Central and peripheral neurologic dysfunction can arise in the setting of conditions with primary endocrine, electrolyte, hematologic, or metabolic causes. Nutritional and toxic factors also contribute to a host of neurologic conditions. Paraneoplastic processes link malignancy and neurologic syndromes through an immune-mediated process. Similarly, rheumatologic diseases with inflammatory (or auto-inflammatory) underpinnings can have neurologic complications. In some cases, the neurologic syndrome is the presenting feature of a systemic condition—and can even predate the “primary” diagnosis by years. It is therefore helpful to understand neurologic disorders in the context of personal and family histories, a comprehensive review of systems, and results of basic investigatory tests. This chapter highlights systemic conditions with neurologic manifestations.

Because the nervous system can reflect injury in a limited number of ways, very different disease processes can cause similar symptoms and signs. The related neurologic dysfunction can be life-threatening—or minor enough that related signs are incidentally noted on a meticulous neurologic exam. Perhaps one of the most important take-home points of this chapter, then, is that non-neurologic causes of neurologic symptoms are important to consider when evaluating patients in any clinical setting.

ENDOCRINE DYSFUNCTION

Diabetes mellitus can have several neurologic manifestations, including the neuropathies detailed in Box 18-1. One of the most easily recognized complications of diabetes is a diabetic polyneuropathy, a distal, symmetric neuropathy affecting sensory and motor nerves. Autonomic fibers can be involved, as well. Diabetes is also a risk factor for stroke. Diabetic lumbosacral radiculoplexus neuropathy (a.k.a. diabetic amyotrophy) and compression neuropathies (e.g., carpal tunnel syndrome) are more common in patients with diabetes. Rarely, muscle infarction can occur in the setting of diabetes. Pain, often in the thigh or calf, associated with warmth, redness, and swelling, in the absence of trauma should raise this possibility—especially when conditions such as infection and deep vein thrombosis have been excluded. Thus, diabetes is associated with deficits at all levels of the neuraxis.

BOX 18-1. Diabetic Neuropathies

In general, the treatment is to optimize control of blood sugar. Of note, lowering glycosylated hemoglobin (HbA1c) too quickly (e.g., a decrease of > 4% HbA1c over 3 months), however, can cause a painful polyneuropathy referred to as treatment-induced diabetic neuropathy or “insulin neuritis.” This is a reminder that both chronic and acute shifts in blood sugar to a range that is too high or too low can have neurologic complications. Similarly, excess or deficient levels of endocrine hormones can be associated with conditions such as myopathy or seizures (Box 18-2). Box 18-2 also gives examples of the neurologic symptoms and signs of hematologic diseases and electrolyte disturbances.

BOX 18-2. Examples of Systemic Conditions with Neurologic Manifestations

Although hyperthyroidism and hyperparathyroidism may have neurologic manifestations, it is particularly important for neurologists to be aware of how hypothyroidism can manifest (Box 18-3). From a central nervous system (CNS) perspective, cognitive slowing can occur. Neuromuscular complications such as carpal tunnel syndrome and a distal symmetric polyneuropathy may also result. Myopathy, characterized by stiffness, myalgias, and elevated creatine kinase (CK) levels, can develop in the context of hypothyroidism—and can improve with return to a euthyroid state.

BOX 18-3. Neurologic Manifestations of Hypothyroidism

ELECTROLYTE, MINERAL, AND NUTrITIONAL FACTORS

Shifts in electrolyte levels can alter mental status, strength, or movement. Disturbances in sodium and calcium balance can cause confusion and seizures, whereas potassium abnormalities can cause weakness (Box 18-2). Abnormal movements, including twitching and tremor, can occur with disturbances of calcium and other electrolytes. Neuro-ophthalmologic dysfunction (including nystagmus, ophthalmoplegia, or optic atrophy), polyneuropathy, or both can be caused by vitamin deficiency or excess, stemming from dietary choices, supplements, medications, renal or hepatic dysfunction, or hematologic conditions (Box 18-2).

Subacute combined degeneration (SCD). Interestingly, anemia need not be present for B₁₂ deficiency to cause neurologic sequelae, including SCD. As outlined in Chapter 22, vitamin B₁₂ deficiency can cause spasticity and paraparesis because of the involvement of dorsolateral white matter tracts in the spinal cord. Patients can also develop concurrent polyneuropathies. Thus, patients may present with a combination of paresthesias, ataxia, and weakness. Correction of the vitamin B₁₂ deficiency can be therapeutic.

When hyponatremia has been present for at least 2 days, it is important that its correction be carried out gradually (e.g., less than 6–8 mEq/L over 24 hours, with serum sodium checks every 2–3 hours at the outset). If hyponatremia is corrected too quickly, central pontine myelinolysis (CPM), also known as osmotic demyelination syndrome, can result. Affected patients may have abnormal speech and swallowing, limb weakness, movement abnormalities (including tremor, myoclonus, dystonia, and choreoathetosis), seizures, and mental status changes. In addition to adventitious movements, pathologically brisk and primitive reflexes may become evident on exam. The time course is important: Symptoms tend to develop 2 to 6 days following sodium correction, and magnetic resonance imaging (MRI) may appear normal for as long as a month before showing the demyelination. Prevention is key, because some of the resultant deficits can be permanent.

Related posts:

The Sensory System The Approach to Coma and Altered Consciousness Head Trauma Neuro-Ophthalmology Demyelinating Diseases of the Central Nervous System Disorders of the Spinal Cord

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