Neurologic Complications in Patients with Cancer

Abstract

Neurologic symptoms are commonly seen in patients with cancer and can be among the most challenging to diagnose and manage. It is often difficult to determine if new neurologic symptoms are secondary to direct effects of a malignant lesion, systemic complications of disease, paraneoplastic disorders, or side effects of cancer treatment itself. However, early diagnosis and treatment of each of these conditions can improve patients' quality of life and long-term functional outcomes. In this review, we describe a systematic approach to the diagnosis of new neurologic symptoms in patients with known malignancy. We have categorized the neurologic complications of cancer through a mechanistic approach, with an emphasis on ascertaining underlying pathophysiology to guide treatment choice. This review focuses on the acute neurologic complications of cancer that require hospital admission.

Altered Mental Status in Cancer

“…63 Cancer Therapy-Related AMS include CNS infections due to acute infection or reactivation of a latent virus secondary to immunosuppression, immune dysregulation in the case of immune-related cancer-directed therapies, posterior reversible encephalopathy syndrome (PRES), seizure, or autoimmune encephalitis in the setting of targeted therapies. 68 In this section, we provide a broad overview of traditional and novel treatments that may cause AMS in a patient with a cancer-treatment history.…”

“…Brain irradiation can induce a multitude of CNS side effects that may result in AMS, including but not limited to seizures, encephalopathy, stroke, radiation necrosis, herniation, and coma over a time course spanning from days to years (►Table 5). 68 Cerebral radiation necrosis, which is an inflammatory necrotic process after radiation therapy, most likely involves vascular changes from endothelial injury mediated by proinflammatory cytokines, though the exact mechanism is not clear. 78 It can present with a vast array of symptoms from headache to focal neurologic deficits, and can manifest as progressive neurologic deterioration over a longer period of time.…”

“…In-depth treatment of ICI-related is discussed elsewhere, but in brief, including corticosteroids as first line, with escalating therapies including intravenous immunoglobulin, plasma exchange, and immunosuppressive medications. 68,91 There are unique CNS complications associated with chimeric antigen receptor therapy (CAR-T). Specifically, AMS can manifest as immune effector cell-associated neurologic syndrome (ICANS), which is a neurologic complication of CAR-T therapy that is characterized by encephalopathy, fatigue, poor attention, and concentration and in some instances focal-neurological deficits.…”

“…[111][112][113] Though any nutritional deficiencies are possible in a patient with very poor oral intake, it is especially important to keep in mind deficiencies in vitamin B1 (thiamine) and vitamin B12 (cobalamin), as they are more common in the for nutrition-based AMS. 68 Nonalcoholic Wernicke's Korsakoff syndrome is caused by severe thiamine deficiency and should be suspected in a patient with encephalopathy with ataxia and confabulations. 114 Similarly, vitamin B12 deficiency usually presents with an initial distal neuropathy, cognitive changes, and weakness.…”

Glycoconjugate Nanoparticle-Based Systems in Cancer Immunotherapy: Novel Designs and Recent Updates

“…However, as with all successes come setbacks and unanticipated factors that can continually be improved. For immunotherapy, these can be due to a host of factors, many that stem from a post-treatment overdriven immune system (cytokine release syndrome, activation of co-inhibitory pathways leading to T-cell exhaustion and effector cell neurotoxicity caused by overactive cytokine release in the cerebral spinal fluid) ( 17 – 19 ). Often, the immunotherapy is not enough to overcome the tumor immunosuppressive environment, led by tumor-associated macrophages and other lymphocytes that secrete cytokines that trigger the production of checkpoint molecules like PD-1 and PD-L1 ( 20 – 23 ).…”