Little information exists on the use of mechanical restraints among nonpsychiatric inpatients. This prospective study evaluates their use among consecutive medical and surgical admissions to an acute care hospital. Daily direct observation of patients and hospital record review provided data on potential predictors of restraint, reasons for their application, complications, and outcome. Cox regression analysis was used to calculate relative risk of restraint while adjusting for duration of hospitalization as well as other variables. Restraints were applied to 37 (17%) of the 222 study patients. Restrained patients were eight times more likely to die during hospitalization (24% v 3%; P less than 0.01). Abnormal mental status exam, diagnosis of dementia, surgery, and presence of monitoring and support devices (eg, intravenous lines) were statistically significant independent predictors of restraint. Mechanical restraint is a common occurrence among nonpsychiatric inpatients particularly those with impaired mentation, requirement for surgery, or intensive medical intervention. Identification of medical and surgical patients at risk for restraint may reduce the use of these devices by concentrating surveillance and prevention on this group.

Whipple's disease is infrequently considered in the differential diagnosis of patients presenting with progressive neurological deterioration. This is in part a result of the relative rarity of this entity and in part due to the more frequent initial presentation of the disease with gastrointestinal, musculoskeletal, or cardiovascular symptoms. A case is described in which the neurological symptoms of progressive dementia and weakness were seen in the relative absence of non-neurological symptomatology. The diagnosis of Whipple's disease was made from a brain biopsy. The neuropathology of Whipple's disease of the central nervous system is described and the importance of considering it as a treatable entity in the differential diagnosis of progressive neurological deterioration, despite the absence of systemic symptomatology, is stressed.

Headache is the most common symptom after closed head injury, persisting for more than 2 months in 60% of patients. Rarely does headache occur in isolation. Cervical pain is a frequent accompaniment. Post-traumatic headache is often one of several symptoms of the postconcussive syndrome, and therefore may be accompanied by additional cognitive, behavioral, and somatic problems. Acute post-traumatic headaches may begin at the time of injury and continue for up to 2 months post-injury. Although onset proximate to the time of injury is most common, any new headache type occurring within this period of time is referred to as an acute post-traumatic headache. If such headaches persist beyond the first two months post-injury, they are subsequently referred to as chronic post-traumatic headaches. Over time, post-traumatic headaches may take on a pattern of daily occurrence. If aggressive treatment is initiated early, posttraumatic headache is less likely to become a permanent problem. Once "windup" of post-traumatic headaches occurs, the cycle of ongoing headaches is more difficult to interrupt. The mechanism of post-traumatic headache is poorly understood. Trauma-induced headaches are usually heterogeneous in nature, often including both tension-type pain and intermittent migraine-like attacks. Rebound-headaches may develop from overuse of analgesic medications, and the occurrence of such may complicate significantly the diagnosis of post-traumatic headache. Adequate treatment typically requires both "peripheral" and "central" measures. Understanding the general principles of treatment, especially appropriate use of preventive and abortive medications, will most usefully guide treatment. There is scant literature with which to direct treatment selection for post-traumatic headache. Consequently, treatments for post-traumatic headache are based on those prescribed for phenomenologically similar but etiologically distinct headache disorders. Delayed recovery from post-traumatic headache may be a result of inadequately aggressive or ineffective treatment, overuse of analgesic medications resulting in analgesia rebound phenomena, or comorbid psychiatric disorders (eg, post-traumatic stress disorder, insomnia, substance abuse, depression, or anxiety).

Migraine in the athlete may occur secondary to effort, prolonged exertion, or trauma or as a posttraumatic event. The chemistry is probably akin to that of spontaneous migraine. The purpose of this discussion is to outline the differential diagnosis of the athlete presenting with headache. Appropriate treatment can enhance athletic performance and enable the migraineur to participate in athletic endeavors.

The International Headache Society applies the term exertional headache to head pain precipitated by exertion. The Society recognizes cough headache and sexual headache as distinct diagnoses. All three types of headache share characteristics and mechanisms, and together may be considered as headache provoked by exertional factors ( Table 1). In distinction to more typical headaches, such as tension-type headaches or migraine, HAPEF is brief, lasting seconds to minutes, and begins immediately following the precipitating exertion. Headache provoked by exertional factors may occur by itself, or in association with headaches that are not exertional. Secondary (or symptomatic) HAPEF arises as a result of an underlying disorder; primary (or benign) HAPEF has no underlying cause. Clinicians must consider HAPEF potentially serious until appropriate investigations are undertaken. Fortunately, disorders that underlie secondary headaches usually become apparent with examination or laboratory testing. Clinical features of the headaches may also offer a clue (Table 2). Several theories have been put forth to explain the underlying mechanism of exertional, cough, and sexual headache. The leading explanation regarding all three involves exertional factors leading to a sudden increase in intracranial pressure or an inappropriate reaction in the cerebral vasculature. Because exertion may also be a migraine trigger, neural hypersensitivity, similar to migraine, may also play a role in HAPEF. The literature contains only several small case studies that deal with treatment of exertional headache, and just one double blind, placebo-controlled study. The consensus to date is that secondary HAPEF resolves if the underlying illness can be treated; primary HAPEF responds well to prophylactic treatment. Treatment strategy varies little among headaches precipitated by cough, sex, or other forms of exertion. Avoidance strategies, sometimes combined with medication (particularly indomethacin), can effectively treat headaches produced by exertional factors in most cases.

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