Clinical neurology epilepsy and seizures

33
EPILEPSY BY DR.Mujahid.A.Abass WKUFOM

Transcript of Clinical neurology epilepsy and seizures

Page 1: Clinical neurology epilepsy and seizures

EPILEPSY

BY DR.Mujahid.A.AbassWKUFOM

Page 2: Clinical neurology epilepsy and seizures

Epilepsy:

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

Page 3: Clinical neurology epilepsy and seizures

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

Page 4: Clinical neurology epilepsy and seizures

CLASSIFICATION OF SEIZURES

1. Focal seizures(Can be further described as having motor,autonomic, cognitive, or other features)2. Generalized seizuresa. Absence Typical Atypicalb. Tonic clonicc. Clonicd. Tonice. Atonicf.Myoclonic3. May be focal, generalized, or unclear Epileptic spasms

Page 5: Clinical neurology epilepsy and seizures

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 partialonset (=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 orcomplex partial seizure), spreads widely, causing a secondary generalized seizure, which is typically convulsive.

Page 6: Clinical neurology epilepsy and seizures

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 bethrown suddenly to the ground, or have a violently disobedient limb: one patientdescribed it as ‘my fl ying-saucer epilepsy’, as crockery which happened to be inthe 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.

Page 7: Clinical neurology epilepsy and seizures

Localizing features of partial (focal) seizures

Temporal lobe •Automatisms—complex motor phenomena, but with impairedawareness 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);

Page 8: Clinical neurology epilepsy and seizures

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

Page 9: Clinical neurology epilepsy and seizures

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

Page 10: Clinical neurology epilepsy and seizures

Parietal lobe

Sensory disturbances—tingling, numbness, pain (rare) •Motorsymptoms (due to spread to the pre-central gyrus).

Occipital lobe Visual phenomena such as spots, lines, fl ashes.

Page 11: Clinical neurology epilepsy and seizures

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 keyconcern here. If the seizure begins with focal features, it is a partial seizure, however rapidly it then generalizes3Any 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.

Page 12: Clinical neurology epilepsy and seizures
Page 13: Clinical neurology epilepsy and seizures

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

Page 14: Clinical neurology epilepsy and seizures

CAUSES OF SEIZURES

CAUSES OF SEIZURESNeonates (<1 month)Perinatal hypoxia and ischemiaIntracranial hemorrhage and traumaAcute CNS infectionMetabolic disturbances (hypoglycemia, hypocalcemia, hypomagnesemia, pyridoxine deficiency)Drug withdrawalDevelopmental disordersGenetic disordersInfants and children (>1 month and <12 years)Febrile seizuresGenetic disorders (metabolic, degenerative, primary epilepsy syn dromes)CNS infectionDevelopmental disordersTraumaIdiopathic

Page 15: Clinical neurology epilepsy and seizures

Adolescents (12–18 years)TraumaGenetic disordersInfectionBrain tumorIllicit drug useIdiopathic

Young adults (18–35 years)TraumaAlcohol withdrawalIllicit drug useBrain tumorIdiopathic

Older adults (>35 years)Cerebrovascular diseaseBrain tumorAlcohol withdrawalMetabolic disorders (uremia, hepaticfailure, electrolyte abnormalities,hypoglycemia, hyperglycemia)Alzheimer’s disease and otherdegenerative CNS diseasesIdiopathic

Page 16: Clinical neurology epilepsy and seizures

DRUGS AND OTHER SUBSTANCES THAT CAN CAUSE SEIZURES

Alkylating agents (e.g.,busulfan, chlorambucil) Immunomodulatory drugsCyclosporineOKT3 (monoclonalantibodies to T cells)TacrolimusInterferons

Antimalarials (chloroquine,mefloquine) PsychotropicsAntidepressantsAntipsychoticsLithium

Antimicrobials/antiviralsβ-lactam and related compoundsQuinolonesAcyclovirIsoniazidGanciclovir

Dietary supplementsEphedra (ma huang)Gingko

Page 17: Clinical neurology epilepsy and seizures

Anesthetics and analgesicsMeperidineTramadolLocal anesthetics

Radiographic contrast agentsTheophylline

Sedative-hypnotic drug withdrawalAlcoholBarbiturates (short-acting)Benzodiazepines(short-acting)

Flumazenila

Drugs of abuseAmphetamineCocainePhencyclidineMethylphenidate

Page 18: Clinical neurology epilepsy and seizures
Page 19: Clinical neurology epilepsy and seizures

MECHANISMS OF SEIZURE INITIATION ANDPROPAGATION

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.

Page 20: Clinical neurology epilepsy and seizures

• 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

Page 21: Clinical neurology epilepsy and seizures

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

Page 22: Clinical neurology epilepsy and seizures

(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 tomore distant areas via long commissural pathways such as the corpus callosum.

Page 23: Clinical neurology epilepsy and seizures

MECHANISMS OF ACTION OFANTIEPILEPTIC 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),

Page 24: Clinical neurology epilepsy and seizures

• 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

Page 25: Clinical neurology epilepsy and seizures

• 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.

Page 26: Clinical neurology epilepsy and seizures

DIFFERENTIAL DIAGNOSIS OF SEIZURES

SyncopeVasovagal syncopeCardiac arrhythmiaValvular heart diseaseCardiac failureOrthostatic hypotension

Psychological disordersPsychogenic seizureHyperventilationPanic attack

Metabolic disturbancesAlcoholic blackoutsDelirium tremensHypoglycemiaHypoxia

Psychoactive drugs (e.g.,hallucinogens)

MigraineConfusional migraineBasilar migraine

Transient ischemic attack (TIA)Basilar artery TIA

Page 27: Clinical neurology epilepsy and seizures

Sleep disordersNarcolepsy/cataplexyBenign sleep myoclonus

Movement disordersTicsNonepileptic myoclonusParoxysmal choreoathetosis

Special considerations inchildrenBreath-holding spellsMigraine with recurrentabdominal pain and cyclicvomitingBenign paroxysmal vertigoApneaNight terrorsSleepwalking

Page 28: Clinical neurology epilepsy and seizures
Page 29: Clinical neurology epilepsy and seizures

Drugs

• Generalized tonic-clonic seizures: Sodium valproate or lamotrigine (often bettertolerated, 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, butavoiding carbamazepine and oxcarbazepine, which may worsen seizures.•Partial seizures ± secondary generalization: Carbamazepine is 1st-line, thensodium valproate, lamotrigine, oxcarbazepine or topiramate. Others: levetiracetam, gabapentin, tiagabine, phenytoin, clobazam

Page 30: Clinical neurology epilepsy and seizures
Page 31: Clinical neurology epilepsy and seizures

Valproate side-ef ectsAppetite , weight gainLiver failure (watch LFTesp. during 1st 6 months)PancreatitisReversible hair loss(grows back curly)OedemaAtaxiaTeratogenicity, tremor,thrombocytopeniaEncephalopathy (due tohyperammonaemia)

Page 32: Clinical neurology epilepsy and seizures
Page 33: Clinical neurology epilepsy and seizures

SPECIAL ISSUES RELATED TO WOMENAND EPILEPSY

1) CATAMENIAL EPILEPSY2) PREGNANCY3) CONTRACEPTION4) BREAST-FEEDING