- Also known as convulsions, epileptic seizures, and if recurrent, epilepsy.
- It is a sudden alterations in normal brain activity that cause distinct changes in behavior and body function. They are thought to result from abnormal, recurrent, uncontrolled electric discharges of neurons in the brain.
- Pathophysiology of seizures is poorly understood but seems to be related to metabolic and electrochemical factors at the cellular level.
- Predisposing factors include head or brain trauma, tumors, cranial surgery, metabolic disorders (hypocalcemia, hypoglycemia or hyperglycemia, hyponatremia, anoxia); central nervous system infection; circulating disorders; drug toxicity; drug withdrawal states (alcohol, barbiturates); and congenital neurodegenerative disorders.
- Seizures are classified as partial or generalized by the origin of the seizure activity and associated clinical manifestations.
a. Simple partial seizures – manifest motor, somatosensory, and psychomotor symptoms without impairment of consciousness.
b. Complex partial seizures – manifest impairment of consciousness with or without simple partial symptoms.
c. Generalized seizures – manifest a loss of consciousness with convulsive or nonconvulsive behaviors and include tonic-clonic, myoclonic, atonic, and absence seizures.
- Simple partial seizures can progress to complex partial seizures, and complex partial seizures can secondarily become generalized.
- Seizures affect all ages. Most cases of epilepsy are identified in childhood, and several seizure types are particular to children.
1. Generalized tonic-clonic (grand mal) seizure
a. May be preceded by an aura such as a peculiar sensation or dizziness; then sudden onset of seizure with loss of consciousness.
b. Rigid muscle contraction in tonic phase which clenched jaw and hands; eyes open with pupils dilated; lasts 30 to 60 seconds.
c. Rhythmic, jerky contraction and relaxation of all muscles in clonic phase with incontinence and frothing at the lips; may bite tongue or cheek, lasts several minutes.
d. Sleeping or dazed postictal state for up to several hours.
2. Absence ( petit mal) seizure
a. Loss of contact with environment for 5 to 30 seconds.
b. Appears to be day dreaming or may roll eyes, nod head, move hands, or smack lips.
c. Resumes activity and is not aware of seizure.
3. Myoclonic seizure (infantile spasm)
a. Seen in children or infants, caused by cerebral pathology, often with mental retardation.
b. Infantile spasms usually disappear by age 4, but child may develop other types of seizures.
c. Brief, sudden, forceful contractions of the muscles of the trunk, neck, and extremities.
d. Extensor type – infant extends head, spreads arms out, bend body backward in “spread eagle” position.
e. Mixed flexor and extensor types may occur in clusters or alternate.
f. May cause children to drop or throw something.
g. Infant may cry out, grunt, grimace, laugh, or appear fearful during an attack.
4. Partial (focal) motor seizure
a. Rhythmic twitching of muscle group, usually hand or face.
b. May spread to involve entire limb, other extremities and face on that side, known as jacksonian seizure.
5. Partial (focal) somatosensory seizure
a. Numbness and tingling in a part of the body.
b. May also be visual, taste, auditory, or olfactory sensation.
6. Partial psychomotor (temporal lobe) seizure
a. May be aura of abdominal discomfort or bad odor or taste.
b. Auditory or visual hallucinations, déjà vu feeling, or sense of fear or anxiety.
c. Repetitive purposeless movements (automatisms) may occur, such as picking at clothes, smacking lips, chewing, and grimacing.
d. Lasts seconds to minutes.
7. Complex partial seizures – begin as partial seizures and progress to impairment of consciousness or impaired consciousness at onset.
8. Febrile seizure
a. Generalized tonic-clonic seizure with fever over 101.8 degrees Fahrenheit.
b. Occurs in children younger than age 5.
c. Treatment is to decrease temperature, treat source of fever, and control seizure.
d. Long-term treatment to prevent recurrent seizures with fever is controversial.
- EEG, with or without video monitoring, locates epileptic focus, spread, intensity, and duration, helps classify seizure type.
- CT scanning or MRI identifies lesion that may cause of seizure.
- Single photon emission CT scanning (SPECT) or positron emission tomography (PET) identifies seizure foci.
- Neuropsychological studies evaluate for behavioral disturbances.
- Serum electrolytes, glucose, and toxicity screen determine the cause of first seizure.
- Lumbar puncture and blood cultures may be necessary if fever is present.
- Antiepileptic drugs (AEDs) may be used singly or in combination to increase effectiveness, treat mixed seizure types, and reduce adverse effects.
- A wide variety of adverse reactions may occur, including hepatic and renal dysfunction, vision disturbances, drowsiness, ataxia, anemia, leukopenia, thrombocytopenia, psychotic symptoms, skin rash, stomach upset, and idiosyncratic reactions.
- Surgical treatment of brain tumor or hematoma may relieve seizures caused by these.
- Temporal lobectomy, extratemporal resection, corpus callosotomy, or hemispherectomy may be necessary in medically intractable seizure disorders.
- Monitor the entire seizure event, including prodromal signs, seizure behavior, and postictal state.
- Monitor complete blood count, urinalysis, and liver function studies for toxicity caused by medications.
- Provide safe environment by padding side rails and removing clutter.
- Place the bed in low position.
- Do not restrain the patient during seizure.
- Do not put anything in the patient’s mouth during seizure.
- Maintain a patent airway until the patient is fully awake after a seizure.
- Provide oxygen during the seizure if the patient become cyanotic.
- Place the patient on side during a seizure to prevent aspiration.
- Protect the patient’s head during the seizure.
- Teach stress reduction techniques that will fit into the patient’s lifestyle.
- Tell the patient to avoid alcohol because it interferes with metabolism of AEDs and adds to sedation.
- Encourage the patient to determine existence of triggering factors for seizures, such as skipped meals, lack of sleep, and emotional stress.
- Remind the family the importance of following medication regimen and maintaining regular laboratory testing, medical check ups, and visual examinations.
- Encourage patient to follow a moderate lifestyle routine, including exercise, mental activity, and nutritious diet.
Nursing Care Plan – Seizure
What Do You Think?
By Dileep Nair, MD, and Juan Bulacio, MD
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For patients with drug-resistant epilepsy and subtle findings on MRI, invasive electrodes are often required for developing a strategy for epilepsy surgery. This is especially likely when eloquent cortex is nearby. How should we choose from the available invasive techniques to optimize outcome in individual cases?
A 29-year-old man presented to Cleveland Clinic’s Epilepsy Center with drug-resistant epilepsy. Seizures began at age 16 as bedwetting episodes. He took antiepileptic medications for three years, then stopped; two years later, seizures recurred. Witnesses described his seizures as periods of staring — with decreased responsiveness, difficulty speaking and hand automatisms — occurring three times daily. In addition, about once a month, a seizure would evolve into a generalized tonic-clonic convulsion. He had tried multiple antiepileptic medications over the years, without relief.
EEG was performed, which showed repetitive spikes in the left frontocentral region interictally.
Ictal EEG showed a burst of fast activity in the same region, then abrupt generalization involving many electrodes. Thirty seconds later, the seizure ended with attenuated activity in the left hemisphere more than the right.
The patient had a normal neurological examination and no epilepsy risk factors. An MRI performed earlier was interpreted as normal. However, a second reading of the same MRI at this time revealed very subtle findings.
Further imaging reveals the likely seizure cause
Focal cortical dysplasia is an important cause of drug-resistant surgically remediable epilepsy, and it may be subtle or invisible on MRI. Often when re-reviewing cases with MRIs initially read as normal, it is possible to find abnormalities when a search is based on other factors in the case.
We had the patient undergo coronal FLAIR imaging, which showed hypointensity in the inferior frontal gyrus on the left side extending from the cortex to white matter.
Axial FLAIR imaging revealed signal changes in the left anterior frontal lobe, in the pars orbitalis. A lesional track communicating from the abnormal gray matter to the ventricle surface indicated a transmantle malformation of cortical development — an abnormality with high epileptogenic potential and the likely cause of the patient’s seizures.
Because of the lesion’s possible proximity to Broca’s language area, functional MRI was performed next. Results showed activation for word generation, listening and rhyming overlying the area of dysplasia.
Is invasive testing needed?
Because invasive evaluation is costly and carries significant risk, it should be undertaken only to confirm or reject a hypothesis and help determine a course of action, not to fish for unexpected results or provide additional evidence for a decision that is already incontrovertible.
When invasive evaluation is decided upon, the choice of techniques must be individualized for every case. Subdural electrodes offer close spatial resolution of the epileptogenic zone in relation to the eloquent cortex, whereas stereotactic depth electrodes enable more-precise recording from regions below the cortical surface. Despite traditional thinking, inserting depth electrodes does not carry a greater risk of complications than subdural evaluation; in fact, with good technique, the opposite may be true.
It was recommended that the patient undergo invasive testing to better determine the lesion’s precise location in relation to language centers and to delineate the area of maximum possible resection.
The area of the lesion was covered by a subdural grid, and two depth electrodes were placed to derive information of the deeper structures at the site of the lesion.
Electrocorticography showed repetitive spikes in the left inferior frontal region interictally and ictally.
Propagation appeared restricted, and the deeper probes appeared more flat. Seizure activity was evident on EEG even without clinical signs.
Continuous repetitive discharges is the most significant and characteristic electrocorticographic finding of focal cortical dysplasia. If areas of continuous repetitive discharges are left behind in surgery, the operation is more likely to fail.
Sublobar resection of the left pars orbitalis was undertaken. The resection was limited to the area defined as abnormal on MRI and epileptogenic on subdural EEG, while sparing language areas identified by cortical stimulation (see map below). Although a common dogma in neurosurgery is to stay at least 1 cm away from eloquent cortex, this is not necessarily justified. In this case, clear anatomical boundaries (the sulci) defined the extent of the language areas and allowed the surgeon to resect to their limit.
Pathology of the resection showed type II cortical dysplasia, with focal cortical architectural disorganization, dysmorphic neurons and balloon cells.
Outcome and conclusions
One year later, the patient has been seizure-free since surgery and without language deficit. His EEG shows no epileptiform discharges.
This case highlights at least two key teaching points and takeaways:
- It is important to revisit an “almost normal” MRI in children and young adults with drug-resistant focal epilepsy and no epilepsy risk factors. In such cases, the most likely cause of a subtle finding on an otherwise normal brain MRI is focal cortical dysplasia, which often arises in the depths of sulci.
- Defining the language-eloquent cortex was extremely important in this case. The three-dimensional picture of a very focal lesion would not have been available without intracranial investigation.
To view a webcast of this and nine other epilepsy cases in the “Hot Topics in Epilepsy for Children and Adults” CME-certified webcast series, visit www.ccfcme.org/EpilepsyCME. This activity has been approved for AMA PRA Category 1 Credit™.
Dr. Nair is Section Head of Adult Epilepsy and Dr. Bulacio is a staff epileptologist, both in Cleveland Clinic’s Epilepsy Center.