Seizures

Stephen Luney

CASE SUMMARY

A 73-year-old man has been found “writhing about” unconscious in the street and brought by an EMS team to the hospital emergency room. He is in a disheveled state, smells of alcohol, and has been incontinent of urine. The staff recognize him as a frequent patient of the department, a homeless person who has been seen for mental health and alcohol-related issues.

On arrival in the department, he has eye opening to speech and is confused but obeys commands. The initial observations show him to have a core temperature of 38°C, heart rate 110 bpm, blood pressure 110/55 mmHg, and oxygen saturation of 92%. While lying semirecumbent on a gurney and before blood samples could be taken, he begins having myoclonic twitching. Immediately thereafter, he proceeds to have a tonic-clonic, grand mal seizure lasting a total of 10 minutes. During this time, the back of the gurney was lowered and his head was cradled to protect him from injury.

Oxygen is administered through a face mask at 12 L per minute, an intravenous catheter is inserted, and an arterial blood gas sample is taken. Venous blood samples are taken and further examination is performed, which show him to have a core temperature of 38°C, heart rate 130 bpm, blood pressure 90/50 mmHg, and an oxygen saturation of 97%. Fluids and a slow intravenous injection of 4 mg of lorazepam are initiated. Arrangements are made to admit him to the intensive care unit for further management.

What Is a Seizure?

By definition, a seizure is the transient clinical manifestations that result from an episode of epileptic neuronal activity. The etiology of seizures is vast (see Table 23.1). One of the characteristic findings is abnormal synchronization of this activity, with either inadequate inhibition, excessive excitation, or both, in large groups (or aggregates) of neurons. How this manifests itself depends on which groups of neurons are involved and the intensity of the discharges. Normally, the clinical manifestation of these events starts suddenly and does not last long.¹

How Does a Seizure Present?

Seizures are usually classified first into partial and generalized, and then each of these is classified further— essentially on the basis of the clinical manifestation of the seizure (see Table 23.2).

A tonic-clonic, or grand mal seizure is the classic form of fit or convulsion that most people imagine when they think of a seizure. Sometimes such a seizure can be preceded by a prodromal period during which the patient may anticipate its onset. It may be that there is an increase in myoclonic jerking. If the patient gets a sensation that a seizure is imminent—termed an aura—technically, it means that the seizure is generalized secondarily. The patient then becomes unconscious and may cry out and fall if standing at the time. For a short period of time, the patient will exhibit tonic flexion, followed by a more prolonged period where they become rigid, and extend axially, with their jaw clamped shut and their eyes rolled up. Their limbs become stiff and adopt a position of adduction and extension, with their fists clenched. During this period, they are apneic and often become cyanotic. This phase lasts up to 30 seconds and leads into the clonic phase. This usually affects all the limbs, jaw, and facial muscles. There can be excessive salivation and partially obstructed respiration, possibly complicated by bleeding from the tongue or lips if they have bitten themselves.

As the seizure continues, the convulsive movements become less frequent and may settle down to around 4 Hz, but become greater in their excursions. Concurrent with these motor manifestations are autonomic phenomena,
including changes in heart rate and blood pressure and cutaneous flushing which last 30 to 60 seconds. These manifestations conclude with a short-lived tonic contraction of all the muscle groups, during which the patient may become incontinent. In the final phase (lasting from a few minutes to half hour), there is generalized muscle flaccidity.

TABLE 23.1 Etiology of Seizures

1.	Metabolic
	a.	Congenital
	b.	Acquired
		(1)	Hypoglycemia
		(2)	Hyperglycemia
		(3)	Hyponatremia
		(4)	Hypoxia
		(5)	Hypocalcemia
		(6)	Uremia
		(7)	Toxins
		(8)	Drugs (either withdrawal or intoxication)
2.	Infection
	a.	Systemic (febrile convulsion/hyperthermia)
	b.	Intracranial
		(1)	Meningitis
		(2)	Encephalitis
		(3)	Abscess
3.	Structural
	a.	Gliotic scarring
		(1)	Temporal lobe sclerosis
		(2)	Posttraumatic
		(3)	Post infection
	b.	Congenital malformations
	c.	Vascular malformations
	d.	Tumor

Consciousness usually returns gradually, although the patient is invariably confused postictally. Oftentimes, patients will complain of severe headache and usually feel dreadful and extremely fatigued. They may also go into a deep sleep (but not unconsciousness), from which they awake later with generalized muscle aches and pains, and frequently report a persisting headache.

How Do I Know It Is Really a Seizure?

In the acute setting in the emergency room or the postanesthesia care unit, one of the questions that runs through one’s mind is “Is this really a seizure or is this guy faking it?” This does not seem like an unreasonable question when you consider that, in an audit of patients referred to a specialized neurology center as status epilepticus, around half were either in a drug-induced coma or in pseudostatus.²

There are a number of things that are helpful in differentiating between pseudoseizure and a valid seizure.³ First of all, clinical signs may be helpful. Evidence of fluctuations of pupillary size (hippus), nystagmus, or stereotypic cyclic motor manifestations greatly aids in confirming the diagnosis, as these are clinical signs that cannot be manufactured. Conversely, clinical signs that should arouse suspicion of (but are not pathognomonic of) pseudoseizure include the following:

TABLE 23.2 International League Against Epilepsy (ILAE) Classification of Seizures

1.	Generalized (convulsive and nonconvulsive)
	a.	Absence seizures
		(1)	Absence seizures
		(2)	Atypical absence seizures
	b.	Myoclonic seizures
	c.	Clonic seizures
	d.	Tonic seizures
	e.	Tonic-clonic seizures
	f.	Atonic seizures
2.	Partial (local, focal seizures)
	a.	Simple partial seizures
		(1)	With motor signs
		(2)	With somatosensory or special sensory signs
		(3)	With autonomic symptoms or signs
		(4)	With psychic symptoms
	b.	Complex partial seizures
		(1)	Simple partial onset followed by impaired consciousness
		(2)	With impaired consciousness from the outset
	c.	Partial seizures evolving to secondary generalized seizures (tonic-clonic, tonic or clonic)
		(1)	Simple partial seizures evolving to generalized seizures
		(2)	Complex partial seizures evolving to generalized seizures
		(3)	Simple partial seizures evolving to complex partial seizures then evolving to generalized seizures
3.	Unclassified epileptic seizures
Data taken from: Shorvon SD. Handbook of epilepsy treatment. Oxford: Blackwell Publishing; 2005.

The patient squeezing the eyes shut or resisting them being opened
Rolling the head
Arching the back
Thrusting the pelvis
Poorly coordinated thrashing

This is by no means an exhaustive list, but includes some of the more common features of pseudoseizure. Another reason to suspect pseudoseizure is if the patient does not respond promptly to initial treatment of the “seizure,” as the vast majority with a seizure do respond. Nonconvulsive seizure is a much more difficult diagnosis to make, and in the presence of coma can only be diagnosed by electroencephalogram (EEG), which should be sought relatively early in the investigation stage.

What Is Status Epilepticus?

For seizures to be classified as status epilepticus, they need to have occurred for at least 30 minutes. Needless to say, one should not wait 30 minutes before treating the seizures. Indeed, if a seizure has been in progress for more than 5 minutes, or if a second seizure occurs without full recovery of consciousness, treatment should be started. There is evidence to show that if there are repeated seizures, and therapy is commenced, status epilepticus can potentially be avoided.⁴

More than half of those who develop status epilepticus are not epileptics and usually have an acute cause for their epilepsy. Those who are known to be epileptic who present with status epilepticus often do so because of either drug withdrawal by their physician or poor compliance on their part. It is important to remember that they, too, may have an acute reason for their seizures, in addition to issues regarding therapy. With children, it is commonly fever that causes their seizures, but in adults, the main causes are stroke, alcohol, metabolic disturbance, and hypoxia.

How Does Anesthesia Relate to the Incidence of Seizures?

Anesthesia providers may come across seizures in a wide variety of settings. Seizures are a potential complication of techniques we perform in our daily anesthesia practice. They may also occur as a complication of surgery. We may be called upon to care for patients in an intensive care setting with the complications of the seizures themselves, or to care for a seizing patient who arrives in our emergency rooms.

Perhaps the most common cause of seizures as a consequence of an anesthesia intervention is following the accidental intravascular injection of a local anesthetic solution. Doses of local anesthetic drugs—anything from a fourth to a seventh of those required to produce cardiac toxicity—generally will produce central nervous system (CNS) toxicity.⁵ The exception to this generalization is with bupivacaine where the CNS and cardiac toxicities may manifest at almost the same dose (see Table 23.3). Local anesthetic-induced seizures can occur in virtually any setting where local anesthetic drugs are used, but the risk increases as we move from field block infiltration through specific nerve blocks to plexus blocks.

Owing to the fact that nerves frequently run within a neurovascular bundle in association with veins and arteries, there is inevitably a risk of inadvertent intravascular injection. For this reason, both the use of a test dose and repeated aspiration during injection of local anesthetic in any site is a vital safety component of the performance of a local anesthetic block. There may be premonitory symptoms, such as perioral tingling, or feelings of dissociation following a test dose. Depending on the block being performed, the severity of risk relates to either the arterial or venous side of the circulation. For example, a brachial plexus block performed by the axillary approach can be inadvertently injected into the axillary vein with subsequent rapid progression to the brain in high concentrations. The performance of a cervical plexus block runs the risk not only of injection into the jugular venous system, but into a carotid or other cervical artery. Because this is then presented directly into the cerebral circulation, it requires much smaller amounts to elicit a seizure. Placement of a central venous catheter with local anesthetic infiltration is another setting where the injection of a local anesthetic runs the risk of intravascular injection.

TABLE 23.3 Mean (±SE) Ratios of Circulatory Collapse (CC) and Convulsive (CNS) Dosages and Blood Concentrations of Bupivacaine, Etidocaine, and Lidocaine in Adult Sheep

	Bupivacaine^a	Etidocaine^a	Lidocaine^a
Dosage ratios (CC/CNS)	3.7 ± 0.5^b	4.4 ± 0.9	7.1 ± 1.1
Blood level ratios (CC/CNS)	1.6 ± 0.1^b	1.7 ± 0.2^b	3.6 ± 0.3
^aCalculated from previously published data. ^bSignificantly different from lidocaine.
SE, standard error; CNS, central nervous system. Modified from: Morishima HO, Pedersen H, Finster M, et al. Bupivacaine toxicity in pregnant and nonpregnant ewes. Anesthesiology. 1985;63:134-139.