TBI and growth hormone

In response to “Traumatic brain injury: Pharmacotherapy options for cognitive deficits” (Med/Psych Update, Current Psychiatry, February 2011, p. 21-37), traumatic brain injury (TBI) has been recognized as a risk factor for cognitive impairment, but TBI also has been shown to be a risk factor for hypopituitarism, presenting most frequently with growth hormone deficiency (GHD). GHD is associated not only with changes in body composition but also with impaired quality of life, cognitive dysfunctions, and psychiatric sequelae, usually classified as “depression.”

In a case study we evaluated the impact of GH therapy on the mental status of TBI patients.¹ Psychiatric and cognitive functions were tested in 6 GHD patients at baseline (minimum 3 years after TBI) and reassessed after 6 months of GH therapy and 12 months after discontinuing GH therapy. Psychiatric and cognitive examinations included semi-structured interviews and 3 instruments: Symptom Checklist-90-Revised, Zung Depression Inventory, and a standard composite neuropsychological battery.

Our results showed that 6 months of GH therapy in GHD TBI patients improved cognitive abilities (particularly verbal and nonverbal memory) and significantly improved psychiatric functioning. Depression severity decreased, as did intensity of interpersonal sensitivity, hostility, paranoid ideation, anxiety, and psychoticism. Somatization, obsessive-compulsive symptoms, and phobic anxiety decreased in all but 1 patient. In 3 GHD patients who stopped GH therapy for 12 months, we observed worsening verbal and nonverbal memory, interpersonal sensitivity, anxiety, and paranoid ideation. Thus, GHD might be associated with affective and cognitive symptoms in TBI patients and GH replacement therapy could be beneficial. Screening for pituitary dysfunction in TBI patients is strongly recommended, particularly in presence of cognitive and affective symptoms.

Nadja Maric, MD, PhD
Associate Professor
Head of Department for Research and Early
Interventions in Psychiatry
Clinic for Psychiatry, Clinical Centre of Serbia
University of Belgrade School of Medicine
Belgrade, Serbia

In response to “Traumatic brain injury: Pharmacotherapy options for cognitive deficits” (Med/Psych Update, Current Psychiatry, February 2011, p. 21-37), traumatic brain injury (TBI) has been recognized as a risk factor for cognitive impairment, but TBI also has been shown to be a risk factor for hypopituitarism, presenting most frequently with growth hormone deficiency (GHD). GHD is associated not only with changes in body composition but also with impaired quality of life, cognitive dysfunctions, and psychiatric sequelae, usually classified as “depression.”

In a case study we evaluated the impact of GH therapy on the mental status of TBI patients.¹ Psychiatric and cognitive functions were tested in 6 GHD patients at baseline (minimum 3 years after TBI) and reassessed after 6 months of GH therapy and 12 months after discontinuing GH therapy. Psychiatric and cognitive examinations included semi-structured interviews and 3 instruments: Symptom Checklist-90-Revised, Zung Depression Inventory, and a standard composite neuropsychological battery.

Our results showed that 6 months of GH therapy in GHD TBI patients improved cognitive abilities (particularly verbal and nonverbal memory) and significantly improved psychiatric functioning. Depression severity decreased, as did intensity of interpersonal sensitivity, hostility, paranoid ideation, anxiety, and psychoticism. Somatization, obsessive-compulsive symptoms, and phobic anxiety decreased in all but 1 patient. In 3 GHD patients who stopped GH therapy for 12 months, we observed worsening verbal and nonverbal memory, interpersonal sensitivity, anxiety, and paranoid ideation. Thus, GHD might be associated with affective and cognitive symptoms in TBI patients and GH replacement therapy could be beneficial. Screening for pituitary dysfunction in TBI patients is strongly recommended, particularly in presence of cognitive and affective symptoms.

Nadja Maric, MD, PhD
Associate Professor
Head of Department for Research and Early
Interventions in Psychiatry
Clinic for Psychiatry, Clinical Centre of Serbia
University of Belgrade School of Medicine
Belgrade, Serbia

In response to “Traumatic brain injury: Pharmacotherapy options for cognitive deficits” (Med/Psych Update, Current Psychiatry, February 2011, p. 21-37), traumatic brain injury (TBI) has been recognized as a risk factor for cognitive impairment, but TBI also has been shown to be a risk factor for hypopituitarism, presenting most frequently with growth hormone deficiency (GHD). GHD is associated not only with changes in body composition but also with impaired quality of life, cognitive dysfunctions, and psychiatric sequelae, usually classified as “depression.”

In a case study we evaluated the impact of GH therapy on the mental status of TBI patients.¹ Psychiatric and cognitive functions were tested in 6 GHD patients at baseline (minimum 3 years after TBI) and reassessed after 6 months of GH therapy and 12 months after discontinuing GH therapy. Psychiatric and cognitive examinations included semi-structured interviews and 3 instruments: Symptom Checklist-90-Revised, Zung Depression Inventory, and a standard composite neuropsychological battery.

Our results showed that 6 months of GH therapy in GHD TBI patients improved cognitive abilities (particularly verbal and nonverbal memory) and significantly improved psychiatric functioning. Depression severity decreased, as did intensity of interpersonal sensitivity, hostility, paranoid ideation, anxiety, and psychoticism. Somatization, obsessive-compulsive symptoms, and phobic anxiety decreased in all but 1 patient. In 3 GHD patients who stopped GH therapy for 12 months, we observed worsening verbal and nonverbal memory, interpersonal sensitivity, anxiety, and paranoid ideation. Thus, GHD might be associated with affective and cognitive symptoms in TBI patients and GH replacement therapy could be beneficial. Screening for pituitary dysfunction in TBI patients is strongly recommended, particularly in presence of cognitive and affective symptoms.

Nadja Maric, MD, PhD
Associate Professor
Head of Department for Research and Early
Interventions in Psychiatry
Clinic for Psychiatry, Clinical Centre of Serbia
University of Belgrade School of Medicine
Belgrade, Serbia