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Like other types of seizures, generalized tonic-clonic seizures are caused by the paroxysmal, uncontrolled discharge of central nervous system neurons, leading to neurologic dysfunction. Unlike most other types of seizures, however, this cerebral hyperactivity isn’t confined to the original focus or to a localized area but extends to the entire brain.
A generalized tonic-clonic seizure may begin with or without an aura. As seizure activity spreads to the subcortical structures, the patient loses consciousness, falls, and may utter a loud cry that’s precipitated by air rushing from the lungs through the vocal cords. His body stiffens (tonic phase), and then undergoes rapid, synchronous muscle jerking and hyperventilation (clonic phase). Tongue biting, incontinence, diaphoresis, profuse salivation, and signs of respiratory distress may also occur. The seizure usually stops after 2 to 5 minutes. The patient then regains consciousness but displays confusion. He may complain of a headache, fatigue, muscle soreness, and arm and leg weakness.
Generalized tonic-clonic seizures usually occur singly. The patient may be asleep or awake and active. (See What happens during a generalized tonic-clonic seizure, page 556.) Possible complications include respiratory arrest due to airway obstruction from secretions, status epilepticus (occurring in 5% to 8% of patients), head or spinal injuries and bruises, Todd’s paralysis and, rarely, cardiac arrest. Life-threatening status epilepticus is marked by prolonged seizure activity or by rapidly recurring seizures with no intervening periods of recovery. It’s most commonly triggered by the abrupt discontinuation of anticonvulsant therapy.
Generalized seizures may be caused by a brain tumor, vascular disorder, head trauma, infection, metabolic defect, drug or alcohol withdrawal syndrome, exposure to toxins, or a genetic defect. Generalized seizures may also result from a focal seizure. With recurring seizures, or epilepsy, the cause may be unknown.
If possible, turn the patient to one side during the seizure to allow secretions to drain and to prevent aspiration. Otherwise, do this at the end of the clonic phase when respirations return. (If they fail to return, check for airway obstruction and suction the patient if necessary. Cardiopulmonary resuscitation, intubation, and mechanical ventilation may be needed.)
Protect the patient after the seizure by providing a safe area in which he can rest. As he awakens, reassure and reorient him. Check his vital signs and neurologic status. Make sure to carefully record these data and your observations during the seizure.
If the seizure lasts longer than 4 minutes or if a second seizure occurs before full recovery from the first, suspect status epilepticus. Establish an airway, start an I.V. line, give supplemental oxygen, and begin cardiac monitoring. Draw blood for appropriate studies. Turn the patient on his side, with his head in a semi-dependent position, to drain secretions and prevent aspiration. Periodically turn him to the opposite side, check his arterial blood gas levels for hypoxemia, and administer oxygen by mask, increasing the flow rate if necessary. Administer diazepam or lorazepam by slow I.V. push, repeated two or three times at 10- to 20-minute intervals, to stop the seizures. If the patient isn’t known to have epilepsy, an I.V. bolus of dextrose 50% (50 ml) with thiamine (100 mg) may be ordered. Dextrose may stop the seizures if the patient has hypoglycemia. If his thiamine level is low, also give thiamine to guard against further damage.
If the patient is intubated, expect to insert a nasogastric (NG) tube to prevent vomiting and aspiration. Be aware that if the patient hasn’t been intubated, the NG tube itself can trigger the gag reflex and cause vomiting. Make sure to record your observations and the intervals between seizures.
If you didn’t witness the seizure, obtain a description from the patient’s companion. Ask when the seizure started and how long it lasted. Did the patient report unusual sensations before the seizure began? Did the seizure start in one area of the body and spread, or did it affect the entire body right away? Did the patient fall on a hard surface? Did his eyes or head turn? Did he turn blue? Did he lose bladder control? Did he have other seizures before recovering?
If the patient may have sustained a head injury, observe him closely for loss of consciousness, unequal or nonreactive pupils, and focal neurologic signs. Does he complain of a headache and muscle soreness? Is he increasingly difficult to arouse when you check on him at 20-minute intervals? Examine his arms, legs, and face (including tongue) for injury, residual paralysis, or limb weakness.
Next, obtain a history. Has the patient ever had generalized or focal seizures before? If so, do they occur frequently? Do other family members also have them? Is the patient receiving drug therapy? Is he compliant? Also, ask about sleep deprivation and emotional or physical stress at the time the seizure occurred.
Generalized seizures may occur in the acute stage of abscess formation or after the abscess disappears. Depending on the size and location of the abscess, a decreased level of consciousness (LOC) varies from drowsiness to deep stupor. Early signs and symptoms reflect increased intracranial pressure (ICP) and include a constant headache, nausea, vomiting, and focal seizures. Typical later features include ocular disturbances, such as nystagmus, impaired vision, and unequal pupils. Other findings vary with the abscess, site but may include aphasia, hemiparesis, abnormal behavior, and personality changes.
Generalized seizures may occur, depending on the tumor’s location and type. Other findings include a slowly decreasing LOC, a morning headache, dizziness, confusion, focal seizures, vision loss, motor and sensory disturbances, aphasia, and ataxia. Later findings include papilledema, vomiting, increased systolic blood pressure, widening pulse pressure and, eventually, a decorticate posture.
End-stage renal failure produces the rapid onset of twitching, trembling, myoclonic jerks, and generalized seizures. Related signs and symptoms include anuria or oliguria, fatigue, malaise, irritability, decreased mental acuity, muscle cramps, peripheral neuropathies, anorexia, and constipation or diarrhea. Integumentary effects include skin color changes (yellow, brown, or bronze), pruritus, and uremic frost. Other effects include an ammonia breath odor, nausea and vomiting, ecchymoses, petechiae, GI bleeding, mouth and gum ulcers, hypertension, and Kussmaul’s respirations.
Generalized seizures are a hallmark of eclampsia. Related findings include a severe frontal headache, nausea and vomiting, vision disturbances, increased blood pressure, a fever of up to 104° (40° C), peripheral edema, and sudden weight gain. The patient may also exhibit oliguria, irritability, hyperactive deep tendon reflexes (DTRs), and a decreased LOC.
Seizures are an early sign of encephalitis, indicating a poor prognosis; they may also occur after recovery as a result of residual damage. Other findings include a fever, a headache, photophobia, nuchal rigidity, neck pain, vomiting, aphasia, ataxia, hemiparesis, nystagmus, irritability, cranial nerve palsies (causing facial weakness, ptosis, dysphagia), and myoclonic jerks.
In most cases, the cause of recurrent seizures is unknown.
In severe cases, generalized seizures may occur at the time of injury. (Months later, focal seizures may occur.) Severe head trauma may also cause a decreased LOC, leading to coma; soft-tissue injury of the face, head, or neck; clear or bloody drainage from the mouth, nose, or ears; facial edema; bony deformity of the face, head, or neck; Battle’s sign; and a lack of response to oculocephalic and oculovestibular stimulation. Motor and sensory deficits may occur along with altered respirations. Examination may reveal signs of increasing ICP, such as a decreased response to painful stimuli, nonreactive pupils, bradycardia, increased systolic pressure, and widening pulse pressure. If the patient is conscious, he may exhibit visual deficits, behavioral changes, and a headache.
Generalized seizures may occur late in hepatic encephalopathy. Associated late-stage findings in the comatose patient include fetor hepaticus, asterixis, hyperactive DTRs, and a positive Babinski’s sign.
Generalized seizures usually occur with severe hypoglycemia, accompanied by blurred or double vision, motor weakness, hemiplegia, trembling, excessive diaphoresis, tachycardia, myoclonic twitching, and a decreased LOC.
Seizures develop when serum sodium levels fall below 125 mEq/L, especially if the decrease is rapid. Hyponatremia also causes orthostatic hypotension, a headache, muscle twitching and weakness, fatigue, oliguria or anuria, cold and clammy skin, decreased skin turgor, irritability, lethargy, confusion, and stupor or coma. Excessive thirst, tachycardia, nausea, vomiting, and abdominal cramps may also occur. Severe hyponatremia may cause cyanosis and vasomotor collapse, with a thready pulse.
Worsening tetany causes generalized seizures. Chronic hypoparathyroidism produces neuromuscular irritability and hyperactive DTRs.
Besides generalized seizures, hypoxic encephalopathy may produce myoclonic jerks and coma. Later, if the patient has recovered, dementia, visual agnosia, choreoathetosis, and ataxia may occur.
Multiple brain lesions from neurofibromatosis cause focal and generalized seizures. Inspection reveals café-au-lait spots, multiple skin tumors, scoliosis, and kyphoscoliosis. Related findings include dizziness, ataxia, monocular blindness, and nystagmus.
Seizures (focal more commonly than generalized) may occur within 6 months of an ischemic stroke. Associated signs and symptoms vary with the location and extent of brain damage. They include a decreased LOC, contralateral hemiplegia, dysarthria, dysphagia, ataxia, unilateral sensory loss, apraxia, agnosia, and aphasia. The patient may also develop visual deficits, memory loss, poor judgment, personality changes, emotional lability, urine retention or urinary incontinence, constipation, a headache, and vomiting.
Besides generalized seizures, arsenic poisoning may cause a garlicky breath odor, increased salivation, and generalized pruritus. GI effects include diarrhea, nausea, vomiting, and severe abdominal pain. Related effects include diffuse hyperpigmentation; sharply defined edema of the eyelids, face, and ankles; paresthesia of the extremities; alopecia; irritated mucous membranes; weakness; muscle aches; and peripheral neuropathy.
In chronically intoxicated patients, barbiturate withdrawal may produce generalized seizures 2 to 4 days after the last dose. Status epilepticus is possible.
Contrast agents used in radiologic tests may cause generalized seizures.
Toxic blood levels of some drugs, such as theophylline, lidocaine, meperidine, penicillins, and cimetidine, may cause generalized seizures. Phenothiazines, tricyclic antidepressants, amphetamines, isoniazid, and vincristine may cause seizures in patients with preexisting epilepsy.
Closely monitor the patient after the seizure for recurring seizure activity. Prepare him for a computed tomography scan or magnetic resonance imaging and EEG.
Generalized seizures are common in children. In fact, between 75% and 90% of epileptic patients experience their first seizure before age 20. Many children between ages 3 months and 3 years experience generalized seizures associated with a fever; some of these children later develop seizures without a fever. Generalized seizures may also stem from inborn errors of metabolism, perinatal injury, brain infection, Reye’s syndrome, Sturge-Weber syndrome, arteriovenous malformation, lead poisoning, hypoglycemia, and idiopathic causes. The pertussis component of the DPT vaccine may cause seizures; however, this is rare.
Read excerpts from these other book chapters related to Seizures:
Copyright Details: Handbook of Signs & Symptoms (Third Edition), Copyright © 2008 Williams & Wilkins.
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More About This Book:
Title: Handbook of Signs & Symptoms (Third Edition) Authors: Springhouse Publisher: Lippincott Williams & Wilkins Copyright: 2006 ISBN: 1-58255-402-1 
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