Pruritus (PDQ®)–Health Professional Version

Pruritus (PDQ®)–Health Professional Version

Overview

Pruritus is usually an unpleasant sensation that elicits a desire to scratch, subjectively quantified by intensity, severity, location, and intractability. It may be proposed that itch is akin to pain because both sensations are thought to be transmitted from the skin to the central nervous system (CNS) through nociceptive small-caliber C nerve fibers.[1] The perception of pruritus, much like the perception of pain, is greatly altered by psychological and CNS factors, accounting for great subjective variability between individuals in perceived pruritus from the same pruritogen. Because of the subjective nature of pruritus, the lack of a precise definition, and only recent development of a suitable murine model, pruritus is a disorder that has not been researched adequately.[2]

This summary will focus on pruritus in the absence of a primary dermatosis, as is often encountered in patients receiving cancer treatment. However, there may still be significant secondary skin changes noted in the form of lichen simplex chronicus, prurigo nodules, linear excoriations, linear petechiae, or superficial erosions in places the patient can reach to scratch (either with fingernails, back scratchers, or makeshift tools).

Pruritus is a manifestation of an underlying systemic disease in approximately 10% to 25% of affected individuals.[3] In a single-institution retrospective review, patients seeking care for pruritus were more likely to have a concomitant diagnosis of cancer than patients without pruritus (odds ratio [OR], 5.76; 95% confidence interval, 5.53–6.00). The OR for malignancy was higher in White patients than in African American patients.[4] Nondermatological conditions that can lead to generalized pruritus include the following:[3]

  • Hepatic, renal, or thyroid dysfunction.
  • Malignancies, including lymphoma, chronic lymphocytic leukemia, and cancers of the liver, gallbladder, biliary tract, and skin.[4]
  • Myeloproliferative neoplasms (e.g., polycythemia vera).
  • HIV or parasitic infections.
  • Neuropsychiatric disorders.

Despite the wide array of diseases that may present with pruritus, a systematic evaluation of the differential using a good history, review of systems, and appropriate blood work will lead to a rational and finite group of etiologies. Then correction of the underlying cause (if possible) and treatment of pruritus may ensue.

In this summary, unless otherwise stated, evidence and practice issues as they relate to adults are discussed. The evidence and application to practice related to children may differ significantly from information related to adults. When specific information about the care of children is available, it is summarized under its own heading.

References
  1. Schmelz M: A neural pathway for itch. Nat Neurosci 4 (1): 9-10, 2001. [PUBMED Abstract]
  2. Feng J, Yang P, Mack MR, et al.: Sensory TRP channels contribute differentially to skin inflammation and persistent itch. Nat Commun 8 (1): 980, 2017. [PUBMED Abstract]
  3. Weisshaar E, Fleischer AB Jr, Bernhard JD, et al.: Pruritus and dysesthesia. In: Bolognia JL, Jorizzo JL, Schaffer JV: Dermatology. 3rd ed. Elsevier Saunders, 2012, pp 111-25.
  4. Larson VA, Tang O, Ständer S, et al.: Association between itch and cancer in 16,925 patients with pruritus: Experience at a tertiary care center. J Am Acad Dermatol 80 (4): 931-937, 2019. [PUBMED Abstract]

Etiology and Pathophysiology

When a primary dermatitis is present, the differential may be narrowed by the history and physical findings, such as:

  • Stigmata of atopic dermatitis.
  • Psoriasis.
  • Scabies.
  • Allergic contact dermatitis.
  • Primary cutaneous lymphoma.

Biopsy of skin dermatitis may be extraordinarily helpful in this scenario if the etiology is not readily evident from history and physical examination alone. Table 1 provides a list of differential diagnoses for when there is little or no primary dermatitis identifiable. Where available, the incidence of pruritus in that condition is given.

Table 1. Pruritus Differential With Little or No Primary Dermatitis
Disease State Prevalence of Pruritus (%)
HMG-CoA = 3-hydroxy-3-methyl-glutaryl–coenzyme A; IgE = immunoglobulin E.
Neoplastic:  
– Hodgkin disease 30 [1]
– Non-Hodgkin lymphoma 15 [2]
– Leukemias 5 [3]
– Carcinoid syndrome  
– Paraproteinemias  
Iron deficiency anemia  
Polycythemia rubra vera ≤50 [4]
Hyper-IgE syndromes  
Parasitic helminthic infection  
Drug-induced eosinophilia  
Chronic renal insufficiency 57 [5]
Liver disease:  
– Primary biliary cirrhosis 69 [6]
– Viral hepatitis infection 15 [7]
– Cholestatic disease  
– Autoimmune hepatitis  
Thyroid dysfunction:  
– Hashimoto thyroiditis  
– Hypothyroidism  
– Hyperthyroidism  
Medication induced:  
– Opioids (codeine, morphine, butorphanol)  
– Hydroxyethyl starch  
– Antimalarials (chloroquine, hydroxychloroquine, quinacrine)  
– 8-methoxypsoralen  
– Beta blockers  
– Hormones (estrogens, testosterone, progestins, anabolic steroids)  
– Phenothiazines  
– Aspirin  
– HMG-CoA reductase inhibitors  
Diabetes mellitus  
HIV infection  
Postherpetic neuralgia ≤60 [8]
Pregnancy 18 [3]
Xerosis  
Psychogenic (somatization, anxiety, depression, neurosis)  
Stroke sequelae  
Multiple sclerosis  

As evident from the differential, a solid history and physical examination are essential for sorting through the possibilities. To corroborate the clinical impression, a limited number of laboratory and radiological examinations also may be used to rule in or rule out many of the possibilities. For more information, see the Assessment section.

Hypothesized mechanisms of pruritus have been inferred from studies of pain because pain and itching share common molecular and neurophysiological mechanisms.[9] Both itch and pain sensations result from the activation of a network of free nerve endings at the dermal-epidermal junction. Activation may be the result of internal or external thermal, mechanical, chemical, or electrical stimulation. The cutaneous nerve stimulation is activated or mediated by several substances, including the following:

  • Histamine.
  • Vasoactive peptides.
  • Enkephalins.
  • Substance P (a tachykinin that affects smooth muscle).
  • Prostaglandins.
  • Interleukins (IL-4, IL-13, IL-31).[10]

It is believed that nonanatomical factors (such as psychological stress, tolerance, and presence and intensity of other sensations and/or distractions) determine itch sensitivity in different regions of the body.

The itch impulse is transmitted along the same neural pathway as pain impulses, i.e., traveling from peripheral nerves to the dorsal horn of the spinal cord, across the cord via the anterior commissure, and ascending along the spinothalamic tract to the laminar nuclei of the contralateral thalamus. Thalamocortical tracts of tertiary neurons are believed to relay the impulse through the integrating reticular activating system of the thalamus to several areas of the cerebral cortex. Factors that are believed to enhance the sensation of itch include:[9,1113]

  • Dryness of the epidermis and dermis.
  • Anoxia of tissues.
  • Dilation of the capillaries.
  • Irritating stimuli.
  • Psychological responses.

The motor response of scratching follows the perception of itch. Scratching is modulated at the corticothalamic center and is a spinal reflex. Itching may be relieved for 15 to 25 minutes after scratching. The mechanism through which the itch is relieved by scratching is unknown. It is hypothesized that scratching generates sensory impulses that break circuits in the relay areas of the spinal cord. However, scratching may actually enhance the sensation of itching, creating a characteristic itch-scratch-itch cycle. Other physical stimuli such as vibration, heat, cold, and ultraviolet radiation diminish itching and increase the release of proteolytic enzymes, potentially eliciting the itch-scratch-itch cycle.

A pinprick near or in the same dermatome as an itchy point will abolish the itch sensation.[12] It is known that hard scratching may substitute pain for the itch, and in some instances, the patient might find pain the more tolerable sensation. It is thought that spinal modulation of afferent stimuli (Gate theory) and central mechanisms may play a role in the relief of itch.[12]

Hypothesized pathogenesis of pruritus associated with underlying disease states is varied. Biliary, hepatic, renal, and malignant diseases are thought to produce pruritus through circulating toxic substances. Histamine released from circulating basophils and the release of leukopeptidase from white blood cells may trigger pruritus associated with lymphomas and leukemias. Elevated blood levels of kininogen in Hodgkin lymphoma, the release of histamine or bradykinin precursors from solid tumors, and the release of serotonin in carcinoids may all be related to pruritus.[11,14]

People receiving cytotoxic chemotherapy, radiation therapy, and/or biologic response modifiers for the treatment of malignancy are likely to experience pruritus. This population is likely to be exposed to many of the other etiological factors related to pruritus, ranging from nutrition-related xerosis (dry skin) to radiation desquamation, chemotherapy-induced and biologic agent–induced side effects, antibiotic reactions, and other drug sensitivities. Because many of these therapies lead to decreased cell turnover, skin can become thin, atrophic, and dehydrated. Long-term xerosis may also occur with poor recovery of sweat, sebaceous, and apocrine gland function after a course of cytotoxic therapy.

References
  1. Gobbi PG, Attardo-Parrinello G, Lattanzio G, et al.: Severe pruritus should be a B-symptom in Hodgkin’s disease. Cancer 51 (10): 1934-6, 1983. [PUBMED Abstract]
  2. Kumar SS, Kuruvilla M, Pai GS, et al.: Cutaneous manifestations of non-Hodgkin’s lymphoma. Indian J Dermatol Venereol Leprol 69 (1): 12-5, 2003 Jan-Feb. [PUBMED Abstract]
  3. Weisshaar E, Dalgard F: Epidemiology of itch: adding to the burden of skin morbidity. Acta Derm Venereol 89 (4): 339-50, 2009. [PUBMED Abstract]
  4. Diehn F, Tefferi A: Pruritus in polycythaemia vera: prevalence, laboratory correlates and management. Br J Haematol 115 (3): 619-21, 2001. [PUBMED Abstract]
  5. Duque MI, Thevarajah S, Chan YH, et al.: Uremic pruritus is associated with higher kt/V and serum calcium concentration. Clin Nephrol 66 (3): 184-91, 2006. [PUBMED Abstract]
  6. Rishe E, Azarm A, Bergasa NV: Itch in primary biliary cirrhosis: a patients’ perspective. Acta Derm Venereol 88 (1): 34-7, 2008. [PUBMED Abstract]
  7. Cribier B, Samain F, Vetter D, et al.: Systematic cutaneous examination in hepatitis C virus infected patients. Acta Derm Venereol 78 (5): 355-7, 1998. [PUBMED Abstract]
  8. Oaklander AL, Bowsher D, Galer B, et al.: Herpes zoster itch: preliminary epidemiologic data. J Pain 4 (6): 338-43, 2003. [PUBMED Abstract]
  9. Greaves MW: Pathophysiology of pruritus. In: Fitzpatrick TB, Eisen AZ, Wolff K, et al., eds.: Dermatology in General Medicine. 3rd ed. McGraw-Hill, 1987, Chapter 7, pp 74-78.
  10. Erickson S, Nahmias Z, Rosman IS, et al.: Immunomodulating Agents as Antipruritics. Dermatol Clin 36 (3): 325-334, 2018. [PUBMED Abstract]
  11. Abel EA, Farber EM: Malignant cutaneous tumors. In: Rubenstein E, Federman DD, eds.: Scientific American Medicine. Scientific American, Inc, Chapter 2: Dermatology, Section XII, 1-20, 1992.
  12. Bernhard JD: Clinical aspects of pruritus. In: Fitzpatrick TB, Eisen AZ, Wolff K, et al., eds.: Dermatology in General Medicine. 3rd ed. McGraw-Hill, 1987, Chapter 7, pp 78-90.
  13. Duncan WC, Fenske NA: Cutaneous signs of internal disease in the elderly. Geriatrics 45 (8): 24-30, 1990. [PUBMED Abstract]
  14. Abel EA, Farber EM: Drug eruptions and urticaria. In: Rubenstein E, Federman DD, eds.: Scientific American Medicine. Scientific American, Inc, Chapter 2: Dermatology, Section VI, 1-11, 1990.

Assessment

Pruritus is a symptom, not a diagnosis or disease. Generalized pruritus should be investigated because of its strong medical significance, as outlined above, particularly if it interferes with daily activities or sleep, and/or is intractable. For more information, see the Etiology and Pathophysiology section. Assessment of pruritus must incorporate an accurate and thorough history and physical examination.[1]

A history includes the following data:

  • Location, onset, duration, and intensity of itching.
  • Effect on activities of daily living or sleep.
  • Factors that relieve and aggravate itching.
  • Other family members or pets affected.
  • History of pruritus.
  • History of malignant disease.
  • Current malignant disease and treatment.
  • Nonmalignant systemic diseases.
  • Use of medications (analgesics, antibiotics, and other prescription and nonprescription drugs, including illicit drugs).
  • Nutritional and fluid level status.
  • Social history (hobbies, occupation, sexual history, and travel).
  • Current skin care practices.
  • Patient’s emotional state.

A physical examination provides data from an assessment of the following:

  • All skin surfaces for signs of infection.
  • All skin surfaces for signs of primary dermatitis (e.g., drug reaction, psoriasis, atopic dermatitis, connective tissue disease, and lichen planus).
  • All skin surfaces for signs of secondary dermatitis (e.g., macular erythema, dryness, excoriation, linear petechiae, prurigo nodules, and lichen simplex chronicus).
  • Environmental factors (temperature, humidity).
  • Physical factors (tight, constrictive clothing).
  • Skin turgor, texture, color, temperature, and cutaneous neoplasms.

First-line studies should include the following:

  • Complete blood count with differential and platelet count.
  • Renal function (blood urea nitrogen, serum creatinine).
  • Hepatic function (transaminases, alkaline phosphatase, bilirubin).
  • Lactate dehydrogenase.
  • Thyroid function (thyroid-stimulating hormone, thyroxin levels).
  • Chest x-ray.
  • Erythrocyte sedimentation rate.

Second-line laboratory studies guided by a review of systems and a physical examination may include the following:

  • Skin biopsy (routine histology with and without direct immunofluorescence).
  • HIV screening.
  • Serum iron, total iron-binding capacity, and ferritin.
  • Fasting glucose and hemoglobin A1C.
  • Parathyroid function (calcium, phosphate, and parathyroid hormone levels).
  • Viral hepatitis screening.
  • Serum immunoglobulin E levels.
  • Serum protein electrophoresis/serum immunofixation electrophoresis.
  • Tissue transglutaminase and endomysial antibodies.
  • Serum tryptase, histamine, and/or chromogranin-A levels.
  • Urine for sediment; 24-hour urine collection for 5-hydroxyindoleacetic acid (serotonin metabolite) and methylimidazoleacetic acid (histamine metabolite).
  • Stool for occult blood, ova, and parasite.
References
  1. Weisshaar E, Fleischer AB Jr, Bernhard JD, et al.: Pruritus and dysesthesia. In: Bolognia JL, Jorizzo JL, Schaffer JV: Dermatology. 3rd ed. Elsevier Saunders, 2012, pp 111-25.

Interventions

Note: Some citations in this section are followed by a level of evidence. The PDQ Editorial Boards use a formal ranking system to help the reader judge the strength of evidence linked to the reported results of a therapeutic strategy. For more information, see Levels of Evidence.

If an underlying cause of pruritus is identified, treatment of the primary disease or correction of the underlying abnormality is the primary therapy. For example, iron supplementation in the setting of iron-deficiency anemia or thyroid supplementation for hypothyroidism should be initiated first. However, gentle skin techniques are considered helpful adjuvant therapies, even if they are not expected to completely alleviate the symptoms.

Interventions for pruritus can be categorized into four distinct groups:

  1. Prevention and elimination of provocative factors.
  2. Topical therapies.
  3. Systemic therapies.
  4. Physical modalities.

Prevention and Elimination of Provocative Factors

Patients and caregivers must be included in planning and providing care to the extent possible. Education is an important aspect of symptom control. Skin care regimens incorporate protection from the environment, good cleansing practices, and internal and external hydration.[1][Level of evidence: IV] The intensity of the regimen and the techniques used will vary according to etiological factors and the degree of distress associated with pruritus.

Adequate nutrition is essential to the maintenance of healthy skin. An optimal diet should include a balance of proteins, carbohydrates, fats, vitamins, minerals, and fluids. Daily fluid intake of at least 3,000 mL is suggested as a guideline but may not be possible for some individuals.[2,3]

Aggravating factors should be avoided, including the following:

  • Fluid loss secondary to fever, diarrhea, nausea and vomiting, or decreased fluid intake.
  • Bathing with hot water.
  • Using bubble baths or soaps that contain detergents.
  • Bathing more than once a day or bathing for longer than 30 minutes.
  • Using soap and adding oil early in a bath.
  • Using a reusable fomite for scrubbing (e.g., buff-puff or loofah sponge).
  • Using scents, fragrances, and perfumes.
  • Dry environment.
  • Laundering sheets and clothing with detergent containing scents, dyes, and preservatives.
  • Using fabric softener sheets.
  • Wearing tight restrictive clothing or clothing made of wool, synthetics, or other harsh/scratchy fabric.
  • Using underarm deodorants or antiperspirants.
  • Applying topical preparations containing scents, dyes, or preservatives.
  • Emotional stress.

Alleviating factors should be promoted, as follows:

  • Applying unscented emollient creams or ointments.
  • Bathing in tepid water.
  • Using mild skin cleansers (nonsoap) or soaps made for sensitive skin (e.g., Cetaphil cleanser, Dove for Sensitive Skin, Oilatum, Basis).
  • Using soap only for dirty areas; otherwise, water is sufficient.
  • Limiting bathing to 30 minutes daily or every other day.
  • Adding oil and using soap at the end of a bath or adding a colloidal oatmeal treatment early to the bath.
  • Gently washing, if needed, with a clean, soft cotton washcloth.
  • Rinsing all residue from bathing with fresh tepid water.
  • Drying off by patting skin instead of rubbing.
  • Maintaining a humid environment (e.g., using a humidifier).
  • Using cotton flannel blankets, if needed.
  • Washing sheets, clothing, and undergarments in mild soaps for infant clothing containing no scents, dyes, or preservatives (e.g., Dreft, All Free Clear, Tide Free and Gentle).
  • Using liquid fabric softener that is rinsed out in the wash (e.g., All Free Clear Fabric Softener) or avoiding fabric softener altogether.
  • Wearing loose-fitting clothing and clothing made of cotton or other soft fabrics.
  • Using distraction, relaxation, positive imagery, or cutaneous stimulation.

Heat increases cutaneous blood flow and may enhance itching. Heat also lowers humidity, and skin loses moisture when the relative humidity falls below 40%. A cool, humid environment may reverse these processes. Extensive bathing aggravates dry skin, and hot baths exacerbate fluid loss by causing vasodilation. The vasodilation results in increased blood flow, which enhances itching. Tepid baths have an antipruritic effect, possibly resulting from capillary vasoconstriction.

The goal of skin cleansing is to remove dirt and prevent odor, but actual hygienic practices are influenced by skin type, lifestyle, and culture. Bathing should be limited to 30 minutes every day or every 2 days.

Many soaps are salts of fatty acids with an alkali base, leading to excessive defatting of the skin lipids and altered skin pH, irritating the skin. Older adults or individuals with dry skin should limit the use of soaps to areas with apocrine glands. Plain water should suffice for cleaning other skin surfaces. Mild soaps have less soap or detergent content. Soap is a degreaser and can also irritate skin. Superfatted soaps deposit a film of oil on the skin surface, but there is no proof that they are less drying than other soaps, and they may be more expensive.

Residue left by detergents after bathing or used in laundering clothes and linens, as well as fabric softeners and antistatic products, may aggravate pruritus. Clothing detergent residue can be neutralized by the addition of vinegar (1 teaspoon per quart of water) to rinse water. Mild laundry soaps marketed for infant items also may offer a solution.

Loose-fitting, lightweight cotton clothes and cotton bed sheets are suggested. The elimination of heavy bedcovers may alleviate itching by decreasing body heat. Wool and some synthetic fabrics may be irritating. Distraction, music therapy, relaxation, and imagery may be useful to relieve symptoms.[4]

Topical Therapies

Over-the-counter products

Some topical agents—including cornstarch, talcum powder, perfumed powders, and bubble baths—can irritate the skin and cause pruritus. Cornstarch has been an acceptable intervention for pruritus associated with dry desquamation related to radiation therapy; however, it should not be applied to moist skin surfaces, areas with hair, sebaceous glands, skin folds (intertriginous zones), or areas close to mucosal surfaces, such as the vagina and rectum.[5,6] Glucose is formed when cornstarch is moistened, providing an excellent medium for fungal growth.[6]

Agents with metal ions (i.e., talcum and aluminum used in antiperspirants) enhance skin reactions during external-beam radiation therapy and should be avoided throughout the course of radiation therapy. Talcum-based agents are otherwise preferred over cornstarch-based modalities when needed, particularly for intertriginous zones. Other common ingredients in over-the-counter lotions and creams that may enhance skin reactions include alcohol, topical antibiotics, and topical anesthetics.

If pruritus is thought to be primarily related to dry skin, interventions to improve skin hydration can be used. The main source of hydration for skin is moisture from the vasculature of underlying tissues. Water, not lipid, regulates the pliability of the epidermis, providing the rationale for using emollients.[7] Emollients reduce evaporation by forming occlusive and semi-occlusive films over the skin surface, encouraging the production of moisture in the layer of epidermis beneath the film.[8][Level of evidence: IV]

Knowledge about the ingredients in skin care products is essential because many ingredients may enhance skin reactions. The three main ingredients of emollients are as follows:

  • Petrolatum, which is poorly absorbed by irradiated skin and is not easily removed. A thick layer could produce an undesired bolus effect when applied within a radiation treatment field.[9][Level of evidence: IV]
  • Lanolin, which may cause allergic sensitization in some individuals.[8][Level of evidence: IV]
  • Mineral oil, which is used in combination with petrolatum and lanolin to create creams and lotions and may be an active ingredient in bath oils.

Other ingredients added to these products—such as thickeners, opacifiers, preservatives, fragrances, and colorings—may cause allergic skin reactions.

Product selection and recommendations must be made in consideration of each patient’s unique needs and should incorporate variables such as the following:[1][Level of evidence: IV]

  • Individual’s skin.
  • Desired effect.
  • Consistency and texture of the preparation.
  • Cost and acceptability to the patient.

Emollient creams or lotions should be applied at least two or three times daily and after bathing. Gels with a local anesthetic (0.5%–5% lidocaine) can be used on some small areas (with the caveat that gels are composed of mostly alcohol-based vehicles) as often as every 2 hours if necessary.[10][Level of evidence: IV]

Over-the-counter products containing menthol, camphor, pramoxine, or capsaicin can be used for certain areas of severe pruritus. These substances soothe, cool, or inhibit itch sensations, raising the threshold for itch perception. Capsaicin-based therapies are more likely to be beneficial in pruritus of neuropathic origin.[11]

Prescription products

Topical steroids can reduce itching, but they reduce blood flow to the skin, resulting in thinning of the skin and increased susceptibility to injury.[12][Level of evidence: IV] Topical steroids should therefore be reserved for pruritic skin with associated primary dermatitis or inflammatory etiologies. Some practitioners may formulate their own mixture of dilute steroid-containing moisturizer by compounding menthol 0.5% and fluocinonide 0.0125% into a Vanicream base (fluocinonide 0.05% 60 g, menthol 480 mg, and Vanicream QSAD 240 g). Topical steroids should not be applied to skin surfaces inside a radiation field during treatment but may be used successfully for radiation-induced dermatitis after the treatment course has concluded.

For more-severe xerosis or keratoderma, humectants may be indicated. These products not only provide an occlusive or semi-occlusive barrier for water, but also chemically exfoliate an excessively cornified layer while drawing dermal fluid into the epidermal compartment. Humectant choices include:[13][Level of evidence: IV]

  • Salicylic acid 6% cream.
  • Ammonium lactate 12% cream.
  • Creams and ointments containing urea 10% to 50%.

Humectants can significantly improve skin pliability and reduce fissuring, but care must be taken that they do not get into fissures because they can cause stinging sensations on open erosions.

Systemic Therapies

Systemic medications used to manage pruritus include those directed toward the underlying disease or control of symptoms. Antibiotics can reduce symptoms associated with infection. Oral antihistamines may provide symptomatic relief in histamine-related itching; however, they are not considered useful in pruritus of neuropathic origin. It is believed that the sedative effect of antihistamines adds to their antipruritic efficacy; therefore, a higher dose of antihistamine at bedtime may produce desirable potentiation of the antipruritic effect by also providing this sedative effect. If one antihistamine is ineffective, one from another class may provide relief (see Table 2).

Second-generation antihistamines have several advantages over first-generation antihistamines.[14] Decreased activity on nonhistamine receptors results in fewer adverse effects. In addition, second-generation antihistamines dissociate slowly from histamine receptors, allowing for once-daily dosing. Compared with first-generation antihistamines, second-generation antihistamines produce less central nervous system penetration and therefore less sedation. Given these advantages, using doses of levocetirizine and desloratadine higher than those approved by the U.S. Food and Drug Administration has been suggested to provide relief for some patients with chronic urticarial conditions.[15] However, studies of cetirizone have produced conflicting results.[16,17]

Table 2. Antihistamines Used to Alleviate Pruritusa
Drug Category Medication Dose Comments Reference
SR = sustained release.
aTable abstracted from Lexicomp Online.[18]
First generation Diphenhydramine 25–100 mg q6h   [19][Level of evidence: IV]
Hydroxyzine 25–50 mg q6–8h Abrupt withdrawal may cause confusion. [20]; [21][Level of evidence: I]
Cyproheptadine 4 mg q6–8h   [20][Level of evidence: IV]
Chlorpheniramine 4 mg q4–6h   [22][Level of evidence: IV]
Second generation Cetirizine 5–10 mg daily Conflicting results when 20–40 mg/day studied. [16][Level of evidence: I]; [17][Level of evidence: II]
Levocetirizine 2.5–5 mg daily Safe to increase dose up to 20 mg daily; may provide better symptom control. [15,23][Level of evidence: I]
Loratadine 10 mg daily   [24][Level of evidence: I]
Desloratadine 5 mg daily Safe to increase dose up to 20 mg daily; may provide better symptom control. [23]
Fexofenadine 60 mg q12h or 180 mg daily (SR tablet)   [25][Level of evidence: I]

Several alternative medications can be used to alleviate pruritus (see Table 3). Antidepressants can have strong antihistamine and antipruritic effects.[22][Level of evidence: IV] Tricyclic antidepressants such as doxepin, amitriptyline, nortriptyline, and trimipramine have additional antihistaminic effects, making them of additional benefit in dermatological conditions such as urticaria. However, the generally more-favorable side-effect profile of selective serotonin reuptake inhibitors and selective norepinephrine reuptake inhibitors has made them the first-line agents in the management of psychogenic pruritus.[26][Level of evidence: II]

Aspirin may reduce pruritus in some individuals with polycythemia vera, while increasing pruritus in others. Patients with thrombocytopenic cancer should be cautioned against using aspirin. Cimetidine alone or in combination with aspirin has been used with some effectiveness for pruritus associated with Hodgkin lymphoma and polycythemia vera.[27][Level of evidence: III]

Novel agents to try in recalcitrant cases of pruritus include gabapentin, pregabalin, and botulinum toxin injection, particularly for neurogenic itch such as post-herpetic neuralgia.[28,29] Aprepitant has been used successfully in the treatment of pruritus by blocking the neurokinin-1 receptor, which is activated by substance P.[30][Level of evidence: III]

Table 3. Alternative Medications Used to Alleviate Pruritusa
Drug Category Medication Dose Comments Reference
ESRD = end-stage renal disease; GABA = gamma-aminobutyric acid; IV = intravenously; tid = 3 times a day.
aTable abstracted from Lexicomp Online.[18]
Tricyclic antidepressant Amitriptyline 25–150 mg daily Start as 10 mg tid or 25 mg at bedtime. [29][Level of evidence: IV]
Doxepin 10–25 mg q8h   [31][Level of evidence: IV]
Selective serotonin reuptake inhibitor Fluvoxamine 50–100 mg daily   [32][Level of evidence: II]
Mirtazapine 7.5–15 mg at bedtime No value to >15 mg. [29][Level of evidence: IV]
Paroxetine 20 mg daily   [33][Level of evidence: I]
Sertraline 75–100 mg daily   [34][Level of evidence: I]
GABA analogue Gabapentin 100–300 mg daily, titrated to effect Dose must be adjusted for renal dysfunction. [35][Level of evidence: I]
Pregabalin 75 mg daily Dose must be adjusted for renal dysfunction. [36][Level of evidence: I]
Sequestrant agent Ursodiol (ursodeoxycholic acid) 10–15 mg/kg of body weight per day For pruritus of cholestasis. [37][Level of evidence: IV]
Cholestyramine 4–16 g daily For pruritus of cholestasis. [37][Level of evidence: IV]
Opioid antagonist Naloxone 0.2 µg/kg of body weight per min IV Efficacy in cholestatic pruritus; conflicting results in ESRD itch. Can cause pain by antagonizing mu-receptor. [38][Level of evidence: I]; [39]
Naltrexone 25–100 mg daily Efficacy in cholestatic pruritus, atopic eczema; conflicting results in ESRD itch. Can cause pain by antagonizing mu-receptor. [39]; [40,41][Level of evidence: I]
Butorphanol 1–4 mg q4–6h intranasally   [42][Level of evidence: II]
Nalbuphine 2.5–5 mg IV For opioid-induced pruritus. [43][Level of evidence: IV]
Miscellaneous agent Aprepitant 80 mg daily   [30][Level of evidence: III]
Aspirin 500 mg q8–24h Only used for polycythemia vera. Positive and negative data. [31][Level of evidence: I]
Botulinum toxin 16–25 units injected into the dermatome   [29][Level of evidence: IV]
Capsaicin 0.025% Apply 5 times daily × 1 week, then 3 times daily For neurological pruritus. [44][Level of evidence: I]
Cimetidine 200 mg q6h Only used for polycythemia vera. [31][Level of evidence: IV]
Cyclosporine 3–4.5 mg/kg of body weight per day Requires close monitoring for renal toxicity. [45][Level of evidence: I]
Pimecrolimus 1% cream Apply twice daily   [46][Level of evidence: I]

Sequestrant agents may be effective in relieving pruritus associated with renal or hepatic disease through binding and removing pruritogenic substances in the gut and reducing bile salt concentration. Choices include ursodeoxycholic acid and cholestyramine; however, cholestyramine is not always effective and produces gastric side effects.[47] Because of the association of pruritus with opioid receptor agonism, increased catabolism of endogenous opioids using rifampin in uremia may be beneficial.[48] Opioid antagonists such as naloxone, naltrexone, nalmefene, butorphanol, and nalbuphine may also have some benefit, particularly in patients with uremic pruritus.[26,40][Level of evidence: III]

Physical Modalities

Alternatives to scratching for the relief of pruritus can help the patient interrupt the itch-scratch-itch cycle. Substituting the application of emollients for scratching may help reduce skin breakdown. The application of a cool washcloth or ice over the site may be useful. Firm pressure at the site of itching, at a site contralateral to the site of itching, and at acupressure points may break the neural pathway. Rubbing, pressure, and vibration can be used to relieve itching.[49][Level of evidence: IV]; [4]

There are anecdotal reports of the use of transcutaneous electronic nerve stimulators (TENS) and acupuncture in the management of pruritus.[50] Ultraviolet phototherapy has been used with limited success to treat pruritus related to uremia.[50]

References
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  2. Lydon J, Purl S, Goodman M: Integumentary and mucous membrane alterations. In: Groenwald SL, Frogge MH, Goodman M, et al., eds.: Cancer Nursing: Principles and Practice. 2nd ed. Jones and Bartlett, 1990, pp 594-635.
  3. Pace KB, Bord MA, McCray N, et al.: Pruritus. In: McNally JC, Stair JC, Somerville ET, eds.: Guidelines for Cancer Nursing Practice. Grune and Stratton, Inc., 1985, pp 85-88.
  4. Yasko JM, Hogan CM: Pruritus. In: Yasko J, ed.: Guidelines for Cancer Care: Symptom Management. Reston Publishing Company, Inc., 1983, pp 125-129.
  5. Hassey KM: Skin care for patients receiving radiation therapy for rectal cancer. J Enterostomal Ther 14 (5): 197-200, 1987 Sep-Oct. [PUBMED Abstract]
  6. Maienza J: Alternatives to cornstarch for itchiness. Oncol Nurs Forum 15 (2): 199-200, 1988 Mar-Apr. [PUBMED Abstract]
  7. Blank L: Factors which influence the water content of the stratum corneum. J Invest Dermatol 18 (2): 133-39, 1952.
  8. Klein L: Maintenance of healthy skin. J Enterostomal Ther 15 (6): 227-31, 1988 Nov-Dec. [PUBMED Abstract]
  9. Hilderley L: Skin care in radiation therapy. A review of the literature. Oncol Nurs Forum 10 (1): 51-6, 1983 Winter. [PUBMED Abstract]
  10. De Conno F, Ventafridda V, Saita L: Skin problems in advanced and terminal cancer patients. J Pain Symptom Manage 6 (4): 247-56, 1991. [PUBMED Abstract]
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  17. Asero R: Chronic unremitting urticaria: is the use of antihistamines above the licensed dose effective? A preliminary study of cetirizine at licensed and above-licensed doses. Clin Exp Dermatol 32 (1): 34-8, 2007. [PUBMED Abstract]
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  20. Levy M: Symptom control manual. In: Cassileth BR, Cassileth PA, eds.: Clinical Care of the Terminal Cancer Patient. Lea and Febiger, 1982, pp 214-262.
  21. Monroe EW, Bernstein DI, Fox RW, et al.: Relative efficacy and safety of loratadine, hydroxyzine, and placebo in chronic idiopathic urticaria. Arzneimittelforschung 42 (9): 1119-21, 1992. [PUBMED Abstract]
  22. Winkelmann RK: Pharmacologic control of pruritus. Med Clin North Am 66 (5): 1119-33, 1982. [PUBMED Abstract]
  23. Staevska M, Popov TA, Kralimarkova T, et al.: The effectiveness of levocetirizine and desloratadine in up to 4 times conventional doses in difficult-to-treat urticaria. J Allergy Clin Immunol 125 (3): 676-82, 2010. [PUBMED Abstract]
  24. Langeland T, Fagertun HE, Larsen S: Therapeutic effect of loratadine on pruritus in patients with atopic dermatitis. A multi-crossover-designed study. Allergy 49 (1): 22-6, 1994. [PUBMED Abstract]
  25. Kaplan AP, Spector SL, Meeves S, et al.: Once-daily fexofenadine treatment for chronic idiopathic urticaria: a multicenter, randomized, double-blind, placebo-controlled study. Ann Allergy Asthma Immunol 94 (6): 662-9, 2005. [PUBMED Abstract]
  26. Zhang H, Yang Y, Cui J, et al.: Gaining a comprehensive understanding of pruritus. Indian J Dermatol Venereol Leprol 78 (5): 532-44, 2012 Sep-Oct. [PUBMED Abstract]
  27. Daly BM, Shuster S: Effect of aspirin on pruritus. Br Med J (Clin Res Ed) 293 (6552): 907, 1986. [PUBMED Abstract]
  28. Scheinfeld N: The role of gabapentin in treating diseases with cutaneous manifestations and pain. Int J Dermatol 42 (6): 491-5, 2003. [PUBMED Abstract]
  29. Yosipovitch G, Samuel LS: Neuropathic and psychogenic itch. Dermatol Ther 21 (1): 32-41, 2008 Jan-Feb. [PUBMED Abstract]
  30. Ständer S, Siepmann D, Herrgott I, et al.: Targeting the neurokinin receptor 1 with aprepitant: a novel antipruritic strategy. PLoS One 5 (6): e10968, 2010. [PUBMED Abstract]
  31. Krajnik M, Zylicz Z: Understanding pruritus in systemic disease. J Pain Symptom Manage 21 (2): 151-68, 2001. [PUBMED Abstract]
  32. Ständer S, Böckenholt B, Schürmeyer-Horst F, et al.: Treatment of chronic pruritus with the selective serotonin re-uptake inhibitors paroxetine and fluvoxamine: results of an open-labelled, two-arm proof-of-concept study. Acta Derm Venereol 89 (1): 45-51, 2009. [PUBMED Abstract]
  33. Zylicz Z, Krajnik M, Sorge AA, et al.: Paroxetine in the treatment of severe non-dermatological pruritus: a randomized, controlled trial. J Pain Symptom Manage 26 (6): 1105-12, 2003. [PUBMED Abstract]
  34. Mayo MJ, Handem I, Saldana S, et al.: Sertraline as a first-line treatment for cholestatic pruritus. Hepatology 45 (3): 666-74, 2007. [PUBMED Abstract]
  35. Gunal AI, Ozalp G, Yoldas TK, et al.: Gabapentin therapy for pruritus in haemodialysis patients: a randomized, placebo-controlled, double-blind trial. Nephrol Dial Transplant 19 (12): 3137-9, 2004. [PUBMED Abstract]
  36. Solak Y, Biyik Z, Atalay H, et al.: Pregabalin versus gabapentin in the treatment of neuropathic pruritus in maintenance haemodialysis patients: a prospective, crossover study. Nephrology (Carlton) 17 (8): 710-7, 2012. [PUBMED Abstract]
  37. Kremer AE, Oude Elferink RP, Beuers U: Pathophysiology and current management of pruritus in liver disease. Clin Res Hepatol Gastroenterol 35 (2): 89-97, 2011. [PUBMED Abstract]
  38. Bergasa NV, Alling DW, Talbot TL, et al.: Effects of naloxone infusions in patients with the pruritus of cholestasis. A double-blind, randomized, controlled trial. Ann Intern Med 123 (3): 161-7, 1995. [PUBMED Abstract]
  39. Wang H, Yosipovitch G: New insights into the pathophysiology and treatment of chronic itch in patients with end-stage renal disease, chronic liver disease, and lymphoma. Int J Dermatol 49 (1): 1-11, 2010. [PUBMED Abstract]
  40. Peer G, Kivity S, Agami O, et al.: Randomised crossover trial of naltrexone in uraemic pruritus. Lancet 348 (9041): 1552-4, 1996. [PUBMED Abstract]
  41. Malekzad F, Arbabi M, Mohtasham N, et al.: Efficacy of oral naltrexone on pruritus in atopic eczema: a double-blind, placebo-controlled study. J Eur Acad Dermatol Venereol 23 (8): 948-50, 2009. [PUBMED Abstract]
  42. Dawn AG, Yosipovitch G: Butorphanol for treatment of intractable pruritus. J Am Acad Dermatol 54 (3): 527-31, 2006. [PUBMED Abstract]
  43. Jannuzzi RG: Nalbuphine for Treatment of Opioid-induced Pruritus: A Systematic Review of Literature. Clin J Pain 32 (1): 87-93, 2016. [PUBMED Abstract]
  44. Wallengren J, Klinker M: Successful treatment of notalgia paresthetica with topical capsaicin: vehicle-controlled, double-blind, crossover study. J Am Acad Dermatol 32 (2 Pt 1): 287-9, 1995. [PUBMED Abstract]
  45. Weisshaar E, Szepietowski JC, Darsow U, et al.: European guideline on chronic pruritus. Acta Derm Venereol 92 (5): 563-81, 2012. [PUBMED Abstract]
  46. Kaufmann R, Bieber T, Helgesen AL, et al.: Onset of pruritus relief with pimecrolimus cream 1% in adult patients with atopic dermatitis: a randomized trial. Allergy 61 (3): 375-81, 2006. [PUBMED Abstract]
  47. Abel EA, Farber EM: Malignant cutaneous tumors. In: Rubenstein E, Federman DD, eds.: Scientific American Medicine. Scientific American, Inc, Chapter 2: Dermatology, Section XII, 1-20, 1992.
  48. Miguet JP, Mavier P, Soussy CJ, et al.: Induction of hepatic microsomal enzymes after brief administration of rifampicin in man. Gastroenterology 72 (5 Pt 1): 924-6, 1977. [PUBMED Abstract]
  49. Dangel RB: Pruritus and cancer. Oncol Nurs Forum 13 (1): 17-21, 1986 Jan-Feb. [PUBMED Abstract]
  50. Bernhard JD: Clinical aspects of pruritus. In: Fitzpatrick TB, Eisen AZ, Wolff K, et al., eds.: Dermatology in General Medicine. 3rd ed. McGraw-Hill, 1987, Chapter 7, pp 78-90.

Latest Updates to This Summary (01/17/2025)

The PDQ cancer information summaries are reviewed regularly and updated as new information becomes available. This section describes the latest changes made to this summary as of the date above.

Editorial changes were made to this summary.

This summary is written and maintained by the PDQ Supportive and Palliative Care Editorial Board, which is editorially independent of NCI. The summary reflects an independent review of the literature and does not represent a policy statement of NCI or NIH. More information about summary policies and the role of the PDQ Editorial Boards in maintaining the PDQ summaries can be found on the About This PDQ Summary and PDQ® Cancer Information for Health Professionals pages.

About This PDQ Summary

Purpose of This Summary

This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about the pathophysiology and treatment of pruritus. It is intended as a resource to inform and assist clinicians in the care of their patients. It does not provide formal guidelines or recommendations for making health care decisions.

Reviewers and Updates

This summary is reviewed regularly and updated as necessary by the PDQ Supportive and Palliative Care Editorial Board, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH).

Board members review recently published articles each month to determine whether an article should:

  • be discussed at a meeting,
  • be cited with text, or
  • replace or update an existing article that is already cited.

Changes to the summaries are made through a consensus process in which Board members evaluate the strength of the evidence in the published articles and determine how the article should be included in the summary.

The lead reviewer for Pruritus is:

  • Larry D. Cripe, MD (Indiana University School of Medicine)

Any comments or questions about the summary content should be submitted to Cancer.gov through the NCI website’s Email Us. Do not contact the individual Board Members with questions or comments about the summaries. Board members will not respond to individual inquiries.

Levels of Evidence

Some of the reference citations in this summary are accompanied by a level-of-evidence designation. These designations are intended to help readers assess the strength of the evidence supporting the use of specific interventions or approaches. The PDQ Supportive and Palliative Care Editorial Board uses a formal evidence ranking system in developing its level-of-evidence designations.

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PDQ is a registered trademark. Although the content of PDQ documents can be used freely as text, it cannot be identified as an NCI PDQ cancer information summary unless it is presented in its entirety and is regularly updated. However, an author would be permitted to write a sentence such as “NCI’s PDQ cancer information summary about breast cancer prevention states the risks succinctly: [include excerpt from the summary].”

The preferred citation for this PDQ summary is:

PDQ® Supportive and Palliative Care Editorial Board. PDQ Pruritus. Bethesda, MD: National Cancer Institute. Updated <MM/DD/YYYY>. Available at: /side-effects/skin-nail-changes/pruritus-hp-pdq. Accessed <MM/DD/YYYY>. [PMID: 26389231]

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Pruritus (PDQ®)–Patient Version

Pruritus (PDQ®)–Patient Version

General Information About Pruritus

Key Points

  • Certain conditions, cancers, and blood disorders may cause pruritus.

Pruritus is an itchy feeling that makes you want to scratch your skin. It may occur without a rash or skin lesions. Pruritus sometimes feels like pain because the signals for itching and pain travel along the same nerve pathways. Scratching may cause breaks in the skin, bleeding, and infection. If your skin feels itchy, let your doctor know so it can be treated and relieved.

The way pruritus feels and how long it lasts is not the same in everyone.

The skin is the largest organ of the body. The most important job of skin is to protect against heat, sunlight, injury, and infection. The skin is also important to self-image and your ability to touch and be touched.

Certain conditions, cancers, and blood disorders may cause pruritus.

Pruritus is a symptom of a certain condition, blood disorder, or a disease. These include:

The cause of pruritus is not always known.

Causes of Pruritus in Cancer Patients

Key Points

  • Certain cancer treatments may cause pruritus.
  • Drugs may be used for supportive care.

Certain cancer treatments may cause pruritus.

Cancer treatments that may cause pruritus include chemotherapy, radiation therapy, and immunotherapy (biologic therapy).

  • When chemotherapy causes pruritus, it may be a sign that you are sensitive to the drugs being used.
  • Radiation therapy can kill skin cells and cause dryness, burning, and itching as the skin peels off.
  • Drugs used in immunotherapy may also cause dryness and itching.

Skin can become thin and dry because many of these therapies make your skin less able to make new cells and heal. Long-term dry skin may occur when hair and sweat gland function does not return to normal right after cancer treatment.

Drugs may be used for supportive care.

Some of the drugs used to prevent or treat cancer symptoms may cause pruritus, including the following:

Assessment of Pruritus

Key Points

  • Finding the cause of the itching is the first step in relieving pruritus.
  • A physical exam, blood tests, and a chest x-ray are done to assess pruritus.

Finding the cause of the itching is the first step in relieving pruritus.

Since pruritus is a symptom of a disease or condition, finding and treating the cause is the first step in bringing you relief.

A physical exam, blood tests, and a chest x-ray are done to assess pruritus.

The following tests and procedures may be done to find the problem that is causing the itching:

  • Physical exam and history: An exam of the body to check general signs of health, including checking for signs of disease, such as lumps or anything else that seems unusual. The doctor will check your skin for the following:

    A history of your health habits, past illnesses, and treatments will also be taken. You may be asked about the following:

    • When the pruritus started, how long it lasts, how bad it is, and what part of your body is itchy.
    • How it affects your daily activities and sleep.
    • What makes the itching better or worse.
    • Whether other family members or pets are affected.
    • Whether you have had pruritus before.
    • Current cancer treatment or past history of cancer.
    • Other diseases you have now or had in the past and their treatment.
    • Pain medicines, antibiotics, or other drugs you are taking, including illegal drugs.
    • Whether your diet is healthy and you drink enough fluids.
    • Social history (hobbies, job, sexual history, and travel).
    • How you care for your skin.
    • Your emotional health.
  • Blood chemistry studies: A procedure in which a blood sample is checked to measure the amounts of certain substances released into the blood by organs and tissues in the body. An unusual (higher or lower than normal) amount of a substance can be a sign of disease. These blood tests include:
  • Complete blood count (CBC) with differential: A procedure in which a sample of blood is drawn and checked for the following:
  • Sedimentation rate: A procedure in which a sample of blood is drawn and checked for the rate at which the red blood cells settle to the bottom of the test tube. The sedimentation rate is a measure of how much inflammation is in the body. A higher than normal sedimentation rate may be a sign of lymphoma or another condition. Also called erythrocyte sedimentation rate, sed rate, or ESR.
  • Chest x-ray: An x-ray of the organs and bones inside the chest. An x-ray is a type of energy beam that can go through the body and onto film, making a picture of areas inside the body.

Depending on the results, further tests, such as a skin biopsy, may be done to diagnose the problem and decide on treatment.

Treatment of Pruritus

Key Points

  • Treatment of pruritus in cancer patients involves learning what the triggers are and taking steps to avoid them.
  • Different types of treatment are used to help treat pruritus.
    • Self-care
    • Over-the-counter treatments
      • Cornstarch and talc
      • Creams and lotions
    • Prescription drugs applied to the skin
    • Systemic therapies
    • Other drug therapies
    • Comfort measures

Treatment of pruritus in cancer patients involves learning what the triggers are and taking steps to avoid them.

It is important for you and for caregivers to know what triggers itching, such as dry skin or hot baths, so you can take steps to prevent it. You may need more than one type of treatment to relieve or prevent pruritus, protect your skin, and keep you comfortable.

Good nutrition is very important for healthy skin. A good diet includes a balance of proteins, carbohydrates, fats, vitamins, minerals, and fluids. Eating a balanced diet and drinking plenty of fluids helps your skin stay healthy. It is best to drink at least 3 liters (about 100 ounces) of fluid each day, but this may not be possible for everyone.

Washing the skin every day or every two days is important to help remove dirt and keep the skin healthy.

Different types of treatment are used to help treat pruritus.

Self-care

Self-care includes avoiding pruritus triggers and taking good care of your skin.

Pruritus triggers include:

  • Dehydration caused by fever, diarrhea, nausea and vomiting, or low fluid intake.
  • Hot baths or bathing more than once a day, or for longer than 30 minutes.
  • Bubble baths or soaps with detergents.
  • Reusable scrubbing sponges for the face or loofahs for the body.
  • Scents, fragrances, and perfumes.
  • Adding oil at the beginning of the bath.
  • Dry indoor air.
  • Laundry detergent with scents, dyes, or preservatives.
  • Fabric softener sheets.
  • Tight clothes or clothes made of wool, synthetics, or other harsh/scratchy fabric.
  • Underarm deodorants or antiperspirants.
  • Skin care or cosmetics with scents, dyes, or preservatives.
  • Emotional stress.

Ways to help lessen itching include:

  • Using unscented, soothing creams or ointments.
  • Bathing in slightly warm water no more than 30 minutes daily or every other day.
  • Using mild skin cleansers (non-soap) or soaps made for sensitive skin (such as Cetaphil cleanser, Dove for Sensitive Skin, Oilatum, Basis).
  • Adding oil and soap at the end of a bath or adding a colloidal oatmeal treatment early to the bath.
  • Using soap only for dirty areas; otherwise water is good enough.
  • Gently washing, if needed, with a clean, fresh, soft cotton washcloth.
  • Rinsing all soap or other residue from bathing with fresh, slightly warm water.
  • Drying off by patting skin instead of rubbing.
  • Keeping home air cool and humid (including use of a humidifier).
  • Washing sheets, clothes, and underwear in mild soap or baby soap that contains no scents, dyes, or preservatives (such as Dreft, All Free Clear, Tide Free and Gentle). Adding vinegar (one teaspoon per quart of water) to rinse water removes traces of detergent.
  • Using liquid fabric softener that gets rinsed out in the wash (such as All Free Clear Fabric Softener) or avoiding fabric softener altogether.
  • Using blankets that are soft, such as cotton flannel.
  • Wearing loose-fitting clothes and clothes made of cotton or other soft fabrics.
  • Using distraction, music therapy, relaxation, or positive imagery.

Over-the-counter treatments

Some over-the-counter treatments (medicines that can be bought without a prescription) help prevent or relieve pruritus. However, you should read labels carefully to look for ingredients that may trigger skin reactions, including alcohol, topical antibiotics, and topical anesthetics.

Cornstarch and talc

Cornstarch can help prevent itching of dry skin caused by radiation therapy but should not be used where skin is moist. When cornstarch becomes moist, fungus may grow. Avoid using it on areas close to mucous membranes, such as the vagina or rectum, in skin folds, and on areas that have hair or sweat glands.

Some powders and antiperspirants, such as those that contain talc and aluminum, cause skin irritation during radiation therapy and should be avoided when you’re receiving radiation treatment.

For itching not related to radiation therapy, talc-based treatments may be better than cornstarch-based treatments, especially where two skin surfaces touch or rub together (such as the underarm or between fingers or toes).

Creams and lotions

If pruritus is related to dry skin, emollient creams or lotions may be used. Emollients help soothe and soften the skin and increase moisture levels in the skin. It is important to know the ingredients in these creams and lotions because some may cause skin reactions. Such ingredients include:

  • Petrolatum, which is not well absorbed in skin treated with radiation therapy and may build up too much or be hard to remove.
  • Lanolin, which may cause allergic reactions in some people.
  • Mineral oil, which may be combined with petrolatum and lanolin in creams and lotions and may be an ingredient in bath oils.

Other ingredients added to emollients, such as thickeners, preservatives, fragrances, and colorings, may also cause allergic skin reactions.

Emollient creams or lotions are applied at least two or three times a day and after bathing. Gels with a local anesthetic (0.5%–5% lidocaine) can be used on some small areas as often as every 2 hours if you aren’t sensitive to alcohol ingredients.

To soothe or cool areas of severe pruritus, over-the-counter products containing menthol, camphor, pramoxine, or capsaicin can be used. These products soothe, cool, and decrease the urge to scratch. Capsaicin-based therapies may work best in pruritus related to nerve signals.

Prescription drugs applied to the skin

Your doctor may prescribe topical steroids (steroids applied to the skin) to reduce itching, but they cause thinning of the skin and make it more sensitive. They should be used only for pruritus related to inflammation. Topical steroids should not be used on skin being treated with radiation therapy, but may be used to relieve inflamed skin after radiation treatment ends.

For xerosis (abnormally dry skin) or keratoderma (a horn-like skin condition), moisturizer creams may be used to seal in moisture and peel off scaly layers of skin. Humectants with ingredients like salicylic acid, ammonium lactate, or urea may improve skin smoothness but can cause stinging if applied to broken skin.

Systemic therapies

Systemic therapies travel through the bloodstream and reach and affect cells all over the body. They may help treat the condition causing your pruritus or help control your symptoms.

Your doctor may prescribe an antibiotic if your pruritus is caused by an infection. You may also be given an oral antihistamine to relieve itching. A larger dose may sometimes be used at bedtime to help you sleep.

Other drug therapies

If other drug treatments do not work to control pruritus, sedatives and antidepressants are sometimes used.

Aspirin may relieve pruritus in some patients with polycythemia vera but may increase pruritus in others. Cimetidine alone or combined with aspirin may help control pruritus in patients with Hodgkin lymphoma and polycythemia vera.

Comfort measures

Other steps may be taken to help you keep from scratching and stop the itch-scratch-itch cycle. These may include:

To Learn More About Pruritus

For more information from the National Cancer Institute about pruritus, see the following:

About This PDQ Summary

About PDQ

Physician Data Query (PDQ) is the National Cancer Institute’s (NCI’s) comprehensive cancer information database. The PDQ database contains summaries of the latest published information on cancer prevention, detection, genetics, treatment, supportive care, and complementary and alternative medicine. Most summaries come in two versions. The health professional versions have detailed information written in technical language. The patient versions are written in easy-to-understand, nontechnical language. Both versions have cancer information that is accurate and up to date and most versions are also available in Spanish.

PDQ is a service of the NCI. The NCI is part of the National Institutes of Health (NIH). NIH is the federal government’s center of biomedical research. The PDQ summaries are based on an independent review of the medical literature. They are not policy statements of the NCI or the NIH.

Purpose of This Summary

This PDQ cancer information summary has current information about the causes and treatment of pruritus. It is meant to inform and help patients, families, and caregivers. It does not give formal guidelines or recommendations for making decisions about health care.

Reviewers and Updates

Editorial Boards write the PDQ cancer information summaries and keep them up to date. These Boards are made up of experts in cancer treatment and other specialties related to cancer. The summaries are reviewed regularly and changes are made when there is new information. The date on each summary (“Updated”) is the date of the most recent change.

The information in this patient summary was taken from the health professional version, which is reviewed regularly and updated as needed, by the PDQ Supportive and Palliative Care Editorial Board.

Clinical Trial Information

A clinical trial is a study to answer a scientific question, such as whether one treatment is better than another. Trials are based on past studies and what has been learned in the laboratory. Each trial answers certain scientific questions in order to find new and better ways to help cancer patients. During treatment clinical trials, information is collected about the effects of a new treatment and how well it works. If a clinical trial shows that a new treatment is better than one currently being used, the new treatment may become “standard.” Patients may want to think about taking part in a clinical trial. Some clinical trials are open only to patients who have not started treatment.

Clinical trials can be found online at NCI’s website. For more information, call the Cancer Information Service (CIS), NCI’s contact center, at 1-800-4-CANCER (1-800-422-6237).

Permission to Use This Summary

PDQ is a registered trademark. The content of PDQ documents can be used freely as text. It cannot be identified as an NCI PDQ cancer information summary unless the whole summary is shown and it is updated regularly. However, a user would be allowed to write a sentence such as “NCI’s PDQ cancer information summary about breast cancer prevention states the risks in the following way: [include excerpt from the summary].”

The best way to cite this PDQ summary is:

PDQ® Supportive and Palliative Care Editorial Board. PDQ Pruritus. Bethesda, MD: National Cancer Institute. Updated <MM/DD/YYYY>. Available at: /side-effects/skin-nail-changes/pruritus-pdq. Accessed <MM/DD/YYYY>. [PMID: 26389398]

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Cognitive Impairment in Adults with Cancer (PDQ®)–Patient Version

Cognitive Impairment in Adults with Cancer (PDQ®)–Patient Version

General Information About Cognitive Problems in Cancer Survivors

Key Points

  • Cognition problems can change the way you think and learn.
  • Memory loss and thinking problems are common in people with cancer and cancer survivors.

Cognition problems can change the way you think and learn.

Cognition is the process of how you learn, remember, and become aware of what is around you.

This process includes being able to do the following:

  • Focus on important information, thoughts, and actions.
  • Pay attention to a task or activity for a long period of time.
  • Predict what may happen, plan, and solve problems.
  • Learn quickly.
  • Have a sense of where objects are around you.
  • Understand and communicate by speaking and writing.
  • Learn and remember new information.

When your cognition changes, you may have problems with daily tasks.

This summary is about cognitive changes that occur in people with cancer and cancer survivors.

Memory loss and thinking problems are common in people with cancer and cancer survivors.

Your thought process may change, and it may be hard for you to focus and remember things the same way as you did before your cancer treatment.

Talk to your doctor about memory loss and thinking problems you have during or after treatment.

Signs of Cognitive Problems

Key Points

  • Signs of cognitive problems include trouble learning or remembering.
  • Cancer treatments or other diseases may cause cognitive problems.
  • Your doctor will examine you to better understand your cognitive problems.

Signs of cognitive problems include trouble learning or remembering.

Other conditions may also cause cognitive problems. Talk to your doctor if you have memory loss or are unable to do the following:

  • Focus on what you are doing.
  • Complete tasks.
  • Understand what people are saying.
  • Remember names and common words.
  • Recognize familiar objects.
  • Follow instructions.
  • Manage your money well. For example, you may have trouble paying bills or balancing your checkbook.

You may also notice the following changes:

  • Disorganized behavior or thinking.
  • Loss of interest.
  • Problems making sense of the world around you.

Cancer treatments or other diseases may cause cognitive problems.

Factors that cause cognitive problems in people with cancer and cancer survivors include the following:

The cognitive effects of endocrine therapy were studied in breast cancer survivors. Patients who received 5 years of treatment with exemestane were compared with those who received 2.5 years of tamoxifen followed by 2.5 years of exemestane, and with healthy participants. Findings suggested that tamoxifen may have more adverse cognitive effects than exemestane. More studies are needed to confirm these results.

Your doctor will examine you to better understand your cognitive problems.

Your doctor will ask about your health history and usual daily activities to find out a cause of your cognitive problems. Your doctor will also do an exam to check for signs of disease.

Treatment of Cognitive Problems

Key Points

  • Treatment of cognitive problems may include activities that help your attention, memory, and thinking.
    • Cognitive rehabilitation
    • Exercise and physical activity
    • Attention restoration
    • Meditation
  • Certain drugs are being studied to treat cognitive problems.

Treatment of cognitive problems may include activities that help your attention, memory, and thinking.

Cognitive rehabilitation

The goal of cognitive rehabilitation is to improve your memory and the way you think, organize, and make decisions. Cognitive rehabilitation involves the following:

  • Learning ways to take in new information and perform new tasks or behaviors.
  • Staying organized by using tools, such as calendars or electronic diaries.
  • Doing activities over and over, usually on a computer, that become more challenging over time.

Exercise and physical activity

Exercise, physical activity, and mind-body practices, such as tai chi, qigong, or yoga, may improve the way you think and focus.

Attention restoration

Activities that restore attention may help you stay focused on what is around you. These activities may include walking, gardening, bird-watching, and caring for pets.

Meditation

Meditation may help improve cognitive function. Meditation is a mind-body practice in which a person focuses his or her attention on something, such as an object, word, phrase, or breathing. This will help keep you from being distracted or having stressful thoughts or feelings. Mindfulness-based stress reduction is a type of meditation that focuses on bringing attention and awareness to each moment.

Certain drugs are being studied to treat cognitive problems.

Several drugs have been studied to treat cognitive problems in people who have or who have had cancer, such as psychostimulants and erythropoietin-stimulating agents, but results are mixed. More research is needed.

About This PDQ Summary

About PDQ

Physician Data Query (PDQ) is the National Cancer Institute’s (NCI’s) comprehensive cancer information database. The PDQ database contains summaries of the latest published information on cancer prevention, detection, genetics, treatment, supportive care, and complementary and alternative medicine. Most summaries come in two versions. The health professional versions have detailed information written in technical language. The patient versions are written in easy-to-understand, nontechnical language. Both versions have cancer information that is accurate and up to date and most versions are also available in Spanish.

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Purpose of This Summary

This PDQ cancer information summary has current information about expert-reviewed information summary about causes and management of cognitive impairment in people with cancer. It is meant to inform and help patients, families, and caregivers. It does not give formal guidelines or recommendations for making decisions about health care.

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Editorial Boards write the PDQ cancer information summaries and keep them up to date. These Boards are made up of experts in cancer treatment and other specialties related to cancer. The summaries are reviewed regularly and changes are made when there is new information. The date on each summary (“Updated”) is the date of the most recent change.

The information in this patient summary was taken from the health professional version, which is reviewed regularly and updated as needed, by the PDQ Supportive and Palliative Care Editorial Board.

Clinical Trial Information

A clinical trial is a study to answer a scientific question, such as whether one treatment is better than another. Trials are based on past studies and what has been learned in the laboratory. Each trial answers certain scientific questions in order to find new and better ways to help cancer patients. During treatment clinical trials, information is collected about the effects of a new treatment and how well it works. If a clinical trial shows that a new treatment is better than one currently being used, the new treatment may become “standard.” Patients may want to think about taking part in a clinical trial. Some clinical trials are open only to patients who have not started treatment.

Clinical trials can be found online at NCI’s website. For more information, call the Cancer Information Service (CIS), NCI’s contact center, at 1-800-4-CANCER (1-800-422-6237).

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The best way to cite this PDQ summary is:

PDQ® Supportive and Palliative Care Editorial Board. PDQ Cognitive Impairment in Adults with Cancer. Bethesda, MD: National Cancer Institute. Updated <MM/DD/YYYY>. Available at: /side-effects/memory/cognitive-impairment-pdq. Accessed <MM/DD/YYYY>.

Images in this summary are used with permission of the author(s), artist, and/or publisher for use in the PDQ summaries only. If you want to use an image from a PDQ summary and you are not using the whole summary, you must get permission from the owner. It cannot be given by the National Cancer Institute. Information about using the images in this summary, along with many other images related to cancer can be found in Visuals Online. Visuals Online is a collection of more than 3,000 scientific images.

Disclaimer

The information in these summaries should not be used to make decisions about insurance reimbursement. More information on insurance coverage is available on Cancer.gov on the Managing Cancer Care page.

Contact Us

More information about contacting us or receiving help with the Cancer.gov website can be found on our Contact Us for Help page. Questions can also be submitted to Cancer.gov through the website’s E-mail Us.

Cognitive Impairment in Adults With Cancer (PDQ®)–Health Professional Version

Cognitive Impairment in Adults With Cancer (PDQ®)–Health Professional Version

General Information About Cognitive Impairment in Cancer Survivors

Cancer survivors report more symptoms of cognitive impairment than people without a history of cancer.[1] Formal neuropsychological testing demonstrates a range of objective cognitive deficits in some but not all survivors who report symptoms, compared with healthy controls. These deficits include the following: [13]

  • Impaired memory.
  • Reduced concentration.
  • Slower information processing.
  • Reduced executive function.

Subjective reports of cognitive impairment often do not correlate with the results of formal neuropsychological testing.[4,5] In addition, the risk factors for subjective or objective cognitive impairment—such as age, preexisting cognitive function, type of cancer, type of chemotherapy, and the natural history of the impairments—remain a matter of active investigation.

The oncology clinician who cares for survivors with objective or subjective cognitive impairment is advised to consider the following:

  • Because abnormal is defined as a significant deviation from population means, formal neuropsychological testing may be insensitive to subtle changes in cognitive function since cancer diagnosis or treatment.
  • There is a strong correlation between a patient’s subjective reports of cognitive impairment and decreased daily functioning [6] or reduced quality of life.[7]
  • It is not known whether cognitive impairment influences or is a sign of psychological distress.[4] However, one study of 226 participants (166 patients with newly diagnosed breast cancer and 60 controls) demonstrated that patients with breast cancer scored consistently worse than controls on cognitive tests. This decline was mediated by post-traumatic stress disorder (PTSD), indicating that PTSD may contribute in part to cognitive decline.[8] Studies have also shown that cognitive impairment is associated with negative emotional states such as anxiety and depression,[6,9,10] the personality trait of negative affectivity,[11] and self-perceived treatment burden.[9]
  • Treatments for patients with cancer-related cognitive impairment have shown minimal to modest benefit. For clinicians, compassionate acknowledgment of a patient’s concerns and a supportive approach are essential.
References
  1. Jean-Pierre P, Winters PC, Ahles TA, et al.: Prevalence of self-reported memory problems in adult cancer survivors: a national cross-sectional study. J Oncol Pract 8 (1): 30-4, 2012. [PUBMED Abstract]
  2. Vardy JL, Dhillon HM, Pond GR, et al.: Cognitive Function in Patients With Colorectal Cancer Who Do and Do Not Receive Chemotherapy: A Prospective, Longitudinal, Controlled Study. J Clin Oncol 33 (34): 4085-92, 2015. [PUBMED Abstract]
  3. Scherwath A, Schirmer L, Kruse M, et al.: Cognitive functioning in allogeneic hematopoietic stem cell transplantation recipients and its medical correlates: a prospective multicenter study. Psychooncology 22 (7): 1509-16, 2013. [PUBMED Abstract]
  4. Pullens MJ, De Vries J, Roukema JA: Subjective cognitive dysfunction in breast cancer patients: a systematic review. Psychooncology 19 (11): 1127-38, 2010. [PUBMED Abstract]
  5. Hutchinson AD, Hosking JR, Kichenadasse G, et al.: Objective and subjective cognitive impairment following chemotherapy for cancer: a systematic review. Cancer Treat Rev 38 (7): 926-34, 2012. [PUBMED Abstract]
  6. Shilling V, Jenkins V: Self-reported cognitive problems in women receiving adjuvant therapy for breast cancer. Eur J Oncol Nurs 11 (1): 6-15, 2007. [PUBMED Abstract]
  7. Von Ah D, Habermann B, Carpenter JS, et al.: Impact of perceived cognitive impairment in breast cancer survivors. Eur J Oncol Nurs 17 (2): 236-41, 2013. [PUBMED Abstract]
  8. Hermelink K, Bühner M, Sckopke P, et al.: Chemotherapy and Post-traumatic Stress in the Causation of Cognitive Dysfunction in Breast Cancer Patients. J Natl Cancer Inst 109 (10): , 2017. [PUBMED Abstract]
  9. Hermelink K, Küchenhoff H, Untch M, et al.: Two different sides of ‘chemobrain’: determinants and nondeterminants of self-perceived cognitive dysfunction in a prospective, randomized, multicenter study. Psychooncology 19 (12): 1321-8, 2010. [PUBMED Abstract]
  10. Hermelink K, Untch M, Lux MP, et al.: Cognitive function during neoadjuvant chemotherapy for breast cancer: results of a prospective, multicenter, longitudinal study. Cancer 109 (9): 1905-13, 2007. [PUBMED Abstract]
  11. Watson D, Pennebaker JW: Health complaints, stress, and distress: exploring the central role of negative affectivity. Psychol Rev 96 (2): 234-54, 1989. [PUBMED Abstract]

Normal Cognition

Cognition is the mental process of acquiring knowledge and understanding through thought, experience, and the senses. The six domains of cognitive function summarized below were proposed in the Diagnostic and Statistical Manual of Mental Disorders, 5th edition, to help establish the etiology and severity of neurocognitive disorders.[1]

  • Attention and concentration: Ability to triage relevant information, thoughts, and actions while ignoring distractions; the ability to maintain attention for an extended period of time.
  • Executive function: Ability to initiate and generate hypotheses, to plan, and to make decisions.
  • Information processing speed: Ability to quickly and efficiently process information.
  • Visuospatial skill: Ability to process and interpret visual information about where things are in space.
  • Language: Ability to understand and communicate symbolic information, both verbally and in writing.
  • Learning and memory: Ability to learn new information; ability to store and recall new information, in either the short term or the long term.

The domains are interdependent, and any proposed taxonomy is provisional and will depend on the specific neuropsychological tests used to assess patients. Furthermore, published studies vary in terms of the cutoff for impairment and which scales are combined into a single score. While the domains reasonably capture the range of concerns experienced by people with cancer, it is important to clarify the specific impairment through a careful history and formal testing. In addition, comparisons between studies are hampered by different scales and definitions.

References
  1. Sachdev PS, Blacker D, Blazer DG, et al.: Classifying neurocognitive disorders: the DSM-5 approach. Nat Rev Neurol 10 (11): 634-42, 2014. [PUBMED Abstract]

Responding to Patient Reports of Cognitive Impairment

Patients with cancer may experience the following cognitive difficulties:

  • Difficulty multitasking; must focus on one thing at a time.
  • Trouble concentrating; inability to focus on tasks.
  • Memory lapses.
  • Difficulty following instructions.
  • Decreased ability to handle personal finances.
  • Disorganized behavior or thinking.
  • Loss of initiative.
  • Difficulty remembering common words and recalling names.
  • Inability to recognize familiar objects.
  • Altered perception.
  • Difficulty finding words.

Before a patient is referred for formal neuropsychological testing, the oncology clinician can perform a complete assessment of the potential contribution of medications and medical comorbidities to the patient’s experience. It is well established that preexisting illness may contribute to cognitive impairment before a patient is diagnosed with or treated for cancer.[1] Patients who report symptoms or concerns suggestive of cognitive impairment may benefit from an evaluation of potentially reversible causes and appropriate measures. Potential contributing factors include the following:

  • Advanced age.
  • Frailty.[2,3]
  • Certain medications and their side effects.
  • Hormone status and menopause status.
  • Emotional distress and/or depressive symptoms and anxiety.
  • Symptoms such as pain, fatigue, and sleep disturbance.[4][Level of evidence: II]
  • Comorbidities.
  • Use of alcohol or other agents that alter cognition.
  • Higher stage of disease, larger tumor size, and markers of tumor aggressivity (e.g., HER2 positivity in breast cancer).[5]
  • Increased levels of C-reactive protein or other proinflammatory cytokines (e.g., interleukin 6).[6,7]

Validation of the Survivor Experience

The experience of cognitive changes after cancer treatment has been documented in qualitative research.[811] Concerns reported by survivors include the following: [8]

  • Memory problems.
  • Inability to concentrate.
  • Decreased ability to function in daily activities, including employment.

Survivors expressed frustration with health care providers’ lack of acknowledgment of their cognitive changes; they also expressed the need to be informed early about the possibility of developing this problem.[9,10] Patients found it comforting that subtle mental changes have been observed widely in cancer survivors and are to be expected. The least helpful response by practitioners was minimizing the changes or not taking them seriously.[9]

Evaluation of Subjective Reports of Cognitive Impairment

As with all patient-reported symptoms and signs, a thorough evaluation will help determine the cause of cognitive impairment and potential interventions to reverse the symptoms or stabilize the patient. A focused history and physical examination can assess the following:

  • Measures of baseline cognitive function, such as educational attainment, job-related responsibilities, and premorbid functioning.
  • Potential risk factors for cognitive impairment such as advanced age, type and stage of cancer, and treatment history, including time since last treatment and drugs used in treatment.
  • Use or misuse of prescription and over-the-counter medications and supplements.
  • Focal neurological deficits. Focal motor defects or discrete cortical defects such as aphasia or apraxia are uncommon in cancer-associated cognitive impairment.[12]
  • Signs of metastatic disease to the brain, meninges, or both.

The routine use of neuroimaging is not warranted unless there are concerns about specific complications from the cancer or its treatment (e.g., metastatic cancer to the brain).

References
  1. Mandelblatt JS, Stern RA, Luta G, et al.: Cognitive impairment in older patients with breast cancer before systemic therapy: is there an interaction between cancer and comorbidity? J Clin Oncol 32 (18): 1909-18, 2014. [PUBMED Abstract]
  2. Mandelblatt JS, Jacobsen PB, Ahles T: Cognitive effects of cancer systemic therapy: implications for the care of older patients and survivors. J Clin Oncol 32 (24): 2617-26, 2014. [PUBMED Abstract]
  3. Mandelblatt JS, Clapp JD, Luta G, et al.: Long-term trajectories of self-reported cognitive function in a cohort of older survivors of breast cancer: CALGB 369901 (Alliance). Cancer 122 (22): 3555-3563, 2016. [PUBMED Abstract]
  4. Huang V, Mackin L, Kober KM, et al.: Distinct sleep disturbance and cognitive dysfunction profiles in oncology outpatients receiving chemotherapy. Support Care Cancer 30 (11): 9243-9254, 2022. [PUBMED Abstract]
  5. Root JC, Zhou X, Ahn J, et al.: Association of markers of tumor aggressivity and cognition in women with breast cancer before adjuvant treatment: The Thinking and Living with Cancer Study. Breast Cancer Res Treat 194 (2): 413-422, 2022. [PUBMED Abstract]
  6. Mandelblatt JS, Small BJ, Zhou X, et al.: Plasma levels of interleukin-6 mediate neurocognitive performance in older breast cancer survivors: The Thinking and Living With Cancer study. Cancer 129 (15): 2409-2421, 2023. [PUBMED Abstract]
  7. Carroll JE, Nakamura ZM, Small BJ, et al.: Elevated C-Reactive Protein and Subsequent Patient-Reported Cognitive Problems in Older Breast Cancer Survivors: The Thinking and Living With Cancer Study. J Clin Oncol 41 (2): 295-306, 2023. [PUBMED Abstract]
  8. Myers JS: Chemotherapy-related cognitive impairment: the breast cancer experience. Oncol Nurs Forum 39 (1): E31-40, 2012. [PUBMED Abstract]
  9. Boykoff N, Moieni M, Subramanian SK: Confronting chemobrain: an in-depth look at survivors’ reports of impact on work, social networks, and health care response. J Cancer Surviv 3 (4): 223-32, 2009. [PUBMED Abstract]
  10. Von Ah D, Habermann B, Carpenter JS, et al.: Impact of perceived cognitive impairment in breast cancer survivors. Eur J Oncol Nurs 17 (2): 236-41, 2013. [PUBMED Abstract]
  11. Munir F, Burrows J, Yarker J, et al.: Women’s perceptions of chemotherapy-induced cognitive side affects on work ability: a focus group study. J Clin Nurs 19 (9-10): 1362-70, 2010. [PUBMED Abstract]
  12. Wefel JS, Witgert ME, Meyers CA: Neuropsychological sequelae of non-central nervous system cancer and cancer therapy. Neuropsychol Rev 18 (2): 121-31, 2008. [PUBMED Abstract]

Proactive Approaches to Cognitive Impairment

In addition to responding respectfully and compassionately to patients’ concerns about cognitive impairment, the oncology clinician faces questions on how best to inform patients about the risks of cognitive impairment and whether to screen all patients routinely or limit screening to patients at higher risk.

Education About the Risk of Cognitive Impairment

In-depth interviews with cancer survivors revealed that few materials were available to educate them about cognitive problems.[1] The amount of information desired by survivors varied from extensive to brief and general.[2] The optimal method of information delivery was also not clear. Patients and survivors described feeling overwhelmed by the amount of written information about treatment and side effects that they received. Some patients expressed the desire to discuss their preferred method of learning with a health care provider who would provide information in a relaxed, unhurried manner.

One study examined the influence of priming patients to associate chemotherapy treatment with cognitive impairment. Via cancer websites, investigators recruited 150 patients with cancer who were receiving or had received chemotherapy and 86 patients who had no experience with chemotherapy to participate in a study on the effects of cancer therapies on individual patients.[3] Volunteers were randomly assigned to receive a neutral introduction or a priming introduction that stated “some patients treated with chemotherapy experience cognitive problems.”

The study found an association between priming and having had chemotherapy. Patients who had chemotherapy and received the priming introduction reported higher levels of cognitive impairment than those who received the neutral introduction. No difference was found for patients not treated with chemotherapy.[3] The volunteers were highly aware of the relationship between chemotherapy and cognitive impairment, but preexisting knowledge of that relationship had no effect on self-reported cognitive complaints and neuropsychological test performance. These study results raise the possibility that the test environment introduced an artifact.

The optimal means and content for educating patients about cognitive impairment are not established. The principle of informed consent applies: the oncology clinician must inform patients of the risk in a manner that respects personal autonomy.

Screening

No large-scale studies of routine screening for cognitive impairment in people with cancer have been published. In the clinical setting, the Mini-Mental State Exam is often used to assess for cognitive impairment [4] but has varying sensitivities of mild cognitive impairment.[5] The National Comprehensive Cancer Network has identified a series of questions and probes to screen for cognitive impairment and rule out other concerns (e.g., depression or sleep disturbances) that can be treated.[6] One challenge in screening for cognitive impairment is the lack of a brief measure that can accurately assess the multiple cognitive domains.[7] Patient-reported outcome scales (e.g., the Patient-Reported Outcomes Measurement Information System [PROMIS] 8-item and 4-point scales and the Functional Assessment of Cancer Therapy—Cognitive [FACT-Cog] version 3) might prove valuable, but further study is required. PROMIS has two scales based on the FACT-cog, including perceived cognitive impairment and perceived cognitive abilities, which measure different dimensions of cognitive impairment.

An additional challenge is the timing of screening activities, given the variable time to onset and the resolution of concerns without intervention for many patients.

References
  1. Myers JS: Chemotherapy-related cognitive impairment: the breast cancer experience. Oncol Nurs Forum 39 (1): E31-40, 2012. [PUBMED Abstract]
  2. Boykoff N, Moieni M, Subramanian SK: Confronting chemobrain: an in-depth look at survivors’ reports of impact on work, social networks, and health care response. J Cancer Surviv 3 (4): 223-32, 2009. [PUBMED Abstract]
  3. Schagen SB, Das E, Vermeulen I: Information about chemotherapy-associated cognitive problems contributes to cognitive problems in cancer patients. Psychooncology 21 (10): 1132-5, 2012. [PUBMED Abstract]
  4. Folstein MF, Folstein SE, McHugh PR: “Mini-mental state”. A practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res 12 (3): 189-98, 1975. [PUBMED Abstract]
  5. Mitchell AJ: A meta-analysis of the accuracy of the mini-mental state examination in the detection of dementia and mild cognitive impairment. J Psychiatr Res 43 (4): 411-31, 2009. [PUBMED Abstract]
  6. Denlinger CS, Ligibel JA, Are M, et al.: Survivorship: cognitive function, version 1.2014. J Natl Compr Canc Netw 12 (7): 976-86, 2014. [PUBMED Abstract]
  7. Wefel JS, Vardy J, Ahles T, et al.: International Cognition and Cancer Task Force recommendations to harmonise studies of cognitive function in patients with cancer. Lancet Oncol 12 (7): 703-8, 2011. [PUBMED Abstract]

Research Studies on the Prevalence, Risk Factors, and Natural History of Cognitive Impairment

This section summarizes the key findings of meta-analyses, systematic reviews, and individual studies of cognitive impairment.

The International Cognition and Cancer Task Force (ICCTF) has identified several methodological differences or shortcomings in published studies:[1,2]

  • Whether patients enrolled in the study had presented with subjective concerns or were recruited to undergo formal testing.
  • Assessment of pretreatment cognitive impairment and interstudy differences in how baseline function was accounted for.
  • Variations in objective neuropsychological testing, including instruments selected, definitions of cognitive domains, and definition of impairment.

The ICCTF has recommended that investigators define a priori cognitive end points, use a core of validated neuropsychological tests, adopt common criteria for cognitive impairment, employ a longitudinal design, and use a control population.[1,2]

Meta-Analyses and Systematic Reviews

Subjective cognitive concerns in patients with breast cancer

One group of researchers identified 27 studies of subjective cognitive impairment in patients with breast cancer that were published between 1960 and April 2009.[3] Only eight studies were high quality. The percentage of patients reporting subjective concerns ranged from 21% to 90%. There was no correlation between subjective concerns and objective findings, and no conclusive information about timing and the contribution of disease versus treatment received.

Subjective concerns were related to health status, fatigue, and psychological distress. The authors pointed out that those subjective concerns may be a marker of anxiety or depression rather than objective cognitive impairment.[3]

In another study of 212 mostly female breast cancer survivors, fatigue and stress were more important than demographic and medical characteristics in self-reported cognitive impairment, whereas other characteristics such as age, smoking history, and number of chemotherapy cycles were more important in objective cognitive impairment in the linear regression models. This finding emphasizes the need to address psychological problems in cancer survivors reporting cognitive impairment.[4]

Relationship between subjective concerns and objective findings

A comprehensive screen for studies comparing rates of subjective cognitive concerns and objective cognitive impairment published between 1980 and 2012 yielded 24 studies.[5] Only 8 of the 24 studies demonstrated a significant correlation, and 6 of these involved patients with breast cancer. The authors pointed out that the lack of correlation may be due to methodological differences (e.g., different assessment methods, different definitions of significant impairment) or the possibility that subjective concerns are a sign of psychological distress.

Cognitive impairment in breast cancer survivors

A group of investigators performed a meta-analysis of data from studies that reported the results of neuropsychological tests in women with breast cancer who were treated for more than 6 months before the study.[6] The investigators identified 17 studies with 807 patients; the mean time since completion of chemotherapy was 2.9 years. Weighted average effect sizes for the studied cognitive domains demonstrated modest impairment in verbal ability (effect size, –0.19; 95% confidence interval [CI], –0.30 to –0.07; P = .002) and visuospatial ability (effect size, –0.27; 95% CI, –0.45 to –0.08; P = .006).

Chemotherapy and cognitive impairment in patients with cancer

A group of researchers calculated effect sizes based on data from 13 high-quality studies published in 2010 and earlier.[7] Key criteria for study inclusion were reports with primary data, statistics to allow calculation of effect sizes, and a control group; studies with patients who had psychological distress were excluded.

Although several domains were affected, the effect sizes were small. The affected domains included:

  • Executive function (effect size, –0.27).
  • Memory (effect size, –0.21).
  • Verbal function and language skills (effect size, –0.17).

Insignificant effect sizes were observed for the following:

  • Construction (the ability to draw and build).
  • Concept formation.
  • Reasoning.
  • Perception.
  • Orientation and attention.

The authors noted a consistent but not universal trend of worse performance by patients who received chemotherapy compared with groups who received other types of treatment, received no treatment, or were healthy. Furthermore, longer time in treatment was associated with increased cognitive impairment, and longer time since completion of treatment was associated with cognitive improvement.[7]

Subjective and objective cognitive deficits in breast cancer survivors receiving endocrine therapy

Researchers identified 12 high-quality studies (including 2,756 patients) published between 1966 and 2015 that examined the impact of endocrine therapy on cognitive functioning.[8] Study eligibility criteria included all prospective and retrospective observational cohort studies and randomized controlled trials that reported the impact of endocrine therapy, including selective estrogen modulators and aromatase inhibitors, on cognitive performance. Cognitive assessments were examined in breast cancer patients over time, from baseline to 6 months to 1 year and/or 2 years.

Treatment with endocrine therapy was accompanied by deficits in verbal memory, verbal fluency, motor speed, attention, and working memory, but not psychomotor speed. However, findings were limited by the methodical heterogeneity of included studies and relatively short follow-up periods (3 months to 2 years).

In the TAILORx trial, 454 women diagnosed with breast cancer were randomly assigned to receive chemotherapy plus endocrine therapy (n = 218) or endocrine therapy alone (n = 236). They also completed the Functional Assessment of Cancer Therapy (FACT)—Cognitive Function-Perceived Cognitive Impairment (FACT-Cog PCI) to assess perceived cognitive function at baseline (pretreatment) and at 3, 6, 12, 24, and 36 months.[9][Level of evidence: I] The FACT-Cog PCI subscale is a well-known, sensitive measure of perceived cognitive impairment and has an empirical-derived, clinically meaningful change score (PCI cutoff, ˃ 0.5) to assess cognitive impairment. In this study, breast cancer survivors in both groups reported significantly poorer perceived cognitive function at 3, 6, 12, 24, and 36 months compared with baseline. Breast cancer survivors who received chemotherapy plus endocrine therapy had statistically significant and clinically meaningful change in perceived cognitive impairment at 3 and 6 months, compared with those who received endocrine therapy alone, but this difference abated over time. The findings suggest that chemotherapy provides early but not sustained contribution to perceived cognitive impairment, indicating that the underlying etiology may be more multifaceted than just chemotherapy use. In addition, since both groups experienced significant perceived cognitive impairment compared with baseline, more studies are needed in the clinical assessment and management of perceived cognitive impairment over the treatment trajectory.

In the Tamoxifen and Exemestane Adjuvant Multinational Trial, breast cancer survivors received 5 years of exemestane treatment (n = 114) or sequential treatment of 2.5 years of tamoxifen treatment, followed by 2.5 years of exemestane treatment (n = 92).[10]  Neuropsychological performance was assessed before endocrine therapy, after 1 year (short-term [ST] follow-up), and at 5 years (long-term [LT] follow-up). A control group of 120 healthy participants were assessed with parallel intervals. After controlling for age, intelligence quotient, attrition, menopausal symptoms, anxiety and/or depression, and fatigue, the sequential group showed ST and LT decline, compared with control participants, on verbal memory (effect size [ES] = 0.26, P = .01; ES = 0.34, P =.003) and executive function (ES = 0.27, P =.007; ES = 0.38, P = .002). In addition, compared with the exemestane group, the sequential group demonstrated ST decline on information processing speed (ES = 0.33, P = .01) and executive function (ES = 0.32, P = .01) and LT decline on verbal memory (ES = 0.33, P = .02). The exemestane group showed no cognitive decline compared with control participants. The apparent cognitive adverse effects of tamoxifen alone and after switching to exemestane suggested that tamoxifen may have a carryover cognitive effect.[10] These findings, if confirmed, suggest that tamoxifen may have more adverse cognitive effects than exemestane.

Objective cognitive deficits in men with prostate cancer receiving androgen deprivation therapy (ADT)

Researchers identified 14 high-quality studies among 157 potentially relevant articles published between 1950 and 2012 by searching PubMed, Medline, PsycINFO, Cochrane Library, and Web of Knowledge/Science.[11] Criteria for study inclusion were an appropriate control group, baseline measurements, and the use of objective neuropsychological tests. Eleven studies were longitudinal; the authors included three cross-sectional studies.

The only significant effect detected was for visuomotor ability. There were no discernible negative effects on the other domains studied, which included the following:[11]

  • Attention/working memory.
  • Executive functioning.
  • Language.
  • Verbal memory.
  • Visual memory.
  • Visuospatial ability.

Individual Research Studies

Neuropsychological tests of patients with early-stage breast cancer receiving adjuvant treatment

Several studies are relevant to an understanding of cognitive impairment in women with early-stage breast cancer who receive chemotherapy.

Using a battery of neuropsychological and psychological tests, investigators assessed healthy controls and women with early-stage breast cancer who were treated with chemotherapy (n = 60) or who did not receive chemotherapy (n = 72), before treatment and again at 1, 6, and 18 months.[12] The primary outcome of interest was processing speed. Results demonstrated that women aged 60 years or older with lower baseline cognitive reserve who received chemotherapy scored lower on processing speed than did healthy controls or women who did not receive chemotherapy. These results are consistent with results from studies of aging.[13] There was also an effect on verbal ability that resolved by 6 months. There were no demonstrable interactions between time, age, and cognitive reserve for the following:[12]

  • Verbal memory.
  • Visual memory.
  • Working memory.
  • Sorting.
  • Distractibility.
  • Reaction time.

Another group of investigators performed neuropsychological assessments for 60 women younger than 66 years who had early-stage breast cancer.[14] The subjects were tested before and after each cycle of adjuvant chemotherapy. The goal was to determine whether there was progressive decline suggesting a dose-response relationship. A control cohort of 60 healthy women matched for age and education was tested at appropriate intervals. The authors observed a dose-related decline in the following:[14]

  • Working memory.
  • Processing speed.
  • Verbal memory.
  • Visual memory.

Subjective reports by patients with early-stage breast cancer receiving adjuvant treatment

Investigators compared subjective cognitive functioning (measured by the Cognitive Failures Questionnaire) and satisfaction with subjective cognitive functioning (measured with the cognitive functioning facet of the World Health Organization Quality of Life instrument) at two times in women with breast cancer—before chemotherapy and 3 months later—and at comparable times in women with benign breast disease.[15] The frequency of subjective concerns did not differ, but women with breast cancer were less satisfied with their cognitive functioning. Psychological factors and diagnosis influenced satisfaction with cognitive functioning.

Self-reported neurocognitive symptoms in women with breast cancer

Investigators conducted a longitudinal study of 581 patients with breast cancer recruited from community cancer clinics and age-matched controls.[16] Patients and controls completed the Functional Assessment of Cancer Therapy—Cognitive Function (FACT-Cog) before receiving chemotherapy, 4 weeks postchemotherapy, and 6 months after the second assessment. Controls were tested within the same time windows as patients. Relevant findings were as follows:

  • At baseline, patients with breast cancer had lower overall quality-of-life scores (on the FACT: General, or FACT-G) than did controls.
  • Mean FACT-G scores declined in patients postchemotherapy but remained stable in controls.
  • Almost half of the patients experienced decline in cognitive function, compared with only 10% of controls.
  • Predictors for decline on the overall FACT-Cog scale included lower reading scores, higher depression, and higher anxiety.
  • Predictors for decline in specific subscales varied.

Neuropsychological tests of patients with early-stage colon cancer

Researchers administered formal neuropsychological tests to 81 patients with early-stage colon cancer who were scheduled to receive oxaliplatin, leucovorin, and fluorouracil . They conducted assessments prechemotherapy (n = 81), postchemotherapy (n = 73), and 6 months after the end of the last cycle of chemotherapy (n = 54).[17] Attention, visuomotor ability, executive function, verbal memory, and verbal learning were evaluated.

More than one-third of patients (37%) had cognitive impairment in processing speed and executive functioning before receiving chemotherapy. More than half of patients (56%) had a decline in verbal memory. At 6 months, 54% of patients had improved, but 33% had worsened. In an exploratory analysis, older age and fewer years of education were risk factors for cognitive impairment. Conversely, quality of life, anxiety, depression, or fatigue levels did not correlate with cognitive dysfunction.[17]

Neuropsychological tests of patients with early- and advanced-stage colon cancer

Longitudinal changes in neuropsychological test results and patient self-reported measures of cognitive symptoms (FACT-Cog version 2) were studied in a cohort of 362 patients with colorectal cancer (289 early-stage and 73 advanced-stage) who received chemotherapy (n = 173) or did not receive chemotherapy (n = 116). Results in these patients were compared with results in a control population of 72 participants.[18] Salient results included the following:

  • Self-reported cognitive impairment was more common in patients who received chemotherapy (32%) than in those who did not receive chemotherapy (16%) or in controls (12.5%) (P = .007) at 6 months. There were no differences at 12 months.
  • Patient self-reported cognitive impairment was moderately associated with fatigue, quality of life, and anxiety/depression.
  • Correlation between neuropsychological test results and self-reported impairment was weak.
  • Based on ICCTF criteria, cognitive impairment was present in approximately 50% of patients with colorectal cancer at baseline and 6 and 12 months later, compared with approximately 15% of controls.
  • There were no differences between patients who had or had not received chemotherapy.

Neuropsychological tests of men with prostate cancer receiving ADT

Investigators studied 58 men with prostate cancer who received ADT at baseline and 6 and 12 months later. They compared their results to those of age-matched and education-level–matched patients with prostate cancer who did not receive ADT (n = 88) and men without prostate cancer (n = 84).[19] The groups were similar at baseline, but at 6 and 12 months, ADT-treated men were more likely to have impaired cognitive performance according to ICCTF criteria, which combine results from individual tests. Rates of impaired cognitive performance on individual tests, however, were not significantly different at 12 months between ADT-treated patients and controls. The following factors did not moderate the effect of ADT on cognitive performance:

  • Age.
  • Cognitive reserve.
  • Depressive symptoms.
  • Fatigue.
  • Hot flashes.

Neuropsychological tests of allogeneic stem cell transplant (SCT) recipients

Researchers tested 102 transplant recipients before and at 12 months after SCT.[20] They used a battery of 14 tests to assess the following cognitive domains:

  • Verbal working memory/fluency.
  • Fine motor function.
  • Visuospatial working memory.
  • Verbal learning and retrieval.
  • Reaction time.

The investigators chose to report the frequency of below-normal test scores for individual tests rather than define domain-specific performance, so comparison with other studies is not possible.[20]

Some evidence of impairment in at least one domain was present in 47% of patients at baseline and 41% of patients at follow-up. Age and premorbid intelligence level were associated with performance. Finally, 16% of patients demonstrated a decline in cognitive function.[20]

References
  1. Wefel JS, Vardy J, Ahles T, et al.: International Cognition and Cancer Task Force recommendations to harmonise studies of cognitive function in patients with cancer. Lancet Oncol 12 (7): 703-8, 2011. [PUBMED Abstract]
  2. Joly F, Giffard B, Rigal O, et al.: Impact of Cancer and Its Treatments on Cognitive Function: Advances in Research From the Paris International Cognition and Cancer Task Force Symposium and Update Since 2012. J Pain Symptom Manage 50 (6): 830-41, 2015. [PUBMED Abstract]
  3. Pullens MJ, De Vries J, Roukema JA: Subjective cognitive dysfunction in breast cancer patients: a systematic review. Psychooncology 19 (11): 1127-38, 2010. [PUBMED Abstract]
  4. Gutenkunst SL, Vardy JL, Dhillon HM, et al.: Correlates of cognitive impairment in adult cancer survivors who have received chemotherapy and report cognitive problems. Support Care Cancer 29 (3): 1377-1386, 2021. [PUBMED Abstract]
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  10. Lee Meeuw Kjoe PR, Kieffer JM, Small BJ, et al.: Effects of tamoxifen and exemestane on cognitive function in postmenopausal patients with breast cancer. JNCI Cancer Spectr 7 (2): , 2023. [PUBMED Abstract]
  11. McGinty HL, Phillips KM, Jim HS, et al.: Cognitive functioning in men receiving androgen deprivation therapy for prostate cancer: a systematic review and meta-analysis. Support Care Cancer 22 (8): 2271-80, 2014. [PUBMED Abstract]
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  18. Vardy JL, Dhillon HM, Pond GR, et al.: Cognitive Function in Patients With Colorectal Cancer Who Do and Do Not Receive Chemotherapy: A Prospective, Longitudinal, Controlled Study. J Clin Oncol 33 (34): 4085-92, 2015. [PUBMED Abstract]
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  20. Scherwath A, Schirmer L, Kruse M, et al.: Cognitive functioning in allogeneic hematopoietic stem cell transplantation recipients and its medical correlates: a prospective multicenter study. Psychooncology 22 (7): 1509-16, 2013. [PUBMED Abstract]

Interventions for Cognitive Impairment

Nonpharmacological Interventions

Evidence-based interventions to manage cognitive impairment in cancer patients and survivors have not been firmly established. Several nonpharmacological approaches have shown promise, including the following:[1]

  • Cognitive rehabilitation.
  • Exercise and physical activity.
  • Psychosocial interventions such as attention-restoring activities and meditation.

All of the interventions in Table 1 have shown some evidence of efficacy but remain active areas of investigation.

Table 1. Nonpharmacological Interventions for Cognitive Impairment
Intervention Dose Comments References
RCT = randomized controlled trial.
Cognitive rehabilitation 4–96 h Multiple RCTs and non-RCTs showed improvement in some components of subjective/objective cognition. Positive results: [213]
Included psychoeducation, compensatory training, and cognitive training. 1 RCT and 2 non-RCTs showed no benefit.
Most RCTs had small samples (<50 participants). Negative results: [1416]
Wide variation in components of intervention, dose, and measures.
Exercise and physical activity 6–65 h Several small RCTs and non-RCTs showed improvement in some components of subjective/objective cognition. Positive results: [17][Level of evidence: I];[2,1822]
Included various types of exercise, yoga, qigong, and tai chi. 2 studies showed no benefit.
Wide variation in type of movement therapy, dose, and measures. Negative results: [23,24]
Attention restoration and meditation 12–22 h 2 large RCTs and 3 small RCTs showed improvement in some components of subjective/objective cognition. Positive results: [2529]
All therapies involved quiet, focused attention in the present moment.

Cognitive rehabilitation

Cognitive rehabilitation has shown promise in reducing the impact of cognitive problems on cancer patients and survivors. This approach originated to treat people with brain injuries such as stroke or traumatic brain injury, and it has been adapted for the cancer setting.[30] Several rehabilitation approaches have been blended to varying degrees, including the following:

  • Psychoeducation provides useful information about brain functioning, cognitive deficits, and their consequences for daily life.[4]
  • Compensatory training focuses on the acquisition of new behaviors and strategies to compensate for chronic dysfunction. This intervention may include modifying or restructuring the environment by substituting external aids (such as calendars and electronic diaries) so that individuals rely less on their cognitive abilities. It may involve learning new coping strategies (such as pacing cognitive activities and minimizing distractions).[8]
  • Cognitive training involves the use of repetitive, increasingly challenging tasks (often via computer) to improve, maintain, or restore cognitive function in the areas of attention, memory, and executive function.[9,13,31]

The modest evidence for the efficacy of cognitive rehabilitation is based on several randomized controlled trials that used a diverse group of objective tests of neuropsychological function and subjective measures of cognitive impairment.[69,11] Cognitive rehabilitation intervention groups showed greater improvement than controls in self-reported cognitive impairment [6,7] and objective neuropsychological measures of attention,[6] memory,[7,8,11] and processing speed.[11] Other cognitive rehabilitation intervention studies provided similar results but were limited by partial or no randomization,[5,14] one-group design,[3,4] or secondary analysis.[10]

Exercise and physical activity

There is increasing interest in physical activity and mind-body exercise to address cognitive impairment in cancer survivors.[18,20,23,32] A systematic review of randomized controlled trials using exercise to address cognitive function in cancer survivors identified 29 potentially relevant trials that were published through 2018. Of these trials, 12 (41%) found benefit in perceived cognitive function. In addition, 3 of the 10 studies (30%) that objectively measured cognitive function found some benefit. A number of limitations in these trials were noted; the type of physical exercise varied, and cognitive function was often not the primary outcome of interest.[33]

In one multicenter randomized clinical trial, 181 breast cancer survivors who had received neoadjuvant or adjuvant chemotherapy reported cognitive problems, which were confirmed by lower-than-expected performance on neuropsychological testing. Participants were randomly assigned to an exercise group or a control group.[34][Level of evidence: I] The 6-month exercise intervention consisted of supervised aerobic exercise and strength training (2 h/wk) and Nordic/power walking (2 h/wk). Notably, two-thirds of the participants attended 80% or more of the exercise sessions, and physical fitness significantly improved for participants in the exercise group, compared with participants in the control group (peak oxygen uptake, 1.4 mL/min/kg, 95% confidence interval, 0.6–2.2). No difference was seen in the primary outcome of memory. However, significant beneficial effects were found for self-reported cognitive functioning, fatigue, quality of life, and depression. In addition, subgroup analysis indicated a positive effect of exercise on tested cognitive functioning in highly fatigued patients.

Similarly, the Exercise Program in Cancer and Cognition Study was a randomized controlled trial designed to determine whether 6 months of 150 minutes or more per week of moderate-intensity aerobic exercise, compared with usual-care control, improved neurocognitive function in 153 women with breast cancer receiving endocrine therapy.[17][Level of evidence: I] Primary outcomes, assessed before baseline and within 2 weeks postintervention, included objective cognitive performance tests of processing speed, learning and memory, verbal memory, and working memory. Secondary outcomes included performance on cognitive tests of attention, executive function, and mental flexibility. Adherence to the exercise intervention was high, with 70.13% of participants who were at least 80% adherent, 67.33% who were at least 90% adherent, and 55.84% who were 100% adherent. However, cardiorespiratory fitness did not differ significantly between treatment groups from baseline to postintervention. Improvements in processing speed were noted for the exercise group compared with the usual-care group, with a significant group-by-time interaction (P = .041) and a trend for the main effect of time (P = .11) for processing speed and no change in the controls. Improvements in processing speed were associated with better intervention adherence (P = .017). In addition, younger women (aged ≤60 years) had a trend for greater processing speed improvements (P = .06), while those with a lower educational level (≤16 years of education) had a significantly greater improvement in processing speed (P = .03).

A randomized controlled trial of qigong—a set of coordinated gentle exercises, meditation, and breathing—demonstrated improved self-reported cognitive impairment in cancer survivors after chemotherapy.[20] Other movement studies used one-group designs,[23] were not randomized,[22] or were secondary analyses.[19,24]

Attention restoration

An intervention focused specifically on restoring and maintaining the capacity to direct attention, actively focus, and concentrate—components of cognitive function—was developed and tested in breast cancer survivors.[25] The intervention consisted of exposure to the natural environment, including activities such as walking or sitting outdoors, tending plants or gardening, watching birds or other wildlife, and caring for pets. Participants contracted in writing to spend 120 minutes per week engaged in one or more of these activities. Neuropsychological tests of attention demonstrated greater improvement in the capacity to direct attention in the group that participated in attention-restoring activities than in the control group.[26]

Meditation

Mindfulness-based stress reduction (MBSR) is an integrative therapy that focuses on bringing attention and awareness to each moment in a nonjudgmental way. The benefits of MBSR have been evaluated in numerous studies of health conditions such as chronic pain, anxiety, and fibromyalgia.[27] A review of MBSR studies in cancer patients found only two randomized trials with positive results, despite a small sample size.[29,35] In one large, adequately powered, randomized trial in breast cancer survivors, the MBSR group showed more improvement in self-reported confusion than did the control group at the end of the intervention period, but there were no long-term effects.[27] No objective measures of cognitive function were used in this trial, and evidence of impairment was not a requirement for study eligibility.

A smaller study showed that MBSR participants experienced more positive effects on self-reported attention and working memory than did a control group. The finding was durable at 6 months.[29] An objective measure of accuracy also showed durable improvement in the MBSR group.

A randomized trial of Tibetan sound meditation demonstrated improvement in objective measures of memory, processing speed, and self-reported cognitive function.[28] Although the sample size was small, eligibility for the study required self-reported cognitive impairment.

Pharmacological Interventions

Several classes of agents have been investigated as potential interventions for managing cognitive impairment. In general, the quality of study design, outcomes studied, and variations in doses and schedules of the agents prevent any firm conclusions. The agents, putative mechanisms of action, and summary of results are provided below and in Table 2.

  • Psychostimulants: Approved by the U.S. Food and Drug Administration primarily for attention-deficit hyperactivity disorder or sleep-wake disorders, psychostimulants are generally well tolerated. These agents have been tested in individuals with drug- or cancer therapy–induced cognitive dysfunction with varying levels of other associated symptoms.[3638] Seven phase II trials of different psychostimulants for treating cognitive impairment and associated symptoms were reviewed. Not all agents showed benefit; the symptoms most likely to improve were alertness, attention, and psychomotor speed. Six trials had control arms, and one reported results in a descriptive fashion. Also, some trials were in limited populations that may have had additional confounders such as individuals with central nervous system tumors, making results difficult to extrapolate to other patient groups.[3739] Finally, the trials were underpowered, in part because of difficulty with enrollment.
  • Erythropoietin-stimulating agents (ESAs): The hypothesized mechanism for ESAs in the improvement of cognitive function is the result of preclinical data demonstrating erythropoietin receptors in brain tissue providing a neuroprotective effect and preventing neuronal apoptosis. The potential for cognitive improvement must be weighed against the risks of ESAs, which include cardiovascular and thrombotic events, the potential for causing tumor progression, and decreases in overall survival.
  • Acetylcholinesterase (AChE) inhibitors: Donepezil, an AChE inhibitor, is approved for Alzheimer disease. It is hypothesized that whole-brain radiation therapy (WBRT) causes neuronal injury that results in a decrease in acetylcholine. This theory is supported clinically by similarities between WBRT cognitive dysfunction and Alzheimer disease. The use of donepezil may increase acetylcholine levels in the brain.

    A large, multisite randomized controlled trial included 276 breast cancer survivors who were at a mean of 29.6 months (standard deviation = 14.2) postchemotherapy. Participants were assigned to receive either 5 mg of donepezil once daily for 6 weeks, titrated up to 10 mg once daily for 18 weeks (n = 140), or a placebo (n = 136).[40][Level of evidence: I] At 24 weeks, the treatment groups did not differ on memory scores (Hopkins Verbal Learning Test-Revised) (donepezil mean = 25.98, placebo = 26.50; P = .32). In addition, there were no statistically significant differences between treatment groups at 12, 24, or 36 weeks for attention, executive function, verbal fluency, processing speed, or self-reported cognitive functioning.

  • N-methyl-D-aspartate (NMDA) receptor antagonists: By inhibiting the NMDA receptor with the antagonist memantine, radiation-induced neuronal stimulation and excitotoxicity may be reduced, preventing WBRT-induced cognitive decline. Memantine has not been studied for reducing cognitive dysfunction in cancer patients outside of the WBRT setting.
Table 2. Agents for Managing Cognitive Impairment
Agent Dose Comments
AChE = acetylcholinesterase; bid = twice a day; ESA = erythropoietin-stimulating agent; NMDA = N-methyl-D-aspartate; qd = every day; RCT = randomized controlled trial; WBRT = whole-brain radiation therapy.
Psychostimulants
Methylphenidate 10–30 mg/d for ≥2 d Phase II studies with varying levels of benefits for different cognitive parameters (alertness, attention, memory, psychomotor speed, and executive function).
Small trials, not always randomized, did not always meet accrual goals; results should be interpreted with caution.[36,37]; [39][Level of evidence: II]
D-methylphenidate 5–10 mg bid Small, underpowered, placebo-controlled experience showed no benefit in verbal learning.
N = 57
Placebo controlled.[41][Level of evidence: II]
Modafinil 200–400 mg/d for 4 d–6 wk Phase II studies with varied trial designs.
Benefit seen in psychomotor speed, memory, executive function, and attention, with largest study showing sustained benefit.[42][Level of evidence: II]
Interpret with caution: accrual problems, short study duration, and inadequate power.
No benefit seen in study in which patients served as their own controls.[37,38,43][Level of evidence: I]
ESAs
Erythropoietin 40,000 U/wk Multiple clinical trials demonstrated conflicting results; no intervention effect on improvement in subjective cognitive function.
Results difficult to generalize: varying assessment tools, small sample sizes, and differences in dosing and length of treatment.[44][Level of evidence: I]; [45][Level of evidence: I]; [46][Level of evidence: II]; [47][Level of evidence: II]; [48][Level of evidence: II]; [49]
AChE Inhibitors
Donepezil 5 mg qd; may increase to 10 mg qd Studied in patients 1–5 y postchemotherapy and >6 mo post-WBRT.
Mixed results of no treatment effect and some improvement in some measures of attention, concentration, and memory in each trial.[50][Level of evidence: I]; [51][Level of evidence: I]; [52][Level of evidence: II]; [40][Level of evidence: I]
NMDA Receptor Antagonists
Memantine 20 mg qd One RCT; primary endpoint of improvement in delayed recall not statistically significant.
Treatment resulted in better cognitive function over time; delayed time to cognitive decline; and reduced rate of decline in memory, executive function, and processing speed.[53]
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  28. Milbury K, Chaoul A, Biegler K, et al.: Tibetan sound meditation for cognitive dysfunction: results of a randomized controlled pilot trial. Psychooncology 22 (10): 2354-63, 2013. [PUBMED Abstract]
  29. Johns SA, Von Ah D, Brown LF, et al.: Randomized controlled pilot trial of mindfulness-based stress reduction for breast and colorectal cancer survivors: effects on cancer-related cognitive impairment. J Cancer Surviv 10 (3): 437-48, 2016. [PUBMED Abstract]
  30. Cicerone KD, Dahlberg C, Malec JF, et al.: Evidence-based cognitive rehabilitation: updated review of the literature from 1998 through 2002. Arch Phys Med Rehabil 86 (8): 1681-92, 2005. [PUBMED Abstract]
  31. Von Ah D, Jansen C, Allen DH, et al.: Putting evidence into practice: evidence-based interventions for cancer and cancer treatment-related cognitive impairment. Clin J Oncol Nurs 15 (6): 607-15, 2011. [PUBMED Abstract]
  32. Lee CE, Kilgour A, Lau YK: Efficacy of walking exercise in promoting cognitive-psychosocial functions in men with prostate cancer receiving androgen deprivation therapy. BMC Cancer 12: 324, 2012. [PUBMED Abstract]
  33. Campbell KL, Zadravec K, Bland KA, et al.: The Effect of Exercise on Cancer-Related Cognitive Impairment and Applications for Physical Therapy: Systematic Review of Randomized Controlled Trials. Phys Ther 100 (3): 523-542, 2020. [PUBMED Abstract]
  34. Koevoets EW, Schagen SB, de Ruiter MB, et al.: Effect of physical exercise on cognitive function after chemotherapy in patients with breast cancer: a randomized controlled trial (PAM study). Breast Cancer Res 24 (1): 36, 2022. [PUBMED Abstract]
  35. Shennan C, Payne S, Fenlon D: What is the evidence for the use of mindfulness-based interventions in cancer care? A review. Psychooncology 20 (7): 681-97, 2011. [PUBMED Abstract]
  36. Bruera E, Miller MJ, Macmillan K, et al.: Neuropsychological effects of methylphenidate in patients receiving a continuous infusion of narcotics for cancer pain. Pain 48 (2): 163-6, 1992. [PUBMED Abstract]
  37. Gehring K, Patwardhan SY, Collins R, et al.: A randomized trial on the efficacy of methylphenidate and modafinil for improving cognitive functioning and symptoms in patients with a primary brain tumor. J Neurooncol 107 (1): 165-74, 2012. [PUBMED Abstract]
  38. Boele FW, Douw L, de Groot M, et al.: The effect of modafinil on fatigue, cognitive functioning, and mood in primary brain tumor patients: a multicenter randomized controlled trial. Neuro Oncol 15 (10): 1420-8, 2013. [PUBMED Abstract]
  39. Meyers CA, Weitzner MA, Valentine AD, et al.: Methylphenidate therapy improves cognition, mood, and function of brain tumor patients. J Clin Oncol 16 (7): 2522-7, 1998. [PUBMED Abstract]
  40. Rapp SR, Dressler EV, Brown WM, et al.: Phase III Randomized, Placebo-Controlled Clinical Trial of Donepezil for Treatment of Cognitive Impairment in Breast Cancer Survivors After Adjuvant Chemotherapy (WF-97116). J Clin Oncol 42 (21): 2546-2557, 2024. [PUBMED Abstract]
  41. Mar Fan HG, Clemons M, Xu W, et al.: A randomised, placebo-controlled, double-blind trial of the effects of d-methylphenidate on fatigue and cognitive dysfunction in women undergoing adjuvant chemotherapy for breast cancer. Support Care Cancer 16 (6): 577-83, 2008. [PUBMED Abstract]
  42. Kohli S, Fisher SG, Tra Y, et al.: The effect of modafinil on cognitive function in breast cancer survivors. Cancer 115 (12): 2605-16, 2009. [PUBMED Abstract]
  43. Lundorff LE, Jønsson BH, Sjøgren P: Modafinil for attentional and psychomotor dysfunction in advanced cancer: a double-blind, randomised, cross-over trial. Palliat Med 23 (8): 731-8, 2009. [PUBMED Abstract]
  44. Chang J, Couture FA, Young SD, et al.: Weekly administration of epoetin alfa improves cognition and quality of life in patients with breast cancer receiving chemotherapy. Support Cancer Ther 2 (1): 52-8, 2004. [PUBMED Abstract]
  45. O’Shaughnessy JA, Vukelja SJ, Holmes FA, et al.: Feasibility of quantifying the effects of epoetin alfa therapy on cognitive function in women with breast cancer undergoing adjuvant or neoadjuvant chemotherapy. Clin Breast Cancer 5 (6): 439-46, 2005. [PUBMED Abstract]
  46. Iconomou G, Koutras A, Karaivazoglou K, et al.: Effect of epoetin alpha therapy on cognitive function in anaemic patients with solid tumours undergoing chemotherapy. Eur J Cancer Care (Engl) 17 (6): 535-41, 2008. [PUBMED Abstract]
  47. Fan HG, Park A, Xu W, et al.: The influence of erythropoietin on cognitive function in women following chemotherapy for breast cancer. Psychooncology 18 (2): 156-61, 2009. [PUBMED Abstract]
  48. Massa E, Madeddu C, Lusso MR, et al.: Evaluation of the effectiveness of treatment with erythropoietin on anemia, cognitive functioning and functions studied by comprehensive geriatric assessment in elderly cancer patients with anemia related to cancer chemotherapy. Crit Rev Oncol Hematol 57 (2): 175-82, 2006. [PUBMED Abstract]
  49. O’Shaughnessy JA: Effects of epoetin alfa on cognitive function, mood, asthenia, and quality of life in women with breast cancer undergoing adjuvant chemotherapy. Clin Breast Cancer 3 (Suppl 3): S116-20, 2002. [PUBMED Abstract]
  50. Lawrence JA, Griffin L, Balcueva EP, et al.: A study of donepezil in female breast cancer survivors with self-reported cognitive dysfunction 1 to 5 years following adjuvant chemotherapy. J Cancer Surviv 10 (1): 176-84, 2016. [PUBMED Abstract]
  51. Rapp SR, Case LD, Peiffer A, et al.: Donepezil for Irradiated Brain Tumor Survivors: A Phase III Randomized Placebo-Controlled Clinical Trial. J Clin Oncol 33 (15): 1653-9, 2015. [PUBMED Abstract]
  52. Shaw EG, Rosdhal R, D’Agostino RB, et al.: Phase II study of donepezil in irradiated brain tumor patients: effect on cognitive function, mood, and quality of life. J Clin Oncol 24 (9): 1415-20, 2006. [PUBMED Abstract]
  53. Brown PD, Pugh S, Laack NN, et al.: Memantine for the prevention of cognitive dysfunction in patients receiving whole-brain radiotherapy: a randomized, double-blind, placebo-controlled trial. Neuro Oncol 15 (10): 1429-37, 2013. [PUBMED Abstract]

Latest Updates to This Summary (11/07/2024)

The PDQ cancer information summaries are reviewed regularly and updated as new information becomes available. This section describes the latest changes made to this summary as of the date above.

Interventions for Cognitive Impairment

Revised Table 1, Nonpharmacological Interventions for Cognitive Impairment, to include information about exercise and physical activity (cited Bender et al. as reference 17 and level of evidence I).

Added text about the results of the Exercise Program in Cancer and Cognition Study, a randomized controlled trial designed to determine whether 6 months of 150 minutes or more per week of moderate-intensity aerobic exercise, compared with usual-care controls, improved neurocognitive function in women with breast cancer receiving endocrine therapy.

Added text about the results of a large, multisite randomized clinical trial, in which breast cancer survivors who were at a mean of 29.6 months postchemotherapy were assigned to receive either 5 mg of donepezil once daily for 6 weeks, titrated up to 10 mg once daily for 18 weeks, or a placebo (cited Rapp et al. as reference 40 and level of evidence I).

This summary is written and maintained by the PDQ Supportive and Palliative Care Editorial Board, which is editorially independent of NCI. The summary reflects an independent review of the literature and does not represent a policy statement of NCI or NIH. More information about summary policies and the role of the PDQ Editorial Boards in maintaining the PDQ summaries can be found on the About This PDQ Summary and PDQ® Cancer Information for Health Professionals pages.

About This PDQ Summary

Purpose of This Summary

This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about expert-reviewed information summary about causes and management of cognitive impairment in adults with cancer. It is intended as a resource to inform and assist clinicians in the care of their patients. It does not provide formal guidelines or recommendations for making health care decisions.

Reviewers and Updates

This summary is reviewed regularly and updated as necessary by the PDQ Supportive and Palliative Care Editorial Board, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH).

Board members review recently published articles each month to determine whether an article should:

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  • be cited with text, or
  • replace or update an existing article that is already cited.

Changes to the summaries are made through a consensus process in which Board members evaluate the strength of the evidence in the published articles and determine how the article should be included in the summary.

The lead reviewers for Cognitive Impairment in Adults With Cancer are:

  • Larry D. Cripe, MD (Indiana University School of Medicine)
  • Diane Von Ah, PhD, RN, FAAN (The Ohio State University)

Any comments or questions about the summary content should be submitted to Cancer.gov through the NCI website’s Email Us. Do not contact the individual Board Members with questions or comments about the summaries. Board members will not respond to individual inquiries.

Levels of Evidence

Some of the reference citations in this summary are accompanied by a level-of-evidence designation. These designations are intended to help readers assess the strength of the evidence supporting the use of specific interventions or approaches. The PDQ Supportive and Palliative Care Editorial Board uses a formal evidence ranking system in developing its level-of-evidence designations.

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The preferred citation for this PDQ summary is:

PDQ® Supportive and Palliative Care Editorial Board. PDQ Cognitive Impairment in Adults With Cancer. Bethesda, MD: National Cancer Institute. Updated <MM/DD/YYYY>. Available at: /side-effects/memory/cognitive-impairment-hp-pdq. Accessed <MM/DD/YYYY>. [PMID: 29112351]

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Low-Fiber Foods

Low-Fiber Foods

If you have diarrhea, your doctor or dietitian may suggest you eat foods that are low in fiber. Get ideas on what to eat from this list of low-fiber foods.

Main meals

  • chicken or turkey (skinless and baked, broiled, or grilled)
  • cooked refined cereals (such as Cream of Rice, instant oatmeal, and grits)
  • eggs
  • fish
  • noodles
  • potatoes, (peeled and boiled or baked)
  • white bread
  • white rice

Fruits and vegetables

  • carrots (cooked)
  • canned fruit, such as peaches, pears, and applesauce
  • fruit juice
  • mushrooms
  • string beans (cooked)
  • vegetable juice

Sweets and snacks

  • angel food cake
  • animal crackers
  • custard
  • gelatin (Jell-O)
  • ginger snaps
  • graham crackers
  • saltine crackers
  • sherbet
  • sorbet
  • vanilla wafers
  • yogurt (plain or vanilla)

Fats

  • oil
  • salad dressing (without seeds)
  • butter
  • mayonnaise

High-Fiber Foods

High-Fiber Foods

If you have constipation or weight gain, your doctor or dietitian may suggest you add foods that are high in fiber to your diet. Get ideas on what to eat from this list of high-fiber foods.

Main meals

  • bran muffins 
  • bran or whole-grain cereals 
  • cooked dried or canned peas and beans, such as lentils or pinto, black, red, or kidney beans
  • peanut butter and other nut butters 
  • soups with vegetables and beans, such as lentil and split pea 
  • whole-grain cereals, such as oatmeal and shredded wheat
  • whole-wheat bread
  • whole-wheat pasta

Fruits and vegetables

  • apples 
  • berries, such as blueberries, blackberries, and strawberries 
  • broccoli 
  • brussels sprouts 
  • cabbage
  • corn 
  • dried fruit, such as apricots, dates, prunes, and raisins 
  • green leafy vegetables, such as spinach, lettuce, kale, and collard greens 
  • peas 
  • potatoes with skins
  • sweet potatoes 
  • yams 

Snacks

  • bran snack bars 
  • granola
  • nuts
  • popcorn
  • seeds, such as pumpkin or sunflower 
  • trail mix

Ways to Add Calories to Your Diet

Ways to Add Calories to Your Diet

If you have appetite loss, weight loss, sore throat, or trouble swallowing, your doctor or dietitian may suggest you add calories to your diet. Use this list to get ideas on how to increase calories in your diet. 

Avocado 

  • spread on toast 
  • mash with spices and lime juice to make guacamole and use as a dip
  • blend into smoothies 
  • add to sandwiches, burgers, salads, or quesadillas 

Milk 

  • use whole milk instead of low-fat 
  • add to hot or cold cereal 
  • pour on chicken and fish while baking 
  • mix in hamburgers, meatloaf, and croquettes 
  • use it to make hot chocolate 

Cheese 

  • melt on top of casseroles, potatoes, and vegetables 
  • add to omelets 
  • add to sandwiches 

Granola 

  • use in cookie, muffin, and bread batters 
  • sprinkle on:
    • vegetables 
    • yogurt 
    • ice cream 
    • pudding 
    • custard 
    • fruit 
  • layer with fruits and bake 
  • mix with dried fruits and nuts for a snack 
  • use in pudding recipes instead of bread or rice 

Dried fruits, such as raisins, prunes, apricots, dates, and figs 

  • soak in warm water to plump them up, then eat for breakfast, dessert, or snack 
  • add to: 
    • muffins 
    • cookies 
    • breads 
    • cakes 
    • rice and grain dishes 
    • cereals 
    • puddings
    • stuffings 
    • cooked vegetables, such as carrots, sweet potatoes, yams, and acorn or butternut squash 
  • bake in pies and turnovers 
  • combine with nuts or granola for snacks 

Eggs

  • add chopped hard-boiled eggs to salads, salad dressings, vegetables, casseroles, and creamed meats, such as chipped cream beef 
  • make a rich custard with eggs, milk, and sugar 
  • add extra hard-boiled yolks to deviled egg filling and sandwich spreads, such as egg or tuna salad
  • beat eggs into mashed potatoes, pureed vegetables, and sauces (make sure to keep cooking these dishes after adding the eggs because raw eggs may contain harmful bacteria). 
  • add extra eggs or egg whites to: 
    • custards
    • puddings 
    • quiches 
    • scrambled eggs or omelets
    • pancake or French toast batter

Easy-to-Digest Foods

Easy-to-Digest Foods

If you have nausea or had vomiting that is now under control, your doctor or dietitian may suggest you eat foods that are easy on the stomach. Get ideas on what to eat from this list of easy-to-digest foods and drinks.

Soups 

  • clear broth, such as chicken, vegetable, or beef 
  • all kinds (strain or puree, if needed), except those made with foods that cause gas, such as dried beans and peas, broccoli, or cabbage 

Drinks 

  • clear carbonated drinks that have lost their fizz 
  • cranberry or grape juice 
  • fruit-flavored drinks 
  • fruit punch 
  • milk 
  • sports drinks, such as Gatorade and Powerade 
  • tea 
  • vegetable juices 
  • water 

Main meals and snacks

  • avocado 
  • beef (tender cuts only) 
  • cheese
    • hard, mild types, such as American 
    • soft or semisoft, such as cottage cheese or cream cheese 
  • chicken or turkey (skinless and broiled or baked) 
  • eggs 
  • fish (poached or broiled) 
  • noodles
  • pasta, plain 
  • peanut butter, creamy, and other nut butters 
  • potatoes (peeled and boiled or baked) 
  • pretzels
  • refined cold cereals, such as corn flakes, Rice Krispies, Rice Chex, and Corn Chex 
  • refined hot cereals, such as Cream of Wheat 
  • saltine crackers 
  • tortillas made with white flour 
  • vegetables, tender, well-cooked 
  • white bread 
  • white rice 

Desserts and sweets

  • angel food cake
  • bananas
  • canned fruit, such as applesauce, peaches, and pears 
  • custard 
  • frozen yogurt 
  • gelatin (Jell-O)
  • ice cream 
  • lemon drop candy 
  • popsicles 
  • pudding 
  • sherbet 
  • sorbet 
  • yogurt (plain or vanilla) 

Protein shakes and supplements 

  • instant breakfast drinks, such as Carnation Breakfast Essentials 
  • liquid protein supplements, such as Ensure 
  • clear nutrition supplements, such as Boost Breeze and Ensure Clear

Easy-to-Chew and Easy-to-Swallow Foods

Easy-to-Chew and Easy-to-Swallow Foods

If you have mouth or throat problems such as dry mouth, sore mouth, sore throat, or trouble swallowing, your doctor or dietitian may suggest you have foods and drinks that are easy to chew and swallow. Get ideas on what to eat from this list of easy-to-chew and easy-to-swallow foods and drinks.

Main meals

  • baby food
  • casseroles
  • chicken salad
  • cooked refined cereals, such as Cream of Wheat, Cream of Rice, instant oatmeal, and grits
  • cottage cheese
  • eggs (soft boiled or scrambled) 
  • egg salad 
  • macaroni and cheese 
  • mashed potatoes 
  • peanut butter (creamy) 
  • pureed, cooked foods 
  • soups 
  • stews 
  • tuna salad
  • custard

Desserts and snacks 

  • flan 
  • fruit
  • pureed fruits or baby food 
  • gelatin (Jell-O)
  • ice cream
  • milkshakes
  • puddings
  • sherbet
  • smoothies
  • soft fruits, such as bananas or applesauce
  • sorbet
  • yogurt (plain or vanilla) 

Protein shakes and supplements

  • instant breakfast drinks, such as Carnation Breakfast Essentials 
  • liquid protein supplements, such as Ensure or Boost 
  • clear nutrition supplements, such as Boost Breeze and Ensure Clear

Full-Liquid Foods and Drinks

Full-Liquid Foods and Drinks

If you have appetite loss, weight loss, or vomiting, your doctor or dietitian may suggest you follow a full-liquid diet. Use this list for ideas on what foods and drinks you can include in a full-liquid diet.

Refined, hot cereals

  • Cream of Wheat
  • Cream of Rice
  • instant oatmeal
  • grits

Soups

  • bouillon
  • broth (such as chicken, vegetable, or beef) 
  • soup that has been strained or put through a blender 

Drinks

  • carbonated drinks 
  • coffee 
  • fruit drinks 
  • fruit punch
  • milk 
  • milkshakes
  • smoothies 
  • sports drinks (such as Gatorade or Powerade)
  • tea 
  • tomato juice 
  • vegetable juice 
  • water

Desserts and snacks 

  • custard (soft or baked) 
  • frozen yogurt 
  • fruit purees that are watered down 
  • gelatin (Jell-O)
  • honey 
  • ice cream with no chunks, such as nuts or cookie pieces 
  • jelly 
  • pudding 
  • sherbet
  • sorbet 
  • syrup 
  • yogurt (plain or vanilla) 

Protein shakes and supplements 

  • instant breakfast drinks, such as Carnation Breakfast Essentials 
  • protein supplements, such as Ensure and Boost
  • clear nutrition supplements, such as Boost Breeze and Ensure Clear