Neural reactivity to a racial trauma cue in an African American woman with alcohol use disorder and PTSD: Case report

Abstract

Alcohol use disorder (AUD) and posttraumatic stress disorder (PTSD) are common co-occurring diagnoses that disproportionately affect racial minorities and women. Black/African American women are more likely to experience racial trauma, which compounds AUD+PTSD comorbidity. Limited research has investigated the effect of racial trauma on AUD+PTSD using functional magnetic resonance imaging (fMRI). We used a novel script-driven imagery procedure during MRI for racial trauma in a 26-year-old, self-identifying Black woman enrolled in a 12-week randomized clinical trial for individuals with AUD+PTSD. During a baseline fMRI scan, the participant listened to personalized audio scripts of an index traumatic event cue (i.e., “PTSD cue”), an alcohol-related cue, a racial trauma cue, and a neutral cue. This case report describes comparisons of brain reactivity between the racial trauma and PTSD cue, and the racial trauma and alcohol cue. In this Black woman with AUD+PTSD, the racial trauma cue elicited unique activation patterns in sensorimotor and interoceptive brain regions. These patterns partially overlapped with but were distinct from activations observed during PTSD and alcohol cues. Racial trauma showed greater activation than the PTSD cue in self-referential (e.g. posterior cingulate cortex) and sensorimotor regions, and broader activation than the alcohol cue across temporal, occipital, and frontal regions. These findings suggest racial trauma may engage unique neural pathways related to emotional pain, self-referential processing, and hypervigilance. While preliminary, this case study offers insights into the neurobiological signature of racial trauma and underscores the need to include culturally specific stressors in trauma and addiction research.

1. Introduction

Alcohol use disorder (AUD) and posttraumatic stress disorder (PTSD) are commonly co-occurring psychiatric disorders. Data from Wave 3 of the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) showed that individuals with PTSD were 1.2 times more likely to meet criteria for AUD after controlling for other psychiatric diagnoses (Smith and Cottler, 2018). Additionally, in clinical populations, 30–50% of adults with AUD also meet criteria for PTSD, and lifetime rates of AUD among adults with PTSD can be as high as 75% in treatment-seeking populations (Petrakis and Simpson, 2017, Ralevski et al., 2014). In comparison to either disorder alone, individuals with AUD+PTSD show a more severe clinical presentation, marked by higher rates of suicide attempts and poorer treatment outcomes (Smith and Cottler, 2018). Within the AUD+PTSD comorbidity, individuals with historically marginalized social identities face additional health disparities likely stemming from inequities in society. For instance, compared to men, women show higher rates of, and more severe comorbid PTSD+AUD; experience more severe lifetime traumas (e.g., sexual assault, rape); show a two-fold greater risk to develop PTSD; and show greater functional impairment when AUD and PTSD co-occur (Smith and Cottler, 2018, Gradus et al., 2017, McHugh et al., 2018, McLean et al., 2011, Torchalla et al., 2014, Saraiya et al., 2023). In addition, relative to their white counterparts, Black individuals show higher rates of trauma exposure, PTSD, AUD, and co-occurring AUD+PTSD (Alegría et al., 2013, Alim et al., 2006, Alim et al., 2006, Brown et al., 2020, Gillespie et al., 2009, Lee and Chen, 2017, Mersky et al., 2013, Smith et al., 2006), and more severe symptomology (McClendon et al., 2020). Black individuals also experience more severe health and social consequences related to alcohol use (e.g., cirrhosis, hypertension, interpersonal violence, financial problems, work and legal issues) than white individuals, and they report more symptoms of alcohol dependence, even though they tend to consume alcohol at lower rates (McClendon et al., 2020, Zapolski et al., 2014, Zemore et al., 2018).

A substantial body of research on health disparities has shown that Black women are at heightened risk for developing severe presentations of AUD+PTSD. Mulia et al. (Mulia et al., 2009) found that compared to white individuals, Black individuals who reported low to moderate levels of heavy drinking—measured by a composite score of the frequency of drinking five or more drinks in a given day, days of drunkenness, and the maximum amount of standard equivalent drinks—were more likely to have negative social consequences and health problems. Another study showed the risk for alcohol dependence is greater at any level of heavy drinking for Black women compared to white women; however, more research is needed to understand this disparity (Witbrodt et al., 2014). Similarly, in the PTSD literature, research has shown that among N = 7,430 Black women, 91% reported trauma exposure and 32.3% met criteria for a probable PTSD diagnosis (Gluck et al., 2021), a rate three times greater than the national prevalence rate of PTSD (10.4%) among women (Kessler et al., 1995). Furthermore, when it comes to trauma exposure and alcohol use, data from the 2010 Behavioral Risk Factor Surveillance System (N = 60,598) showed that non-Hispanic Black women with adverse childhood experiences (ACEs) were three times more likely to drink heavily (e.g., > 1 drink for women in one drinking occasion) than individuals with no ACEs (Lee and Chen, 2017).

Although race has been examined in AUD and PTSD, less work has focused on how racism as a structure operates within the individual and thereby influences the development and presentation of AUD+PTSD (Komaromy et al., 2021). Racial trauma—the cumulative effect of traumatizing racism on racial minorities (e.g. racial discrimination, systemic racism, historical trauma, intergenerational trauma, cultural trauma, and community trauma)—has been shown to produce stress reactions similar to, but not typically labeled as, post-traumatic stress disorder (Carter et al., 2020, Sibrava et al., 2019). Extant literature has shown that some Black individuals who experience racial trauma exhibit PTSD symptoms and that chronic exposure to racial trauma contributes to PTSD vulnerability among Black individuals (Bird et al., 2021, Dale and Safren, 2019, Mekawi et al., 2021). Recent neuroimaging studies further distinguish neural responses associated with racial trauma from typical PTSD neural signatures. For example, Fani et al. (Fani et al., 2022) identified unique structural brain alterations in individuals exposed to racial discrimination, including reduced cortical thickness in regions important for emotional regulation and threat appraisal (e.g., rostral anterior cingulate cortex, posterior cingulate cortex). Webb et al. (Webb et al., 2022) similarly found altered resting-state connectivity patterns specifically linked to racial discrimination, involving heightened connectivity within salience network regions (e.g., amygdala, insula, and thalamus). Expanding on these findings, Webb et al. (Webb et al., 2024) later demonstrated differential impacts of personally mediated and structural racism on neural circuits underlying threat detection and social processing. Specifically, personally mediated racism elicited heightened neural vigilance and reactivity, reflected in greater activation of the amygdala, anterior insula, and doral anterior cingulate cortex, whereas structural racism was associated with blunted emotional and physiological threat responses, evidenced by reduced ventromedial prefrontal cortex activation—potentially reflecting adaptive responses to chronic racial stress. Fani et al. (Fani et al., 2021) examined neural reactivity to trauma-related versus neutral imagery among Black/African American females, finding that greater racial discrimination was associated with increased activation in brain networks related to emotion regulation and fear inhibition (ventromedial prefrontal cortex) and visual attention (middle occipital cortex), even after controlling for trauma exposure and PTSD symptoms. The authors suggest these findings reflect participants’ increased hypervigilance toward threats as well as active inhibition of the threat response, ultimately depleting cognitive resources and increasing risk for negative health outcomes (e.g. substance use disorders).

Experiences of racial trauma have also been linked to steeper increases in alcohol consumption, binge drinking, negative drinking consequences, greater risk for developing AUD, and more alcohol-related problems despite equivalent alcohol consumption (Desalu et al., 2019, Marks et al., 2021). Glass et al. (Glass et al., 2020) found that racially-minoritized adults (34.9% Black) who experienced racial discrimination (i.e., racial trauma) had greater risk for mild (1.5×), moderate (1.6×) and severe (2.3×) AUD, highlighting strong associations between racial trauma and risk of AUD among Black individuals. In parallel, meta-analytic and task-based neuroimaging studies in individuals with AUD have consistently implicated the ventral striatum, amygdala, anterior insula, and dorsal anterior cingulate cortex (dACC) in response to alcohol cues, with activation in these regions predictive of craving intensity and relapse risk (Schacht et al., 2013, Courtney et al., 2016) Notably, Webb et al. (Webb et al., 2022) found that racial discrimination was associated with heightened connectivity in the same salience network regions—including the amygdala, anterior insula, and dACC—during resting state fMRI. These overlapping patterns suggest possible neurobiological convergence in the brain’s response to racial trauma and alcohol-related stimuli, highlighting the salience network as a potential transdiagnostic mechanism linking chronic racial stress to substance use vulnerability. However, the research directly linking racial discrimination, trauma-related neural circuitry, and alcohol cue reactivity remains limited. This area of inquiry is still in its early stages, and further investigation is needed to fully understand the intricate relationships among racial discrimination, neural mechanisms, and alcohol use behavior.

Despite disparities in AUD+PTSD, race, and gender have been largely conceptualized as singular demographic factors with less attention paid to (1) adopting an intersectional framework that examines identities synergistically and (2) exploring how experiences of racism (i.e., racial discrimination) are associated with comorbid AUD and PTSD. For minoritized individuals with AUD+PTSD, there is little research that examines the impact of racism in the etiology and treatment for this comorbid condition. Functional magnetic resonance imaging (fMRI) is one methodology, consistent with the Research Doman Criteria (RDoC) Initiative, that allows researchers to focus their investigations on physiological and behavioral elements of mental illnesses so as to “… [contribute] to a more precise understanding of—and thus better assessment, treatment, and prevention of—mental disorders (Developing and RDoC study 2025).” While research has used fMRI technology to examine AUD and PTSD, little research has leveraged fMRI to examine the impact of racial trauma (Fani et al., 2022, Webb et al., 2022, Fani et al., 2021, Fani et al., 2022, Harnett et al., 2023) using script-driven imagery of racially traumatic events. Given recent findings that suggest distinct neurobiological mechanisms of racial trauma, this novel paradigm (i.e., script-driven imagery) may provide new information on the neural similarities and differences of how individuals respond to racial trauma versus PTSD and AUD cues. This proof-of-concept case study uses an intersectional lens and translational (i.e., fMRI) approach to examine brain reactivity to a novel script-driven imagery procedure for racial trauma in a Black woman starting treatment for AUD+PTSD.

1.1. Current case

The patient was a 26-year-old Black/African American woman who, at the time of treatment, resided in the southeastern United States in a sober living community with three roommates. The patient identified as a mother and had shared custody of her 6-year-old son with his father. During her initial therapy sessions, the patient reported that she was distant from her family members, but that her sponsor from Alcoholics Anonymous and her son’s father were major sources of social support. At baseline, the participant reported a frequency of drinking alcohol and using e-cigarettes. Her self-identified index trauma was sexual assault from a family friend who molested her when she was 16 years old. The patient reported two additional sexual assaults, which occurred after the age of 16; she reported that she was raped by multiple individuals while intoxicated and reported being raped by a former boyfriend. She also reported directly experiencing three race-related stressors, categorized as events that involved physical confrontation or violence.

2. Methods

This current case study reports on one participant enrolled in a larger, double-blind, 12-week randomized controlled trial (RCT) evaluating the efficacy of N-acetylcysteine (NAC) in reducing alcohol use and PTSD symptoms among individuals with AUD+PTSD. Eligible participants were: 18–65 years old, fluent in English, and met DSM-5 criteria for AUD+PTSD. Participants were randomized to receive NAC or placebo, and regardless of treatment condition, received 12 weeks of relapse prevention therapy for AUD (Caroll, 1997). Participants were also given the opportunity to undergo fMRI where personalized imagery scripts were developed at baseline prior to medication initiation and at week 12 before medication discontinuation (only baseline data presented here). All study procedures were approved by the affiliated IRB; the study was conducted in the southeastern United States. Additional details about the RCT can be found in <masked for review>

Stimuli and design for fMRI measurement:

We developed personalized imagery script cues for the participant based on validated procedures (Sinha and Tuit, 2012). Specifically, the scripts were developed following the Sinha & Tuit Imagery Script Development Procedure Manual (Sinha and Tuit, 2012, Sinha, 2009), which provides structured guidance on eliciting detailed, emotionally evocative narratives across trauma, substance, and neutral conditions. For the racial trauma script, race-related stressors were defined as personally experienced events of race-based discrimination, exclusion, harassment, or marginalization that elicited distress (e.g., anxiety, anger, sadness, hopelessness). These were identified through participant interviews and incorporated into a first-person narrative format designed to maximize emotional and physiological engagement. To assist us in developing scripts, the participant provided: 1) a detailed narrative of her Criterion A index trauma (i.e., “PTSD cue”); 2) a situation wherein she wanted to have an alcoholic drink and went ahead and had one (i.e., “alcohol cue”); 3) a race-related stressor, namely a racially motivated situation she experienced that made her feel upset and that still causes distress (e.g., anxiety, irritability/anger, sadness/depression, hopelessness) (i.e., “racial trauma cue”); and 4) a situation she found relaxing (i.e., “neutral cue”). These scripts were read aloud and audio recorded by a member of the study team.

During the baseline scan, the participant listened to audio recordings of her personalized scripts in the scanner. Cues for the scripts were two minutes long each and presented in a block design (i.e., neutral, alcohol, neutral, trauma, neutral, racial trauma). Scanning was conducted in a Siemens 3 Tesla Prisma MRI scanner (Siemens Medical, Erlangen, Germany). T2*-weighted gradient-echo planar images (EPI) were acquired with the following parameters: TR = 1100 ms, TE = 30 ms, flip angle = 65°, ipat factor = 3, matrix 64 × 64, field of view = 19.2 cm, slice thickness = 3.0 mm with no gap, with 51 slices to cover the entire brain.

fMRI analyses:

We performed post-acquisition preprocessing and analysis of the fMRI data from each scan using FSL’s (FMRIB’s Software Library) FEAT (FMRI Expert Analysis Tool), Version 6.00. Preprocessing consisted of skull stripping using the Brain Extraction Tool (BET), high-pass temporal filtering (cutoff=440s), MCFLIRT motion correction, and spatial smoothing (Gaussian kernel of FWHM 6 mm

Images were transformed to standard space (Montreal Neurological Institute; MNI) to aid interpretation. Mean blood oxygen level dependent (BOLD) time series was examined in a whole-brain analysis using a general linear model framework. Onsets and durations of each block (i.e., imagery script) were included in the model as explanatory variables.

For this report, we examined activation by racial trauma, PTSD cue, and alcohol cue as well as racial trauma > PTSD cue and racial trauma > alcohol cue. A statistical map for each contrast of interest was generated for the participant, which was cluster thresholded at z =5.3 with p< .01. Due to the high cluster threshold cut-off, there were numerous clusters with fewer than 10 voxels for some contrasts. Therefore, only regions associated with a cluster size (in voxels) greater than or equal to 10, and local maxima within clusters are reported in Table 2. To fully present activation patterns, however, the activation maps presented in the Fig.s are based on the statistical activation maps (z > 5.3, p < .01). This allows visualization of the full spatial extent of suprathreshold activation.

Table 2.

Baseline fMRI Scan Areas of Activation.

Cue type and Brain region	Cluster Size (in voxels)	Z-statistic	p-value	MNI Standard Space Coordinates			Brodmann Area
				X	Y	Z
Racial Trauma Cue
Left precentral gyrus	29	7.46	<0.001	−53.40	−2.28	25.40	6
Cerebellum/Posterior cingulate	14	6.19	<0.001	1.06	−47.0	0.62	0
Left precentral gyrus	11	6.35	<0.001	−43.80	−7.37	56.20	6
Right precentral gyrus	10	6.21	<0.001	59.40	−2.12	17.60	48
Right precentral gyrus	10	6.47	<0.001	47.80	−3.85	56.40	6
PTSD Trauma Cue
Left Heschl’s gyrus	665	12.10	<0.001	−50.70	−21.80	6.92	48
Right planum temporale	304	11.30	<0.001	62.30	−24.30	13.00	22
Left inferior frontal gyrus	26	7.52	<0.001	−47.30	13.30	22.30	48
Left middle frontal gyrus	23	7.54	<0.001	−40.80	1.94	53.00	6
Left frontal orbital cortex	16	6.54	<0.001	−41.70	27.90	−8.70	47
Alcohol Cue
Left Heschl’s gyrus	1758	13.30	<0.001	−50.70	−21.80	6.92	48
Right frontal pole	789	12.60	<0.001	34.90	78.80	1.13	11
Right posterior supramarginal gyrus	303	9.01	<0.001	71.50	−43.00	15.30	22
Right cerebral white matter	223	10.60	<0.001	31.70	−40.30	6.46	0
Cerebellum	137	7.45	<0.001	−17.70	−41.90	−30.20	0
Brain stem	131	10.00	<0.001	3.71	−10.40	−29.60	0
Cerebellum	83	8.05	<0.001	24.70	−67.30	−43.40	0
Left cerebral white matter	42	8.61	<0.001	−29.50	−75.20	3.75	19
Right inferior lateral occipital cortex	34	7.47	<0.001	40.50	−84.70	−6.32	19
Right precentral gyrus	28	8.34	<0.001	56.50	−1.86	24.70	43
Cerebellum	27	8.50	<0.001	−27.20	−89.60	−45.90	0
Right precuneus cortex	26	7.45	<0.001	14.00	−54.50	48.40	5
Cerebellum	25	8.13	<0.001	36.90	−55.00	−50.30	0
Left insular cortex	25	6.30	<0.001	−38.60	9.16	−6.15	44
Left temporal pole	24	9.40	<0.001	−60.40	17.50	−32.90	38
Left precentral gyrus	18	7.54	<0.001	−38.10	4.18	28.60	48
Right putamen	17	8.17	<0.001	13.20	6.15	−8.25	25
Right insular cortex	17	7.64	<0.001	34.70	0.31	1.16	48
Right cerebral white matter	17	7.47	<0.001	1.25	3.50	6.06	0
Occipital pole	16	8.50	<0.001	−5.44	−101.00	−15.80	18
Left cerebral white matter	13	8.03	<0.001	−1.75	19.20	6.87	0
Left frontal operculum cortex	12	7.01	<0.001	−29.10	25.60	11.70	48
Cerebellum	11	7.22	<0.001	61.70	−69.50	−20.40	0
Right inferior frontal gyrus	11	6.32	<0.001	40.90	28.60	2.18	47
Left frontal pole	10	8.37	<0.001	−37.90	54.60	34.30	46
Cerebellum	10	6.73	<0.001	−18.00	−76.90	−42.20	0
Right middle frontal gyrus	10	8.26	<0.001	62.80	26.70	32.70	45
Right frontal pole	10	10.90	<0.001	32.50	49.20	48.80	9
Racial Trauma Cue > PTSD Trauma Cue
Posterior cingulate gyrus	42	7.66	<0.001	1.65	−26.80	36.20	23
Left precentral gyrus	16	6.12	<0.001	−53.30	−5.17	32.20	4
Left posterior cingulate / precuneus	13	6.20	<0.001	−13.50	−29.70	43.60	0
Racial Trauma Cue > Alcohol Cue
Left postcentral gyrus	353	9.70	<0.001	−46.80	−29.30	58.90	3
Left superior lateral occipital cortex	313	9.96	<0.001	23.30	−66.60	61.50	7
Right postcentral gyrus	248	10.20	<0.001	38.70	−38.10	65.70	3
Posterior cingulate gyrus	62	7.89	<0.001	1.59	−26.90	32.70	23
Right postcentral gyrus	52	7.54	<0.001	53.90	−13.30	55.70	4
Left precentral gyrus	49	7.49	<0.001	−40.70	−13.50	59.30	6
Right middle frontal gyrus	48	8.33	<0.001	29.60	5.80	64.50	6
Left frontal pole	40	7.61	<0.001	−20.30	59.10	−15.10	11
Left frontal pole	37	7.79	<0.001	−41.40	53.60	6.40	46
Left frontal orbital cortex	32	7.41	<0.001	−35.80	24.20	−23.10	38
Right frontal pole	30	8.39	<0.001	22.30	43.50	−17.40	11
Right superior lateral occipital cortex	21	6.43	<0.001	35.10	−70.60	36.40	19
Right frontal pole	17	7.12	<0.001	29.10	67.00	21.80	10
Left frontal pole	17	7.75	<0.001	−22.90	69.60	13.40	10
Left superior lateral occipital cortex	15	7.04	<0.001	−22.40	−60.30	67.00	7
Cerebellum	15	7.24	<0.001	−54.40	−70.30	−30.00	0
Left temporal pole	15	6.65	<0.001	−50.80	18.40	−8.77	38
Right inferior frontal gyrus	14	6.75	<0.001	53.60	14.10	32.50	44
Left superior frontal gyrus	13	7.29	<0.001	−19.10	−0.36	73.10	6
Right frontal pole	13	6.57	<0.001	3.98	58.90	−23.00	11
Right frontal pole	12	6.67	<0.001	28.50	62.40	−16.80	11
Left middle frontal gyrus	11	6.27	<0.001	−47.00	20.30	40.10	44
Right frontal medial cortex	11	6.80	<0.001	7.14	40.50	−13.50	11
Left precentral gyrus	10	7.03	<0.001	−65.90	6.33	5.24	6

Measures.

PTSD was assessed with the Clinician-Administered PTSD Scale for the DSM-5 (CAPS-5), a 30-item semi-structured diagnostic interview considered a gold standard for assessing PTSD at baseline and end of treatment (Weathers et al., 2013). PTSD symptoms were also assessed weekly by the PTSD Checklist for DSM-5 (PCL-5), a 20-item self-report measure that assesses PTSD severity (Weathers et al., 2013). AUD was assessed at baseline with the MINI International Neuropsychiatric Interview for DSM-5 (Sheehan et al., 1998). Past 60-day alcohol consumption was assessed at baseline by the Timeline Follow-back (Sobell and Sobell, 1992), a measure that uses calendar prompts to recall alcohol use. In addition, the Alcohol Use Disorders Identification Test (AUDIT) (Babor et al., 2001) was used to assess drinking behavior and problems.

The participant’s self-reported experiences of racial discrimination were captured at baseline by the Race-related Events Scale (Waelde et al., 2010). The RES is a 22-item checklist with yes/no items that assess frequency of lifetime exposure to different race-related stressors. Discriminatory stress (i.e., anxiety symptoms, trauma symptoms) was assessed using the Trauma Symptoms of Discrimination Scale (TSDS), a 21-item self-report measure that focuses on anxiety-related trauma symptoms due to experiences of racial discrimination (Williams et al., 2018).

3. Results

3.1. Clinical data

Demographic and clinical data can be found in Table 1. At baseline, the participant reported drinking alcohol for 53% of the past 60 days, averaging 8.1 standard drinks per drinking day. Her AUDIT score was 33 (range = 0–40), indicating moderate to severe AUD and hazardous alcohol consumption. She also scored in the clinical range for PTSD (CAPS-5 severity = 44, range = 0–80; PCL-5 score = 69, range = 0–80). The participant did not endorse, nor meet DSM-5 criteria for, any other substance use disorders. On the day of the fMRI scan, her blood alcohol concentration was 0.00.

Table 1.

Participant clinical data.

Variable	Score
Percent Days Drinking (past 60 days)	53%
Average Drinks per Drinking Day	8.1
Alcohol Use Disorders Identification Test (AUDIT)	33a
Clinician-Administered PTSD Scale for DSM-5 (CAPS-5)	44b
PTSD Checklist 5 Sum Score (PCL-5)	69
Racial Trauma Measures
Race-related Events Scale (RES)	17
Everyday Discrimination Events	11
Direct RES	3
Indirect or Vicarious RES	3
Trauma Symptoms of Discrimination Scale	70

^aModerate-severe AUD and hazardous alcohol consumption.

^bClinical range.

3.2. Description of trauma scripts and reactions

Her self-identified index trauma was sexual assault from a family friend who molested her when she was 16-years-old. The patient reported two additional sexual assaults, which occurred after the age of 16; she reported that she was raped by multiple individuals while intoxicated and reported being raped by a former boyfriend. The trauma narrative for her PTSD-trauma imagery script focused on the sexual assault perpetrated by a family friend. During and immediately following the traumatic incident, the participant experienced intense emotional and physiological responses. Emotional reactions included fear, helplessness, confusion, disbelief, and deep emotional pain, as well as intrusive thoughts questioning the perpetrator’s motives and actions. Physiologically, the participant described a rapid heartbeat, trembling hands, tension throughout her body (especially in her back, arms, and legs), shaking, nausea, tightness in her chest, labored breathing, gasping for air, a lump in her throat, pounding headache, and sharp internal pain. After the assault concluded, the participant reported feeling violated, deeply hurt, emotionally numb, and experiencing profound distress and despair (“it hurts to be alive”). These acute reactions highlight significant psychological trauma and distress extending beyond the immediate event itself, underscoring the severe impact on the participant’s mental health and emotional well-being.

The participant’s reported racial trauma involved an emotionally charged classroom incident from Spring 2012, shortly after the murder of Trayvon Martin. The participant experienced significant racial distress triggered by racist comments made by White classmates about Trayvon Martin’s murder. Classmates equated Black physical features to animals, joked about harming Black individuals, and openly mocked Trayvon Martin’s death. They directly questioned the participant’s family’s financial means and used explicitly racist language. Throughout the event, the participant reported intense emotional reactions, including anger, rage, frustration, betrayal, emptiness, and helplessness. Physiological reactions described in the script included rapid heartbeat, trembling hands, muscle tension, a pounding headache, labored breathing, jaw clenching, feelings of hollowness, and tearfulness. These reactions persisted beyond the immediate incident, resulting in feelings of self-blame and ongoing frustration about the inability to adequately respond or defend oneself against racial degradation, highlighting the traumatic and lingering psychological impact of the experience.

On measures that correspond to symptoms associated with racial trauma, such as the RES, the patient endorsed directly experiencing and witnessing 17 (range = 0 to 23) race-related events in her lifetime, including but not limited to rude treatment, general harassment, and secondhand knowledge of race-based cruelty. Her TSDS score of 70 suggested a high level of anxiety-related trauma symptoms due to racial discrimination (range = 21 to 81).

3.3. Baseline scan

Results from the fMRI scan suggest that each of the three cues examined was associated with widespread activation in multiple brain regions (see Table 2). The racial trauma cue was associated with activation in the right and left precentral gyrus and the posterior cingulate / cerebellum (see Fig. 1). The PTSD trauma cue was associated with activation in the left Heschl’s gyrus, right planum temporale, left inferior and middle frontal gyri, and the left frontal orbital cortex. The alcohol cue elicited activation in numerous regions, including the left Heschl’s gyrus, the right and left frontal pole, the right posterior supramarginal gyrus and inferior lateral occipital cortex, right and left precentral gyri, right precuneus cortex, left and right insular cortex, left temporal pole, right putamen, occipital pole, left frontal operculum cortex, and right inferior and middle frontal gyri, as well as white matter, cerebellar, and brain stem regions.

Fig. 1.

Areas of neural activation for racial trauma cue rendered on a high-resoloution T1-weighted anatomical scan. Note: N = 1; statistically significant activation (z > 5.3) is shown.

The participant showed greater activation in response to the racial trauma cue than the PTSD trauma cue in the posterior cingulate cortex, left precentral gyrus, and in precuneus (Fig. 2). Relative to the alcohol cue, the participant elicted activation to the racial trauma cue in the left and right postcentral gyrus, left and right superior lateral occipital cortex, posterior cingulate gyrus, right and left middle frontal gyri, right and left frontal pole, left frontal orbital cortex, and right and left superior lateral occipital cortices, cerebellum, left temporal pole, right inferior frontal gyrus, left superior frontal gyrus, right frontal medial cortex, and left precentral gyrus (Fig. 3).

Fig. 2.

Areas of neural activation for racial trauma cue > PTSD trauma cue rendered on a high-resolution T1-weighted anatomical scan. Note: N = 1; statistically significant activation (z > 5.3) is shown.

Fig. 3.

Areas of neural activation for racial trauma cue > alcohol cue rendered on a high-resolution T1-weighted anatomical scan. Note: N = 1; statistically significant activation (z > 5.3) is shown.

4. Discussion

This proof-of-concept case study demonstrated unique brain reactivity to a personalized imagery script based on a racial trauma relative to other cues during an fMRI scan in a Black woman with AUD+PTSD. Across the three script-driven auditory cues (racial trauma, PTSD trauma, and alcohol-related event), we observed both overlapping and distinct neural activation in sensory and motor brain regions implicated in processing emotionally salient cues (i.e., temporal, occipital, frontal regions). We found: 1) activation specific to the PTSD trauma cue in planum temporale and left frontal orbital cortex; and 2) activation specific to the alcohol cue in parietal (posterior supramarginal gyrus, precuneus) regions, the temporal pole, occipital (inferior lateral occipital cortex, occipital pole) regions, and frontal (frontal pole, inferior frontal gyrus, middle frontal gyrus) regions as well as cerebellar, brain stem, and white matter regions. However, greater activation was demonstrated for the racial trauma cue in the posterior cingulate cortex and left precentral gyrus, relative to the PTSD trauma cue. Compared to the alcohol cue, the racial trauma cue elicited greater activation in numerous regions including parietal (postcentral gyrus, posterior cingulate), occipital (superior lateral occipital cortex), frontal (precentral gyrus, middle frontal gyrus, frontal pole, inferior frontal gyrus), cerebellum, and temporal (temporal pole) regions. These results offer preliminary insights for better understanding the neural reactivity of racial trauma in patients with AUD+PTSD.

Although both the racial trauma and the PTSD cue activated frontal regions of the brain, they were distinct in which frontal regions were activated. Racial trauma scripts activated the precentral gyrus. While this region is typically more associated with motor movement, recent research on context-sensitive engagement of motor-related areas during emotional perception indicates that emotion and action interact in important ways in the brain. For example, activation of motor-related areas during emotional stimuli may reflect fight or flight responses that are prompted in response to emotional stimuli (Lima Portugal et al., 2020). Additionally, greater activation of the precentral gyrus may also reflect more intense emotional pain (e.g., pain associated with social rejection, as seen in most forms of racial discrimination; (Kross et al., 2011)) due to the chronic nature of racial discrimination for many Black individuals.

Activation to the racial trauma cue was observed in the posterior cingulate cortex (PCC), a region strongly implicated in memory retrieval and internally focused thought processes such as autobiographical memory and self-referential processing (Yoshii, 2021). This activation may reflect the cognitive and emotional processing that occurs when recalling personal experiences of racial trauma. Previous work has demonstrated that discrimination-related experiences can elicit heightened functional connectivity within brain networks involved in salience detection and threat monitoring, including the PCC. For example, in a sample of Black Americans who had recently experienced an acute traumatic injury, racial discrimination was associated with greater connectivity between the amygdala and thalamus, even after accounting for PTSD symptoms and lifetime trauma exposure (Webb et al., 2022). Although thalamic activation was not observed in the current study, the involvement of the PCC may similarly reflect hypervigilance and persistent cognitive engagement with past discriminatory experiences — a hallmark symptom of racial trauma. These findings suggest that the experience of racial trauma may activate neural systems responsible for evaluating the personal relevance of past events and preparing for future threats. Additionally, activation was observed in the posterior cingulate cortex, specifically within the retrosplenial region. This area has been strongly associated with autobiographical memory retrieval and self-referential processing (Cavanna and Trimble, 2006, Etkin and Wager, 2007). Its consistent activation across all contrasts involving the racial trauma cue may suggest that exposure to race-related stress elicits deeply personal, memory-linked responses that may underlie persistent and intrusive experiences of racial trauma. This pattern aligns with emerging findings linking racial discrimination to alterations in memory and salience-related networks (Webb et al., 2022).

Further, the racial trauma cue had significantly greater activation in the posterior cingulate, left precentral gyrus compared to the PTSD trauma cue. The posterior cingulate is often implicated in self-referential processing and emotional memory, suggesting that racial trauma may engage neural networks tied to both embodied and autobiographical memory (Leech and Sharp, 2014, Northoff et al., 2006, Spreng et al., 2009, Maddock et al., 2003, Svoboda et al., 2006).

Racial trauma and alcohol cues activated some overlapping brain regions, suggesting similar neural pathways associated with racial trauma and alcohol cues. It should be noted, however, that the findings here are less clear in how racial trauma relates to alcohol cues and neural reactivity given that this study is one of the first to examine the relationship between alcohol use and racial trauma through fMRI. Overlapping regions of activation for the racial trauma and alcohol cue included the precentral gyrus. As noted above, previous research has shown that the precentral gyrus may be implicated in motor-related areas during emotional stimuli, such as emotional pain, and additional research shows that the precentral gyrus is correlated with alcohol craving during alcohol cue tasks among participants with AUD (Kross et al., 2011, Park et al., 2007).

In addition to the shared regions of activation, the racial trauma cue elicited greater activation in numerous regions, including the parietal (postcentral gyrus, posterior cingulate) occipital (superior lateral occipital cortex), frontal (precentral gyrus, frontal pole, frontal orbital gyrus, inferior frontal gyrus, superior frontal gyrus, middle frontal gyrus, frontal medial cortex), temporal (left temporal pole) cortices, and cerebellum, compared to the alcohol cue. As previously stated when constrasting the racial trauma and PTSD cues, these additional areas may reflect some of the same processes that more closely tied to autobiographical memory, self-referential thinking, and heightened vigilance (Leech and Sharp, 2014, Northoff et al., 2006, Spreng et al., 2009)—functions often implicated in racial trauma—whereas alcohol cue reactivity may more strongly reflect interoceptive awareness and reward salience (Schacht et al., 2013, Naqvi and Bechara, 2010, Craig, 2009). Given the broad span of activation, the functional significance of these differences remain unclear and warrants further study, particularly in relation to how racial trauma may influence alcohol cue reactivity and broader substance use outcomes.

Together, these findings point to both shared and distinct neural processes engaged by racial trauma and alcohol-related cues and underscore the importance of considering the sociocultural context in understanding neural responses to trauma. Clarifying the neurobiological mechanisms underlying this overlap remains an important direction for future research.

Previous studies suggest that PTSD can be a major risk factor for the development of AUD, as PTSD symptoms drive excessive alcohol consumption, and AUD worsens PTSD symptoms (Smith and Cottler, 2018, Back and Jones, 2018). Neuroimaging studies show changes in fear/anxiety and reward/addiction circuitry that occur in overlapping brain areas in persons with comorbid AUD and PTSD, suggesting that these two disorders share neurobiological etiology (Suh and Ressler, 2018). Given this information, it is plausible that the same could be true for racial trauma and AUD. However, additional work is needed to confirm a shared etiology.

4.1. Limitations

As this is a proof-of-concept case study, findings and subsequent interpretations are focused on a single participant. These exploratory results should therefore be interpreted with caution given the inherent limitations of single-case research—namely limited generalizability and the inability to test for between-subject variability. Additionally, the relatively high activation thresholds and corresponding p-values selected for this case study may have resulted in more fractionated, small clusters of activation; these data are intended for descriptive purposes and should not be interpreted as evidence of generalizable statistical significance.

To more comprehensively understand how racial trauma is related to AUD and PTSD symptoms at the neural level, future research in larger more diverse samples is needed to test for reliable similarities and differences in neural activation for racial trauma, PTSD, and alcohol cues. Furthermore, while the racial trauma imagery script was developed using procedures based on validated methods, the application of these methods specifically to racial trauma has not yet been psychometrically validated, though it draws from established methods.

The research on this topic is still evolving, and further investigation is needed to fully understand the intricate relationship between racial discrimination, trauma, neural mechanisms, and alcohol use behavior.

5. Conclusions

Although preliminary and exploratory, this proof-of-concept study suggests that racial trauma cues activated regions of the brain that overlap with PTSD trauma cues in this participant. Both PTSD trauma cue and racial trauma cues activated brain regions associated with flashbacks and re-experiencing. However, unlike PTSD trauma cues, racial trauma scripts activated brain regions associated with emotional pain. This activation suggests racial trauma may also be associated with emotional pain, an area of important future investigation. In addition, racial trauma cues shared similar regional activity as alcohol cues. Although there is limited literature on this overlap, this shared activation may point to shared neurocircuitry between racial trauma and alcohol craving.

Given that Black individuals are at increased risk of PTSD, substance use, and co-occurring PTSD/AUD, it is imperative to continue this line of work (Torchalla et al., 2014, Alegría et al., 2013, Gillespie et al., 2009, Lee and Chen, 2017, Smith et al., 2006). For Black individuals, such as this participant, the mental strain of hypervigilance and ostracism—of being perceived as “the other”—due to racial trauma, may not only take a toll on physical and mental health but also increase the likelihood of negative alcohol-related and trauma outcomes, further widening the health disparities gap. Thus, investigating how racial trauma additively and uniquely contributes to the progression of AUD+PTSD is critical, as it may reflect not only overlapping neural mechanisms but also distinct neural processes specific to the chronic, identity-based nature of racial stress.