香港大学：癫痫和癫痫发作（PPT讲稿）Seizures & Epilepsy

Seizures Epilepsy MBBS V Group C Tutor: Prof V Wong 16hFeb2004

Seizures & Epilepsy MBBS IV Group C Tutor: Prof. V. Wong 16th Feb 2004

Outline Definitions n PathophysIology Aetiology Classification Video demonstration Diagnostic approach Treatment

Outline  Definitions  Pathophysiology  Aetiology  Classification  Video demonstration  Diagnostic approach  Treatment  Quiz

Definition t Seizure(Convulsion) Clinical manifestation of synchronised electrical discharges of neurons Epilepsy Present when 2 or more unprovoked seizures occur at an interval greater than 24 hours apart

Definition Seizure (Convulsion) • Clinical manifestation of synchronised electrical discharges of neurons Epilepsy • Present when 2 or more unprovoked seizures occur at an interval greater than 24 hours apart

Definition Provoked seizures Seizures induced by somatic disorders originating outside the brain E.g. fever, infection, syncope, head trauma hypoxia, toxins, cardiac arrhythmias

Definition  Provoked seizures  Seizures induced by somatic disorders originating outside the brain  E.g. fever, infection, syncope, head trauma, hypoxia, toxins, cardiac arrhythmias

Definition * Status epilepticus (SE) Continuous convulsion lasting longer than 30 minutes or occurrence of serial convulsions between which there is no return of consciousness Idiopathic SE Seizure develops in the absence of an underlying CNS lesion/insult SymptomatIc SE e Seizure occurs as a result of an underlying neurological disorder or a metabolic abnormality

Definition  Status epilepticus (SE)  Continuous convulsion lasting longer than 30 minutes OR occurrence of serial convulsions between which there is no return of consciousness  Idiopathic SE  Seizure develops in the absence of an underlying CNS lesion/insult  Symptomatic SE  Seizure occurs as a result of an underlying neurological disorder or a metabolic abnormality

Aetiology of seizures epileptic Idiopathic(70-80%) Cerebral tumor Neurodegenerative disorders Neurocutaneous syndromes Secondary to Cerebral damage: e.g. congenital infections HIE, intraventricular hemorrhage Cerebral dysgenesis/malformation: e.g hydrocephalus

Aetiology of seizures ▪ Epileptic ▪ Idiopathic (70-80%) ▪ Cerebral tumor ▪ Neurodegenerative disorders ▪ Neurocutaneous syndromes ▪ Secondary to ▪ Cerebral damage: e.g. congenital infections, HIE, intraventricular hemorrhage ▪ Cerebral dysgenesis/malformation: e.g. hydrocephalus

Aetiology of seizures Non-epileptic Febrile convulsions Metabolic Hypoglycemia HypoCa, HypoMg, HyperNa, HypoNa Head trauma Meningitis Encephalitis Poisons/toxins

Aetiology of seizures ▪ Non-epileptic ▪ Febrile convulsions ▪ Metabolic ▪ Hypoglycemia ▪ HypoCa, HypoMg, HyperNa, HypoNa ▪ Head trauma ▪ Meningitis ▪ Encephalitis ▪ Poisons/toxins

t Aetiology of Status Epilepticus Prolonged febrile seizure a Most common cause Idiopathic status epilepticus Non-compliance to anti-convulsants Sudden withdrawal of anticonvulsants Sleep deprivation e Intercurrent infection Symptomatic status epilepticus e Anoxic encephalopathy Encephalitis, meningitis e Congenital malformations of the brain e Electrolyte disturbances, drug/lead intoxication, extreme hyperpyrexia, brain tumor

Aetiology of Status Epilepticus  Prolonged febrile seizure  Most common cause  Idiopathic status epilepticus  Non-compliance to anti-convulsants  Sudden withdrawal of anticonvulsants  Sleep deprivation  Intercurrent infection  Symptomatic status epilepticus  Anoxic encephalopathy  Encephalitis, meningitis  Congenital malformations of the brain  Electrolyte disturbances, drug/lead intoxication, extreme hyperpyrexia, brain tumor

Pathophysiology still unknown Some proposals EXcitatory glutamatergic synapses EXcitatory amino acid neurotransmitter (glutamate, aspartate) Abnormal tissues tumor. avm, dead area Genetic factors Role of substantia nigra and gaba

Pathophysiology  Still unknown  Some proposals:  Excitatory glutamatergic synapses  Excitatory amino acid neurotransmitter (glutamate, aspartate)  Abnormal tissues — tumor, AVM, dead area  Genetic factors  Role of substantia nigra and GABA

Pathophysiology t EXcitatory glutamatageric synapses t And, excitatory amino acid neurotransmitter(glutamate, aspartate These are for the neuronal excitation e In rodent models of acquired epilepsy and in human temporal lobe epilepsy, there is evidence for enhanced functional efficacy of ionotropic N-methyl-D-aspartate (NMDA)and metabotropic(Group I)receptors ChapmanAG Glutatmate and Epilepsy. J Nutr. 2000 Apr; 1304 S Supp):1043S-5S

Pathophysiology  Excitatory glutamatageric synapses  And, excitatory amino acid neurotransmitter (glutamate, aspartate)  These are for the neuronal excitation  In rodent models of acquired epilepsy and in human temporal lobe epilepsy, there is evidence for enhanced functional efficacy of ionotropic N-methyl-D-aspartate (NMDA) and metabotropic (Group I) receptors Chapman AG. Glutatmate and Epilepsy. J Nutr. 2000 Apr; 130(4S Suppl): 1043S-5S