Hydrogen peroxide poisoning, usually by accidental ingestion, causes multiple small cerebral infarcts through a mechanism of gas embolus (Ijichi et al). Most cases have been reversible. According to Humberson and colleagues (cited by Ijichi et al) 120 mL of 35 percent hydrogen peroxide releases 14 L of oxygen on contact with organic tissue. The lung is involved, and the unmistakable brain lesions consist of tiny gas bubbles concentrated in parasagittal watershed areas.
The increasing use of potent antineoplastic agents has given rise to a diverse group of neurologic complications, the most important of which are summarized here. A more detailed account of these agents—as well as the neurologic complications of corticosteroid therapy, immunosuppression, and radiation—can be found in the monograph edited by Rottenberg and in the review of Tuxen and Hansen and in appropriate chapters of the book. The neurotoxic effects of certain agents used in the treatment of brain tumors are specifically considered in Chap. 30.
This drug is used in the treatment of acute lymphoblastic leukemia, lymphomas, and some solid tumors. Its most important toxic side effect, and the one that limits its use as a chemotherapeutic agent, is a peripheral neuropathy. Paresthesias of the feet, hands, or both may occur within a few weeks of the beginning of treatment; with continued use of the drug, a progressive symmetrical neuropathy evolves (mainly sensory with reflex loss). Cranial nerves are affected less frequently, but ptosis and lateral rectus, facial, and vocal cord palsies have been observed. Autonomic nervous system function may also be affected: constipation and impotence are frequent complications; orthostatic hypotension, atonicity of the bladder, and adynamic ileus are less frequent. The polyneuropathy caused by vincristine is described more fully in Chap. 43. Inappropriate antidiuretic hormone secretion and seizures have been reported but are uncommon.
Although rarely noted in the literature, the authors have seen an instance of reversible posterior leukoencephalopathy with cortical blindness and headache after a single dose of vincristine, identical to the syndrome reported with the use of calcineurin inhibitors (see further on).
The neural complications of vinblastine are similar to those of vincristine but are usually avoided because bone marrow suppression limits the dose of the drug that can safely be employed. Vinorelbine is a more recently introduced semisynthetic vinca alkaloid. It has much the same antitumor activity as vincristine but is supposedly less toxic.
Cisplatin, a heavy metal that inhibits DNA synthesis, is effective in the treatment of gonadal and head and neck tumors, as well as carcinoma of the bladder, prostate, and breast. The dose-limiting factors in its use are nephrotoxicity and vomiting and a peripheral neuropathy (see
Chap. 43). The latter manifests itself by numbness and tingling in fingers and toes, sometimes painful—symptoms that are being observed with increasing frequency. This toxic manifestation appears to be related to the total amount of drug administered, and it usually improves slowly after it has been discontinued. Biopsies of peripheral nerve have shown a primary axonal degeneration. Approximately one-third of patients receiving this drug also experience tinnitus or high-frequency hearing loss or both. Ototoxicity is also dose related, cumulative, and only occasionally reversible. Retrobulbar neuritis occurs rarely. Seizures associated with drug-induced hyponatremia and hypomagnesemia have been reported.