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The Inner Workings Of Grief


Bereavement has been a primary concern in psychotherapy for decades. However, making the appropriate distinctions between complicated grief (CG) or Prolonged Grief Disorder (PGD) and acute grief have provided much difficulty for clinicians. As more patients become debilitated by chronic bereavement, there has been a greater need for understanding what factors complicate the healing process. Therefore, the purpose herein is to use a neurobiological approach to conceptualize the bereavement process. More importantly, we plan to use this approach to formulate better assessment and treatment options for the use of psychotherapy, cognitive behavioral therapy, psychotropic medicines.

Keywords: Complicated Grief (CG), Prolonged Grief Disorder (PGD), Dopamine (DA), Nucleus Accumbens (NAcc).


Most individuals in their lifetime experience loss of a loved one. Regardless of the circumstances surrounding death, it can be life-changing. That devastation may initiate a cycle of grief with no clear end or beginning. For those who have not endured death, this concept may seem foreign. However, exploring the bereavement process provides insight into what many people face everyday. Grief is defined as deep sorrow and pain that is caused by someone’s death. Yet this definition just barely scratches the surface of what some people actually endure in the months and years following death.

As initially proposed by Elisabeth Kubler-Ross in her 1969 book entitled Death and Dying, grief can include, but is not limited to Denial, Anger, Depression, Bargaining, and Acceptance. Collectively, these stages are known as the bereavement period. During the stage of denial, the individual struggles to cope and refuses to accept that their loved one has actually passed on. This stems from being unable to address the magnitude of pain that comes with acceptance. In this stage, individuals actively deny loss by employing distractions. For example, you will see someone burying themselves in work to prevent subconscious feelings of sadness from emerging.

In comparison to denial, anger manifests itself in various forms. For example, unresolved matters with the person who has died can lead to a sense of resentment and blame. In the midst of anger, friendships and family relationships can be destroyed by irrational thoughts such as: “Why did you have to enable your sister’s drinking? It’s your fault that she died.” In fact, feelings of anger during mourning may lead to maladaptive coping strategies such as excessive drug use, partying, and even isolation. The emotional complexities within this stage are endless, but it is imperative to become aware of these issues in order to become that non-judgmental, loyal, and supportive clinicians. Having a sense of awareness about the bereavement process prevents any undue stigma.

Kubler-Ross has defined bargaining as the victim pleading for the return of their loved one in exchange for doing something. Often times you will hear someone saying: “I would trade anything in the world just to have my mother back, even if it is just for one second.” This stage is also where feelings of guilt creep in. People may blame themselves for things they didn’t say or do to improve the situation. That guilt propels the need to bargain or try to reiterate different scenarios in their minds that would have changed the outcome of death. This is one of the most difficult stages of grief to endure because the circular thinking leads to sleep deprivation, depression, and unrelenting feelings of anger towards oneself.

The Stage of Acceptance comes into fruition when the individual who experienced loss is able to not only obtain a sense of closure, but also come to accept the reality of death. In this stage there is the ability to compartmentalize the loss as outside of one’s own control and eliminate sense of guilt, blame, or depression because that person has been able to properly deal, rather than resorting to maladaptive coping strategies.

Although Kubler-Ross’ work has provided great insight to support a generalized understanding of grief, research has displayed that 10% of all bereaved persons end up with complicated grief (Middleton et. al, 1993 & Prigerson et. al, 2009). In fact, for some individuals, bereavement can be much more complex than initially thought. Therefore, it has become critical for clinicians to make diagnostic criterion that distinguish complicated grief from recurring traumatic memories consistent with Post-Traumatic Stress Disorder (PTSD), and Major Depressive Disorder (MDD). We plan to delineate the neurobiological mechanisms that empirically support the proposed core symptoms of complicated grief.

Acute Grief

According to Prigerson et. al (2009), acute grief commonly occurs within 6-12 months following the loss of a loved one. Common symptoms include, recurrent and strong feelings of yearning, pangs of deep sadness or remorse (episodes of crying), steady and vivid thoughts and images of the deceased, a struggle to accept the reality of the death concurrent with feelings of anger. However, there may also be somatic symptoms such as uncontrollable sighing, digestive symptoms, loss of appetite, sleep disturbances, exhaustion and weakness, restlessness, and difficulty initiating or maintaining organized activities. There is also a sense of feeling disconnected from the world or other people, whereby the individual becomes indifferent and irritable with others. Grief becomes considered complicated when there is persistence of symptoms of acute grief. Furthermore, there is a presence of thoughts, feelings and behaviors reflecting distracting concerns about the circumstances surrounding death.

Complicated versus Non-Complicated Grief

According to (O'Connor et. al, 2008), complicated grief (CG) refers to prolonged, unabated grief where strong attachments to the deceased activate rewards systems that evoke yearning concurrent with pain when presented with stimuli regarding death. On the other hand, uncomplicated grief (NCG) patients display the ability to experience brief pain and do not have prolonged yearning or reward activation in response to loss related stimuli. Earlier work on grief supports the framework for current classifications of NCG and CG by presenting a model of reunion versus detachment, whereby the loss of a loved one evokes either a strong desire to reunite or an ability to accept the loss and move forward by detaching oneself from the outcome of death (Bowlby, 1979).

Absent Grief

In the book entitled Bereavement, Reactions, Consequences, and Care(1984), it is considered a pathological outcome to experience little or no grief at all. These individuals typically experience minimal or no feelings of distress. In fact, they are described (Bowlby, 1980) to carry on as if the death had never occurred and may even appear to be coping splendidly. A sensitive observer will notice, however, that they appear tense and oftentimes, short-tempered. As Bowlby asserts, even though these individuals may appear to be coping effectively, there are usually clues that not all is well. For example, the person who experienced the loss may be intolerant and even forbid of mentions of the event. It has been found that denial in this form, may be a form of coping that is temporarily useful for the purposes of moving forward. But denial that persists for months, it may be considered pathological to never address or face the reality of the loss (Horowitz et al., 2003).

DSM-5 Criterion for Persistent Complex Bereavement- Related Disorder

  • The patient experienced the death of a loved one at least six months previously

At least one of the following symptoms have been present longer than expected, taking into account the person’s social or cultural environment:

  • Intense and persistent yearning for the deceased

  • Frequent preoccupation with the deceased

  • Intense feelings of emptiness or loneliness

  • Recurrent thoughts that life is meaningless or unfair without the deceased

  • A frequent urge to join the deceased in death

At least two of the following symptoms have been recorded for at least one month:

  • Feelings of disbelief or inability to accept the loss

  • Rumination about the circumstances or consequences of the death

  • Anger or bitterness about the death

  • Experiencing pain that the deceased suffered, or hearing/seeing the deceased

  • Trouble trusting or caring about others

  • Intense reactions to memories or reminders of the deceased

  • Avoidance of reminders of the deceased, or the opposite - seeking out reminders to feel close to the deceased

Symptoms cause substantial distress for the sufferer or impact significantly on areas of functioning and cannot be attributed to other causes.

Criticisms Of DSM-IV Diagnostic Criteria

The primary concern with the proposed criteria for Persistent Complex Bereavement is over the core characteristics required to be present to yield a diagnosis. First and foremost, the DSM requires that at least one of the four core symptoms to be present within a six month time period. The issue with this is that these symptoms tend to coexist with degrees of severity which can become more problematic when all four symptoms are present.

Neurobiological Mechanisms of Grief

Because love and attachments are neurobiologically similar to drug addiction, the absence of those bonds can elicit intense withdrawal symptoms that produce cravings (Burkett & Young, 2012). According to O'Connor, the Nucleus Accumbens (NAC), is responsible for not only reward signalling during drug-taking, but also plays a role in social attachment, maternal behavior via the mesolimbic dopamine (DA) system. In other words, the same structures responsible for drug cravings may also invoke yearning during complicated grief. This may suggest that those who have already been diagnosed with alcohol or drug-dependency issues will be more likely to develop symptoms of complicated grief following a loss. Given the nature of the addiction, it may be possible that the memories or loved ones become intermingled with drug cues that lead to protracted drug-taking. Because drugs have already hijacked the brain, this may lead an individual to spiral out of control. In other words, tolerance levels increase, while the ability to maintain the high begins to decrease. This inverse relationship may result in enormous downregulation of the brain's natural dopamine (DA) levels, whereby the absence of drugs and a loved one leads to anhedonia and lethargic depression due to that depletion. This only compounds the ability for clinicians and psychiatrists to treat not only CG, but also the addiction itself. Changes in DA levels may lead to other comorbid conditions such as, bipolar I and II, depression, anxiety, schizophrenia, and autoimmune diseases.

In order to account for the presence of these comorbid conditions, we have to make the assumption that changes in personality are probable. When anhedonia occurs, other structures such as the Orbital Prefrontal Cortex (OBFC) and the Dorsolateral Prefrontal Cortex (DLPFC) also undergo Dopamine depletion and that not only alters personality, but also increases the likelihood for development of psychiatric conditions (Walker & Roberts, 2008). As a consequence of these biochemical changes, there are noticeable differences in the way we process information regarding decision making. In other words, subjects are more likely to become impulsive and engage in risky behavior, increasing the probability of drug relapse. As these structural, chemical, and personality becomes more abberhant, there is more of a possibility that those who are enduring grief will make the transition to prolonged grief, wherein treatment becomes increasingly difficult as comorbid conditions interact.

Reward System Processing During Chronic Drug Use

With the introduction of drugs into a naive subject, there are numerous behavioral changes that occur in accordance with reward processing through the mesolimbic dopamine system. The normal behavioral response to natural rewards such as food, sex, and water become secondary as first time drug use leads to repeated self-administration. Drugs hijack the brain making these natural rewards or simple pleasures become secondary. It is important to further investigate the role of the amygdala in order to understand how these changes take place (Koob, 2003; 2009).

Genetic Changes in Reward Systems During Chronic Drug Use as a Predictor For Prolonged Grief

According to Nestler & Aghajanian (1997) chronic opiate use leads to a compensatory up-regulation of Cyclic Adenosine Monophosphate (cAMP). This causes an increase adenylyl cyclase and cAMP dependent in the Protein Kinase A (PKA). Whereas acute opiate exposure results in inhibition of the cAMP pathway. As Nestler and colleagues assert, up-regulation of this pathway as opposed to acute opiate inhibition, is an indicator of marked increases in physiological tolerance. In the absence of the opiate, the up-regulated pathway becomes fully functional and enhances the features of dependence and withdrawal. The absence of drugs following chronic drug use causes a yearning for drug-seeking and taking. These neurochemical pathways may possibly resemble the changes that occur during late stages of grief, where patients may in return feel the need to self-medicate or find a surrogate. If researchers constructed a paradigm allowing for experimentation of control versus bereaved subjects, evaluating cAMP may serve as a useful measure.

Final Thoughts

Although research on the relationship between prolonged grief and genetics is in its infancy, biological changes within reward systems may be an underlying mechanism by which the primary symptoms of bereavement persist. Understanding the relationships between reward, genetics, and behavior is only one critical component required for advancements in treatment. Furthermore, it is necessary to acknowledge those enduring chronic grief during primary evaluations in order to prompt focused research. Thus, in order to aid those suffering, there would need to be more specificity in the diagnostic criterion. In concordance with this, researchers can guide clinicians on bereavement in a similar fashion to strategies employed for treatment of chronic drug addiction. If feelings of yearning, wanting, and withdrawal can be adequately managed using similar techniques employed for preventing drug relapse, patients have a better chance at making improvements. This proposed solution does not exclude the need for benefits provided by treatment of other comorbid conditions. In other words, other forms of therapy would serve as an adjunct to techniques used for absolving patients from long-term grief. We should hold steadfast in our work towards educating ourselves as friends, clinicians, and researchers, so that those fighting the battle against devastation have the opportunity to overcome it.


Abnormal Grief Reactions: Complicated Mourning. (2008). Grief Counseling and Grief Therapy. doi:10.1891/9780826101211.0005

Bowlby, J. (1979). The Bowlby-Ainsworth attachment theory. Behavioral and Brain Sciences, 2(4), 637-638. doi:10.1017/s0140525x00064955

Bowlby, R. (2018). Fifty Years of Attachment Theory. Fifty Years of Attachment Theory, 11-26. doi:10.4324/9780429474736-2

Burkett, J. P., & Young, L. J. (2012). The behavioral, anatomical and pharmacological parallels between social attachment, love and addiction. Psychopharmacology, 224(1), 1-26. doi:10.1007/s00213-012-2794-x

Diagnostic and statistical manual of mental disorders DSM-5. (2013). American Psychiatric Publ.

Grief Therapy: Resolving Complicated Mourning. (2008). Grief Counseling and Grief Therapy. doi:10.1891/9780826101211.0006

Horowitz, M. J., Siegel, B., Holen, A., Bonanno, G. A., Milbrath, C., & Stinson, C. H. (2003). Diagnostic Criteria for Complicated Grief Disorder. Focus, 1(3), 290-298. doi:10.1176/foc.1.3.290

Koob, G. F. (2009). Brain stress systems in the amygdala and addiction. Brain Research, 1293, 61-75. doi:10.1016/j.brainres.2009.03.038

Koob, G. F. (2003). Neuroadaptive mechanisms of addiction: Studies on the extended amygdala. European Neuropsychopharmacology, 13(6), 442-452. doi:10.1016/j.euroneuro.2003.08.005

Kubler-Ross, E. (1969). On death and dying. Macmillan.

Middleton, W., Raphael, B., Martinek, N., & Misso, V. (1993). Pathological grief reactions. Handbook of Bereavement, 44-61. doi:10.1017/cbo9780511664076.004

Nestler, E. J., & Aghajanian, G. K. (1997). Molecular and Cellular Basis of Addiction. Science, 278(5335), 58-63. doi:10.1126/science.278.5335.58

Walker, S. C., Robbins, T. W., & Roberts, A. C. (2008). Differential Contributions of Dopamine and Serotonin to Orbitofrontal Cortex Function in the Marmoset. Cerebral Cortex, 19(4), 889-898. doi:10.1093/cercor/bhn136

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