Sudden loss of consciousness

In most cases of sudden loss of consciousness, it is rather difficult to obtain anamnestic information about the events immediately preceding this. The long-term history, which may contain diagnostically useful information, may also be unknown. A sudden loss of consciousness can be short-term or persistent and can have both neurogenic (neurogenic syncope, epilepsy, stroke), and somatogenic (cardiac abnormalities, hypoglycemia, etc.).

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

The main causes of sudden loss of consciousness:

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

Fainting

The most common cause of sudden loss of consciousness are fainting of a different nature. Often there is not only the fall of the patient (acute postural insufficiency), but also loss of consciousness for a period measured in seconds. Prolonged loss of consciousness with fainting is rarely observed. The most common types of syncope are: vasovagal (vasodepressor, vasomotor) syncope; hyperventilation syncope; syncope associated with carotid sinus hypersensitivity (GCS syndrome); cough syncope; nocturic; hypoglycemic; orthostatic syncope of different genesis. For all fainting, the patient notes the lipotymic (pre-unconscious) state: feeling of nausea, nonsystematic dizziness, and foreboding of loss of consciousness.

The most common type of fainting is a vasodepressor (simple) syncope, usually provoked by certain stressful effects (waiting for pain, blood type, 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 impairment, muscle spasms (tetanic convulsions), palpitations.

Nikturic syncope is characterized by a typical clinical picture: it is usually night episodes of unconsciousness that occur during or (more often) immediately after urination, due to the need for which the patient has to stand up at night. They sometimes have to be differentiated from epileptic seizures with the help of a traditional EEG study.

Massage of the carotid sinus helps to reveal the hypersensitivity of the carotid sinus. A history of such patients often reveals poor tolerance of tight collars and ties. Compression of the carotid sinus with the doctor’s hand in such patients can provoke dizziness and even faint with a decrease in blood pressure and other vegetative manifestations.

Orthostatic hypotension and syncope can have both neurogenic (in the picture of primary peripheral autonomic failure) and somatogenic origin (secondary peripheral failure). The first variant of peripheral autonomic insufficiency (PVN) is also called progressive autonomic insufficiency. It has a chronic course and is represented by such diseases as idiopathic orthostatic hypotension, stri-nigral degeneration, Shaya-Drader syndrome (variants of multiple systemic atrophy). Secondary PVN has an acute course and develops on the background of somatic diseases (amyloidosis, diabetes, alcoholism, chronic renal failure, porphyria, bronchus carcinoma, leprosy, and other diseases). Dizziness in the pattern of PVN is always accompanied by other characteristic manifestations of PVN: anhidrosis, fixed heart rhythm, etc.

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

The deficit of adrenergic effects and, consequently, the clinical manifestations of orthostatic hypotension are possible in the picture of adisson's disease, in some cases the use of pharmacological agents (gnbgloblokatory, hypotensive agents, dopaminomimetiki type nakoma, madopar and some dopamine receptors agonost).

Orthostatic circulatory disorders also occur with organic pathology of the heart and blood vessels. Thus, syncope may be a frequent manifestation of obstructed aortic current in aortic stenosis, ventricular arrhythmia, tachycardia, fibrillation, sick sinus syndrome, bradycardia, atrioventricular blockade, myocardial infarction, long QT interval syndrome, etc. Almost every patient with significant aortic stenosis has a systolic murmur and a “cat's purr” (it is easier to listen in standing 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 of development of orthostatic hypotension and syncope occurs when using ganglioblokatorov, some tranquilizers, antidepressants and anti-adrenergic agents.

With a drop in blood pressure against the background of a current cerebrovascular disease, ischemia often develops in the brain stem region (cerebrovascular syncope), manifested by characteristic stem phenomena, non-systemic vertigo, and fainting (Unterharnscheidt syndrome). Drop attacks are not accompanied by lipotymia and fainting. Such patients need careful examination to rule out cardiogenic syncope (cardiac arrhythmias), epilepsy, and other diseases.

Predisposing factors to lipo-chemistry 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 a suspected or existing deficit of blood volume (hypovolemic syncope), unusual tachycardia is of diagnostic importance while sitting in bed. Hypoglycemia is another important factor predisposing to syncope.

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

The Valsalva maneuver is most informative in patients with nykturicheskie, cough fainting 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 of difficulties should not cause. In fact, the situation is often complicated by the fact that 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 be confusing to the doctor when it comes to a young patient. Useful diagnostic information provides an increase in blood creatine phosphokinase level. Post-attack drowsiness, epileptic activity in EEG (spontaneous or provoked by enhanced hyperventilation or sleep deprivation) and observation of an attack help correct diagnosis.

[12], [13], [14]

Intracerebral hemorrhage

Intracerebral hemorrhage occurs, as a rule, in patients with chronic arterial hypertension. The reason is rupture of the aneurysm of a sclerotic modified small caliber vessel; the most frequent localization is the basal ganglia, the bridge and the cerebellum. The patient is in a somnolent or unconscious state. Most likely the presence of hemiplegia, which can be detected in a patient in a comatose state, by unilateral reduction of muscle tone. Deep reflexes on the side of paralysis can be reduced, but Babinski’s symptom is often positive. In hemispheric hemorrhage, it is often possible to identify friendly withdrawal of the eyeballs in the direction of the lesion. With hemorrhage in the area of the bridge is observed tetraplegia with bilateral extensor reflexes and various oculomotor disorders. With a friendly eye abstraction, the gaze is directed to the side opposite to the bridge lesion, in contrast to the hemispheric hemorrhage, when the gaze is directed to the lesion side (the safe hemispheric oculomotor system pushes the eyeballs to the opposite side). "Floating" friendly or non-friendly eye movements are often observed and do not represent diagnostic value in the sense of determining the localization of the lesion within the brainstem. Spontaneous nystagmus is more often horizontal with a bridging lesion and vertical with localization of a lesion in the region of the midbrain.

Ocular bobbing is most often observed during compression of the lower sections of the brain stem by the cerebellar volumetric process. This symptom is often (but not absolutely unequivocal) a sign of irreversible dysfunction of the brain stem. The extinction of the oculocephalic reflex corresponds to the deepening of the coma.

Often there are pupillary disorders. Bilateral miosis with intact photoreactions indicates damage at the level of the bridge, and sometimes the safety of photoreactions can be ascertained only with a magnifying glass. Unilateral mydriasis is observed with damage to the nucleus of the third cranial nerve or its vegetative efferent fibers in the lid of the midbrain. Bilateral mydriasis is a formidable, prognostic unfavorable sign.

Liquor is in most cases stained with blood. In neuroimaging studies, the location and size of the hemorrhage and its impact on brain tissue are clearly defined, and the need for neurosurgical intervention is resolved.

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

Subarachnoid hemorrhage (SAH)

Note that some patients after subarachnoid hemorrhage are found in an unconscious state. Rigidity of the occipital muscles is almost always detected, and with lumbar puncture, liquor stained with blood is obtained. Centrifugation of the cerebrospinal fluid is necessary, since during the puncture the needle can get into the blood vessel, and the cerebrospinal fluid will contain ground blood. Neuroimaging reveals a subarachnoid hemorrhage, the volume and localization of which sometimes can even be judged on the prognosis. With a large volume of blood spilled, the development of arterial spasm should be expected in the next few days. Neuroimaging also allows timely detection of reported hydrocephalus.

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

Basilar artery thrombosis

Thrombosis of the basilar artery with no prior symptoms is rare. Such symptoms usually occur for several days before the disease; this is speech blurring, doubling, ataxia, or paresthesias in the limbs. The severity of these precursor symptoms usually fluctuate until suddenly or quickly there is a loss of consciousness. Collecting anamnesis in such cases is very essential. Neurological status is similar to that of hemorrhage into the bridge. In such cases, Doppler ultrasound is most valuable, since it allows to reveal the characteristic pattern of impaired blood flow in large vessels. The diagnosis of basilar artery thrombosis is particularly likely when high resistance is detected in the vertebral arteries, which is found even with occlusion of the basilar artery. Transcranial Doppler Ultrasound directly measures the blood flow in the basilar artery and is an extremely useful diagnostic procedure for patients who need angiographic examination.

When 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 genesis.

In acute massive stenosis or occlusion of a vertebrobasilar vessel, urgent measures can help a patient — 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 missing (there may be no witnesses). The patient is found in a coma with the symptoms described above, presented in various combinations. Each patient who is in a coma should be examined and examined in order to identify possible damage to the soft tissues of the head and bones of the skull. With traumatic brain injury may develop epi- or subdural hematoma. These complications should be suspected if coma deepens and hemiplegia develops.

Metabolic disorders

Hypoglycemia (insulinoma, alimentary hypoglycemia, post-operation gastrectomy, severe damage to the parenchyma of the liver, insulin overdose in diabetic patients, hypofunction of the adrenal cortex, hypofunction and atrophy of the anterior pituitary gland) can develop a neurogenic form of neuropathy, hypofunction and atrophy of the anterior pituitary gland), if it is developed, can contribute to the neurogenic of the adrenal gland, hypofunction and atrophy of the anterior pituitary gland), if it is developed, can contribute to the neurogenic of the adrenal gland, hypofunction and atrophy of the anterior pituitary anterior lobe; lead to soporous and coma. Another common metabolic cause is uremia. But it leads to a gradual deterioration of the state of consciousness. In the absence of anamnesis, the state of stunning and stupor is sometimes seen. Laboratory tests of blood for screening metabolic disorders are crucial in diagnosing the metabolic causes of sudden loss of consciousness.

[35], [36], [37]

Exogenous intoxication

More often it leads to subacute episodes of 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 a coma, this cause of loss of consciousness should be considered with the exclusion of other possible etiological factors of a sudden unconscious state.

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

Psychogenic seizure (psychogenic areactivity)

Typical signs of a psychogenic “coma” are: forcibly closing the eyes when the doctor tries to open them for the study of oculomotor functions and pupillary disorders, friendly looking away when the doctor opens the patient’s squint eyelids (rolling eyes), the patient does not respond to painful stimuli while the blink reflex is intact when touched up lashes. A description of all possible behavioral markers for a patient with a psychogenic seizure is beyond the scope of this chapter. We only note that the doctor must develop a certain intuition, allowing to catch some of the "absurdities" in the neurological status of the patient, demonstrating an unconscious state. The EEG, as a rule, clarifies the situation if the doctor is able to distinguish the reactive EEG during alpha-coma from the wakeful EEG with easily determined activation reactions on it. Vegetative activation in terms of RAG, heart rate and blood pressure is also characteristic.

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

Diagnostic tests for sudden loss of consciousness

When a sudden loss of consciousness is carried out the following diagnostic tests:

Laboratory diagnosis

• general and biochemical blood test;
• fasting blood sugar;
• Analysis of urine;
• liquor study;
• screening for metabolic disorders.

Instrumental diagnostics:

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

The consultations of the following specialists are shown:

• general practitioner consultation;
• examination of the oculist (fundus and field of view).

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