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INTRODUCTION

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Diseases of the nervous system are known for their diverse clinical manifestations. When the central nervous system is affected, symptoms may include headache, cognitive and psychiatric disturbances, visual changes, seizures, ataxia, tremors, rigidity, weakness, and sensory loss. In peripheral nervous system diseases, pain, weakness, paresthesias, and numbness are common, and in some instances, there may be additional autonomic disturbances.

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The pattern of neurologic symptoms depends on the nature of the insult. For instance, excessive exposure to many industrial or environmental chemicals causes a generalized disorder of peripheral nerves, that is, peripheral neuropathy. This presents usually as a diffuse and symmetric clinical syndrome. In contrast, some occupations may predispose workers to physical injuries to peripheral nerves. Common examples are carpal tunnel syndrome from median nerve entrapment and lumbar radiculopathy from compression of the spinal roots. Single nerves or spinal roots are affected in these instances, leading to a localized pattern of neurologic symptoms and signs. Focal nerve injuries are discussed in Chapters 9 and 10 and are not further covered in this chapter.

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GENERAL PRINCIPLES

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Neurologic evaluation of patients largely depends on bedside history and physical examination, supplemented by traditional diagnostic tests such as computed tomography (CT) and magnetic resonance imaging (MRI) of the brain or spine, electroencephalography (EEG), nerve conduction study, electromyography (EMG), lumbar puncture, and neuropsychological testing.

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With few exceptions, the pathophysiology of most neurotoxic injuries is not well understood. Animal models of toxin exposure provide at best a rough guide to human disease. Moreover, it is nearly impossible to study the effects of toxins under controlled conditions in humans. Much of our current knowledge is gained from clinical observations of intense exposures during accidents or chronic heavy occupational exposures. Extrapolation of these classic observations to other situations is problematic. For instance, for many compounds, there is considerable uncertainty concerning the exposure level and duration necessary to cause neurologic injury. It has been especially difficult to ascertain the sequelae of chronic low-level exposure, a situation particularly likely to be encountered by today's physicians.

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Despite our incomplete understanding in many of these diseases, several generalizations have been useful in the clinical approach to these disorders.

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  1. A dose-toxicity relationship exists in the majority of neurotoxic exposures. In general, neurologic symptoms appear only after a cumulative exposure reaches a threshold level. Individual susceptibility varies over a limited range, but idiosyncratic reactions seldom occur.

  2. Exposure to toxins typically leads to a nonfocal or symmetric neurologic syndrome. Significant asymmetry such as weakness or sensory loss of one limb or one side of the body with complete sparing of the contralateral side should suggest an alternate cause.

  3. There is usually a strong temporal relationship between exposure and the onset of symptoms. Immediate symptoms after acute exposure are often a consequence of the physiologic effects of the chemical (eg, the cholinergic effects of organophosphates). These symptoms subside quickly with ...

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