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Toxic Encephalopathy

Toxic encephalopathy is a distinct clinical entity characterized by brain injury following exposure to a toxic substance, predominantly organic solvents, heavy metals, and other occupational compounds. Exposure in the work setting is the primary risk factor, and the clinical presentation depends on the dose and potency of the substance. A thorough clinical workup, with an emphasis on patient history, is the key step in making the diagnosis.


Toxic encephalopathy is a term denoting brain injury and potentially life-threatening central nervous system (CNS) damage that can be induced by various toxic compounds. In the literature, the majority of patients suffer from this condition as a result of exposure to organic solvents or other lipophilic neurotoxins in the occupational setting [1] [2] [3], whereas several gases, chemotherapeutic drugs (such as L-asparagine, methotrexate), bacterial neurotoxins, recreational drugs, and ethanol can all be the underlying cause [4] [5] [6] [7]. Signs and symptoms of toxic encephalopathy appear in proportion to the amount of toxin that reaches the CNS, as well as the rate at which it damages the brain, thus a broad classification into acute and chronic forms has been made [1] [2] [3] [6]:

  • Acute toxic encephalopathy is characterized by the development of acute alterations in consciousness, euphoria, seizures, stupor and in most severe cases, coma and even sudden death [1] [7]. Symptoms appear within days or weeks after the initial toxin exposure. Some of the most important toxins are gasses (such as carbon monoxide (CO), cyanide, and hydrogen sulfide) and heavy metals, both inorganic and organic (mercury, lead, and tin) [1] [2].
  • Chronic toxic encephalopathy, on the other hand, causes a slowly progressive cognitive, intellectual, emotional and physical decline due to chronic exposure (months or even years) to a neurotoxic substance [1] [3] [6]. The severity of toxicity is divided into three stages. Initial symptoms (stage I) include mood changes and trouble concentrating, while attention and memory deficits, together with impaired learning, are typically encountered in stages II and III when a severe decline in psychomotor function is observed [1] [2] [3] [6].

In addition, toxic encephalopathy can also manifest through a specific subset of symptoms, such as cerebellar dysfunction (gait disturbances, ataxia, nystagmus, etc.) in methyl mercury (known as Minamata disease), methyl bromide, or organic tin toxicity, whereas chronic exposure to manganese produces Parkinson-like complaints accompanied by psychosis and various other neuropsychiatric symptoms, as it greatly interferes with the function of globus pallidus [1].

  • Persistent symptoms developed, an average, 16 years after exposure onset and included impaired memory (38), altered mood (21), imbalance (18), and headache (17).[ncbi.nlm.nih.gov]
  • A 41 yr-old male presented with dizziness, headache, and diplopia after exposure to the detergent without protective equipment.[ncbi.nlm.nih.gov]
  • The main clinical manifestation is headache accompanied by intracranial hypertension.[ncbi.nlm.nih.gov]
  • In particular they suffered less from fatigue, headache, and dizziness. When diagnosed they had an average of seven out of ten typical neurasthenic symptoms included in the toxic encephalopathy syndrome.[ncbi.nlm.nih.gov]
  • All were female workers who had been in contact with DCE and subsequently had had seizures or symptoms of intracranial hypertension, including headache, nausea, and vomiting.[ncbi.nlm.nih.gov]
  • Encephalopathy causes confusion, abnormal thought processes, poor memory, hallucinations, and psychotic thinking.[healthcare-online.org]
  • Alcohol intoxication can cause __ in the nervous system Euphoria, ataxia, confusion, coma, death Alcohol withdrawal can cause __ in the nervous system Delirium tremens (Tremor, hallucinations, confusion, autonomic features); Seizures within 48 hours Wernicke's[quizlet.com]
  • The clinical presentation of toxic leukoencephalopathy is extremely variable, ranging from minor cognitive impairment, easily confused with psychiatric illnesses, to severe neurological dysfunction.[radiopaedia.org]
  • He was intubated and spent 4 days in intensive care; on extubation he was confused and paranoid but was discharged after 10 days in hospital ( day 12 ), ‘99% back to normal’. Figure 1 Time line depicting the patient's clinical status.[pn.bmj.com]
  • If patients with hypoglycemia are given glucose at the first signs of encephalopathy (for example, irritability, mild confusion), most patients recover completely.[medicinenet.com]
  • Two patients lost their consciousness, while two patients had typical extrapyramidal tremor symptoms. Further neurological examination revealed various degrees of muscle strength impairment in these patients.[ncbi.nlm.nih.gov]
  • […] encephalopathy is: Impaired ATTENTION (early finding in delirium, late finding in dementia) Symptoms of encephalopathy include: Hallucinations, delusions, agitation or lethargy; Irritation to light touch; Withdraw limbs unequally; Asterixis, myoclonus, tremor[quizlet.com]
  • Significant tremors were present at rest, which increased on intention. There was lack of co-ordination of rapid alternating movements. The rest of the physical exam was non-contributory.[ijri.org]
  • Other neurological symptoms may include myoclonus (involuntary twitching of a muscle or group of muscles), nystagmus (rapid, involuntary eye movement), tremor, muscle atrophy and weakness, dementia, seizures, and loss of ability to swallow or speak.[web.archive.org]
Personality Change
  • The symptoms of acute and chronic toxic encephalopathy do not resolve with cessation of exposure and can include memory loss, small personality changes/increased irritability, insidious onset of concentration difficulties, involuntary movements (parkinsonism[en.wikipedia.org]
  • This exposure to toxic substances can cause a wide variety of symptoms, including: Visual problems Altered mental status Memory loss Personality changes, including increased irritability Difficulty concentrating Seizures Dizziness Fatigue Lightheadedness[keefelaw.com]
  • Depending on the type and severity of encephalopathy, common neurological symptoms are progressive loss of memory and cognitive ability, subtle personality changes, inability to concentrate, lethargy, and progressive loss of consciousness.[web.archive.org]
  • A toxic encephalopathy characterized by depressed level of consciousness, marked irritability, and ataxia developed in seven children, 5 years of age and younger, following administration of an antiemetic combination of pentobarbital and pyrilamine maleate[ncbi.nlm.nih.gov]
  • We describe a 77-year-old man undergoing adjuvant treatment of colon cancer with capecitabine and oxaliplatin who presented with acute cerebellar ataxia and encephalopathy that progressed to coma.[ncbi.nlm.nih.gov]
  • Need WIDE variations to change neuronal and glial dysfunction Because the brain is location-based, global disruption of metabolic homeostasis can result in: Behavior change, poor coordination, ataxia, confusion, seizures, stupor and coma; May be a lag[quizlet.com]
  • In addition, toxic encephalopathy can also manifest through a specific subset of symptoms, such as cerebellar dysfunction (gait disturbances, ataxia, nystagmus, etc.) in methyl mercury (known as Minamata disease), methyl bromide, or organic tin toxicity[symptoma.com]
  • Other persistent neurologic sequelae include cerebellar ataxia, cognitive dysfunction, optic neuropathy, sensori-neural hearing loss and equilibrium disorders. The most common syndrome is multifocal CNS involvement.[ijri.org]


Acute toxic encephalopathy can often be fatal and brain damage caused by chronic exposure to neurotoxic substances may be irreversible in the absence of an early diagnosis, implying that clinical suspicion toward this syndrome must exist early on. Several reports have emphasized the vital role of a properly obtained patient history, which will assess the patient's occupancy, potential exposure to substances that may induce CNS-related symptoms (both in acute or chronic forms), as well as the course and progression of symptoms [1] [2] [3] [6]. Furthermore, a complete neurological examination, including the examination of cranial nerves, muscle tone, sensation, cerebellar function and evaluation of mental function should be subsequently conducted [1]. When there is a clinical suspicion of a primary CNS disorder, electroencephalography (EEG) and imaging studies of the brain must be carried out promptly [1] [3] [6]. Computed tomography (CT) is a useful initial method to rule out hemorrhage and other acute vascular incidents in the brain, while magnetic resonance imaging (MRI), magnetic resonance spectroscopy (MRS), functional MRI (fMRI), single photon emission tomography (SPECT) and positron emission tomography (PET) have all been described as important modalities in the evaluation of toxic encephalopathy [1] [3]. However, clinical criteria and findings obtained during history taking remain the cornerstone in diagnosing this condition.

Triphasic Waves
  • Furthermore, in these cases, other epileptic patterns in the form of spikes or sharp waves can also be detected. [39] However, triphasic waves are not specific only for hepatic encephalopathy.[neurologyindia.com]
Brain Edema
  • Death occurred following rapid neurological detoriation resulting in brain edema despite intensive treatment. Evidence of brain edema may be a prediction factor for death.[ncbi.nlm.nih.gov]
  • The cranial MRI showed extensive brain edema in either the subcortical white matter, bilateral globus pallidus, and cerebellar nucleus dendatus, or the cortices.[ncbi.nlm.nih.gov]
  • Links: brain tissue brain edema central nervous system hbot[oxy.hr]
  • The typical cranial CT/MR scan of DCE toxic encephalopathy shows extensive brain edema and diffuse, symmetric, abnormal signal intensities in the cerebellar dentate nucleus, basal ganglia, and white matter in the bilateral cerebral hemispheres.[ncbi.nlm.nih.gov]


  • RESULTS: Ninety-five patients started treatment, 84 patients had complete data. Treatment satisfaction was high.[ncbi.nlm.nih.gov]
  • All tremor symptoms were completely resolved in these patients at 30 min, 50 min, and 70 min following treatment, respectively. After the hemoperfusion treatment, encephalopathy symptoms of two patients had completely disappeared.[ncbi.nlm.nih.gov]
  • Capecitabine is a fluoropyrimidine commonly used in the treatment of colorectal cancer which may cause central nervous system toxicity, namely cerebellar dysfunction.[ncbi.nlm.nih.gov]
  • Dehydrating agents and glucocorticoids are the primary treatments. With early diagnosis and prompt treatment, promising results and recovery can be achieved. Effective prevention is expected to reduce the incidence of DCE toxic encephalopathy.[ncbi.nlm.nih.gov]
  • High-dose intravenous haloperidol for severe agitation has been reported as an effective and safe treatment option for the hospitalized patient.[ncbi.nlm.nih.gov]


  • Prognosis is usually good but fatalities and neurological deficits have been reported. We report here two infants with Margosa Oil poisoning presenting with encephalopathy.[ncbi.nlm.nih.gov]
  • Thirty-eight patients and 21 family members participated in a 1-day education scheduled with short lectures on the clinical examination of chronic toxic encephalopathy and the prognosis.[ncbi.nlm.nih.gov]
  • Abstract The prognosis of chronic toxic encephalopathy in former house painters was examined in a prospective study with a two-year observation period.[ncbi.nlm.nih.gov]
  • […] showed a loss of hearing, 7 patients complained about tinnitus, and all patients had a history of exposure to both noise and organic solvents, which had not been observed at the initial examination, but seemed to have serious implications for their prognosis[ncbi.nlm.nih.gov]
  • Consequently, the prognosis varies from patient to patient and ranges from complete recovery to a poor prognosis that often leads to permanent brain damage or death.[medicinenet.com]


  • Other alternative etiological entities were also excluded. Our findings indicate that long-term exposure to organic solvents may lead to a chronic brain syndrome.[ncbi.nlm.nih.gov]
  • The quality of the EEG changes gives prognostic signs, but is of restricted value in establishing the etiology without the anamnestic data of salicylate ingestion.[ncbi.nlm.nih.gov]
  • Abstract A … More Psychosis possibly linked to an occupational disease: an e-patient’s participatory approach to consideration of etiologic factors Summary: The purpose of … More[psychoticdisorders.wordpress.com]
  • Applicable To Toxic encephalitis Toxic metabolic encephalopathy Code First Code First Help Certain conditions have both an underlying etiology and multiple body system manifestations due to the underlying etiology.[icd10data.com]
  • Etiology There are numerous agents implicated in toxic leukoencephalopathy.[radiopaedia.org]


  • To be able to properly diagnose toxic encephalopathy, the professor believes doctors must have a specialized knowledge of the central and peripheral nervous systems, as well as toxicology, epidemiology and occupational medicine in order to understand[gesinjuryattorneys.com]
  • Page 69 - Epidemiology is defined as the study of the distribution and determinants of health-related states or events in specified populations, and the application of this study to control of health problems. ‎[books.google.com]
  • […] and Demographic Data Demographic and epidemiological data suggest that encephalopathy correlates with age.[neurologyindia.com]
Sex distribution
Age distribution


  • Health science Providing basic knowledge of medical terminology, anatomy and physiology, and pathophysiology of diseases and conditions.[icd-10online.com]
  • The Centers for Medicare & Medicaid Services (CMS) assigns a lower severity to the nonspecific behavioral diagnosis of delirium than for the pathophysiological diagnosis of encephalopathy.[icd10monitor.com]
  • Encephalopathy may also develop in primary infections of CNS, as well as due to the prolonged effect of anesthetics and sedatives. [13] Pathophysiological mechanisms Pathophysiological mechanisms of encephalopathy are not fully understood.[neurologyindia.com]


  • According to the results of the study, conditions at work places ought to be changed in such a way that harmful exposure can be prevented in the future.[ncbi.nlm.nih.gov]
  • Early recognition of encephalopathy and measures to prevent brain edema may improve patient outcome. Copyright 2011. Published by Elsevier B.V.[ncbi.nlm.nih.gov]
  • Active therapeutic measures including exchange transfusions are needed to prevent irreversible metabolic and pressure changes in the brain.[ncbi.nlm.nih.gov]
  • Effective prevention is expected to reduce the incidence of DCE toxic encephalopathy.[ncbi.nlm.nih.gov]
  • Rapid diagnosis is important to attempt to prevent further damage to the brain and further neurologic deficits.[en.wikipedia.org]



  1. Kim Y, Kim JW. Toxic Encephalopathy. Saf Health Work. 2012;3(4):243-256.
  2. Triebig G, Hallermann J. Survey of solvent related chronic encephalopathy as an occupational disease in European countries. Occupational and Environmental Medicine. 2001;58(9):575-581.
  3. Ramos A, Jardim SR, Silva-Filho JF. Solvent-related chronic toxic encephalopathy as a target in the worker's mental health research. An Acad Bras Cienc. 2004;76(4):757-769.
  4. Frantzeskaki F, Rizos M, Papathanassiou M, et al. L-asparaginase fatal toxic encephalopathy during consolidation treatment in an adult with acute lymphoblastic leukemia. Am J Case Rep. 2013;14:311-314.
  5. Müller J1, Kralovánszky J, Adleff V, et al. Toxic encephalopathy and delayed MTX clearance after high-dose methotrexate therapy in a child homozygous for the MTHFR C677T polymorphism. Anticancer Res. 2008;28(5B):3051-3054.
  6. Sørensen AM, Shapiro AU, Lund SP, Brun B, Rosenberg T, Lykke J. Toxic encephalopathy and noise-induced hearing loss. Noise Health. 2006;8(33):139-46.
  7. Pourakbari B, Mamishi S, Kohan L, et al. Lethal toxic encephalopathy due to childhood shigellosis or Ekiri syndrome. J Microbiol Immunol Infect. 2012;45(2):147-150.

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Last updated: 2019-07-11 21:12