by Mohammad Ibrahim, MBBS; Hassam Nasir Khan Alizai, MBBS; Izma Shahid, MBBS; and Muhammad Hannan Malik, MBBS, MCPS

All authors are with Shaikh Zayed Hospital, Lahore in Lahore, Punjab, Pakistan.

FUNDING: No funding was provided for this article.

DISCLOSURES: The authors declare no conflicts of interest relevant to the content of this article.

Innov Clin Neurosci. 2025;22(1–3):51–53.

Abstract

This case report presents a 35-year-old male patient from Lahore, Pakistan, who experienced recurring seasonal depressive symptoms from May to September for seven years. The patient exhibited symptoms including feelings of worthlessness, low mood, loss of appetite, decreased energy, anhedonia, and psychomotor retardation during the summer months, with a return to normal functioning outside of these months. The patient remained undiagnosed throughout this time. After multiple unsuccessful treatments from various facilities, he presented to our outpatient clinic for evaluation. Subsequently, he was admitted to the inpatient unit, where regular assessments diagnosed him with summer seasonal affective disorder (SAD), a rare and less-recognized form of SAD. After further evaluation, a treatment plan was devised that included slowly tapering off previous medications and initiating bupropion (a United States Food and Drug Administration [FDA]-approved medication for SAD) along with cognitive behavioral therapy. The patient subsequently fully recovered on bupropion and returned to normal functioning. The case highlights the challenges in diagnosing and treating summer SAD, particularly in tropical climates, where it is less recognized than winter SAD due to the scarcity of literature and awareness regarding it. Additionally, the positive response to bupropion suggests its potential efficacy for summer SAD. This report emphasizes the importance of considering regional and seasonal factors in psychiatric diagnoses and calls for increased awareness of and research on summer SAD, especially in countries such as Pakistan. The authors note this as potentially the first reported case of summer SAD in Pakistan, the sixth-most populous country globally. This highlights the need for a better understanding and management of seasonal disorders in diverse geographical contexts. 

Keywords: Antidepressants therapy, bupropion, psychiatry, depression, summer seasonal affective disorder

Seasonal affective disorder (SAD) is a subtype of major depressive disorder (MDD) with seasonal attributes. Typically, patients with SAD experience depressive episodes during a particular season, but present with normal mental health throughout the remainder of the year.¹ Traditional accounts of SAD attribute it to a scarcity of light in the autumn and winter. Another, rarer form of SAD occurs during the summer.² An individual experiencing summer SAD might experience problems with sleep; feel restlessness, anxious, or agitated; have reduced appetite; and lose weight.³ In contrast, symptoms of winter SAD include oversleeping, increased eating, and weight gain.⁴

SAD is more prevalent in some geographical locations than others, which might be due to seasonal changes and the amount of light received.⁵ Women are four times more likely than men to experience SAD, with onset typically occurring between the ages of 20 and 40 years. Those residing farther from the equator are also at higher risk of SAD.⁶ The conventional approach to treating winter SAD includes phototherapy, pharmacotherapy with antidepressant drugs, and psychological intervention incorporating cognitive behavioral therapy (CBT). Treatment of summer SAD might require environmental changes to help avoid heat, medication, and psychotherapy.⁷

Most studies on SAD are based on the winter subtype, while there is comparatively scant literature on summer SAD. Diagnosing SAD can be challenging because it can resemble conditions such as chronic fatigue syndrome, underactive thyroid, low blood glucose, viral illnesses, or other mood disorders.⁸ This can lead to it being underreported and, therefore, underdiagnosed.⁹ 

The following case report is of a patient from Pakistan, a country with a primarily hot and humid climate, who experienced summer SAD. Through this case presentation and a literature review, this report aims to contribute to the existing knowledge of summer SAD, as well as the cultural aspects of the disorder. By filling the gaps in our understanding, this report can help clinicians provide patients with more effective treatment, potentially improving patient care.

Case Report

A 35-year-old unmarried male individual, the fourth child of five siblings, who lived in Lahore, Pakistan, presented to the outpatient department in July with complaints of persistent feelings of apprehension, worthlessness, decreased interest in daily activities, and overwhelming fatigue. The patient reported a history of experiencing worthlessness, low mood, loss of appetite, weight loss, reduced energy, loss of interest, guilt, anhedonia, and psychomotor retardation, with a notable seasonal aggravation from May to September. The patient started to feel low during May with a rapid onset of symptoms, which caused him to be confined to his bed. This also caused him to resign from his job, rendering it difficult for him to earn money and provide for his family, which further aggravated his feelings of worthlessness. Suicidal ideation during that time was also present. These feelings persisted until September, when the monsoon rains caused a shift in temperature, after which he started to feel better. 

The seasonal onset of symptoms was persistent for the past seven years. There were reports of visits to multiple psychiatrists and the use of multiple psychiatric medications, with minimal effects on his mental state; reports indicated failed trials of sertraline, clomipramine, paroxetine, and escitalopram. When the patient presented to the outpatient department, he had been taking venlafaxine, olanzapine, and trifluoperazine. Venlafaxine was previously initiated at 75mg and increased to 150mg after one week, followed by a further increase to 225mg after three weeks. Despite this dose escalation, the patient stated that he did not exhibit significant clinical improvement. Consequently, olanzapine was added as an augmentation therapy, starting at 2.5mg and increasing to 10mg over one month. However, this combination also failed to produce meaningful benefits. Two weeks before coming to our facility, he was started on trifluoperazine 5mg. The day he presented to our outpatient department, he was taking 225mg of venlafaxine, 10mg of olanzapine, and 5mg of trifluoperazine. While trifluoperazine provided some improvement, the therapeutic gains were limited by the onset of extrapyramidal side effects. On arrival at our outpatient department, the patient had not previously undergone psychotherapy; the only prior treatment modality was medication use. 

Due to the prolonged history of polypharmacy and functional impairment, the patient was advised to be admitted to the psychiatric ward for further evaluation and management. Upon admission, baseline tests, thyroid profile, and vitamin D levels were measured, and all were within normal ranges, ruling out any organic cause. There was no history suggestive of hallucinations, delusions, negative symptoms, or substance abuse. During his mental state examination, the patient exhibited a dysphoric state, low energy, loss of motivation, low self-esteem, and negative view of himself. The Patient Health Questionnaire-9 (PHQ-9) and Generalized Anxiety Disorder-7 (GAD-7) yielded scores of 18 and 12, respectively. These scores were interpreted as the patient having moderately severe depression and moderate anxiety.

The patient’s account, as well as the collateral account from his attendants, who were interveiwed on the day of the patient’s admission, revealed no history of manic or hypomanic episodes, which effectively ruled out bipolar disorder and cyclothymic disorder. No significant psychosocial stressors were identified at the onset of symptoms in any given year. The patient’s symptoms appeared only for five months every year, ruling out dysthymia and chronic fatigue syndrome. Notable seasonal aggravation of symptoms from May until September aligned with The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) diagnostic criteria for SAD. The Seasonal Pattern Assessment Questionnaire (SPAQ) developed by Rosenthal et al, which is a widely used tool for screening SAD, was applied.¹⁰ A Global Seasonality Score (GSS) of 13 on the SPAQ further supported the diagnosis of SAD. 

When the diagnosis was established, a plan was made to take the patient off polypharmacy and start him on bupropion, which is approved by the United States Food and Drug Administration (FDA) for the treatment of SAD. The patient was given informational care regarding the nature of his illness and the treatment objectives. The potential side effects were explained to him, especially the fact that bupropion can lower seizure threshold. His concerns and queries regarding his treatment were addressed. After getting verbal consent from the patient, treatment was initiated with bupropion 150mg, which was titrated up to 300mg over seven days. A short (2-week) course of clonazepam 2mg was also initiated for acute management of the patient’s symptoms. At the time of medication initiation, the patient was also enrolled in an inpatient CBT program. During this time, the clinicians also started to slowly and cautiously taper off his other medications.  

The patient reported rapid improvement in his affective symptoms on the 15th day of admission. His sleep improved, and negative thoughts were replaced by hopefulness. His depressive and anxiety symptoms also improved significantly. A risk assessment was done and revealed no risk to self. The patient was subsequently discharged with instructions for weekly follow-up. 

The follow-up assessment after one month revealed significant reductions in the PHQ-9 and GAD-7 scores to 3 and 3, respectively. The patient showed adherence with the prescribed medications and reported a complete resolution of symptoms, with no adverse effects observed.

Discussion

SAD is not classified as a distinct diagnostic condition but is recognized as a form of recurring major depression that follows a seasonal pattern. As outlined in the DSM-5, the criteria for a seasonal pattern of depression include experiencing depressive episodes that consistently start and resolve during a specific season each year for a minimum of two consecutive years, along with having more seasons marked by depression than those without it over a lifetime. While seasonal pattern disorders are most commonly observed in winter, they can also manifest during the summer.¹¹ 

While much literature is on the winter subtype of SAD, the literature on summer SAD  is scarce.¹² In some places, it has been named reverse SAD or summer depression.¹³ Most of the theories concerning seasonal depression focus on the decreased production of serotonin and overproduction of melatonin during the winter owing to decreased sunlight exposure, which causes symptoms typical of SAD.^14,15 However, there is less information on the causes of depressive symptoms in summer. Some theories suggest that increased temperature plays a role in its symptomatology.¹⁶ In contrast, others suggest that there exists a reasonable possibility that a physiologic process is responsible for summer depressive symptoms because of the endogenous vegetative findings, including decreased appetite and insomnia, that are distinct to the summer subtype of SAD, compared to winter SAD.¹⁷

The symptoms of summer SAD can range from typical nonseasonal depressive symptoms, such anhedonia, worthlessness, excessive guilt, fatigue, loss of interest, and psychomotor slowing, to weight loss, insomnia, agitation, restlessness, anxiety, and even episodes of violent behavior.¹⁸ In our case, our patient experienced the typical endogenous vegetative symptoms of insomnia and loss of appetite, and showed no episodes of anger, restlessness, or agitation. 

Literature shows that summer SAD is underreported due to its less frequent occurrence, lack of prominent atypical vegetative features, and the focus on winter SAD in research.¹⁹ Also, most studies on SAD have been carried out on populations in temperate climates. This is because very little research considers people living in tropical zones. When compared with the pattern of SAD in temperate zones, based on the few studies available, there appears to be an opposite trend of seasonality in tropical zones, such as in the context of the climate of North India.²⁰ 

The fact that our patient visited several different psychiatrists and was treated with various medications, including, but not limited to, mood stabilizers, antipsychotics, and antidepressants, with little success, illustrates a challenge in treating summer SAD. There is a need to define seasonal psychiatric illnesses in a regional context so that clinicians following the guidelines are made well aware of them, thus reducing the likelihood of a missed diagnosis. Robust diagnostic criteria that consider the regional dynamics are needed to help prevent underdiagnosis.

Bupropion has been widely promoted and accepted as a popular treatment option for winter SAD.^21,22 However, there is not much data regarding its efficacy on the summer subtype of SAD. Through this case report, we would like to highlight bupropion’s efficacy in treating summer SAD when combined with CBT. Although more research is warranted, it is recommended that bupropion with CBT should be considered as a potential first-line treatment for patients diagnosed with the summer subtype of SAD. 

Lastly, it is worth mentioning that, according to our literature search, this is the first case of summer SAD reported from Pakistan, a country of approximately 250 million people, in 2024.²³

Conclusion

This case report emphasizes the need to detect the less common summer subtype of SAD, especially in tropical countries such as Pakistan and India. It is for these reasons that we have endeavored to highlight the diagnostic factors of summer SAD, given that it presents in a manner different from winter SAD and the information regarding summer SAD is scarce. The effectiveness of treating our patient with bupropion, which is approved for the treatment of SAD, in combination with CBT demonstrates that this combination should be considered as the first-line treatment for summer SAD. There is a need to raise awareness of and conduct research on summer SAD to realize the necessity of developing diagnostic criteria for seasonal diseases based on geographical area and appropriate treatment regimens to provide suitable treatment as early as possible. We hope this report can generate discussions regarding seasonal disorders so that clinicians can be more informed about comprehending, diagnosing, and managing SAD.

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