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Etiology:
-Idiopathic
-Familial incidence
-Physical stimuli (head trauma,
loud noises or bright lights)
-Biochemical stimuli (stress, CNS
infection, brain tumor, high fever,
hypertension, metabolic and toxic
conditions, drug and alcohol
withdrawal, excessive
premenstrual fluid retention, etc.)
Altered
permeability of
neuronal
Reduced inhibitory
for control of
neurons
Lower threshold for
stimulation
Hyperexcitable
epileptogenic focus
Sudden, spontaneous,
uncontrolled depolarization
of neurons
Depolarization spreads
through focal cells
stimulating the surrounding
cells via cortical synapses
Neurotransmitter
imbalance
SEIZURE PATHOPHYSIOLOGY
Depolarization spreads
through intrahemospheric
tracts to contralateral cortex,
basal ganglia, thalamus and
brainstem
Spread of
depolarization to
the spinal cord
Abnormal motor or
sensory activity
Inhibitory neurons
in cortex, anterior
thalamus and basal
ganglia begin to
inhibit cortical
excitation
Seizure
Status Epilepticus
Complications:
-severe hypoxia
-hypoglycemia
-acidosis
-injury
Cerebral
hypoglyce
mia
Metabolic
acidosis
Reference:
Gould, B. E. (2007). Pathophysiology for the health professions. Elsevier Singapore PTE LTD.
Smeltzer, S. C., Brenda, B. G., Hinkle, J. L., & Cheever, K. H. (2008). Brunner & suddarth's
textbook of medical-surgical nursing. Philadephia: Lippincott Williams & Wilkins.