Emotional Effects

The most common emotional consequences of stroke are depression, emotional lability, anxiety, sleep disturbance, and fatigue. Clinical depression occurs in approximately 40% of patients after stroke; its incidence peaks 6 months to 2 years after the ictus. It is more likely in those with a prior history of alcoholism or depression and in patients who have suffered a severe stroke.

Depression can be difficult to identify in aphasic patients who cannot respond reliably to questions about mood and in those with motor aprosodia (loss of emotional tone in facial expression and voice) due to right hemispheric stroke. Patients tend to become more socially isolated after stroke because of language, cognitive, and physical deficits. Loss of social interaction and support increases the likelihood of depression. Stress related to marital role reversal after one member of the pair has a stroke is common, as is depression in caregivers.

Neurologically mediated emotional lability, also known as pseudobulbar affect or emotional incontinence, in which the patient has abrupt episodes of crying or laughing in response to mention of an affectively charged topic, may be a source of distress to the patient and family. It may also complicate evaluation of the patient’s true emotional state.

Patients may experience heightened anxiety chronically after stroke. In some cases, specific triggers of the anxiety—such as fear of falling while walking with a cane or fear of being left alone—can be identified in the history. The prevalence and severity of anxiety symptoms were comparable to those of depression symptoms, and the prevalence of both mood symptoms was similar during the acute period and 1 year after stroke. Both mood disturbances were also associated with a poorer health-related quality of life at 1 year, whereas only symptoms of depression influenced functional recovery. More emphasis should be given to the role of anxiety in stroke rehabilitation interventions.

Pain

Pain is a common problem after stroke in young patients. It usually affects the hemiparetic extremities and may be centrally or peripherally mediated. Shoulder pain occurs in up to 67% to 72% of stroke patients, usually during the 12 months after stroke. The history should address its many potential causes ( Table 160.1 ). In addition, younger individuals with partially recovered motor function may have secondary musculoskeletal injuries and nerve palsies in the paretic extremities as these are pushed beyond their physiologic limits in the effort to resume normal activities. The unaffected arm and leg may suffer similar overuse injuries in the course of compensating for the weak side. Heavy use of assistive devices—including canes, walkers, braces, and splints—may contribute to these injuries and consequent pain.

Muscle Stiffness Due to Spasticity

Stiffness and heaviness of muscles and joints are common complaints of young stroke patients in the post-acute setting. These symptoms are often due to the evolution of muscle tone from the flaccid to the spastic state that occurs during the first several months following a stroke, as described by the Brunnstrom stages of motor recovery. Although it is occasionally helpful in allowing weight bearing on a leg with little voluntary motor return, spasticity more often complicates the patient’s efforts to resume normal motor function. The reader is referred to Chapter 154 for further discussion of spasticity symptoms. Joint stiffness may also be due to joint contractures (see Chapter 127 ). This is common in the finger joints of the affected hand. Frozen shoulder, with contracture of the glenohumeral joint capsule, also occurs.

Bladder Dysfunction

Chronically diminished bladder control with urge incontinence occurs commonly in younger stroke patients. The history should ascertain the chronicity and frequency of the problem, diurnal pattern, and presence or absence of the sensation of needing to void; a relationship to coughing, laughing, or straining is noted. The patient should be queried about abdominal pain and pain on urination.

Sexual Dysfunction

Whether the physiologic process of sexual function changes as a result of stroke, and if so, how it changes, has not been scientifically established. Nonetheless, most patients report diminished sexual function after stroke. This may involve diminished libido or decreased erectile or ejaculatory function. Decreased libido may correlate with the presence of depression and reduced physiologic sexual function with medical comorbidity. Neither clearly relates to the size or location of stroke. There is evidence that patients’ partners—through fear of relapse, anguish, and lack of excitation—play a significant role in the decline of sexual activity. A small number of patients report increased libido after stroke and, rarely, troublesome hypersexuality. The history should note change in interest and frequency of sexual activity, alteration in ability to achieve erection or ejaculation in men and lubrication or orgasm in women, and presence of depression or active medical comorbidities that may influence sexual activity levels. Medications that may hinder sexual function and possibly fertility should be identified.

Fatigue

Increased fatigue after stroke has been reported in 39% to 68% of patients and is frequently influenced by coexisting depression. Young adults who never before needed naps now do. Patients become fatigued, physically and mentally, with less effort than before the stroke. Return to active work and family life may be limited by fatigue. Both fatigue and depression are associated with long-term mortality in young adults with ischemic stroke. Depression may be linked to higher mortality because of psychosocial factors and unhealthy lifestyles, whereas the link between fatigue and mortality is broader, including connection to diabetes mellitus, myocardial infarction, and psychosocial factors. The history should document symptoms of insomnia, sleep apnea, and the many medical conditions that produce fatigue. Medications are reviewed to identify sedative agents. Depression and loss of physical conditioning may affect energy levels, as may the increased energy cost of hemiplegic gait.