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Understanding Seizure Pathophysiology

Altered neuronal permeability and neurotransmitter imbalance can lower the threshold for neuronal stimulation, leading to a hyperexcitable epileptogenic focus. This focus causes sudden, uncontrolled depolarization of neurons that spreads to other neurons via synapses and tracts, potentially involving the entire brain. The seizure involves tonic and clonic muscular contractions along with autonomic symptoms. After the seizure, patients experience confusion and fatigue. Without treatment, continued and prolonged seizures can lead to hypoxia, hypoglycemia, acidosis and brain injury.

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677 views2 pages

Understanding Seizure Pathophysiology

Altered neuronal permeability and neurotransmitter imbalance can lower the threshold for neuronal stimulation, leading to a hyperexcitable epileptogenic focus. This focus causes sudden, uncontrolled depolarization of neurons that spreads to other neurons via synapses and tracts, potentially involving the entire brain. The seizure involves tonic and clonic muscular contractions along with autonomic symptoms. After the seizure, patients experience confusion and fatigue. Without treatment, continued and prolonged seizures can lead to hypoxia, hypoglycemia, acidosis and brain injury.

Uploaded by

qwertyuiop
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as DOCX, PDF, TXT or read online on Scribd

SEIZURE PATHOPHYSIOLOGY

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

SIGNS AND SYMPTOMS


TONIC PHASE:
-loss of consciousness
-muscle contraction and brief flexion
-extension of limbs and rigid trunk
-abdominal and thoracic muscle contract
forcing air out of the lungs, then jaws are
clenched tightly and respiration ceases
-AUTONOMIC SYMPTOMS: increase blood
pressure, heart rate and bladder pressure,
flushing, sweating, increased salivation and
bronchial secretion, and apnea
CLONIC PHASE:
-Alternate muscle contraction and relaxation
-forceful rhythmic jerky movements
-increased salivation
-biting of tongue, cheek or lip
-bowel and bladder incontinence
POST-ICTAL PHASE:
-confusion, fatigue, aching muscle
-may fall into deep sleep

Seizure

Status Epilepticus

Complications:
-severe hypoxia
-hypoglycemia
-acidosis
-injury

Increased cerebral blood


flow, Increased oxygen
and glucose
consumption
Cerebr
al
hypoxi

Cerebral
hypoglyce
mia

Metabolic
acidosis

Brain damage and


mental retardation

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.

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