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Seizure Disorder

Seizure –

  1. Paroxysmal event due to abnormal, excessive and hypersynchronous discharges from an aggregate of CNS neurons.
  2. The term epilepsy describes a syndrome characterized by recurrent seizures.
  3. Manifestation of a seizure can include impairment or loss of consciousness, sensory, motor or behavioral abnormalities.
  4. A seizure is said to be convulsive if it is accompanied by motor manifestation.
  5. So a convulsion is a type of seizure but all seizures are not convulsion.

Extra Edge: Single seizure does not constitute epilepsy but there are 40 – 80 % chances of seizure with in next 12 months so driving is not allowed during this period.

Classification –

  1. Partial seizures
    1. Simple partial              
    2. Complex partial (Temporal lobe epilepsy)
    3. Partial seizures with secondary generalization.
  2. Primary generalized seizures
    1. Absence (Petit mal)              
    2. Tonic – clonic (Grand mal)    
    3. Tonic   
    4. Atonic          
    5. Myoclonic
  3. Unclassified
    1. Neonatal Seizure            
    2. Infantile Spasm.
  4. Post traumatic
  5. Status epilepticus

Partial Seizures Seizure activity is restricted to discrete areas of cerebral cortex. Partial seizures are often associated with structural abnormalities of the brain. In such case CT/MRI of brain is mandatory.

  1. Simple partial seizure The consciousness is fully preserved during the seizure simple partial seizure cause motor, sensory autonomic or psychic symptoms.
  2. Complex partial seizure (Temporal lobe epilepsy) Focal seizure activity accompanied by a transient impairment of patient’s ability to maintain normal contact with the environment. Automatism is a feature of CPS.
  3. Partial seizures with secondary generalization Partial seizure can spread to involve both hemisphere and produce generalized seizure. Aura is an important feature. It is frequently observed following simple partial seizure.

Extra Edge:

Jacksonian march – Movements begin in a very restricted region and gradually progress to include a larger area.

Todd’s paralysis – Localized paresis in the involved region.

Epilepsia partialis continua – Seizure activity continue for hours – days.

Generalized Seizures – Arise from both cerebral hemisphere simultaneously. Result from cellular, biochemical or structural abnormalities.

Absence seizures/Petit mal seizures:


Clinical Hallmarks

  1. Almost always begin in childhood and cease by age of 20.
  2. Sudden brief lapses of consciousness without loss of postural control
  3. Seizure typically lasts only for seconds. Impairment is so brief that patient may be unaware of it.
  4. Consciousness returns as suddenly as it was lost i.e. onset and termination of attack, both are abrupt.
  5. Usually accompanied by subtle bilateral motor signs such as
    1. Rapid blinking of eye lids
    2. Chewing movements
    3. Small amplitude, clonic movements of hands
  6. There is no postictal confusion
  7. The seizure can occur hundreds of times per day.
  8. First clue to absence seizure is often unexplained 'day dreaming' and a decline in school performance recognized by a teacher.

Electrophysiological hallmark

  1. Electrophysiological hallmark of typical absence seizure is a generalized symmetric, 3 Hz spike and wave discharge that begins and ends suddenly superimposed on a normal EEG background.
    Hyperventilation tends to provoke these electrographic discharges and even the seizures themselves.
  2. Atypical absence seizure – Lapse of consciousness is longer duration, less abrupt in onset and cessation.
    EEG 2.5HZ.
    Mental retardation positive.
  3. Atonic seizures Loss of postural muscle tone lasting 1 to 2 second.
    Consciousness is briefly impaired but there is no post ictal confusion.
    Ranging from quick head drop to collapse.
    EEG Brief generalized spike and wave discharge followed by diffuse slow waves that correlate with loss of ms. tone.
  4. Myoclonic seizures Sudden and brief ms contraction that may involve one part of the body or the entire body.
    Causes – Metabolic disorders, degenerative CNS disorder, Anoxic brain damage. Creutzfeldt Jacob disease. Myoclonus may occur in normal person also
    EEG B/L Synchronous spike and wave discharges.
  5. GTCS (Generalized Tonic Clonic Seizure)

Epilepsy Syndromes


Epilepsy syndromes are disorders in which epilepsy is a predominant feature and there is sufficient evidence to suggest a common underlying mechanism.

Three important epilepsy syndromes are – 
(Ref. Hari. 18th ed., Pg- 3253)

  1. Juvenile myoclonic epilepsy (JME) also known as JANZ syndrome. It is an epilepsy syndrome.
    It is characterized by:
    1. Appearance in early adolescence
    2. Bilateral myoclonic jerks that may be single or repetitive
    3. Most frequent in morning after awakening
    4. Can be provoked by sleep deprivation
    5. Consciousness is usually preserved unless myoclonus is specially severe
    6. Association with generalized tonic-clonic seizures and absence seizure is seen
    7. Benign condition although complete remission is uncommon
    8. Seizure responds well to appropriate anticonvulsant medication
    9. Family history of epilepsy is common
    10. Treatment is with valproate
  2. Lennox – Gastaut syndrome Occur in children and consist of triad of
    1. Multiple seizure type (GTCS, atonic, atypical absence)
    2. EEG <3HZ spike & wave discharge
    3. Impaired cognitive function.
Causes – Developmental ab normal. Perinatal hypoxia/ ischemia, trauma, infection. Response to therapy is poor.
  1. Mesial Temporal Lobe Epilepsy H/O febrile seizure. Family h/o positive. Complex partial seizure.
    Poor response to therapy. Characteristic hippocampal sclerosis. Surgery is curative.

Causes of epilepsy

  1. Neonates (<1month) – Perinatal hypoxia/ ischemia, Intracranial hmg. CNS infection.
  2. Infants / children (<12) – Febrile seizures, metabolic. CNS infection, Idiopathic
  3. Adolescents (12 – 18) – Trauma, infection
  4. Young adults (<35) – Trauma, alcohol
  5. Older (>35) – Cerebrovascular disease (Most common cause in elderly), Brain tumor, Degenerative CNS disorders.
  6. Epileptogenic factors – Head trauma (50% risk in case of penetrating injury)

Table: Features that distinguish generalized tonic – clonic seizure from syncope




Immediate precipitating factors

Usually none

Emotional stress, Valsalva, orthostatic hypotension, cardiac etiologies

Posture at onset



Transition to unconsciousness

Often immediate

Gradual over seconds

Duration of unconsciousness



Disorientation and sleepiness after event

Many minutes to hours


Return of consciousness

After many minutes or hrs

Almost immediately (AIPG 07)

Biting of tongue









Post traumatic epilepsy


The term post traumatic epilepsy should be used if repeated seizures occur after first week of head injury and are recurrent. (AIIMS NOV 2011)

Neonatal Seizures


Subtypes of neonatal seizures

  1. Subtle (commonest subtype)        
  2. Clonic (Focal / Multifocal)
  3. Tonic (Focal / Generalized)           
  4. Myoclonic (Focal / Multifocal / Generalized)

Extra Edge: Hypsarrhythmia are seen in infantile spasm (salaam seizure)

Factors which may trigger seizures

  1. Sleep deprivation                         
  2. Emotional stress
  3. Physical and mental exhaustion                    
  4. Infection, pyrexia
  5. Drug or alcohol ingestion, or withdrawal               
  6. Flickering light, visual patterns, proximity to television screens
  7. Uncommon triggers                             
  8. Loud noise, Hot baths, Music, Reading

Table 369-8 Selection of Antiepileptic Drugs

Generalized-onset Tonic-Clonic


Typical Absence

Atypical Absence, Myoclonic, Atonic


Valproic acid


Valproic acid

Valproic acid



(AIIMS May 08)




(LQ 2012)




















Valproic acid




























Extra Edge: Valproate is the drug which is effective in most types of epilepsy. (LQ 2012) 

Recent Advances: Newer Drugs in neurology (Not given in Harrisin 18th edition  also !!!)

  1. Stiripentol
    1. Stiripentol is used in the treatment of epilepsy.
    2. Mechanism of action
      1. It increases GABA transmission.
  2. Retigabine
    1. It  is an anticonvulsant used as a treatment for partial epilepsies.
    2. It is a potassium channel opener—that is, by activating a certain family of voltage-gated potassium channels in the brain. 
    3. This mechanism of action is unique among antiepileptic drugs.
  3. Ramelteon
    It is the first in a new class of sleep agents that selectively binds to the MT1 and MT2 receptors in the suprachiasmatic nucleus (SCN), instead of binding to GABA A receptors, such as with drugs like zolpidem, eszopiclone, and zaleplon.
  4. Agomelatine
    1. It is used for the treatment of major depressive disorder and has a reduced level of sexual side effects.
    2. It also has positive effects on sleep.
  5. Perampanel is an antiepileptic drug that acts as a selective noncompetitive antagonist of AMPA receptors, the major subtype of ionotropic glutamate receptors.
    Perampanel is effective in the treatment of refractory partial-onset seizures
  6. Retigabine, is an anticonvulsant used as an adjunctive treatment for partial epilepsies. It is a potassium channel opener.
  7. Rufinamide is an anticonvulsant medication. It is used in combination with other medication and therapy to treat Lennox–Gastaut syndrome and various other seizure disorders.
  8. Progabide is an analog and prodrug of GABA used in the treatment of epilepsy. Specifically, generalized tonic-clonic, myoclonic, partial, and Lennox-Gastaut syndrome seizures—in both children and adults.. It is a new drug not given in Harrison 18th edition also !!!

Surgical Treatment of Epilepsy
Procedures done are –

  1. Temporal lobectomy – In temporal lobe epilepsy
  2. Lesionectomy –
  3. Multiple subpial transection
  4. Hemispherectomy – In pt. of hemi megalencephaly
  5. Corpus callosotomy – In Lennox – Gastaut syndrome.

Anti Epileptic Drugs –


Side effects

1. Phenytoin

Dizziness, diplopia, cerebellar ataxia, Gum hyperplasia, Lymphadenopathy, Hirsutism, osteomalacia.

2. Carbamazepine

Ataxia, vertigo, Dizziness, Aplastic anemia
Leukopenia, Hepatotoxicity, Hyponatremia

3. Valproic acid

Ataxia, tremor, Sedation, Hepatotoxicity, weight gain
Thrombocytopenia, Transient alopecia

4. Lamotrigine

Skin rash, Stevens. Johnson syndrome, Dizziness, diplopia
Sedation, Ataxia, Headache

5. Ethosuximide

Ataxia, Lethargy, Bone marrow suppression, Skin rash

6. Topiramate

Psychomotor slowing, Language disorder, Renal stones.

7. Phenobarbital

Sedation, ataxia, Confusion, dizziness
Decreased libido, Depression, Skin rash         


Extra Edge: 

  1. Carbamazepine reduces phenobarbitone level Carbamazepine and Phenobarbitone are strong inducer of each others metabolism by inducing CYP3A4.
  2. Lymphadenopathy 'Pseudolymphoma' is a complication associated with use of phenytoin.
  3. Causes of Gum hyperplasia – Phenytoin, cyclosporin, nifedipine, AML, Pregnancy, Wegener’s granulomatosis, Sarcoidosis. (LQ 2012).

Status Epilepticus –
Continuous seizures or repetitive, discrete seizures with impaired consciousness in the interictal period.


  1. Anticonvulsant drug withdrawal            
  2. Metabolic disorder                
  3. Drug toxicity  
  4. CNS infection                               
  5. CNS tumors                         
  6. Head trauma

Anticonvulsant therapy for status epilepticus:

First choice drugs

Second choice drugs

Alternative/Add on drugs

Lorazepam (I.V)

Phenytoin (I.V)

General Anaesthetic e.g.

Clonozepam (I.V)

Phenobarbitone (I.V. I.M.)

Thiopentone sodium

Diazepam (I.V)




Extra Edge:
  1. Thiopentone sodium can occasionally be used for rapid control of convulsions.
  2. No role of carbamazepine in status epilepticus. 

Figure 369-3

Pharmacologic treatment of generalized tonic-clonic status epilepticus in adults. The horizontal bars indicate the approximate duration of drug infusions. IV, intravenous; PE, phenytoin equivalents

Important Points:

Catamenial Epilepsy –

  1. Increased seizure frequency around the time of menstruation.
  2. This is due to effects of estrogen and progesterone on neuronal excitability or change in antiepileptic drug levels due to altered protein binding.
  3. Treatment - (Ref. Hari. 18th ed., Pg- 3269)
    1. Some patients may benefit from increases in antiepileptic drug dosages during menses.
      Natural progestins or intramuscular medroxyprogesterone may be of benefit to a subset of women.
    2. Acetazolamide as adjunctive therapy.

Narcolepsy and Cataplexy

  1. Narcolepsy (sudden irresistible urge to sleep) cataplexy (sudden loss of muscle tone following strong emotional disturbance) HLA DR-2 is characteristic (Ref. Hari. 18th ed., Pg -220)
  2. A lateral hypothalamic (LQ 2012) neuropeptide called hypocretin (orexin) is implicated in narcolepsy.
  3. Narcolepsy is both a disorder of the ability to sustain wakefulness voluntarily and a disorder of REM sleep regulation.
  4. The classic “Narcolepsy tetrad: consists of excessive daytime somnolence plus three specific symptoms are-
    1. Cataplexy            
    2. Hypnagogic hallucination      
    3. Sleep paralysis.
  5. REM sleep occurs with in 15 min of onset of sleep in narcolepsy.
  6. Polysomnography is used for diagnosis.
  7. Treatment of narcolepsy: (Ref. Hari. 18th ed., Pg- 220)
    1. Modafinil is the drug of choice
    2. Older drugs such as methylphenidate or dextroamphetamine are still used as alternatives.
  8. Treatment of the REM-related phenomena of cataplexy, hypnagogic hallucinations, and sleep paralysis requires the potent REM sleep suppression produced by antidepressant medications.
    1. The tricyclic antidepressants [Protriptyline and Clomipramine]
    2. SSRIs (Fluoxetine)

Recent Advances:


Armodafinil is approved by the FDA for the treatment of narcolepsy and as an adjunctive treatment for obstructive sleep apnea.

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