Vocal cord dysfunction (VCD) is a respiratory condition characterized by adduction of the vocal cords with resultant airflow limitation at the level of the larynx. Previously, this condition was described in case reports and in small series. This study reviews all patients hospitalized from 1984 through 1991 in whom VCD was diagnosed. Demographic, historical, physiologic, laboratory, and psychiatric factors were statistically analyzed. Ninety-five patients met the criteria for proved VCD; of these, 53 also had asthma. All patients had laryngoscopic evidence of paradoxical vocal cord motion, with inspiratory and/or early expiratory vocal cord adduction. The patients with VCD without asthma were predominantly young women. In these patients, asthma had been misdiagnosed for an average of 4.8 years. Their medications were identical to those of a control group of patients with severe asthma. Thirty-four of the 42 patients with VCD without asthma were receiving prednisone regularly at an average daily dose of 29.2 mg. Medical utilization was enormous with the VCD group, averaging 9.7 emergency room visits and 5.9 admissions in the year prior to presentation. Also, 28% of the patients with VCD had been intubated. We conclude that VCD can masquerade as asthma and that it often coexists with asthma. This study helps to define the historical and clinical features of VCD.

The pathology of disseminated Mycobacterium avium-intracellulare (MAI) was studied in 20 specimens from 11 patients. The patients ranged from 28 to 65 years and included 8 immunosuppressed and 3 immunocompetent hosts. Specimens of lymph node (five), spleen (one), liver (four), bone (three), pulmonary tissue (three), skin (three), and an aortic aneurysm were included. All cultured specimens grew MAI, but only two-thirds of these showed acid-fast bacilli (AFB) on staining. Some tissues (liver, spleen) showed granulomas similar to those seen in tuberculosis. Other tissues (skin, bone, bronchus) showed necrotizing acute and chronic inflammation with histiocytes but no definite granulomas. Lymph nodes showed a variety of nonnecrotizing and necrotizing granulomatous lesions. In skin, bone, and some lymph nodes, MAI infection appears to be histopathologically distinguishable from tuberculosis. The cases reported here are distinct from those reported in some children and patients with the acquired immunodeficiency syndrome who have massive histiocytic infiltrates with innumerable intracellular AFB. This difference may be due to a specific defect in host response involving T-cell macrophage interaction.

Thirteen cases of disseminated Mycobacterium avium-intracellulare (MAI), representing a total of 27 bone marrow specimens, were studied. The patients ranged from 25 to 46 years of age and included ten immunocompromised and three immunocompetent hosts. Peripheral blood findings included anemia in all patients, leukopenia in 73%, thrombocytopenia in 45%, and pancytopenia in 45%. Fourteen of the specimens (52%) showed granulomas ranging from small, subtle lymphohistiocytic aggregates to larger lymphohistiocytic lesions and clusters of epithelioid histiocytes; almost half of these lesions were missed initially. Rare acid-fast bacilli were seen in only one case, but 53% grew MAI on culture. In one case of the acquired immunodeficiency syndrome, culture was positive in the absence of inflammation or AFB on staining. These findings are not significantly different from those reported in disseminated Mycobacterium tuberculosis infection.