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Clinical neurology epilepsy and seizures
Epilepsy is characterized by recurrent seizures due to abnormal electrical activity in the brain, with diagnosis based on seizure frequency, EEG changes, and postictal symptoms. Seizures are classified into focal and generalized types, with specific subtypes including absence, tonic-clonic, and myoclonic seizures, and the classification of epilepsy syndromes is based on various factors including age of onset and EEG findings. The document also details possible causes, mechanisms of seizure initiation, the action of antiepileptic drugs, differential diagnosis of seizures, and specific considerations for treatment in different demographics.
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Similar to Clinical neurology epilepsy and seizures
Clinical neurology epilepsy and seizures
- 1.
- 2. Epilepsy: is a recurrenttendency to spontaneous, intermittent, abnormal electrical activity in part of the brain, manifesting as seizures.
- 3. E S SE 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 Focalonset, 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 seizuresSimultaneous 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 ofpartial (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 involvementmay 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 reallyseizures? 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 OFSEIZURES 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 Geneticdisorders 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 ANDOTHER 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 Localanesthetics 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 SEIZUREINITIATION 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 burstingactivity 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 spreadof 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 relatedto 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 ACTIONOF 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 ofglutamate 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 contrastto 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 OFSEIZURES 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 sleepmyoclonus 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-clonicseizures: 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-efects 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 RELATEDTO WOMEN AND EPILEPSY 1) CATAMENIAL EPILEPSY 2) PREGNANCY 3) CONTRACEPTION 4) BREAST-FEEDING