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Biomedical subjects

Robert W Pratt

Publications and source records attributed to Robert W Pratt.

2 recordsLinked to original sources

Medication and toxin-induced peripheral neuropathy.

Medication and toxin-induced neuropathies, although uncommon, are important to identify because of potential reversibility. Numerous medications and toxins are implicated with neuropathy, but objective proof is lacking for many. Chemotherapeutic agents, nucleoside analogs, and other medications and toxins have clear causative links with neuropathy, but many agents have only rare temporal associations. Neuropathies are being recognized from new medications approved for use and other medications, which have expanded indications. Some established associations with neuropathy are less widely known while others are overestimated. Peripheral neuropathy from chronic drug exposure is more problematic to determine. Axonal pathology is most common, but some agents cause demyelination and even conduction block, mimicking immune-mediated neuropathies. Multiple and varied toxic mechanisms are implicated. Neuropathy is a dose-limiting complication of some critical treatments and preventative agents are being actively pursued.

Anti-Bacterial Agents↗

Normal pressure "herniation".

INTRODUCTION: Hydrocephalus with normal intracranial pressure has rarely been reported to result in herniation. METHODS: Case report. RESULTS: A 52-year-old man became acutely comatose with extensor posturing and ventriculomegaly 17 days after experiencing a primary ventricular hemorrhage. An external ventricular drain revealed normal intracranial pressure. After 24 hours without improvement with the drain set at a level of 5 mm H2O, negative-pressure siphoning (50 mL of cerebrospinal fluid [CSF] removed) reduced ventricular size and led to dramatic clinical recovery. CONCLUSION: Normal pressure hydrocephalus can result in delayed brainstem herniation after ventricular hemorrhage. CSF siphoning in these patients can reverse the syndrome.

Acute Disease↗