There was no medical/family history of bronchial asthma or epilepsy for either patient. On admission, the body mass index (BMI) values of patients 1 and 2 were 20.1 and 17.8, respectively. We performed several medical examinations, such as blood tests, chest X-ray, echocardiogram, electrocardiogram, and cephalic CT, to rule out organic diseases that could cause hyperventilation. There were no abnormalities in the blood test results of either patient(WBC: 4800/μL and 5200/μL, Hb: 13.1 g/dL and 11.3 g/dL, platelet: 20.1 × 10
4/μL and 28.9 × 10
4/μL, AST: 23 IU/L and 18, ALT: 13 IU/L and 17 IU/L,s-AMY: 66 IU/L and 97 IU/L,CRP: none and o.1 mg/dL, creatinine: 0.7 mg/dL and o.9 mg/dL, Na: 143 mEq/L and 141 mEq/L, K: 3.9 mEq/L and 4.3 mEq/L, fT
4: 1.2 ng/dL and i.0 ng/dL, fT
3: 1.2 pg/dL and 3.3 pg/dL,TSH: 0.41 μIU/mL and 1.08 μIU/mL). There were no abnormal findings in the chest X-ray, electrocardiogram, echocardiogram, or cephalic CT, so lung, heart and brain disease were ruled out. A hyperventilation attack was identified based on respiration that obviously exceeded the usual breathing rate (about 12 to 20 breaths per minute) and clinical symptoms such as tetany. A physician used a stethoscope to confirm that there were no airway stenosis sounds or abnormal alveolar sounds. We could not analyze arterial blood-gas to prove hypocapnia because the hospital did not possess the device needed to perform this analysis. Neither patient presented with hypoxemia during the hyperventilation attacks or normal respiration. Therefore, the possibility of a hyperventilation attack being caused by other disorders was ruled out. Although the arterial PCO
2 level was not measured for either patient, the clinical presentation left little doubt that over-breathing resulted in HVS. To examine the psychological aspects, the Minnesota multiphasic personality inventory(MMPI)was performed. The MMPI showed high scores of Hs: 30, D: 48 and Hy: 33 for Patient 1 and Sc: 54, Pt: 49 and D:35 for Patient 2. These data suggest a depressive state for both patients, namely anxiety about her physical symptoms by Patient 1 and unreasonable fears or anxiety and obsessions by Patient 2. In both patients, some stressors were present prior to the hyperventilation attacks. In case 1, acute tonsillitis induced the hyperventilation attacks, which occurred frequently and increased her anxiety level. Immediately on hospitalization, she developed frequent hyperventilation attacks before fasting therapy [
14,
15] was begun. She agreed to undergo fasting therapy but had considerable anxiety over receiving the therapy. Hospitalization and anxiety about the fasting therapy became the stressors and triggers of her hyperventilation attacks after admission to the hospital. In case 2, a co-worker’s visit to her in the hospital evoked memories of the sexual harassment in the office and induced hyperventilation attacks. Both cases were diagnosed with HVS because they had preceding stressors and no organic abnormalities that could cause hyperventilation attacks.