There are congenital and acquired encephalopathies.

The congenital ones can result from genetic defects and developmental brain malformations or be connected with prenatal exposures to damaging factors mainly being brain hypoxia and intracranial birth injury.

As to acquired encephalopathies, they derive from brain exposures to damaging factors all through patient’s life.

There are several types of acquired encephalopathies depending on etiology and pathogenic mechanism:

1. Post-traumatic encephalopathies represent late or remote effects of head injuries.
2. Toxic encephalopathies result from regular exposures to neurotropic agents such as ethyl alcohol, chloroform, barbiturates, lead etc., as well as bacterial poisons.
3. Radiation encephalopathy develops as a result of brain exposure to ionizing radiation.
4. Encephalopathies induced by metabolic disorders resulting from visceral diseases. Various liver diseases accompanied by hepatocytes necrosis and hepatic vascular changes prevent the liver from neutralization of toxic substances which enter the greater blood circulation, poisoning brain and causing hepatic encephalopathy. Metabolic encephalopathies also include nephropathological encephalopathy. Pancreatic encephalopathy is related to pancreatic pathology and often takes form of acute pancreatitis complication.
5. Encephalopathies induced by frequent exposure to higher pressures, frequent jet lags, change of climate conditions.
6. Another yet the most common group comprises so-called vascular encephalopathies which are etiologically connected to inveterate brain blood supply disturbances:

• cerebral atherosclerosis
• arterial hypertension
• cerebral venous stasis (often due to herniated intervertebral disc in the cervical region)
• vegetative-vascular dystonia
• systemic hemodynamic disorders
• systemic diseases of connective tissue
• vasculitides
• blood problems etc.

So what happens in the early stages of cerebral affection?/p>

Diffuse structural brain abnormalities and, accordingly, functional brain disorders.

Precursory symptoms of encephalopathy include nonspecific symptoms such as decline of mental capacity, hypomnesia (especially with recent events), difficulty changing activity types, sleep problem, daytime atony, general fatigue. Complains of diffuse headaches, tinnitus, general weakness, mood swings, irritancy, ill-founded dysphoria, and depression are also often.

Regretfully, at this stage which is also known as the first stage of dyscirculatory encephalopathy, objective diagnostic methods (neurological examination, brain imaging, EEG etc.) might not show any visible changes.

The disease often flows under the cover of Da Costa’s syndrome, depression, insomnia syndrome, chronic fatigue syndrome etc.

As a rule, in these cases a short administration course of vascular, nootropic drugs, vitamins is prescribed. Mostly, it’s a one-time course without patient’s orientation towards further treatment and prevention of deterioration in the condition.

Unfortunately, it’s far too often that the beginning of this formidable process remains underestimated both by the physician and the patient.

If the disease is allowed to advance further, the second stage of dyscirculatory encephalopathy develops. The pathognomonic symptoms continue to persist but in a more distinct way. Idiophrenic symptoms become apparent because of frequent transitory ischemic attacks, strokes etc. A neurological examination can reveal nystagmus, impaired visual and auditory acuity, high muscle tone and tendon reflexes, presence of pathologic pyramidal signs and oral reflexes, coordination disturbances, autonomic imbalances. These disturbances can advance as the underlying disease progresses that comes with encephalopathy. Electroencephalography (EEG) registers disorganization of background rhythms, emergence of pathologic slow waves, and seizure patterns. Computer tomography (CT) and MRI registers signs of diffuse cerebral atrophy: enlargement of cerebral ventricles, subarachnoid space, deepening of sulci cerebri. Distinct neurologic syndromes such as the parkinsonian and pseudobulbar syndromes become apparent. In some patients, mental disabilities can be observed. At this disease stage, both the patients and their family members note significant deterioration in the condition. Patients often need external assistance. Treatment at this stage can improve the condition and contribute to some regression of symptoms. However, it is too late to talk about full restoration of the previous life quality.

The third stage of dyscirculatory encephalopathy is characterized by inherent presence and advancement of neurologic syndromes (amyostatic syndrome, dyscirculatory syndrome, pyramidal signs, pseudobulbar syndrome etc.). Complains persist about headache, loss of memory, tinnitus, insomnia, motor dysfunction. Development of seizures, mental deficiency and loss of the patient’s criticism as to his or her own condition, as well as so-called dementia, is also typical.

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