Although these drugs are generally considered safer and less toxic than conventional chemotherapy, off-target toxicities (e.g., neurotoxicity) may emerge, particularly during prolonged use. In fact, physicians should be trained not only at the use of treatments but also at the recognition and proper assessment of the first signs of neurotoxicity, and patients should be made aware of it to report early symptoms with the common goal of preventing irreversible damage. Although treatment with steroids has been advocated, this syndrome is frequently self-limiting and patients usually recover completely over the course of several weeks without specific therapy. Patients report problems with memory retrieval, learning, and concentration, which may persist after treatment has finished or never fully resolve.1 The incidence of acute problems during treatment ranges from 15% to 70%, with 50% of patients in one study identifying persistent problems a year after treatment.2 Cross-sectional studies also suggest persistent cognitive dysfunction in 20% to 30% of patients 2 to 10 years posttreatment.3,4. Chemotherapy-induced neurotoxicity is a serious consequence of cancer treatment, which occurs with some of the most commonly used chemotherapies 1,2.Chemotherapy-induced peripheral neuropathy produces symptoms of numbness and paraesthesia in the limbs and may progress to difficulties with fine motor skills and walking, leading to functional impairment. Acta Obstet Gynecol Scand. JCO Oncology Practice Paola Marmiroli, Shire (I), Acetylon Pharmaceuticals (I), Methys (I). Guido Cavaletti. JCO Clinical Cancer Informatics ASCO Meetings In patients with CIPN who are treated with platinum drugs, a peculiar temporal pattern can be observed, which is represented by symptoms that worsen months after chemotherapy suspension—the so-called coasting phenomenon. A dying-back process that starts from distal nerve endings and is followed by disturbed axonal flow has been demonstrated in models of CIPN associated with taxanes.19 However, macrophage activation in both the DRG and the peripheral nerve, and microglial activation within the spinal cord, also have been demonstrated.20 In an animal study, paclitaxel-induced swelling and vacuolation of axonal mitochondria in A and C fibers was demonstrated.21, Competition studies with paclitaxel demonstrated that epothilones might act on the same or on an overlapping binding site on tubulin. Acute neurotoxicity symptoms, most commonly cold-induced paraesthesiae and jaw or throat tightness, were reported by all patients treated with oxaliplatin (n = 22) and none of those treated with carboplatin plus paclitaxel or cisplatin (n = 6). Consulting or Advisory Role: Guido Cavaletti, Shire Pharmaceuticals. DOI: 10.14694/EdBook_AM.2015.35.e553 American Society of Clinical Oncology Educational Book Among the reasons for this situation, the insufficient knowledge of the pathogenesis of cancer treatment–related neurotoxicity is definitely one of the most important issues. MRI scanning reveals diffuse high-intensity lesions within the central matter on T2-weighting that may be reversible.18 The encephalopathy should rapidly resolve entirely on stopping cytarabine; however, damage may be permanent and progress to leukoencephalopathy in a minority of patients, usually those with preexisting organ dysfunction or neurological problems.8 Less commonly, optic neuropathy, anosmia, and an incompletely reversible myelopathy have been reported.14 As with methotrexate, the intrathecal administration of cytarabine may cause ascending myelitis.8,79–81 There have also been case reports of sensory peripheral neuropathy following cytarabine exposure.82, Etoposide, a topoisomerase II inhibitor used in treatment of hematological, lung, ovarian, and testicular cancers,69 causes very little neurotoxicity, although at very high doses there have been reports of peripheral neuropathy, headache, seizures, and somnolence, in bone marrow transplant recipients and patients with malignant gliomas.83,84, Neurotoxicity with the antimetabolite fludarabine is uncommon, but somnolence, acute encephalopathy, and chronic leukoencephalopathy progressing to coma and death have all been reported.85. 2019 Feb;98(2):240-249. doi: 10.1111/aogs.13477. To achieve a proper understanding of the long-term effects of CIPN, knowledge of the basic pathogenetic and clinical features related to the use of the different neurotoxic dugs is necessary. More rarely, motor, autonomic, or cranial nerve involvement also can be observed. The ASCO Post Typical Clinical Features of Chemotherapy-Induced Peripheral Neurotoxicity Associated with Standard Chemotherapeutic Agents. Histologically, these patches contain an intense inflammatory infiltration with demyelination but axonal sparing. In this clinical setting, a formal trial (the CI-PeriNomS study) demonstrated the actual reliability of physician-assessed and patient-reported outcome measures in patients with stable CIPN. Peripheral neuropathies are the most common neurological complications in patients receiving chemotherapy, especially with regimens containing taxanes (taxol, docataxel), platinum (cisplatin, carboplatin, oxaliplatin), and vinca alkaloids (vincristine). It is more common after oral administration, and is also more frequent with short intravenous infusion durations.89–91 The mechanism of toxicity is unclear but may be related to accumulation of metabolites such as chloracetaldehyde and chloro- ethylamine, which deplete intracellular glutathione and NAD and impair mitochondrial electron transport.92 Methylene blue, 300 mg IV in 6 divided doses, is used in the treatment of ifosfamide-induced encephalopathy and 50 mg IV qds may be given prophylatically.93–96 It is thought to act primarily as an alternative electron acceptor restoring mitochondrial respiratory chain function, but may also oxidate NADH and inhibits plasma monoamine oxidases. Over the last decades, improvement in early diagnosis, precise subtype characterization, and more effective treatment plans allowed clinicians to achieve complete cures or remarkable increases in long-term survival in patients living with cancer in developed countries. Cytarabine and 5-fluorouracil are the cytotoxics most likely to cause cerebellar dysfunction including truncal ataxia, gait disturbance, and ataxia.8,14,21,22 Acutely, the MRI tends to be normal, but subsequent scans may show chronic atrophy due to irreversible Purkinje cell loss.15–18. Mols et al performed a systematic review of the available literature and found 11 studies that assessed the relationship that exists between CIPN and QoL.45 Eight of these studies reported an association, whereas three failed to observe any association between CIPN and QoL. Cognitive effects of cancer and its treatments at the intersection of aging: what do we know; what do we need to know? However, considerable input from the multidisciplinary team is required in the holistic care of the patient,53 including analgesia for neuropathic pain, maximization of mobility (with occupational and physiotherapist involvement where there is loss of balance, sensory loss, or muscle weakness), and good nursing care to manage bowel or bladder dysfunction, protection of pressure areas in immobilized patients, and maintenance of a safe environment if patients are confused. To overcome some of these problems, a transition to rationally designed, molecularly targeted drugs, which aims at a much more specific effect on cancer cells and a sparing of normal tissues, has occurred in chemotherapy. The first methodological study designed to address this relevant issue has been reported recently,4 and marked differences in perceptions of CIPN by patients versus by treating physicians have been demonstrated.14 These apparently conflicting results actually represent two sides of the same coin, and they should always be coupled in the planning and interpretation of any study devoted to CIPN investigation or treatment. The symptoms may seem vague and unconnected, lead… Despite these efforts, knowledge about this problem is still largely incomplete, and further studies are necessary to clarify the several still-unsettled aspects of long-term peripheral neurotoxicity of conventional and targeted anticancer chemotherapy. It may cause cerebrovascular accidents during the first few weeks of its administration. Paola Marmiroli, Kedrion (I). The epidemiology of CIPN is still unclear, and one of the main reasons for this uncertainty is the lack of a gold standard in its assessment.5 In fact, the reliability and reproducibility of a CIPN assessment in patients with cancer are still unmet clinical and scientific needs. Buy Membership for Hematology, Oncology and Palliative Medicine Category to continue reading. Cancer patients have frequently recognized decreased cognitive function (“chemo-brain”) during chemotherapy, which, in the past, was attributed by their physicians to stress or depression. The effect is cumulative. Despite these challenges, the proper design of a reliable assessment plan is now easier for patients with CIPN. The previously accepted paradigm that CIPN, in nearly all cases, is a reversible clinical condition has recently been challenged by several studies performed mainly in patients with breast, colorectal, and ovarian cancer, in which the use of neurotoxic drugs is frequent and survival for greater than 5 years is increasingly frequent. Cerebellar signs in an oncology patient are usually due to direct spread of cancer, particularly if it is asymmetric. Speakers' Bureau: None. Cancer patients have frequently recognized decreased cognitive function (“chemo-brain”) during chemotherapy, which, in the past, was attributed by their physicians to stress or depression. Paola Alberti. MRI shows patchy abnormalities within the white matter that enhance with gadolinium. Second, the pathogenesis of the clinical signs of PNS damage is unknown for most chemotherapy-related conditions. However, with the aging population, cancer (and treatment-related toxicities) in the primary care setting are very likely to increase in the future. Overall, the importance of chemotherapy-related toxicity caused by PNS damage is underestimated. A number of trials have investigated the benefits of agents such as calcium-magnesium infusions, carbamazepine, gabapentin, amifostine, and glutathione.7,35–52 However, the trials are small studies and no specific prophylaxis can be routinely recommended. Radiation patients may experience neuropathic side effects as well. Patients present with cognitive deficits, which may progress to dementia, coma, and death. Some of the effects of neurotoxicity may appear immediately, while others can take months or years to manifest.The effects of neurotoxicity depends on various different factors such as the characteristics of the neurotoxin, the dose a person has been exposed to, ability to metabolise and excrete the toxin, the ability of affected mechanism and structures to recover and how vulnerable a cellular target is.Some of the symptoms of neurotoxicity include: 1. Currently there are few therapies able to prevent neurological toxicity preemptively. They also cause cell-cycle kinetics alterations: postmitotic DRG neurons would reenter into the cell cycle and be induced into apoptosis.15 Other pathogenetic hypotheses have been proposed, which involve oxidative stress, mitochondrial dysfunction, reduction in the activity of enzymes involved in DNA base excision, repair of oxidative damage, redox regulation, and cellular transport.16–18, The most obvious mechanism of PNS damage by taxanes is related to their hyper-polymerizing action on microtubules. Abstract. But if you’re anything like me, that simple sounding “neuro check” can be an overwhelmingly daunting task, … Jordi Bruna. If focal neurological deficit is present, CT or MRI imaging may be helpful and, in any case, should be undertaken prior to a lumbar puncture. Patients with HIV-related malignancies are also at increased risk of cytotoxic-induced neuropathy, since both HIV and the drugs used to treat it (highly active antiretroviral therapy, or HAART) can cause neurological damage independently.34 Distal sensory neuropathy is the commonest form of HIV-associated neuropathy and can be difficult to distinguish from that caused by specific nucleoside antiretrovirals. Spinal cord toxicity can occur following intrathecal administration of certain cytotoxics in acute leukemias, lymphomas, and brain tumors. (May 14, 2015) In addition to the immune-mediated effect on the PNS, clinical pictures compatible with classical CIPN also have been described with cancer-targeted drugs. This is mostly because of the less efficient blood–nervous system barrier in the PNS, namely at the dorsal root ganglia (DRG) level, which allows easy access to nerve fibers and neurons. Patients present with cognitive deficits, which may progress to dementia, coma, and death.10–14 MRI imaging shows widespread changes throughout the white matter,15–18 and histologically, there is axonal swelling, demyelination, and neuronal death.19 Those most at risk are patients treated with methotrexate or cytarabine, particularly if given intrathecally or if cranial radiotherapy preceded cytotoxic administration.9 Elderly patients with primary central nervous system lymphoma undergoing treatment with high-dose methotrexate and whole-brain radiotherapy (WBRT) are at particularly high risk of developing this complication.20 There is no specific therapy that can halt the progressive decline, and overall the prognosis is poor. With subsequent treatment cycles, symptoms may progress to permanent paresthesia, with decreased sensation to pinprick, light touch, and vibration on formal testing.9,25–29 At this stage, chemotherapy should be stopped or the dose reduced, as continuing can lead to difficulty with activities of daily living. In rarer situations, this can be due to paraneoplastic syndromes, which tend to have a subacute onset and may be associated with the presence of antineuronal antibodies. The neuropathy tends to be predominantly sensory in nature, with a glove and stocking distribution. Another study was reported in 2014 by Ezendam et al,47 who investigated a cohort of patients with ovarian cancer by using two EORTC QoL scales; the results demonstrated that CIPN symptoms were significantly associated with QoL impairment. Neurotoxicity is not that simple. Central neurotoxicity of chemotherapy, neurotoxic agents & consequences. Neurotoxic side effects of chemotherapy occur frequently and are often a reason to limit the dose of chemotherapy. Paola Marmiroli. Employment: None. Acute encephalopathy is associated with the administration of high-dose methotrexate (>3 mg/m, Medical Complications in the Management of Brain Tumors, Neurological Complications of Radiation Therapy. e553-e560. From the Experimental Neurology Unit and Milan Center for Neuroscience, Department of Surgery and Translational Medicine, University of Milano-Bicocca, Monza, Italy. Neurotoxicity with chemotherapy is common and second only to myelosuppression as a reason to limit dosing. Since bone marrow toxicity, as the major limiting factor in most chemotherapeutic regimens, can be overcome with growth factors or bone marrow transplantation, the use of higher doses of chemotherapy is possible, which increases the risk of neurotoxicity. Apart from dose reduction or discontinuing the drugs implicated in the development of neurotoxicity, there is very little in the way of specific pharmacological management to reverse their side effects. Long-term effects of chemo on the cognitive function of cancer patients, Chemotherapy-induced neuropathy: a comprehensive survey, Chemotherapy-induced peripheral neurotoxicity (CIPN): an update, Chemotherapy-induced peripheral neurotoxicity in the era of pharmacogenomics, Chemotherapy-induced peripheral neurotoxicity, Physician-assessed and patient-reported outcome measures in chemotherapy-induced sensory peripheral neurotoxicity: two sides of the same coin, Cisplatin-induced apoptosis in rat dorsal root ganglion neurons is associated with attempted entry into the cell cycle, Oxaliplatin-induced neurotoxicity is dependent on the organic cation transporter OCT2, Neuronal drug transporters in platinum drugs-induced peripheral neurotoxicity, Mechanisms underlying chemotherapy-induced neurotoxicity and the potential for neuroprotective strategies, Morphological and morphometric analysis of paclitaxel and docetaxel-induced peripheral neuropathy in rats, Intravenous paclitaxel administration in the rat induces a peripheral sensory neuropathy characterized by macrophage infiltration and injury to sensory neurons and their supporting cells, Prevention of paclitaxel-evoked painful peripheral neuropathy by acetyl-l-carnitine: effects on axonal mitochondria, sensory nerve fiber terminal arbors, and cutaneous Langerhans cells, Damage to the cytoskeleton of large diameter sensory neurons and myelinated axons in vincristine-induced painful peripheral neuropathy in the rat, Bortezomib-induced painful peripheral neuropathy: an electrophysiological, behavioral, morphological and mechanistic study in the mouse, Bortezomib-induced painful neuropathy in rats: a behavioral, neurophysiological and pathological study in rats, Bortezomib induces the formation of nuclear poly(A) RNA granules enriched in Sam68 and PABPN1 in sensory ganglia neurons, Preclinical and clinical development of the proteasome inhibitor bortezomib in cancer treatment, Proteasome inhibitors increase tubulin polymerization and stabilization in tissue culture cells: a possible mechanism contributing to peripheral neuropathy and cellular toxicity following proteasome inhibition, Evaluation of tubulin polymerization and chronic inhibition of proteasome as citotoxicity mechanisms in bortezomib-induced peripheral neuropathy, Thalidomide sensory neurotoxicity: a clinical and neurophysiologic study, Lenalidomide in patients with chemotherapy-induced polyneuropathy and relapsed or refractory multiple myeloma: results from a single-centre prospective study, Interventions for preventing neuropathy caused by cisplatin and related compounds, Prevention and management of chemotherapy-induced peripheral neuropathy in survivors of adult cancers: American Society of Clinical Oncology clinical practice guideline, Neurological complications following alemtuzumab-based reduced-intensity allogeneic transplantation, Guillain-Barré syndrome after use of alemtuzumab (Campath) in a patient with T-cell prolymphocytic leukemia: a case report and review of the literature, A phase I weekly dosing study of brentuximab vedotin in patients with relapsed/refractory CD30-positive hematologic malignancies, Results of a pivotal phase II study of brentuximab vedotin for patients with relapsed or refractory Hodgkin's lymphoma, Severe peripheral motor neuropathy in a patient with Hodgkin lymphoma treated with brentuximab vedotin, Long-term neuropathy after oxaliplatin treatment: challenging the dictum of reversibility, Leucovorin and fluorouracil with or without oxaliplatin as first-line treatment in advanced colorectal cancer, Oxaliplatin, fluorouracil, and leucovorin as adjuvant treatment for colon cancer, Chemotherapy-induced neuropathy and its association with quality of life among 2- to 11-year colorectal cancer survivors: results from the population-based PROFILES registry, Peripheral neuropathy in colorectal cancer survivors: the influence of oxaliplatin administration. 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