The Journal of Family Practice

The Centers for Disease Control and Prevention (CDC) and the World Health Organization are investigating an outbreak of monkeypox cases that have occurred around the world in countries that do not have endemic monkeypox virus.^1,2 As of July 5, there have been 6924 cases documented in 52 countries, including 560 cases that have occurred in the United States.² In the United States, as well as globally, a large proportion of cases have been in men who have sex with men.

First, what is monkeypox? Monkeypox is an orthopox virus that is closely related to variola (smallpox) and vaccinia (the virus used in the smallpox vaccine). It is endemic in western and central Africa and is contracted by contact with an infected mammal (including humans). Transmission can occur through direct contact with infected body fluids or lesions, via infectious fomites, or through respiratory secretions (although this usually requires prolonged exposure).

What is the disease course? The incubation period is 4 to 17 days. The initial symptoms include fever, malaise, headache, sore throat, and lymphadenopathy. A rash erupts 1 to 4 days after the prodrome and progresses synchronously from macules to papules to vesicles and then to pustules, which eventually scab over and fall off. In some cases reported in the United States, the rash started in the groin and genital area.

Don’t be fooled by other exanthems. Monkeypox can be confused with chickenpox and molluscum contagiosum (MC). However, the lesions in chickenpox appear asynchronously (all 4 stages present at the same time) and the papules of MC contain a central pit.

Can monkeypox be prevented? There are currently 2 vaccines against orthopox viruses: ACAM2000 and Jynneos. Currently, these vaccines are routinely recommended only for those at occupational risk of orthopox exposure.³

What you should know—and do. Be alert for any patient who presents with a suspicious rash; if there is a possibility of monkeypox, the local public health department should be contacted. They will investigate and collect samples for laboratory testing and will elicit contact names and locations. If monkeypox is confirmed, they may offer close contacts 1 of the 2 vaccines, which if administered within 4 days of exposure can prevent infection.

Advise all patients confirmed to have monkeypox to self-isolate until all skin lesions have healed. Good infection control practices in the clinical setting will prevent spread to staff and other patients.

More information about monkeypox, including images of typical lesions—as well as an update on the current investigation in the United States and worldwide—can be found on the CDC website.⁴

The Centers for Disease Control and Prevention (CDC) and the World Health Organization are investigating an outbreak of monkeypox cases that have occurred around the world in countries that do not have endemic monkeypox virus.^1,2 As of July 5, there have been 6924 cases documented in 52 countries, including 560 cases that have occurred in the United States.² In the United States, as well as globally, a large proportion of cases have been in men who have sex with men.

First, what is monkeypox? Monkeypox is an orthopox virus that is closely related to variola (smallpox) and vaccinia (the virus used in the smallpox vaccine). It is endemic in western and central Africa and is contracted by contact with an infected mammal (including humans). Transmission can occur through direct contact with infected body fluids or lesions, via infectious fomites, or through respiratory secretions (although this usually requires prolonged exposure).

What is the disease course? The incubation period is 4 to 17 days. The initial symptoms include fever, malaise, headache, sore throat, and lymphadenopathy. A rash erupts 1 to 4 days after the prodrome and progresses synchronously from macules to papules to vesicles and then to pustules, which eventually scab over and fall off. In some cases reported in the United States, the rash started in the groin and genital area.

Don’t be fooled by other exanthems. Monkeypox can be confused with chickenpox and molluscum contagiosum (MC). However, the lesions in chickenpox appear asynchronously (all 4 stages present at the same time) and the papules of MC contain a central pit.

Can monkeypox be prevented? There are currently 2 vaccines against orthopox viruses: ACAM2000 and Jynneos. Currently, these vaccines are routinely recommended only for those at occupational risk of orthopox exposure.³

What you should know—and do. Be alert for any patient who presents with a suspicious rash; if there is a possibility of monkeypox, the local public health department should be contacted. They will investigate and collect samples for laboratory testing and will elicit contact names and locations. If monkeypox is confirmed, they may offer close contacts 1 of the 2 vaccines, which if administered within 4 days of exposure can prevent infection.

Advise all patients confirmed to have monkeypox to self-isolate until all skin lesions have healed. Good infection control practices in the clinical setting will prevent spread to staff and other patients.

More information about monkeypox, including images of typical lesions—as well as an update on the current investigation in the United States and worldwide—can be found on the CDC website.⁴

The Centers for Disease Control and Prevention (CDC) and the World Health Organization are investigating an outbreak of monkeypox cases that have occurred around the world in countries that do not have endemic monkeypox virus.^1,2 As of July 5, there have been 6924 cases documented in 52 countries, including 560 cases that have occurred in the United States.² In the United States, as well as globally, a large proportion of cases have been in men who have sex with men.

First, what is monkeypox? Monkeypox is an orthopox virus that is closely related to variola (smallpox) and vaccinia (the virus used in the smallpox vaccine). It is endemic in western and central Africa and is contracted by contact with an infected mammal (including humans). Transmission can occur through direct contact with infected body fluids or lesions, via infectious fomites, or through respiratory secretions (although this usually requires prolonged exposure).

What is the disease course? The incubation period is 4 to 17 days. The initial symptoms include fever, malaise, headache, sore throat, and lymphadenopathy. A rash erupts 1 to 4 days after the prodrome and progresses synchronously from macules to papules to vesicles and then to pustules, which eventually scab over and fall off. In some cases reported in the United States, the rash started in the groin and genital area.

Don’t be fooled by other exanthems. Monkeypox can be confused with chickenpox and molluscum contagiosum (MC). However, the lesions in chickenpox appear asynchronously (all 4 stages present at the same time) and the papules of MC contain a central pit.

Can monkeypox be prevented? There are currently 2 vaccines against orthopox viruses: ACAM2000 and Jynneos. Currently, these vaccines are routinely recommended only for those at occupational risk of orthopox exposure.³

What you should know—and do. Be alert for any patient who presents with a suspicious rash; if there is a possibility of monkeypox, the local public health department should be contacted. They will investigate and collect samples for laboratory testing and will elicit contact names and locations. If monkeypox is confirmed, they may offer close contacts 1 of the 2 vaccines, which if administered within 4 days of exposure can prevent infection.

Advise all patients confirmed to have monkeypox to self-isolate until all skin lesions have healed. Good infection control practices in the clinical setting will prevent spread to staff and other patients.

More information about monkeypox, including images of typical lesions—as well as an update on the current investigation in the United States and worldwide—can be found on the CDC website.⁴

This patient was given a diagnosis of Gianotti Crosti syndrome (GCS; also called infantile acrodermatitis of childhood), which is a self-resolving (often dramatic) dermatosis triggered by a viral infection or immunization. Patients with this syndrome develop papules, vesicles, and plaques on their face, hands, feet, and extremities a week (or more) after having a viral illness or receiving an immunization. In patients with darker skin types, lesions may appear purple to brown rather than bright red to red/orange. The syndrome typically occurs in children between the ages of 1 to 4 years, but almost all patients are under the age of 15.¹ Scratching and sleep disturbance are common. The condition typically resolves on its own after 3 or 4 weeks.

Globally, the hepatitis B virus (HBV) is the most common cause of GCS.¹ Other reported triggering viruses include hepatitis A and C, cytomegalovirus, Epstein-Barr virus, enteroviruses, HIV, parainfluenza viruses, parvoviruses, rubella, and COVID-19.²

Since the cause of this patient’s case of GCS was likely linked to a viral infection that produced the loose stools in a population with low-HBV risk, no further serologic testing was performed. Serologic testing may have been necessary if other infections, disease risks, or symptoms were identified. To relieve itching, topical triamcinolone 0.1% cream was prescribed for use once to twice daily on the extremities and hydrocortisone 1% cream was prescribed once to twice daily for use on the child’s face. At the 6-week follow-up visit, the lesions had resolved; light pink discoloration remained but was expected to further fade. In patients with darker skin, post-inflammatory hyperpigmentation may take several months to resolve.

‌

Text courtesy of Jonathan Karnes, MD, medical director, MDFMR Dermatology Services, Augusta, ME. Photos courtesy of Jonathan Karnes, MD (copyright retained).

This patient was given a diagnosis of Gianotti Crosti syndrome (GCS; also called infantile acrodermatitis of childhood), which is a self-resolving (often dramatic) dermatosis triggered by a viral infection or immunization. Patients with this syndrome develop papules, vesicles, and plaques on their face, hands, feet, and extremities a week (or more) after having a viral illness or receiving an immunization. In patients with darker skin types, lesions may appear purple to brown rather than bright red to red/orange. The syndrome typically occurs in children between the ages of 1 to 4 years, but almost all patients are under the age of 15.¹ Scratching and sleep disturbance are common. The condition typically resolves on its own after 3 or 4 weeks.

Globally, the hepatitis B virus (HBV) is the most common cause of GCS.¹ Other reported triggering viruses include hepatitis A and C, cytomegalovirus, Epstein-Barr virus, enteroviruses, HIV, parainfluenza viruses, parvoviruses, rubella, and COVID-19.²

Since the cause of this patient’s case of GCS was likely linked to a viral infection that produced the loose stools in a population with low-HBV risk, no further serologic testing was performed. Serologic testing may have been necessary if other infections, disease risks, or symptoms were identified. To relieve itching, topical triamcinolone 0.1% cream was prescribed for use once to twice daily on the extremities and hydrocortisone 1% cream was prescribed once to twice daily for use on the child’s face. At the 6-week follow-up visit, the lesions had resolved; light pink discoloration remained but was expected to further fade. In patients with darker skin, post-inflammatory hyperpigmentation may take several months to resolve.

‌

Text courtesy of Jonathan Karnes, MD, medical director, MDFMR Dermatology Services, Augusta, ME. Photos courtesy of Jonathan Karnes, MD (copyright retained).

This patient was given a diagnosis of Gianotti Crosti syndrome (GCS; also called infantile acrodermatitis of childhood), which is a self-resolving (often dramatic) dermatosis triggered by a viral infection or immunization. Patients with this syndrome develop papules, vesicles, and plaques on their face, hands, feet, and extremities a week (or more) after having a viral illness or receiving an immunization. In patients with darker skin types, lesions may appear purple to brown rather than bright red to red/orange. The syndrome typically occurs in children between the ages of 1 to 4 years, but almost all patients are under the age of 15.¹ Scratching and sleep disturbance are common. The condition typically resolves on its own after 3 or 4 weeks.

Globally, the hepatitis B virus (HBV) is the most common cause of GCS.¹ Other reported triggering viruses include hepatitis A and C, cytomegalovirus, Epstein-Barr virus, enteroviruses, HIV, parainfluenza viruses, parvoviruses, rubella, and COVID-19.²

Since the cause of this patient’s case of GCS was likely linked to a viral infection that produced the loose stools in a population with low-HBV risk, no further serologic testing was performed. Serologic testing may have been necessary if other infections, disease risks, or symptoms were identified. To relieve itching, topical triamcinolone 0.1% cream was prescribed for use once to twice daily on the extremities and hydrocortisone 1% cream was prescribed once to twice daily for use on the child’s face. At the 6-week follow-up visit, the lesions had resolved; light pink discoloration remained but was expected to further fade. In patients with darker skin, post-inflammatory hyperpigmentation may take several months to resolve.

‌

Text courtesy of Jonathan Karnes, MD, medical director, MDFMR Dermatology Services, Augusta, ME. Photos courtesy of Jonathan Karnes, MD (copyright retained).

Pyogenic granulomas (PGs), also called lobular capillary hemangiomas, manifest as friable, moist or glistening, papules. PGs are a benign vascular proliferation. They often have a collarette, which is subtle in this lesion, and they bleed with minimal trauma. They are commonly seen on the gingiva during pregnancy, the umbilical area in newborns, or at sites of trauma.

Since PGs often occur during pregnancy, it’s been suggested that their development is related to hormonal changes.¹ It’s also been suggested that PGs are the result of an abnormal hypertrophic healing response, as they can occur in men, infants (at the umbilical stump), and even within blood vessels.¹

Although benign and painless, PGs are usually hard to ignore due to their raised appearance, tendency to bleed, and the low likelihood that they will resolve on their own. There are multiple physical treatment options available, including excision with primary closure, curettage followed by electrodessication, laser treatment, and cryosurgery. Topical therapies include timolol (a beta-blocker that has been used successfully with congenital hemangiomas), imiquimod, and trichloroacetic acid.¹ These topical medications do not require any anesthetic, which may make them an appealing option for children. Unfortunately, topical medications require multiple applications over a period of 2 or more weeks.

In this case, the lesion was shaved off and sent out to pathology to rule out amelanotic melanoma. The pathology for this patient confirmed PG. Immediately following the lesion’s removal, the physician performed 2 cycles of curettage and electrodessication. Thus, the patient’s treatment was completed on the same day as her evaluation.

‌

Photo courtesy of Daniel Stulberg, MD. Text courtesy of Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.

Pyogenic granulomas (PGs), also called lobular capillary hemangiomas, manifest as friable, moist or glistening, papules. PGs are a benign vascular proliferation. They often have a collarette, which is subtle in this lesion, and they bleed with minimal trauma. They are commonly seen on the gingiva during pregnancy, the umbilical area in newborns, or at sites of trauma.

Since PGs often occur during pregnancy, it’s been suggested that their development is related to hormonal changes.¹ It’s also been suggested that PGs are the result of an abnormal hypertrophic healing response, as they can occur in men, infants (at the umbilical stump), and even within blood vessels.¹

Although benign and painless, PGs are usually hard to ignore due to their raised appearance, tendency to bleed, and the low likelihood that they will resolve on their own. There are multiple physical treatment options available, including excision with primary closure, curettage followed by electrodessication, laser treatment, and cryosurgery. Topical therapies include timolol (a beta-blocker that has been used successfully with congenital hemangiomas), imiquimod, and trichloroacetic acid.¹ These topical medications do not require any anesthetic, which may make them an appealing option for children. Unfortunately, topical medications require multiple applications over a period of 2 or more weeks.

In this case, the lesion was shaved off and sent out to pathology to rule out amelanotic melanoma. The pathology for this patient confirmed PG. Immediately following the lesion’s removal, the physician performed 2 cycles of curettage and electrodessication. Thus, the patient’s treatment was completed on the same day as her evaluation.

‌

Photo courtesy of Daniel Stulberg, MD. Text courtesy of Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.

Pyogenic granulomas (PGs), also called lobular capillary hemangiomas, manifest as friable, moist or glistening, papules. PGs are a benign vascular proliferation. They often have a collarette, which is subtle in this lesion, and they bleed with minimal trauma. They are commonly seen on the gingiva during pregnancy, the umbilical area in newborns, or at sites of trauma.

Since PGs often occur during pregnancy, it’s been suggested that their development is related to hormonal changes.¹ It’s also been suggested that PGs are the result of an abnormal hypertrophic healing response, as they can occur in men, infants (at the umbilical stump), and even within blood vessels.¹

Although benign and painless, PGs are usually hard to ignore due to their raised appearance, tendency to bleed, and the low likelihood that they will resolve on their own. There are multiple physical treatment options available, including excision with primary closure, curettage followed by electrodessication, laser treatment, and cryosurgery. Topical therapies include timolol (a beta-blocker that has been used successfully with congenital hemangiomas), imiquimod, and trichloroacetic acid.¹ These topical medications do not require any anesthetic, which may make them an appealing option for children. Unfortunately, topical medications require multiple applications over a period of 2 or more weeks.

In this case, the lesion was shaved off and sent out to pathology to rule out amelanotic melanoma. The pathology for this patient confirmed PG. Immediately following the lesion’s removal, the physician performed 2 cycles of curettage and electrodessication. Thus, the patient’s treatment was completed on the same day as her evaluation.

‌

Photo courtesy of Daniel Stulberg, MD. Text courtesy of Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.

THE COMPARISON

A Nodular basal cell carcinoma (BCC) with a pearly rolled border, central pigmentation, and telangiectasia on the forehead of an 80-year-old Hispanic woman (light skin tone).

B Nodular BCC on the cheek of a 64-year-old Black man. The dark nonhealing ulcer had a subtle, pearly, rolled border and no visible telangiectasia.

Basal cell carcinoma (BCC) is most prevalent in individuals with lighter skin tones and rarely affects those with darker skin tones. Unfortunately, the lower incidence and lack of surveillance frequently result in a delayed diagnosis and increased morbidity for the skin of color population.1

Epidemiology

BCC is the most common skin cancer in White, Asian, and Hispanic individuals and the second most common in Black individuals. Squamous cell carcinoma is the most common skin cancer in Black individuals.²

Although BCCs are rare in individuals with darker skin tones, they most often develop in sun-exposed areas of the head and neck region.¹ In one study in an academic urban medical center, BCCs were more likely to occur in lightly pigmented vs darkly pigmented Black individuals.³

Key clinical features in people with darker skin tones

The classic BCC manifestation of a pearly papule with rolled borders and telangiectasia may not be seen in the skin of color population, especially among those with darker skin tones.⁴ In patient A, a Hispanic woman, these features are present along with hyperpigmentation. More than 50% of BCCs are pigmented in patients with skin of color vs only 5% in White individuals. ^5-7 The incidence of a pigmented BCC is twice as frequent in Hispanic individuals (FIGURE, A) as in non- Hispanic White individuals.⁷ Any skin cancer can present with ulcerations. So, while this is not specific to BCC, it is a reason to consider biopsy.

Worth noting

Pigmented BCC can mimic melanoma clinically and even when viewed with a dermatoscope, but such a suspicious lesion should prompt the clinician to perform a biopsy regardless of the type of suspected cancer. With experience and training, however, physicians can use dermoscopy to help make this distinction.

Note that skin of color is found in a heterogeneous population with a spectrum of skin tones and genetic/ethnic variability. In my practice in San Antonio (RPU), BCC is uncommon in Black patients and relatively common in Hispanic patients with lighter skin tones (FIGURE, A).

There is speculation that a lower incidence of BCC in the skin of color population leads to a low index of suspicion, which contributes to delayed diagnoses with poorer outcomes.¹ There are no firm data to support this because the rare occurrence of BCC in darker skin tones makes this a challenge to study.

Health disparity highlight

In general, barriers to health care include poverty, lack of education, lack of health insurance, and systemic racism. One study on keratinocyte skin cancers including BCC and squamous cell carcinoma found that these cancers were more costly to treat and required more health care resources, such as ambulatory visits and medication costs, in non-Hispanic Black and Hispanic White patients compared to non-Hispanic White patients.⁸

Final thoughts

Efforts are needed to achieve health equity through education of patients and health care providers about the appearance of BCC in skin of color with the goal of earlier diagnosis. Any nonhealing ulcer on the skin (FIGURE, B) should prompt consideration of skin cancer—regardless of skin color.

THE COMPARISON

A Nodular basal cell carcinoma (BCC) with a pearly rolled border, central pigmentation, and telangiectasia on the forehead of an 80-year-old Hispanic woman (light skin tone).

B Nodular BCC on the cheek of a 64-year-old Black man. The dark nonhealing ulcer had a subtle, pearly, rolled border and no visible telangiectasia.

Basal cell carcinoma (BCC) is most prevalent in individuals with lighter skin tones and rarely affects those with darker skin tones. Unfortunately, the lower incidence and lack of surveillance frequently result in a delayed diagnosis and increased morbidity for the skin of color population.1

Epidemiology

BCC is the most common skin cancer in White, Asian, and Hispanic individuals and the second most common in Black individuals. Squamous cell carcinoma is the most common skin cancer in Black individuals.²

Although BCCs are rare in individuals with darker skin tones, they most often develop in sun-exposed areas of the head and neck region.¹ In one study in an academic urban medical center, BCCs were more likely to occur in lightly pigmented vs darkly pigmented Black individuals.³

Key clinical features in people with darker skin tones

The classic BCC manifestation of a pearly papule with rolled borders and telangiectasia may not be seen in the skin of color population, especially among those with darker skin tones.⁴ In patient A, a Hispanic woman, these features are present along with hyperpigmentation. More than 50% of BCCs are pigmented in patients with skin of color vs only 5% in White individuals. ^5-7 The incidence of a pigmented BCC is twice as frequent in Hispanic individuals (FIGURE, A) as in non- Hispanic White individuals.⁷ Any skin cancer can present with ulcerations. So, while this is not specific to BCC, it is a reason to consider biopsy.

Worth noting

Pigmented BCC can mimic melanoma clinically and even when viewed with a dermatoscope, but such a suspicious lesion should prompt the clinician to perform a biopsy regardless of the type of suspected cancer. With experience and training, however, physicians can use dermoscopy to help make this distinction.

Note that skin of color is found in a heterogeneous population with a spectrum of skin tones and genetic/ethnic variability. In my practice in San Antonio (RPU), BCC is uncommon in Black patients and relatively common in Hispanic patients with lighter skin tones (FIGURE, A).

There is speculation that a lower incidence of BCC in the skin of color population leads to a low index of suspicion, which contributes to delayed diagnoses with poorer outcomes.¹ There are no firm data to support this because the rare occurrence of BCC in darker skin tones makes this a challenge to study.

Health disparity highlight

In general, barriers to health care include poverty, lack of education, lack of health insurance, and systemic racism. One study on keratinocyte skin cancers including BCC and squamous cell carcinoma found that these cancers were more costly to treat and required more health care resources, such as ambulatory visits and medication costs, in non-Hispanic Black and Hispanic White patients compared to non-Hispanic White patients.⁸

Final thoughts

Efforts are needed to achieve health equity through education of patients and health care providers about the appearance of BCC in skin of color with the goal of earlier diagnosis. Any nonhealing ulcer on the skin (FIGURE, B) should prompt consideration of skin cancer—regardless of skin color.

THE COMPARISON

A Nodular basal cell carcinoma (BCC) with a pearly rolled border, central pigmentation, and telangiectasia on the forehead of an 80-year-old Hispanic woman (light skin tone).

B Nodular BCC on the cheek of a 64-year-old Black man. The dark nonhealing ulcer had a subtle, pearly, rolled border and no visible telangiectasia.

Basal cell carcinoma (BCC) is most prevalent in individuals with lighter skin tones and rarely affects those with darker skin tones. Unfortunately, the lower incidence and lack of surveillance frequently result in a delayed diagnosis and increased morbidity for the skin of color population.1

Epidemiology

BCC is the most common skin cancer in White, Asian, and Hispanic individuals and the second most common in Black individuals. Squamous cell carcinoma is the most common skin cancer in Black individuals.²

Although BCCs are rare in individuals with darker skin tones, they most often develop in sun-exposed areas of the head and neck region.¹ In one study in an academic urban medical center, BCCs were more likely to occur in lightly pigmented vs darkly pigmented Black individuals.³

Key clinical features in people with darker skin tones

The classic BCC manifestation of a pearly papule with rolled borders and telangiectasia may not be seen in the skin of color population, especially among those with darker skin tones.⁴ In patient A, a Hispanic woman, these features are present along with hyperpigmentation. More than 50% of BCCs are pigmented in patients with skin of color vs only 5% in White individuals. ^5-7 The incidence of a pigmented BCC is twice as frequent in Hispanic individuals (FIGURE, A) as in non- Hispanic White individuals.⁷ Any skin cancer can present with ulcerations. So, while this is not specific to BCC, it is a reason to consider biopsy.

Worth noting

Pigmented BCC can mimic melanoma clinically and even when viewed with a dermatoscope, but such a suspicious lesion should prompt the clinician to perform a biopsy regardless of the type of suspected cancer. With experience and training, however, physicians can use dermoscopy to help make this distinction.

Note that skin of color is found in a heterogeneous population with a spectrum of skin tones and genetic/ethnic variability. In my practice in San Antonio (RPU), BCC is uncommon in Black patients and relatively common in Hispanic patients with lighter skin tones (FIGURE, A).

There is speculation that a lower incidence of BCC in the skin of color population leads to a low index of suspicion, which contributes to delayed diagnoses with poorer outcomes.¹ There are no firm data to support this because the rare occurrence of BCC in darker skin tones makes this a challenge to study.

Health disparity highlight

In general, barriers to health care include poverty, lack of education, lack of health insurance, and systemic racism. One study on keratinocyte skin cancers including BCC and squamous cell carcinoma found that these cancers were more costly to treat and required more health care resources, such as ambulatory visits and medication costs, in non-Hispanic Black and Hispanic White patients compared to non-Hispanic White patients.⁸

Final thoughts

Efforts are needed to achieve health equity through education of patients and health care providers about the appearance of BCC in skin of color with the goal of earlier diagnosis. Any nonhealing ulcer on the skin (FIGURE, B) should prompt consideration of skin cancer—regardless of skin color.

Dermoscopy revealed multiple small white structures around a central pore and tortuous, but not arborizing, blood vessels around the periphery (frequently called a crown pattern). These features pointed to the diagnosis of sebaceous gland hyperplasia (SGH).

SGH is a common benign condition seen predominantly in middle- to older-age people and patients on immunosuppressant drugs (especially ciclosporin). SGH tends to manifest as multiple lesions on the face and forehead, although the lesions can appear elsewhere.¹

As the name implies, SGH is hyperplasia of the sebocytes of the hair follicle, which results in white-to-yellow clusters around the dilated opening of the follicle.¹ In contrast to BCCs, which have arborizing blood vessels that can occur throughout the lesion, the vessels in SGH have a lower propensity for branching and tend to follow the periphery instead of crossing into the central pore.² This characteristic pattern, as well as the appearance of multiple similar lesions elsewhere on a patient’s body, suggests a diagnosis of SGH. If the lesion is atypical, solitary, or has other features that make the diagnosis uncertain, a biopsy is recommended.

SGH is not malignant and is asymptomatic, so treatment is not required. However, the cosmetic appearance can be distressing or undesirable for some patients.¹ The most common cosmetic remedies are destructive and include electrodessication, cryosurgery, and treatments with laser and intense pulsed light. Unfortunately, if there is residual tissue after treatment, recurrence is common, and due to the destructive nature of treatment, scarring is possible. It is important to counsel the patient regarding both of these possibilities and to balance the extent of destruction.

In patients with multiple lesions, oral isotretinoin may be used, but SGH will recur if treatment is discontinued. Additionally, isotretinoin, which is also used for cystic acne, is a high-risk medication due its potential to cause fetal anomalies and death if used during pregnancy. Patients usually get cheilitis and dyshidrosis due to its drying effect, but those symptoms are manageable with topical emollients.

This patient declined treatment, as he already had scars from previous NMSCs and was not concerned about the appearance of SGH.

‌

Photo courtesy of Daniel Stulberg, MD. Text courtesy of Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.

Dermoscopy revealed multiple small white structures around a central pore and tortuous, but not arborizing, blood vessels around the periphery (frequently called a crown pattern). These features pointed to the diagnosis of sebaceous gland hyperplasia (SGH).

SGH is a common benign condition seen predominantly in middle- to older-age people and patients on immunosuppressant drugs (especially ciclosporin). SGH tends to manifest as multiple lesions on the face and forehead, although the lesions can appear elsewhere.¹

As the name implies, SGH is hyperplasia of the sebocytes of the hair follicle, which results in white-to-yellow clusters around the dilated opening of the follicle.¹ In contrast to BCCs, which have arborizing blood vessels that can occur throughout the lesion, the vessels in SGH have a lower propensity for branching and tend to follow the periphery instead of crossing into the central pore.² This characteristic pattern, as well as the appearance of multiple similar lesions elsewhere on a patient’s body, suggests a diagnosis of SGH. If the lesion is atypical, solitary, or has other features that make the diagnosis uncertain, a biopsy is recommended.

SGH is not malignant and is asymptomatic, so treatment is not required. However, the cosmetic appearance can be distressing or undesirable for some patients.¹ The most common cosmetic remedies are destructive and include electrodessication, cryosurgery, and treatments with laser and intense pulsed light. Unfortunately, if there is residual tissue after treatment, recurrence is common, and due to the destructive nature of treatment, scarring is possible. It is important to counsel the patient regarding both of these possibilities and to balance the extent of destruction.

In patients with multiple lesions, oral isotretinoin may be used, but SGH will recur if treatment is discontinued. Additionally, isotretinoin, which is also used for cystic acne, is a high-risk medication due its potential to cause fetal anomalies and death if used during pregnancy. Patients usually get cheilitis and dyshidrosis due to its drying effect, but those symptoms are manageable with topical emollients.

This patient declined treatment, as he already had scars from previous NMSCs and was not concerned about the appearance of SGH.

‌

Photo courtesy of Daniel Stulberg, MD. Text courtesy of Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.

Dermoscopy revealed multiple small white structures around a central pore and tortuous, but not arborizing, blood vessels around the periphery (frequently called a crown pattern). These features pointed to the diagnosis of sebaceous gland hyperplasia (SGH).

SGH is a common benign condition seen predominantly in middle- to older-age people and patients on immunosuppressant drugs (especially ciclosporin). SGH tends to manifest as multiple lesions on the face and forehead, although the lesions can appear elsewhere.¹

As the name implies, SGH is hyperplasia of the sebocytes of the hair follicle, which results in white-to-yellow clusters around the dilated opening of the follicle.¹ In contrast to BCCs, which have arborizing blood vessels that can occur throughout the lesion, the vessels in SGH have a lower propensity for branching and tend to follow the periphery instead of crossing into the central pore.² This characteristic pattern, as well as the appearance of multiple similar lesions elsewhere on a patient’s body, suggests a diagnosis of SGH. If the lesion is atypical, solitary, or has other features that make the diagnosis uncertain, a biopsy is recommended.

SGH is not malignant and is asymptomatic, so treatment is not required. However, the cosmetic appearance can be distressing or undesirable for some patients.¹ The most common cosmetic remedies are destructive and include electrodessication, cryosurgery, and treatments with laser and intense pulsed light. Unfortunately, if there is residual tissue after treatment, recurrence is common, and due to the destructive nature of treatment, scarring is possible. It is important to counsel the patient regarding both of these possibilities and to balance the extent of destruction.

In patients with multiple lesions, oral isotretinoin may be used, but SGH will recur if treatment is discontinued. Additionally, isotretinoin, which is also used for cystic acne, is a high-risk medication due its potential to cause fetal anomalies and death if used during pregnancy. Patients usually get cheilitis and dyshidrosis due to its drying effect, but those symptoms are manageable with topical emollients.

This patient declined treatment, as he already had scars from previous NMSCs and was not concerned about the appearance of SGH.

‌

Photo courtesy of Daniel Stulberg, MD. Text courtesy of Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.

I enjoyed reading “How to identify balance disorders and reduce fall risk” (J Fam Pract. 2022;71:20-30) from the January/February issue. I was, however, disappointed to see that normal pressure hydrocephalus (NPH) was not discussed in the article or tables.

Recently, I took care of a 72-year-old patient who presented after multiple falls. In conjunction with Neurology, the presumptive diagnosis of Parkinson disease was made. However, the patient continued to experience a health decline that included cognitive changes, nocturia, and the classic “magnetic gait” of NPH (mnemonic for diagnosing this triad of symptoms: weird, wet, wobbly). The presumptive diagnosis was then changed when the results of a fluorodopa F18 positron emission tomography scan (also known as a DaT scan) returned as normal, essentially excluding the diagnosis of Parkinson disease.

The patient has since seen a dramatic improvement in gait and cognitive and urinary symptoms following a high-volume lumbar puncture and placement of a ventriculoperitoneal shunt. 

This case demonstrates the importance of considering NPH in the differential diagnosis for patients with balance disorders. Prompt diagnosis and management can result in a variable, but at times dramatic, reversal of symptoms. 

Ernestine Lee, MD, MPH
Austin, TX

I enjoyed reading “How to identify balance disorders and reduce fall risk” (J Fam Pract. 2022;71:20-30) from the January/February issue. I was, however, disappointed to see that normal pressure hydrocephalus (NPH) was not discussed in the article or tables.

Recently, I took care of a 72-year-old patient who presented after multiple falls. In conjunction with Neurology, the presumptive diagnosis of Parkinson disease was made. However, the patient continued to experience a health decline that included cognitive changes, nocturia, and the classic “magnetic gait” of NPH (mnemonic for diagnosing this triad of symptoms: weird, wet, wobbly). The presumptive diagnosis was then changed when the results of a fluorodopa F18 positron emission tomography scan (also known as a DaT scan) returned as normal, essentially excluding the diagnosis of Parkinson disease.

The patient has since seen a dramatic improvement in gait and cognitive and urinary symptoms following a high-volume lumbar puncture and placement of a ventriculoperitoneal shunt. 

This case demonstrates the importance of considering NPH in the differential diagnosis for patients with balance disorders. Prompt diagnosis and management can result in a variable, but at times dramatic, reversal of symptoms. 

Ernestine Lee, MD, MPH
Austin, TX

I enjoyed reading “How to identify balance disorders and reduce fall risk” (J Fam Pract. 2022;71:20-30) from the January/February issue. I was, however, disappointed to see that normal pressure hydrocephalus (NPH) was not discussed in the article or tables.

Recently, I took care of a 72-year-old patient who presented after multiple falls. In conjunction with Neurology, the presumptive diagnosis of Parkinson disease was made. However, the patient continued to experience a health decline that included cognitive changes, nocturia, and the classic “magnetic gait” of NPH (mnemonic for diagnosing this triad of symptoms: weird, wet, wobbly). The presumptive diagnosis was then changed when the results of a fluorodopa F18 positron emission tomography scan (also known as a DaT scan) returned as normal, essentially excluding the diagnosis of Parkinson disease.

The patient has since seen a dramatic improvement in gait and cognitive and urinary symptoms following a high-volume lumbar puncture and placement of a ventriculoperitoneal shunt. 

This case demonstrates the importance of considering NPH in the differential diagnosis for patients with balance disorders. Prompt diagnosis and management can result in a variable, but at times dramatic, reversal of symptoms. 

Ernestine Lee, MD, MPH
Austin, TX

I cannot agree more with Dr. Hickner’s editorial, “The power of the pause to prevent diagnostic error” (J Fam Pract. 2022;71:102). In 1974, when I started at the Medical College of Virginia, I thought I was going to be a medical researcher. By mid-1978, I had completely changed my focus to family medicine. Fortunately, my drive for detail and accuracy remained, albeit at odds with a whirlwind residency and solo practice. I drove my staff (and wife) crazy because I frequently spent more than the “allotted” time with a patient. The time was not wasted; it was most important for me to gain the trust of the patient and then to get it right—or find a path to the answer.

Jeff Ginther, MD
Bristol, VA

I cannot agree more with Dr. Hickner’s editorial, “The power of the pause to prevent diagnostic error” (J Fam Pract. 2022;71:102). In 1974, when I started at the Medical College of Virginia, I thought I was going to be a medical researcher. By mid-1978, I had completely changed my focus to family medicine. Fortunately, my drive for detail and accuracy remained, albeit at odds with a whirlwind residency and solo practice. I drove my staff (and wife) crazy because I frequently spent more than the “allotted” time with a patient. The time was not wasted; it was most important for me to gain the trust of the patient and then to get it right—or find a path to the answer.

Jeff Ginther, MD
Bristol, VA

I cannot agree more with Dr. Hickner’s editorial, “The power of the pause to prevent diagnostic error” (J Fam Pract. 2022;71:102). In 1974, when I started at the Medical College of Virginia, I thought I was going to be a medical researcher. By mid-1978, I had completely changed my focus to family medicine. Fortunately, my drive for detail and accuracy remained, albeit at odds with a whirlwind residency and solo practice. I drove my staff (and wife) crazy because I frequently spent more than the “allotted” time with a patient. The time was not wasted; it was most important for me to gain the trust of the patient and then to get it right—or find a path to the answer.

Jeff Ginther, MD
Bristol, VA

Evidence summary

Surgical repair: Re-injury risk goes down, complications risk goes up

A 2021 network meta-analysis including 38 RCTs (N = 2480) reported outcomes in patients ages 18 and older with acute Achilles tendon rupture (AATR) and 3 or more months of follow-up.¹ A significant increase in re-rupture rate was shown in patients who underwent nonoperative vs open repair (risk ratio [RR] = 2.41; 95% CI, 1.12-5.18). There was a significant decrease in wound-related complications in nonoperative vs open-repair patients (RR = 0.23; 95% CI, 0.06-0.88). There was also a significant difference in incidence of sural nerve injury in nonoperative vs open repair (RR = 0.27; 95% CI, 0.08-0.94). There were no significant differences in return to sport between open repair and nonoperative repair (RR = 0.62; 95% CI, 0.22-1.77). Insufficient data were reported to calculate the number needed to treat (NNT) and number needed to harm (NNH) for these outcomes.

Additionally, the authors looked at traditional standard rehabilitation and accelerated functional rehabilitation in both the operative and the nonoperative setting. The type of rehabilitation program did not have a significant impact on complications of re-rupture, wound, or sural nerve injury.

The included studies had an overall low risk of publication bias based on Begg’s funnel plot test (Pr > |z| = 0.86). The highest risk was performance bias, as neither the participants nor personnel were blinded to treatment in 71% of the studies.

Functional outcomes are similar for surgical vs nonoperative repair

In a 2019 meta-analysis of 9 RCTs (N = 822), adults ages 18 and older with AATR and a minimum of 12 months’ follow-up were randomized to either operative or nonoperative repair. There was a decreased rate of rupture with surgical repair and an associated increased rate of complications (ie, superficial wound infections and nerve injury). However, there was no significant difference in Physical Activity Scale (PAS) score between the 2 groups (mean difference, –0.05; 95% CI, –0.37 to 0.27).² With surgical intervention, the NNT for Achilles tendon re-rupture was 15, and the NNH for superficial wound infection and nerve injury, respectively, were 22 and 28. Limitations of the study included different operative techniques and rehab protocols, which may have affected the results of the included studies.

Large data sets with consistent results show that nonoperative treatment of Achilles tendon rupture is an excellent option.

A third meta-analysis consisted of 10 RCTs and 19 observational studies (N = 15,862) with patients ages 16 years and older treated operatively vs nonoperatively. Function and return-to-activity rates in both the short term (≤ 1 year) and long term (> 1 year) were evaluated using the Achilles tendon Total Rupture Score (ATRS).³ Surgical management was associated with decreased re-rupture rates but increased complication rates. However, when the analysis was limited to studies using accelerated functional rehabilitation programs, there was no significant difference in re-rupture rate (RR = 0.26 to 1.37; P = .23). Only 1 observational study found a statistically significant difference in short-term functional outcomes favoring operative management, and no studies found a significant difference in long-term functional outcomes. These functional outcomes were not pooled for statistical analysis due to high interrater variability of the ATRS.

An RCT showed equal “customer satisfaction”

One RCT randomized 61 patients to either surgical or nonsurgical management and followed them for a mean of 15.7 years.⁴ Patient-reported outcomes of function, symptoms, and impact on daily life were measured using various surveys. There was no statistically significant difference in the function and impact on daily life after treatment according to the Short Musculoskeletal Function Assessment or the ATRS (P = .289 and .313, respectively). When assessed using the Net Promoter Score (a single-question metric used in consumer industry to assess whether an individual would recommend the product to others), there was no statistical significance for the patients to recommend one treatment over another: 79% of operatively managed patients vs 87% of nonoperatively managed patients would recommend their treatment to others (P = .225).

Recommendations from others

The American College of Foot and Ankle Surgeons consensus statement finds no difference between operative and nonoperative management with regard to complications, functional outcome, and return to activity long term, when looking at available Level 1 evidence.⁵ They do acknowledge that although some Level III studies suggest operative intervention will return high-­functioning patients to full activity sooner, there should be discussion regarding the risks and complications of both operative and nonoperative management. Patients with increased risk factors for postoperative complications (diabetes, obesity, cigarette smoking) should have special considerations regarding the decision to operate.

Editor’s takeaway

Large data sets with consistent results show that nonoperative treatment of Achilles tendon rupture is an excellent option. However, we cannot say if it is better or worse than operative treatment, because both options have advantages and disadvantages. One must weigh the alternatives with individual patient preferences and circumstances.

Evidence summary

Surgical repair: Re-injury risk goes down, complications risk goes up

A 2021 network meta-analysis including 38 RCTs (N = 2480) reported outcomes in patients ages 18 and older with acute Achilles tendon rupture (AATR) and 3 or more months of follow-up.¹ A significant increase in re-rupture rate was shown in patients who underwent nonoperative vs open repair (risk ratio [RR] = 2.41; 95% CI, 1.12-5.18). There was a significant decrease in wound-related complications in nonoperative vs open-repair patients (RR = 0.23; 95% CI, 0.06-0.88). There was also a significant difference in incidence of sural nerve injury in nonoperative vs open repair (RR = 0.27; 95% CI, 0.08-0.94). There were no significant differences in return to sport between open repair and nonoperative repair (RR = 0.62; 95% CI, 0.22-1.77). Insufficient data were reported to calculate the number needed to treat (NNT) and number needed to harm (NNH) for these outcomes.

Additionally, the authors looked at traditional standard rehabilitation and accelerated functional rehabilitation in both the operative and the nonoperative setting. The type of rehabilitation program did not have a significant impact on complications of re-rupture, wound, or sural nerve injury.

The included studies had an overall low risk of publication bias based on Begg’s funnel plot test (Pr > |z| = 0.86). The highest risk was performance bias, as neither the participants nor personnel were blinded to treatment in 71% of the studies.

Functional outcomes are similar for surgical vs nonoperative repair

In a 2019 meta-analysis of 9 RCTs (N = 822), adults ages 18 and older with AATR and a minimum of 12 months’ follow-up were randomized to either operative or nonoperative repair. There was a decreased rate of rupture with surgical repair and an associated increased rate of complications (ie, superficial wound infections and nerve injury). However, there was no significant difference in Physical Activity Scale (PAS) score between the 2 groups (mean difference, –0.05; 95% CI, –0.37 to 0.27).² With surgical intervention, the NNT for Achilles tendon re-rupture was 15, and the NNH for superficial wound infection and nerve injury, respectively, were 22 and 28. Limitations of the study included different operative techniques and rehab protocols, which may have affected the results of the included studies.

Large data sets with consistent results show that nonoperative treatment of Achilles tendon rupture is an excellent option.

A third meta-analysis consisted of 10 RCTs and 19 observational studies (N = 15,862) with patients ages 16 years and older treated operatively vs nonoperatively. Function and return-to-activity rates in both the short term (≤ 1 year) and long term (> 1 year) were evaluated using the Achilles tendon Total Rupture Score (ATRS).³ Surgical management was associated with decreased re-rupture rates but increased complication rates. However, when the analysis was limited to studies using accelerated functional rehabilitation programs, there was no significant difference in re-rupture rate (RR = 0.26 to 1.37; P = .23). Only 1 observational study found a statistically significant difference in short-term functional outcomes favoring operative management, and no studies found a significant difference in long-term functional outcomes. These functional outcomes were not pooled for statistical analysis due to high interrater variability of the ATRS.

An RCT showed equal “customer satisfaction”

One RCT randomized 61 patients to either surgical or nonsurgical management and followed them for a mean of 15.7 years.⁴ Patient-reported outcomes of function, symptoms, and impact on daily life were measured using various surveys. There was no statistically significant difference in the function and impact on daily life after treatment according to the Short Musculoskeletal Function Assessment or the ATRS (P = .289 and .313, respectively). When assessed using the Net Promoter Score (a single-question metric used in consumer industry to assess whether an individual would recommend the product to others), there was no statistical significance for the patients to recommend one treatment over another: 79% of operatively managed patients vs 87% of nonoperatively managed patients would recommend their treatment to others (P = .225).

Recommendations from others

The American College of Foot and Ankle Surgeons consensus statement finds no difference between operative and nonoperative management with regard to complications, functional outcome, and return to activity long term, when looking at available Level 1 evidence.⁵ They do acknowledge that although some Level III studies suggest operative intervention will return high-­functioning patients to full activity sooner, there should be discussion regarding the risks and complications of both operative and nonoperative management. Patients with increased risk factors for postoperative complications (diabetes, obesity, cigarette smoking) should have special considerations regarding the decision to operate.

Editor’s takeaway

Large data sets with consistent results show that nonoperative treatment of Achilles tendon rupture is an excellent option. However, we cannot say if it is better or worse than operative treatment, because both options have advantages and disadvantages. One must weigh the alternatives with individual patient preferences and circumstances.

Evidence summary

Surgical repair: Re-injury risk goes down, complications risk goes up

A 2021 network meta-analysis including 38 RCTs (N = 2480) reported outcomes in patients ages 18 and older with acute Achilles tendon rupture (AATR) and 3 or more months of follow-up.¹ A significant increase in re-rupture rate was shown in patients who underwent nonoperative vs open repair (risk ratio [RR] = 2.41; 95% CI, 1.12-5.18). There was a significant decrease in wound-related complications in nonoperative vs open-repair patients (RR = 0.23; 95% CI, 0.06-0.88). There was also a significant difference in incidence of sural nerve injury in nonoperative vs open repair (RR = 0.27; 95% CI, 0.08-0.94). There were no significant differences in return to sport between open repair and nonoperative repair (RR = 0.62; 95% CI, 0.22-1.77). Insufficient data were reported to calculate the number needed to treat (NNT) and number needed to harm (NNH) for these outcomes.

Additionally, the authors looked at traditional standard rehabilitation and accelerated functional rehabilitation in both the operative and the nonoperative setting. The type of rehabilitation program did not have a significant impact on complications of re-rupture, wound, or sural nerve injury.

The included studies had an overall low risk of publication bias based on Begg’s funnel plot test (Pr > |z| = 0.86). The highest risk was performance bias, as neither the participants nor personnel were blinded to treatment in 71% of the studies.

Functional outcomes are similar for surgical vs nonoperative repair

In a 2019 meta-analysis of 9 RCTs (N = 822), adults ages 18 and older with AATR and a minimum of 12 months’ follow-up were randomized to either operative or nonoperative repair. There was a decreased rate of rupture with surgical repair and an associated increased rate of complications (ie, superficial wound infections and nerve injury). However, there was no significant difference in Physical Activity Scale (PAS) score between the 2 groups (mean difference, –0.05; 95% CI, –0.37 to 0.27).² With surgical intervention, the NNT for Achilles tendon re-rupture was 15, and the NNH for superficial wound infection and nerve injury, respectively, were 22 and 28. Limitations of the study included different operative techniques and rehab protocols, which may have affected the results of the included studies.

Large data sets with consistent results show that nonoperative treatment of Achilles tendon rupture is an excellent option.

A third meta-analysis consisted of 10 RCTs and 19 observational studies (N = 15,862) with patients ages 16 years and older treated operatively vs nonoperatively. Function and return-to-activity rates in both the short term (≤ 1 year) and long term (> 1 year) were evaluated using the Achilles tendon Total Rupture Score (ATRS).³ Surgical management was associated with decreased re-rupture rates but increased complication rates. However, when the analysis was limited to studies using accelerated functional rehabilitation programs, there was no significant difference in re-rupture rate (RR = 0.26 to 1.37; P = .23). Only 1 observational study found a statistically significant difference in short-term functional outcomes favoring operative management, and no studies found a significant difference in long-term functional outcomes. These functional outcomes were not pooled for statistical analysis due to high interrater variability of the ATRS.

An RCT showed equal “customer satisfaction”

One RCT randomized 61 patients to either surgical or nonsurgical management and followed them for a mean of 15.7 years.⁴ Patient-reported outcomes of function, symptoms, and impact on daily life were measured using various surveys. There was no statistically significant difference in the function and impact on daily life after treatment according to the Short Musculoskeletal Function Assessment or the ATRS (P = .289 and .313, respectively). When assessed using the Net Promoter Score (a single-question metric used in consumer industry to assess whether an individual would recommend the product to others), there was no statistical significance for the patients to recommend one treatment over another: 79% of operatively managed patients vs 87% of nonoperatively managed patients would recommend their treatment to others (P = .225).

Recommendations from others

The American College of Foot and Ankle Surgeons consensus statement finds no difference between operative and nonoperative management with regard to complications, functional outcome, and return to activity long term, when looking at available Level 1 evidence.⁵ They do acknowledge that although some Level III studies suggest operative intervention will return high-­functioning patients to full activity sooner, there should be discussion regarding the risks and complications of both operative and nonoperative management. Patients with increased risk factors for postoperative complications (diabetes, obesity, cigarette smoking) should have special considerations regarding the decision to operate.

Editor’s takeaway

Large data sets with consistent results show that nonoperative treatment of Achilles tendon rupture is an excellent option. However, we cannot say if it is better or worse than operative treatment, because both options have advantages and disadvantages. One must weigh the alternatives with individual patient preferences and circumstances.

THE CASE

Declan M*, a 42-year-old man, presents as a new patient for general medical care. One year ago, he sustained a severe frontal traumatic brain injury (TBI) when he was hit by a car while crossing a street. He developed a subdural hematoma and was in a coma for 6 days. He also had fractured ribs and a fractured left foot. When he regained consciousness, he had posttraumatic amnesia. He also had executive function deficits and memory difficulties, so a guardian was appointed.

Mr. M no longer works as an auto mechanic, a career he once greatly enjoyed. Mr. M’s guardian reports that recently, Mr. M has lost interest in activities he’d previously enjoyed, is frequently irritable, has poor sleep, is socially isolated, and is spending increasing amounts of time at home. When his new primary care physician (PCP) enters the examining room, Mr. M is seated in a chair with his arms folded across his chest. He states that he is “fine” and just needs to “get a doctor.”

● HOW WOULD YOU PROCEED WITH THIS PATIENT?

*This patient is an amalgam of patients for whom the author has provided care.

TBI ranges from mild to severe and can produce a number of profound effects that are a direct—or indirect—result of the physical injury.¹ The location and the severity of the injury affect symptoms.² Even mild TBI can cause impairment, and severe TBI can lead to broad cognitive, behavioral, and physical difficulties. As numbers of TBI cases increase globally, primary care providers need to recognize the symptoms and assess accordingly.¹ The Acute Concussion Evaluation (ACE; Physician/Clinician Office Version) facilitates a structured evaluation for patients presenting with possible TBI symptoms. It can easily be accessed on the Centers for Disease Control and Prevention website.³

Direct effects of TBI include impulsivity, depression, reduced frustration tolerance, reduced motivation, low awareness, and insomnia and other sleep difficulties.^4,5 Depression may also result indirectly from, or be exacerbated by, new posttraumatic limitations and lifestyle changes as well as loss of career and community.⁴ Both direct and indirect depression often manifest as feelings of hopelessness and worthlessness and a lack of interest in once enjoyable activities. Depression can worsen other TBI sequelae such as difficulty concentrating, lack of initiation, flat affect, irritability, reduced independence, reduced functional performance, loss of inhibition, and physical pain.⁶

Suicidality in TBI is a chronic concern. Assess for its presence no matter how long ago the TBI occurred.

Nationwide, most mental health concerns continue to be addressed in the primary care setting.⁷ Individuals with TBI experience major depression at a rate 5 to 6 times higher than those in the general population, with a prevalence rate of 45%.⁸

Suicide. The subject of suicide must be explored with survivors of TBI; evidence suggests a correlation between TBI, depression, and increased risk for suicide.⁹ Among those who have TBI, as many as 22% experience suicidal ideation; the risk of suicide in survivors of severe TBI is 3 to 4 times the risk in the general population.¹⁰ Additionally, suicidality in this context appears to be a chronic concern; therefore, carefully assess for its presence no matter how long ago the TBI occurred.¹⁰

Additional TBI-associated health concerns

Grief and loss. We so often focus on death as the only cause for grief, but grief can occur for other types of loss, as well. Individuals with TBI often experience a radical negative change in self-concept after their injury, which is associated with feelings of grief.¹¹ Helping patients recognize that they are grieving the loss of the person they once were can help set a framework for their experience.

Continue to: Relationship loss

Relationship loss. Many people with TBI lose close relationships.¹² This can be due to life changes such as job loss, loss of function or ability to do previously enjoyed activities, or personality changes. These relationship losses can affect a person profoundly.¹² Going forward, they may have difficulty trusting others, for example.

Existential issues. Many people with TBI also find that cognitive deficits prevent them from engaging in formerly meaningful work. For example, Mr. M lost his longstanding career as an auto mechanic and therefore part of his identity. Not being able to find purpose and meaning can be a strong contributor to coping difficulties in those with TBI.¹³

Chronic pain. More than half of people with TBI experience chronic pain. Headaches are the most common pain condition among all TBI survivors.¹⁴

Substance use disorders. The directionality of substance use disorders and TBI is not always clear; however, most evidence suggests that substance abuse is highly prevalent, premorbid, and often a contributing factor in TBI (eg, car accidents).¹⁵ Alcohol abuse is the most common risk factor, followed by drug abuse.¹⁶ Substance abuse may be exacerbated after TBI when it becomes a coping mechanism under worsening stressors; additionally, executive function deficits or other neurologic problems may result in poor decision-making with regard to substance use.¹⁵ While substance abuse may decline in the immediate post-TBI period, it can return to pre-injury levels within a year.¹⁷

Selective serotonin reuptake inhibitors may help

Few studies have explored the efficacy of antidepressant medication in TBI survivors. In a controlled study of patients with TBI, Fann and colleagues¹⁸ found no significant improvement in depression symptoms between sertraline and a placebo. However, they did note some possibilities for this lack of significance: socially isolated TBI survivors in the placebo group may have demonstrated improvement in depression symptoms because of increased social interaction; members of both the sertraline and placebo groups had many psychosocial difficulties; and the study had a relatively small sample size. Worth noting: Subjects given sertraline did demonstrate improvement in information processing.

Continue to: Other research has found...

Other research has found that sertraline improved both depression and quality of life for men with post-TBI depression.¹⁹ In a ­meta-analysis of 4 studies, Paraschakis and Katsanos²⁰ found that sertraline demonstrated a “trend toward significance” in the treatment of depression among patients with TBI. Silverberg and Panenka²¹ argue that selective serotonin reuptake inhibitors should be used as first-line treatment for depression in survivors of TBI. They note that in non-randomized studies, treatment effects with antidepressants are significant. Additionally, patients who do not respond to the first antidepressant prescribed will often respond to adjunctive or different medications. Finally, they argue that depression measures can capture symptoms related to the physical brain injury, in addition to symptoms of depression, thus confounding results.

THE CASE

Mr. M’s chart showed that he was not taking any medication and that he had no history of substance abuse or tobacco use. He refused to fill out the Patient Health Questionnaire (PHQ)-2. His guardian said that Mr. M was spending much of his time at home, and that he used to be an avid painter and guitar player but had not engaged in either activity for months. Furthermore, Mr. M used to enjoy working out but did so rarely now.

During the interview, the PCP was careful to make eye contact with Mr. M as well as his guardian, thereby making sure Mr. M was part of the conversation about his care. Pacing of questions was deliberate and unhurried; a return visit would be scheduled to further explore any concerns not covered in this visit. This collaborative, inclusive, patient-centered approach to the clinical interview seemed to place Mr. M at ease. When his guardian said he thought Mr. M was depressed, Mr. M agreed. Although Mr. M still refused to fill out the PHQ-2, he was now willing to answer questions about depression. He acknowledged that he was feeling hopeless and took little pleasure in activities he used to enjoy, thereby indicating a positive screen for depression.

The PCP opted to read the PHQ-9 questions aloud, and Mr. M agreed with most of the items but strongly denied suicidal ideation, citing his religious faith.

The PCP determined that Mr. M’s depression was likely a combination of the direct and indirect effects of his TBI. A quantitative estimate based on Mr. M’s report yielded a PHQ-9 score of 17, indicating moderately severe depression.

Continue to: In addition to building rapport...

In addition to building rapport, careful listening garnered important information about Mr. M. For example, until his accident and subsequent depression, Mr. M had long prioritized his physical health through diet and exercise. He followed a vegetarian diet but recently had little appetite and was eating one microwaveable meal a day. He had an irregular sleep schedule and struggled with insomnia. He lost his closest long-term relationship after his accident due to difficulties with affect regulation. He also lost his job as he could no longer cognitively handle the tasks required.

Hearing Mr. M’s story provided the opportunity to customize education about self-management skills including regular diet, exercise, and sleep hygiene. Due to limited visit time, the PCP elected to use this first visit to focus on sleep and depression. As cognitive behavioral therapy (CBT) for insomnia is first-line treatment for both primary insomnia and insomnia due to a medical condition such as TBI,⁵ a sleep aid was not prescribed. Fortunately, the clinic psychologist who offered CBT was able to join the interview to meet Mr. M and explain the treatment.

Mr. M expressed some initial reluctance to try an antidepressant. However, acknowledging he “just hasn’t been the same” since his TBI, he agreed to a prescription for sertraline and said he hoped it could make him “more like [he] was.”

RETURN VISIT

Four weeks after Mr. M began taking sertraline and participating in weekly CBT sessions, he returned for a follow-up visit with his PCP. He had a noticeably brighter affect, and his guardian reported that he had been playing the guitar again. Mr. M said that he had more energy as a result of improved sleep and mood, and that he felt like his “thinking was clearer.” Mr. M noted that he never thought he would meet with a psychologist but was finding CBT for insomnia helpful.

Patients who do not respond to the first antidepressant prescribed will often respond to adjunctive or different medications.

The psychologist’s notes proposed a treatment plan that would also include targeted grief and existential therapies to address Mr. M’s sudden life changes. At this visit, Mr. M admitted that his reading comprehension and speed were negatively affected by the accident and said this is why he did not wish to fill out the PHQ-2. But he was again willing to have the PHQ-9 questions read to him with his guardian’s support. Results showed a score of 6, indicating mild depression.

A follow-up appointment with Mr. M was scheduled for 6 weeks later, and the team was confident he was getting the behavioral and mental health support he needed through medication and therapy.

CORRESPONDENCE
Elizabeth Imbesi, PhD, VA Ann Arbor Healthcare System, 2215 Fuller Road, Ann Arbor, MI 48105; [email protected]

THE CASE

Declan M*, a 42-year-old man, presents as a new patient for general medical care. One year ago, he sustained a severe frontal traumatic brain injury (TBI) when he was hit by a car while crossing a street. He developed a subdural hematoma and was in a coma for 6 days. He also had fractured ribs and a fractured left foot. When he regained consciousness, he had posttraumatic amnesia. He also had executive function deficits and memory difficulties, so a guardian was appointed.

Mr. M no longer works as an auto mechanic, a career he once greatly enjoyed. Mr. M’s guardian reports that recently, Mr. M has lost interest in activities he’d previously enjoyed, is frequently irritable, has poor sleep, is socially isolated, and is spending increasing amounts of time at home. When his new primary care physician (PCP) enters the examining room, Mr. M is seated in a chair with his arms folded across his chest. He states that he is “fine” and just needs to “get a doctor.”

● HOW WOULD YOU PROCEED WITH THIS PATIENT?

*This patient is an amalgam of patients for whom the author has provided care.

TBI ranges from mild to severe and can produce a number of profound effects that are a direct—or indirect—result of the physical injury.¹ The location and the severity of the injury affect symptoms.² Even mild TBI can cause impairment, and severe TBI can lead to broad cognitive, behavioral, and physical difficulties. As numbers of TBI cases increase globally, primary care providers need to recognize the symptoms and assess accordingly.¹ The Acute Concussion Evaluation (ACE; Physician/Clinician Office Version) facilitates a structured evaluation for patients presenting with possible TBI symptoms. It can easily be accessed on the Centers for Disease Control and Prevention website.³

Direct effects of TBI include impulsivity, depression, reduced frustration tolerance, reduced motivation, low awareness, and insomnia and other sleep difficulties.^4,5 Depression may also result indirectly from, or be exacerbated by, new posttraumatic limitations and lifestyle changes as well as loss of career and community.⁴ Both direct and indirect depression often manifest as feelings of hopelessness and worthlessness and a lack of interest in once enjoyable activities. Depression can worsen other TBI sequelae such as difficulty concentrating, lack of initiation, flat affect, irritability, reduced independence, reduced functional performance, loss of inhibition, and physical pain.⁶

Suicidality in TBI is a chronic concern. Assess for its presence no matter how long ago the TBI occurred.

Nationwide, most mental health concerns continue to be addressed in the primary care setting.⁷ Individuals with TBI experience major depression at a rate 5 to 6 times higher than those in the general population, with a prevalence rate of 45%.⁸

Suicide. The subject of suicide must be explored with survivors of TBI; evidence suggests a correlation between TBI, depression, and increased risk for suicide.⁹ Among those who have TBI, as many as 22% experience suicidal ideation; the risk of suicide in survivors of severe TBI is 3 to 4 times the risk in the general population.¹⁰ Additionally, suicidality in this context appears to be a chronic concern; therefore, carefully assess for its presence no matter how long ago the TBI occurred.¹⁰

Additional TBI-associated health concerns

Grief and loss. We so often focus on death as the only cause for grief, but grief can occur for other types of loss, as well. Individuals with TBI often experience a radical negative change in self-concept after their injury, which is associated with feelings of grief.¹¹ Helping patients recognize that they are grieving the loss of the person they once were can help set a framework for their experience.

Continue to: Relationship loss

Relationship loss. Many people with TBI lose close relationships.¹² This can be due to life changes such as job loss, loss of function or ability to do previously enjoyed activities, or personality changes. These relationship losses can affect a person profoundly.¹² Going forward, they may have difficulty trusting others, for example.

Existential issues. Many people with TBI also find that cognitive deficits prevent them from engaging in formerly meaningful work. For example, Mr. M lost his longstanding career as an auto mechanic and therefore part of his identity. Not being able to find purpose and meaning can be a strong contributor to coping difficulties in those with TBI.¹³

Chronic pain. More than half of people with TBI experience chronic pain. Headaches are the most common pain condition among all TBI survivors.¹⁴

Substance use disorders. The directionality of substance use disorders and TBI is not always clear; however, most evidence suggests that substance abuse is highly prevalent, premorbid, and often a contributing factor in TBI (eg, car accidents).¹⁵ Alcohol abuse is the most common risk factor, followed by drug abuse.¹⁶ Substance abuse may be exacerbated after TBI when it becomes a coping mechanism under worsening stressors; additionally, executive function deficits or other neurologic problems may result in poor decision-making with regard to substance use.¹⁵ While substance abuse may decline in the immediate post-TBI period, it can return to pre-injury levels within a year.¹⁷

Selective serotonin reuptake inhibitors may help

Few studies have explored the efficacy of antidepressant medication in TBI survivors. In a controlled study of patients with TBI, Fann and colleagues¹⁸ found no significant improvement in depression symptoms between sertraline and a placebo. However, they did note some possibilities for this lack of significance: socially isolated TBI survivors in the placebo group may have demonstrated improvement in depression symptoms because of increased social interaction; members of both the sertraline and placebo groups had many psychosocial difficulties; and the study had a relatively small sample size. Worth noting: Subjects given sertraline did demonstrate improvement in information processing.

Continue to: Other research has found...

Other research has found that sertraline improved both depression and quality of life for men with post-TBI depression.¹⁹ In a ­meta-analysis of 4 studies, Paraschakis and Katsanos²⁰ found that sertraline demonstrated a “trend toward significance” in the treatment of depression among patients with TBI. Silverberg and Panenka²¹ argue that selective serotonin reuptake inhibitors should be used as first-line treatment for depression in survivors of TBI. They note that in non-randomized studies, treatment effects with antidepressants are significant. Additionally, patients who do not respond to the first antidepressant prescribed will often respond to adjunctive or different medications. Finally, they argue that depression measures can capture symptoms related to the physical brain injury, in addition to symptoms of depression, thus confounding results.

THE CASE

Mr. M’s chart showed that he was not taking any medication and that he had no history of substance abuse or tobacco use. He refused to fill out the Patient Health Questionnaire (PHQ)-2. His guardian said that Mr. M was spending much of his time at home, and that he used to be an avid painter and guitar player but had not engaged in either activity for months. Furthermore, Mr. M used to enjoy working out but did so rarely now.

During the interview, the PCP was careful to make eye contact with Mr. M as well as his guardian, thereby making sure Mr. M was part of the conversation about his care. Pacing of questions was deliberate and unhurried; a return visit would be scheduled to further explore any concerns not covered in this visit. This collaborative, inclusive, patient-centered approach to the clinical interview seemed to place Mr. M at ease. When his guardian said he thought Mr. M was depressed, Mr. M agreed. Although Mr. M still refused to fill out the PHQ-2, he was now willing to answer questions about depression. He acknowledged that he was feeling hopeless and took little pleasure in activities he used to enjoy, thereby indicating a positive screen for depression.

The PCP opted to read the PHQ-9 questions aloud, and Mr. M agreed with most of the items but strongly denied suicidal ideation, citing his religious faith.

The PCP determined that Mr. M’s depression was likely a combination of the direct and indirect effects of his TBI. A quantitative estimate based on Mr. M’s report yielded a PHQ-9 score of 17, indicating moderately severe depression.

Continue to: In addition to building rapport...

In addition to building rapport, careful listening garnered important information about Mr. M. For example, until his accident and subsequent depression, Mr. M had long prioritized his physical health through diet and exercise. He followed a vegetarian diet but recently had little appetite and was eating one microwaveable meal a day. He had an irregular sleep schedule and struggled with insomnia. He lost his closest long-term relationship after his accident due to difficulties with affect regulation. He also lost his job as he could no longer cognitively handle the tasks required.

Hearing Mr. M’s story provided the opportunity to customize education about self-management skills including regular diet, exercise, and sleep hygiene. Due to limited visit time, the PCP elected to use this first visit to focus on sleep and depression. As cognitive behavioral therapy (CBT) for insomnia is first-line treatment for both primary insomnia and insomnia due to a medical condition such as TBI,⁵ a sleep aid was not prescribed. Fortunately, the clinic psychologist who offered CBT was able to join the interview to meet Mr. M and explain the treatment.

Mr. M expressed some initial reluctance to try an antidepressant. However, acknowledging he “just hasn’t been the same” since his TBI, he agreed to a prescription for sertraline and said he hoped it could make him “more like [he] was.”

RETURN VISIT

Four weeks after Mr. M began taking sertraline and participating in weekly CBT sessions, he returned for a follow-up visit with his PCP. He had a noticeably brighter affect, and his guardian reported that he had been playing the guitar again. Mr. M said that he had more energy as a result of improved sleep and mood, and that he felt like his “thinking was clearer.” Mr. M noted that he never thought he would meet with a psychologist but was finding CBT for insomnia helpful.

Patients who do not respond to the first antidepressant prescribed will often respond to adjunctive or different medications.

The psychologist’s notes proposed a treatment plan that would also include targeted grief and existential therapies to address Mr. M’s sudden life changes. At this visit, Mr. M admitted that his reading comprehension and speed were negatively affected by the accident and said this is why he did not wish to fill out the PHQ-2. But he was again willing to have the PHQ-9 questions read to him with his guardian’s support. Results showed a score of 6, indicating mild depression.

A follow-up appointment with Mr. M was scheduled for 6 weeks later, and the team was confident he was getting the behavioral and mental health support he needed through medication and therapy.

CORRESPONDENCE
Elizabeth Imbesi, PhD, VA Ann Arbor Healthcare System, 2215 Fuller Road, Ann Arbor, MI 48105; [email protected]

THE CASE

Declan M*, a 42-year-old man, presents as a new patient for general medical care. One year ago, he sustained a severe frontal traumatic brain injury (TBI) when he was hit by a car while crossing a street. He developed a subdural hematoma and was in a coma for 6 days. He also had fractured ribs and a fractured left foot. When he regained consciousness, he had posttraumatic amnesia. He also had executive function deficits and memory difficulties, so a guardian was appointed.

Mr. M no longer works as an auto mechanic, a career he once greatly enjoyed. Mr. M’s guardian reports that recently, Mr. M has lost interest in activities he’d previously enjoyed, is frequently irritable, has poor sleep, is socially isolated, and is spending increasing amounts of time at home. When his new primary care physician (PCP) enters the examining room, Mr. M is seated in a chair with his arms folded across his chest. He states that he is “fine” and just needs to “get a doctor.”

● HOW WOULD YOU PROCEED WITH THIS PATIENT?

*This patient is an amalgam of patients for whom the author has provided care.

TBI ranges from mild to severe and can produce a number of profound effects that are a direct—or indirect—result of the physical injury.¹ The location and the severity of the injury affect symptoms.² Even mild TBI can cause impairment, and severe TBI can lead to broad cognitive, behavioral, and physical difficulties. As numbers of TBI cases increase globally, primary care providers need to recognize the symptoms and assess accordingly.¹ The Acute Concussion Evaluation (ACE; Physician/Clinician Office Version) facilitates a structured evaluation for patients presenting with possible TBI symptoms. It can easily be accessed on the Centers for Disease Control and Prevention website.³

Direct effects of TBI include impulsivity, depression, reduced frustration tolerance, reduced motivation, low awareness, and insomnia and other sleep difficulties.^4,5 Depression may also result indirectly from, or be exacerbated by, new posttraumatic limitations and lifestyle changes as well as loss of career and community.⁴ Both direct and indirect depression often manifest as feelings of hopelessness and worthlessness and a lack of interest in once enjoyable activities. Depression can worsen other TBI sequelae such as difficulty concentrating, lack of initiation, flat affect, irritability, reduced independence, reduced functional performance, loss of inhibition, and physical pain.⁶

Suicidality in TBI is a chronic concern. Assess for its presence no matter how long ago the TBI occurred.

Nationwide, most mental health concerns continue to be addressed in the primary care setting.⁷ Individuals with TBI experience major depression at a rate 5 to 6 times higher than those in the general population, with a prevalence rate of 45%.⁸

Suicide. The subject of suicide must be explored with survivors of TBI; evidence suggests a correlation between TBI, depression, and increased risk for suicide.⁹ Among those who have TBI, as many as 22% experience suicidal ideation; the risk of suicide in survivors of severe TBI is 3 to 4 times the risk in the general population.¹⁰ Additionally, suicidality in this context appears to be a chronic concern; therefore, carefully assess for its presence no matter how long ago the TBI occurred.¹⁰

Additional TBI-associated health concerns

Grief and loss. We so often focus on death as the only cause for grief, but grief can occur for other types of loss, as well. Individuals with TBI often experience a radical negative change in self-concept after their injury, which is associated with feelings of grief.¹¹ Helping patients recognize that they are grieving the loss of the person they once were can help set a framework for their experience.

Continue to: Relationship loss

Relationship loss. Many people with TBI lose close relationships.¹² This can be due to life changes such as job loss, loss of function or ability to do previously enjoyed activities, or personality changes. These relationship losses can affect a person profoundly.¹² Going forward, they may have difficulty trusting others, for example.

Existential issues. Many people with TBI also find that cognitive deficits prevent them from engaging in formerly meaningful work. For example, Mr. M lost his longstanding career as an auto mechanic and therefore part of his identity. Not being able to find purpose and meaning can be a strong contributor to coping difficulties in those with TBI.¹³

Chronic pain. More than half of people with TBI experience chronic pain. Headaches are the most common pain condition among all TBI survivors.¹⁴

Substance use disorders. The directionality of substance use disorders and TBI is not always clear; however, most evidence suggests that substance abuse is highly prevalent, premorbid, and often a contributing factor in TBI (eg, car accidents).¹⁵ Alcohol abuse is the most common risk factor, followed by drug abuse.¹⁶ Substance abuse may be exacerbated after TBI when it becomes a coping mechanism under worsening stressors; additionally, executive function deficits or other neurologic problems may result in poor decision-making with regard to substance use.¹⁵ While substance abuse may decline in the immediate post-TBI period, it can return to pre-injury levels within a year.¹⁷

Selective serotonin reuptake inhibitors may help

Few studies have explored the efficacy of antidepressant medication in TBI survivors. In a controlled study of patients with TBI, Fann and colleagues¹⁸ found no significant improvement in depression symptoms between sertraline and a placebo. However, they did note some possibilities for this lack of significance: socially isolated TBI survivors in the placebo group may have demonstrated improvement in depression symptoms because of increased social interaction; members of both the sertraline and placebo groups had many psychosocial difficulties; and the study had a relatively small sample size. Worth noting: Subjects given sertraline did demonstrate improvement in information processing.

Continue to: Other research has found...

Other research has found that sertraline improved both depression and quality of life for men with post-TBI depression.¹⁹ In a ­meta-analysis of 4 studies, Paraschakis and Katsanos²⁰ found that sertraline demonstrated a “trend toward significance” in the treatment of depression among patients with TBI. Silverberg and Panenka²¹ argue that selective serotonin reuptake inhibitors should be used as first-line treatment for depression in survivors of TBI. They note that in non-randomized studies, treatment effects with antidepressants are significant. Additionally, patients who do not respond to the first antidepressant prescribed will often respond to adjunctive or different medications. Finally, they argue that depression measures can capture symptoms related to the physical brain injury, in addition to symptoms of depression, thus confounding results.

THE CASE

Mr. M’s chart showed that he was not taking any medication and that he had no history of substance abuse or tobacco use. He refused to fill out the Patient Health Questionnaire (PHQ)-2. His guardian said that Mr. M was spending much of his time at home, and that he used to be an avid painter and guitar player but had not engaged in either activity for months. Furthermore, Mr. M used to enjoy working out but did so rarely now.

During the interview, the PCP was careful to make eye contact with Mr. M as well as his guardian, thereby making sure Mr. M was part of the conversation about his care. Pacing of questions was deliberate and unhurried; a return visit would be scheduled to further explore any concerns not covered in this visit. This collaborative, inclusive, patient-centered approach to the clinical interview seemed to place Mr. M at ease. When his guardian said he thought Mr. M was depressed, Mr. M agreed. Although Mr. M still refused to fill out the PHQ-2, he was now willing to answer questions about depression. He acknowledged that he was feeling hopeless and took little pleasure in activities he used to enjoy, thereby indicating a positive screen for depression.

The PCP opted to read the PHQ-9 questions aloud, and Mr. M agreed with most of the items but strongly denied suicidal ideation, citing his religious faith.

The PCP determined that Mr. M’s depression was likely a combination of the direct and indirect effects of his TBI. A quantitative estimate based on Mr. M’s report yielded a PHQ-9 score of 17, indicating moderately severe depression.

Continue to: In addition to building rapport...

In addition to building rapport, careful listening garnered important information about Mr. M. For example, until his accident and subsequent depression, Mr. M had long prioritized his physical health through diet and exercise. He followed a vegetarian diet but recently had little appetite and was eating one microwaveable meal a day. He had an irregular sleep schedule and struggled with insomnia. He lost his closest long-term relationship after his accident due to difficulties with affect regulation. He also lost his job as he could no longer cognitively handle the tasks required.

Hearing Mr. M’s story provided the opportunity to customize education about self-management skills including regular diet, exercise, and sleep hygiene. Due to limited visit time, the PCP elected to use this first visit to focus on sleep and depression. As cognitive behavioral therapy (CBT) for insomnia is first-line treatment for both primary insomnia and insomnia due to a medical condition such as TBI,⁵ a sleep aid was not prescribed. Fortunately, the clinic psychologist who offered CBT was able to join the interview to meet Mr. M and explain the treatment.

Mr. M expressed some initial reluctance to try an antidepressant. However, acknowledging he “just hasn’t been the same” since his TBI, he agreed to a prescription for sertraline and said he hoped it could make him “more like [he] was.”

RETURN VISIT

Four weeks after Mr. M began taking sertraline and participating in weekly CBT sessions, he returned for a follow-up visit with his PCP. He had a noticeably brighter affect, and his guardian reported that he had been playing the guitar again. Mr. M said that he had more energy as a result of improved sleep and mood, and that he felt like his “thinking was clearer.” Mr. M noted that he never thought he would meet with a psychologist but was finding CBT for insomnia helpful.

Patients who do not respond to the first antidepressant prescribed will often respond to adjunctive or different medications.

The psychologist’s notes proposed a treatment plan that would also include targeted grief and existential therapies to address Mr. M’s sudden life changes. At this visit, Mr. M admitted that his reading comprehension and speed were negatively affected by the accident and said this is why he did not wish to fill out the PHQ-2. But he was again willing to have the PHQ-9 questions read to him with his guardian’s support. Results showed a score of 6, indicating mild depression.

A follow-up appointment with Mr. M was scheduled for 6 weeks later, and the team was confident he was getting the behavioral and mental health support he needed through medication and therapy.

CORRESPONDENCE
Elizabeth Imbesi, PhD, VA Ann Arbor Healthcare System, 2215 Fuller Road, Ann Arbor, MI 48105; [email protected]