Medical Leadership in Inpatient Rehabilitation Facilities in the United States.

OBJECTIVE: Inpatient rehabilitation facilities treat patients with extensive postacute care rehabilitation needs. Physiatrists are uniquely trained in the complexities of such patients; however, not all inpatient rehabilitation facilities use physiatrists as medical leadership. This study identifies the training background and credentials of medical directors in all inpatient rehabilitation facilities within the United States. DESIGN: Using Internet search, e-mail, and telephone communication, the following data were collected: medical director credential and specialty information, board certification rates and years of practice experience, as well as bed numbers for each inpatient rehabilitation facilities listed on The Centers for Medicare and Medicaid Services Website. Data were collected between November 2019 and November 2020. RESULTS: Of the 1114 open facilities, 85% have medical directors with a doctor of medicine degree, while 13% have a doctor of osteopathic medicine degree. Two percent reported no physician medical director. Physiatry is the most common specialty (80%), followed by internal medicine, family medicine, neurology, orthopedic surgery, general surgery, and medicine/pediatrics. The mean number of beds per facility is 35.6 (median, 24; range, 4-350). There is an average of 11.4 inpatient rehabilitation facility beds per 100,000 people nationally. CONCLUSIONS: Physiatry is the predominant specialty to fulfill medical leadership at inpatient rehabilitation facilities, although there remains room for growth. In addition, doctor of medicine degrees greatly outnumber doctor of osteopathic medicine degrees in medical leadership.

Patient Sleep Quality in Acute Inpatient Rehabilitation.

BACKGROUND: Sleep is an important component of neurorehabilitation. This study evaluates sleep quality in the acute inpatient rehabilitation setting and is the first to compare sleep quality in acute rehabilitation versus the acute care hospital and home settings. OBJECTIVE: To assess patient sleep quality in the acute inpatient rehabilitation setting. DESIGN: Cross-sectional survey study. SETTING: Acute inpatient rehabilitation unit. PATIENTS: Seventy-three patients admitted to the acute rehabilitation unit participated in the study. INTERVENTIONS: A validated sleep questionnaire was provided on admission regarding sleep at home and in the acute care hospital. The questionnaire was repeated on discharge from the acute rehabilitation unit regarding sleep during their rehabilitation admission. MAIN OUTCOME MEASURES: Visual analog scale of sleep depth, falling asleep, number of awakenings, percentage of time awake, and quality of sleep were obtained through use of the Richards-Campbell Sleep Questionnaire. These values were averaged to obtain "overall sleep perception." An additional question on environmental noise was added. Scores ranged from 0 for "worst sleep possible" to 100 for "best sleep possible." RESULTS: Patients reported significantly better sleep in all domains and overall in the acute rehabilitation unit compared to the acute care hospital, with the exception of percentage of time awake. Patients also reported significantly better sleep depth but worse noise in the acute rehabilitation unit when compared to home. Similarly, patients reported significantly better sleep in all domains and overall at home in comparison to the acute care hospital with the exception of percentage of time awake. CONCLUSIONS: Patient in the acute rehabilitation unit experience sleep quality that matches their experience at home and exceeds that in the hospital.

Combined deficiency of dystrophin and beta1 integrin in the cardiac myocyte causes myocardial dysfunction, fibrosis and calcification.

The dystrophin-glycoprotein complex is a large complex of membrane-associated proteins linking the cytoskeleton to the extracellular matrix in muscle. Transmembrane heterodimeric (alphabeta) integrins serve also as cellular adhesion molecules and mechanotransducers. In the animal model for Duchenne muscular dystrophy, the mdx mouse, loss of dystrophin causes more severe abnormalities in skeletal than in cardiac muscle. We hypothesized that ablation of cardiac myocyte integrins in the mdx background would lead to a severe cardiomyopathic phenotype. Mdx mice were crossed to ones with cardiac myocyte-specific deletion of beta1 integrin (beta1KO) to generate beta1KOmdx. Unstressed beta1KOmdx mice were viable and had normal cardiac function; however, high mortality was seen in peri- and postpartum females by 6 months of age, when severe myocardial necrosis and fibrosis and extensive dystrophic calcification was seen. Decreased ventricular function and blunted adrenergic responsiveness was found in the beta1KOmdx mice compared with control (Lox/Lox, no Cre), beta1KO, and mdx. Similarly, adult beta1KOmdx males were more prone to isoproterenol-induced heart failure and death compared with control groups. Given the extensive calcification, we analyzed transcript levels of genes linked to fibrosis and calcification and found matrix gamma-carboxyglutamic acid protein, decorin, periostin, and the osteoblast transcription factor Runx2/Cbfa1 significantly increased in beta1KOmdx cardiac muscle. Our data show that combined deficiency of dystrophin and integrins in murine cardiac myocytes results in more severe cardiomyopathic changes in the stressed myocardium than reduction of either dystrophin or integrins alone and predisposes to myocardial calcification.