Medical complications of stroke …

Susan Law DO MPH

Stroke & Vascular Disorders

Updated 05.03.2026
Released 06.07.2001
Expires For CME 05.03.2029

Medical complications of stroke

Author: Susan Law DO MPH

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Editor: Steven R Levine MD

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Medical complications of stroke

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Introduction

Overview

Medical complications of stroke account for significant morbidity and mortality. Early recognition and management result in favorable outcomes. During the first week, the direct effects of ischemic stroke are responsible for most deaths. Other medical complications, including cardiac, infectious, and venous thromboembolism, increase mortality thereafter. In this article, the author discusses the medical complications of stroke-related deficits, their workup, and treatment modalities.

Key points

	• Venous thromboembolism is one of the most common and serious complications of stroke.
	• During acute stroke, thrombolysis for the treatment of pulmonary embolism is contraindicated.
	• Limited mobility following stroke is associated with osteoporosis, fractures, pressure sores, painful arthritis, and peripheral neuropathy.
	• Post-stroke pain may be severely debilitating and refractory to conventional analgesics. Invasive neurosurgical procedures and noninvasive transcranial magnetic stimulation have shown promising results but require further testing.

Classification scheme for medical complications of stroke

Prospective studies suggest that direct effects of ischemic stroke, such as hemorrhagic conversion or cerebral edema, account for most deaths within the first week. However, medical complications account for at least 50% of mortality thereafter (161; 66).

Medical complications of stroke decrease survival by several years (07). Admission to stroke units significantly reduces these complications, including immobility and mortality within the first 4 weeks (05). Later, the predominant complications are venous thromboembolism, pneumonia, urosepsis, cardiac arrhythmias, and myocardial infarction. Other late complications include mechanical falls, pressure sores, psychiatric disorders, and central post-stroke pain. Some of the most beneficial measures are swallowing evaluation to prevent aspiration, avoidance of urinary catheters, early mobility, and prophylaxis of thromboembolism (161).

Table 1 outlines the medical complications of stroke (90). The topics discussed in this article are listed in Table 2. Several of these topics are discussed in other MedLink Neurology articles.

Table 1. Medical Complications of Stroke: A Classification Scheme

I. Neurologic complications
	(A) Seizures (B) Vascular dementia
II. Infections
	(A) Urinary tract infection (B) Dysphagia, aspiration pneumonia
III. Complications of immobility
	(A) Falls (B) Hemiosteoporosis, fractures (C) Pressure ulcer (D) Spasticity
IV. Thromboembolism
	(A) Deep venous thrombosis (B) Pulmonary embolism
V. Pain
	(A) Shoulder pain (B) Central post-stroke pain
VI. Psychological complications
	(A) Depression (B) Anxiety (C) Confusion (D) Emotional incontinence
VII. Miscellaneous
	(A) Gastrointestinal hemorrhage (B) Constipation (C) Cardiac failure, arrhythmias (D) Arthritis (E) Sleep apnea (F) Nutritional deficiencies
Adapted from (90).

Table 2. Medical Complications of Stroke

I. Disorders of immobility

(A) Deep venous thrombosis and pulmonary embolus
(B) Hemiosteoporosis and hip fractures
(C) Falls
(D) Pressure sores, skin ulcers
(E) Peripheral nerve injury

II. Pain

(A) Shoulder pain
(B) Central post-stroke pain

III. Incontinence

Deep venous thrombosis and pulmonary embolism

Epidemiology. Venous thromboembolism after acute ischemic stroke is a significant cause of morbidity and mortality. Deep venous thrombosis typically appears on the second day after stroke onset. At 2 weeks, deep venous thrombosis occurs in up to 50% of patients (16). In a case series of 30 patients with stroke, only four of whom received deep venous thrombosis prophylaxis, sudden death occurred in 50% of patients with pulmonary embolism (196). Prompt and early administration of chemical prophylaxis remains a hallmark of standard of care in hospitals.

Among patients with ischemic stroke discharged between 1979 and 2003, 1.17% had venous thromboembolism, 0.74% had deep venous thrombosis, and 0.51% had pulmonary embolism. Hemorrhagic stroke was associated with higher rates: 1.93%, 1.37%, and 0.68%, respectively (162).

The etiology of venous thromboembolism is multifactorial: endothelial damage, blood flow stasis, and hypercoagulability (156). Endothelial damage promotes coagulation. Thrombosis risk factors include severe paralysis and hypercoagulability (88).

Following a stroke, the paretic leg is preferentially affected due to immobility, venous stasis, accumulation of activated coagulation factors, and repeated trauma (76). A systematic review of Medline and Embase searches from January 1990 onwards, including 26 studies, identified the venous thromboembolism risk factors reported by two or more studies as previous venous thromboembolism, pre-stroke disability, large infarct, low Barthel index, age, dehydration, delayed preventing measures, infection, prolonged hospital stay, cancer, infection, elevated C-reactive protein, and D-dimer (178).

Pulmonary embolism may be asymptomatic, but if severe, it may cause respiratory failure and sudden death. In patients with asymptomatic deep venous thrombosis, 40% of lung scans detect pulmonary emboli (124). Although 90% of pulmonary emboli originate in the legs, ultrasound is positive in only 29% of cases (179).

Venous thromboembolism increases the risk of cardiovascular death. A systematic review and meta-analysis that included 13 observational studies enrolling 22,251 patients found that cardiovascular death is more frequent in patients with venous thromboembolism than in the general population without venous thromboembolism (risk ratio: 3.85, 95% CI: 2.75–5.39) (133).

Differential diagnosis. Edema of the paretic limb may mimic deep venous thrombosis. Respiratory failure may be caused by cerebral herniation or a brainstem lesion. The post-thrombotic syndrome (PTS) attributed to venous hypertension and abnormal microcirculation is characterized by edema and pain with or without venous ulceration (15; 76).

Diagnostic workup. Most patients with pulmonary embolism have at least one of these symptoms: sudden onset dyspnea, chest pain, syncope, and hemoptysis (119).

Index scores can be calculated to best predict pretest clinical probability of pulmonary embolism (Tables 3 and 4) and several scoring systems (189; 120; 191). A normal D-dimer level combined with low pretest clinical probability excludes thrombotic disease.

A high pretest probability should not affect the clinical decision (190). A normal D-dimer level does not exclude venous thromboembolism if the clinical probability is high. Lower limb ultrasound or helical chest CT is needed to exclude venous thromboembolism (155).

Table 3. Wells Prediction Rule for Diagnosing Deep Venous Thrombosis

Clinical Features	Score
Recently bedridden for more than 3 days or major surgery within 12 weeks Localized tenderness along the deep veins Paralysis or immobilization of lower extremities Entire leg swollen Calf swelling 3 cm larger than normal Pitting edema confined to symptomatic leg Active cancer Collateral superficial veins (non-varicose) Alternative diagnosis less likely to be deep venous thrombosis	+1 +1 +1 +1 +1 +1 +1 +1 -2
Clinical probability of deep venous thrombosis: Low = less than 0; intermediate = 1 to 2; high = 3 or higher From: (189)

Table 4. Wells Prediction Rule for Diagnosing Pulmonary Embolism

Clinical Features	Score
Previous pulmonary embolism or deep venous thrombosis Heart rate greater than 100/min Recent surgery or immobilization Deep venous thrombosis clinical signs Alternative diagnosis less likely than pulmonary embolism Hemoptysis Cancer	+1.5 +1.5 +1.5 +3 +3 +1 +1
Clinical probability of pulmonary embolism: Low = 0 to 1; intermediate = 2 to 6; high = 7 or higher From: (23)

Prevention of thromboembolism

General measures. Nonpharmacologic prevention includes early mobilization, graduated compression stockings, and pneumatic sequential compression devices. Bed rest following stroke should be limited to patients with large cerebellar or cerebral lesions and increased intracranial pressure, severe angina and myocardial infarction, deep venous thrombosis (before anticoagulation), and postural ischemia due to large-vessel carotid or vertebrobasilar artery disease. If possible, avoid intravenous lines in the paretic arm due to the increased risk of deep venous thrombosis.

Compression stockings. Thigh-length graduated compression stockings (GCS) failed to prevent proximal deep venous thrombosis after stroke and caused skin complications (30). However, intermittent compression stockings prevent deep venous thrombosis and increase survival in patients with acute stroke (29). The American College of Chest Physicians recommends intermittent pneumatic compression devices or elastic stockings if anticoagulation is contraindicated (75).

Anticoagulation. During an acute stroke, either low-dose unfractionated heparin, low molecular weight heparin, or danaparoid may be used (75). Thromboprophylaxis for up to 4 to 5 weeks is more beneficial than short-term prophylaxis (181).

Unfractionated heparin 5000 IU sc thrice daily reduces the risk of venous thromboembolism after acute stroke from 73% to 22%, along with a decrease in the combined rate for deep venous thrombosis, pulmonary embolism, and death (112).

Low molecular weight heparin (LMWH) administered once daily is safer and more cost-effective than unfractionated heparin (70; 160; 148).

Fondaparinux, an indirect factor Xa inhibitor, is a safe alternative in patients at risk for heparin-induced thrombocytopenia (54).

Direct oral anticoagulation (DOAC) agents are easier to administer. However, DOACs are not superior to postoperative LMWH for venous thromboembolism prevention. For acute treatment and secondary prevention of venous thromboembolism, DOAC agents have a lower risk of hemorrhagic complications but are not more efficacious than warfarin (166).

After intracerebral hemorrhage, preventive anticoagulation is delayed until hemorrhage expansion stops. A meta-analysis of eight studies including 3893 patients found a decreased risk of pulmonary embolism, but the risk of deep venous thrombosis and venous thromboembolism was not modified (159). The risk of increased intracerebral hemorrhage, rebleeding, or poor outcome was not increased.

Treatment of venous thromboembolism in stroke patients. If clinical suspicion of venous thromboembolism is high, intravenous anticoagulation is indicated while waiting for diagnostic confirmation. Intermediate suspicion warrants intravenous anticoagulation if confirmation of venous thromboembolism is delayed for more than 4 hours. In patients with a low suspicion, parenteral anticoagulation should be deferred if the confirmatory test result is expected within 24 hours.

Anticoagulation alone is the preferred treatment for acute leg deep venous thrombosis. Isolated, distal deep venous thrombosis without severe symptoms and unlikely to extend may be monitored by serial imaging for 2 weeks. However, severe symptoms and risk or evidence of proximal thrombus extension by ultrasound warrant anticoagulation.

Patients with acute pulmonary embolism and systolic blood pressure less than 90 mmHg, who do not have a high risk of bleeding, may benefit from intravenous thrombolysis. Catheter-directed thrombolysis is associated with fewer cerebral hemorrhagic complications than systemic thrombolysis but similar mortality (100). In the case of thrombolysis, failure or shock surgical thrombectomy may be beneficial (75).

DOACs (dabigatran, rivaroxaban, apixaban, and edoxaban) are the preferred anticoagulants for the treatment of acute deep venous thrombosis and pulmonary embolism as they are noninferior to warfarin and were associated with fewer hemorrhagic complications (157; 40; 41; 03; 59).

Bridging with LMWH or fondaparinux is initiated on the same day as warfarin. Parenteral anticoagulation is continued for a minimum of 5 days or at least 24 hours after INR is 2 or above. The ideal INR target is 2 to 3. Warfarin dosage should begin with 5 mg (56; 33). Anticoagulation clinics improve warfarin anticoagulation control, patient outcomes, and health care costs (25). If compliance is unreliable, long-term subcutaneous LMWH or DOACs can be used.

Unprovoked venous thromboembolism is treated for 3 months if the risk of bleeding is high and for longer if the risk of bleeding is low or moderate. At the end of 3 months, the risk-benefit ratio should be reassessed. Provoked venous thromboembolism is treated for 3 months and for longer if the provoking factor persists. Extended anticoagulation is recommended at a lower dose with a DOAC or warfarin in those patients who are not candidates for DOAC. Malignancy requires extended anticoagulation regardless of the bleeding risk.

Warfarin is teratogenic. During pregnancy, heparin is used instead. Early mobilization and avoiding procoagulant agents (eg, hormone-replacement therapy or oral contraceptives) are advisable.

Intracerebral hemorrhage is a transient contraindication for thrombolysis and anticoagulation. A temporary inferior vena cava filter may be used instead until anticoagulation can be resumed. However, the inferior vena cava filter is not recommended in addition to anticoagulation.

Post-thrombotic syndrome development can be avoided by using systemic or catheter-directed thrombolysis. A trial of compression stockings is indicated in patients with post-thrombotic syndrome. Persisting post-thrombotic syndrome may benefit from an intermittent compression device.

Further recommendations on acute venous thromboembolism treatment are detailed by the American College of Chest Physicians (168).

Bone disease: osteoporosis and fractures

Stroke impairs mobility, leading to osteoporosis, falls, and fractures. Most fractures occur late, on the hemiplegic side (154). Sequential bilateral hip fractures were seen more frequently in institutionalized patients with a history of stroke and osteomalacia (26). Hip fractures are associated with an increased risk of institutionalization and death (43).

Epidemiology. Out of 130,000 discharged acute stroke patients, 2.0% suffered fractures in 1 year and 10.6% in 10 years (37). The risk of hip fracture increases 4-fold after stroke (71).

Pathophysiology. Bone strength is a composite of bone density and bone quality, with the latter thought to include bone architecture, bone damage (eg, microfractures), and mineralization. Immobilization after stroke leads to osteoporosis (154). After a stroke, approximately 30% of fractures occur in the upper extremities (139).

Clinical risk factors that contribute to fracture risk independent of bone mineral density are presented in Table 5 (72).

Table 5. Risk Factors for Osteoporotic Fractures in Women

• Age
• Premature menopause
• Primary amenorrhea or amenorrhea associated with low estrogen
• Asian or white ethnic origin
• Previous fragility fracture
• Low bone mineral density
• Glucocorticoid therapy
• High bone turnover
• Family history of hip fracture
• Poor visual acuity
• Low body weight
• Neuromuscular disorders
• Cigarette smoking
• Excessive alcohol consumption
• Long-term immobilization
• Low dietary calcium intake
• Vitamin D deficiency

Adapted from (72)

Bone loss in the paretic limb after stroke results from lack of exertion. A retrospective study of 1139 patients followed for a median time of 2.9 years found that most fractures occur in the paretic hip. Fracture incidence was two to four times higher than in the general population (154). In another study, the risk factors of fractures after stroke are weakness, numbness, neglect, imbalance, and decreased awareness (150).

Vitamin D deficiency increases the risk of fracture in disabled elderly patients (142). Nutrition, light exposure, and medications are additional contributors. Proton pump inhibitors increase the risk of osteoporosis (102). Dabigatran, a direct oral thrombin inhibitor, is associated with a lower risk of osteoporotic fractures compared to warfarin (91).

Clinical features. Vertebral fractures may cause back pain, spinal deformity, functional limitations, and increased risk of hospitalization and mortality (69; 44).

Osteoporosis is defined as bone mineral density of 2.5 SD or more below the average value for premenopausal women (T score, less than -2.5 SD). In the presence of one or more fragility fractures, osteoporosis is considered severe (72).

Table 6. World Health Organization (WHO) Definition of Osteoporosis

Diagnostic Category	T-score	Bone Mineral Density
Normal	Greater than –1	Within 1 SD of a young normal adult
Low bone mass	–1 to –2.5	Between 1 and 2.5 SD below that of a young normal adult
Osteoporosis	Less than –2.5	More than 2.5 SD below that of a young normal adult
Severe osteoporosis	Less than –2.5 and 1 or more fragility fractures	More than 2.5 SD below that of a young normal adult and one or more osteoporotic fractures

Treatment. Osteoporosis management aims to prevent fractures by increasing bone strength and physical function (132). A single-center registry database of 1307 consecutively registered patients with acute ischemic stroke shows that osteoporosis pharmacotherapy may improve the functional outcomes at 3 months and 1 year after ischemic stroke onset (163).

A pyramidal approach has been recommended. The base is represented by lifestyle changes: calcium and vitamin D intake, physical activity, and fall prevention (134). Physical activity promotes bone formation and maintenance. However, walking alone is insufficient. Exercises that improve mobility, muscle function, and balance may reduce the fracture risk (46). Reversal of osteoporosis after hemiplegia requires daily weight training for a minimum of 60 and 90 minutes for males and females, respectively (55).

Calcium and vitamin D supplementation help prevent fractures (36). The recommended intake of calcium is 1000 mg/day for men and women aged 50 years or younger and 1200 mg/day for those older than 50 years of age (NIH Dietary Supplement Fact Sheet--Calcium). The recommended dose of vitamin D is 400 IU/day for men and women aged 51 to 70 years and 600 IU/day for those 71 years or older (NIH Dietary Supplement Fact Sheet—Vitamin D). The second level includes addressing and treating secondary causes of osteoporosis. The third level includes pharmacotherapeutic interventions to improve bone density and reduce the risk of fracture.

Bisphosphonates inhibit bone resorption. Zoledronate administered as a single dose of 4 mg intravenously within 5 weeks of stroke onset helps preserve bone mineral density (149).

Denosumab is a monoclonal antibody with an affinity for the receptor activator of nuclear factor-kappaB ligand (RANKL). Denosumab given as a subcutaneous injection every 6 months inhibits osteoclastic activity and increases bone mass in patients with osteoporosis (113).

Several antiresorptive agents increase the risk of thromboembolism and are contraindicated in patients with stroke. These include raloxifene, strontium ranelate, and romosozumab (98; 185; 89).

Complications of stroke

Falls. Traumatic brain injury is responsible for 78% of fall-related deaths and 79% of the cost (167). Stroke doubles the risk of falling (67). Most falls occurred during transfers between the wheelchair and bed (144). Predictors of falls are executive dysfunction, imbalance while dressing, and depression (87; 106; 170). Depression and anxiety predominantly affect young women with low socioeconomic status (17). Comorbidities, polypharmacy, decreased vision, and decreased cognition in stroke patients often increase the risk of falling.

The Postural Assessment Scale for Stroke (PASS) and the Postural Control and Balance for Stroke test (PCBS) evaluate postural control and assess the risk of fall after stroke (09; 151).

Fall prevention programs emphasize supervision of high-risk patients, proper seating, wheelchair transfers, and regular toileting.

Pressure sores. Pressure sores may develop rapidly in bedridden stroke patients. Sustained pressure due to limited mobility results in skin ischemia over the weight-bearing points, usually the bony prominences. If infected, they can result in significant morbidity and mortality (20).

A Swedish retrospective study of 161 patients with stroke recorded 116 pressure ulcers, 30 of whom had multiple ulcers (57). The sacrum and the lower body are most often affected (52).

Other risk factors include diabetes, peripheral vascular disease, urinary incontinence, and low body mass index (11).

Pressure sores are classified according to stages (128):

	Stage I—non-blanchable erythema on intact skin.
	Stage II—partial thickness skin loss of the dermis presenting as a shallow open ulcer with a red or pink wound bed, without slough.
	Stage III—full thickness tissue loss involving the subcutaneous tissue or fascia. Bone, tendon, and muscle are not exposed.
	Stage IV—full thickness tissue loss with exposed bone, tendon, or muscle.

The Braden Scale predicts the risk of developing pressure sores. The scores range from 6 to 23, with higher risk associated with lower scores (10; 14).

Bed sores can be prevented by turning every 2 hours. A Cochrane review found that higher‐specification foam mattresses, rather than standard hospital foam mattresses, or the use of medical grade sheepskin reduce the incidence of pressure ulcers (116). Managing incontinence, daily checks, and high protein nutritional intake help maintain the skin barrier integrity (176). Pressure sore treatment consists of wound dressing and cleaning to prevent infection (50).

Peripheral nerve injury. Compression peripheral nerve injury in stroke patients results from limb malposition and may cause additional disability or pain. The risk is increased by sensory loss, weakness, neglect, and limb edema. In addition, using a manual wheelchair increases the likelihood of median and ulnar nerve injury in the arm nerve (12). Hematoma, a complication of anticoagulation, may result in brachial plexus injury or femoral nerve entrapment (42).

Electrodiagnostic studies help establish the injury site and severity and the need for surgical intervention. In most cases, splinting and other supportive devices as well as pain management may be sufficient.

Pain syndromes

After a stroke, many patients experience pain that affects their quality of life. A prospective study of 443 patients with stroke showed that 29.56% suffered from pain (14.06% in acute, 42.73% in the subacute, and 31.90% in the chronic stroke stage). Headache after stroke manifests acutely. Musculoskeletal and central pain occurs more often in the subacute and chronic stages, whereas spasticity-related pain appears in the chronic stage (140).

Central post-stroke pain. Also called thalamic pain syndrome or Dejerine-Roussy syndrome, central post-stroke pain is a delayed complication of stroke. Central nervous system pain has a burning, aching, throbbing, cramping, or combination character. Central pain triggers may be innocuous stimuli. Elderly patients tend to experience nonburning pain. Characteristically, the sensitivity to pinprick and temperature is decreased in the same region. However, the spinothalamic sensation may persist in many patients (85).

In a systematic review of 69 papers, central pain was reported in 11% of strokes in any location and in 50% of patients with medulla and thalamus strokes. Central pain coincides with acute stroke in 26% of patients and may appear up to 12 months later (99). Symptoms can occur months or even years after stroke onset; the timing of symptoms can complicate decision making during diagnosis. Prevalence of central post-stroke pain is up to 8% of stroke patients in the United States and 11% for stroke patients over 80 years of age.

Lesions of the ventral posterolateral, ventral medial, and medial dorsal nucleus and the trigeminal and spinothalamocortical pathways, including the brainstem, and cerebral cortex lead to post-stroke pain (13; 32; 130). Pure central post-stroke pain, sometimes mistaken for malingering or psychogenic pain, is related to the spinothalamic tracts from the posterolateral mesencephalon (31). Central post-stroke pain should be considered after other causes of pain are excluded.

Medial lemniscus has a modulatory role. Well-controlled central pain due to lateral medullary stroke may recur after a second infarct involving the ipsilateral medial medullary region (78). Lesions of the ventral caudal nucleus suggest a role for other pathways in central pain development (121; 77).

The pattern of central pain correlates with the site of the lesion. Ventroposterior thalamic nuclear lesions are more likely to produce half-body pain. The supratentorial lesions cause the most severe pain in the extremities, whereas the infratentorial lesions cause pain in the face (13). Imaging injured spinothalamic strokes may be achieved with diffusion tensor tractography (62).

There is a lack of high-quality clinical trials of central pain treatment. Post-stroke pain may be refractory to standard analgesics and opioids. First-line therapies include minimizing triggers that cause pain.

Amitriptyline has been effective in a small, randomized controlled study (94); however, there is a need for more data (122). Amitryptyline continues to remain the most widely used agent. Other considerations include trazodone and venlafaxine. Selective serotonin reuptake inhibitors are considered to be ineffective; however, case reports are mixed. Should a trial of antidepressants and serotonin and norepinephrine reuptake inhibitors fail, a trial of psychostimulants has been reported to be helpful if risks and benefits are properly assessed. Amitriptyline remains the first-line agent for spinal cord injury and comorbid depression (169).

Pregabalin is effective at escalating doses of 150, 300, and 600 mg/day (186). In addition, it may improve pain-related anxiety and sleep disturbances (80). Duloxetine was also studied with success in a small study (82), but a prior clinical randomized double-blind placebo-controlled trial did not show a significant decrease in pain intensity (187). Newer studies suggest a more effective role for duloxetine in multiple sclerosis–related neuropathies. Similarly, the cannabinoid class of medications have been shown to be helpful as well.

Carbamazepine is probably effective for chronic neuropathic pain, but there is a lack of information beyond 4 weeks (194). The effect of gabapentin on neuropathic pain is probably not superior to carbamazepine (192).

Lamotrigine in a dose of 200 mg daily was moderately effective in a small, randomized study (184), but a Cochrane review provided no convincing evidence of benefit at doses of 200 to 400 mg/day. In addition, its titration is difficult because of the risk of rash (193). The current literature recommends lamotrigine as the most effective anticonvulsant agent for the treatment of central post-stroke pain (169).

Levetiracetam is not effective for post-stroke pain treatment (68; 195).

Intravenous lidocaine and morphine have a limited role in treating central pain due to the delivery method and side effects (06). Intrathecal baclofen improved central post-stroke pain in a small case series (172). Fluvoxamine and mexiletine may also be used as adjuvants for pain treatment (79). Botulinum toxin, BTX-A, has been used with some success for neuropathic pain; however, a clinical trial is needed to confirm the initial results (60).

Graded motor imagery, like limb laterality recognition, imagined movements, mirror movements, and mirror therapy may improve pain and function in patients with phantom limb and complex regional pain syndrome type 1 (123; 175).

Cold caloric stimulation modulates the nociceptive evoked potentials (115; 45). In small studies, caloric stimulation improved central pain (152; 114; 115; 129). However, controlled randomized studies are needed to validate this observation.

Stellate ganglion blockade can reduce refractory thalamic pain (101). In one case report, the stellate ganglion blockade with lidocaine analgesia persisted for 9 months (105).

Scrambler therapy, a form of noninvasive electroanalgesia, showed a reduction of post-stroke pain in a small study of 20 patients (171).

Repetitive transcranial magnetic stimulation (rTMS) is a potentially useful noninvasive method for pain control (95). Fiber tracking with diffusion tensor imaging may predict response to rTMS (49). However, there is a significant publication bias (38). A systematic review of transcranial direct current stimulation (tDCS) on neuropathic pain in patients with stroke shows promise, but there is high heterogeneity (35; 153). rTMS may control chronic as well as acute pain after stroke (96; 108). A systematic review of five studies, including 119 patients who underwent rTMS, found that stimulation of the M1 area only reduced central pain significantly (111).

Prefrontal cortex stimulation is preferred because it is less invasive and more effective than deep brain and spinal cord stimulation (74). Motor cortex stimulation is also useful for central pain from the brainstem and spinal cord lesions (173). Pain relief may persist for 12 months (165; 183). Long-term, over 80% reduction in pain was seen in 31% of patients, 50% to 80% reduction in 23% of patients, and no improvement in 15% of patients (164). The main complications are epidural hematoma and subdural effusion. The presumed mechanism is increased regional blood flow to the ipsilateral corticothalamic connections or reduced inflammation (18; 158).

For nonthalamic lesions, spinal cord stimulation achieved relief for more than 12 months in 44.4% of patients (174). Other useful locations for electrical stimulation include periventricular grey matter and the centromedian thalamic nucleus (127; 147; 04).

The data on neurosurgical management of central post-stroke pain are limited, and further studies are needed to confirm these findings (34; 47). Procedures like thalamotomy have been evaluated but are considered to be of last resort. Dorsal root entry zone lesioning has been reported; however, limited studies also showed a very high recurrence rate of symptoms.

Shoulder pain. Shoulder pain occurs in 22% of patients within the first 4 months of the first stroke; 79% have moderate to severe pain. Weakness and a high NIHSS score correlate with pain. Pain is disabling and limits rehabilitation (104). Shoulder pain frequency has decreased over the last 15 years, suggesting an improvement in stroke care and rehabilitation (118).

The causes of shoulder pain are adhesive capsulitis, subluxation, spasticity, local trauma, shoulder-hand syndrome, and complex regional pain syndrome. The severity and stage of paralysis alter the shoulder joint configuration and the type of pain differently (180). Adhesive capsulitis and shoulder subluxation are the most common causes of shoulder pain (107). They occur in 50% and 44% of patients, respectively A meta-analysis of 23 studies found that ultrasound of the hemiparetic shoulder may reveal pathology in the biceps long head tendon (41.4%), followed by the supraspinatus tendon (33.2%). These abnormalities occur more often than in the contralateral shoulder (103).

In the flaccid stage, inferior subluxation may benefit from shoulder support and muscle electrical stimulation. In the spastic stage, muscle relaxants and range of motion improve mobility (180). Pain resolves spontaneously only in some patients despite similar functional status. Persistence of shoulder pain suggests a decreased adaptation to pain (73).

Shoulder subluxation. Shoulder subluxation results from the inferior displacement of the paretic arm (180). Glenohumeral subluxation was present in nearly 50% of patients in a case-control study of 107 hemiplegic adults with stroke (137).

Subluxation is diagnosed by palpation, plain radiographs of the shoulder, or ultrasonography (141). Careful manipulation of the weak limb during transfers is important for preventing subluxation (188). Support slings have produced mixed results (136). Moreover, one study showed that subluxation correction was impaired by wearing an arm sling (182). Observational studies suggest that shoulder orthoses reduce vertical subluxation and pain (126). In a multicenter randomized controlled trial, the elastic dynamic sling was superior to the Bobath sling (81).

Theoretical benefits of electrical stimulation of the shoulder include maintenance of muscle bulk and tone and enhancement of functional recovery (180). Long-term follow-up was limited, however. A meta-analysis of seven clinical trials showed that electrical stimulation added to conventional therapy reduced subluxation early, but not late, after stroke (01). A randomized pilot study of 31 stroke survivors showed that the addition of kinesio-tape or neuromuscular electric stimulation (NEMS) to conventional therapy did not further improve shoulder pain (58). Another randomized controlled study of 28 patients showed that adding NMES to standard therapy and external shoulder support improved the subluxation and arm function but not the pain level (92).

Intramuscular electrical stimulation in 61 chronic stroke survivors with shoulder pain and subluxation significantly reduced pain levels up to 12-month follow-up (22). Another single-blind randomized trial of 38 patients with subacute or chronic stroke showed better pain control with EMG-triggered neuromuscular electric stimulation compared to transcutaneous electrical nerve stimulation (TENS), both immediately and at 1-month follow-up (28). In a case series of five patients, a fully implantable peripheral nerve stimulator was safe and significantly reduced shoulder pain after 12 months (197).

A systematic review of neuromuscular electric stimulation showed a reduction of shoulder subluxation in the acute and subacute phase but not in the chronic stroke or reduction of shoulder pain (93).

Spasticity. Spasticity of the shoulder following stroke is painful and disabling. The arm posture is adducted and rotated medially with flexion at the elbow, wrist, and fingers. Analgesics and muscle relaxants may alleviate the symptoms.

Botulinum toxin type A injection has been assessed in several small short-term studies with mixed results. Injection in the pectoralis major reduced pain caused by spasticity in the first week after stroke in a double-blind, randomized clinical trial of 31 patients (110). Injection in the subscapularis muscle improved pain control (199). A prospective randomized, double-blind, placebo-controlled trial found that botulinum toxin A reduced disability but not the pain (109). Moreover, a meta-analysis of 950 patients showed that the overall effectiveness of botulinum toxin type A does not differ from placebo for post-stroke patients with upper limb spasticity (63). A higher dose of botulinum toxin A was also studied; however, there are insufficient data to recommend this approach (61).

IncobotulinumtoxinA is a highly purified form of botulinum toxin with lower immunogenicity. A pooled analysis of data from six phase 2 or 3 studies, including 415 patients treated with incobotulinumtoxinA, showed that it is effective against spastic shoulder pain, especially if used in multiple injection cycles (198).

Although botulinum toxin A may reduce spasticity and pain associated with stroke, it is unknown if it improves the functional capacity (97). Botulinum toxin is not indicated for non-spastic causes of shoulder pain (84).

Other promising therapeutic modalities include repetitive transcranial magnetic stimulation (27), suprascapular nerve block (02; 146), modified wheelchair arm support (138), extracorporeal shock wave therapy (64), and mirror therapy (125).

Frozen shoulder. Also known as adhesive capsulitis, frozen shoulder is caused by recurrent local injuries and is characterized by shoulder pain and limited motion in all directions. It may be exacerbated by immobility and is often associated with rotator cuff tear. Contrast arthrogram is diagnostic in 50% of hemiplegic patients with shoulder pain (107). A placebo-controlled study showed that intra-articular injection of a corticosteroid in addition to physiotherapy improves pain control and mobility (21).

Shoulder-hand syndrome. This form of complex regional pain syndrome following stroke is characterized by severe shoulder and hand pain associated with dysautonomia (edema, changes in skin color and temperature, and excessive sweating). Atrophy of the skin and muscles of the shoulder and hand with sparring of the elbow often follows. The mechanism is probably central and peripheral sensitization due to stroke. However, involvement of the sympathetic system has not been demonstrated (145). Furthermore, shoulder subluxation and peripheral nerve damage increase the likelihood of developing complex regional pain syndrome (48).

The diagnosis of complex regional pain syndrome is primarily clinical. Bone scintigraphy may show increased periarticular uptake, particularly at the shoulder and wrist, and decreased bone mineral density in the paretic limb when compared to matched healthy controls (51; 86).

Preventative measures consist of avoidance of shoulder trauma. Treatment consists of physical therapy and pain management. Mirror therapy may reduce pain and improve the function of the upper limb (19).

Severe sympathetic dysfunction may benefit from regional block, although strong evidence is lacking. Investigations into neuromodulation through spinal cord stimulation and administration of intrathecal analgesia have been undertaken in patients with complex regional pain syndrome (86).

Two systematic reviews of acupuncture found several heavily biased studies, suggesting the need for further randomized clinical studies (24; 143).

Heterotopic ossification. Heterotopic ossification of the soft tissue of the paretic limb contributes to post-stroke pain and dysfunction (135). Calcification may also occur in the nonparetic limb (83; 53). Nonsteroidal anti-inflammatory drugs and radiation therapy may prevent its occurrence (08). If heterotopic ossification impairs rehabilitation and medical treatment fails, surgical resection is an option (117).

Urinary incontinence. Urinary incontinence within the first 7 days of stroke was noted in 53% of patients. One third of these patients remained incontinent at 12-month follow-up. Furthermore, those who were incontinent in the acute phase were four times more likely to be institutionalized after 1 year and a predictor of death (65).

Post-stroke urinary incontinence can be described based on etiology (167):

(1) Urge urinary incontinence: urgency followed by involuntary leakage that can result from a lesion of the central micturition pathways.

(2) Functional urinary incontinence: inability to achieve self-toileting due to impaired mobility from stroke.

(3) Stress urinary incontinence: involuntary leakage during effort such as coughing. This is usually present before stroke onset but is exacerbated by coughing associated with dysphagia and aspiration.

There are insufficient data from clinical trials to guide incontinence care in patients with stroke (177). Urinary incontinence after stroke is managed similarly to the general population. Treatment begins with behavioral interventions like timed voiding, prompted voiding, bladder retraining with urge suppression, pelvic floor muscle retraining, and compensatory rehabilitation approaches (39). Pharmacological treatment and urologic consultation with surgical intervention may be necessary. OnabotulinumtoxinA decreases the neurogenic detrusor overactivity and control of the overactive bladder (131).

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Medical complications of stroke

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Anterior cerebral artery stroke syndromes
Complex regional pain syndrome
Depression after stroke
Hypertensive intracerebral hemorrhage
Ischemic stroke
- Nontraumatic intracerebral hemorrhage
- Stroke: supportive care
- Stroke therapy
- Vascular dementia

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Stroke & Vascular Disorders

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Stroke (hemorrhagic)

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Medical complications of stroke …

Medical complications of stroke

Cite this article

Introduction

Overview

Key points

Classification scheme for medical complications of stroke

Table 1. Medical Complications of Stroke: A Classification Scheme

Table 2. Medical Complications of Stroke

Deep venous thrombosis and pulmonary embolism

Table 3. Wells Prediction Rule for Diagnosing Deep Venous Thrombosis

Table 4. Wells Prediction Rule for Diagnosing Pulmonary Embolism

Prevention of thromboembolism

Bone disease: osteoporosis and fractures

Table 5. Risk Factors for Osteoporotic Fractures in Women

Table 6. World Health Organization (WHO) Definition of Osteoporosis

Complications of stroke

Pain syndromes

References

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Fusiform and dolichoectatic aneurysms

Neoplastic and infectious aneurysms

Aortic atherosclerosis and stroke

Stroke associated with cerebral angiography

Sneddon syndrome

Cerebral venous thrombosis

Fibromuscular dysplasia

Brainstem hemorrhage

Medical complications of stroke

Cite this article

Introduction

Overview

Key points

Classification scheme for medical complications of stroke

Table 1. Medical Complications of Stroke: A Classification Scheme

Table 2. Medical Complications of Stroke

Deep venous thrombosis and pulmonary embolism

Table 3. Wells Prediction Rule for Diagnosing Deep Venous Thrombosis

Table 4. Wells Prediction Rule for Diagnosing Pulmonary Embolism

Prevention of thromboembolism

Bone disease: osteoporosis and fractures

Table 5. Risk Factors for Osteoporotic Fractures in Women

Table 6. World Health Organization (WHO) Definition of Osteoporosis

Complications of stroke

Pain syndromes

References

Contributors

Author

Editor

Former Authors

Patient Profile

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Fusiform and dolichoectatic aneurysms

Neoplastic and infectious aneurysms

Aortic atherosclerosis and stroke

Stroke associated with cerebral angiography

Sneddon syndrome

Cerebral venous thrombosis

Fibromuscular dysplasia

Brainstem hemorrhage

This is an article preview.
Start a Free Account
to access the full version.