Medical complications of stroke …

Adrian Marchidann MD

Stroke & Vascular Disorders

Updated 10.26.2023
Released 06.07.2001
Expires For CME 10.26.2026

Medical complications of stroke

Author: Adrian Marchidann MD

See Contributor Disclosures

Editor: Steven R Levine MD

Medical complications of stroke

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Introduction

Overview

Medical complications following stroke account for significant morbidity and mortality. Early recognition and management result in a more favorable outcome. 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 because of impaired limb mobility. In the case of intracerebral hemorrhage, early anticoagulation is of concern.
	• Although promising, the new oral anticoagulants require further testing.
	• During the acute stroke phase, thrombolysis should be avoided for treatment of severe pulmonary embolism.
	• 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 (168; 69).

Medical complications of stroke decrease survival by several years (08). 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 falls, pressure sores, psychiatric disorders, and central poststroke pain. Some of the most beneficial measures are swallowing evaluation to prevent aspiration, avoidance of urinary catheters, and prophylaxis of thromboembolism (168).

The classification scheme for post-stroke medical complications is outlined in Table 1 (95). Several of these topics are discussed in other clinical summaries. The topics discussed in this article are listed in Table 2.

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 (95).

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 is a major cause of morbidity and mortality after acute ischemic stroke. In the absence of prophylaxis, thrombus formation is seen on the second day after stroke. At 2 weeks, thrombosis may affect up to 50% of patients (18). The risk of thrombosis increases with severity of paralysis and hypercoagulability (93). Before routine prophylaxis, 37% of patients with clinically apparent venous thrombosis died from pulmonary embolism (21). Pulmonary embolism accounts for 5% to 10% of deaths in the acute period of stroke and 25% later (74). In a small series of patients with stroke, sudden death occurred in 50% of patients with pulmonary embolism (201).

Among patients with ischemic stroke discharged between 1979 to 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 (169).

Etiology of venous thromboembolism is multifactorial and is described by the Virchow triad: vessel wall damage, venous stasis, and hypercoagulability (163; 79). Damage to the vessel wall prevents the endothelium from inhibiting coagulation and initiating local fibrinolysis.

Virchow triad

In 1862, Rudolf Virchow proposed the pathophysiology triad of thrombosis: blood vessel wall lesion, blood flow stasis, and alterations in blood coagulability. (Contributed by Dr. Steven Lentz.)

The risk factors for arterial stroke and venous thromboembolism overlap significantly. Obesity, cigarette smoking, and hypertension are independent risk factors for pulmonary embolism (52). Following stroke, the paretic leg is preferentially affected due to repeated minor trauma, loss of the muscle contractility, venous stasis, and accumulation of activated coagulation factors (81). Additionally, atrial fibrillation, oral contraceptives, hormone-replacement therapy, and thrombophilias (hyperhomocysteinemia and activated protein C resistance) predispose to both venous thromboembolism and ischemic strokes (135; 51).

A systematic review of Medline and Embase searches from January 1990 onwards highlights more risk factors, including previous venous thromboembolism, pre-stroke disability, large infarct, low Barthel index, age, dehydration, delayed institution of preventive measures, infection, prolonged hospital day, cancer, infection, and elevated C-reactive protein and D-dimer (183).

Pulmonary embolism may be asymptomatic or cause severe respiratory failure and even sudden death. The lung scans of asymptomatic patients with deep venous thrombosis demonstrate pulmonary emboli in 40% of cases (128). Although 90% of pulmonary embolism originates in the legs, ultrasound detects venous thrombosis in only 29% of these patients (184). Most remainder emboli arise from the pelvic deep veins (74).

Differential diagnosis. Edema of the paretic limb may mimic deep venous thrombosis. Respiratory failure may be due to 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 (17; 81).

Diagnostic workup. Most patients with pulmonary embolism have at least one of these symptoms: sudden onset dyspnea, chest pain, syncope, and hemoptysis (123).

Pretest clinical probability of pulmonary embolism (Tables 3 and 4) and the scoring developed, Wells (194), Geneva (196), and Pisa (124), are used to determine the need further studies.

D-dimer level is elevated in myocardial infarction, pneumonia, heart failure, cancer, recent surgery, and stroke (51). Normal D-dimer level combined with low pretest clinical probability excludes thrombotic disease.

A high pretest probability should not affect clinical decision (195). If clinical probability is high, a normal D-dimer level does not exclude venous thromboembolism. This needs to be confirmed with lower limbs ultrasonography or helical CT scan of the chest (162). However, CT alone may not be sensitive enough to exclude pulmonary embolism in these patients (158).

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 asymptomatic side 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: (194)

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: (26)

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 (prior to anticoagulation), and postural ischemia due to large-vessel carotid or vertebrobasilar artery disease. If possible, avoid intravenous lines in the paretic arm as they may increase the risk of deep venous thrombosis.

Compression stockings. The thigh-length graduated compression stockings (GCS) do not reduce the incidence of proximal deep venous thrombosis after stroke and caused skin complications (33).

However, intermittent compression stockings prevent deep venous thrombosis and increase survival in patients with acute stroke (32). In an observational study, sequential compression devices added to unfractionated heparin reduced the risk of deep vein thrombosis more than 40-fold (74). The American College of Chest Physicians recommends intermittent pneumatic compression devices or elastic stockings for patients who have contraindications to anticoagulants (80).

Anticoagulation. During acute stroke, either low-dose unfractionated heparin, low molecular weight heparin, or danaparoid may be used (80). Extension of thromboprophylaxis up to 4 to 5 weeks seems to be more beneficial than short-term prophylaxis (186).

Unfractionated heparin 5000 IU sc given three times 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 (116).

Low molecular weight heparins (LMWH) are administered once daily. The risk for developing thrombocytopenia and osteoporosis is lower than with unfractionated heparin. A meta-analysis showed that LMWH had the best benefit-to-risk ratio in patients with acute stroke and is cost-effective (73; 167; 154).

In patients at risk for heparin-induced thrombocytopenia (HIT), fondaparinux, an indirect factor Xa inhibitor, 2.5 mg sc is a safe alternative (58).

Direct oral anticoagulation (DOAC) agents have the advantage of convenience over heparin or warfarin. Four systematic reviews, network meta-analyses, and cost-effectiveness analyses of randomized controlled trials have not shown strong evidence that DOACs should replace postoperative LMWH in primary prevention of venous thromboembolism. 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 (174).

After intracerebral hemorrhage, preventive anticoagulation is delayed until hemorrhage expansion stops. In a small, randomized study, initiation of low-dose unfractionated heparin (5000 IU subcutaneously three times daily) on the second day from ictus significantly lowered the incidence of pulmonary embolism, compared with delayed therapy on day 4 or day 10 (13). In another prospective randomized study of 75 patients, low-dose enoxaparin (40 mg sc daily) initiated 2 days after onset was as effective and safe as the compression stockings (138). However, a Cochrane review found two randomized controlled trials totaling 120 patients that failed to provide evidence for or against the use of anticoagulants for venous thromboembolism prophylaxis (150). A randomized controlled trial, stopped prematurely because of low recruitment, and a meta-analysis that included these patients showed that anticoagulation for venous thromboembolism prevention is safe but did not significantly reduce the incidence of venous thromboembolism, pulmonary embolism, or death (142).

Treatment of venous thromboembolism in stroke patients. Initiation of treatment for suspected venous thromboembolism depends on the strength of the clinical suspicion, timing of the confirmatory tests, and location of the deep venous thrombosis or pulmonary embolism.

For high clinical suspicion, parenteral anticoagulant is indicated while waiting for the results of diagnostic tests. If the suspicion is intermediate, initiation of parenteral anticoagulation is indicated if the confirmatory tests are delayed for more than 4 hours. In patients with low suspicion, there is no need to initiate parenteral anticoagulation provided the results will be available within 24 hours.

Deep venous thrombosis that is isolated, distal, without severe symptoms, and unlikely to extend may only benefit from serial imaging for 2 weeks. However, severe symptoms and the risk of or extension on serial ultrasound warrant anticoagulation. Once-daily LMWH or fondaparinux is preferred over unfractionated heparin.

The post-thrombotic syndrome may be avoided by systemic or catheter-directed thrombolysis, which are associated with a higher hemorrhagic risk.

If anticoagulation is contraindicated due to intracerebral hemorrhage, a temporary inferior vena cava (IVC) filter is recommended. Anticoagulation should be resumed if the contraindication no longer exists. However, insertion of IVC filter is not recommended in addition to anticoagulation.

The first 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 before further recommendations are made. Provoked venous thromboembolism by either surgery or a transient nonsurgical factor is treated for 3 months. If cancer is present, extended anticoagulation is recommended regardless of the bleeding risk.

Compression stockings for 2 years or more are indicated in patients with symptomatic deep venous thrombosis of the leg or post-thrombotic syndrome. If they fail to relieve the symptoms, a trial of intermittent compression device is reasonable.

Severe acute pulmonary embolism causing hypotension benefits from intravenous thrombolysis. Catheter-directed thrombolysis is associated with fewer cerebral hemorrhagic complications than systemic thrombolysis but does not decrease mortality (105). If intravenous thrombolysis or catheter-assisted thrombectomy fail or the patient is in shock and likely to die within a few hours, surgical thrombectomy may be beneficial (80).

Intravenous unfractionated heparin and oral warfarin are initiated on the same day. Heparin is continued for a minimum of 5 days or at least 24 hours of INR 2 or above. The ideal INR target is 2 to 3. Warfarin dosage should begin with 5 mg (60; 36). Anticoagulation clinics improve warfarin anticoagulation control, patient outcomes, and health care costs (28).

During pregnancy, warfarin is teratogenic and replaced by heparin. Early mobilization and stopping procoagulant agents (eg, hormone-replacement therapy or oral contraceptives) are both advisable.

Active cancer is another situation in which heparin is preferred to warfarin. Additionally, if the patient is unreliable, long-term subcutaneous injections of a low molecular weight heparin is an alternative.

Dabigatran was non-inferior to warfarin and was associated with fewer hemorrhagic complications (165).

Rivaroxaban is also effective for the treatment of venous thromboembolism. A dose of 15 mg po twice daily for 3 weeks followed by 20 mg daily was noninferior to enoxaparin followed by warfarin (43; 44).

Moreover, apixaban was not inferior to enoxaparin followed by warfarin, yet caused fewer clinically relevant bleeding. The dose of apixaban was 10 mg po bid for 7 days, followed by 5 mg po bid for 6 months (03).

The American College of Chest Physicians recommends LMWH or vitamin K antagonists to the newer oral agents (80).

Bone disease: osteoporosis and fractures

Stroke impairs mobility and stability, leading to osteoporosis, falls, and fractures. Most fractures occur late, on the hemiplegic side (161). Sequential bilateral hip fractures were seen more frequently in institutionalized patients with history of stroke and osteomalacia (29). Hip fractures are associated with an increased risk of institutionalization and death (46).

Epidemiology. Out of 130,000 discharged acute stroke patients, 2.0% suffered fractures by 1 year and 10.6% by 10 years (40). The risk of hip fracture increases 4-fold after stroke (75).

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 (161). After stroke, approximately 30% of fractures occur in the upper extremities (144).

Clinical risk factors that contribute to fracture risk independent of bone mineral density are presented in Table 5 (76).

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 (76)

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 the paretic hip was most commonly fractured after stroke. Fracture incidence was two to four times higher than in the general population (161). In another study, the risk factors of fractures after stroke are weakness, numbness, neglect, imbalance, and decreased awareness (156).

Vitamin D deficiency increases the risk of fracture in disabled elderly patients (147). Nutrition, light exposure, and medications are additional contributors. Proton pump inhibitors increase the risk of osteoporosis (107). Dabigatran, a direct oral thrombin inhibitor, is associated with a lower risk of osteoporotic fractures compared to warfarin (96).

Clinical features. Vertebral fractures may cause chronic back pain, spinal deformity, functional limitations, and increased risk of hospitalization and mortality (72; 47).

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 (76).

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 1 or more osteoporotic fractures

Treatment. Osteoporosis management aims at prevention of fractures, increased bone strength, and physical function (136). A single-center registry database of 1307 consecutively registered patients with acute ischemic stroke shows that osteoporosis pharmacotherapy may reduce poor function and improve functional outcomes at 3 months and 1 year after ischemic stroke onset (171).

A pyramidal approach has been recommended in which the base represents lifestyle changes: calcium and vitamin D intake, physical activity, and fall prevention (137). 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 (48). Reversal of osteoporosis after hemiplegia requires daily weight training for a minimum of 60 and 90 minutes for males and females, respectively (59).

Calcium and vitamin D supplementation help prevent fractures (39). 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 (155).

Denosumab (formerly known as AMG 162) 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 (117).

Romosozumab, administered 210 mg subcutaneously monthly, is a new promising antiresorptive agent (164). This is a monoclonal antibody against sclerostin, a natural inhibitor of the Wnt signaling pathway that promotes bone mineral density. One important contraindication of romosozumab is stroke in the past year (94).

Other antiresorptive agents that increase the risk of thromboembolism are raloxifene and strontium ranelate (103; 190).

Complications of stroke

Falls. Traumatic brain injury is responsible for 78% of fall-related deaths and 79% of the cost (175). Stroke doubles the risk of falling (70). Most falls occurred during transfers between a wheelchair and bed (149). Predictors of falls after stroke are executive dysfunction, imbalance while dressing, and depression (92; 111; 176). Depression and anxiety predominantly affect young women with low socioeconomic status (19). Comorbidities, polypharmacy, decreased vision, and decreased cognition in stroke patients often increase the risk of falling.

The Postural Assessment Scale for Stroke patients (PASS) and the Postural Control and Balance for Stroke test (PCBS) evaluate postural control and assess the risk of fall after stroke (10; 157).

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 ischemia of the skin over the weight-bearing points, usually the bony prominences. If infected, they can cause great morbidity and mortality (23).

A Swedish retrospective study of 161 patients with stroke recorded 116 pressure ulcers, 30 patients having more than one ulcer (61). Sacrum and the lower body are most often affected (56).

Other risk factors include diabetes, peripheral vascular disease, urinary incontinence, and low body mass index (12).

Pressure sores are classified according to stages (132):

	Stage I—nonblanchable 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 (11; 16).

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 use of medical grade sheepskins reduce the incidence of pressure ulcers (120). Managing incontinence, daily checks, and high protein nutritional intake help maintain the skin barrier integrity (181).

Pressure sore treatment consists of using proper wound dressing and removal of the necrotic debris to prevent bacterial growth and infection (54). Electrical stimulation for sore treatment has uncertain utility and cannot be recommended outside a clinical trial (06).

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, use of manual wheelchairs increases the likelihood of an upper limb nerve injury like the median and ulnar nerves (14). Hematoma, a complication of anticoagulation, may result in brachial plexus injury or femoral nerve entrapment (45).

Electrodiagnostic studies help establish the nerve injury site and assess the severity of injury 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 stroke, many patients experience pain that affects the 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 manifests acutely; musculoskeletal and central pain occur more often in the subacute and chronic stage, and spasticity-related pain appears in the chronic stage (145).

Central post-stroke pain. Central nervous system pain feels like burning, aching, throbbing, cramp, or a combination of these and is often triggered by a non-noxious stimulus. Elderly patients tend to experience nonburning pain. Characteristic to central pain is the sensory loss to pinprick or temperature in the same region; however, the spinothalamic sensation may persist in many patients (90).

In a systematic review of 69 papers, central pain was reported in 11% of strokes in any locations and in 50% of patients with medulla and thalamus strokes. Central pain coincided with acute stroke in 26% of patients and may occur up to 12 months afterwards (104).

Lesions of the ventral posterolateral, ventral medial, and medial dorsal nucleus and the trigemino- and spinothalamocortical pathways, including the brainstem and cerebral cortex, lead to post-stroke pain (15; 35; 133). Pure central post-stroke pain, sometimes mistaken for malingering or psychogenic pain, is related to the spinothalamic tracts from the posterolateral mesencephalon (34). 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 (83). Lesions of the ventral caudal nucleus suggest involvement of other pathways in central pain development (125; 82).

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 most severe pain in an extremity, whereas the infratentorial lesions are in the face (15). Imaging injured spinothalamic strokes may be achieved with diffusion tensor tractography (65).

There is a lack of high-quality clinical trials of central pain treatment. Post-stroke pain can be resistant to standard use of analgesics and opioids.

Amitriptyline has been effective in a small, randomized controlled study (99); however, there is a need for more data (126).

Pregabalin is effective at escalating doses of 150, 300, and 600 mg/day (191). In addition, it may improve pain-related anxiety and sleep disturbances (85). Duloxetine was also studied with success in a small study (87), but a prior clinical randomized double-blind placebo-controlled trial did not show a significant decrease in pain intensity (192).

Carbamazepine is probably effective for chronic neuropathic pain, but there is a lack of information beyond 4 weeks (199). The effect of gabapentin on neuropathic pain is probably not superior to carbamazepine (197).

Lamotrigine in a dose of 200 mg daily was moderately effective in a small, randomized study (189), 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 for rash (198).

Levetiracetam is not effective for post-stroke pain treatment (71; 200).

Intravenous lidocaine and morphine have a limited role in treating central pain due to the delivery method and side-effects (07). Intrathecal baclofen improved central post-stroke pain in a small case series (177). Fluvoxamine and mexiletine may also be used as adjuvants for pain treatment (84). Botulinum toxin, BTX-A, has been used with some success for neuropathic pain; however, a clinical trial is needed to confirm the initial results (63).

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 (127; 180). For multimodal physiotherapy, electrotherapy, and manual lymphatic drainage, the evidence is absent or of very low quality (170).

The cold caloric stimulation can rapidly relieve thalamic pain (159; 118; 119). Refractory thalamic pain was successfully treated by stellate ganglion block (106). In one case report, ultrasound guided block of the stellate ganglion with lidocaine had a lasting effect at 9 months (110).

Repetitive transcranial magnetic stimulation (rTMS) is a potentially useful noninvasive method for pain control (100). Fiber tracking with diffusion tensor imaging may predict response to rTMS (53). However, there is a significant publication bias (41). A systematic review of transcranial direct current stimulation (tDCS) on neuropathic pain in patients with stroke shows promise, but there is high heterogeneity (38; 160). rTMS may control chronic as well as acute pain after stroke (101; 113).

Motor cortex stimulation was used successfully for intractable central pain. The motor prefrontal cortex is preferred because the procedure is less invasive, achieves better pain control (48% vs. 25% for deep brain stimulation vs. 7% for spinal cord stimulation), and is less likely to trigger painful sensations (78). Motor cortex stimulation is also useful for painful brainstem and spinal cord lesions (178). Pain relief may persist for 12 months (173; 188). 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 (172). Epidural hematoma and subdural effusion are potential complications. Motor cortex stimulation is thought to work by increasing regional cerebral blood flow to the ipsilateral corticothalamic connections or by anti-inflammatory effects (20; 166).

For nonthalamic lesion, spinal cord stimulation achieved relief for more than 12 months in 44.4% of patients (179). Other useful locations for electrical stimulation include periventricular grey matter and the centromedian thalamic nucleus (131; 153; 04).

The data on neurosurgical management of central post-stroke pain are limited, and further studies are needed to confirm these findings (37; 49).

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 (109). Shoulder pain frequency has decreased over the last 15 years, suggesting an improvement in stroke care and rehabilitation (122).

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 (185). Adhesive capsulitis and shoulder subluxation, which occurs in 50% and 44% of patients, respectively, are the most common causes of shoulder pain (112). 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 (108).

In the flaccid stage, inferior subluxation may benefit from shoulder support and electrical stimulation of the muscle. In the spastic stage, reduced mobility should be addressed by muscle relaxants and maintenance of range of motion (185). Pain resolves spontaneously in some but not all patients with similar functional status. Persistence of shoulder pain suggests a decreased adaptation to pain (77).

Shoulder subluxation. Shoulder subluxation results from the inferior displacement of the paretic arm (185). Glenohumeral subluxation was present in nearly 50% of patients in a case-control study of 107 hemiplegic adults with stroke (141).

Subluxation is diagnosed by palpation, plain radiographs of the shoulder, or ultrasonography (146). Careful manipulation of the weak limb during transfers is important for preventing subluxation (193). Support slings have produced mixed results (140). Moreover, one study showed that subluxation correction was impaired by wearing an arm sling (187). Observational studies suggest that shoulder orthoses reduce vertical subluxation and pain (130). In a multicenter randomized controlled trial, the elastic dynamic sling was superior to the Bobath sling (86).

Theoretical benefits of electrical stimulation of the shoulder include maintenance of muscle bulk and tone and enhancement of functional recovery (185). 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 (62). 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 (97).

Intramuscular electrical stimulation in 61 chronic stroke survivors with shoulder pain and subluxation significantly reduced pain levels up to 12-month follow-up (25). Another single-blinded 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 (31). In a case series of five patients, a fully implantable peripheral nerve stimulator was safe and significantly reduced shoulder pain at 12-month follow-up (202).

A systematic review of neuromuscular electric stimulation showed reduction of shoulder subluxation in the acute and subacute phase but not in the chronic stroke or reduction of shoulder pain (98).

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 (115). Injection in the subscapularis muscle improved pain control (204). A prospective randomized, double-blind, placebo-controlled trial found that botulinum toxin A reduced disability but not the pain (114). 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 (66). A higher dose of botulinum toxin A was also studied; however, there are insufficient data to recommend this approach (64).

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 (203).

Although botulinum toxin A may reduce spasticity and pain associated with stroke, it is yet undetermined if it improves the functional capacity, as this is related more with weakness than spasticity. Long-term studies are needed to make this determination (102). Botulinum toxin is not indicated for nonspastic causes of shoulder pain (89).

Other promising therapeutic modalities include repetitive transcranial magnetic stimulation (30), suprascapular nerve block (02; 152), modified wheelchair arm support (143), extracorporeal shock wave therapy (67), and mirror therapy (129).

Frozen shoulder. Also known as adhesive capsulitis, frozen shoulder is caused by recurrent local injuries and 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 enhanced arthrogram is diagnostic in 50% of hemiplegic patients with shoulder pain (112). A placebo-controlled study showed that a combination of intra-articular corticosteroids and physiotherapy was effective in improving pain and mobility (24).

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 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 (151). Furthermore, shoulder subluxation and peripheral nerve damage increase the likelihood of developing complex regional pain syndrome (50).

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 (55; 91).

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 (22).

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 (91).

Two systematic reviews of acupuncture found several heavily biased studies, suggesting the need for further randomized clinical studies (27; 148).

Heterotopic ossification. Heterotopic ossification of the soft tissue of the paretic limb contributes to post-stroke pain and dysfunction (139). Calcification may also occur in the nonparetic limb (88; 57). Nonsteroidal anti-inflammatory drugs and radiation therapy may prevent its occurrence (09). If heterotopic ossification impairs rehabilitation and medical treatment fails, surgical resection is an option (121).

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 (68).

Post-stroke urinary incontinence can be described based on etiology (175):

(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 on effort such as coughing. This is usually present prior to 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 (182). Management of urinary incontinence after stroke is like that of the general population. Treatment begins with behavioral interventions like timed voiding, prompted voiding, bladder retraining with urge suppression, and pelvic floor muscle retraining and compensatory rehabilitation approaches (42). Pharmacological treatment and urologic consultation with surgical intervention may be necessary. OnabotulinumtoxinA has been used with success for neurogenic detrusor overactivity and overactive bladder (134).

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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
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- Stroke: supportive care
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- Vascular dementia

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Medical complications of stroke …

Medical complications of stroke

Introduction

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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

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Vein of Galen malformations

Patent foramen ovale

Neuroimaging in acute stroke

Atrial myxoma

Anterior cerebral artery stroke syndromes

Hemorrhagic transformation of ischemic stroke

Intracerebral hemorrhage due to thrombolytic therapy

White matter abnormalities in the brain

Medical complications of stroke

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

Media

References

Contributors

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Editor

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Vein of Galen malformations

Patent foramen ovale

Neuroimaging in acute stroke

Atrial myxoma

Anterior cerebral artery stroke syndromes

Hemorrhagic transformation of ischemic stroke

Intracerebral hemorrhage due to thrombolytic therapy

White matter abnormalities in the brain

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