Progressive clouding of consciousness: causes, symptoms, diagnosis

Unlike fainting, hemorrhagic stroke or epilepsy, in which consciousness is disturbed suddenly, a slowly progressive impairment of consciousness down to a deep coma is characteristic of such diseases as exogenous and endogenous intoxication, intracranial volumetric processes, inflammatory lesions of the nervous system, and less often other causes.

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

The main causes of progressive obscuration of consciousness:

1. Exogenous intoxication
2. The intracranial volumetric process
3. Thrombosis of the cerebral sinus (s) and stroke
4. Diffuse cerebral ischemia
5. Encephalitis, meningitis
6. Encephalopathy Wernicke
7. Epileptic status (simple and complex partial seizures)
8. Metabolic disorders
9. Increase in blood viscosity (dehydration)

Exogenous intoxication

Undoubtedly, the most frequent cause of progressive obscuration of consciousness (stunning, sopor, coma) is intoxication. The increase in symptoms and their severity are due to the continued absorption of a toxic agent (including drug or alcohol) and its cumulative dose. The presence and nature of the response to external stimuli determines the depth of loss of consciousness. The patient can observe slow floating movements of eyeballs, which can be friendly or not friendly. There may be no oculocephalic reflex, that is, a reflex eye-opening away from the stimulated labyrinth with a passive rotation of the patient's head in the lateral or vertical plane. There may be no oculocaloric reflex (nystagmus in the side opposite to the side of the stimulated labyrinth). Pupils are narrowed, pupillary photoreactions are usually preserved. As the coma progresses, pupils expand and lose photoreactions. In the limbs, there may be a phenomenon of decerebrate rigidity. With the progression of the disorder of consciousness, muscle hypotension, areflexia (atonic coma), and critical disruption of vital functions (blood circulation and respiration) develop. Such a dynamics of symptoms indicates a progressive dysfunction (oppression) of the main systems of the brain stem.

Complete absence of clinical signs of the functional activity of the brain (lack of independent breathing, loss of ability to thermoregulation, extinction of all cerebral reflexes - corneal, cough, oculocardial, oculovestibular, photoreaction of pupils, swallowing) usually (but not always) indicates its irreversible damage, is defined as a transcendental coma and is considered as one of the criteria for the state of brain death. The diagnostic criteria for brain death also include bioelectric silence of the brain (isoelectric line on the EEG); absence of cerebral blood flow (phenomenon of pseudothrombosis with carotid and vertebral angiography); absence of a cerebral arteriovenous difference in oxygen.

Some of these criteria (in particular, bioelectric silence of the brain, absence of cerebral reflexes, independent breathing and thermoregulation) are not sufficient for diagnosing brain death if the patient has had hypothermia or if the coma is caused by poisoning with sedatives. In these cases, it is possible to restore the cerebral functions even after a sufficiently long (hours) stay in a state corresponding to the clinical characteristics of the transcendental coma. Due to the fact that this condition is not irreversible, it is defined as a coma with loss of vegetative functions and is not considered as an indicator of brain death.

Intoxication as a cause of impaired consciousness should be considered in the absence of other possible etiological factors of sopor or coma.

Without further research, the diagnosis of intoxication is often impossible. With neuroimaging and transcranial dopplerography, there are no pathological changes. When an overdose of barbiturates and benzodiazepines on the EEG, the predominant beta activity is recorded; when intoxication with other drugs, diffuse changes in brain electrical activity are detected. These electrophysiological studies reveal only the dysfunction of cortical and stem structures. It is useful to search for traces of the substances or preparations taken in the pockets of clothing, in places where medicines are stored, in the bedside table, etc. The key diagnostic methods are blood and urine tests for the presence of toxic agents; in the case of sufficient grounds to assume intoxication, forced diuresis, administration of antidotes, hemodialysis is used.

The intracranial volumetric process

The presence of symptoms of focal brain lesions indicates the possibility of intracranial volumetric process (tumor, hematoma, abscess). The cause of the confusion of consciousness may be the rupture of the vessel feeding the tumor, or the buildup of cerebral edema, the violation of venous outflow. Anamnestic information indicating the possibility of cerebral pathology may be absent, and edema of optic discs is not always observed. On the EEG, focal and diffuse changes in electrical activity are revealed. Carrying out a lumbar puncture is fraught with risk - it is possible to infringe the temporal lobe or wedge the cerebellum into the large occipital foramen and squeeze the brainstem.

Diagnosis is established in neuroimaging studies or cerebral angiography.

Thrombosis of the cerebral sinus (s) and stroke

In rare cases, a progressive obscuration of consciousness may be the only symptom of thrombosis of the cerebral sinus. The onset of the disease can be acute, subacute or chronically progressive. In most cases, the first symptoms are epileptic seizures and mono- or hemiparesis. If these symptoms occur during labor, thrombosis of the venous sinus is the most likely diagnosis. However, cases of "spontaneous" thrombosis are not uncommon, in such situations, immediate clinical diagnosis is significantly hampered. In the cerebrospinal fluid, erythrocyte pleocytosis can be detected (which, as a rule, gives rise to the erroneous assumption of subarachnoid hemorrhage).

Causes of aseptic thrombosis of large sinuses of the brain: pregnancy and postpartum period, Behcet's disease, systemic lupus erythematosus, oral contraceptive use, polycythemia, antiphospholipid syndrome, deficiency of antithrombin III, protein C, hemolytic anemia, brain injury, brain tumors, severe dehydration, cerebral arterial occlusions.

Causes of septic thrombosis: general and local infections, diseases of the ear, throat, nose, teeth; furuncles of the face, brain abscesses, osteomyelitis, pneumonia, postpartum endometritis, septic conditions.

Differential diagnosis of thrombosis of dural sinuses is performed with violation of the arterial blood circulation of the brain, brain tumor, meningoencephalitis, eclampsia.

Hemorrhagic stroke is often accompanied by rapid (sometimes instantaneous) development of a coma, but a slow (subacute) deterioration in the condition and growth of neurological symptoms is possible. There are hemisyndromes, bilateral pyramidal signs, meningeal syndrome and defeats of cranial nerves. Like ischemic strokes, all other vascular brain accidents are more common in mature and older age and develop against the background of known risk factors.

The diagnosis is based on the results of neuroimaging or angiographic studies, with particular attention to the blood flow velocity and the visualization of sinuses during the late phase of the pulse wave. In case of confirmation of the diagnosis of sinus thrombosis, a detailed study of the hemostatic system should be mandatory.

Diagnosis is especially assisted by methods of neurovisualization ("delta mark" in CT: the contrast medium, surrounding the thrombosed sine, forms a figure A, reminiscent of the Greek letter delta).

Diffuse cerebral ischemia

Diffuse cerebral ischemia associated with an anoxia in case of atrioventricular block or ventricular fibrillation, or, for example, with carbon monoxide poisoning, can lead to a progressive diminution of the condition. An anamnesis with an indication of heart disease, an analysis of clinical symptoms, an ECG is important for diagnosis.

Encephalitis, meningitis

Diagnosis of encephalitis in the acute phase is often not easy. It is important to consider the existence of two variants of encephalitis. Postinfectious encephalitis (encephalomyelitis) usually develops after an unclear viral infection that usually affects the respiratory tract and is more common in children. It manifests itself primarily by cerebral symptoms, the most striking of which are inhibition, generalized epileptic seizures and diffuse slowing of EEG activity without or with minimal focal changes. Neurological symptoms vary and reflect the localization of the primary lesion. The signs of demyelination predominate.

In contrast to postinfection encephalitis in viral acute encephalitis, focal damage occurs to the brain tissue of one of the hemispheres by a viral agent, which manifests (in addition to progressive obscuration of the mind) focal symptoms, for example - aphasia or hemiplegia. We do not consider slow viral infections here.

Any viral encephalitis is characterized by acute onset and fever. Clinical manifestations of most viral encephalitis include headaches, fever, impaired consciousness, disorientation, speech and behavioral disorders, and neurological signs such as hemiparesis or epileptic seizures. These symptoms distinguish viral encephalitis from viral meningitis, which usually reveals only rigidity of the neck muscles, headaches, photophobia and fever. Individual viruses have tropism in relation to particular types of cells in the brain (poliovirus primarily affects motoneurons, rabies virus - neurons of the limbic system, damage to cortical neurons leads to epileptic seizures and focal symptoms, herpes symplex affects mainly temporal lobes (aphasia, anosmia, temporal seizures, other focal symptoms.) The epidemiological situation can help in the detection of the nature of the virus.In the cerebrospinal fluid, pleocytosis (predominantly mononuclear cells), increased with squirrel holding. Sometimes cerebrospinal fluid may be normal. EEG and MRI detected focal changes in the brain. Serological studies of CSF during the acute period is not always assist diagnosis.

Diagnosis of meningitis

Diagnosis of meningitis is less difficult task. The clinical picture of the unconscious state is dominated by the meningeal syndrome. Analysis of cerebrospinal fluid resolves almost all diagnostic issues.

Encephalopathy Wernicke

Acute or subacute appearance in the patient of such pupillary disorders as uneven dilatation of pupils with photoreaction disturbance should facilitate recognition of Wernicke's encephalopathy. The diagnosis is confirmed by the appearance of oculomotor disorders, ataxia, nystagmus, deafness. These symptoms result from damage to the midbrain. At this stage of the disease there is only a slight disturbance of consciousness, since the activating reticular system has not been severely damaged yet. Almost all patients have clinical signs of chronic alcohol abuse: mild icterus of the integument, widening of the veins, tremor of the fingers, loss of achilles reflexes. An objective anamnesis, collected from relatives or friends of the patient, is important.

Epileptic status (simple and complex partial seizures)

With a series of partial epileptic seizures (simple or complex), progressive obscuration of consciousness may not be. This condition is discussed in this chapter because the very moment of a sudden change in the level of consciousness can elude the doctor's attention and the doctor states only an increasing deterioration in the state. Epileptic syndrome rarely debuts with epileptic status; if the doctor is aware of the presence of epileptic seizures in a given patient, then the diagnosis of the status epilepticus should not be called for. The leading symptoms are characteristic stereotyped convulsions and movements. In the case of an epileptic status with simple partial seizures, this is a nystagmoid eye twitching upwards with a frequency of about 3 per second and, sometimes, a contraction of the facial muscles. In complex partial seizures, there are well-known chewing or swallowing movements and (or) any stereotyped movements produced by both hands, sometimes vocalization. The diagnosis is confirmed by the results of the EEG study: the periods of generalized spike-wave activity at a frequency of 3 per second or bilateral complexes are observed, an acute wave-slow wave in the temporal leads. Although this condition develops sharply, with non-presentation for some reason of help, the status epilepticus can lead to progressive brain edema and the patient's death.

Metabolic disorders

Clinical manifestations of metabolic disturbances are very nonspecific, and their diagnosis is possible only with a wide range of laboratory tests. The most common cause is hyperglycemia (diabetes mellitus), with a hyperosmolar, rather than a ketoacidotic form, more common. With the exception of diabetes, consultation of the therapist and screening of other metabolic disorders (uremia, liver failure, etc.) is necessary.

Increase in blood viscosity (dehydration)

Often, elderly patients who do not receive adequate care are taken to the hospital at the stage of progressive obscuration of consciousness, which develops as a result of dehydration. This is possible, for example, in patients suffering from dementia - they just may forget to drink. However, this syndrome can develop not only in a patient who is at home. With such a situation, a neurologist may encounter in a surgical hospital, when in a postoperative period a patient who is on parenteral nutrition does not receive enough fluid. Excessive use of diuretics in an elderly patient, especially suffering from diabetes mellitus (sometimes unrecognized), is always fraught with deterioration.

Progressive deterioration of consciousness may be due to other physical diseases (heart failure, pneumonia), which are usually accompanied by a characteristic clinical picture and the corresponding results of a paraclinical examination (ECG, chest X-ray, etc.).