A 77- year- old male with past medical history Non Hodgkin’s Lymphoma (NHL) Stage IV presented to emergency room with difficulty in breathing at rest, of 1 day duration. He was diagnosed with NHL 1 year ago and was receiving chemotherapy with vincristine, prednisone, rituximab and cyclophosphamide. He had completed seven cycles of chemotherapy 4 -weeks prior to presentation. Clinical examination revealed patient was restless and dyspneic. There was no obvious neck swelling, masses, jugular venous distension or peripheral edema. Respiratory system exam revealed reduced bilateral air entry and the remainder of the examination revealed no abnormalities. Computerized Tomography (CT) scan of chest and neck was unremarkable. Patient developed stridor and was emergently intubated and placed on mechanical ventilation. Emergent bronchoscopy showed bilateral vocal cord paralysis with no endobronchial lesion. In the absence of any identifiable pathology presumptive diagnosis of vincristine related recurrent laryngeal nerve paralysis was made.

Vinca alkaloids (vincristine, vinblastine) can cause peripheral, autonomic or central neuropathies. Neuropathy is due to the disruption of microtubules and interference with axonal transport. The peripheral and autonomic neuropathies are more common as compared to central neuropathy. Earliest and most consistent peripheral neuropathy indication is asymptomatic depression of the Achilles reflex.1 The motor involvement is characterized by wrist drop, foot drop, atrophy, cramps, ataxia, slapping gait, and inability to walk. Autonomic neuropathy can result in constipation, abdominal cramps, urinary retention or incontinence. Cranial nerve neuropathy can result in ophthalmoplegia¹, optic atrophy, blindness, sensineural deafness and hoarseness of voice due to vocal cord palsy.² Neurotoxicity is greatest with vincristine as compared to other vinca alkaloids. However vocal cord paralysis has been reported with vinblastine treatment.^3,4 The vocal cord paralysis in a patient with systemic cancer can be due to pressure on the recurrent laryngeal nerve by enlarged lymph nodes, jugular foramen syndrome, leptomeningeal metastasis or upper respiratory tract infection. We believe vincristine led to the development of vocal cord paralysis due to temporal association with the drug, clinical plausibility, and lack of alternate explanation.

The vincristine toxicity has a cumulative effect. Frequent (more than once a week) and higher doses (>2 mg/m2/wk) increases the toxicity.¹ At present, there are no known methods of preventing or decreasing the toxic effects that are associated with vincristine therapy. Vincristine-induced vocal cord paralysis is usually reversible two to nine months after discontinuation of therapy.⁴ In case of suspected vincristine toxicity the dose should be reduced or therapy should be discontinued.  Vocal cord paralysis should be suspected in patients who develop stridor while receiving treatment with vincristine.
S Besur, SK Talluri
Department of Internal Medicine, McLaren Regional Medical Centre, Flint, Michigan, USA
Email: [email protected]

Acknowledgements
Dr. Shivani Bishnoi & Dr. Rohit Bishnoi 
References 
1. Holland JF, Scharlau C, Gailani S,Krant MJ, Olson KB, Horton J, Shnider BI, Lynch JJ, Owens A, Carbone PP, Colsky J, Grob D, Miller SP, Hall TC. Vincristine treatment of advanced cancer: a cooperative study of 392 cases. Cancer Res. 1973 Jun; 33:1258-64.
2. Bohannon RA, Miller DG, Diamond HD. Vincristine in the treatment of lymphomas and leukemias Cancer Res. 1963 May; 23:613-21.
3. Brook J, Schreiber W. Vocal cord paralysis: a toxic reaction to vinblastine (NSC-49842) therapy. Cancer Chemotherapy Rep. 1971 Dec; 55:591-3.
4.  Whittaker JA, Griffith IP. Recurrent laryngeal nerve paralysis in patients receiving vincristine and vinblastine.Br Med J. 1977 May 14; 1:1251-2