SEARCH RESULTS FOR: hyperventilation

generalized-absence-seizures-petit-mal

Typical Absence (Petit Mal) Seizure Hyperventilation: A common trigger of absence seizures in pediatric patients with existing absence seizures ↑ respirationà↑ CO2 expelled from body & blood ↓ acidic CO2 levels in bloodà↑ blood pH (↓ blood acidity) Predisposes neurons to fire spontaneously and asynchronouslyà↓ seizure threshold Pathogenesis of absence seizure is complex and not yet fully elucidated, but evidence supports the cortical focus theory: Hyperexcitable focal neurons on cerebral cortex send activation signals down to thalamocortical neuron network Activated neurons in thalamus interact with cortical neurons to produce rhythmic oscillatory neuronal firing (brain waves) between these two regions of the brain Abnormal rhythmic and bilaterally synchronous activation of the cerebral cortex during wakefulness Between seizures (inter-ictal) Inter-ictal changes in neuronal firing patterns and connectivity in sensorimotor cortices (mechanism unclear) First degree relative with absence epilepsy Genetic predisposition/idiopathic (>90%) No single identified cause such as a structural lesion or single genetic mutation Multiple gene mutations that predispose to epilepsy when occurring together Authors: Alyssa Federico, Davis Maclean, Erika Russell, Harjot Atwal Reviewers: Ario Mirian, Shaily Singh*, Kim Smyth*, Yan Yu* * MD at time of publication Monogenetic mutation (<10%) Single gene mutation predisposing to epilepsy Mutations involve genes encoding voltage-gated calcium channels and gamma aminobutyric acid (GABA) receptors, which are important in regulating thalamocortical activity Absence Seizure: Brief lapse of consciousness with a vacant stare lasting 3-10 seconds, without convulsions or loss of motor tone. May occur up to 100 times per day. Seizure features (ictal phase) Absence seizures generally occur in the context of an epilepsy syndrome and present in childhood Childhood absence epilepsy: Most common form of pediatric epilepsy, characterized by absence seizures Juvenile absence epilepsy: Characterized by absence seizures +/- generalized tonic-clonic seizures Juvenile myoclonic epilepsy: Characterized by myoclonic seizures +/- absence seizures Post-seizure (post-ictal) Mechanisms unclear Consciousness regained immediately after seizure No post-ictal symptoms No memory of event Neuropsychiatric symptoms (poor attention, memory, mood, cognition) seen in 60% of children Smooth/rapid transition to seizure No aura (warning sign) prior to seizures Seizure activity directly or indirectly impairs communication between neural networksà alters activity of brain structures involved in maintaining awareness Some simple response to internal or external stimuli may remain intact (mechanisms unclear) Automatisms: Eye movements (fluttering), oral (lip smacking, swallowing, chewing), manual (finger tapping, scratching) Brain wave oscillations generated in the thalamus EEG findings: Generalized 3 Hz spike-wave activity with maximum amplitude in both frontal lobes Impaired awareness Inhibition of response to external stimuli Impaired school performance and social interactions Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published January 2, 2021 on www.thecalgaryguide.com

Febrile Seizures

Febrile Seizures: Pathogenesis and clinical findings Factors that ↓ seizure threshold Immunizations (DTaP, MMR) activate host immune system Immune cells release pro-inflammatory interleukin (IL)-1β, IL-6 & TNF-α cytokines that reach the central nervous system Viral infections (primarily HHV-6 & H1N1) activate host immune system Immature nervous system in children between 6 Family history of febrile seizures months & 5 years old (peak 12-18 months old) (genetic predisposition) Hypothalamus releases prostaglandin E2 (PGE2) to ↑ body temperature Fever reaches ≥380C ↑ Voltage gated Na+ & Ca2+ channel excitability ↑ Susceptibility to fevers Fever ↑ metabolic rate & ↑ oxygen demand ↑ Respiratory rate Hyperventilation ↑ volume of CO2 exhaled ↓ Serum CO2 leads to respiratory alkalosis Inherited mutations in genes encoding the GABAA receptor subunit ↓ GABAA receptor expression ↓ GABAergic inhibition Inherited mutations in genes encoding the Na+ channels IL-1β ↑ glutamate release & ↓ GABAergic inhibition Pro-inflammatory mediators ↑ sensitivity of N-methyl-D-aspartate (NMDA) (glutamate) receptors on medial temporal lobe neurons Imbalances between excitatory glutamate & inhibitory gamma- aminobutyric acid (GABA) neurotransmission ↑ Neuronal Na+ channel activity Neurons become more excitable & generate action potentials more readily Large groups of neurons fire simultaneously (synchronize) in the medial temporal lobe (hippocampus) Activity spreads to other subcortical or cortical brain regions via synapses & gap junctions Excessive excitatory signaling disrupts normal brain activity Authors: Merry Faye Graff Catherine Beyak, Dasha Mori Reviewers: Michelle J. Chen, Calvin Howard Emily J. Doucette, Gary Klein* Jean K. Mah* * MD at time of publication Simple Febrile Seizure Complex Febrile Seizure Focal seizure, associated with a fever, that lasts > 15 minutes or has multiple recurrences in a 24-hour period Generalized seizure, associated with a fever, that lasts < 15 minutes & does not recur in a 24-hour period Generalized (bilateral cortical involvement) tonic-clonic seizure Temporary post-ictal Temporary post-ictal weakness or ↓ Threshold for future febrile seizures Prolonged (> 30 mins) or recurrent seizures without full return to consciousness in between (Febrile status epilepticus) Focal (localized) seizures Damages to neuronal circuits in affected regions drowsiness or confusion **See corresponding Calgary Guide slide paralysis (Todd’s paralysis) Epilepsy** Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published Jan 21, 2019; updated Mar 20, 2025 on www.thecalgaryguide.com