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   , whereas several gases, chemotherapeutic drugs (such as L-asparagine, methotrexate), bacterial neurotoxins, recreational drugs, and ethanol can all be the underlying cause    . 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    :
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 .
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    . 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 . When there is a clinical suspicion of a primary CNS disorder, electroencephalography (EEG) and imaging studies of the brain must be carried out promptly   . 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  . However, clinical criteria and findings obtained during history taking remain the cornerstone in diagnosing this condition.