Epilepsy Final MBBS theory presentation- Medicine Neurology

2. What is a seizure?
A seizure is the manifestation of an abnormal, paroxysmal discharge of
a group of cortical neurons. This discharge may produce subjective
symptoms or objective signs.

3. What are the key features of a seizure?
• Paroxysmal nature of the event.
• Associated abnormal movements.
• Altered responsiveness or impairment of consciousness / awareness.

5. Classifications
Partial

6. Generalized
• There is simultaneous involvement of bot hemispheres,always
associated with loss of consciousness or awareness.
• Tonic clonic (grand mal)
• Absence (petit mal)
• Myoclonic
• Tonic clonic atonic

7. Focal (Partial)
Electrical discharge restricted to a
limited part of the cortex of one
cerebral hemisphere.
Focal seizures are further characterized
according to whether or not there is:
Aura
e.g. smell or auditory hallucination, déjà
vu, fear, visual distortion, sensory
symptoms such as tingling, abdominal
rising sensation
Motor features
e.g. one limb jerking (a Jacksonian
seizure)
Loss of awareness or responsiveness,
e.g. in many temporal lobe seizures.
Old class.
• Simple –without loss of awareness
• Complex- with loss of awareness
• With secondary generalization

8. Focal seizures with electrical activity confined to
one part of the brain may spread after a few
seconds, due to failure of inhibitory mechanisms, to
involve the whole of both hemispheres, causing a
bilateral tonic–clonic seizure.

10. Generalized seizure type

11. Generalized tonic–clonic seizures (grand mal
seizures)
Prodrome. There is often no warning before generalized tonic– clonic
seizures (GTCS), or there may be an aura prior to a bilateral
tonic–clonic seizure.
Tonic–clonic phase. -An initial tonic (stiffening) is followed by the clonic
phase with synchronous (twisting or jerking) of the limbs, reducing in
frequency over about 2 minutes until the convulsion stops.
The patient may utter an initial cry and then falls, sometimes suffering
serious injury.

12. The eyes remain open and the tongue is often bitten.
There may be incontinence of urine or faeces.
Post-ictal phase.
A period of flaccid unresponsiveness is followed by gradual return of
awareness with confusion and drowsiness lasting 15 minutes to an
hour or longer.
Headache is common after a GTCS.

15. Myoclonic, tonic and atonic seizures
• Myoclonic seizures or ‘jerks’ (sudden shock like contraction of the
muscle) take the form of momentary brief contractions of a muscle or
muscle groups:
for example,
Causing a sudden involuntary twitch of a finger or hand. They are
common in primary generalized epilepsies.

16. Atonic Seizure
Atonic seizures involve a sudden collapse with loss of muscle tone and
consciousness.
Tonic seizure
Consist of stiffening of the body, not followed by jerking.

17. Typical absence seizures (petit mal)
Almost invariably begins in childhood.
Each attack is accompanied by 3 Hz spike-and-wave EEG activity. (The EEG
shows generalised 3/second spike and wave discharge, which is bilaterally
synchronous during and sometimes between episodes)
There is loss of awareness and a vacant expression for less than 10 seconds
before returning abruptly to normal and continuing as though nothing had
happened.
Apart from slight fluttering of the eyelids, there are no motor manifestations.
Patients often do not realize they have had an attack but may have many per
day.

18. Typical absence attacks are never due to acquired lesions such as
tumours; they are a manifestation of primary generalized epilepsy.
Children with absence seizures may go on to develop generalized
convulsive seizures.
Absence seizures are often confused with temporal lobe seizures
causing transient alteration of awareness.

19. Focal seizure type

20. Focal seizures with aura
The nature of the aura helps to localize the seizure focus.
Temporal-lobe auras include
• déjà vu (a feeling of having already experienced the present situation)
or jamais vu (phenomenon of experiencing a situation that one
recognizes in some fashion, but that nevertheless seems novel and
unfamiliar)
• Olfactory hallucination
• Formed visual hallucination or misperception eg: micropsia or
macropsia ( object appear larger or smaller)
• Fear may be mistaken for panic attack

21. frontal lobe
• Motor phenomena
Occipital lobe auras-
• include visual phenomena such as zigzag lines and coloured
scotomas.
Parietal lobe
• Contralateral altered sensation (dysaesthesia)

23. Focal motor seizures
These originate within the motor cortex.
Jerking typically begins on one side of the mouth or in one hand,
sometimes spreading to involve the entire side.
This visible spread of activity is called the Jacksonian march of a
seizure.
Local temporary paralysis of the limbs affected sometimes follows:
Todd’s paralysis.

24. Focal seizures with altered awareness or
responsiveness
These usually arise from the temporal lobe (60%) or the frontal lobe.
There is often a preceding aura followed by a period of complete or partial loss of
awareness of surroundings, lasting for 1–2 minutes on average (as opposed to 10
seconds in absence seizures), which the patient generally does not remember
subsequently.
This stage is accompanied by speech arrest and often by automatisms: semi-
purposeful stereotyped motions such as lip smacking or dystonic limb posturing,
or more complex motor behaviours such as walking in a circle or undressing.
The attacks may be followed by a short period of post-ictal confusion or may
develop into a bilateral tonic– clonic seizure.

25. Epilepsy syndromes and aetiology of epilepsy
The range of causes of epilepsy is different at different ages and in
different countries.
• Children and teenagers: genetic, perinatal and congenital disorders
predominate.
• Younger adults: trauma, drugs and alcohol are common.
• Older ages (>60 years): vascular disease and mass lesions such
as neoplasms are important.

27. Causes of Epilepsy
• Primary generalized epilepsy, e.g. juvenile myoclonic epilepsy,
childhood absent seizure, monogenic disorder.
• Developmental, e.g. neuronal migration abnormalities, cortical
dysplasia
• Hippocampal sclerosis (major cause)
• Brain trauma and surgery (ICH, depressed skull #, penetrating injury)
• Intracranial mass lesions, e.g. tumour
• Vascular, e.g. cerebral infarction, arteriovenous malformation, venous
sinus thrombosis
• Infectious, e.g. viral encephalitis, meningitis, cerebral tuberculosis,
HIV, cerebral toxoplasmosis, neurocysticercosis

28. • Immune, e.g. NMDA receptor antibody and potassium channel antibody
encephalitis
• Genetic, e.g. channelopathies
• Metabolic abnormalities, e.g. hyponatraemia, hypocalcaemia,
hypoglycaemia, acute hypoxia, uremia, hepatic encephalopathy, porphyria.
• Neurodegenerative disorders, e.g. Alzheimer’s
• Drugs, e.g. ciclosporin, lidocaine, quinolones, tricyclic antidepressants,
antipsychotics, lithium, stimulant drugs such as cocaine
• Alcohol withdrawal

29. • Perinatal brain injury and cerebral palsy (leukomalasia, brain
haemorrhage associated with prematurity and fetal hypoxia) – early
onset epilepsy.

31. Differential diagnosis of seizure
Acute symptomatic seizure
Is he well between seizures
YES NO
Epilepsy Acute symptomatic seizure

32. IF NO….
• Encephalitis : Fever with LOC
• Meningitis
• Cerebral abscess - low grade fever, subacute
• Hx of bronchiectasis, IE, valvular disease, HIV, CSF shunt, splenectomy
• Past History of head trauma, history of previous brain surgeries
• Stroke : Hemiparesis
• Hypoglycaemia
• Electrolyte abnormalities
• Intracranial SOL
• SAH
• SDH
• Multiple sclerosis

33. Differentiating pseudo seizures from epilepsy

34. Differentiating syncope from seizures

35. • Gradual onset
• Vasovagal – following prolonged periods of standing, stress
• Cardiogenic – increased emotion
• Have time to tell someone/ sit / park the car if driving usually
• Syncope – cold clammy peripheriesn,Pale, hypotensive ,Vasovagal –
bradycardia

37. Diagnosis of the first fit and investigations
The diagnosis of a seizure is
essentially a clinical one, based on
taking a history from the patient and
any witnesses.
Investigations have a limited role in
distinguishing between a seizure and
other causes of a blackout or attack
The majority of patients referred to a
first fit clinic have not had a seizure.
The most common error is to
misdiagnose a syncopal blackout for
a seizure.

38. Investigation
Basic
• FBC – infection
• CBS – hypoglycemia
• BU/SE, S.Ca, S. Mg – uraemia, electrolyte abnormality
• S. Creatinine
• LFT
• 12 lead ECG (as cardiac arrhythmias can mimic seizure)
• Urine- toxicology, amino acid and organic acid measurement*
• Non contrast CT – chronic SDH

39. EEG
• Useful for evaluating interictal abnormalities
• Occasionally useful for determining nature of a clinical symptom
(absence seizures, tics or other frequent movements)
• Helpful in predicting recurrence of seizures.
• A normal EEG does not exclude a diagnosis of seizure.

41. Ambulatory EEG
• Allows for Ictal recording- ie, EEG activity during a suspected episode:-
Drawbacks- technical, availability, depends on patient to indicate when the
episodes are occurring
Videotelemetery
• Simultaneous recording of EEG and video of patient
• Can be done as a day procedure or as in patient
• Episodes must occur with some frequent

43. Imaging procedures
• CTT is not the procedure of choice but is appropriate in emergencies,
especially trauma
• MRI is the imaging procedure of choice
o Abnormal neurological examination
o Focal seizure activity
o Focal findings on EEG
• PET scanning is a specialized procedure done in limited circumstances
(usually as part of evaluation of intractable seizures or when a surgical
treatment is proposed.

44. Approach to a first seizure

46. Management
• The first seizure is not generally treated exceptions :-
oPatient has a predisposing factor
oOccupational demands
oUnderlying brain problem
oFamily history
• Usually treatment is started after second episode
• Recommendation 2-5 years. At least 3 years from last seizure.
• Started with monotherapy, gradually increased to achieve control and
then tailed off.
• Focal and 2ry generalized-drug of choice- CBZ
• All other seizures 1stline sodium valporate

50. Drug side effect

53. What advise will you give?
• All drugs once started need to be continued for Minimum 2-3 years
• Abrupt withdrawal can precipitate status epilepticus – do not
discontinue for any reason
Eg:- inter-current illness w/o medical advise
• Ask to avoid –
oDriving – Heavy vehicles – NEVER
oOwn car – avoid till fit free for 2-3yrs
oSwimming, contact sports, precipitant factors
• S/E – esp. Steven Johnson Xn, anaemia, liver toxicity

54. If 1st mono-therapy fails
• If seizure continues despite the maximally tolerated dose of 1st AED
• - Review the diagnosis
• - Review seizure type/syndrome
• - Review dosage and frequency
• - Review the compliance

55. Acceptable combinations of AED treatment
• Carbamazipine + valporate (leads to an enhanced therapeutic
efficacy)
• Valporate + ethosuximide (control absent seizures which is not
controlled by either drug alone)
• Valporate + clonazepam (used for myoclonic seizures)
Combinations of AED should be avoided
• Carbamazepine + phenytoin (enzyme inducers cause reduction of
drug levels of each others)
• Carbamazepine + lamotrigine (enhance each other’s side effects)

56. Antiepileptic Drug Interactions
• Drugs that induce metabolism of other drugs: carbamazepine,
phenytoin, phenobarbital.
• Drugs that inhibit metabolism of other drugs: valproate
• Drugs that are highly protein bound: valproate, phenytoin,
carbamazepine
• Other drugs may alter metabolism or protein binding of antiepileptic
drugs

57. When to consider Rx withdrawal?
• Withdrawal of AED therapy
considered only after seizure
free period of at least 3 yrs
• Rx withdrawn over period of 6
months
• If relapse during withdrawal
continue Rx for another 2yrs

59. Management of Status epilepsy
This medical emergency means continuous seizures for 30 minutes or longer
(or two or more seizures without recovery of consciousness between them
over a similar period).
The longer the duration of status, the greater the risk of permanent cerebral
damage.
Rhabdomyolysis may lead to acute kidney injury in convulsive status
epilepticus.
Over 50% of cases occur without a previous history of epilepsy. Some 25%
with apparent refractory status have pseudostatus (non-epileptic attack
disorder).

60. Management

65. Pregnancy and Epilepsy
• Most pregnancies in mothers with epilepsy produce normal children
• Fetal anomalies (up to 10% of pregnancies) are multifactorial
oDrug effects
oConsequences of the mother’s underlying diseases
oConsequence of maternal seizures during pregnancy
• All antiepileptic drugs carry teratogenic risks
• Polytherapy increases risk

66. If possible, avoidance of VPA and AED polytherapy during the first
trimester of pregnancy should be considered to decrease the risk of
MCMs.

67. Epilepsy in elderly
• Because elderly people are the most rapidly growing segment of the
population and
• Because incidence and prevalence of epilepsy are higher in this age
group a marked increase in epilepsy in the elderly is expected.