Clinical neurology epilepsy and seizures essential description about all (common things occurs commonly)

1. EPILEPSY
BY DR.Mujahid.A.Abass
WKUFOM

2. Epilepsy:
is a recurrent tendency to spontaneous, intermittent, abnormal
electrical activity in part of the brain, manifesting as seizures.

3. E S S E N T I A L S O F D I A G N O S I S
▶ Recurrent seizures.
▶ Characteristic electroencephalographic changes
accompany seizures.
▶ Mental status abnormalities or focal neurologic
symptoms may persist for hours postictally

4. CLASSIFICATION OF SEIZURES
1. Focal seizures
(Can be further described as having motor,
autonomic, cognitive, or other features)
2. Generalized seizures
a. Absence
Typical
Atypical
b. Tonic clonic
c. Clonic
d. Tonic
e. Atonic
f.Myoclonic
3. May be focal, generalized, or unclear
Epileptic spasms

5. Partial seizures Focal onset, with features referable to a part of one hemisphere.
Often seen with underlying structural disease.
Simple partial seizure: Awareness is unimpaired, with focal motor, sensory
(olfactory, visual, etc), autonomic or psychic symptoms. No post-ictal symptoms.
Complex partial seizures: Awareness is impaired. May have a simple partial
onset (=aura), or impaired awareness at onset. Most commonly arise from the temporal
lobe. Post-ictal confusion is common with seizures arising from the temporal lobe,
whereas recovery is rapid after seizures in the frontal lobe.
Partial seizure with secondary generalization: In ⅔ of patients with
partial seizures, the electrical disturbance, which starts focally (as either a simple or
complex partial seizure), spreads widely, causing a secondary generalized seizure, which is
typically convulsive.

6. Primary generalized seizures Simultaneous onset of electrical
dischargethroughout cortex, with no localizing features referable to only one hemisphere.
throughout cortex, with no localizing features referable to only one hemisphere.
•Absence seizures: Brief (≤10s) pauses, eg suddenly stops talking in mid-sentence, then
carries on where left of . Presents in childhood.
•Tonic–clonic seizures: Loss of consciousness. Limbs stif en (tonic), then jerk (clonic).
May have one without the other. Post-ictal confusion and drowsiness.
•Myoclonic seizures: Sudden jerk of a limb, face or trunk. The patient may be
thrown suddenly to the ground, or have a violently disobedient limb: one patient
described it as ‘my fl ying-saucer epilepsy’, as crockery which happened to be in
the hand would take of .
•Atonic (akinetic) seizures: Sudden loss of muscle tone causing a fall, no LOC.
•Infantile spasms: Commonly associated with tuberous sclerosis.
NB: the classifi cation of epileptic syndromes is separate to the classifi cation of seizures, and
is based on seizure type, age of onset, EEG fi ndings and other features such as family history.
Seizure classifi cations based on semiology also exist.

7. Localizing features of partial (focal) seizures
Temporal lobe •Automatisms—complex motor phenomena, but with impaired
awareness and no recollection afterwards, varying from primitive oral (lip smacking,
chewing, swallowing) or manual (fumbling, fi ddling, grabbing) movements,to complex
actions (singing, kissing, driving a car and violent acts); 213 •Abdominal rising sensation or
pain (± ictal vomiting; or rarely episodic fevers 214 or D&V 215);
 Dysphasia (ictal or post-ictal);
 Memory phenomena—déjà vu (when everything seems strangely familiar), or jamais
vu (everything seems strangely unfamiliar);

8.  Hippocampal involvement may cause emotional disturbance, eg sudden terror, panic,
anger or elation, and derealization (out-of-body experiences) 216, which in combination
may manifest as excessive religiosity;1 217
 Uncal involvement may cause hallucinations of smell or taste and a dreamlike state, 218
and seizures in auditory cortex may cause complex auditory hallucinations, eg music or
conversations, or palinacousis 219;
 Delusional behaviour;
 Finally, you may find yourself not believing your patient’s bizarre story—eg “Canned
music at Tesco’s always makes me cry and then pass out, unless I wear an earplug in one
ear” 220 or “I get orgasms when I brush my teeth” (right temporal lobe hyper- and
hypoperfusion, respectively).22

9.  Frontal lobe
 Motor features such as posturing, versive movements of the head and eyes,222 or peddling
movements of the legs
 Jacksonian march (a spreading focal motor seizure with retained awareness, often starting
with the face or a thumb)
 Motor arrest
 Subtle behavioural disturbances (often diagnosed as psychogenic)
 Dysphasia or speech arrest
 Post-ictal Todd’s palsy

10.  Parietal lobe
 Sensory disturbances—tingling, numbness, pain (rare) •Motor
symptoms (due to spread to the pre-central gyrus).
Occipital lobe Visual phenomena such as spots, lines, fl ashes.

11. Diagnosis:
1Are these really seizures? A detailed description from a witness of
‘the fi t’ is vital (but ask yourself: “Are they reliable?
2What type of seizure is it—partial or generalized? The attack’s onset
is the key
concern here. If the seizure begins with focal features, it is a partial
seizure, however rapidly it then generalizes
3Any triggers? Eg alcohol, stress, fevers, certain sounds, fl ickering
lights/TV, contrasting patterns, reading/writing? Does he recognize
warning events (eg twitches) so he can abort the fi t before it
generalizes? TV-induced fi ts rarely need drugs.

13.  EPILEPSY SYNDROMES
i. Epilepsy syndromes are disorders in which epilepsy is
apredominant feature, and there is sufficient evidence (e.g.,
through clinical, EEG, radiologic, or genetic observations) to
suggest a common underlying mechanism.
• JUVENILE MYOCLONIC EPILEPSY
• LENNOX-GASTAUT SYNDROME
• MESIAL TEMPORAL LOBE EPILEPSY
SYNDROME

14.  CAUSES OF SEIZURES
CAUSES OF SEIZURES
Neonates (<1 month)
Perinatal hypoxia and ischemia
Intracranial hemorrhage and trauma
Acute CNS infection
Metabolic disturbances (hypoglycemia, hypocalcemia, hypomagnesemia, pyridoxine deficiency)
Drug withdrawal
Developmental disorders
Genetic disorders
Infants and children (>1 month and <12 years)
Febrile seizures
Genetic disorders (metabolic, degenerative, primary epilepsy syn dromes)
CNS infection
Developmental disorders
Trauma
Idiopathic

15. Adolescents (12–18 years)
Trauma
Genetic disorders
Infection
Brain tumor
Illicit drug use
Idiopathic
Young adults (18–35 years)
Trauma
Alcohol withdrawal
Illicit drug use
Brain tumor
Idiopathic
Older adults (>35 years)
Cerebrovascular disease
Brain tumor
Alcohol withdrawal
Metabolic disorders (uremia, hepatic
failure, electrolyte abnormalities,
hypoglycemia, hyperglycemia)
Alzheimer’s disease and other
degenerative CNS diseases
Idiopathic

16.  DRUGS AND OTHER SUBSTANCES THAT CAN CAUSE
SEIZURES
Alkylating agents (e.g.,busulfan, chlorambucil) Immunomodulatory drugs
Cyclosporine
OKT3 (monoclonalantibodies to T cells)
Tacrolimus
Interferons
Antimalarials (chloroquine,mefloquine) Psychotropics
Antidepressants
Antipsychotics
Lithium
Antimicrobials/antivirals
β-lactam and related compounds
Quinolones
Acyclovir
Isoniazid
Ganciclovir
Dietary supplements
Ephedra (ma huang)
Gingko

17. Anesthetics and analgesics
Meperidine
Tramadol
Local anesthetics
Radiographic contrast agents
Theophylline
Sedative-hypnotic drug withdrawal
Alcohol
Barbiturates (short-acting)
Benzodiazepines
(short-acting)
Flumazenila
Drugs of abuse
Amphetamine
Cocaine
Phencyclidine
Methylphenidate

19. MECHANISMS OF SEIZURE INITIATION AND
PROPAGATION
 Focal seizure activity can begin in a very discrete region of cortex and then
spread to neighboring regions, i.e., there is a seizure initiation phase and a
seizure propagation phase
 The initiation phase is characterized by two concurrent events in an aggregate
of neurons:
(1) high-frequency bursts of action potentials .
(2) hypersynchronization.

20. • The bursting activity is caused by a relatively long-lasting depolarization of
the neuronal membrane due to influx of extracellular calcium (Ca2 +), which
leads to the opening of voltage-dependent sodium (Na +) channels, influx of
Na +, and generation of repetitive action potentials. This is followed by a
hyperpolarizing afterpotential mediated by γ-aminobutyric acid (GABA)
receptors or potassium (K+) channels, depending on the cell type. The
synchronized bursts from a sufficient number of neurons result in a so-called
spike discharge on the EEG

21. Normally, the spread of bursting activity is prevented by intact hyperpolarization
and a region of “surround” inhibition created by inhibitory neurons.
 With sufficient activation there is a recruitment of surrounding neurons via a
number of synaptic and nonsynaptic mechanisms, including:
(1) an increase in extracellular K+, which blunts hyperpolarization and
depolarizes neighboring neurons.
(2) accumulation of Ca2 + in presynaptic terminals, leading to enhanced
neurotransmitter release.
(3) depolarization-induced activation of the N-methyl- D-aspartate (NMDA)
subtype of the excitatory amino acid receptor, which causes additional Ca2 +
influx and neuronal activation

22. (4) ephapticninteractions related to changes in tissue osmolarity and cell
swelling.
 The recruitment of a sufficient number of neurons leads to the propagation of
seizure activity into contiguous areas via local cortical connections, and to
more distant areas via long commissural pathways such as the corpus
callosum.

23. MECHANISMS OF ACTION OF
ANTIEPILEPTIC DRUGS
• Antiepileptic drugs appear to act primarily by blocking the initiation or spread
of seizures. This occurs through a variety of mechanisms that modify the
activity of ion channels or neurotransmitters, and in most cases the drugs have
pleiotropic effects. The mechanisms include inhibition of Na +-dependent
action potentials in a frequency-dependent manner (e.g., phenytoin,
carbamazepine, lamotrigine, topiramate, zonisamide, lacosamide, rufinamide),
inhibition of voltage-gated Ca2 + channels (phenytoin, gabapentin, pregabalin),

24. • attenuation of glutamate activity (lamotrigine, topiramate, felbamate),
potentiation of GABA receptor function (benzodiazepines and barbiturates),
increase in the availability of GABA (valproic acid, gabapentin, tiagabine),
and modulation of release of synaptic vesicles (levetiracetam). The two most
effective drugs for absence seizures, ethosuximide and valproic acid,
probably act by inhibiting T-type Ca2 + channels in thalamic neurons

25. • In contrast to the relatively large number of antiepileptic drugs that can
attenuate seizure activity, there are currently no drugs known to prevent the
formation of a seizure focus following CNS injury. The eventual
development of such “antiepileptogenic” drugs will provide an important
means of preventing the emergence of epilepsy following injuries such as
head trauma, stroke, and CNS infection.

26. DIFFERENTIAL DIAGNOSIS OF SEIZURES
Syncope
Vasovagal syncope
Cardiac arrhythmia
Valvular heart disease
Cardiac failure
Orthostatic hypotension
Psychological disorders
Psychogenic seizure
Hyperventilation
Panic attack
Metabolic disturbances
Alcoholic blackouts
Delirium tremens
Hypoglycemia
Hypoxia
Psychoactive drugs (e.g.,hallucinogens)
Migraine
Confusional migraine
Basilar migraine
Transient ischemic attack (TIA)
Basilar artery TIA

27. Sleep disorders
Narcolepsy/cataplexy
Benign sleep myoclonus
Movement disorders
Tics
Nonepileptic myoclonus
Paroxysmal choreoathetosis
Special considerations inchildren
Breath-holding spells
Migraine with recurrent
abdominal pain and cyclic
vomiting
Benign paroxysmal vertigo
Apnea
Night terrors
Sleepwalking

29. Drugs
• Generalized tonic-clonic seizures: Sodium valproate or lamotrigine (often better
tolerated, and less teratogenic) are 1st-line, then carbamazepine or topiramate.
Others: levetiracetam, oxcarbazepine, clobazam.
•Absence seizures: Sodium valproate, lamotrigine or ethosuximide.
•Tonic, atonic and myoclonic seizures: As for generalized tonic-clonic seizures, but
avoiding carbamazepine and oxcarbazepine, which may worsen seizures.
•Partial seizures ± secondary generalization: Carbamazepine is 1st-line, then
sodium valproate, lamotrigine, oxcarbazepine or topiramate. Others: levetiracetam,
gabapentin, tiagabine, phenytoin, clobazam

31.  Valproate side-ef ects
Appetite , weight gain
Liver failure (watch LFTesp. during 1st 6 months)
Pancreatitis
Reversible hair loss(grows back curly)
Oedema
Ataxia
Teratogenicity, tremor,
thrombocytopenia
Encephalopathy (due tohyperammonaemia)

33. SPECIAL ISSUES RELATED TO WOMEN
AND EPILEPSY
1) CATAMENIAL EPILEPSY
2) PREGNANCY
3) CONTRACEPTION
4) BREAST-FEEDING