Encephalopathy

Main nosological forms

The pathology includes several key syndromes depending on the cause of nervous tissue damage:

• Alcoholic encephalopathy. Develops against the background of alcohol consumption. The acute form is associated with a sharp metabolic disturbance, while the chronic form is associated with gradual neurodegeneration. It is often accompanied by polyneuropathy and myelopathy.
• Wernicke's encephalopathy (Gayet-Wernicke syndrome). A life-threatening condition caused by acute or chronic vitamin B1 (thiamine) deficiency. It can be of alcoholic or other origin. The main danger is brainstem edema, which requires emergency treatment to prevent death or severe disability.
• Toxic encephalopathy. Develops upon exposure to various poisons and toxicants, causing complex psychoneurological disorders.
• Angiospastic encephalopathy (renal eclampsia). One of the complications of acute nephritic syndrome, occurring alongside muscle cramps, dyspepsia, and acute left ventricular failure.
• Reversible syndromes. These include posterior reversible encephalopathy syndrome and reversible cerebral vasoconstriction syndrome.

Pathogenesis of hepatic encephalopathy (HE)

In acute liver failure, CNS depression occurs due to a complex neurochemical imbalance and swelling of glial cells (astrocytes).

1. Synthesis of "false" neurotransmitters. An excess of aromatic amino acids penetrates the brain. Octopamine and β-phenylethanolamine are formed from them. They are structurally similar to catecholamines, but have weak activity. By displacing dopamine, adrenaline, and noradrenaline from receptors, they cause suppression of the nervous system.
2. Imbalance of true mediators. The accumulation of tryptophan leads to an excess of serotonin and an increase in the number of 5-HT1 receptors, which directly disrupts sleep-wake cycles. Simultaneously, the level of the main inhibitory neurotransmitter, GABA, increases.
3. Astrocyte swelling. Glial cells accumulate fluid under the action of pro-inflammatory cytokines (in particular, TNF-α) and electrolyte shifts. For example, in viral hepatitis, cells lose potassium while compensatingly accumulating sodium and calcium.

Clinical stages of HE

Symptomatology progresses gradually, affecting intelligence, behavior, and neuromuscular transmission:

• HE-I (Precoma I). Psychoemotional shifts come to the fore: euphoria is quickly replaced by apathy, thinking slows down, and memory lapses appear. Sleep inversion (insomnia at night and drowsiness during the day) is characteristic. Somatic micro-symptoms include frequent yawning, hiccups, dizziness, a tendency to fainting, and mild speech disorders.
• HE-II (Precoma II). Pronounced neurological disorders join in. The patient is disoriented in space, time, and their own personality. Delirium and psychomotor agitation alternating with drowsiness are possible. A specific motor symptom of this stage is asterixis (non-rhythmic, "flapping" tremor of outstretched hands).

CNS involvement in infective endocarditis (IE)

Neurological complications in IE are most often (in 50–80% of cases) of ischemic nature, with small focal lesions predominating. Less frequently (less than 10%), parenchymal or subarachnoid hemorrhages, abscesses, and mycotic aneurysms occur.

Brain MRI is critically important for diagnostics (ESC level of evidence I B).

• Advantages of MRI: The method is more sensitive than CT in detecting infarctions, transient ischemic attacks, and encephalopathy. In complex cases, MRI increases the number of established IE diagnoses by 25%.
• Clinical significance: In patients without neurological symptoms, MRI detects hidden lesions in at least half of the cases, which helps confirm the diagnosis (acts as a Duke minor diagnostic criterion). In symptomatic patients, MRI results directly affect treatment tactics, particularly the timing of cardiac surgery.
• Microhemorrhages: Small areas of hemosiderin deposition are found in 50–60% of patients. This is small vessel pathology which, despite its association with IE, should not be considered a Duke minor criterion.

Class and exam questions

What else to study on this topic

• Mechanisms of development of acute left ventricular failure in acute nephritic syndrome.
• Differential diagnostics of ischemic infarctions and mycotic aneurysms based on MRI data.
• The role of pro-inflammatory cytokines (TNF-α) in astrocyte hyperhydration.
• The impact of brain MRI results on the choice of timing for surgical treatment of infective endocarditis.

Other topics in the "Additional Topics" section

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.