Generalized tonic–clonic seizure

A generalized tonic–clonic seizure, or GTCS, previously known as a Grand mal seizure,[1] is a type of generalized seizure that produces bilateral, convulsive tonic and then clonic muscle contractions.[2] Tonic-clonic seizures are the seizure type most commonly associated with epilepsy and seizures in general and the most common seizure associated with metabolic imbalances.[2] It is a misconception that they are the sole type of seizure, as they are the main seizure type in approximately 10% of those with epilepsy.[2]

Generalized tonic–clonic seizure
Other namesGrand mal seizure, tonic–clonic seizure
Generalized 3 Hz spike-and-wave discharges on an electroencephalogram
SpecialtyNeurology

These seizures typically initiate abruptly with either a focal or generalized onset, the former being known as focal to bilateral tonic-clonic seizure.[3] The seizure itself includes tonic (sustained) and then clonic (repetitive short) contractions.[4] In some seizures, the tonic phase may be preceded by brief, arrhythmic muscle jerks (myoclonus), by a clonic phase or by an absence seizure.[4] After the GTCS, there is an extended postictal state where the person is unresponsive and commonly sleeping with loud snoring.[4] There is usually pronounced confusion upon awakening.[4]

Causes

The vast majority of generalized tonic-clonic seizures have a focal origin[5] they start as a smaller seizure that occurs solely on one side of the brain and is referred to as a focal (or partial) seizure.[3] These unilateral seizure types (formerly known as simple partial seizure or a complex partial seizure and now referred to as focal aware seizure and focal impaired awareness seizure, respectively) can then spread to both hemispheres of the brain and cause a generalized tonic-clonic seizure.[3] This type of seizure has a specific term called "focal to a bilateral tonic-clonic seizure.[3] Other generalized tonic-clonic seizures are idiopathic, start in large networks involving both hemispheres, and have a presumed genetic cause. Precipitating factors include chemical and neurotransmitter imbalances and a genetically or situationally determined seizure threshold, both of which have been implicated. The seizure threshold can be altered by fatigue, malnutrition, lack of sleep or rest, hypertension, stress, diabetes, the presence of strobe-flashes or simple light/dark patterns, raised estrogen levels at ovulation, fluorescent lighting, rapid motion or flight, blood sugar imbalances, anxiety, antihistamines and other factors.[6] Tonic–clonic seizures can also be induced deliberately with electroconvulsive therapy.[7]

In the case of symptomatic focal epilepsy, the cause is often determined by MRI or other neuroimaging techniques showing that there is some degree of damage to a large number of neurons.[8] The lesions (i.e., scar tissue) caused by the loss of these neurons can result in groups of neurons forming a seizure "focus" area with episodic abnormal firing that can cause seizures if the focus is not abolished or suppressed via anticonvulsant drugs.[8]

Mechanism

Prodrome

Most generalized tonic–clonic seizures begin without warning and abruptly, but some epileptic patients describe a prodrome. The prodrome of a generalized tonic–clonic seizure is a sort of premonitory feeling hours before a seizure. This type of prodrome is distinct from stereotypic aura of focal seizures that become generalized seizures.

Phases

A tonic–clonic seizure comprises three phases: the tonic phase, clonic phase and postictal phase.

  • The tonic phase is usually the first phase.[4] Consciousness will quickly be lost and the skeletal muscles will suddenly tense, often causing the extremities to be pulled towards the body or rigidly pushed away from it, which will cause the patient to fall if standing or sitting.[4] There may also be upward deviation of the eyes with the mouth open.[4] The tonic phase is usually the shortest part of the seizure, normally lasting only 10–20 seconds.[2] The patient typically expresses brief vocalizations like a loud moan upon entering the tonic stage, due to air being forcefully expelled from the lungs.[4] This vocalization is commonly referred to as an "ictal cry".[4] Starting in the tonic phase, there may also be bluing of the skin from respiration impairment and pooling of saliva in the back of the throat.[4] Increased blood pressure, pupillary size and heart rate (sympathetic response) may also be noted with clenching of the jaw possibly resulting in biting the tongue.[4] The initial tonic phase may be preceded by repetitive rhythmic or arrhythmic jerks or by the absence seizure.[4]
  • The clonic phase is an evolution of the tonic phase and is caused by muscle relaxations superimposed on the tonic phase muscle contractions. This phase is longer than the tonic phase with the total ictal period usually lasting no longer than 1 minute.[9] Skeletal muscles will start to contract and relax rapidly, causing convulsions. These may range from exaggerated twitches of the limbs to violent shaking or vibrating of the stiffened extremities. The patient may roll and stretch as the seizure spreads. Initially, these contractions are of a high frequency and low amplitude, which will gradually progress to decreased frequency and high amplitude. An eventual decrease in contraction amplitude just before seizure cessation is also typical.[9]
  • The postictal phase causes are multifactorial to include alteration of cerebral blood flow and effects on multiple neurotransmitters.[6] These changes after a generalized tonic–clonic seizure cause a period of postictal sleep with stertorous breathing.[2] Confusion and total amnesia upon regaining consciousness are also usually experienced and slowly wear off as the patient becomes gradually aware that a seizure occurred and remembers their identity and location.[2] Most often, patients regain consciousness within 30 minutes.[2] Rarely, impaired consciousness duration can last several hours after a seizure, especially with a compounding central nervous system condition or a prolonged seizure.[2] Occasionally the patient may vomit or burst into tears from the experienced mental trauma.[10]

An additional smaller seizure can also occur several minutes after the main seizure, particularly if the patient's seizure threshold has been brought unusually low by known factors or combinations of such.[10] Examples include: severe hangovers, sleep deprivation, elevated estrogen at ovulation, prolonged physical tiredness, and drug use or abuse (including, but not limited to, stimulants, alcohol and caffeine).[10]

Rarely, the respiration is inhibited during the postictal phase, leading to sudden unexpected death in epilepsy (SUDEP).[11] Generalized tonic–clonic seizures represent the most important risk factor for SUDEP, especially in patients with nocturnal seizures, who are living alone or do not share a bedroom.[11]

Diagnosis

Diagnosis can be made definitively by video recordings of the seizures and Electroencephalography (EEG), which records the electrical activity of the brain.[2] This is typically done after a seizure episode in a clinical setting with an attempt to "capture" a seizure while it happens.[2] According to the "Harrison's Manual of Medicine," the EEG during the tonic phase will show a "progressive increase in low-voltage fast wave activity, followed by generalized high-amplitude, poly spike discharges."[2] The clonic phase EEG will show "high amplitude activity that is typically interrupted by slow waves to create a spike-and-slow-wave pattern."[2] Additionally, the postictal phase will show suppression of all brain activity, then slowing that gradually recovers as the patient awakens.[2]

Management

For a person experiencing a tonic–clonic seizure, first-aid treatment includes rolling the person over into the recovery position, which can prevent asphyxiation by preventing fluid from entering the lungs.[12] Other general actions to take as recommended by the Epilepsy Foundation include staying with a person until a seizure is over, paying attention to length of seizure as a possible indication for status epilepticus and/or indication to give rescue medication and call for emergency help, moving close objects out of the way to prevent injury.[12] It is also not recommended to hold a person down that is having a seizure, as that can lead to injury.[12] Nor should anything be put in a person's mouth, as these items can become choking hazards and, depending on what is put in, can potentially break the person's teeth.[12]

Long-term therapy may include the use of antiepileptic drugs, surgical therapy, diet therapy (ketogenic diet), vagus nerve stimulation, or deep brain stimulation.[12]

Terminology

Generalized tonic–clonic seizures can have a focal onset (described above) that progresses into a generalized seizure or be a generalized seizure at the onset.[12] The term "Grand Mal" is outdated and nonspecific, referring to generalized tonic-clonic seizures with either a focal or generalized onset.[12]

See also

References
  1. "Grand mal seizure - Symptoms and causes". Mayo Clinic.
  2. Harrison, Tinsley Randolph (2016). Harrison's Manual of medicine (19th ed.). New York. ISBN 978-0071828529.
  3. "2017 Revised Classification of Seizures". Epilepsy Foundation.
  4. Bradley's neurology in clinical practice (6th ed.). Philadelphia, PA: Elsevier/Saunders. 2012. ISBN 9781437704341.
  5. "Generalized Tonic-Clonic Seizures: Background, Pathophysiology, Etiology". 11 March 2022.
  6. "Seizure Triggers". Epilepsy Foundation.
  7. "Looking at the Brain : Epilepsy.com". web.archive.org. 12 October 2007. Archived from the original on 2007-10-12.
  8. Fisher, RS; Schachter, SC (February 2000). "The postictal state: a neglected entity in the management of epilepsy". Epilepsy & Behavior. 1 (1): 52–9. doi:10.1006/ebeh.2000.0023. PMID 12609127. S2CID 20393636.
  9. Herausgeber., Kasper, Dennis L., Herausgeber. Fauci, Anthony S., Herausgeber. Hauser, Stephen L., Herausgeber. Longo, Dan L., 1949– Herausgeber. Jameson, J. Larry, Herausgeber. Loscalzo, Joseph (2016-05-27). Harrisons manual of medicine. ISBN 978-0071828529. OCLC 956960804.
  10. Michael, GE; O'Connor, RE (February 2011). "The diagnosis and management of seizures and status epilepticus in the prehospital setting". Emergency Medicine Clinics of North America. 29 (1): 29–39. doi:10.1016/j.emc.2010.08.003. PMID 21109100.
  11. Sveinsson, O; Andersson, T; Mattsson, P; Carlsson, S; Tomson, T (28 January 2020). "Clinical risk factors in SUDEP: A nationwide population-based case-control study". Neurology. 94 (4): e419–e429. doi:10.1212/WNL.0000000000008741. PMC 7079690. PMID 31831600.
  12. "Seizure First Aid Training and Certification". Epilepsy Foundation.
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