Figure 15-4. Medial temporal sclerosis. A. T1-weighted MRI in the coronal plane, showing reduced volume of the left hippocampus (shown by arrow) and secondary enlargement of the adjacent temporal horn of the lateral ventricle. B. Coronal T2-FLAIR image showing abnormal hyperintense signal within the left hippocampus (shown by arrow).
Figure 15-5. Distribution of the main causes of epilepsy at different ages. Evident is the prevalence of congenital causes in childhood and the emergence of cerebrovascular disease in older patients. (Adapted from several sources including Hauser and Annegers and the texts of Engel and Pedley.)
Figure 15-6. Schematic depiction of sites and mechanisms of action of antiepileptic drugs on excitatory and inhibitory synapses. GABA, gamma amino butyric acid; GAD: glutamic acid decarboxylase; GATI: GABA transporter (also known as SLC6A1). (Adapted by permission of Nature Publishing Group and authors from Bialer M, White HS: Key factors in the discovery and development of new antiepileptic drugs. Nat Rev Drug Discov 9:68–82, 2010.)
Generalized seizuresArising within and rapidly engagingbilaterally distributed networksFocal seizuresOriginating within networkslimited to one hemisphereTonic-ClonicTypicalAtypicalTonicAtonicMyoclonicClonicAbsenceMyoclonicMyoclonic-atonicMyoclonic-tonicAbsence withspecial featuresCharacterized according toone or more features:AuraMotorAutonomicAwareness/responsiveness:altered (dyscognitive) or retainedUnknownInsufficient evidence to characterizeas focal, generalized or bothEpileptic spasmsOtherBilateral convulsive seizureMay evolve toMyoclonic absenceEyelid myoclonia
BAInhibitory SynapseGlutamateGABAGABA-TGABA-TGABAGATISuccinicsemialdehydeSuccinicsemialdehydeGABAGABAAreceptorCl–GADPostsynapticneuronInhibitorypresynapticterminalGlial cellFelbamate,topiramate,zonisamideBenzodiazepinesVigabatrinTiagabineBarbituratesPropagatedaction potentialNa+DepolarizationVesicularrelease˜2° subunitof L-type Ca2+channelSV2AGlutamateAMPA andkainate receptorsNa+ (Ca2+)K+K+NMDAreceptorCa2+, Na+ Voltage-gatedNa+ channelPostsynapticneuronExcitatorypresynapticterminalTopiramateFelbamateLevetiracetamPhenytoin, carbamazepine,valproic acid, felbamate,rufinamide, lamotrigine,lacosamide, topiramate,zonisamide, oxcarbazepineGabapentin,PregabalinExcitatory Synapse
Coma and Related Disorders of Consciousness
In hospital and emergency neurology, the clinical analysis of unresponsive and comatose patients becomes a practical necessity. There is an urgent need to determine the disease underlying a diminished state of consciousness and the direction in which it is evolving in order to protect the brain against irreversible damage. When called upon, the physician must therefore be prepared to implement a rapid, systematic investigation of the comatose patient and prompt action that allows little time for deliberate, leisurely investigation.