Periodic Catatonia Marked by Hypercortisolemia and Exacerbated by the Menses: A Case Report and Literature Review

Kahlbaum first described catatonia; later Kraepelin, Gjessing, and Leonhard each defined periodic catatonia differently. A 48-year-old female with catatonia, whose grandmother probably died from it, was prospectively followed for \u3e4 years in a US psychiatric state hospital. Through 4 catatonic episodes (one lasting 17 months) there were menstrual exacerbations of catatonia and increases in 4 biological variables: (1) creatine kinase (CK) up to 4,920 U/L, (2) lactate dehydrogenase (LDH) up to 424 U/L, (3) late afternoon cortisol levels up to 28.0 mcg/dL, and (4) white blood cell (WBC) counts up to 24,200/mm3 with neutrophilia without infections. Records from 17 prior admissions documented elevations of WBC and LDH and included an abnormal dexamethasone suppression test (DST) which normalized with electroconvulsive therapy. Two later admissions showed CK and WBC elevations. We propose that these abnormalities reflect different aspects of catatonic biology: (1) the serum CK, the severity of muscle damage probably exacerbated by the menses; (2) the hypercortisolemia, the associated fear; (3) the leukocytosis with neutrophilia, the hypercortisolemia; and (4) the LDH elevations, which appear to be influenced by other biological abnormalities. Twentieth-century literature was reviewed for (1) menstrual exacerbations of catatonia, (2) biological abnormalities related to periodic catatonia, and (3) familial periodic catatonia

Periodic Catatonia Marked by Hypercortisolemia and Exacerbated by the Menses: A Case Report and Literature Review

Kahlbaum first described catatonia; later Kraepelin, Gjessing, and Leonhard each defined periodic catatonia differently. A 48-year-old female with catatonia, whose grandmother probably died from it, was prospectively followed for >4 years in a US psychiatric state hospital. Through 4 catatonic episodes (one lasting 17 months) there were menstrual exacerbations of catatonia and increases in 4 biological variables: (1) creatine kinase (CK) up to 4,920 U/L, (2) lactate dehydrogenase (LDH) up to 424 U/L, (3) late afternoon cortisol levels up to 28.0 mcg/dL, and (4) white blood cell (WBC) counts up to 24,200/mm3 with neutrophilia without infections. Records from 17 prior admissions documented elevations of WBC and LDH and included an abnormal dexamethasone suppression test (DST) which normalized with electroconvulsive therapy. Two later admissions showed CK and WBC elevations. We propose that these abnormalities reflect different aspects of catatonic biology: (1) the serum CK, the severity of muscle damage probably exacerbated by the menses; (2) the hypercortisolemia, the associated fear; (3) the leukocytosis with neutrophilia, the hypercortisolemia; and (4) the LDH elevations, which appear to be influenced by other biological abnormalities. Twentieth-century literature was reviewed for (1) menstrual exacerbations of catatonia, (2) biological abnormalities related to periodic catatonia, and (3) familial periodic catatonia