Although malabsorption is generally considered to be a gastrointestinal problem, the effects of malabsorption extend far beyond the gastrointestinal tract and can include
neurologic dysfunction. Malabsorption may occur by a variety of mechanisms, both genetic and acquired, that interfere with the absorption of basic nutrients,
vitamins, minerals, and
trace elements. Disorders that interfere with fat absorption can lead to
neurologic dysfunction as a consequence of associated impairment of fat-soluble
vitamin absorption. Thus, individuals with genetic
vitamin E deficiency and the familial hypocholesterolemias may develop symptoms of
peripheral neuropathy,
cerebellar ataxia, and other
neurologic signs and symptoms. Disease processes that damage the enteric mucosa and produce malabsorption can trigger
neurologic dysfunction both by immune-related processes, as in
celiac disease, and by impairing absorption of essential
vitamins and other nutrients, as in
tropical sprue. Deficiencies of water-soluble
vitamins, such as
thiamine and
niacin, can also develop in the setting of malabsorption and lead to
neurologic dysfunction. Neurologists are aware of the neurologic damage that
copper excess can cause in
Wilson's disease, but
copper deficiency due to malabsorption can also produce
neurologic dysfunction in the form of
myelopathy. It is vitally important for neurologists to be aware of the potential for malabsorptive processes to produce
neurologic dysfunction, because effective treatment for such disorders is often available.