Neurologic Effect

Abstract: PURPOSE: Oxaliplatin is a novel platinum compound with clinical activity in several malignancies. Neurotoxicity is dose-limiting and occurs in two distinct forms, an acute neurologic symptom complex that occurs within hours or days of therapy and a chronic, cumulative sensory neuropathy. PATIENTS AND METHODS: Patients were treated in a phase I study designed to establish the maximum-tolerated dose of capecitabine given with oxaliplatin. Because of the unusual neurosensory toxicity of oxaliplatin, detailed neurologic examination, needle electromyography (EMG), and nerve conduction studies (NCS) were performed before and the day after oxaliplatin in a subset of 13 patients. Carbamazepine therapy was tried in 12 additional patients to determine whether the neurologic effects might be relieved. RESULTS: All patients experienced acute, reversible neurotoxicities with oxaliplatin. Symptoms included paresthesias, dysesthesias, cold hypersensitivity, jaw pain, eye pain, pain in the arm used for drug infusion, pto...

Abstract: Neurologic abnormalities were seen in 13 of 20 patients with a history of chronic solvent vapor (primarily toluene) abuse for 2 or more years. The patients were evaluated after an abstinence period of at least 4 weeks, to avoid neurologic effects of acute intoxication. Neurologic signs included cognitive (60%), pyramidal (50%), cerebellar (45%), and brainstem/ cranial nerve (25%) findings. Eight of nine CTs revealed diffuse atrophy of cerebral hemispheres, cerebellum, and brainstem. BAERs were abnormal in three of four patients, and EEG abnormalities were seen in three of seven patients. Chronic exposure to solvent vapor may cause persistent neurologic impairment.

Abstract: Purpose This review focuses on the neurologic issues concerning the treatment of hypo- or hyperglycemia in the critically ill patient. Data sources Articles written in English and identified through the Bibliographic Retrieved Service Colleague database. Study selection Articles chosen on the basis of their relevance to the issue of blood glucose management and its neurologic effects in critically ill patients. Data extraction Data from articles were analyzed to obtain a scientific foundation and rationale for treating abnormal blood glucose levels. Data synthesis Moderate hypoglycemia may evoke a significant stress response, behavioral changes, and alterations in cerebral blood flow and metabolism. It is unclear what effect prolonged or repeated episodes of moderate hypoglycemia may have on patient outcome. However, alterations in cerebral vascular physiology must be addressed when caring for patients with cerebral ischemia or intracranial compliance problems. Depending on its severity, hypoglycemia has varying influences on neurologic damage after ischemia. Hyperglycemia may impair neuronal recovery following cerebral ischemia. However, the detrimental effects of hyperglycemia vary depending on the types of brain ischemia sustained (focal or global). Evidence suggests that hyperglycemia during global and incomplete global ischemia events is detrimental to neurologic outcome. However, the relationship between hyperglycemia and outcome after focal ischemia is controversial. Conclusion Because both hypo- and hyperglycemia may produce neurologic changes, aggressive management of abnormal glucose values is warranted.