Vocal fold palsy following vinca alkaloid treatment

Burns, B. V.; Shotton, J. C.

doi:10.1017/s002221510014085x

Cited by 26 publications

(8 citation statements)

References 15 publications

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“…Mononeuropathies (femoral, peroneal), cranial nerve lesions, diplopia, vocal cord paralysis ( Burns and Shotton, 1998 ) facial nerve palsy, and sensoneurial hearing loss have been described in individual case reports ( Sanderson et al, 1976; Lugassy and Shapira, 1990; Kalcioglu et al, 2003 ) . Autonomic changes can result in constipation, paralytic ileus, or megacolon ( Low et al, 2003 ) .…”

Section: Individual Classes Of Chemotherapy Drugs Associated With Cinmentioning

confidence: 99%

Chemotherapy‐induced neuropathy

Windebank

Grisold

2008

J Peripheral Nervous Sys

559

401

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Neurotoxic side effects of cancer therapy are second in frequency to hematological toxicity. Unlike hematological side effects that can be treated with hematopoietic growth factors, neuropathies cannot be treated and protective treatment strategies have not been effective. For the neurologist, the diagnosis of a toxic neuropathy is primarily based on the case history, the clinical and electrophysiological findings, and knowledge of the pattern of neuropathy associated with specific agents. In most cases, toxic neuropathies are length-dependent, sensory, or sensorimotor neuropathies often associated with pain. The platinum compounds are unique in producing a sensory ganglionopathy. Neurotoxicity is usually dependent on cumulative dose. Severity of neuropathy increases with duration of treatment and progression stops once drug treatment is completed. The platinum compounds are an exception where sensory loss may progress for several months after cessation of treatment ("coasting"). As more effective multiple drug combinations are used, patients will be treated with several neurotoxic drugs. Synergistic neurotoxicity has not been extensively investigated. Pre-existent neuropathy may influence the development of a toxic neuropathy. Underlying inherited or inflammatory neuropathies may predispose patients to developing very severe toxic neuropathies. Other factors such as focal radiotherapy or intrathecal administration may enhance neurotoxicity. The neurologist managing the cancer patient who develops neuropathy must answer a series of important questions as follows: (1) Are the symptoms due to peripheral neuropathy? (2) Is the neuropathy due to the underlying disease or the treatment? (3) Should treatment be modified or stopped because of the neuropathy? (4) What is the best supportive care in terms of pain management or physical therapy for each patient? Prevention of toxic neuropathies is most important. In patients with neuropathy, restorative approaches have not been well established. Symptomatic and other management are necessary to maintain and improve quality of life.

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Section: Individual Classes Of Chemotherapy Drugs Associated With Cinmentioning

confidence: 99%

Chemotherapy‐induced neuropathy

Windebank

Grisold

2008

J Peripheral Nervous Sys

559

401

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“…More than one third of the patients develop signs of autonomic nervous system dysfunction characterised by orthostatic hypotension, constipation, paralytic ileus, urinary bladder dysfunction and erectile impotence. Some of the patients show disturbances of eye movements and paralysis of the vocal cords [7]. Most of these symptoms are reversible after months or years.…”

Section: Vincristinementioning

confidence: 99%

Chemotherapy-induced peripheral neuropathy

Quasthoff¹,

Hartung²

2002

J Neurol

823

552

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The induction of peripheral neuropathy is a common factor in limiting therapy with chemotherapeutic drugs. Little is known about the mechanisms responsible for the development of neuropathy. Depending on the substance used, a pure sensory and painful neuropathy (with cisplatin, oxaliplatin, carboplatin) or a mixed sensorimotor neuropathy with or without involvement of the autonomic nervous system (with vincristine, taxol, suramin) can ensue. Neurotoxicity depends on the total cumulative dose and the type of drug used. In individual cases neuropathy can evolve even after a single drug application. A general predisposition for developing a chemotherapy-induced neuropathy has been observed in nerves previously damaged by diabetes mellitus, alcohol or inherited neuropathy. The recovery from symptoms is often incomplete and a long period of regeneration is required to restore function. Up to now, no drug is available to reliably prevent or cure chemotherapy-induced neuropathy.

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“…Besides our patient, there are only four other reported cases of reintroduction of vincristine at full dose [11,14,16,17] and in two of them there was a relapse [11,14,16] (Table 1). The reason for continuing vincristine at full dose in our case was that at that point our differential for vocal cord palsy was mainly infection, and the mass at the right aryepiglottic fold was a red herring.…”

Section: Discussionmentioning

confidence: 74%

Vincristine-induced vocal cord palsy and successful re-treatment in a patient with diffuse large B cell Lymphoma: a case report

Samoon

Shabbir-Moosajee

2014

BMC Res Notes

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BackgroundVincristine, a type of vinca alkaloid, is widely used in the treatment of various childhood and adult malignancies. A well-known side effect of vincristine is its neurotoxicity and it is rarely indicted in vagus nerve involvement. Vincristine induced vocal cord palsy is a potentially reversible condition, with the mainstay of therapy being withdrawal of the offending drug. However, there are no clear guidelines regarding the possibility of re-treatment with the causative agent.Case presentationA 58 year old Asian male presented with constipation and abdominal distension. Diagnostic investigations revealed stage IVB diffuse large B cell lymphoma (DLBCL). The patient was subsequently started on R-CHOP (Rituximab, Cyclophosphamide, Doxorubicin, Vincristine, and Prednisolone). On day twelve of receiving course four of R-CHOP, our patient presented to the hospital with a history of hoarseness of voice. Clinical and radiological examination revealed bilateral vocal cord palsy. Tracheostomy was done in view of a compromised airway. The patient subsequently went on to receive two more cycles of R-CHOP. Two weeks later Flexible laryngoscopy showed no lesion and the vocal cords were moving normally. The tracheostomy was removed. His voice has improved since and the patient is currently in remission.ConclusionThe occurrence of vincristine induced vocal cord palsy has been well reported in the literature. We strongly believe that our patient developed vocal cord palsy secondary to vincristine. The uniqueness of our patient’s case lies in successful re-treatment of our patient with the offending drug. To the best of our knowledge this is the third instance where a patient was successfully re-treated with vincristine after having developed vocal cord palsy as a result of its use.

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Vocal fold palsy following vinca alkaloid treatment

Cited by 26 publications

References 15 publications

Chemotherapy‐induced neuropathy

Chemotherapy‐induced neuropathy

Chemotherapy-induced peripheral neuropathy

Vincristine-induced vocal cord palsy and successful re-treatment in a patient with diffuse large B cell Lymphoma: a case report

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