Epilepsy week 7 Flashcards
What are the general triggers for seizure? What other triggers are person/epilepsy type specific?
What general trigger is specific to absence seizures?
● General:
○ Fatigue, sleep deprivation, emotional stress, hypoglycemia, fevers, alcohol, certain drugs and antibiotics, menstruation, hyperventilation: specific to absence seizures
● Person/Epilepsy Type specific:
○ Odors, flashing lights, certain types of music
What are the etiologies of seizures?
What are some metabolic causes of seizure?
Etiology of seizures
● Genetic
● Congenital/Perinatal
● Acquired
○ Intracranial – AVM, aneurysm, infection, cyst, stroke, hemorrhage, tumor
○ Metabolic – fluid/electrolyte disturbance, hypoxia, acidosis, drugs, heavy metal, hepatic dysfunction
○ Post-traumatic head injury
● The cause is unknown in at least a third of patients
In what age group(s) is epilepsy most common?
What is the most common type of seizure?
Age distribution: incidence is markedly elevated in the young and the old
Seizure type distribution: partial seizures (especially complex partial seizures) are the most common
What are the seizure types? (classification)
What part of the brain is affected in simple partial seizures?
How is conciousness affected?
Where are the localizing signs and symptoms?
SIMPLE PARTIAL
● Anatomical substrate: Neocortical
● Awareness maintained***
● Localizing signs and symptoms depend on cortical region:
○ sensory or motor or certain higher functions, e.g. vision or hearing or focal clonic activity or language disruption (can’t speak or can’t understand)
What are the potential motor and sensory disturbances in simple partial seizures?
What is Jacksonian March? What seizure type(s) is it observed in?
SIMPLE PARTIAL
● MOTOR – motor strip, symptoms/signs dependent on anatomical onset
○ Focal vs Spread (Jacksonian March)
○ Versive head turning (contralateral to ictus)
○ Continuous (epilepsia partialis continua)
● SENSORY (aura) – sensory strip, symptoms/signs dependent on anatomical onset
○ Paresthesias or Sensory disturbance
○ Special sensory symptoms: visual/auditory hallucinations, gustatory symptoms (metallic taste), vertigo.
Jacksonian seizure or march
● partial seizure (simple or complex) starts in one anatomic site and then spreads to anatomically connected sites.
● first described for motor seizures by Hughlings Jackson
○ Motor cortex: start at one site in the body, clonic movement
○ FACE → ARM → LEG “marching” along the primary motor cortex.
○ behavioral manifestations reflecting the areas of cortex successively engaged
What part of the brain is affected in complex partial seizures?
What is the core symptom? What are the other symptoms and what parts of the brain is associated with each?
COMPLEX PARTIAL
● Anatomical substrate: Limbic: hippocampus or amygdala, orbital frontal cortex or cingulate gyrus
● Core symptom: alteration of consciousness
● Other symptoms:
○ Automatisms: motor, involuntary, purposeless
• lip smacking, chewing, fidgeting, picking at clothes
○ amnesia (hippocampus)
○ autonomic or visceral sensations, fear (amygdala)
○ smell-olfaction (uncus, amygdala)
○ taste-gustation (insula)
○ vertigo
○ hallucinations or delusions
What is Todd’s paralysis? During what period is it observed in? (pre-ictal, ictal, post-ictal). What type of seizure is it observed in?
Todd’s Paralysis: impaired motor function during the post-ictal period in the affected body area due to inhibition or exhaustion in the affected brain region. Seen in partial seizures.
● Following a focal seizure there may be postictal loss of function reflecting the site of onset
○ e.g. a clonic seizure of the arm may be followed by a postictal (post-seizure) weakness of the arm lasting minutes to a few hours.
● Comparable postictal deficits of other behaviors may be seen appropriate to the site of onset
○ e.g. a temporary visual field loss after a seizure discharge in the visual cortex.
Differentiation of an epileptic seizure from psychogenic experiences is important since the underlyng pathology and the treatments are very different.
How can one tell the difference btwn a complex partial seizure and a psychiatric disease?
For a given person the behaviors and subjective experiences during seizures tend to be highly stereotyped in character, psychogenic behaviors are more variable.
For example: A person may have the same hallucination during each seizure
In primary generalized seizures, what area(s) of the brain are affected?
What is the core symptom?
PRIMARY GENERALIZED
● Physiologic substrate: bilateral cortex and thalamus
● Core symptoms: loss of consciousness, bilaterality.
What kind of seizures are petit mal (absence) and tonic clonic (grand mal) seizures?
What are the symptoms of each?
Approximately how long does each seizure type last?
In what age group are absence seizures more common? How many times per day do they often occur?
Absence and tonic clonic seizures are primary generalized seizures.
○ petit mal (absence): brief loss of consciousness with arrest of behavior, eyes stare and often turn upward, the eyelids may blink rapidly, usually last seconds
○Common in children
○ Genetic predisposition
○ Loss of awareness → Interruption of activity → Staring, blinking, eye rolling, eyelid fluttering, lasting 3-30 seconds
○ +/- Automatisms or Mild clonic movements
○ Multiple times per day (10’s-100’s)
○ generalized tonic clonic (grand mal): sudden, bilaterally symmetrical major motor seizure/ convulsion (muscle spasm) with loss of consciousness, often lasts a few minutes. Tonic phase involves sustained contraction of muscles, clonic phase involves intermittent contraction and relaxation of muscles
○ Tonic phase: sudden loss of consciousness
- Arms/legs extended
- Fall to ground
- Jaw tightening +/- tongue biting
- “Epileptic cry”
- +/- bladder or bowel incontinence
- Pupillary dilatation
- Apnea → pale or dusky appearance
- Lasts <1 min
○ Clonic phase: gradual transition
- Inhibitory neurons activate → interrupt tonic phase → violent, rhythmic contractions
- Face contorts, eyes roll, salivation/frothing, sweating, tachycardia
What is a secondary generalized seizure?
What seizure type are they common in?
Secondary generalized seizure
● A partial seizure (simple or complex) starts in one anatomic site and may become secondarily generalized
● Involves both hemispheres and at that point may be indistinguishable from a primary generalized seizure.
○ This is particularly common for frontal lobe seizures.
● Primary and secondary generalized seizures share the features of being bilateral and having loss of consciousness as a manifestation.
What is status epilepticus?
What can cause status epilepticus?
What is the mortality rate? What are the possible causes of mortality?
Status epilepticus
● Definition:
○ Seizures lasting >5 minutes
○ 2+ seizures without interictal return to baseline
● Causes:
○ Discontinue medications abruptly
○ ETOH, sedatives, fever
● Types:
○ Clinical vs Subclinical (need EEG)
● 20% mortality
○ Cardiopulmonary failure
○ Hyperthermia
○ Rhabdomyolysis
○ Neuronal ischemia and infarction/cerebral edema→ herniation
What is the cause of seizures? (pathophysiology)
What is paroxysmal depolarization shift? What receptor is involved in this process? What part of the brain are these receptors particularly abundant in?
● Excitation & Inhibition of CNS: IMBALANCE
○ Too much Excitation not checked by Inhibitory mechanisms → high rate of neuronal firing and synchronization between neurons → hyperexcitable neurons →SEIZURE
● High frequency firing of action potentials that is not dependent on normal synaptic input
SEIZURES
- high-frequency bursts of action potentials
- Long-lasting depolarization (influx of Ca→ Open Na channel→ AP’s)
- Increased firing rate and amplitude
- Recruitment
• Nearby neurons, synapses
- hypersynchronization
● Intracellular manifestation: Paroxysmal depolarization shift (PDS) - giant synaptic potential or intrinsic alteration of membrane properties. This process is facilitated by activation of NMDA receptors, which are particularly abundant in the hippocampus
What is the celluar mechanism behind paroxysmal depolarization shift?
How is this visualed on the EEG?
● In epileptic neurons the Paroxysmal Depolarization Shift (PDS) results when the normal sodium action potential is supplanted by calcium action potentials through activation of NMDA receptors.
● This leads to a prolonged depolarization due to calcium influx followed by an afterhyperpolarization due to potassium efflux.
● This cellular event corresponds to the interictal epileptic spike seen in the scalp EEG.
What is the EEG pattern for an absence seizure?
Absence: 3/sec spike and slow wave
• bilateral poly spike and slow wave
