Sudden loss of consciousness

In most cases of sudden loss of consciousness, it is difficult to obtain anamnestic information about the events immediately preceding it. Remote anamnesis, which may contain diagnostically useful information, may also be unknown. Sudden loss of consciousness may be short-term or persistent and may have both neurogenic (neurogenic syncope, epilepsy, stroke) and somatogenic (cardiac disorders, hypoglycemia, etc.) origin.

[ 1 ], [ 2 ], [ 3 ], [ 4 ], [ 5 ], [ 6 ], [ 7 ]

The main causes of sudden loss of consciousness:

1. Fainting of neurogenic and other origin
2. Epilepsy
3. Intracerebral hemorrhage
4. Subarachnoid hemorrhage
5. Basilar artery thrombosis
6. Traumatic brain injury
7. Metabolic disorders (most often hypoglycemia and uremia)
8. Exogenous intoxication (usually develops subacutely)
9. Psychogenic seizure

Fainting

The most common cause of sudden loss of consciousness is fainting of various types. Often, not only does the patient fall (acute postural insufficiency), but also loss of consciousness for a period measured in seconds. Long-term loss of consciousness during fainting is rare. The most common types of fainting are: vasovagal (vasodepressor, vasomotor) fainting; hyperventilation syncope; fainting associated with carotid sinus hypersensitivity (GCS syndrome); cough syncope; nocturic; hypoglycemic; orthostatic fainting of various origins. With all types of fainting, the patient notes a lipothymic (pre-fainting) state: a feeling of nausea, non-systemic dizziness, and a premonition of loss of consciousness.

The most common type of fainting is vasodepressor (simple) syncope, usually provoked by one or another stressful event (anticipation of pain, sight of blood, fear, stuffiness, etc.). Hyperventilation syncope is provoked by hyperventilation, which is usually accompanied by dizziness, mild headache, numbness and tingling in the limbs and face, visual disturbances, muscle spasms (tetanic spasms), and palpitations.

Nocturic syncope is characterized by a typical clinical picture: usually nocturnal episodes of loss of consciousness, occurring during or (more often) immediately after urination, due to the need for which the patient is forced to get up at night. They sometimes have to be differentiated from epileptic seizures using a traditional EEG study.

Carotid sinus massage helps to identify carotid sinus hypersensitivity. Such patients often have a history of poor tolerance to tight collars and ties. Compression of the carotid sinus area by the doctor's hand in such patients can provoke dizziness and even fainting with a decrease in blood pressure and other vegetative manifestations.

Orthostatic hypotension and fainting may be of both neurogenic (in the picture of primary peripheral autonomic failure) and somatogenic origin (secondary peripheral failure). The first variant of peripheral autonomic failure (PAF) is also called progressive autonomic failure. It has a chronic course and is represented by such diseases as idiopathic orthostatic hypotension, stria-nigral degeneration, Shy-Drager syndrome (variants of multiple system atrophy). Secondary PAF has an acute course and develops against the background of somatic diseases (amyloidosis, diabetes mellitus, alcoholism, chronic renal failure, porphyria, bronchial carcinoma, leprosy and other diseases). Dizziness in the picture of PAF is always accompanied by other characteristic manifestations of PAF: anhidrosis, fixed heart rhythm, etc.

In the diagnosis of any variants of orthostatic hypotension and fainting, in addition to special cardiovascular tests, it is important to take into account the orthostatic factor in their occurrence.

Deficiency of adrenergic effects and, consequently, clinical manifestations of orthostatic hypotension are possible in the picture of Addison's disease, in some cases of the use of pharmacological agents (hyperglycemic blockers, antihypertensive agents, dopamine mimetics such as nacom, madopar and some dopamine receptor agonists).

Orthostatic circulatory disorders also occur with organic pathology of the heart and blood vessels. Thus, syncope can be a frequent manifestation of obstructed aortic flow with aortic stenosis, ventricular arrhythmia, tachycardia, fibrillation, sick sinus syndrome, bradycardia, atrioventricular block, myocardial infarction, long QT syndrome, etc. Almost every patient with significant aortic stenosis has a systolic murmur and a "cat purr" (easier to hear in a standing position or in a "vous" position).

Sympathectomy may result in insufficient venous return and, as a consequence, orthostatic circulatory disorders. The same mechanism of development of orthostatic hypotension and syncope occurs with the use of ganglion blockers, some tranquilizers, antidepressants and anti-adrenergic agents.

When blood pressure drops against the background of an ongoing cerebrovascular disease, ischemia in the brainstem area (cerebrovascular syncope) often develops, manifested by characteristic brainstem phenomena, non-systemic dizziness and fainting (Unterharnscheidt syndrome). Drop attacks are not accompanied by lipothymia and fainting. Such patients require a thorough examination to exclude cardiogenic fainting (cardiac arrhythmia), epilepsy and other diseases.

Predisposing factors to lipothymia and orthostatic syncope are somatic disorders associated with a decrease in circulating blood volume: anemia, acute blood loss, hypoproteinemia and low plasma volume, dehydration. In patients with suspected or actual blood volume deficit (hypovolemic syncope), unusual tachycardia while sitting in bed is of great diagnostic importance. Hypoglycemia is another important factor predisposing to syncope.

Orthostatic syncope often requires differential diagnosis with epilepsy. Syncope is extremely rare in the horizontal position and never occurs during sleep (at the same time, it is possible when getting out of bed at night). Orthostatic hypotension can be easily detected on a turntable (passive change of body position). Postural hypotension is considered established when systolic blood pressure drops by at least 30 mm Hg when moving from a horizontal to a vertical position. A cardiological examination is necessary to exclude the cardiogenic nature of these disorders. The Aschner test has a certain diagnostic value (a slowing of the pulse by more than 10-12 beats per minute during the Aschner test indicates increased reactivity of the vagus nerve, which often occurs in patients with vasomotor syncope), as well as such techniques as compression of the carotid sinus, the Valsalva test, and a 30-minute standing test with periodic measurement of blood pressure and heart rate.

The Valsalva test is most informative in patients with nocturic, cough syncope and other conditions accompanied by a short-term increase in intrathoracic pressure.

[ 8 ], [ 9 ], [ 10 ], [ 11 ]

Generalized epileptic seizure

At first glance, the diagnosis of the postictal state should not cause difficulties. In fact, the situation is often complicated by the fact that the convulsions themselves during an epileptic seizure may go unnoticed, or the seizure may be non-convulsive. Such characteristic symptoms as biting the tongue or lips may be absent. Involuntary urination can occur for many reasons. Postictal hemiparesis can mislead the doctor if the patient is young. Useful diagnostic information is provided by an increase in the level of creatine phosphokinase in the blood. Postictal drowsiness, epileptic activity in the EEG (spontaneous or provoked by increased hyperventilation or sleep deprivation) and observation of the seizure help in the correct diagnosis.

[ 12 ], [ 13 ], [ 14 ]

Intracerebral hemorrhage

Intracerebral hemorrhage usually occurs in patients with chronic arterial hypertension. The cause is a rupture of an aneurysm of a sclerotically altered small-caliber vessel; the most common localization is the basal ganglia, pons, and cerebellum. The patient is somnolent or unconscious. Hemiplegia is most likely to be present, which can be detected in a patient in a comatose state by a unilateral decrease in muscle tone. Deep reflexes on the side of paralysis may be decreased, but Babinski's symptom is often positive. With hemispheric hemorrhage, it is often possible to detect concomitant abduction of the eyeballs toward the lesion. With hemorrhage in the pons, tetraplegia with bilateral extensor reflexes and various oculomotor disorders is observed. With concomitant abduction of the eyes, the gaze is directed to the side opposite to the side of the pontine lesion, in contrast to hemispheric hemorrhage, when the gaze is directed toward the lesion (the intact hemispheric oculomotor system "pushes" the eyeballs to the opposite side). "Floating" concomitant or nonconcomitant eye movements are observed frequently and do not have diagnostic value in terms of determining the localization of the lesion within the brainstem. Spontaneous nystagmus is more often horizontal with pontine lesions and vertical with the lesion localized in the midbrain.

Ocular bobbing is most often seen with compression of the lower brainstem by a cerebellar space-occupying process. This symptom is often (but not always) a sign of irreversible brainstem dysfunction. The loss of the oculocephalic reflex corresponds to a deepening coma.

Pupillary disorders are often present. Bilateral miosis with intact photoreactions indicates damage at the level of the pons, and sometimes the preservation of photoreactions can only be verified with a magnifying glass. Unilateral mydriasis is observed with damage to the nucleus of the third cranial nerve or its autonomic efferent fibers in the tegmentum of the midbrain. Bilateral mydriasis is a formidable, prognostically unfavorable sign.

In most cases, the cerebrospinal fluid is stained with blood. Neuroimaging studies clearly determine the location and size of the hemorrhage and its impact on brain tissue, and decide on the need for neurosurgical intervention.

[ 15 ], [ 16 ], [ 17 ], [ 18 ], [ 19 ], [ 20 ], [ 21 ]

Subarachnoid hemorrhage (SAH)

It should be noted that some patients after subarachnoid hemorrhage are found unconscious. Neck rigidity is almost always detected, and lumbar puncture yields blood-stained cerebrospinal fluid. Centrifugation of the cerebrospinal fluid is necessary, since during the puncture the needle may enter a blood vessel, and the cerebrospinal fluid will contain travel blood. Neuroimaging reveals subarachnoid hemorrhage, the volume and location of which can sometimes even be used to judge the prognosis. With a large volume of spilled blood, arterial spasm should be expected to develop over the next few days. Neuroimaging also allows for the timely detection of communicating hydrocephalus.

[ 22 ], [ 23 ], [ 24 ], [ 25 ], [ 26 ]

Basilar artery thrombosis

Basilar artery thrombosis without prior symptoms is rare. Such symptoms are usually present for several days before the onset of the disease and include slurred speech, double vision, ataxia, or paresthesias in the extremities. The severity of these premonitory symptoms usually fluctuates until sudden or rapid loss of consciousness occurs. History taking is essential. The neurologic status is similar to that seen in pontine hemorrhage. Doppler ultrasound is most valuable in such cases because it reveals the characteristic pattern of abnormal blood flow in the large vessels. The diagnosis of basilar artery thrombosis is particularly likely when high resistance is detected in the vertebral arteries, which is detectable even in basilar artery occlusion. Transcranial Doppler ultrasound directly measures basilar artery flow and is an extremely useful diagnostic procedure in patients requiring angiographic evaluation.

During angiography of the vessels of the vertebrobasilar system, stenosis or occlusion in this basin is revealed, in particular, “occlusion of the apex of the basilar artery”, which has an embolic genesis.

In acute massive stenosis or occlusion of the vertebrobasilar vessel, the patient may benefit from urgent measures - either intravenous infusion therapy with heparin or intra-arterial thrombolytic therapy.

[ 27 ], [ 28 ], [ 29 ], [ 30 ], [ 31 ], [ 32 ], [ 33 ], [ 34 ]

Traumatic brain injury

Information about the injury itself may be absent (there may be no witnesses). The patient is found in a coma with the symptoms described above, presented in various combinations. Every patient in a comatose state should be examined and examined to detect possible damage to the soft tissues of the head and bones of the skull. In case of traumatic brain injury, the development of an epi- or subdural hematoma is possible. These complications should be suspected if the coma deepens and hemiplegia develops.

Metabolic disorders

Hypoglycemia (insulinoma, alimentary hypoglycemia, condition after gastrectomy, severe liver parenchyma lesions, insulin overdose in patients with diabetes mellitus, hypofunction of the adrenal cortex, hypofunction and atrophy of the anterior pituitary gland) with its rapid development can contribute to neurogenic syncope in individuals predisposed to it or lead to a soporous and comatose state. Another common metabolic cause is uremia. But it leads to a gradual deterioration in the state of consciousness. In the absence of anamnesis, the state of stupor and sopor is sometimes visible. Laboratory blood tests for screening metabolic disorders are decisive in the diagnosis of metabolic causes of sudden loss of consciousness.

[ 35 ], [ 36 ], [ 37 ]

Exogenous intoxication

Most often it leads to subacute deterioration of consciousness (psychotropic drugs, alcohol, drugs, etc.), but sometimes it can create the impression of sudden loss of consciousness. In the case of a comatose state, this cause of loss of consciousness should be considered when excluding other possible etiological factors of a sudden unconscious state.

[ 38 ], [ 39 ], [ 40 ], [ 41 ], [ 42 ]

Psychogenic seizure (psychogenic unresponsiveness)

Typical signs of psychogenic "coma" are: forced closing of the eyes when the doctor tries to open them to examine oculomotor functions and pupillary disorders, consensual upward aversion of the eyes when the doctor opens the patient's closed eyelids (eye rolling), the patient's failure to respond to painful stimuli while maintaining the blink reflex when touching the eyelashes. A description of all possible behavioral markers of the presence of a psychogenic seizure in a patient is beyond the scope of this chapter. We will only note that the doctor must develop a certain intuition that allows him to detect some "absurdities" in the neurological status of a patient demonstrating an unconscious state. EEG, as a rule, clarifies the situation if the doctor is able to distinguish an areactive EEG in alpha coma from an EEG of wakefulness with easily detectable activation reactions. Vegetative activation is also characteristic according to the GSR, HR and BP indicators.

[ 43 ], [ 44 ], [ 45 ], [ 46 ], [ 47 ], [ 48 ], [ 49 ]

Diagnostic tests for sudden loss of consciousness

In case of sudden loss of consciousness, the following diagnostic tests are performed:

Laboratory diagnostics

• general and biochemical blood analysis;
• fasting blood sugar;
• urine analysis;
• cerebrospinal fluid analysis;
• screening for metabolic disorders.

Instrumental diagnostics:

• ECG, including Holter monitoring;
• echocardiography;
• cardiovascular tests;
• EEG;
• CT and MRI;
• Aschner's test;
• carotid sinus massage;
• 30-minute standing test;
• Ultrasound Doppler imaging of the main vessels of the head;
• Orthostatic and clinostatic tests;
• angiography of cerebral vessels.

Consultations with the following specialists are shown:

• consultation with a therapist;
• ophthalmologist examination (fundus and visual fields).

[ 50 ], [ 51 ], [ 52 ], [ 53 ]