These vital trace substances are generally associated with vitamin deficiency syndromes, but because health enthusiasm has reached passionate proportions for many individuals, physicians are encountering neurotoxic syndromes from overdosage. The first recognized toxicity of vitamins was related to the fat-soluble vitamins, but water-soluble vitamins have been found to be harmful at times when they are ingested in large quantities.
Vitamin A toxicity results in a syndrome of increased intracranial pressure, headaches, blurred vision, and sixth nerve palsy. On fundoscopic examination, gradual papilledema develops.y , y The mechanism whereby increased intracranial pressure develops is not known, although biochemically, the vitamin stimulates the synthesis of glycoproteins
and mucopolysaccharides, which may alter fluid balance centrally. The generally recommended daily vitamin A allowance is 5000 IU, and toxicity occurs with intake as little as four times that dose. y Similar toxicity has been noted with one of the vitamin A-like substances, c/s-retinoic acid, when used for acne in a person taking recommended intakes of vitamin A.y In addition there is considerable evidence of the teratogenic effects of vitamin A in the mouse, rat, hamster, and guinea pig. Malformations include cleft palate, fused ribs, spina bifida, meningocele, hydronephrosis, and heart and genitourinary abnormalities. y
Massive amounts of vitamin D mobilize bone calcium and phosphorus. Where there is bone demineralization and degeneration, nerve root and spinal cord compression can occur. Meningeal symptoms and trigeminal neuralgia are two additional reported findings without clear pathogenesis. Trigeminal neuralgia may relate to bony foraminal changes. Alterations in the calcium balance in the form of hypercalcemia can produce metastatic calcifications in the brain with resultant mental retardation or a clinical picture of generalized weakness, muscle aches, cramps, and mild metabolic encephalopathy. y When renal impairment occurs, progressive secondary encephalopathy, not directly related to the vitamin, develops. Vitamin D, like vitamin A, is a teratogen, and when the vitamin consumed in large amounts by pregnant women, it can produce specific abnormalities of the facies, brain, heart, and kidney of the fetus. y
Excessive vitamin E ingestion may produce subtle signs and symptoms of toxicity, such as easy fatigability, muscle weakness, headache, and delayed wound healing. Symptoms usually disappear with cessation of excessive intake. Increased bleeding tendencies have also been reported with large amounts of vitamin E, but no intracranial bleeding has been reported as resulting from it. No toxic effects have been reported at doses of 800 IU daily. y Even with supraclinical doses, associated with high levels of plasma tocopherol, ventricular CSF levels are exceedingly low. y
Effects of excess thiamine on the CNS include nervousness, convulsions, headache, weakness, trembling, and neuromuscular paralysis. y The decreased use of thiamine, especially parenterally for various functional disorders, appears to have resulted in a reduction of toxic reactions.
Pyridoxine, previously considered benign, has been found to have direct toxic effects on the peripheral nervous system. Animals treated with high doses of pyridoxine develop vacuolation and degeneration of dorsal root and ganglion cells, along with a widespread degeneration of sensory nerve fibers. When consumed in daily doses of 2 g or more, it has been reported to produce a syndrome consisting of difficulty walking with lightning-like dysesthesias in the back. Numbness of the extremities occurs, and most important, facial dysesthesias, so uncommon with most toxic neuropathies other than trichloroethane, quickly develop. Areflexia, stocking-and-glove sensory loss, and profound sensory ataxia with preserved strength are typical. On EMG, marked slowing of the sensory nerve conduction is seen with normal motor conduction.^1 , y Treatment consists of cessation of pyridoxine, and in some cases there is a dramatic, although often slow, recovery.
When low to moderate doses of pyridoxine are added to the diet of a parkinsonian patient receiving levodopa, without carbidopa supplementation (e.g., Sinemet), it will precipitiously cause an exacerbation of the disease. Pyridoxine is a co-factor for dopa decarboxylase and enhances the systemic conversion of dopa to dopamine: Because dopamine cannot cross the blood-brain barrier, this enhanced peripheral synthesis of dopamine in fact diminishes central delivery of dopa for effective antiparkinsonian therapy. When sufficient carbidopa is added to levodopa (usually at least 100 mg/day), this pyridoxine toxicity is probably insignificant.
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