Literally translated, the word encephalopathy means brain disease. Enképhalos = brain, páthos = disease. Encephalopathy belongs to the diffuse brain injury types.
Encephalopathy is a general term without specifying the cause. The cause is often written before the word encephalopathy.
- Metabolic encephalopathy is a collective term for a reduced functioning of the brain due to an accumulation of waste products from the body, such as in uremic encephalopathy and hepatic encephalopathy. An EEG can show diffuse delay in metabolic encephalopathy; brainwaves with a frequency of 0–4 Hz, or delta waves.
- Uremic encephalopathy is a reduced functioning of the brain due to renal failure with an accumulation of breakdown substances, including serum calcium, which causes uremia to develop. It is the main complication of acute and chronic renal failure and requires urgent dialysis treatment. There is an imbalance in the neurotransmitter amino acids. Glycine levels rise and glutamine and gamma-aminobutyric acid (GABA) levels fall. Dopamine and serotonin levels also change. The symptoms vary from sensory disturbance, severe organic fatigue, seizures to coma, depending on the severity of the kidney failure.
- Viral encephalopathy is a reduced functioning of the brain due to a rare complication of the flu (influenza) and other viral infections. This also includes the corona virus. It is also called an acute necrotizing encephalopathy. Necrotizing means that brain cells die. See also viral encephalitis.
- Hepatic Encephalopathy (HE) is a reduced functioning of the brain due to severe liver failure, for example due to liver cirrhosis. As a result, certain breakdown products can enter the blood circulation, such as ammonia, and the astrocyte brain cells 'swell'. Due to the swelling, the brain cells are less able to transmit signals. A sliding, sometimes not clearly noticeable deterioration in functioning can be seen, sometimes with periodic complaints (episodes). If someone shows a decreased level of consciousness without clear brain area related complaints (focal symptoms), a metabolic encephalopathy (due to accumulation of waste products) should always be kept in mind.
Possible complaints: reduced alertness, confusion, confused speech, dysarthria, word finding problems, change in fine motor skills and coordination, dizziness, daily activities are performed less well (apraxia), mood changes, sleep arrhythmias, sleepiness (hypersomnia) and insomnia, slowness, tremors (flapping tremor in which the fingers of the outstretched arm rise and fall sharply, also called asterixis or negative myoclonus; sudden loss of tone (muscle tone) of wrist and hand muscles and therefore an inability to maintain a fixed position of the hands), increasing disorientation , changed sense of time, fears, decreasing consciousness and finally hepatic coma. Other causes of an increase in ammonia include swallowing too many diuretics or benzodiazepines, valproic acid use (anti-epileptic drug), taking apparently harmless dietary supplements that can lead to liver damage and failure weeks to months after ingestion, infection, constipation and bleeding high in the gastrointestinal tract. A neurological examination and MRI scan do not have to show any abnormalities, diffuse brain damage can be detectable on an EEG. Abnormal laboratory values, such as elevated transaminase levels and elevated ammonia concentration, may not be present in every patient with HE.
- Minimal Hepatic Encephalopathy (MHE) is a lighter variant of hepatic encephalopathy, in which patients with cirrhosis of the liver function apparently well, but in which cognitive impairments can occur.
- Portal Systemic Encephalopathy is the milder variant of hepatic encephalopathy caused by chronic liver disease, usually due to liver cirrhosis, is often characterized by a more insidious development. Subtle cognitive dysfunction or periods (episodes) of "mild" neurological symptoms.
- Anoxic encephalopathy is the acute form of reduced brain function due to oxygen deprivation. This may be as a result of resuscitation, near-drowning, suffocation, cardiac arrhythmias, heart failure, status epilepticus (prolonged seizure of seizures), shock, accident. It can also occur in infants due to oxygen deficiency during pregnancy or at birth (perinatal asphyxia = oxygen deficiency around birth).
Other names are:
- Hypoxic ischemic encephalopathy (HIE)
Brain cells, kidney cells and liver cells are sensitive to oxygen deficiency. Of the brain areas, in particular the basal nuclei (basal ganglia) and in case of extensive oxygen deficiency, the cerebral cortex (especially the temporal lobe), hippocampus, brainstem and thalamus are very sensitive to oxygen deficiency. Damage to the basal nuclei can cause difficulty in movement, dystonia and spasticity. Damage in the cerebral cortex can cause difficulty moving, hearing, seeing and speaking. Brainstem damage can cause problems with all autonomic functions, such as temperature regulation, heart rate, blood pressure, breathing, sucking (in infants) and swallowing. Epilepsy can be a result of anoxic encephalopathy. Damage is not always visible on an MRI scan. Detectable abnormalities on an MRI scan can sometimes only be visible after a few days, but they can also disappear. Read more on our page on oxygen deficiency.
- Post anoxic encephalopathy; the chronic situation of a reduced functioning of the brain due to lack of oxygen, or local and temporary bloodlessness of a brain blood vessel. For a detailed description see above for anoxic encephalopathy. This situation may also occur after circulatory arrest (cardiac arrest and respiratory arrest), near drowning, severe respiratory failure and severe low blood pressure, shock.
- Chronic Traumatic Encephalopathy (CTE); progressive neurological deterioration of the brain due to much head trauma, as can occur in many types of sports. The accumulating effect of repeated head injuries with or without obvious symptoms such as a concussion and how long the exposure to the repeated head injuries took place (for example during the sports career) are determining factors.
Amodio P, del Piccolo F, Marchetti P, Angeli P, Iemmolo R, Caregaro L, et al. Clinical features and survival of cirrhotic patients with subclinical cognitive alterations detected by the number connection test and computerized psychometric tests. Hepatology. 1999;29:1662-7.
Canan Akman, Dilek Ülker Çakır, Serkan Bakırdö˘,Serdal Balcı (May 2019). The Effect of Serum Calcium Levels on Uremic Encephalopathy in Patients with Acute Kidney Injury in the Emergency Department. Medicina (Kaunas, Lithuania) 55(5):204 · May 2019 DOI: 10.3390/medicina55050204
Fraser, C.L.; Arie, A.L. Nervous system complications in uremia. Ann. Intern. Med. 1988, 109, 143–153.
Lameire, N.; Van Biesen,W.; Vanholder, R. Acute renal failure. Lancet 2005, 365, 417–430.
Lizardi-Cervera J, Almeda P, Guevara L, Uribe M. Hepatic encephalopathy: a review. Ann Hepatol. 2003;2:122-30.
Lohr, James W., Batuman, Vecihi. (May 2017). Uremic Encephalopathy: Medscape
Mas A. Hepatic encephalopathy: from pathophysiology to treatment. Digestion. 2006;73 Suppl 1:86-93.
Häussinger D, Schliess F. Astrocyte swelling and protein tyrosine nitration in hepatic encephalopathy. Neurochem Int. 2005;47:64-70.
Häussinger D, Schliess F, Kircheis G. Pathogenesis of hepatic encephalopathy. J Gastroenterol Hepatol. 2002;17 Suppl 3:S256-9.
Smogorzewski, M.J. Central nervous dysfunction in uremia. Am. J. Kidney Dis. 2001, 38 (Suppl. 1), 122–128.
Vaquero J, Chung C, Blei AT. Brain edema in acute liver failure. A window to the pathogenesis of hepatic encephalopathy. Ann Hepatol. 2003;2:12-22.