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Toxic Encephalopathy Toxic Encephalopathy Michael R. Dobbs, M.D.1,2 ABSTRACT Neurotoxic exposures are common. Although there are myriad substances that can cause encephalopathy, this review focuses on common environmental neurotoxins, such as select heavy metals, organic industrial toxins, and pesticides. The central nervous system is susceptible to toxic injury, and many environmental neurotoxins are capable of causing encephalopathy. When a patient presents with toxic encephalopathy, the differential diagnosis is initially broad. The clinical presentation after exposure to a toxin varies in severity among patients. Arriving at the correct diagnosis is often a diagnostic challenge. The importance of taking a good history and performing a comprehensive examination cannot be overemphasized. Neuroimaging and neurophysiologic testing typically play ancillary roles. Confirmatory laboratory testing is available for some toxins. Treatment of most toxic encephalopathies is not supported by clinical trials; additional research is needed in the field. KEYWORDS: Toxic encephalopathy, neurotoxin, neurotoxicology, encephalopathy BACKGROUND fusion, attention deficits, seizures, and coma. CNS Neurotoxins have been known to cause disease since capillary damage, hypoxia, and cerebral edema antiquity.1 In modern times, we estimate that millions of play major roles.7 Depending on the toxin, the dose, people around the world work with neurotoxic substan- and the individual, neurologic symptoms may resolve ces.2 Many others are exposed at home or through other with removal from exposure. However, a single ex- inadvertent mechanisms. There are hundreds of sub- posure to some toxins can result in permanent deficits 3–5 stances known to be neurotoxic. There are probably or death. Downloaded by: Emory University. Copyrighted material. many unrecognized neurotoxins in our environments as The chronic toxic encephalopathy may exhibit well.6 insidious symptoms and signs that go unrecognized as The central nervous system (CNS) is to some being due to a toxic exposure. Sometimes, clinical extent protected from toxic exposure by the blood–brain symptoms may not manifest until years after exposure barrier, but remains vulnerable to many toxins nonethe- begins.8 Mood disturbances, fatigue, and cognitive dys- less. Nonpolar, lipid-soluble substances gain the easiest function may be seen. Significant recovery may take access to the CNS. Once a toxin gains access to the months or years after removal of the toxin. Sometimes CNS, neurons are easy targets due to their high lipid recovery may never occur. content and high metabolism. White matter can also be Most classes of neurotoxins have encephalopathic easily damaged by lipophilic toxins. effects. Some classic examples include neuromanganism Acute toxic encephalopathies exhibit symptoms and lead encephalopathy from the metals, encephalop- and signs along a spectrum that includes mild con- athy in carbon monoxide (CO) survivors, mixed solvent Departments of 1Neurology and 2Preventive Medicine, University of Samuels, M.D. Kentucky, College of Medicine, College of Public Health, Lexington, Semin Neurol 2011;31:184–193. Copyright # 2011 by Thieme Kentucky. Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, Address for correspondence and reprint requests: Michael R. USA. Tel: +1(212) 584-4662. Dobbs, M.D., 740 South Limestone Street, Wing D Kentucky Clinic DOI: http://dx.doi.org/10.1055/s-0031-1277989. L-412, Lexington, KY 40536 (e-mail: [email protected]). ISSN 0271-8235. Acute and Subacute Encephalopathies; Guest Editor, Martin A. 184 TOXIC ENCEPHALOPATHY/DOBBS 185 encephalopathy, Korsakoff’s alcoholic encephalopathy, With toxic leukoencephalopathy, the clinical pre- acute ethylene glycol poisoning, and the encephalopathy sentation will usually parallel the degree of white matter of chemotherapy. damage. The clinical severity may therefore range from This review will focus on important and common mild confusion to coma. Neurobehavioral function may environmental causes of toxic encephalopathy. Iatro- be the sphere most often affected in toxic leukoence- genic (pharmaceutic) causes of encephalopathy, though phalopathy.17 very important, will not be addressed in detail. Nor will the neurologic complications of ethanol be reviewed. Illicit recreational drugs will be briefly discussed as they Mixed Toxic Encephalopathy pertain to important agents that cross over into the The symptoms that follow toxic cerebral injury gener- industrial arena. For additional information on the ally reflect damage to both gray and white matter neurotoxic effects of pharmaceuticals, ethanol, and illicit processes. Common complaints include memory dis- drugs, there are several excellent chapters and reviews turbance, impaired cognition, mood disturbance, fa- available.9–12 tigue, and headache. It is rare to see prominent gray matter signs such as aphasia, apraxia, or agnosia on examination of patients with pure toxic encephalop- RECOGNIZING TOXIC ENCEPHALOPATHY athy. Cortical blindness might be an exception, although cortical blindness due to neurotoxicity is Toxic Cortical Encephalopathy controversial. A pure cortical encephalopathy results from toxic dam- Posterior reversible encephalopathy syndrome age to neurons. The cerebral and cerebellar cortices, as (PRES) may be the etiology in some cases of toxic well as deep gray matter nuclei, may be involved in the cortical blindness, and PRES has been reported with process. Cortical encephalopathy may result from expo- toxic exposures.18 In a study of 120 patients diagnosed sure to CO, carbon disulfide, hydrogen sulfide, ethanol, with PRES, 47 patients (42%) were being treated with organophosphates, lead, manganese, aluminum, and immunosuppressive agents. The authors concluded others. However, a pure cortical encephalopathy is that PRES is common in patients with autoimmune probably rare. Most toxins that cause cortical damage conditions, which were present in 51 (45%) of the also cause injury to white matter tracts. This includes patients, and did not correlate PRES with toxic effects CO.13 of medication.19 Aradiologystudyof30patients Injury to the basal ganglia may produce parkin- with PRES that included 24 hypertensive patients, sonism. Cerebellar injury causes typical cerebellar signs, and 6 patients without hypertension in whom PRES such as ataxia and poor balance. Focal cerebral cortical was associated with neurotoxic exposures, found no signs of prominence such as aphasia, apraxia, and agnosia difference in magnetic resonance imaging (MRI) find- are rare in toxic encephalopathy, but may be seen on ings between the hypertensive and toxic groups.20 careful examination. Frontal release signs are possible. PRES may sometimes be due to toxic mechanisms of The syndrome of cortical blindness can result from multiple cancer chemotherapeutic agents, especially exposure to many substances, including organic mercury, in children with hematopoietic disorders.21–24 Cyclo- Downloaded by: Emory University. Copyrighted material. vincristine,14 interferon,15 and other cancer chemother- sporine administration is frequently associated with apeutic agents.16 PRES.25–27 Whether PRES can be a consequence of primary neurotoxicity will remain a point of debate for now. Toxic Leukoencephalopathy White matter lesions, like gray matter lesions, can present with distinct clinical pictures depending on the Complex Toxic Encephalopathy location of the lesion. White matter tends to be more One might define complex encephalopathy as an ence- resistant to ischemia and hypoxia than gray matter, phalopathy in which there is an underlying brain lesion although many areas of white matter lack collateral that contributes to the clinical encephalopathic picture. blood flow. Perhaps the most common complex encephalopathy Because so many disease categories can preferen- (nontoxic) would be the condition of stroke re-exacer- tially affect white matter, the differential diagnosis of a bation with mild infection. leukoencephalopathy is extensive, of which neurotoxicity Little has been specifically written about the is but one facet. However, in the patient with diffuse patient with complex toxic encephalopathy. However, white matter lesions and encephalopathy, who has it stands to reason that in those patients with toxic known or suspected exposure to potentially neurotoxic encephalopathy and underlying brain lesions that the agents, toxic leukoencephalopathy should be investi- degree of encephalopathy might be intensified, or at least gated. be mixed with focal findings. 186 SEMINARS IN NEUROLOGY/VOLUME 31, NUMBER 2 2011 CONFIRMING TOXIC ENCEPHALOPATHY PRES, one expects to see focal and symmetrical paren- A good first step in confirming toxic encephalopathy is chymal edema. The parietal and occipital lobes are most narrowing down the list of differential diagnoses. This often affected, but also sometimes the frontal lobes, the may prove challenging because most of the disorders in temporooccipital junction, and the cerebellum.33,34 the differential diagnosis are not toxic. Neurophysiologic Testing The Clinical Examination Electroencephalography (EEG) may provide useful The examination may contain several clues pointing nonspecific information in cases of suspected toxic en- toward a toxic cause of encephalopathy. Many signs cephalopathy. EEG can be used to objectively quantify are general rather than neurologic, and so one cannot the degree of encephalopathy present and perhaps mon- afford to rush through the general physical exam. Exam-
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