Epilepsy (Physiology) - Block 1 Flashcards
How many lobes are in the brain?
5: frontal, parietal, occipital, temporal, insula
What is cerebral white matter?
Myelinated fibers bundled into large tracts
What is the decussation of the pyramids?
Where fibers cross over to the opposite side before contnuing into the spinal cord which is the crossover point
* Each hemisphere controls the opposite side of the body
What is an ambulatory EEG?
Records brain waves continuously for up to 72 hrs
What is a seizure?
Discrete clinical event of abnormal electrical discharge from neurons in the cerebral cotex leading to involuntary movement and/or behavior and sensory alterations
What age group are seizures more common?
Children
* first seizure is expereinced before 20 for most people
What is epilepsy?
Chronic disorder of recurrent discharges from neurons due to a CNS disorder/disruption
How are seizure classified?
- Clinical sx
- EEG activity
What are the 2 classes of seizure disorders?
Focal (partial): Limited to 1 hemisphere and discretely localized or widely discributed
Generalized: Bilaterally distributed networks
Epileptic spasms
What is an idiopathic seizure?
Cause is unknown
What are some known causes of seizures?
- Metabolic derangement
- Infection
- Tumors
- Drug abuse
- Vascular lesions
- Congenital deformities
- Brain injury
List some of the theories that can cause abnormal brain activity?
- Alterations in cell permeability or distribution of ions
- Decreased inhibion of cortical or thalamic neuronal activity (excitiability of neurons)
- Neurotransmitter imbalances
- Genetic mutations (channelopathy)
- Immunopathogenesi
Describe some of the neurotrasmitter imbalances associated wit seizures?
What is the normal function of VGNCs?
- Progresses from closed to open states
- Largetransient Ns influx (INaP)
- Small percentage of Na influx persists at steady state
What is channelopathy?
Point mutation that impairs inactivatio of the VGNC -> increased INaP and excessive sodium influx at steady state
Describe the 5 anticonvulsant targets?
- Enhance GABAergic neural activity (Na+ channel inactivation)
- Inhibit glutamatergic neural activity (Cl- channel activation)
- Inhibition of Ca2+ current (Ca2+ channel inhibition)
- Potentiate GABAergic signaling at inhibitory presynaptic nerve terminals (Promotes IPSPs)
- Inhibit glutamate signaling at excitatory presynaptic nerve terminals (Prevents EPSPs)
WHat is the most common type of seizure among newly diagnosed cases?
Focal (partial)
Describe the Immunopathogenesis of seizure disorders?
- Elevated levels of immune mediators
- Neurons, glia, and endothelial cells of the blood-brain barrier (BBB) take part in inflammatory processes
- Elevated cytokine levels in serum and brain tisse
- IL-1b, IL-6, TNF-a are most common
What are the types of focal sz?
- Simple partial: without impairment of consiousness, memory, awareness
- Complx partial: memory impairment or behavior changes
Sz with observable motor or autonomic components?
Simple partial sz (focal motor and autonomic)
Sz subjective sensory or psychic phenomena only?
Aura
What are the clinical manifestations of focal without impairment?
Abnormal neural discharge corresponds to location of onset on the contralateral side of the body:
Motor area: motor movement
Sensory area:
* Somatic sensoy disturbance: tingling, crawling
* Special sensory disturbances: visual, auditory, gustatory, olfactory
How does abnormal cortical discharge affect the ANS?
Flushng, tachy, diaphoresis, hypo and hypertension, pupillary changes
What are the warning signs of impending seizure activity?
Prodrome and aura
What is aura?
Sx that may occurs before seizure (visual changes, bright lights, zigzags)
What are the manifestations of focal with impairment?
Focal seizures envolving to a bilateral convulsive seizures (complex partial sz)
* Impairment of consciousness
* Often arise from temporal lobe
Sx: psychomotor seizures with automtisms and postictal state
What are automatisms?
Repetitive, purposeful activates such as lip smacking, grimacing, patting, rubbing clothing
What is postictal state?
COnfusion after seizure
What are generalized sz? Categories?
Effects both hemispheres at onset
1. Tonic-clonic
2. Absence
3. Myoclonic
4. Clonic
5. Tonic
6. Atonic
What are the phases of a tonic clonic seizure?
Tonic: vague warnings with sharp tnic contraction f the muscles
* Pupil fixed and dilated
* Incontinence of bladder and bowel
* Hypoxia, skin pallor, cyanosis
* 15-60 seconds
Clonic:
* Alternating periods of muscular contraction and relaxation
* 60-90 sec
Postictal:
* Level of consciousness is decreased
What are typical absence sz?
- Non-convulsive epileptic events
- Disturbances in consciousness
3, Petit mal
What are the automatisms of absense sz?
- Lip smacking
- Mild clonic motion
- Increased or decreaed postural tone
- Autonomic phenomena
- few seconds
What are atypical absence sz?
Similar to typical absence seizures except for greater alterations in muscle tone and less abrupt onset and cessation.
What are myoclonic sz?
Involves brief involuntary muscle contractions induced by stimuli or cerebral origin (bilateral jerking of muscles)
What are clonic sz?
Begin with a loss of consciousness and sudden hypotonia (limb jerking)
What are tonic sz?
Sudden onset of increased tone, which is maintained in the extensor muscles (falling)
What are atonic sz?
Sudden, split second loss of muscle tone leading to slackening limbs (drop attacks)
What are status epilepticus?
Acute symptomatic sz that is a medical emergency
Duration: >30 minutes
What are febrile sz?
Seizures that occur as a result of a rapid body temperature rise above 102.2°F, often in association with an acute illness.
Most common in 6 months to 5 yrs old
What are intractable sz?
Seizures that are refractory
What is the Pharmacokinetic Hypothesis?
: Overexpression of drug efflux transporters in peripheral organs decreases ASD plasma levels, reducing the amount of ASD available to enter the brain and reach the epileptic focus.
What is the neuronal network hypothesis?
: Seizure-induced degeneration and remodeling of the neural network suppresses the brain’s seizure control system and restricts ASDs from accessing neuronal targets.
What is the intrinsic severity hypothesis?
Common neurobiological factors contribute to both epilepsy severity and pharmacoresistance.
What are gene variant hypothesis?
Variations in genes (e.g., metabolic enzymes, ion channels, and certain neurotransmitter receptors that are targets for ASDs) associated with ASD pharmacokinetics and pharmacodynamics cause inherent pharmacoresistance.
What are target hypothesis?
Alterations in the properties of ASD targets such as changes in voltage-gated ion channels and neurotransmitter receptors (e.g., GABAA receptor) result in decreased drug sensitivity and lead to refractoriness.
What are transporter hypothesis?
Overexpression of ASD efflux transporters at the blood–brain barrier in epilepsy leads to decreased ASD brain uptake and ASD resistance.
