For millions of patients undergoing aggressive medical therapies, the mere thought, smell, or visual perception of a treatment environment can trigger visceral physical suffering long before pharmacological agents enter the bloodstream. Anticipatory nausea stands as one of medicine’s most poignant illustrations of the deep, bidirectional integration between cognitive processing, affective expectation, and autonomic physiology.
Anticipatory Nausea
1. Concise Definition
Anticipatory nausea is a conditioned, psychophysiological response characterized by the subjective sensation of impending emesis that occurs prior to the administration of a noxious or emetogenic treatment, most commonly cytotoxic chemotherapy. It emerges not as a direct pharmacological side effect, but as a learned reflex triggered by environmental or cognitive stimuli previously paired with visceral distress.
In clinical oncology, anticipatory nausea reflects a profound manifestation of associative learning, typically appearing after a patient has experienced repeated episodes of post-treatment nausea or vomiting. Unlike acute or delayed chemotherapy-induced emesis, anticipatory nausea operates primarily through neural circuits involved in sensory processing, memory consolidation, and threat appraisal, bypassing primary gastrointestinal chemotransduction pathways during its onset.
Though most frequently documented in cancer care, the phenomenon highlights a broader neurobiological vulnerability wherein sensory cues become potent elicitors of complex autonomic, endocrine, and somatic symptoms. Understanding this state requires an interdisciplinary analysis spanning classical conditioning paradigms, visceral neuroscience, psychopharmacology, and cognitive-behavioral interventions.
2. Etymology & Linguistic Origin
The term anticipatory derives from the Latin verb anticipare, meaning “to take beforehand,” “to forestall,” or “to experience in advance,” constructed from the prefix ante- (“before”) and capere (“to take” or “to seize”). Historically used in philosophy and rhetoric to denote the act of addressing an objection or conceptualizing an outcome prior to its occurrence, its modern scientific sense refers to physiological and psychological preparations for anticipated future events.
The noun nausea traces directly back to the classical Latin nausea, an adaptation of the ancient Greek nausia (ναυσία) or nautia (ναυτία), which literally translated to “seasickness” or “ship-sickness,” rooted in naus (ναῦς), meaning “ship.” Over centuries of medical evolution, the word expanded beyond maritime motion sickness to delineate any generalized sensation of gastric discomfort, malaise, and the urge to vomit.
The compounding of these two terms into “anticipatory nausea” entered formal medical and psychological lexicons during the late 1970s and early 1980s. As modern oncology introduced highly emetogenic cytotoxic regimens such as high-dose cisplatin, researchers recognized that a substantial subset of patients developed severe prodromal nausea prior to subsequent infusions, prompting behavioral psychologists and oncologists to formally categorize the syndrome under the rubric of conditioned physiological responses.
3. Pronunciation & Grammatical Form
Pronunciation: /ænˌtɪs.ɪ.pəˈtɔːr.i ˈnɔː.zi.ə/ or /ænˌtɪs.ə.pə.tɔːr.i ˈnɔː.ʃə/
Grammatical Form: Compound noun phrase, uncountable. It functions primarily as the subject or object of clinical, psychological, and biological statements (e.g., “The patient exhibited severe anticipatory nausea prior to the fourth chemotherapy cycle”). The adjectival component (“anticipatory”) modifies the physiological symptom (“nausea”), distinguishing it categorically from acute, delayed, breakthrough, or refractory variants.
4. Detailed Conceptual Explanation
To fully grasp anticipatory nausea, one must differentiate its etiology from that of standard chemotherapy-induced nausea and vomiting (CINV). Standard acute nausea arises when cytotoxic agents directly trigger the release of neurotransmitters, such as serotonin (5-hydroxytryptamine, or 5-HT) and substance P, from enterochromaffin cells in the gastrointestinal mucosa. These substances stimulate vagal afferent fibers that terminate in the solitary tract and the area postrema—a circumventricular organ in the medulla oblongata lacking a tight blood-brain barrier, functionally recognized as the chemoreceptor trigger zone (CTZ).
In contrast, anticipatory nausea emerges through central neurobiological pathways independent of concurrent peripheral chemotransduction. Through associative mechanisms, environmental stimuli—such as the clinical smell of isopropyl alcohol, the hum of an infusion pump, the sight of a specific nurse, the fluorescent lighting of an oncology floor, or even the turn into the hospital parking lot—become linked with the visceral suffering endured during prior post-infusion states. When the individual re-encounters these contextual elements, the sensory input projects through the primary thalamic relays directly into the insular cortex, the anterior cingulate cortex, and the basolateral amygdala, reconstructing the visceral representation of nausea.
The boundaries of anticipatory nausea are governed strictly by chronology and conditioning history. It cannot occur prior to a patient’s initial exposure to emetogenic stimuli, as an unconditioned association must first be established. Furthermore, anticipatory symptoms typically present within the 24 hours preceding scheduled treatment, escalating in intensity as temporal and spatial proximity to the clinic increases. If gastrointestinal symptoms occur prior to treatment without prior emetogenic exposure, clinicians must look toward other biological etiologies, such as mechanical bowel obstruction, cerebral metastases, hypercalcemia, or pre-existing gastrointestinal illness.
The intensity and chronicity of anticipatory nausea vary widely among individuals, demonstrating clear interactions between physiological susceptibility and cognitive-affective traits. Individuals who metabolize antiemetics rapidly, those who experience intense acute or delayed post-chemotherapy emesis, and those with a strong propensity toward somatic amplification or baseline trait anxiety are markedly more vulnerable. Once established, this learned aversion displays resistance to conventional antiemetics, representing an intractable cycle of conditioned physiological arousal, interoceptive hypervigilance, and conditioned distress.
5. Historical Development
The formal investigation of anticipatory nausea closely tracks the introduction of potent chemotherapeutic agents in systemic oncology throughout the latter half of the twentieth century. Before the late 1960s, early chemotherapy regimens demonstrated limited anti-tumor potency and variable emetogenicity. However, the introduction of platinum-based agents—specifically cisplatin in the 1970s—fundamentally transformed oncology care. While cisplatin markedly improved cure rates for malignancies such as testicular cancer, it carried an emetogenic potential exceeding 90% in the absence of robust antiemetics.
During the late 1970s, clinicians began noticing a striking pattern: patients returning for subsequent courses of cisplatin or high-dose anthracyclines began retching and vomiting in waiting rooms, inside taxicabs en route to clinics, or immediately upon hearing their oncologist’s voice. Initial psychiatric models erroneously categorized this behavior as psychoneurotic hysteria, malingering, or a subconscious somatic defense mechanism against treatment. However, experimental psychologists recognized that these symptoms mirrored the foundational learning models pioneered decades earlier.
Seminal investigations conducted by researchers such as Gary Morrow, William Redd, and Paul Jacobsen in the late 1970s and 1980s reframed the phenomenon through the rigorous empirical framework of Pavlovian learning. By demonstrating that environmental cues served as conditioned stimuli capable of eliciting visceral changes, these investigators stripped the condition of its psychiatric stigma. Their studies showed that anticipatory nausea affected between 25% and 35% of all cancer patients undergoing moderately to highly emetogenic regimens during an era before advanced antiemetics.
The late 1980s and 1990s brought profound structural shifts to this landscape. The commercial development of first-generation 5-HT3 receptor antagonists (such as ondansetron and granisetron), followed in the early 2000s by neurokinin-1 (NK-1) receptor antagonists (such as aprepitant), drastically reduced the incidence of acute unconditioned emesis. Because the strength of conditioned learning correlates with the magnitude of the unconditioned response, modern antiemetic protocols drastically reduced the baseline incidence of anticipatory nausea. Nevertheless, recent clinical epidemiologic surveys confirm that anticipatory nausea remains a persistent, disabling issue for approximately 10% to 15% of oncology patients, surviving despite advanced pharmacological prophylaxis and cementing its place as a distinct neuropsychological challenge.
6. Theoretical Foundations
The predominant theoretical architecture explaining anticipatory nausea is Pavlovian classical conditioning. Within this paradigm, the cytotoxic chemotherapy agent operates as the unconditioned stimulus (UCS). The physiological cascade of nausea, autonomic activation, and emesis triggered by the direct chemical stimulation of the gastrointestinal tract and chemoreceptor trigger zone constitutes the unconditioned response (UCR).
During treatment, neutral environmental, sensory, and temporal markers present within the therapeutic milieu act as conditioned stimuli (CS). These markers include visual inputs (hospital architecture, the color of chemotherapy bags, clinical attire), olfactory cues (the distinct odors of surface disinfectants, medical tape, hand sanitizer), auditory stimuli (the chiming of intravenous pumps, elevator bells), and internal temporal states (waking up on the morning of an infusion). Through repetitive pairings (CS-UCS temporal contiguity), the previously neutral cues acquire the capacity to evoke the gastrointestinal sensations and subjective distress of nausea as a conditioned response (CR), even in the complete absence of the cytotoxic drug.
Complementing Pavlovian mechanics is the evolutionary model of taste aversion learning, often termed the Garcia Effect or the sauce béarnaise effect, identified by John Garcia in the 1950s and 1960s. Garcia demonstrated that unlike arbitrary sensory-motor conditioning, which typically requires dozens of temporal pairings and precise millisecond intervals, organisms possess biologically prepared evolutionary hardware that links gustatory and visceral stimuli over hours-long delays. This specialized mechanism evolved to prevent toxic ingestion by establishing rapid, powerful, and persistent conditioned aversions following a single toxic episode. Anticipatory nausea in modern clinical settings can be viewed as an evolutionary misapplication of this preparedness: the human nervous system interprets systemic chemotherapy as systemic poisoning, thereby permanently tagging all surrounding environmental cues as toxic hazards.
Cognitive and interoceptive models offer a further layer of theoretical depth. According to cognitive appraisal theories, the development and maintenance of anticipatory nausea are heavily moderated by catastrophic thinking, expectancy theory, and interoceptive sensitivity. Expectancy theory posited by Irving Kirsch highlights that subjective physiological responses are actively shaped by the explicit expectation of those responses. When a patient hyper-focuses on the potential for nausea, ambiguous gastrointestinal signals (such as normal gastric motility or slight anxiety-induced visceral contractions) are cognitively appraised and amplified as the onset of emesis. This attentional capture initiates an escalating biobehavioral feedback loop: negative expectation promotes autonomic sympathetic activation and parasympathetic withdrawal, dysregulating the gastric slow-wave rhythm (gastric dysrhythmia or tachygastria) and producing true, subjectively debilitating nausea.
7. Key Components, Types & Dimensions
Anticipatory nausea is a multidimensional construct comprising sensory, cognitive, autonomic, and behavioral components. It can be characterized along several key axes:
- Sensory-Triggered Variant: Evoked directly and immediately by discrete external stimuli that were present during previous unconditioned episodes (e.g., catching the scent of the disinfectant used on the port-a-cath site or seeing the oncology clinic sign).
- Temporal/Cognitive Variant: Develops autonomously without direct sensory exposure, driven by internal timekeeping and prospective cognitive anticipation (e.g., an individual beginning to experience severe nausea at home the evening before an appointment).
- Autonomic Profile: Accompanied by objective physical dysregulation, including cutaneous pallor, cold diaphoresis, pupillary dilation, salivary alterations (either hypersalivation or xerostomia), tachycardia, and electrogastrographic dysrhythmia (gastric tachygastria).
- Affective and Cognitive Dimension: Marked by catastrophic rumination, feeling helpless, interoceptive hypervigilance, and intense situational anxiety that mirrors panic spectrum symptomatology.
- Behavioral Dimension: Characterized by active avoidance behaviors, such as procrastinating before clinic appointments, missed infusions, treatment non-adherence, or outright refusal of potentially curative medical therapies.
8. Examples & Illustrative Cases
Case Illustration 1: Pure Sensory Conditioning
A 48-year-old female receiving adjuvant chemotherapy for early-stage breast cancer experienced severe, poorly controlled acute and delayed nausea during her first two cycles of doxorubicin and cyclophosphamide. Prior to her third cycle, she drove toward the comprehensive cancer center. While stopping at an intersection approximately two miles away, she spotted the architectural outline of the hospital’s outpatient pavilion. Within seconds, she experienced severe epigastric churning, cold sweats, and overwhelming nausea, forcing her to pull her vehicle over. Laboratory values and clinical assessments revealed no metabolic abnormalities; the visual silhouette of the facility acted as a robust conditioned stimulus eliciting a physiological conditioned response.
Case Illustration 2: Olfactory and Temporal Association
A 62-year-old male with non-Hodgkin lymphoma underwent inpatient infusions of a multi-agent regimen. During his inpatient stays, a distinct brand of pine-scented floor cleanser was routinely applied in the corridors. Three months following the completion of his entire chemotherapy protocol, he visited a local hardware store where a spill of identical pine cleanser occurred in an adjacent aisle. Upon inhaling the fragrance, the patient immediately developed profound nausea, dry-heaving, and intense autonomic panic. This illustrates the robust longevity of biological preparedness and conditioned aversions, which can persist for months or years in the absence of therapeutic extinction.
9. Measurement & Assessment
Assessing anticipatory nausea requires isolating it temporally and phenomenologically from post-treatment CINV, anxiety disorders, and unrelated gastrointestinal pathology. Standardized psychometric and clinical tools are employed to evaluate its incidence, frequency, and severity:
- Morrow Assessment of Nausea and Emesis (MANE): Developed by Gary Morrow, this is one of the most widely validated and utilized instruments in behavioral oncology. The MANE systematically tracks the timing, duration, and intensity of nausea and emesis across three distinct phases: before treatment (anticipatory), within 24 hours of treatment (acute), and from 24 hours to 7 days post-treatment (delayed). It employs Likert-type scales to assess physical severity and psychological distress.
- Functional Living Index – Emesis (FLIE): A validated, disease-specific, patient-reported outcome instrument designed to assess the functional impact of nausea and vomiting on daily life. Although frequently applied to acute and delayed phases, its subscales offer valuable insight into how anticipatory symptoms impair social, physical, and emotional functioning.
- Visual Analogue Scales (VAS) and Numerical Rating Scales (NRS): Single-item dimensional measures, ranging from 0 (“no nausea at all”) to 10 or 100 (“nausea as bad as it could possibly be”). Patients rate their symptoms immediately prior to chemotherapy administration, providing an immediate snapshot of anticipatory symptom severity.
- Electrogastrography (EGG): An objective physiological research tool using cutaneous electrodes placed across the epigastrium to track the electrical slow-wave activity of the stomach. While a normal gastric pacemaker operates at approximately 3 cycles per minute (normogastria), the emergence of anticipatory nausea frequently correlates with an abrupt shift to 4–9 cycles per minute (tachygastria), providing an empirical physiological biomarker of visceral dysregulation.
10. Applications & Practical Significance
Anticipatory nausea is clinically significant because it challenges traditional pharmacotherapy. Because standard antiemetic agents—such as 5-HT3 receptor antagonists, corticosteroids (e.g., dexamethasone), and NK-1 antagonists—primarily act on peripheral visceral afferents and brainstem chemoreceptor zones, they show minimal efficacy in treating anticipatory nausea once it has been established. Treating it effectively requires psychological, behavioral, and integrated neurobiological strategies.
The primary clinical priority is primary prevention through aggressive early antiemetic management. By completely suppressing acute and delayed nausea during cycle one of chemotherapy, clinicians remove the unconditioned stimulus-response pairing, preventing the associative bridge from forming in the first place.
When anticipatory nausea does emerge, non-pharmacological behavioral therapies serve as the primary line of treatment:
- Systematic Desensitization: Developed within behavioral psychology, systematic desensitization involves constructing a graded hierarchy of anxiety- and nausea-provoking cues (e.g., thinking about the clinic, packing a bag, entering the parking garage, sitting in the waiting area, entering the infusion room). The patient is trained in deep somatic relaxation techniques, progressively pairing relaxed physiological states with increasingly vivid visualizations of these triggers to extinguish the conditioned visceral response.
- Progressive Muscle Relaxation (PMR) with Guided Imagery: Initiated prior to and during the infusion, PMR directly interrupts the sympathetic autonomic surge and vagal dysregulation that exacerbate gastric dysrhythmia, actively altering the interoceptive feedback sent to the insular cortex.
- Hypnosis and Cognitive Reframing: Clinical hypnosis uses intense, focused attention and guided suggestions to alter interoceptive sensory perceptions. Meta-analyses demonstrate that clinical hypnosis significantly mitigates both the severity and frequency of anticipatory nausea, especially in pediatric and adolescent oncology populations.
- Virtual Reality (VR) Distraction: Immersive VR technology acts as an attentional interruptor during clinical intake and pre-infusion preparations. By saturating the patient’s sensory processing channels with rich visual and auditory landscapes, VR prevents environmental cues from accessing the associative neural circuits that trigger conditioned nausea.
- Acupuncture and Acupressure: Targeted mechanical or electrical stimulation of the PC6 (Neiguan) pericardium meridian point on the anterior forearm has been shown to modulate autonomic tone and suppress centrally mediated visceral discomfort, functioning as a non-invasive adjunct to behavioral interventions.
11. Research & Empirical Evidence
Early empirical breakthroughs were spearheaded by Gary R. Morrow and colleagues throughout the 1980s. Morrow demonstrated in multi-center clinical trials that standard pharmacological interventions (such as prochlorperazine or high-dose metoclopramide) failed to suppress conditioned anticipatory symptoms, whereas behavioral interventions employing systematic desensitization and relaxation training produced statistically and clinically significant reductions in symptom incidence and intensity.
William H. Redd and his team at Memorial Sloan Kettering Cancer Center explored cognitive and behavioral interventions, particularly in pediatric oncology. In an influential series of clinical investigations, Redd et al. proved that video game-based distraction and guided hypnosis systematically attenuated pre-chemotherapy nausea in children and young adults, demonstrating that cognitive resource competition could block conditioned sensory retrieval.
In the modern era of antiemetics, clinical trials orchestrated by cooperative groups such as the Multinational Association of Supportive Care in Cancer (MASCC) and the American Society of Clinical Oncology (ASCO) have clarified the epidemiology of anticipatory nausea. Landmark trials evaluating neurokinin-1 receptor antagonists (such as aprepitant, fosaprepitant, and rolapitant) indicated that regimens combining an NK-1 antagonist, a 5-HT3 antagonist, and dexamethasone dramatically reduced anticipatory nausea in later cycles primarily by eliminating acute and delayed unconditioned emetic episodes in the first cycle. Additional neuroimaging studies using functional Magnetic Resonance Imaging (fMRI) have shed light on the neurobiology, showing that conditioned nausea cues selectively light up the anterior insula, the dorsal anterior cingulate cortex, and the amygdala, confirming that the condition is driven by interoceptive and affective circuits rather than simple brainstem reflexes.
12. Cultural & Cross-Cultural Considerations
While the underlying neurobiology of classical conditioning is universal across human populations, the expression, reporting, and psychological modulation of anticipatory nausea are influenced by cultural contexts. Cross-cultural research shows that symptom reporting patterns often reflect distinct cultural norms regarding emotional restraint, somatic amplification, and the clinical expression of suffering.
In many Western cultural settings, patients are encouraged to express emotional and physical distress directly, which may lead to higher self-reported rates of anticipatory nausea on standardized inventories. Conversely, in cultures that prioritize emotional stoicism or view illness through fatalistic frameworks, patients may underreport subjective nausea, presenting instead with generalized somatic complaints like headaches, dizziness, or profound fatigue prior to medical treatments.
Furthermore, cultural context affects how hospital environments and sensory cues are experienced. Olfactory associations, dietary staples, and architectural layouts vary globally; for example, the scents and visual motifs of traditional healing facilities versus Western-style oncology clinics create different conditioning triggers. Cultural attitudes toward non-pharmacological therapies also influence treatment success: populations with traditional familiarity with mind-body practices, such as acupuncture, meditation, and rhythmic breathwork, frequently demonstrate higher adoption of and response rates to behavioral therapies for anticipatory nausea.
13. Criticisms, Debates & Limitations
Despite strong empirical consensus, anticipatory nausea research has seen persistent debate regarding theoretical models, categorization, and best therapeutic approaches. One long-standing debate centers on whether anticipatory nausea is purely a conditioned Pavlovian reflex or whether it is primarily driven by state anxiety and catastrophic thinking.
Proponents of the strict classical conditioning model argue that anticipatory nausea can develop in patients with low baseline trait anxiety, triggered entirely by sensory exposure and biological taste-aversion preparedness. Conversely, cognitive theorists argue that anxiety and expectancy are essential mediators, demonstrating that patients with high anticipatory anxiety develop the condition at significantly higher rates, and that managing anxiety alone can eliminate symptoms. This tension complicates clinical assessment: is the practitioner treating an autonomic reflex or an acute anxiety response presenting with visceral symptoms?
Another issue concerns the pharmacological management of established anticipatory nausea. When behavioral interventions prove insufficient, clinicians often prescribe benzodiazepines (such as lorazepam or alprazolam). While benzodiazepines can reduce anticipatory distress through anxiolysis, sedation, and short-term anterograde amnesia, critics highlight substantial limitations: they do not target the underlying conditioning, carry risks of cognitive impairment, dependency, and paradoxical agitation, and can occasionally disrupt the cognitive engagement required for behavioral therapies like systematic desensitization.
Finally, there is an ongoing debate regarding the diagnostic classification of anticipatory nausea in psychiatric nosologies. While some argue that severe, intractable cases meet criteria for a Specific Phobia (Medical/Blood-Injection-Injury Type) or an Adjustment Disorder under the DSM-5, others maintain that medicalizing this learned visceral response risks pathologizing a natural evolutionary survival mechanism triggered by toxic oncology treatments.
14. Related Terms & Distinctions
To avoid diagnostic confusion, anticipatory nausea must be distinguished from related clinical phenomena:
- Acute Chemotherapy-Induced Nausea and Vomiting (CINV): Visceral nausea and emesis occurring within the first 0 to 24 hours following drug infusion, driven primarily by serotonin (5-HT3) release from enterochromaffin cells stimulating vagal afferents and the area postrema. In contrast, anticipatory nausea occurs prior to drug administration.
- Delayed CINV: Nausea and emesis presenting more than 24 hours post-infusion (peaking between 48 and 72 hours), primarily mediated by substance P signaling at neurokinin-1 (NK-1) receptors in the central and peripheral nervous systems.
- Anticipatory Vomiting (AV): The physical act of emetic expulsion occurring prior to treatment. While anticipatory nausea and anticipatory vomiting share an identical conditioning etiology, anticipatory vomiting represents a rarer, more severe motor manifestation that is coordinated by the medullary vomiting center.
- Anticipatory Anxiety: A state of cognitive apprehension, physiological hyperarousal, and dread regarding an upcoming event. While anticipatory anxiety frequently co-occurs with and exacerbates anticipatory nausea, it lacks the specific epigastric, gastrointestinal, and emetic sensations that define nausea.
- Vasovagal Syncope: A neurocardiogenic reflex characterized by an abrupt drop in heart rate and blood pressure leading to loss of consciousness, often triggered by blood, needles, or medical trauma. While vasovagal reactions can involve prodromal nausea, diaphoresis, and pallor, their cardinal endpoint is cerebral hypoperfusion and fainting, distinct from conditioned nausea.
15. Summary & Key Takeaways
Anticipatory nausea is an acquired, conditioned psychophysiological state in which patients experience the sensation of pending emesis prior to receiving a noxious medical treatment, most commonly cytotoxic cancer chemotherapy. Rooted in Pavlovian conditioning and evolutionary food aversion learning, the condition develops when previously neutral environmental sights, sounds, smells, or temporal intervals become paired with the severe gastrointestinal distress triggered by toxic therapeutic agents.
The condition highlights the profound clinical importance of the mind-body connection, demonstrating how higher-order cognitive processing and sensory inputs directly dysregulate peripheral autonomic and gastric function. Standard antiemetics show limited success once anticipatory nausea is established; optimal management requires primary prevention through aggressive antiemetic prophylaxis during the very first treatment cycle, complemented by behavioral interventions such as systematic desensitization, clinical hypnosis, progressive muscle relaxation, and virtual reality distraction.
By reframing anticipatory nausea not as a psychiatric weakness but as a learned biological response, interdisciplinary clinicians can address this visceral distress with targeted behavioral and neurobiological care, protecting both treatment adherence and overall quality of life.
References
- Morrow, G. R., & Roscoe, J. A. (1997). Anticipatory nausea and vomiting: Models and mechanisms. Oncology, 11(11A), 14–18.
- Redd, W. H., Montgomery, G. H., & DuHamel, K. N. (2001). Behavioral intervention for cancer treatment side effects. Journal of the National Cancer Institute, 93(11), 810–823. https://doi.org/10.1093/jnci/93.11.810
- Hesketh, P. J. (2008). Chemotherapy-induced nausea and vomiting. New England Journal of Medicine, 358(23), 2482–2494. https://doi.org/10.1056/NEJMra0706547
- Jacobsen, P. B., Bovbjerg, D. H., Schwartz, M. D., Andrykowski, M. A., Furlong, M. A., Marks, P. B., & Redd, W. H. (1993). Conditioned emotional distress in cancer patients: A relation to anticipatory nausea. Journal of Consulting and Clinical Psychology, 61(1), 131–139. https://doi.org/10.1037/0022-006X.61.1.131
- Roscoe, J. A., Morrow, G. R., Aapro, M. S., Molassiotis, A., & Olver, I. (2011). Anticipatory nausea and vomiting. Supportive Care in Cancer, 19(10), 1533–1538. https://doi.org/10.1007/s00520-010-0980-0