The depth and duration of unconsciousness vary. Sometimes the person is not completely oblivious to his surroundings; he may still hear voices or see the blurred outlines of people. More often there is a complete lack of awareness and responsiveness. The patient lies motionless, with skeletal muscles fully relaxed. Sphincteric control is maintained in nearly all cases. The pupils are dilated. The pulse is thin and slow or cannot be felt; or they may be tachycardic, the systolic blood pressure is reduced (to 60 mm Hg or less as a rule), and breathing may be almost imperceptible. It is the brief period of hypotension and cerebral hypoperfusion that is the unifying feature of the various forms of syncope. The depressed vital functions, striking facial pallor, and unconsciousness almost simulate death.
Once the patient is horizontal, the flow of blood to the brain is restored. The strength of the pulse soon improves and color begins to return to the face. Breathing becomes quicker and deeper. Then the eyelids flutter and consciousness is quickly regained. However, should unconsciousness persist for 15 to 20 s, some motor activity is commonly observed. The term convulsive syncope has been used to describe this phenomenon, but it has also been used for an authentic seizure caused by a prolonged period of brain hypoxia. These movements, which are often mistaken for a seizure, usually take the form of brief clonic jerks of the limbs and trunk and twitchings of the face or a tonic extension of the trunk, clenching of the jaw or turning of the eyes to either direction or upward. Occasionally, the extensor rigidity and jerking flexor movements are more severe, but very rarely is there urinary incontinence or biting of the tongue, features that characterize a generalized tonic-clonic convulsion. These movements are displayed in the exercise carried out with medical students, who induced syncope by hyperventilation followed by the Valsalva maneuver. Nearly all had myoclonic jerks and ocular deviation as syncope commenced as demonstrated in a video (Bauer, Lempert, and Schmidt; https://www.youtube.com/watch?v=KPewaYFWsrE&feature=youtu.be).
Gastaut and Fischer-Williams used the oculocardiac inhibitory reflex to study the pattern of electroencephalographic (EEG) changes in syncope. They found that the heightened vagal discharge produced by compression of the eyeballs (oculovagal reflex, a cause of syncope in acute glaucoma) could produce brief periods of cardiac arrest and syncope. This effect was produced in 20 of 100 patients who had a history of syncopal attacks. These investigators found that after a 7to 13-s period of cardiac arrest, there was a loss of consciousness, pallor, and muscle relaxation and changes in EEG activity. Toward the end of this period, runs of bilaterally synchronous theta and delta waves appeared in the EEG, predominantly in the frontal lobes; in some patients there were one or more myoclonic jerks, synchronous with the slow waves. If the hypotension persisted beyond 14 or 15 s, the EEG became flat. This period of electrical silence lasted for 10 to 20 s and was sometimes accompanied by a generalized tonic spasm with incontinence. Following the spasm, heartbeats and large-amplitude delta waves reappeared, and after another 20 to 30 s, the EEG reverted to normal. It is noteworthy that rhythmic clonic seizures or epileptiform EEG activity was not observed at any time during the periods of cardiac arrest, syncope, and tonic spasm.
From the moment that consciousness is regained, there is a correct perception of the environment. Confusion, headache, and drowsiness, the common sequelae of a convulsive seizure, do not follow a syncopal attack. Nevertheless, the patient often feels weak and groggy after a vasodepressor faint and, by arising too soon, may precipitate another faint.