Severe vincristine neuropathy in charcot‐marie‐tooth disease type 1A

  title={Severe vincristine neuropathy in charcot‐marie‐tooth disease type 1A},
  author={William D. Graf and Phillip F. Chance and M. William Lensch and L J Eng and Hillary P. Lipe and Thomas D. Bird},
A general predisposition for vincristine‐related neuropathy has been observed in persons with a family history of hereditary neuropathies. 

Severe peripheral neuropathy secondary to vincristin therapy

Two patients with unrecognized hereditary neuropathy who developed foot drop following low dose vincristine therapy are described, highlighting the importance of detailed neurologic examination and history taking before initiating therapy.

Vincristine treatment revealing asymptomatic hereditary motor sensory neuropathy type 1A

Neurophysiological and genetic analysis at age 8 years indicated that vincristine had induced symptoms of a hereditary sensory motor neuropathy type 1A, which had previously been asymPTomatic; his genetically affected mother was also asymptomatic.

Vincristine‐induced acute neurotoxicity versus Guillain–Barré syndrome: a diagnostic dilemma

The case of a patient with acute lymphoblastic leukaemia who developed a fulminant motor polyradiculoneuropathy resembling an axonal variant of Guillain‐Barré syndrome is reported.

Coexistence of two chronic neuropathies in a young child: Charcot–marie–tooth disease type 1A and chronic inflammatory demyelinating polyneuropathy

An 18‐month‐old Charcot–Marie–Tooth type 1A (CMT1A) patient who developed a rapid‐onset neuropathy responded well to immunomodulation, confirming the coexistence of an inherited and an inflammatory neuropathy.

Charcot-Marie-Tooth hereditary neuropathy revealed after administration of docetaxel in advanced breast cancer

This case stresses again the necessity to obtain a complete personal and familial anamnesis and to perform a neurologic examination before the administration of neurotoxic chemotherapeutical agents to prevent the clinical expression of these hereditary neuropathies.

Acute motor and sensory axonal neuropathy in Burkitt‐like lymphoma

It is hypothesized that immune mechanisms triggered by the lymphoma initiated damage to the peripheral nervous system and enhanced its vulnerability to the toxic effects of vincristine.

Uneventful administration of vincristine in Charcot–Marie–Tooth disease type 1X

CMT should be excluded in any patient who develops a profound, acute neuropathy following vincristine, as many patients in the cases reviewed were asymptomatic prior to treatment.

Acute deterioration of Charcot-Marie-Tooth disease IA (CMT IA) following 2 mg of vincristine chemotherapy.

Prior to administration of vincristine family and patient history as well as physical examination should be performed carefully to look for underlying hereditary neuropathy to prevent serious neurologic complications.

Cisplatin-based chemotherapy for testicular cancer in a patient with spinal muscular atrophy: a case report.

The authors report the successful treatment of a patient with testicular cancer and spinal muscular atrophy, an inherited degenerative neuromuscular disease with cisplatin-based chemotherapy.

Peripheral neurotoxic disorders.




Vincristine neurotoxicity in Charcot‐Marie‐Tooth syndrome

The case of a patient with Charcot‐Marie‐Tooth syndrome and diffuse large‐cell lymphoma, in whom a severe generalized weakness developed after the intravenous administration of vincristine (2 mg)

Vincristine neuropathy in type I and type II Charcot-Marie-Tooth disease (hereditary motor sensory neuropathy).

A patient with Ewing's sarcoma and demyelinating type Charcot-Marie-Tooth disease and axonal type CMT developed severe neuropathy after receiving a total vincristine dose of 6 mg and recovered quickly.

Polyneuropathy following vincristine therapy in two patients with Charcot-Marie-Tooth syndrome.

Two patients with nodular sclerosing Hodgkin's disease are described in whom a rapidly progressive, but reversible, severe polyneuropathy developed when they were given a total of 4 mg of vincristine sulfate, which suggests that the use of vINCristine is contraindicated in patients with the demyelinating form of Charcot-Marie-Tooth syndrome.

Gene dosage is a mechanism for Charcot-Marie-Tooth disease type 1A

It is demonstrated that a patient with a cytogenetically visible duplication, dup(17)(p11.2p12), has decreased NCV, which supports the hypothesis that the CMT1A phenotype can result from a gene dosage effect.

Assignment of the Charcot-Marie-Tooth neuropathy type 1 (CMT 1a) gene to 17p11.2-p12.

The results indicated that the CMT 1a mutation is localized in the chromosomal region 17p11.2-p12 between the marker D17S71 and the gene for myosin heavy polypeptide 2 of adult skeletal muscle.

Neurotoxicity of commonly used antineoplastic agents (first of two parts).

The broad concept of "carcinomatous neuromyopathy" is frequently invoked to explain obscure neurologic symptoms in patients with cancer, but it is also important to realize that neurologic dysfunction may be iatrogenic — i.e., caused by the treatment of cancer.

Analysis of the DNA duplication 17p11.2 in Charcot‐Marie‐Tooth neuropathy type 1 pedigrees

It is confirmed that the CMT1 locus in these two pedigrees does not map to chromosome 17p11.2 or 1q, and further evidence for the existence of a third autosomal locus for C MT1 is provided.

Charcot–Marie–Tooth neuropathy type 1B is associated with mutations of the myelin P0 gene

The results indicate that P0 is a gene responsible for CMT1B, and point mutations found are located in the extracellular domain, which plays a significant role in myelin membrane adhesion.

Studies on the pathogenesis of vincristine‐induced neuropathy

The microtubule changes were associated with malorientation of microtubules and neurofilaments, accompanied by free vesicle accumulation and fragmentation of the smooth endoplasmic reticulum, and support the possibility that micro Tubules consist of both stable and labile segments.

Trisomy 17p associated with Charcot‐Marie‐Tooth neuropathy type 1A phenotype

Observations in this patient with trisomy 17p are relevant to an understanding of the genetic mechanism in CMT1A and provide strong evidence that gene dosage through segmentai trisomie for 17p11.2 results in the C MT1A phenotype.