Medical complications of any type of stroke are common and often lead to poor clinical outcome. Their frequency must be recognized so that preventive strategies and appropriate treatment may be timely employed. Stroke may disrupt breathing either by causing a disturbance of central rhythm generation, interrupting the descending respiratory pathways leading to a reduced respiratory drive, or causing bulbar weakness leading to aspiration. The pathophysiology and clnical patterns of hemispheric (affecting the cortex), brainstem and cervical cord strokes are widely different: Patients with bilateral hemispheric cerebrovascular disease show an increased respiratory responsiveness to carbon dioxide and are liable to develop Cheyne-Stokes respiration. In patients with vascular bulbar lesions, impaired swallowing, abnormalities of the respiratory rhythm, reduced vital capacity, and reduced or even absent triggering of cough reflex all increase the risk of aspiration pneumonia. Nocturnal upper airway occlusion may also contribute to respiratory impairment. Unilateral or bilateral lateral tegmental infarcts in the pons (at or below the level of the trigeminal nucleus) may lead to apneustic breathing and impairment of carbon dioxide responsiveness, while similar lesions in the medulla (for example, lateral medullary syndrome) may result in acute failure of the automatic respiration. Infarction of the spinal cord at high cervical levels may selectively affect respiratory control. Pneumonia is one of the most common respiratory complications of acute stroke, occurring in >5% of patients. It is associated with higher mortality and poorer long-term outcome. Risk factors for in-hospital pneumonia include older age, dysarthria, aphasia, stroke severity, cognitive impairment, and abnormal swallowing. Intubation and mechanical ventilation of patients with ischemic stroke may be necessary to treat pulmonary edema or for inability to protect the airway. The morbidity and mortality in patients intubated after acute stroke is high. Neurogenic pulmonary edema (NPE) may occur in severe cerebral injury, like stroke, particularly subarachnoid hemorrhage. It often develops abruptly and progresses quickly after the onset of the neurologic insult. The patient with NPE is dyspneic, tachycardic, and hypertensive, with bilateral rales. Many casesmay resolve spontaneously, but NPE can be fatal in severe cases. Treatment is largely supportive and directed mainly towards treatment of the underlying neurologic condition. Abnormal breathing patterns are a common consequence of stroke. Among the recognized abnormal respiratory patterns are Cheyne-Stokes breathing, periodic breathing, apneustic breathing, central sleep apnea, ataxic breathing, and failure of automatic breathing. The relationship of sleep disordered breathing (including both obstructive sleep apnea and central sleep apnea syndrome) as a possible risk factor for stroke and as a possible complication of stroke has been discussed extensively in recent literature.