Epilepsy. Southern Neurology. Classification of seizures 1. Partial – arises from an epileptic focus , that is, a localised region of the cerebral cortex in which the excessive discharge of neurons occurs.
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Partial – arises from an epileptic focus , that is, a localised region of the cerebral cortex in which the excessive discharge of neurons occurs.
Partial seizures may be simple (consciousness not impaired) – motor symptoms, somatosensory symptoms, autonomic or psychic symptoms; complex (with impairment of consciousness) – may or may not have reactive or stereotyped automatisms; or secondarily generalised.
Partial epilepsy syndromes include – idiopathic forms eg benign childhood epilepsy with centro-temporal spikes; childhood epilepsy with occipital paroxysms and primary reading epilepsy; symptomatic forms eg temporal, frontal, parietal and occipital lobe epilepsies; and cryptogenic. (Cryptogenic refers to idiopathic partial but cause obscure).
A 6-year old girl has episodic staring spells of sudden onset which are typically characterized by a statue-like facial expression, cessation of ongoing activity, unresponsiveness, eye-blinking and lip-smacking; the spell stops abruptly and the child has no memory of the event. EEG shows 3 Hz spike-and-wave activity.
Epidemiology – incidence 6-8/100,00 children aged < 15 years; 10-12% of children with epilepsy ages 5-14 years; F>M (3:2); family history in 15-44%; 30-40% after age 7 years develop generalised tonic-clonic seizures; spontaneous remission in approximately 50% (no GTCS 75% vs GTCS 35% seizure free).
Treatment – ethosuximide age < 6 years; valproate age > 6 years or ethosuximide failure. Tegretol, tiagabine and vigabatrin may exacerbate absence seizures.
>50% of partial seizures originate from the temporal lobe.
Auras (or simple partial seizures) occur in approximately 80% of patients with TLE. They may be useful in localisation but not necessarily reliable as ictal discharges may begin in a clinically silent area but manifest as auras after spreading to adjacent regions.
An aura typically lasts shorter duration than period of altered consciousness (or complex partial seizure) which may follow the aura.
Auras can be psychic/cognitive phenomena (eg déjà vu jamais vu, dreamy state, fear, pleasure, altered sense of reality, mind-body dissociation or depersonalisation), speech phenomena (eg dysphasia, speech arrest), illusions and hallucinations (eg distortion of size-macropsia/micropsia, shape, colour, distance, olfactory and auditory hallucinations), and autonomic phenomena (eg nausea, irregular cardio-respiratory patterns, GI hypermotility, chest discomfort).
Automatisms occur in 50-100% of temporal lobe seizures and may occur in the ictal or post-ictal phases. They typically appear during impaired consciousness. They may be stereotyped (eg lip smacking and chewing as seen with mesial temporal involvement or tonic/dystonic as seen with frontal lobe seizures) or reactive to environmental stimuli (eg fumbling with clothing, touching objects, looking around).
Post-ictal confusion, lethargy and/or aphasia may occur and often can last up to 30 minutes
35% of patients with epilepsy show interictal epileptiform activity in all routine waking EEGs, 15% do not show abnormalities even after multiple EEGs and 50% show epileptiform activity in some but not all recordings.
An EEG is of little help in predicting a subsequent relapse although in children, an active interictal EEG probably indicates an increased risk of recurrence.
The commonest cause of failure of carbamazepine therapy is non-compliance as a result of unpleasant adverse effects (dizziness, drowsiness, nausea, vomiting).
It is reasonable to start slow (eg 100-200 mg twice daily) and increase by 100-200 mg/day every 4-7 days until a final desired dose (ranging from 600-1600 mg/day) is obtained. Final dose depends in part on type and severity of epilepsy
If the first drug fails, particular attention should be paid as to whether the diagnosis is correct, whether there are triggering factors (eg sleep deprivation, alcohol), and whether compliance is an issue.
Assuming these are satisfactory, the recommended approach is to commence another appropriate drug and gradually withdraw the initial agent. If the second agent also fails, then combination therapy is recommended.
If seizure control is achieved, consider gradual withdrawal of first agent.
Commenced tegretol 200 mg bd but ongoing seizures and not tolerated well. Changed to epilim 500 mg bd. Further CPS. Depressed as both unable and too afraid to drive again. Lamotrigine added – reports dizziness, drowsiness, diplopia. Still having CPS. Wants complete seizure freedom.
Changed to topiramate – no better. Changed to trileptal –some improvement. Referred for surgical consideration.
First synthesized in 1953 as part of a programme investigating analogues of chlorpromazine.
In an early study (Rodin et al 1974), carbamazepine or placebo was administered to 37 chronically hospitalized patients with intractable epilepsy and 44% of patients given carbamazepine became seizure-free, 55% had reduced ‘grand mal’ seizures and 83% had reduced ‘psychomotor’ attacks.
Comparison studies in the 1970 and 80s with phenytoin showed similar efficacy (up to 80% of patients with newly diagnosed epilepsy seizure free)