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

The main causes of sudden loss of consciousness:

  • Syncope of neurogenic and other nature
  • Epilepsy
  • intracerebral hemorrhage
  • subarachnoid hemorrhage
  • Thrombosis of the basilar artery
  • Traumatic brain injury
  • Metabolic disorders (most often hypoglycemia and uremia)
  • Exogenous intoxication (more often develops subacutely)
  • Psychogenic seizure

Fainting as a cause of sudden loss of consciousness

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. Prolonged loss of consciousness during fainting is rare. The most common types of fainting are:

  • vasovagal (vasodepressor, vasomotor) syncope;
  • hyperventilation syncope;
  • fainting associated with hypersensitivity of the carotid sinus (GCS syndrome);
  • cough syncope;
  • nocturic;
  • hypoglycemic;
  • orthostatic fainting of various origins.

With all fainting, the patient notes a lipothymic (pre-fainting) state: a feeling of lightheadedness, unsystematic dizziness and a premonition of loss of consciousness.

The most common type of fainting is vasodepressor (simple) syncope, usually provoked by certain stressful influences (anticipation of pain, the sight of blood, fear, stuffiness, etc.). Hyperventilation syncope is caused 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 these are nocturnal episodes of loss of consciousness that occur 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 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 can have both neurogenic (in the picture of primary peripheral autonomic failure) and somatogenic origin (secondary peripheral failure). The first variant of peripheral autonomic failure (PVF) is also called progressive autonomic failure. It has a chronic course and is represented by diseases such as idiopathic orthostatic hypotension, strionigral degeneration, Shy-Drager syndrome (variants of multiple system atrophy). Secondary PVN 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 PVN is always accompanied by other characteristic manifestations of PVN: anhidrosis, fixed heart rate, 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.

A deficiency of adrenergic influences and, therefore, clinical manifestations of orthostatic hypotension are possible in the picture of Addison’s disease, in some cases, the use of pharmacological agents (gpnglioblockers, antihypertensive drugs, dopaminomimetics such as Nakoma, 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’s purr” (easier to hear in a standing position or in the “a la your” position).

Sympathectomy can lead to insufficient venous return and, as a result, to orthostatic circulatory disorders. The same mechanism for the development of orthostatic hypotension and fainting occurs when using ganglion blockers, some tranquilizers, antidepressants and anti-adrenergic agents.

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

Predisposing factors to lipothymia and orthostatic fainting 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 existing blood volume deficiency (hypovolemic syncope), unusual tachycardia while sitting in bed is of important diagnostic value. Hypoglycemia is another important predisposing factor to fainting.

Orthostatic syncope often requires a differential diagnosis with epilepsy. Fainting is extremely rare in a horizontal position and never occurs during sleep (at the same time, they are possible when getting out of bed at night). Orthostatic hypotension can be easily detected on a rotary table (passive repositioning). Postural hypotension is considered established when systolic blood pressure drops by at least 30 mmHg. column when moving from a horizontal to a vertical position. A cardiac examination is necessary to exclude the cardiogenic nature of these disorders. The Aschner test has a certain diagnostic value (a slowdown of the pulse by more than 10 – 12 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, performing the Valsalva maneuver, 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.

Generalized epileptic seizure as a cause of sudden loss of consciousness

At first glance, diagnosing the postictal state should not cause any 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. Characteristic symptoms such as biting the tongue or lips may be absent. Involuntary urination can occur for many reasons. Post-attack hemiparesis can mislead the doctor if we are talking about a young patient. Useful diagnostic information is provided by an increase in blood creatine phosphokinase levels. Post-ictal somnolence, epileptic EEG activity (spontaneous or provoked by increased hyperventilation or sleep deprivation) and observation of the seizure help in the correct diagnosis.

intracerebral hemorrhage

Intracerebral hemorrhage occurs, as a rule, in patients with chronic arterial hypertension. The cause is a rupture of an aneurysm of a small-caliber sclerotically modified vessel; the most common locations are the basal ganglia, pons, and cerebellum. The patient is in a doubtful or unconscious state. The most likely presence is hemiplegia, which can be detected in a comatose patient by a unilateral decrease in muscle tone. Deep reflexes on the side of the paralysis may be reduced, but the Babinski sign is often positive. With hemispheric hemorrhage, it is often possible to detect a concomitant abduction of the eyeballs towards the lesion. With hemorrhage in the area of ​​the bridge, tetraplegia with bilateral extensor reflexes and various oculomotor disorders is observed. With concomitant eye abduction, gaze is directed in the direction opposite to the side of the pontine lesion, in contrast to hemispheric hemorrhage, when gaze is directed towards the lesion (the intact hemispheric oculomotor system “pushes” the eyeballs to the opposite side). “Floating” friendly or unfriendly eye movements are often observed and do not represent diagnostic value in the sense of determining the localization of the lesion within the brain stem. Spontaneous nystagmus is more often horizontal with pontine lesions and vertical with localization of the lesion in the midbrain region.

Ocular bobbing is most often observed when the lower brainstem is compressed by a cerebellar space-occupying process. This symptom is often (but not absolutely) a sign of irreversible brainstem dysfunction. The extinction of the oculocephalic reflex corresponds to the deepening of the coma.

There are often pupillary abnormalities. Bilateral miosis with intact photoreactions indicates damage at the level of the bridge, and sometimes the integrity of photoreactions can only be verified with the help of 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.

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

Subarachnoid hemorrhage (SAH)

Note that some patients are found unconscious after subarachnoid hemorrhage. Almost always, a stiff neck is detected, and a lumbar puncture produces blood-stained cerebrospinal fluid. Centrifugation of the cerebrospinal fluid is necessary, since during a puncture the needle may enter a blood vessel, and the cerebrospinal fluid will contain blood. Neuroimaging reveals subarachnoid hemorrhage, the volume and location of which can sometimes even determine the prognosis. With a large volume of bleeding, arterial spasm should be expected to develop over the next few days. Neuroimaging also allows early detection of communicating hydrocephalus.

Thrombosis of the basilar artery

Basilar artery thrombosis without previous symptoms is rare. Such symptoms usually exist for several days before illness; this is slurred speech, double vision, ataxia or paresthesia in the limbs. The severity of these warning symptoms usually fluctuates until sudden or rapid loss of consciousness occurs. Taking an anamnesis in such cases is very important. The neurological status is similar to that of hemorrhage into the pons. In such cases, Doppler ultrasound is most valuable, since it allows one to identify a characteristic pattern of blood flow disturbances in large vessels. The diagnosis of basilar artery thrombosis is especially likely when recording high resistance in the vertebral arteries, which is found even with occlusion of the basilar artery. Transcranial Doppler ultrasound allows direct measurement of blood flow in the basilar artery and is an extremely useful diagnostic procedure for patients who require angiographic testing.

Angiography of the vessels of the vertebrobasilar system reveals stenosis or occlusion in this basin, in particular, “occlusion of the apex of the basilar artery,” which has an embolic origin.

In case of acute massive stenosis or occlusion of the vertebrobasilar vessel, the patient can be helped by urgent measures – either intravenous infusion therapy with heparin or intra-arterial thrombolytic therapy.

Traumatic brain injury

Information about the injury itself may be missing (there may be no witnesses). The patient is found in a coma with the symptoms described above, presented in various combinations. Each patient in a comatose state should be examined and examined to identify possible damage to the soft tissues of the head and bones of the skull. With 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, nutritional hypoglycemia, condition after gasterectomy, severe damage to the liver parenchyma, 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 persons predisposed to it or lead to stuporous and comatose states. Another common metabolic cause is uremia. But it leads to a gradual deterioration in the state of consciousness. In the absence of anamnesis, a state of stupor and stupor is sometimes visible. Laboratory blood tests to screen for metabolic disorders are crucial in diagnosing the metabolic causes of sudden loss of consciousness.

Exogenous intoxication

More often it leads to subacute deterioration of consciousness (psychotropic drugs, alcohol, drugs, etc.), but sometimes it can create the impression of a sudden loss of consciousness. In the case of coma, this cause of loss of consciousness should be considered to the exclusion of other possible etiological factors of sudden unconsciousness.

Psychogenic seizure (psychogenic unresponsiveness)

Typical signs of a psychogenic “coma” are: forced closing of the eyes when the doctor tries to open them to study oculomotor functions and pupillary disorders, friendly upward movement of the eyes when the doctor opens the patient’s closed eyelids (rolling the eyes), the patient’s non-reaction to painful stimuli while the blink reflex is preserved when touched up to 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. Let us 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. An EEG, as a rule, clarifies the situation if the doctor is able to distinguish a non-reactive EEG during alpha coma from a waking EEG with easily detectable activation reactions on it. Autonomic activation in terms of GSR, heart rate and blood pressure is also characteristic.

Diagnostic tests for sudden loss of consciousness

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

Laboratory diagnosis

  • general and biochemical blood test;
  • fasting blood sugar;
  • Analysis of urine;
  • cerebrospinal fluid examination;
  • screening for metabolic disorders.

Instrumental diagnostics:

  • ECG, including Holter monitoring;
  • echocardiography;
  • cardiovascular tests;
  • EEG;
  • CT and MRI;
  • Aschner sample;
  • carotid sinus massage;
  • 30-minute standing test;
  • Doppler ultrasound 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;
  • examination by an ophthalmologist (fundus and visual field).

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