine: often considered the least teratogenic of the older antiepileptics
  • phenytoin: associated with cleft palate
  • lamotrigine: studies to date suggest the rate of congenital malformations may be low. The dose of lamotrigine may need to be increased in pregnancy

Breast feeding is generally considered safe for mothers taking antiepileptics with the possible exception of the barbiturates

It is advised that pregnant women taking phenytoin are given vitamin K in the last month of pregnancy to prevent clotting disorders in the newborn

Sodium valproate

The November 2013 issue of the Drug Safety Update also carried a warning about new evidence showing a significant risk of neurodevelopmental delay in children following maternal use of sodium valproate.

The update concludes that sodium valproate should not be used during pregnancy and in women of childbearing age unless clearly necessary. Women of childbearing age should not start treatment without specialist neurological or psychiatric advice.

46
Q

epilepsy: contraception

A

Epilepsy: contraception

There are a number of factors to consider for women with epilepsy:

the effect of the contraceptive on the effectiveness of the anti-epileptic medication

the effect of the anti-epileptic on the effectiveness of the contraceptive

the potential teratogenic effects of the anti-epileptic if the woman becomes pregnant

Given the points above, the Faculty of Sexual & Reproductive Healthcare (FSRH) recommend the consistent use of condoms, in addition to other forms of contraception.

For women taking phenytoin,carbamazepine, barbiturates, primidone, topiramate, oxcarbazepine:

UKMEC 3: the COCP and POP

UKMEC 2: implant

UKMEC 1: Depo-Provera, IUD, IUS

For lamotrigine:

UKMEC 3: the COCP

UKMEC 1: POP, implant, Depo-Provera, IUD, IUS

If a COCP is chosen then it should contain a minimum of 30 µg of ethinylestradiol.

47
Q

status epilepticus: definition

A
  • Seizure lasting >30min, or
  • Repeated seizures w/o intervening consciousness
48
Q

status epilepticus: what’s the risk

A
  • Mortality/permanent brain damage: ↑ w/ length of attack (stop <20min)
  • Typically occurs in known epileptics
  • Pregnant women – pre-eclampsia – call obstetrics may need an emergency delivery
49
Q

SE: classification

A

Classification of status epilepticus (SE)

SE can be divided according to semiology, duration and underlying aetiology (1).

The most commonly used is the semiologic classification

convulsive status epilepticus (CSE)

  • generalized convulsive SE (GCSE) - the most common type of SE..S/S:
    • generalized tonic - clonic activity of the extremities.
    • impaired mental status e.g. - coma, lethargy, confusion
    • may demonstrate focal neurological impairments in the post ictal period e.g., Todd’s paralysis,

nonconvulsive status epilepticus (NCSE)

=is when a patient has seizure activity seen on electroencephalogram (EEG) without the associated clinical features of genralised convulsive status epilepticus (GCSE)

  • absence SE
  • simple partial SE (SPSE)
  • complex partial SE (CPSE)
  • subtle SE (2)

Spectrum of non-convulsive seizures is highly variable and can be divided into:

🎀 negative symptoms - include anorexia, aphasia/mutism, amnesia, catatonia, coma, confusion, lethargy, and staring.

🎀 positive symptoms - include agitation/aggression, automatisms, blinking, crying, delirium, delusions, echolalia, facial twitching, laughter, nausea/vomiting, nystagmus/eye deviation, perseveration, psychosis, and tremulousness.

refractory SE (RSE)

50
Q

diagnosis

A

diagnosis of generalized convulsive status epilepticus is usually straightforward with the patient presenting with generalized tonic or clonic activity (1)

The following investigations should be carried out as soon as possible and should accompany pharmacological interventions simultaneously (2).

in all patients

  • fingerstick glucose (BM)
  • monitor vital signs
  • computed tomography (CT) scan (appropriate for most cases) of the head- once the patients is stabilised
  • laboratory studies:
    • blood glucose
    • complete blood count
    • basic metabolic panel e.g. - serum electrolytes, blood urea nitrogen (BUN), creatinine,
    • calcium (total and ionized)
    • magnesium
    • AED levels
  • continuous electroencephalograph (EEG) monitoring

according to the clinical presentation (patient’s history and events leading up to presentation)

  • brain MRI
  • lumbar puncture - in suspected cases of CNS infection or subarachnoid hemorrhage
  • comprehensive toxicology screen to identify toxins which may be responsible for seizures e.g - isoniazid, tricyclic antidepressants, theophylline cocaine, sympathomimetics, alcohol, organophosphates, and cyclosporine
  • other laboratory tests e.g. - liver function tests,
51
Q

SE- acute mx

A
  • Acute management:
  • Airways: open + maintain, lie in recovery position, remove false teeth, insert oral/nasal airway, intubate if necessary
  • Breathing: O2 + suction[as required]
  • Circulation: IV access and bloods – U+E, LFT, FBC, glucose, ca2+, toxicology screen if indicated, anticonvulsant levels
  • Stop seizure: slow IV bolus phase - lorazepam – 2-4mg à 2nd dose if no response in 10min
  • Alcoholism/malnourishment[if suspected]: Thiamine 250mg IV
  • If hypoglycaemia: Glucose 50mL 50% (w/v) saline IV
  • Treat acidosis if severe
  • Hypotension: fluids
  • Continuous seizure:
    • IV infusion phase: phenytoin 15-20mg/kg IVI – rate <50mg/min

· CI: dysrhythmia or Heart block

  • Maintenancedose: 100mg/6-8h
  • Monitor: ECG (length QT-interval), BP
  • Alternative: diazepam infusion 100mg in 500mL of 5% glucose: infusion at ~40mL/h

Continuing seizure: ICU, GA (expert help with paralysis and ventilation)