CHAPTER 159
Stroke in Young Adults
Definition
Four percent of strokes in the United States occur in adults younger than 45 years, and a collective review of reports provides estimates that range up to 21% or greater [1]. Although the 28,000 strokes in this age group are a small fraction of the 731,000 total events in the United States each year, stroke is an important cause of neurologic impairment in this group. Stroke occurs in those younger than 45 years more than twice as frequently as spinal cord injury (11,000 per year, all ages), and yet there has been limited awareness in American society of stroke as a disease affecting younger adults. As overall stroke incidence declines, there is evidence that stroke is occurring at a younger age, with the incidence increasing in younger adults [2]. Before the age of 30 years, more women than men have strokes because of the risks of pregnancy, childbirth, and oral contraceptive use [3,4]; this trend reverses with advancing age. In the United States, the incidence of stroke is two to five times higher in young urban blacks and twice as high in Hispanics than in whites [5]. Strokes in young adults are particularly devastating events because they often occur in otherwise healthy-seeming individuals who are in the prime of life and fully involved with family, community, and workplace responsibilities. Young adults also have high expectations of recovery and consequent difficulty in adjusting to residual disability.
Although more than 60 different disorders causing stroke in young adults have been identified, they can be grouped into several broad categories. Atherosclerotic disease accounts for approximately 20%; cardiac emboli, 20%; arteriopathies (particularly large-vessel dissection), 10%; coagulopathy, 10%; and peripartum cerebrovascular accidents, 5%. Another 20% may be related to mitral valve prolapse, migraine, and oral contraceptive use, and 15% remain unexplained after full evaluation [6]. In American studies, illicit drug use has been associated with stroke in 4% to 12% of cases [5,7]. The main clinical challenge in the management of young adults with acute stroke is the identification of its cause. Whereas cryptogenic stroke was the most common cause in the past, today specific causes are more readily identified resultant to improved capability in noninvasive imaging of brain vessels and heart arteries and valves, aortic electrophysiology, and genetic diagnostic instruments developed in recent decades [8,9]. The rate of thrombolysis use among young acute ischemic stroke patients has increased in the past decade, in part owing to stroke center certification and the availability of the stroke networks [10].
Approximately 75% of patients younger than 65 years will survive 5 years or more after their stroke [1]. Individual survival depends, of course, on the specific cause of the stroke and its treatment. In general, two thirds of young survivors achieve good functional recovery, although a history of diabetes mellitus, severe deficit at onset, or stroke involving the total anterior circulation may reduce that likelihood. Overall, the risk for recurrence in those who have suffered a first stroke averages 5% per year and varies with the survivor’s burden of risk factors [11–13].
Symptoms
The presenting neurologic symptoms of stroke are the same in young as in elderly patients and are reviewed in Chapter 158. The clinician caring for young adult stroke survivors in the post-acute phase is likely to encounter, in addition to neurologic residua of the stroke, a number of secondary symptoms that will require ongoing management. The most common of these are emotional effects, pain, spasticity, bladder dysfunction, sexual dysfunction, and fatigue. These symptoms may also occur in older stroke patients; however, this chapter focuses on the impact they have on the young stroke survivor.
Emotional Effects
The common emotional consequences of stroke are depression, emotional lability, and anxiety. 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 [14,15].
Depression can be difficult to identify in aphasic patients who cannot respond reliably to questions about mood and in patients 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 a stroke in one member of a couple is common, as is depression in caregivers [15].
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 depression symptoms influenced functional recovery. More emphasis should be given to the role of anxiety in stroke rehabilitation interventions [16].
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 85% of stroke patients, usually during the first 6 to 12 months after stroke [17]. The history should address its many potential causes [18] (Table 159.1). In addition, younger individuals with partially recovered motor function may have secondary sprains, tendinitis, skin breakdown, and nerve palsies in the paretic extremities as these are pushed beyond their physiologic limits in the effort to resume normal activities. The normal 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.
Table 159.1
Post-Stroke Shoulder Pain [18]
Disorder | Inferior Subluxation | Rotator Cuff Tear | CRPS I (Shoulder-Hand) | Frozen Shoulder | Impingement Syndrome | Biceps Tendinitis |
Examination | Acromiohumeral separation Flaccid |
Positive abduction test result Positive drop arm test result Flaccid or spastic |
Metacarpophalangeal joint compression test Skin color changes Flaccid or spastic |
External rotation < 15 degrees Early scapular motion Spastic |
Pain with abduction of 70-90 degrees End-range pain with forward flexion Spastic |
Positive Yergason test result Flaccid or spastic |
Diagnostic test | Standing radiograph in scapular plane | Arthrography Subacromial injection of lidocaine Magnetic resonance imaging |
Triple-phase bone scan Stellate ganglion block |
Arthrography | Subacromial injection of lidocaine | Tendon sheath injection of lidocaine |
Treatment | ||||||
Initial | Analgesics, nonsteroidals | Nonsteroidals, analgesics | Oral corticosteroids | Analgesics | Nonsteroidals, analgesics | Nonsteroidals, analgesics |
Rehabilitation | Harris hemi-sling or wheelchair arm board | AAROM Electrical stimulation to supraspinatus |
AAROM Heat modalities |
PROM Manipulation |
AAROM Scapular mobilization |
AAROM |
Procedures | Steroid injection Surgical repair |
Stellate ganglion block | Subacromial, intra-articular steroids Débridement Reduction of internal rotator tone |
Subacromial steroids Reduction of internal rotator tone |
Tendon sheath injection of steroids |
AAROM, active-assisted range of motion; CRPS I, chronic regional pain syndrome type I; PROM, passive range of motion.
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 that follow a stroke. 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 153 for further discussion of spasticity symptoms. Joint stiffness may also be due to contracture, which is shortening of the muscles, ligaments, or tendons around a joint due to rheologic changes in the tissues. 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 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 is queried about abdominal pain and pain on urination.