My journey with mental illness

I am a retired advanced practice psychiatric nurse who has lived and worked on “both sides of the door.” This wording is paraphrased from psychologist and therapist Lauren Slater, PhD, who wrote about a time she went to McLean Hospital in Belmont, Massachusetts, as a therapist after staying there as a patient years earlier: “And now I am standing on the other—the wrong, I mean the right side of the door and I ring the buzzer.”¹ Here I tell my story of the physical and emotional effects of my mental illness and treatment.

Onset of bipolar disorder. My bipolar illness started with a bout of depression in 1963 at age 13, which resulted in a low-key summer of often staying inside. I received no medication, and no one sent me for evaluation. In the fall, I went back to school and finished the year without incident. I continued as a quiet, shy kid through high school in the late 1960s. In my senior year, I decided to take an overload of difficult courses and run on the varsity cross-country team. The amount and intensity of these activities were too much. This resulted in my first manic episode, which started during a weekend visit to a college I hoped to attend. I became excitable, grandiose, and had delusions. A day later, I returned home, and my parents had me admitted to a psychiatric hospital, where I remained for 3 months.

At first, my diagnosis was unclear, and initially no one considered what at the time was called manic depression. At that point, I was unaware of my extensive family psychiatric history. My pharmacologic treatment consisted of chlorpromazine, trifluoperazine, and procyclidine. I returned home just before Christmas and barely finished my senior year of high school. A good college accepted me. But during the orientation, I was asked to leave because I experienced a second manic episode. After 4 more psychiatric hospitalizations, I finally stabilized.

During one of my hospitalizations, I had the good fortune to be interviewed by Dr. Thomas Detre. During this interview, I talked expansively about Don Quixote, Aldonza, and Sancho Panza. Dr. Detre diagnosed me with manic depression, and suggested that I see Dr. Christiaan van der Velde, who was researching lithium carbonate.² In 1970, I was hospitalized at Norwich State Hospital in Preston, Connecticut and was started on lithium, even though it had not yet been FDA-approved. I responded well to lithium monotherapy.

An extensive family history. Having bipolar disorder was not something I would discuss with others because I felt ashamed. I commonly hid my medication during college, especially from my roommates or other friends. By then, I had learned a little about my family’s psychiatric history, but I knew few specifics. Over time, I became aware of a dense familial cluster of affective illness going back several generations. My maternal grandmother was hospitalized for depression in 1921 after her husband suddenly died during her fourth pregnancy. She became bereft and suicidal because she had no one to support her 4 children. During my grandmother’s hospitalization, her sister and sister’s husband took care of her children. My grandmother remained hospitalized until she died in 1943. At that time, no medications were available to treat her illness. Over the next 2 generations, 2 of her 4 children and 6 of her 12 grandchildren (including me) developed bipolar disorder.

A career and family. In 1970, I started to work as a nursing assistant, then as a nursing technician for 1.5 years in a specialty hospital in New England. In 1973, I began nursing school at a junior college. I received my RN in 1975, a BS in nursing in 1979, and an MS in psychiatric nursing in 1982. I worked steadily as a psychiatric nurse in both inpatient and outpatient settings from 1975 until I retired in 2019.

In the early 1980s, I married my first wife and had 2 wonderful children. During our courtship in 1981 and 1982, I became hypomanic, which perhaps made me more outgoing and sociable. In 1985, after my father required open heart surgery, I had a manic episode that lasted 1 week. Over the next 20 years, although I was not happy with my marriage, I remained euthymic and productive at work. My marriage ended in 2012.

Continue to: By the end of 2012...

By the end of 2012, I had been taking lithium continuously for 42 years. My laboratory tests showed peak lithium levels between 0.6 and 1.2 mmol/L. I remained otherwise healthy, as demonstrated by annual physical exams and laboratory test results. In 2015, I developed an increase in my blood pressure and my primary care physician (PCP) prescribed oral lisinopril, initially 10 mg/d, and later 10 mg twice daily. My blood pressure improved and ranged from 120/74 to 130/82 mm Hg.

Hyperparathyroidism. By 2016, my psychiatrist, PCP, and nephrologist all urged me to consider parathyroid surgery.^3-5 Hypercalcemia and hyperparathyroidism caused the most worry. Laboratory tests indicated calcium 11.2 mg/dL, parathyroid hormone (PTH) 88 pg/mL, estimated glomerular filtration rate (eGFR) 59 mL/min, and thyroid-stimulating hormone (TSH) 0.78 mIU/L. Electrocardiographysometimes showed a slight QT elongation. A right bundle branch block, which was first noted in 2015, continued. Due to my elevated calcium levels, I eliminated most calcium from my diet. My psychiatrist began to speak more strongly of parathyroid surgery. I then consulted a senior endocrinologist and a senior nephrologist, who each recommended parathyroid surgery.

I remarried in July 2016, and we moved to a different area of the country. My second wife became a stabilizing force for me. My new PCP, however, found elevated high-density lipoproteins during a routine physical examination, and started me on simvastatin, 10 mg/d. My calcium and PTH levels continued to be elevated. My PCP, nephrologist, therapist, and wife urged me to proceed with the parathyroidectomy. After a short period of watchful waiting and a second consultation with a nephrologist, I agreed to schedule a subtotal parathyroidectomy.

Surgery. In spring 2017, I began preparation for parathyroidectomy. At the time, my lithium carbonate dose was 600 mg/d, alternating with 900 mg/d. My peak level of lithium was 0.6 mmol/L. Lisinopril is synergistic, which allowed me to take a smaller effective dose of lithium.

My parathyroid surgery occurred on June 28, 2017 at Norman Parathyroid Center in Tampa, Florida.⁶ The surgeon recorded my parathyroid glands as 136, 602, and 348 units using a measure developed at Norman Parathyroid Center. No reading was given for my fourth parathyroid gland, which they did not remove. Following the surgery, I resumed my previous functions, including employment as a visiting nurse. I initially took calcium supplements after surgery, and my lithium dose was reduced to 300 mg orally, twice daily, which I have continued. I have remained euthymic. On August 3, 2017 my laboratory workup showed an eGFR of 64 mL/min, calcium 10.0 mg/dL, and PTH 17 pg/mL. Vitamin D25 OH 33, glucose, BUN/Cr, electrolytes, complete blood count, and albumin were all within normal limits. Repeat bloodwork on September 19, 2017 showed Ca⁺⁺ 10.1 mg/dL and PTH 18 pg/mL. Nine months after the surgery, I showed an incredibly positive physical and mental response, which has continued to this day.

Continue to: Clinical implications

Clinical implications. This is a single case study. However, it is important for clinicians treating patients with lithium carbonate to regularly order laboratory testing, including for lithium levels, PTH, and calcium, to detect early signs of complications from treatment, including hyperparathyroidism and hypercalcemia.⁷ These levels could be obtained every 6 months. If a patient’s PTH levels are >70 pg/mL and calcium levels are >11.0 mg/dL, it would be prudent to refer him/her for further medical evaluation. Additionally, it would be helpful to counsel the patient about considering alternative medication and adjunct mental health treatment. At some future point, it could be useful for the clinician and his/her patient to explore the idea of parathyroid surgery.

In addition to chronic lithium use, other causes of hyperparathyroidism include an adenoma on a gland, hyperplasia of ≥2 parathyroid glands, a malignant tumor, severe calcium deficiency, severe vitamin D deficiency, chronic renal failure, and (rarely) an inherited gene that causes hyperparathyroidism.

How I’m doing today. Currently, I am euthymic and in a happy marriage. My laboratory workup in May 2020 included glucose 107 mg/dL, Ca⁺⁺ 9.5 mg/dL, eGFR 61 mL/min, PTH 32 pg/mL, lithium 0.3 mmol/L (300 mg twice daily), and TSH 1.79 mIU/L. A comprehensive metabolic panel, complete blood count, and lipid panel were all within normal limits.

I am fortunate to continue having excellent care provided by my PCP, nephrologist, urologist, and psychiatric APRN. Together with these wonderful professionals, I have been able to maintain my physical and mental health.

Acknowledgment: I gratefully acknowledge the help and skills of Robin Scharak and Gary Blake for providing some of the editing on this article.

Bill Greenberg MS, RN, APRN
Delray Beach, Florida

I am a retired advanced practice psychiatric nurse who has lived and worked on “both sides of the door.” This wording is paraphrased from psychologist and therapist Lauren Slater, PhD, who wrote about a time she went to McLean Hospital in Belmont, Massachusetts, as a therapist after staying there as a patient years earlier: “And now I am standing on the other—the wrong, I mean the right side of the door and I ring the buzzer.”¹ Here I tell my story of the physical and emotional effects of my mental illness and treatment.

Onset of bipolar disorder. My bipolar illness started with a bout of depression in 1963 at age 13, which resulted in a low-key summer of often staying inside. I received no medication, and no one sent me for evaluation. In the fall, I went back to school and finished the year without incident. I continued as a quiet, shy kid through high school in the late 1960s. In my senior year, I decided to take an overload of difficult courses and run on the varsity cross-country team. The amount and intensity of these activities were too much. This resulted in my first manic episode, which started during a weekend visit to a college I hoped to attend. I became excitable, grandiose, and had delusions. A day later, I returned home, and my parents had me admitted to a psychiatric hospital, where I remained for 3 months.

At first, my diagnosis was unclear, and initially no one considered what at the time was called manic depression. At that point, I was unaware of my extensive family psychiatric history. My pharmacologic treatment consisted of chlorpromazine, trifluoperazine, and procyclidine. I returned home just before Christmas and barely finished my senior year of high school. A good college accepted me. But during the orientation, I was asked to leave because I experienced a second manic episode. After 4 more psychiatric hospitalizations, I finally stabilized.

During one of my hospitalizations, I had the good fortune to be interviewed by Dr. Thomas Detre. During this interview, I talked expansively about Don Quixote, Aldonza, and Sancho Panza. Dr. Detre diagnosed me with manic depression, and suggested that I see Dr. Christiaan van der Velde, who was researching lithium carbonate.² In 1970, I was hospitalized at Norwich State Hospital in Preston, Connecticut and was started on lithium, even though it had not yet been FDA-approved. I responded well to lithium monotherapy.

An extensive family history. Having bipolar disorder was not something I would discuss with others because I felt ashamed. I commonly hid my medication during college, especially from my roommates or other friends. By then, I had learned a little about my family’s psychiatric history, but I knew few specifics. Over time, I became aware of a dense familial cluster of affective illness going back several generations. My maternal grandmother was hospitalized for depression in 1921 after her husband suddenly died during her fourth pregnancy. She became bereft and suicidal because she had no one to support her 4 children. During my grandmother’s hospitalization, her sister and sister’s husband took care of her children. My grandmother remained hospitalized until she died in 1943. At that time, no medications were available to treat her illness. Over the next 2 generations, 2 of her 4 children and 6 of her 12 grandchildren (including me) developed bipolar disorder.

A career and family. In 1970, I started to work as a nursing assistant, then as a nursing technician for 1.5 years in a specialty hospital in New England. In 1973, I began nursing school at a junior college. I received my RN in 1975, a BS in nursing in 1979, and an MS in psychiatric nursing in 1982. I worked steadily as a psychiatric nurse in both inpatient and outpatient settings from 1975 until I retired in 2019.

In the early 1980s, I married my first wife and had 2 wonderful children. During our courtship in 1981 and 1982, I became hypomanic, which perhaps made me more outgoing and sociable. In 1985, after my father required open heart surgery, I had a manic episode that lasted 1 week. Over the next 20 years, although I was not happy with my marriage, I remained euthymic and productive at work. My marriage ended in 2012.

Continue to: By the end of 2012...

By the end of 2012, I had been taking lithium continuously for 42 years. My laboratory tests showed peak lithium levels between 0.6 and 1.2 mmol/L. I remained otherwise healthy, as demonstrated by annual physical exams and laboratory test results. In 2015, I developed an increase in my blood pressure and my primary care physician (PCP) prescribed oral lisinopril, initially 10 mg/d, and later 10 mg twice daily. My blood pressure improved and ranged from 120/74 to 130/82 mm Hg.

Hyperparathyroidism. By 2016, my psychiatrist, PCP, and nephrologist all urged me to consider parathyroid surgery.^3-5 Hypercalcemia and hyperparathyroidism caused the most worry. Laboratory tests indicated calcium 11.2 mg/dL, parathyroid hormone (PTH) 88 pg/mL, estimated glomerular filtration rate (eGFR) 59 mL/min, and thyroid-stimulating hormone (TSH) 0.78 mIU/L. Electrocardiographysometimes showed a slight QT elongation. A right bundle branch block, which was first noted in 2015, continued. Due to my elevated calcium levels, I eliminated most calcium from my diet. My psychiatrist began to speak more strongly of parathyroid surgery. I then consulted a senior endocrinologist and a senior nephrologist, who each recommended parathyroid surgery.

I remarried in July 2016, and we moved to a different area of the country. My second wife became a stabilizing force for me. My new PCP, however, found elevated high-density lipoproteins during a routine physical examination, and started me on simvastatin, 10 mg/d. My calcium and PTH levels continued to be elevated. My PCP, nephrologist, therapist, and wife urged me to proceed with the parathyroidectomy. After a short period of watchful waiting and a second consultation with a nephrologist, I agreed to schedule a subtotal parathyroidectomy.

Surgery. In spring 2017, I began preparation for parathyroidectomy. At the time, my lithium carbonate dose was 600 mg/d, alternating with 900 mg/d. My peak level of lithium was 0.6 mmol/L. Lisinopril is synergistic, which allowed me to take a smaller effective dose of lithium.

My parathyroid surgery occurred on June 28, 2017 at Norman Parathyroid Center in Tampa, Florida.⁶ The surgeon recorded my parathyroid glands as 136, 602, and 348 units using a measure developed at Norman Parathyroid Center. No reading was given for my fourth parathyroid gland, which they did not remove. Following the surgery, I resumed my previous functions, including employment as a visiting nurse. I initially took calcium supplements after surgery, and my lithium dose was reduced to 300 mg orally, twice daily, which I have continued. I have remained euthymic. On August 3, 2017 my laboratory workup showed an eGFR of 64 mL/min, calcium 10.0 mg/dL, and PTH 17 pg/mL. Vitamin D25 OH 33, glucose, BUN/Cr, electrolytes, complete blood count, and albumin were all within normal limits. Repeat bloodwork on September 19, 2017 showed Ca⁺⁺ 10.1 mg/dL and PTH 18 pg/mL. Nine months after the surgery, I showed an incredibly positive physical and mental response, which has continued to this day.

Continue to: Clinical implications

Clinical implications. This is a single case study. However, it is important for clinicians treating patients with lithium carbonate to regularly order laboratory testing, including for lithium levels, PTH, and calcium, to detect early signs of complications from treatment, including hyperparathyroidism and hypercalcemia.⁷ These levels could be obtained every 6 months. If a patient’s PTH levels are >70 pg/mL and calcium levels are >11.0 mg/dL, it would be prudent to refer him/her for further medical evaluation. Additionally, it would be helpful to counsel the patient about considering alternative medication and adjunct mental health treatment. At some future point, it could be useful for the clinician and his/her patient to explore the idea of parathyroid surgery.

In addition to chronic lithium use, other causes of hyperparathyroidism include an adenoma on a gland, hyperplasia of ≥2 parathyroid glands, a malignant tumor, severe calcium deficiency, severe vitamin D deficiency, chronic renal failure, and (rarely) an inherited gene that causes hyperparathyroidism.

How I’m doing today. Currently, I am euthymic and in a happy marriage. My laboratory workup in May 2020 included glucose 107 mg/dL, Ca⁺⁺ 9.5 mg/dL, eGFR 61 mL/min, PTH 32 pg/mL, lithium 0.3 mmol/L (300 mg twice daily), and TSH 1.79 mIU/L. A comprehensive metabolic panel, complete blood count, and lipid panel were all within normal limits.

I am fortunate to continue having excellent care provided by my PCP, nephrologist, urologist, and psychiatric APRN. Together with these wonderful professionals, I have been able to maintain my physical and mental health.

Acknowledgment: I gratefully acknowledge the help and skills of Robin Scharak and Gary Blake for providing some of the editing on this article.

Bill Greenberg MS, RN, APRN
Delray Beach, Florida

I am a retired advanced practice psychiatric nurse who has lived and worked on “both sides of the door.” This wording is paraphrased from psychologist and therapist Lauren Slater, PhD, who wrote about a time she went to McLean Hospital in Belmont, Massachusetts, as a therapist after staying there as a patient years earlier: “And now I am standing on the other—the wrong, I mean the right side of the door and I ring the buzzer.”¹ Here I tell my story of the physical and emotional effects of my mental illness and treatment.

Onset of bipolar disorder. My bipolar illness started with a bout of depression in 1963 at age 13, which resulted in a low-key summer of often staying inside. I received no medication, and no one sent me for evaluation. In the fall, I went back to school and finished the year without incident. I continued as a quiet, shy kid through high school in the late 1960s. In my senior year, I decided to take an overload of difficult courses and run on the varsity cross-country team. The amount and intensity of these activities were too much. This resulted in my first manic episode, which started during a weekend visit to a college I hoped to attend. I became excitable, grandiose, and had delusions. A day later, I returned home, and my parents had me admitted to a psychiatric hospital, where I remained for 3 months.

At first, my diagnosis was unclear, and initially no one considered what at the time was called manic depression. At that point, I was unaware of my extensive family psychiatric history. My pharmacologic treatment consisted of chlorpromazine, trifluoperazine, and procyclidine. I returned home just before Christmas and barely finished my senior year of high school. A good college accepted me. But during the orientation, I was asked to leave because I experienced a second manic episode. After 4 more psychiatric hospitalizations, I finally stabilized.

During one of my hospitalizations, I had the good fortune to be interviewed by Dr. Thomas Detre. During this interview, I talked expansively about Don Quixote, Aldonza, and Sancho Panza. Dr. Detre diagnosed me with manic depression, and suggested that I see Dr. Christiaan van der Velde, who was researching lithium carbonate.² In 1970, I was hospitalized at Norwich State Hospital in Preston, Connecticut and was started on lithium, even though it had not yet been FDA-approved. I responded well to lithium monotherapy.

An extensive family history. Having bipolar disorder was not something I would discuss with others because I felt ashamed. I commonly hid my medication during college, especially from my roommates or other friends. By then, I had learned a little about my family’s psychiatric history, but I knew few specifics. Over time, I became aware of a dense familial cluster of affective illness going back several generations. My maternal grandmother was hospitalized for depression in 1921 after her husband suddenly died during her fourth pregnancy. She became bereft and suicidal because she had no one to support her 4 children. During my grandmother’s hospitalization, her sister and sister’s husband took care of her children. My grandmother remained hospitalized until she died in 1943. At that time, no medications were available to treat her illness. Over the next 2 generations, 2 of her 4 children and 6 of her 12 grandchildren (including me) developed bipolar disorder.

A career and family. In 1970, I started to work as a nursing assistant, then as a nursing technician for 1.5 years in a specialty hospital in New England. In 1973, I began nursing school at a junior college. I received my RN in 1975, a BS in nursing in 1979, and an MS in psychiatric nursing in 1982. I worked steadily as a psychiatric nurse in both inpatient and outpatient settings from 1975 until I retired in 2019.

In the early 1980s, I married my first wife and had 2 wonderful children. During our courtship in 1981 and 1982, I became hypomanic, which perhaps made me more outgoing and sociable. In 1985, after my father required open heart surgery, I had a manic episode that lasted 1 week. Over the next 20 years, although I was not happy with my marriage, I remained euthymic and productive at work. My marriage ended in 2012.

Continue to: By the end of 2012...

By the end of 2012, I had been taking lithium continuously for 42 years. My laboratory tests showed peak lithium levels between 0.6 and 1.2 mmol/L. I remained otherwise healthy, as demonstrated by annual physical exams and laboratory test results. In 2015, I developed an increase in my blood pressure and my primary care physician (PCP) prescribed oral lisinopril, initially 10 mg/d, and later 10 mg twice daily. My blood pressure improved and ranged from 120/74 to 130/82 mm Hg.

Hyperparathyroidism. By 2016, my psychiatrist, PCP, and nephrologist all urged me to consider parathyroid surgery.^3-5 Hypercalcemia and hyperparathyroidism caused the most worry. Laboratory tests indicated calcium 11.2 mg/dL, parathyroid hormone (PTH) 88 pg/mL, estimated glomerular filtration rate (eGFR) 59 mL/min, and thyroid-stimulating hormone (TSH) 0.78 mIU/L. Electrocardiographysometimes showed a slight QT elongation. A right bundle branch block, which was first noted in 2015, continued. Due to my elevated calcium levels, I eliminated most calcium from my diet. My psychiatrist began to speak more strongly of parathyroid surgery. I then consulted a senior endocrinologist and a senior nephrologist, who each recommended parathyroid surgery.

I remarried in July 2016, and we moved to a different area of the country. My second wife became a stabilizing force for me. My new PCP, however, found elevated high-density lipoproteins during a routine physical examination, and started me on simvastatin, 10 mg/d. My calcium and PTH levels continued to be elevated. My PCP, nephrologist, therapist, and wife urged me to proceed with the parathyroidectomy. After a short period of watchful waiting and a second consultation with a nephrologist, I agreed to schedule a subtotal parathyroidectomy.

Surgery. In spring 2017, I began preparation for parathyroidectomy. At the time, my lithium carbonate dose was 600 mg/d, alternating with 900 mg/d. My peak level of lithium was 0.6 mmol/L. Lisinopril is synergistic, which allowed me to take a smaller effective dose of lithium.

My parathyroid surgery occurred on June 28, 2017 at Norman Parathyroid Center in Tampa, Florida.⁶ The surgeon recorded my parathyroid glands as 136, 602, and 348 units using a measure developed at Norman Parathyroid Center. No reading was given for my fourth parathyroid gland, which they did not remove. Following the surgery, I resumed my previous functions, including employment as a visiting nurse. I initially took calcium supplements after surgery, and my lithium dose was reduced to 300 mg orally, twice daily, which I have continued. I have remained euthymic. On August 3, 2017 my laboratory workup showed an eGFR of 64 mL/min, calcium 10.0 mg/dL, and PTH 17 pg/mL. Vitamin D25 OH 33, glucose, BUN/Cr, electrolytes, complete blood count, and albumin were all within normal limits. Repeat bloodwork on September 19, 2017 showed Ca⁺⁺ 10.1 mg/dL and PTH 18 pg/mL. Nine months after the surgery, I showed an incredibly positive physical and mental response, which has continued to this day.

Continue to: Clinical implications

Clinical implications. This is a single case study. However, it is important for clinicians treating patients with lithium carbonate to regularly order laboratory testing, including for lithium levels, PTH, and calcium, to detect early signs of complications from treatment, including hyperparathyroidism and hypercalcemia.⁷ These levels could be obtained every 6 months. If a patient’s PTH levels are >70 pg/mL and calcium levels are >11.0 mg/dL, it would be prudent to refer him/her for further medical evaluation. Additionally, it would be helpful to counsel the patient about considering alternative medication and adjunct mental health treatment. At some future point, it could be useful for the clinician and his/her patient to explore the idea of parathyroid surgery.

In addition to chronic lithium use, other causes of hyperparathyroidism include an adenoma on a gland, hyperplasia of ≥2 parathyroid glands, a malignant tumor, severe calcium deficiency, severe vitamin D deficiency, chronic renal failure, and (rarely) an inherited gene that causes hyperparathyroidism.

How I’m doing today. Currently, I am euthymic and in a happy marriage. My laboratory workup in May 2020 included glucose 107 mg/dL, Ca⁺⁺ 9.5 mg/dL, eGFR 61 mL/min, PTH 32 pg/mL, lithium 0.3 mmol/L (300 mg twice daily), and TSH 1.79 mIU/L. A comprehensive metabolic panel, complete blood count, and lipid panel were all within normal limits.

I am fortunate to continue having excellent care provided by my PCP, nephrologist, urologist, and psychiatric APRN. Together with these wonderful professionals, I have been able to maintain my physical and mental health.

Acknowledgment: I gratefully acknowledge the help and skills of Robin Scharak and Gary Blake for providing some of the editing on this article.

Bill Greenberg MS, RN, APRN
Delray Beach, Florida