Progressive obscuration: causes, symptoms, diagnosis

Unlike fainting, hemorrhagic stroke or epilepsy, in which consciousness is suddenly impaired, slowly progressing impairment of consciousness up to deep coma is characteristic of diseases such as exogenous and endogenous intoxication, intracranial space-occupying processes, inflammatory lesions of the nervous system, and, less commonly, other causes.

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The main causes of progressive clouding of consciousness:

1. Exogenous intoxication
2. Intracranial space-occupying process
3. Cerebral sinus(es) thrombosis and stroke
4. Diffuse cerebral ischemia
5. Encephalitis, meningitis
6. Wernicke's encephalopathy
7. Status epilepticus (simple and complex partial seizures)
8. Metabolic disorders
9. Increased blood viscosity (dehydration)

Exogenous intoxication

Undoubtedly, the most common cause of progressive clouding of consciousness (stupor, sopor, coma) is intoxication. The increase in symptoms and their severity are due to the ongoing absorption of the toxic agent (including a 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 may have slow floating movements of the eyeballs, which may be consensual or non-consensual. The oculocephalic reflex, i.e., the reflex diverting of the eyes to the side opposite to the stimulated labyrinth during passive rotation of the patient's head in the lateral or vertical plane, may be absent. The oculocaloric reflex (nystagmus to the side opposite to the side of the stimulated labyrinth) may be absent. The pupils are constricted, pupillary photoreactions are usually preserved. As the coma progresses, the pupils dilate and photoreactions are lost. The phenomenon of decerebrate rigidity may be observed in the extremities. As the impairment of consciousness progresses, muscular hypotonia, areflexia (atonic coma) and critical impairment of vital functions (circulation and respiration) develop. Such dynamics of symptoms indicate progressive dysfunction (inhibition) of the main systems of the brainstem.

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

Some of the above criteria (in particular, bioelectrical silence of the brain, absence of cerebral reflexes, spontaneous breathing and thermoregulation) are not sufficient to diagnose brain death if the patient has been treated with hypothermia or if the comatose state is caused by poisoning with sedatives. In these cases, restoration of cerebral functions is possible even after a fairly long (hours) stay in a state corresponding to the clinical characteristics of extreme 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 an indicator of brain death.

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

Without additional studies, intoxication diagnostics are often impossible. Neuroimaging and transcranial Doppler sonography do not reveal any pathological changes. In case of overdose of barbiturates and benzodiazepines, EEG records predominant beta activity; in case of intoxication with other drugs, diffuse changes in the electrical activity of the brain are detected. These electrophysiological studies reveal only dysfunction of the cortical and stem structures. It is useful to search for traces of the substances or drugs taken in pockets of clothing, in places where medications are stored, in a nightstand, etc. The key diagnostic methods are blood and urine tests for toxic agents; in case of sufficient grounds to suspect intoxication, forced diuresis, administration of antidotes, and hemodialysis are used.

Intracranial space-occupying process

The presence of symptoms of focal brain damage indicates the possibility of an intracranial volumetric process (tumor, hematoma, abscess). The cause of clouding of consciousness may be a rupture of a vessel feeding the tumor, or an increase in cerebral edema, or a violation of venous outflow. Anamnestic information indicating the possibility of brain pathology may be absent, and edema of the optic discs is not always observed. EEG reveals focal and diffuse changes in electrical activity. Lumbar puncture is associated with risk - it is possible to infringe the temporal lobe or wedge the cerebellum into the foramen magnum and compress the brainstem.

The diagnosis is established by neuroimaging studies or cerebral angiography.

Cerebral sinus(es) thrombosis and stroke

In rare cases, progressive clouding of consciousness may be the only symptom of cerebral sinus thrombosis. The onset of the disease may 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, venous sinus thrombosis is the most likely diagnosis. However, cases of "spontaneous" thrombosis are not uncommon, in which case immediate clinical diagnosis is significantly complicated. Erythrocyte pleocytosis may be detected in the cerebrospinal fluid (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 the postpartum period, Behcet's disease, systemic lupus erythematosus, oral contraceptive use, polycythemia, antiphospholipid syndrome, deficiency of antithrombin III, protein C, hemolytic anemia, traumatic brain injury, brain tumors, severe dehydration, cerebral arterial occlusions.

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

Differential diagnosis of dural sinus thrombosis is carried out with impaired cerebral arterial circulation, brain tumor, meningoencephalitis, and eclampsia.

Hemorrhagic stroke is often accompanied by rapid (sometimes instantaneous) development of a comatose state, but slow (subacute) deterioration of the condition and increase in neurological symptoms are possible. Hemisyndromes, bilateral pyramidal signs, meningeal syndrome and cranial nerve damage are revealed. Like ischemic strokes, all other cerebrovascular accidents are more common in mature and old age and develop against the background of known risk factors.

The diagnosis is based on neuroimaging or angiographic studies, with particular attention to blood flow velocity and visualization of the sinuses during the late phase of the pulse wave. If the diagnosis of sinus thrombosis is confirmed, a detailed study of the hemostasis system is mandatory.

Neuroimaging methods are particularly helpful in the diagnosis (the "delta sign" in CT: the contrast agent surrounding the thrombosed sinus forms an A-shape, resembling the Greek letter delta).

Diffuse cerebral ischemia

Diffuse cerebral ischemia associated with anoxia in atrioventricular block or ventricular fibrillation, or, for example, with carbon monoxide poisoning, can lead to progressive clouding of the condition. For diagnosis, anamnesis indicating heart disease, analysis of clinical symptoms, and ECG are important.

Encephalitis, meningitis

Diagnosis of encephalitis in the acute phase is often difficult. It is important to consider the existence of two types of encephalitis. Postinfectious encephalitis (encephalomyelitis) usually develops following an unclear viral infection, usually affecting the respiratory tract and is more often observed in children. It manifests itself primarily by general cerebral symptoms, the most striking of which are lethargy, generalized epileptic seizures and diffuse slowing of EEG activity with no or minimal focal changes. Neurological symptoms vary and reflect the localization of the predominant lesion. Signs of demyelination predominate.

Unlike postinfectious encephalitis, acute viral encephalitis involves focal damage to the brain tissue of one of the hemispheres by a viral agent, which manifests itself (in addition to progressive clouding of consciousness) by focal symptoms, such as aphasia or hemiplegia. We are not considering slow viral infections here.

All viral encephalitis is characterized by an acute onset and fever. The clinical manifestations of most viral encephalitides include headaches, fever, altered level of consciousness, disorientation, speech and behavioral disturbances, and neurological signs such as hemiparesis or epileptic seizures. These symptoms distinguish viral encephalitis from viral meningitis, which usually only presents with neck stiffness, headaches, photophobia, and fever. Some viruses have a tropism for certain types of cells in the brain (poliovirus preferentially affects motor neurons; rabies virus - neurons of the limbic system; damage to cortical neurons leads to epileptic seizures and focal symptoms; herpes symplex affects mainly the temporal lobes (aphasia, anosmia, temporal seizures, other focal symptoms). The epidemiological situation can help in identifying the nature of the virus. Pleocytosis (mainly mononuclear cells) and increased protein content are usually present in the cerebrospinal fluid. Sometimes the cerebrospinal fluid may be normal. EEG and MRI reveal focal changes in the brain. Serological studies of cerebrospinal fluid in the acute period do not always help in diagnosis.

Diagnosis of meningitis

Diagnosis of meningitis is less difficult. In the clinical picture of unconsciousness, meningeal syndrome dominates. Analysis of cerebrospinal fluid solves almost all diagnostic issues.

Wernicke's encephalopathy

Acute or subacute appearance of such pupillary disturbances in a patient as uneven pupil dilation with impaired photoreactions should facilitate the recognition of Wernicke encephalopathy. The diagnosis is confirmed by the appearance of oculomotor disturbances, ataxia, nystagmus, and confusion. These symptoms arise due to damage to the midbrain. At this stage of the disease, only a slight impairment of consciousness is observed, since the activating reticular system has not yet been significantly damaged. Almost all patients have clinical signs of chronic alcohol abuse: mild jaundice of the integument, varicose veins, finger tremors, loss of Achilles reflexes. An objective anamnesis collected from relatives or acquaintances of the patient is important.

Status epilepticus (simple and complex partial seizures)

In a series of partial epileptic seizures (simple or complex), progressive clouding of consciousness may not occur. This condition is discussed in this chapter because the moment of sudden change in the level of consciousness may escape the physician's attention, and the physician may only note a progressive deterioration in the condition. Epileptic syndrome very rarely debuts with status epilepticus; if the physician knows that the patient has a history of epileptic seizures, then the diagnosis of status epilepticus should not cause difficulties. The leading symptoms are characteristic stereotypical convulsions and movements. In the case of status epilepticus in simple partial seizures, these are nystagmoid upward twitching of the eyes at a frequency of about 3 per second and, sometimes, contraction of the facial muscles. In complex partial seizures, well-known chewing or swallowing movements and/or any stereotypical movements made by both hands are observed, sometimes vocalization. The diagnosis is confirmed by the results of an EEG study: periods of generalized spike-wave activity with a frequency of 3 per second or bilateral acute wave-slow wave complexes in the temporal leads are recorded. Although this condition develops acutely, if no help is provided for some reason, epileptic status can lead to progressive cerebral edema and death of the patient.

Metabolic disorders

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

Increased blood viscosity (dehydration)

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

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