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Subacute toxic encephalopathies are challenging to identify due to their often insidious tempo of evolution, nonspecific manifestations, relative infrequency as individual entities, and frequent lack of specific diagnostic testing. Yet they are crucial to recognize-in aggregate, subacute toxic encephalopathies are a common problem that can lead to severe, irreversible harm if not diagnosed and treated efficiently. This article reviews the clinically relevant aspects of some of the more important subacute toxic encephalopathy syndromes caused by inorganic toxins, carbon monoxide, antibiotics, antineoplastic agents, and psychiatric medications., Competing Interests: Disclosure Dr D.P. Lerner receives royalty payments from McGraw-Hill for editorial services. Dr A. Tadevosyan and Dr J.D. Burns have nothing to disclose., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Clinical neurotoxicology is an unrecognized neurologic subspecialty. Few neurology residency programs offer an organized education or training in the field. Nevertheless, neurotoxic exposures and subsequent injuries are common. This article provides a basic approach to clinical assessment and causal inference. It addresses the knowledge gap for clinical practice and provides a thematic structure to use interdisciplinary resources., Competing Interests: Disclosure The authors have no commercial or financial conflicts of interest to disclose., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Peripheral neuropathies secondary to neurotoxicants are frequently considered but can be difficult to diagnose. Accurate diagnosis is important to avoid unnecessary testing, prevent further exposure, and initiate treatment when available. This article reviews key features of some of the more common or representative toxic neuropathies, including those caused by occupational and environmental exposure, medications, and chemotherapeutic agents., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Many medications and toxins may induce central nervous system (CNS) depression. Even when the intention is to induce CNS depression, other nervous system adverse effects may occur, such as with anesthetics. Pain medications produce characteristic CNS toxicities. Sedative hypnotics may induce altered mentation among systemic toxicities. Stimulants may mimic coma when discontinued abruptly. Acute and chronic carbon monoxide poisoning can lead to altered mental status and prolonged cognitive difficulties. Some medications and environmental toxins can mimic brain death. High clinical suspicion and early recognition of these effects is vital to treatment, most of which is supportive., Competing Interests: Disclosure The authors have nothing to disclose., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Acute delirium is a transient state of cerebral dysfunction reflecting an underlying medical decompensation. Toxicity from medications and other substances are a common cause of delirium. History and laboratory testing may be limited by alteration and lack of specific tests for certain compounds. Classes of compounds produce a constellation of symptoms and examination findings recognized as a toxidrome. Cessation of the offending agent, supportive care, and specific antidotal therapy are key to treatment. This article reviews the presentations of the anticholinergic toxidrome, sympathomimetic toxidrome, hallucinogenic toxidrome, γ-aminobutyric acid withdrawal, and Wernicke encephalopathy, as well as their mechanisms and basic management., Competing Interests: Disclosure A. Cai has nothing to disclose. X. Cai is an employee of Pfizer, Inc., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Neurologic complications of systemic cancer therapy encompass a range of symptoms that can affect the central nervous system (CNS), peripheral nervous system (PNS), or both. Their incidence will likely increase as novel agents, such as targeted therapy and immunotherapy, become incorporated into standard treatment regimens, and the number of long-term cancer survivors rises. Recognizing the common adverse effects of treatment is important to avoid misdiagnosis of cancer recurrence in the nervous system or paraneoplastic disease. Ongoing has focused on identifying patient-specific risk factors that predispose to drug toxicity and the development of appropriate preventive and therapeutic strategies., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Among commercial and industrial chemicals, cosmetics, food additives, pesticides, and medicinal drugs, there are more than 50,000 substances distributed. Neurotoxic insults to the brain can manifest in many different ways, especially involving cognition. Given many possible differences in the pathophysiology of neurotoxic exposure and related cognitive sequelae, a systematic method of cognitive assessment is important for appropriate management of neurotoxic exposure. In the context of Neurotoxicology, this article briefly reviews the contemporary literature and the utility of cognitive assessment tools that are used in neuropsychology., (Copyright © 2011 Elsevier Ltd. All rights reserved.)

Neurotoxic emergencies are depicted by severe disruption of critical central or peripheral nervous system functions caused by xenobiotics with rapid mechanisms of action. This article reviews 4 categories of neurotoxic emergency: drug-induced and toxin-induced seizures, acute depressed mental status, acute excited mental status, and peripheral neurotoxic agents. Selected xenobiotics, representing the frontiers of neurotoxic emergencies, are discussed in detail based on the major neurotransmitters involved., (Published by Elsevier Inc.)

The effects of several substances known to produce peripheral neuropathy are reviewed, as are the criteria espoused to be useful in establishing their neurotoxicity. Included is a description of systemic and neurologic symptoms and signs important in identification of the neurotoxic disorder, and a description of the resultant electrodiagnostic abnormalities.

The epidemiology, clinical features, pathology, and mechanisms of action of basal ganglia neurotoxins are reviewed. Manganese, cyanide, hydrogen sulfide, methanol, carbon monoxide, 3-nitropropionic acid, MPTP, and annonaceae alkaloids are discussed. The probable mechanism of action for almost all basal ganglia neurotoxins is inhibition of mitochondrial function with destruction of the pallidum and putamen. MPTP produces selective loss of dopaminergic neurons because of selective uptake of a toxic metabolite in dopaminergic neurons. The basis for selective vulnerability of the putamen and pallidum is unknown.

An ideal classification of neurotoxic substances should link the vulnerable target of chemical attack to alterations in neural function. There is little basis for classifying agents based on their common use or physico-chemical properties. Outlined in this article are the principal cellular targets of substances that perturb the nervous system structure and function.

The development of imaging technology over the past 25 years has had a profound impact on the clinical practices of a number of medical disciplines. In this article, the author reviews the various neuroimaging modalities and the neurologic processes that they can address.

Epidemiology is the study of the patterns of disease and patterns of exposures in human populations. The main goals of epidemiology are to determine whether specific population groups have an increased risk of developing particular diseases and to determine what factors may be associated with increased risks of disease. In this article, the author focuses on epidemiologic studies of potential neurotoxic exposures, reviewing the basic principles involved and the special challenges associated with providing evidence of causal relationships between exposure and adverse health conditions.

The use of the clinical neurological examination to document abnormal signs in suspected neurotoxic disorders is described, recognizing that identifying an abnormal examination does not establish the cause of the problem. Several forms of quantitative tests of neurological function are discussed, and their application to the evaluation of neurotoxic disorders is reviewed. Although results of such testing are rarely specific for toxic exposure, these measures have important application in sequential evaluations to document small changes in neurologic function over time.

Several controversial neurotoxic syndromes have received notoriety in the past several decades. For each, the controversy involves the most fundamental question about the existence of the disorder as a clinically diagnosable entity. Interestingly, the most controversial of these syndromes share several features, including argument about the existence of each syndrome in the courtroom. The authors focus their discussion on three problems (painter's encephalopathy, silicone breast implant neurotoxicity, and the Gulf War syndrome) for which no scientific consensus has been reached that would establish them as diagnosable disorders. These syndromes do not meet traditional disease criteria, and until a clear set of symptoms and objective signs can be defined, a definite course and clear cause demonstrated, and specific tests and treatments identified, these syndromes are likely to remain highly controversial.

In this article, the author provides an overview of the neuropsychologic approach to evaluation of neurologic dysfunction. The various strengths and weaknesses of this methodology are discussed, and the steps of the neuropsychologic evaluation are detailed.

This article deals with disorders of mood and the interaction between mood and cognitive function. The various ways in which environmental toxins can lead to disorders of mood are presented, and discussions regarding the neurobiology of mood are presented.

In this article, the authors provide a conceptual framework in which to consider alternative approaches to identify the developmental consequences of exposing the developing brain to neurotoxic substances. Concepts underlying brain development and issues regarding neurobehavioral testing in children are reviewed. In addition, the authors selectively review preclinical data identifying mechanisms contributing to neurobehavioral compromise, and clinical data identifying deficits resulting from exposure to two classes of neurotoxins: exposure to drugs of abuse, including alcohol, nicotine, and cocaine; and exposure to environmental agents, including lead, methyl-mercury, PCBs, and organophosphorus compounds.

Electrophysiologic testing in concert with the neurologic history and physical examination can be useful for evaluating the patient with suspected neurotoxicity. Procedures are selected depending on whether the central or peripheral nervous system, or both, are considered to be affected. Extensive data is available on the use of nerve conduction studies to substantiate and serially follow patients with peripheral neuropathy, and the electrophysiologic findings can be used to predict the most likely focus of pathology in the peripheral nervous system. With this information in hand, the electrodiagnostician can guide the clinical neurotoxicologist towards a broad differential diagnosis of the most likely neurotoxins.