Stroke is the leading cause of serious long-term disability in the US, leaving less than half of survivors able to return directly home. 1 Stroke recurrence, estimated as high as 17% over 5 years, also remains unacceptably high. 1 The use of lytic drugs and endovascular devices have revolutionized the care of select stroke patients in the acute setting. However, enormous challenges remain in changing the trajectory of stroke recovery for the vast majority of patients who do not qualify or remain disabled after these treatments, and also in preventing the accumulating disability associated with stroke recurrence. The role of sleep disorders in stroke outcome and recurrence has become a pressing question. Despite estimates of greater than 50% prevalence of sleep disorders after stroke, only about 6% of stroke survivors are offered formal sleep testing and an estimated 2% complete such testing in the 3-month post-stroke period. 2 The reasons for the low rate of screening are at least partly related to the lack of awareness regarding sleep disorders among stroke providers (Figure 1). This review evaluates the role of sleep disorders, including sleep disordered breathing (SDB) and sleep-wake cycle disorders, in stroke etiology and examines the impact of their treatment on stroke outcome. Physiology and anatomy of breathing during sleep During sleep, ventilation is reduced compared to wake, in parallel with the restorative and toning-down changes that occur to heart rate, temperature and blood pressure. Volitional or behavioral input on breathing are absent during sleep; only brainstem neurons, peripheral chemoreceptors and respiratory muscle afferents regulate breathing. 3 Groups of chemoreceptive neurons in the brainstem, including those of the dorsolateral pons, nucleus solitarius and ventral medullary respiratory column, respond to changes in the partial pressure of carbon dioxide and oxygen and thereby serve as a pacemaker regulating the breathing rhythm. 4 Along with effects on the breathing pattern, these brainstem neurons cause a reduction in the upper airway tone at sleep onset through reduced activity of airway dilator muscles, especially the genioglossus, which forms the bulk of the tongue. 3 Alternatively, the chemoreceptive neurons of the brainstem can detect increased carbon

Hypoxic-ischemic encephalopathy accompanying cardiac arrest is a common cause of long-term neurological dysfunction. With the improvement in prehospital emergency systems, larger numbers of people are resuscitated from cardiac arrests, although with the increased prospect of neurological sequelae. Neurological impairment after cardiac arrest is dependent on the degree of brain damage suffered during the arrest. Although the duration and severity of brain ischemia is often difficult to determine, clinicians are often faced with difficult issues related to predicting outcome related to awakening and long-term neurological deficits after the arrest. Neurological impairments range from mild cognitive deficits to severe motor and cognitive deficits that preclude independence in many activities of daily living. Several neurological syndromes have been described in patients who awaken from hypoxic-ischemic coma with lasting motor and cognitive deficits. This review will address many of the common syndromes after hypoxic-ischemic encephalopathy, including persistent vegetative states, seizures, myoclonus, movement disorders, cognitive dysfunction, and other neurological abnormalities.

Objective Statistical models predicting outcome after intraparenchymal hemorrhage (IPH) include patients irrespective of do-not-attempt-resuscitation (DNAR) orders. We built a model to explore how the inclusion of patients with DNAR orders affects IPH prognostic models. Design Retrospective, observational cohort study from May 2001 until September 2003 Setting University-affiliated tertiary referral hospital in Seattle, Washington Patients 424 consecutive patients with spontaneous intraparenchymal hemorrhage Measurements We retrospectively abstracted information from medical records of IPH patients admitted to a single hospital. Using multivariate logistic regression of presenting clinical characteristics, but not DNAR status, we generated a prognostic score for favorable outcome (FO, defined as moderate disability or better at discharge). We compared observed probability of FO with that predicted, stratified by DNAR-status. We then generated a modified prognostic score using only non-DNAR patients. Main Results Records of 424 patients were reviewed: 44% had FO, 43% had a DNAR-order and 38% died in hospital. Observed and predicted probability of FO agreed well with all patients taken together. Observed probability of FO was significantly higher than predicted in non-DNAR patients and significantly lower in DNAR patients. Results were similar when applying a previously published and validated prognostic score. Our modified prognostic score was no longer pessimistic in non-DNAR patients, but remained overly optimistic in DNAR patients. Conclusions Although our prognostic model was well calibrated when assessing all IPH patients, predictions were significantly pessimistic in patients without, and optimistic in those with DNAR orders. Such pessimism may drive decisions to make patients DNAR in whom a FO may have been possible, thereby creating a self-fulfilling prophecy. To be most useful in clinical decision-making, IPH prognostic models should be calibrated to large IPH cohorts in whom DNAR orders were not used.

Although numerous treatments are available to improve cerebral perfusion after acute stroke and prevent recurrent stroke, few rehabilitation treatments have been conclusively shown to improve neurologic recovery. The majority of stroke survivors with motor impairment do not recover to their functional baseline, and there remains a need for novel neurorehabilitation treatments to minimize long-term disability, maximize quality of life, and optimize psychosocial outcomes. In recent years, several novel therapies have emerged to restore motor function after stroke, and additional investigational treatments have also shown promise. Here, we familiarize the neurohospitalist with emerging treatments for poststroke motor rehabilitation. The rehabilitation treatments covered in this review will include selective serotonin reuptake inhibitor medications, constraint-induced movement therapy, noninvasive brain stimulation, mirror therapy, and motor imagery or mental practice.