Post-stroke rehabilitation. A review of the guidelines for patient management.

A comprehensive, intense rehabilitation program is key to successful convalescence for patients who have experienced stroke. A guideline on post-stroke rehabilitation published by the Agency for Healthcare Research and Quality provides clinicians with detailed recommendations for managing patients who have sustained a brain attack. Rehabilitation should begin following diagnosis and after any life-threatening issues have been effectively managed. The key steps include patient management during the acute phase, screening for rehabilitation and choice of setting, managing rehabilitation, and facilitating the patient's transition back into the community. The timeliness of rehabilitation interventions and the intensity of rehabilitation services are important factors in maximizing a patient's functional outcome at hospital discharge and on follow-up.

Brainstem infarct with pharyngeal dysmotility and paralyzed vocal cord: management with a multidisciplinary approach.

An unusual case of right posterior brainstem infarction with isolated deficits of severe dysphagia and ataxia is presented. Neurological examination revealed dysfunction of the pharyngeal and laryngeal branches of cranial nerves IX, X, and a paralyzed right vocal cord. The patient was unable to swallow 1/4 teaspoon of applesauce. Modified barium swallow revealed extremely sluggish pharyngeal peristalsis and absent swallowing reflex. Percutaneous esophageal gastrostomy tube was inserted and an intensive dysphagia rehabilitation program was initiated. Pharyngeal-phase-oriented protocol was used. Results were significantly improved compensatory pharyngeal and laryngeal function with restoration of swallowing and no aspiration. This case illustrates successful management of dysphagia associated with brainstem infarction and the benefits of a coordinated multidisciplinary protocol.

Thromboxane, prostacyclin, beta-thromboglobin, and diabetes mellitus.

Plasma levels of beta-thromboglobin (beta-TH) and of thromboxane B2 (TXB2) and 6-keto-prostaglandin F1-alpha, the stable metabolites of thromboxane A2 and prostacyclin, were determined by radioimmunoassay methods in eight patients with noninsulin-dependent diabetes before and after dietary treatment and after administration of the sulfonylurea drug glibenclamide. Blood examinations were performed when hyperglycemia was detected for the first time, four weeks after a dietary regimen was started, and four and eight weeks after glibenclamide treatment was begun. Drug treatment was instituted because, despite a suitable diet, patients' postprandial blood sugar was higher than 8 mmol/L (145 mg/dl). At the initial examination, elevated TXB2 and beta-TH levels indicating platelet hyperactivity and hyperglycemia were found. TXB2 and beta-TH levels decreased significantly after glibenclamide treatment was started, as did the blood glucose level. There was no change in 6-keto-PGF1-alpha. We interpret these results to indicate that diabetes is associated with hyperactivity of platelet aggregation and that control of blood glucose is important because a lower blood glucose level attenuates platelet hyperactivity. Whether the decrease in platelet hyperactivity is a direct result of the lowered blood sugar or reflects the influence of the drug treatment requires clarification.