Stroke is one of the leading causes of mortality, with an annual total of 6 million fatal events worldwide. In the United States, approximately 10% of strokes occur in patients below 50 years of age. There is limited awareness of stroke as a disease affecting younger adults. 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. More than 60 different disorders have been found to cause stroke in young adults. The presentation of ischemic stroke in the young can be missed if it is nontraditional and includes generalized weakness and fatigue, altered mental status, altered gait, and dizziness. Missed diagnosis occurred in more than 50% of the patients presenting to emergency departments. Approximately 75% of patients below 65 years of age will survive 5 years or more after stroke. The common emotional consequences of stroke are depression, emotional lability, anxiety, sleep disturbances, and fatigue. Stroke can cause pain, bladder dysfunction, and speech impairments, among other complications. However, many young stroke survivors can return to a productive life with appropriate rehabilitation.
Key Wordsdepression, fatigue, stroke, young
|G81.00||Flaccid hemiplegia affecting unspecified side|
|G81.01||Flaccid hemiplegia affecting right dominant side|
|G81.02||Flaccid hemiplegia affecting left dominant side|
|G81.03||Flaccid hemiplegia affecting right nondominant side|
|G81.04||Flaccid hemiplegia affecting left nondominant side|
|G81.10||Spastic hemiplegia affecting unspecified side|
|G81.11||Spastic hemiplegia affecting right dominant side|
|G81.12||Spastic hemiplegia affecting left dominant side|
|G81.13||Spastic hemiplegia affecting right nondominant side|
|G81.14||Spastic hemiplegia affecting left nondominant side|
|G82.51||Quadriplegia, C1-C4 complete|
|G82.52||Quadriplegia, C1-C4 incomplete|
|G82.53||Quadriplegia, C5-C7 complete|
|G82.54||Quadriplegia, C5-C7 incomplete|
|I69.30||Unspecified sequelae of cerebral infarction|
|R41.89||Other symptoms and signs involving cognitive functions and awareness|
|G81.90||Hemiplegia, unspecified affecting unspecified side|
|G81.91||Hemiplegia, unspecified affecting right dominant side|
|G81.92||Hemiplegia, unspecified affecting left dominant side|
|G81.93||Hemiplegia, unspecified affecting right nondominant side|
|G81.94||Hemiplegia, unspecified affecting left nondominant side|
Stroke is one of the leading causes of mortality, with an annual total of 6 million fatal events worldwide. Stroke mainly affects elderly people, yet approximately 10% of strokes occur in patients below 50 years of age. Each year stroke affects nearly 800,000 individuals in the United States. Three percent of strokes in the United States occur in adults below 40 years of age. Stroke is an important cause of neurologic impairment in this group. However, there has been limited awareness in American society of stroke as a disease affecting younger adults. As the incidence of stroke declines, there is evidence that stroke is occurring at a younger age, with the incidence increasing in younger adults. More women than men suffer strokes because of the risks of pregnancy, childbirth, and oral contraceptive use before age 30. However, the correlation between the oral contraceptives and the incidence of stroke is now in doubt. In the United States, the incidence of stroke is two to five times greater among young urban blacks and twice as high in Hispanics than in whites. The effects of strokes in young adults are particularly devastating 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.
There are more than 60 different disorders causing stroke in young adults. They are grouped into several broad categories. Spontaneous arterial dissection is one of the most common causes of stroke in young adults : 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. In studies in the United States, the use of illicit drugs has been associated with stroke in 4% to 12% of cases. The main clinical challenge in the management of young adults with acute stroke is identification of its cause. Young adults with stroke do not have the same vascular risk factors as patients greater than 55 years.Whereas cryptogenic stroke was the most common cause in the past, today specific causes are more readily identified owing to improvements over recent decades in the noninvasive imaging of brain vessels and heart arteries and valves, aortic electrophysiology, and genetic diagnostic instruments. One must keep in mind that the differential diagnosis—including multiple sclerosis, somatoform disorders, migraine with prolonged aura, postictal focal deficit, neoplasms, and less often encephalitis—should be considered. The rate of thrombolysis use among young patients with acute ischemic stroke has increased in the past decade, in part owing to stroke center certification and the availability of the stroke networks. There has been a decrease in the death rate with the increased rehabilitation placement of young adults.
Approximately 75% of patients younger than 65 years will survive 5 years or more after stroke. Individual survival depends 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, Fabry disease (x-linked lysosomal storage dysfunction), severe deficit at onset, or stroke involving the anterior cerebral artery (ACA) may reduce that likelihood. Strokes affecting the posterior cerebral artery (PCA) have had better outcomes than those affecting the middle cerebral artery (MCA) or the ACA. Overall, the risk for recurrence in those who have suffered a first stroke averages 3% per year and varies with the survivor’s burden of risk factors; it is 11.7% in those with a history of transient ischemic attack (TIA).
In most cases, presenting neurologic symptoms of stroke are the same in young as in elderly patients; they are reviewed in Chapter 159 . The presentation of ischemic stroke in the young can be missed if it is nontraditional and includes symptoms such as generalized weakness and fatigue, altered mental status, altered gait, and dizziness. Missed diagnosis occurred in more than 50% of the patients with nontraditional symptoms presenting to an emergency room. 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 (SD), fatigue, and sleep disturbance.
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 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.
|Disorder||Inferior Subluxation||Rotator Cuff Tear||CRPS I (Shoulder-Hand)||Frozen Shoulder||Impingement Syndrome||Biceps Tendinitis|
|Examination||Acromiohumeral separation |
|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
|Pain with abduction of 70–90 degrees |
End-range pain with forward flexion
|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|
|Initial||Analgesics, nonsteroidals||Nonsteroidals, analgesics||Oral corticosteroids||Analgesics||Nonsteroidals, analgesics||Nonsteroidals, analgesics|
|Rehabilitation||Harris hemisling or wheelchair arm board||AAROM |
Electrical stimulation to supraspinatus
|Procedures||Steroid injection |
|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|
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.
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.
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.
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.