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).

References

01: Ada L, Foongchomcheay A. Efficacy of electrical stimulation in preventing or reducing subluxation of the shoulder after stroke: a meta-analysis. Aust J Physiother 2002;48(4):257-67. PMID 12443520
02: Adey-Wakeling Z, Crotty M, Shanahan EM. Suprascapular nerve block for shoulder pain in the first year after stroke: a randomized controlled trial. Stroke 2013;44(11):3136-41. PMID 23970790
03: Agnelli G, Buller HR, Cohen A, et al. Oral apixaban for the treatment of acute venous thromboembolism. N Engl J Med 2013;369(9):799-808. PMID 23808982
04: Alves RV, Asfora WT. Deep brain stimulation for Dejerine-Roussy syndrome: case report. Minim Invasive Neurosurg 2011;54(4):183-6. PMID 21922448
05: Anonymous. How do stroke units improve patient outcomes? A collaborative systematic review of the randomized trials. Stroke Unit Trialists Collaboration. Stroke 1997;28(11):2139-44. PMID 9368554
06: Arora M, Harvey LA, Glinsky JV, et al. Electrical stimulation for treating pressure ulcers. Cochrane Database Syst Rev 2020;1(1):CD012196. PMID 31962369
07: Attal N, Gaude V, Brasseur L, et al. Intravenous lidocaine in central pain: a double-blind, placebo-controlled, psychophysical study. Neurology 2000;54(3):564-74. PMID 10680784
08: Bae HJ, Yoon DS, Lee J, et al. In-hospital medical complications and long-term mortality after ischemic stroke. Stroke 2005;36(11):2441-5. PMID 16224097
09: Balboni TA, Gobezie R, Mamon HJ. Heterotopic ossification: athophysiology, clinical features, and the role of radiotherapy for prophylaxis. Int J Radiat Oncol Biol Phys 2006;65(5):1289-99. PMID 16863921
10: Benaim C, Perennou DA, Villy J, Rousseaux M, Pelissier JY. Validation of a standardized assessment of postural control in stroke patients: the Postural Assessment Scale for Stroke Patients (PASS). Stroke 1999;30(9):1862-8. PMID 10471437
11: Bergstrom N, Demuth PJ, Braden BJ. A clinical trial of the Braden Scale for Predicting Pressure Sore Risk. Nurs Clin North Am 1987;22(2):417-28. PMID 3554150
12: Berlowitz DR, Brandeis GH, Anderson JJ, et al. Evaluation of a risk-adjustment model for pressure ulcer development using the Minimum Data Set. J Am Geriatr Soc 2001;49(7):872-6. PMID 11527477
13: Boeer A, Voth E, Henze T, Prange HW. Early heparin therapy in patients with spontaneous intracerebral haemorrhage. J Neurol Neurosurg Psychiatry 1991;54(5):466-7. PMID 1865215
14: Boninger ML, Impink BG, Cooper RA, Koontz AM. Relation between median and ulnar nerve function and wrist kinematics during wheelchair propulsion. Arch Phys Med Rehabil 2004;85(7):1141-5. PMID 15241765
15: Bowsher D, Leijon G, Thuomas KA. Central poststroke pain: correlation of MRI with clinical pain characteristics and sensory abnormalities. Neurology 1998;51(5):1352-8. PMID 9818859
16: Braden BJ, Maklebust J. Preventing pressure ulcers with the Braden scale: an update on this easy-to-use tool that assesses a patient's risk. Am J Nurs 2005;105(6):70-2. PMID 15930875
17: Brandjes DP, Buller HR, Heijboer H, et al. Randomised trial of effect of compression stockings in patients with symptomatic proximal-vein thrombosis. Lancet 1997;349(9054):759-62. PMID 9074574
18: Brandstater ME, Roth Ej, Siebens HC. Venous thromboembolism in stroke: literature review and implications for clinical practice. Arch Phys Med Rehabil 1992;73(5-S):S379-91. PMID 1301012
19: Broomfield NM, Quinn TJ, Abdul-Rahim AH, Walters MR, Evans JJ. Depression and anxiety symptoms post-stroke/TIA: prevalence and associations in cross-sectional data from a regional stroke registry. BMC Neurol 2014;14:198. PMID 25269762
20: Brown JA. Motor cortex stimulation. Neurosurg Focus 2001;11(3):E5. PMID 16519425
21: Byrne JJ. Phlebitis: a study of 748 cases at the Boston City Hospital. New Engl J Med 1955;253(14):579-86. PMID 13265999
22: Cacchio A, De Blasis E, De Blasis V, Santilli V, Spacca G. Mirror therapy in complex regional pain syndrome type 1 of the upper limb in stroke patients. Neurorehabil Neural Repair 2009;23(8):792-9. PMID 19465507
23: Capon A, Pavoni N, Mastromattei A, Di Lallo D. Pressure ulcer risk in long-term units: prevalence and associated factors. J Adv Nurs 2007;58(3):263-72. PMID 17474915
24: Carette S, Moffet H, Tardif J, et al. Intraarticular corticosteroids, supervised physiotherapy, or a combination of the two in the treatment of adhesive capsulitis of the shoulder: a placebo-controlled trial. Arthritis Rheum 2003;48(3):829-38. PMID 12632439
25: Chae J, Yu DT, Walker ME, et al. Intramuscular electrical stimulation for hemiplegic shoulder pain: a 12-month follow-up of a multiple-center, randomized clinical trial. Am J Phys Med Rehabil 2005;84(11):832-42. PMID 16244520
26: Chagnon I, Bounameaux H, Aujesky D, et al. Comparison of two clinical prediction rules and implicit assessment among patients with suspected pulmonary embolism. Am J Med 2002;113(4):269-75. PMID 12361811
27: Chau JPC, Lo SHS, Yu X, et al. Effects of acupuncture on the recovery outcomes of stroke survivors with shoulder pain: a systematic review. Front Neurol 2018;9:30. PMID 29445354
28: Chiquette E, Amato MG, Bussey HI. Comparison of an anticoagulation clinic with usual medical care: anticoagulation control, patient outcomes, and health care costs. Arch Intern Med 1998;158(15):1641-7. PMID 9701098
29: Chiu KY, Pun WK, Luk KD, Chow SP. Sequential fractures of both hips in elderly patients--a prospective study. J Trauma 1992;32(5):584-7. PMID 1588646
30: Choi GS, Chang MC. Effects of high-frequency repetitive transcranial magnetic stimulation on reducing hemiplegic shoulder pain in patients with chronic stoke: a randomized controlled trial. Int J Neurosci 2018;128(2):110-6. PMID 28805107
31: Chuang LL, Chen YL, Chen CC, et al. Effect of EMG-triggered neuromuscular electrical stimulation with bilateral arm training on hemiplegic shoulder pain and arm function after stroke: a randomized controlled trial. J Neuroeng Rehabil 2017;14(1):122. PMID 29183339
32: CLOTS Trials Collaboration, Dennis M, Sandercock P, et al. Effectiveness of intermittent pneumatic compression in reduction of risk of deep vein thrombosis in patients who have had a stroke (CLOTS 3): a multicentre randomised controlled trial. Lancet 2013;382(9891):516-24. PMID 23727163
33: CLOTS Trials Collaboration, Dennis M, Sandercock PA, et al. Effectiveness of thigh-length graduated compression stockings to reduce the risk of deep vein thrombosis after stroke (CLOTS trial 1): a multicentre, randomised controlled trial. Lancet 2009;373(9679):1958-65. PMID 19477503
34: Convers P, Creac'h C, Beschet A, Laurent B, Garcia-Larrea L, Peyron R. A hidden mesencephalic variant of central pain. Eur J Pain 2020;24(7):1393-99. PMID 32419231
35: Craig AD. Distribution of trigeminothalamic and spinothalamic lamina I terminations in the macaque monkey. J Comp Neurol 2004;477(2):119-48. PMID 15300785
36: Crowther MA, Ginsberg JB, Kearon C, et al. A randomized trial comparing 5-mg and 10-mg warfarin loading doses. Arch Intern Med 1999;159(1):46-8. PMID 9892329
37: Cruccu G, Aziz TZ, Garcia-Larrea L, et al. EFNS guidelines on neurostimulation therapy for neuropathic pain. Eur J Neurol 2007;14(9):952-70. PMID 17718686
38: David MCMM, Moraes AA, Costa MLD, Franco CIF. Transcranial direct current stimulation in the modulation of neuropathic pain: a systematic review. Neurol Res 2018:1-9. PMID 29600889
39: Dawson-Hughes B, Harris SS, Krall EA, Dallal GE. Effect of calcium and vitamin D supplementation on bone density in men and women 65 years of age or older. N Engl J Med 1997;337(10):670-6. PMID 9278463
40: Dennis MS, Lo KM, McDowall M, West T. Fractures after stroke: frequency, types, and associations. Stroke 2002;33(3):728-34. PMID 11872896
41: Dufka FL, Munch T, Dworkin RH, Rowbotham MC. Results availability for analgesic device, complex regional pain syndrome, and post-stroke pain trials: comparing the RReADS, RReACT, and RReMiT databases. Pain 2015;156(1):72-80. PMID 25599303
42: Dumoulin C, Korner-Bitensky N, Tannenbaum C. Urinary incontinence after stroke: does rehabilitation make a difference? A systematic review of the effectiveness of behavioural therapy. Top Stroke Rehabil 2005;12(3):66-76. PMID 16110429
43: EINSTEIN Investigators, Bauersachs R, Berkowitz SD, et al. Oral rivaroxaban for symptomatic venous thromboembolism. N Engl J Med 2010;363(26):2499-2510. PMID 21128814
44: EINSTEIN-PE Investigators, Büller HR, Prins MH, et al. Oral rivaroxaban for the treatment of symptomatic pulmonary embolism. N Engl J Med 2012;366(14):1287-97. PMID 22449293
45: Elesber AA, Kent PD, Jennings CA. Compressive neuropathy of the brachial plexus and long thoracic nerve: a rare complication of heparin anticoagulation. Chest 2001;120(1):309-11. PMID 11451857
46: Empana JP, Dargent-Molina P, Breart G, EPIDOS Group. Effect of hip fracture on mortality in elderly women: the EPIDOS prospective study. J Am Geriatr Soc 2004;52(5):685-90. PMID 15086646
47: Ensrud KE, Thompson DE, Cauley JA, et al. Prevalent vertebral deformities predict mortality and hospitalization in older women with low bone mass. Fracture Intervention Trial Research Group. J Am Geriatr Soc 2000;48(3):241-9. PMID 10733048
48: Fiatarone MA, Marks EC, Ryan ND, Meredith CN, Lipsitz LA, Evans WJ. High-intensity strength training in nonagenarians. Effects on skeletal muscle. JAMA 1990;263(22):3029-34. PMID 2342214
49: Fontaine D, Hamani C, Lozano A. Efficacy and safety of motor cortex stimulation for chronic neuropathic pain: critical review of the literature. J Neurosurg 2009;110(2):251-6. PMID 18991496
50: Gokkaya NK, Aras M, Yesiltepe E, Koseoglu F. Reflex sympathetic dystrophy in hemiplegia. Int J Rehabil Res 2006;29(4):275-9. PMID 17106342
51: Goldhaber SZ. Pulmonary embolism. N Engl J Med 1998;339(2):93-104. PMID 9654541
52: Goldhaber SZ, Grodstein F, Stampfer MJ, et al. A prospective study of risk factors for pulmonary embolism in women. JAMA 1997;277(8):642-5. PMID 9039882
53: Goto T, Saitoh Y, Hashimoto N, et al. Diffusion tensor fiber tracking in patients with central post-stroke pain; correlation with efficacy of repetitive transcranial magnetic stimulation. Pain 2008;140(3):509-18. PMID 19004554
54: Grey JE, Harding KG, Enoch S. Pressure ulcers. BMJ 2006;332(7539):472-5. PMID 16497764
55: Greyson ND, Tepperman PS. Three-phase bone studies in hemiplegia with reflex sympathetic dystrophy and the effect of disuse. J Nucl Med 1984;25(4):423-9. PMID 6544813
56: Groeneveld A, Anderson M, Allen S, et al. The prevalence of pressure ulcers in a tertiary care pediatric and adult hospital. J Wound Ostomy Continence Nurs 2004;31(3):108-20; quiz 121-2. PMID 15867739
57: Gurcay E, Ozturk EA, Erdem T, Gurcay AG, Cakci A. Heterotopic ossification as rare complication of hemiplegia following stroke: two cases. Brain Inj 2013;27(13-14):1727-31. PMID 24088051
58: Hackett CT, Ramanathan RS, Malhotra K, et al. Safety of venous thromboembolism prophylaxis with fondaparinux in ischemic stroke. Thromb Res 2015;135(2):249-54. PMID 25554497
59: Han L, Li SG, Zhai HW, Guo PF, Chen W. Effects of weight training time on bone mineral density of patients with secondary osteoporosis after hemiplegia. Exp Ther Med 2017;13(3):961-5. PMID 28450926
60: Harrison L, Johnston M, Massicotte MP, Crowther M, Moffat K, Hirsh J. Comparison of 5-mg and 10-mg loading doses in initiation of warfarin therapy. Ann Intern Med 1997;126(2):133-6. PMID 9005747
61: Hede GW, Faxén-Irving G, Olin AÖ, Ebbeskog B, Crisby M. Nutritional assessment and post-procedural complications in older stroke patients after insertion of percutaneous endoscopic gastrostomy - a retrospective study. Food Nutr Res 2016;60:30456. PMID 27487849
62: Hochsprung A, Domínguez-Matito A, López-Hervás A, et al. Short- and medium-term effect of kinesio taping or electrical stimulation in hemiplegic shoulder pain prevention: A randomized controlled pilot trial. NeuroRehabilitation 2017;41(4):801-10. PMID 29254115
63: Intiso D, Basciani M, Santamato A, Intiso M, Di Rienzo F. Botulinum toxin type A for the treatment of neuropathic pain in neuro-rehabilitation. Toxins (Basel) 2015;7(7):2454-80. PMID 26134256
64: Intiso D, Centra AM, Gravina M, Chiaramonte A, Bartolo M, Di Rienzo F. Botulinum toxin-A high-dosage effect on functional outcome and spasticity-related pain in subjects with stroke. Toxins (Basel) 2023;15(8):509. PMID 37624266
65: Jang SH, Lee J, Yeo SS. Central post-stroke pain due to injury of the spinothalamic tract in patients with cerebral infarction: a diffusion tensor tractography imaging study. Neural Regen Res 2017;12(12):2021-4. PMID 29323041
66: Jia S, Liu Y, Shen L, et al. Botulinum toxin type A for upper limb spasticity in poststroke patients: a meta-analysis of randomized controlled trials. J Stroke Cerebrovasc Dis 2020a;29(6):104682. PMID 32305277
67: Jia G, Ma J, Wang S, et al. Long-term effects of extracorporeal shock wave therapy on poststroke spasticity: a meta-analysis of randomized controlled trials. J Stroke Cerebrovasc Dis 2020b;29(3):104591. PMID 31899073
68: John G, Bardini C, Mégevand P, Combescure C, Dällenbach P. Urinary incontinence as a predictor of death after new-onset stroke: a meta-analysis. Eur J Neurol 2016;23(10):1548-55. PMID 27425212
69: Johnston KC, Li JY, Lyden PD, et al. Medical and neurological complications of ischemic stroke: experience from the RANTTAS trial. RANTTAS Investigators. Stroke 1998;29(2):447-53. PMID 9472888
70: Jorgensen L, Engstad T, Jacobsen BK. Higher incidence of falls in long-term stroke survivors than in population controls: depressive symptoms predict falls after stroke. Stroke 2002;33(2):542-7. PMID 11823667
71: Jungehulsing GJ, Israel H, Safar N, et al. Levetiracetam in patients with central neuropathic post-stroke pain--a randomized, double-blind, placebo-controlled trial. Eur J Neurol 2013;20(2):331-7. PMID 22925226
72: Kado DM, Browner WS, Palermo L, Nevitt MC, Genant HK, Cummings SR. Vertebral fractures and mortality in older women: a prospective study. Study of Osteoporotic Fractures Research Group. Arch Intern Med 1999;159(11):1215-20. PMID 10371229
73: Kamphuisen PW, Agnelli G. What is the optimal pharmacological prophylaxis for the prevention of deep-vein thrombosis and pulmonary embolism in patients with acute ischemic stroke. Thromb Res 2007;119(3):265-74. PMID 16674999
74: Kamran SI, Downey D, Ruff RL. Pneumatic sequential compression reduces the risk of deep vein thrombosis in stroke patients. Neurology 1998;50(6):1683-8. PMID 9633711
75: Kanis J, Oden A, Johnell O. Acute and long-term increase in fracture risk after hospitalization for stroke. Stroke 2001;32(3):702-6. PMID 11239190
76: Kanis JA. Diagnosis of osteoporosis and assessment of fracture risk. Lancet 2002;359(9321):1929-36. PMID 12057569
77: Kashi Y, Ratmansky M, Defrin R. Deficient Pain Modulation in patients with chronic hemiplegic shoulder pain. Pain Pract 2018;18(6):716-28. PMID 29136315
78: Katayama Y, Yamamoto T, Kobayashi K, et al. Motor cortex stimulation for post-stroke pain: comparison of spinal cord and thalamic stimulation. Stereotact Funct Neurosurg 2001;77(1-4):183-6. PMID 12378074
79: Kearon C. Epidemiology of venous thromboembolism. Semin Vasc Med 2001;1(1):7-26. PMID 15199510
80: Kearon C, Akl EA, Comerota AJ, et al. Antithrombotic therapy for VTE disease: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest 2012;141(2 Suppl):e419S-94S. PMID 22315268
81: Kelly J, Rudd A, Lewis R, Hunt BJ. Venous thromboembolism after acute stroke. Stroke 2001;32(1):262-7. PMID 11136946
82: Kim JH, Greenspan JD, Cognill RC, Ohara S, Lenz FA. Lesions limited to the human thalamic principal somatosensory nucleus (ventral caudal) are associated with loss of cold sensations and central pain. J Neurosci 2007a;27(18):4995-5004. PMID 17475808
83: Kim JS. Medial medullary infarct aggravates central poststroke pain caused by previous lateral medullary infarct. Eur Neurol 2007b;58(1):41-3. PMID 17483584
84: Kim JS. Pharmacological management of central post-stroke pain: a practical guide. CNS Drugs 2014;28(9):787-97. PMID 25112542
85: Kim JS, Bashford G, Murphy TK, Martin A, Dror V, Cheung R. Safety and efficacy of pregabalin in patients with central post-stroke pain. Pain 2011;152(5):1018-23. PMID 21316855
86: Kim MG, Lee SA, Park EJ, et al. Elastic dynamic sling on subluxation of hemiplegic shoulder in patients with subacute stroke: a multicenter randomized controlled trial. Int J Environ Res Public Health 2022;19(16):9975. PMID 36011613
87: Kim NY, Lee SC, Kim YW. Effect of duloxetine for the treatment of chronic central poststroke pain. Clin Neuropharmacol 2019;42(3):73-6. PMID 31085946
88: Kocaağa Z, Bal S, Gurgan A. Hemiplegia and heterotopic ossification on the non-paretic extremity: a case report. J Rehabil Med 2007;39(6):500-2. PMID 17624486
89: Kong KH, Neo JJ, Chua KS. A randomized controlled study of botulinum toxin A in the treatment of hemiplegic shoulder pain associated with spasticity. Clin Rehabil 2007;21(1):28-35. PMID 17213238
90: Kumar A, Bhoi SK, Kalita J, Misra UK. Central post stroke pain can occur with normal sensation. Clin J Pain 2016;21(11):955-60. PMID 26710220
91: Kumar V, Kalita J, Gujral RB, Sharma VP, Misra UK. A study of bone densitometry in patients with complex regional pain syndrome after stroke. Postgrad Med J 2001;77(910):519-22. PMID 11470933
92: Lamb SE, Ferrucci L, Volapto S, Fried LP, Guralnik JM, Women’s Health and Aging Study. Risk factors for falling in home-dwelling older women with stroke: the Women's Health and Aging Study. Stroke 2003;34(2):494-501. PMID 12574566
93: Landi G, D’Angelo A, Boccardi E, et al. Venous thromboembolism in acute stroke. Prognostic importance of hypercoagulability. Arch Neurol 1992;49(3):279-83. PMID 1536631
94: Langdahl BL, Hofbauer LC, Forfar JC. Cardiovascular safety and sclerostin inhibition. J Clin Endocrinol Metab 2021;106(7):1845-53. PMID 33755157
95: Langhorne P, Stott DJ, Robertson L, et al. Medical complications after stroke: a multicenter study. Stroke 2000;31(6):1223-9. PMID 10835436
96: Lau WC, Chan EW, Cheung CL, et al. Association between dabigatran vs warfarin and risk of osteoporotic fractures among patients with nonvalvular atrial fibrillation. JAMA 2017;317(11):1151-8. PMID 28324091
97: Lavi C, Elboim-Gabyzon M, Naveh Y, Kalichman L. A combination of long-duration electrical stimulation with external shoulder support during routine daily activities in patients with post-hemiplegic shoulder subluxation: a randomized controlled study. Int J Environ Res Public Health 2022;19(15):9765. PMID 35955118
98: Lee JH, Baker LL, Johnson RE, Tilson JK. Effectiveness of neuromuscular electrical stimulation for management of shoulder subluxation post-stroke: a systematic review with meta-analysis. Clin Rehabil 2017;31(11):1431-44. PMID 28343442
99: Leijon G, Boivie J. Central post-stroke pain--a controlled trial of amitriptyline and carbamazepine. Pain 1989;36(1):27-36. PMID 2465530
100: Leung A, Donohue M, Xu R, et al. rTMS for suppressing neuropathic pain: a meta-analysis. J Pain 2009;10(12):1205-16. PMID 19464959
101: Leung A, Shirvalkar P, Chen R, et al. Transcranial magnetic stimulation for pain, headache, and comorbid depression: INS-NANS Expert Consensus Panel Review and Recommendation. Neuromodulation 2020;23(3):267-90. PMID 32212288
102: Levy J, Molteni F, Cannaviello G, Lansaman T, Roche N, Bensmail D. Does botulinum toxin treatment improve upper limb active function? Ann Phys Rehabil Med 2019;62(4):234-240. PMID 29960017
103: Lewiecki EM, Miller PD, Harris ST, et al. Understanding and communicating the benefits and risks of denosumab, raloxifene, and teriparatide for the treatment of osteoporosis. J Clin Densitom 2014;17(4):490-5. PMID 24206867
104: Liampas A, Velidakis N, Georgiou T, et al. Prevalence and management challenges in central post-stroke neuropathic pain: a systematic review and meta-analysis. Adv Ther 2020;37(7):3278-91. PMID 32451951
105: Liang NL, Avgerinos ED, Singh MJ, Makaroun MS, Chaer RA. Systemic thrombolysis increases hemorrhagic stroke risk without survival benefit compared with catheter-directed intervention for the treatment of acute pulmonary embolism. J Vasc Surg Venous Lymphat Disord 2017;5(2):171-6.e1. PMID 28214483
106: Liao C, Yang M, Liu P, Zhong W, Zhang W. Thalamic pain alleviated by stellate ganglion block: a case report. Medicine (Baltimore). 2017;96(5):e6058. PMID 28151918
107: Lin SM, Yang SH, Liang CC, Huang HK. Proton pump inhibitor use and the risk of osteoporosis and fracture in stroke patients: a population-based cohort study. Osteoporos Int 2018;29(1):153-62. PMID 29032384
108: Lin TY, Shen PC, Chang KV, Wu WT, Özçakar L. Shoulder ultrasound imaging in the post-stroke population: a systematic review and meta-analysis. J Rehabil Med 2023;55:jrm13432. PMID 37615388
109: Lindgren I, Jonsson AC, Norrving B, Lindgren A. Shoulder pain after stroke: a prospective population-based study. Stroke 2007;38(2):343-8. PMID 17185637
110: Liu Q, Zhong Q, Tang G, Ye L. Ultrasound-guided stellate ganglion block for central post-stroke pain: a case report and review. J Pain Res 2020;13:461-4. PMID 32161490
111: Liu-Ambrose T, Pang MY, Eng JJ. Executive function is independently associated with performances of balance and mobility in community-dwelling older adults after mild stroke: implications for falls prevention. Cerebrovasc Dis 2007;23(2-3):203-10. PMID 17143004
112: Lo SF, Chen SY, Lin HC, Jim YF, Meng NH, Kao MJ. Arthrographic and clinical findings in patients with hemiplegic shoulder pain. Arch Phys Med Rehabil 2003;84(12):1786-91. PMID 14669184
113: Malfitano C, Rossetti A, Scarano S, Malloggi C, Tesio L. Efficacy of repetitive transcranial magnetic stimulation for acute central post-stroke pain: a case study. Front Neurol 2021;12:742567. PMID 34858311
114: Marciniak CM, Harvey RL, Gagnon CM, et al. Does botulinum toxin type A decrease pain and lessen disability in hemiplegic survivors of stroke with shoulder pain and spasticitiy? A randomized, double-blind, placebo-controlled trial. Am J Phys Med Rehabil 2012;91(12):1007-19. PMID 23064478
115: Marco E, Duarte E, Vila J, et al. Is botulinum toxin type A effective in the treatment of spastic shoulder pain in patients after stroke. A double-blind randomized clinical trial. J Rehabil Med 2007;39(6):440-7. PMID 17624477
116: McCarthy ST, Turner J. Low-dose subcutaneous heparin in the prevention of deep-vein thrombosis and pulmonary emboli following acute stroke. Age Ageing 1986;15(2):84-8. PMID 3962762
117: McClung MR, Lewiecki EM, Cohen SB, et al. Denosumab in postmenopausal women with low bone mineral density. N Engl J Med 2006;354(8):821-31. PMID 16495394
118: McGeoch PD, Williams LE, Lee RR, Ramachandran VS. Behavioural evidence for vestibular stimulation as a treatment for central post-stroke pain. J Neurol Neurosurg Psychiatry 2008;79(11):1298-301. PMID 18550629
119: McGeoch PD, Williams LE, Song T, Lee RR, Huang M, Ramachandran VS. Post-stroke tactile allodynia and its modulation by vestibular stimulation: a MEG case study. Acta Neurol Scand 2009;119(6):404-9. PMID 18853944
120: McInnes E, Jammali-Blasi A, Bell-Syer SE, et al. Support surfaces for pressure ulcer prevention. Cochrane Database Syst Rev 2015;2015(9):CD001735. PMID 26333288
121: Melamed E, Robinson D, Halperin N, Wallach N, Keren O, Groswasser Z. Brain injury-related heterotopic bone formation: treatment strategy and results. Am J Phys Med Rehabil 2002;81(9):670-4. PMID 12172519
122: Menoux D, Jousse M, Quintaine V, Tlili L, Yelnik AP. Decrease in post-stroke spasticity and shoulder pain prevalence over the last 15 years. Ann Phys Rehabil Med 2019;62(6):403-8. PMID 29604351
123: Miniati M, Cenci C, Monti S, Poli D. Clinical presentation of acute pulmonary embolism: survey of 800 cases. PLoS One 2012;7(2):e30891. PMID 22383978
124: Miniati M, Prediletto R, Formichi B, et al. Accuracy of clinical assessment in the diagnosis of pulmonary embolism. Am J Respir Crit Care Med 1999;159(3):864-71. PMID 10051264
125: Montes C, Magnin M, Maarrawi J, et al. Thalamic thermo-algesic transmission: ventral posterior (VP) complex versus VMpo in the light of a thalamic infarct with central pain. Pain 2005;113(1-2):223-32. PMID 15621383
126: Moore RA, Derry S, Aldington D, Cole P, Wiffen PJ. Amitriptyline for neuropathic pain and fibromyalgia in adults. Cochrane Database Syst Rev 2012;12:CD008242. PMID 23235657
127: Moseley GL. Graded motor imagery for pathologic pain: a randomized controlled trial. Neurology 2006;67(12):2129-34. PMID 17082465
128: Moser KM, Fedullo PF, LitteJohn JK, Crawford R. Frequent asymptomatic pulmonary embolism in patients with deep venous thrombosis. JAMA 1994;271(3):223-5. PMID 8277550
129: Munoz-Gomez E, Inglés M, Aguilar-Rodríguez M, Sempere-Rubio N, Mollà-Casanova S, Serra-Añó P. Effects of mirror therapy on spasticity and sensory impairment after stroke: systematic review and meta-analysis. PM R 2023;15(11):1478-92. PMID 36787183
130: Nadler M, Pauls M. Shoulder orthoses for the prevention and reduction of hemiplegic shoulder pain and subluxation: systematic review. Clin Rehabil 2017;31(4):444-53. PMID 27184582
131: Nandi D, Smith H, Owen S, Joint C, Stein J, Aziz T. Peri-ventricular grey stimulation versus motor cortex stimulation for post stroke neuropathic pain. J Clin Neurosci 2002;9(5):557-61. PMID 12383415
132: National Pressure Ulcer Advisory Panel. Library of Medicine. Pressure Ulcer Stages. Revised by NPUAP. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5098472/. Accessed October 2007.
133: Nicholson BD. Evaluation and treatment of central pain syndromes. Neurology 2004;62(5 Suppl 2):S30-6. PMID 15007162
134: Nitti V, Haag-Molkenteller C, Kennelly M, Chancellor M, Jenkins B, Schurch B. Treatment of neurogenic detrusor overactivity and overactive bladder with Botox (onabotulinumtoxinA): development, insights, and impact. Medicine (Baltimore) 2023;102(S1):e32377. PMID 37499088
135: Noel P, Gregoire F, Capon A, Lehert P. Atrial fibrillation as a risk factor for deep venous thrombosis and pulmonary emboli in stroke patients. Stroke 1991;22(6):760-2. PMID 2057976
136: North American Menopause Society. Management of osteoporosis in postmenopausal women: 2006 position statement of The North American Menopause Society. Menopause 2006;13(3):340-67;quiz 368-9. PMID 16735931
137: Office of the Surgeon General. Bone health and osteoporosis: a report of the surgeon general. Rockville, MD: Office of the Surgeon General, 2004. PMID 20945569
138: Orken DN, Kenangil G, Ozkurt H, et al. Prevention of deep venous thrombosis and pulmonary embolism in patients with acute intracerebral hemorrhage. Neurologist 2009;15(6):329-31. PMID 19901711
139: Ozen S, Bölük Şenlikci H, Ümit Yemişci O. Post-stroke bilateral heterotopic ossification: an acute problem with long-lasting consequences. Jt Dis Relat Surg 2020;31(2):386-9. PMID 32584742
140: Paci M, Nannetti L, Rinaldi LA. Glenohumeral subluxation in hemiplegia: An overview. J Rehabil Res Dev 2005;42(4):557-68. PMID 16320150
141: Paci M, Nannetti L, Taiti P, Baccini M, Rinaldi L. Shoulder subluxation after stroke: relationships with pain and motor recovery. Physiother Res Int 2007;12(2):95-104. PMID 17536647
142: Paciaroni M, Agnelli G, Alberti A, et al. PREvention of VENous thromboembolism in hemorrhagic stroke patients - PREVENTIHS study: a randomized controlled trial and a systematic review and meta-analysis. Eur Neurol 2020;83(6):566-75. PMID 33190135
143: Pan R, Zhou M, Cai H, et al. A randomized controlled trial of a modified wheelchair arm-support to reduce shoulder pain in stroke patients. Clin Rehabil 2018;32(1):37-47. PMID 28629270
144: Pang MY, Eng JJ. Muscle strength is a determinant of bone mineral content in the hemiparetic upper extremity: implications for stroke rehabilitation. Bone 2005;37(1):103-11. PMID 15869927
145: Paolucci S, Iosa M, Toni D, et al. Prevalence and time course of post-stroke pain: a multicenter prospective hospital-based study. Pain Med 2016;17(5):924-30. PMID 26814255
146: Park GY, Kim JM, Sohn SI, Shin IH, Lee MY. Ultrasonographic measurement of shoulder subluxation in patients with post-stroke hemiplegia. J Rehabil Med 2007;39(7):526-30. PMID 17724551
147: Passeri G, Pini G, Troiano L, et al. Low vitamin D status, high bone turnover, and bone fractures in centenarians. J Clin Endocrinol Metab 2003;88(11):5109-15. PMID 14602735
148: Peng L, Zhang C, Zhou L, Zuo HX, He XK, Niu YM. Traditional manual acupuncture combined with rehabilitation therapy for shoulder hand syndrome after stroke within the Chinese healthcare system: a systematic review and meta-analysis. Clin Rehabil 2018;32(4):429-39. PMID 28901172
149: Perennou D, El Fatimi A, Masmoudi M, et al. [Incidence, circumstances and consequences of falls in patients undergoing rehabilitation after a first stroke]. Ann Readapt Med Phys 2005;48(3):138-45. PMID 15833261
150: Perry LA, Berge E, Bowditch J, et al. Antithrombotic treatment after stroke due to intracerebral haemorrhage. Cochrane Database Syst Rev 2017;5(5):CD012144. PMID 28540976
151: Pertoldi S, Di Benedetto P. Shoulder-hand syndrome after stroke. A complex regional pain syndrome. Eura Medicophys 2005;41(4):283-92. PMID 16474282
152: Picelli A, Bonazza S, Lobba D, et al. Suprascapular nerve block for the treatment of hemiplegic shoulder pain in patients with long-term chronic stroke: a pilot study. Neurol Sci 2017;38(9):1697-701. PMID 28699104
153: Pickering AE, Thornton SR, Love-Jones SJ, Steeds C, Patel NK. Analgesia in conjunction with normalisation of thermal sensation following deep brain stimulation for central post-stroke pain. Pain 2009;147(1-3):299-304. PMID 19833434
154: Pineo GF, Lin J, Annemans L. The economic impact of enoxaparin versus unfractionated heparin for prevention of venous thromboembolism in acute ischemic stroke patients. Clinicoecon Outcomes Res 2012;4:99-107. PMID 22570556
155: Poole KES, Loveridge N, Rose CM, Warburton EA, Reeve J. A single infusion of zoledronate prevents bone loss after stroke. Stroke 2007;38(5):1519-25. PMID 17395868
156: Poole KES, Reeve J, Warburton EA. Falls, fractures, and osteoporosis after stroke: time to think about protection. Stroke 2002;33(5):1432-6. PMID 11988628
157: Pyoria O, Talvitie U, Nyrkko H, Kautianinen H, Pohjolainen T. Validity of the postural control and balance for stroke test. Physiother Res Int 2007;12(3):162-74. PMID 17631637
158: Qaseem A, Snow V, Barry P, et al. Current diagnosis of venous thromboembolism in primary care: a clinical practice guideline from the American Academy of Family Physicians and the American College of Physicians. Ann Fam Med 2007;5(1):57-62. PMID 17261865
159: Ramachandran VS, McGeoch PD, Williams L, Arcilla G. Rapid relief of thalamic pain syndrome induced by vestibular caloric stimulation. Neurocase 2007;13(3):185-8. PMID 17786778
160: Ramger BC, Bader KA, Davies SP, et al. Effects of non-invasive brain stimulation on clinical pain intensity and experimental pain sensitivity among individuals with central post-stroke pain: a systematic review. J Pain Res 2019;12:3319-29. PMID 31853195
161: Ramnemark A, Nyberg L, Borssen B, Olsson T, Gustafson Y. Fractures after stroke. Osteoporos Int 1998;8(1):92-5. PMID 9692083
162: Righini M, Perrier A, De Moerloose P, Bounameaux H. D-dimer for venous thromboembolism diagnosis: 20 years later. J Thromb Haemost 2008;6(7):1059-71. PMID 18419743
163: Rosendaal FR. Venous thrombosis: a multicausal disease. Lancet 1999;353(9159):1167-73. PMID 10209995
164: Saag KG, Petersen J, Brandi ML, et al. Romosozumab or alendronate for fracture prevention in women with osteoporosis. N Engl J Med 2017;377(15):1417-27. PMID 28892457
165: Schulman S, Kearon C, Kakkar AK, et al. Dabigatran versus warfarin in the treatment of acute venous thromboembolism. N Engl J Med 2009;361(24):2342-52. PMID 19966341
166: Silva GD, Lopes P, Fonoff ET, Pagano RL. The spinal anti-inflammatory mechanism of motor cortex stimulation: cause of success and refractoriness in neuropathic pain? J Neuroinflammation 2015;12(1):10. PMID 25600429
167: Shorr AF, Jackson WL, Sherner JH, Moores LK. Differences between low-molecular-weight and unfractionated heparin for venous thromboembolism prevention following ischemic stroke: a metaanalysis. Chest 2008;133(1):149-55. PMID 17925410
168: Silver FL, Norris JW, Lewis AJ, Hachinski VC. Early mortality following stroke: a prospective review. Stroke 1984;15(3):492-6. PMID 6729878
169: Skaf E, Stein PD, Beemath A, Sanchez J, Bustamante MA, Olson RE. Venous thromboembolism in patients with ischemic and hemorrhagic stroke. Am J Cardiol 2005;96(12):1731-3. PMID 16360366
170: Smart KM, Wand BM, O'Connell NE. Physiotherapy for pain and disability in adults with complex regional pain syndrome (CRPS) types I and II. Cochrane Database Syst Rev 2016;2:CD010853. PMID 26905470
171: Sohn JH, Kim C< Kim Y, Park SY, Lee SH. Impact of osteoporosis pharmacotherapy on functional outcomes after ischemic stroke. J Clin Med 2023;12(15):4905. PMID 37568307
172: Sokal P, Harat M, Zieliński P, Furtak J, Paczkowski D, Rusinek M. Motor cortex stimulation in patients with chronic central pain. Adv Clin Exp Med 2015;24(2):289-96. PMID 25931362
173: Son BC, Lee SW, Choi ES, Sung JH, Hong JT. Motor cortex stimulation for central pain following a traumatic brain injury. Pain 2006;123(1-2):210-6. PMID 16616421
174: Sterne JA, Bodalia PN, Bryden PA, et al. Oral anticoagulants for primary prevention, treatment and secondary prevention of venous thromboembolic disease, and for prevention of stroke in atrial fibrillation: systematic review, network meta-analysis and cost-effectiveness analysis. Health Technol Assess 2017;21(9):1-386. PMID 28279251
175: Stevens JA, Corso PS, Finkelstein EA, Miller TR. The costs of fatal and non-fatal falls among older adults. Inj Prev 2006;12(5):290-5. PMID 17018668
176: Stroke Unit Trialists Collaboration. How do stroke units improve patient outcomes? A collaborative systematic review of the randomized trials. Stroke 1997;28(11):2139-44. PMID 9368554
177: Taira T, Tanikawa T, Kawamura H, Iseki H, Takakura K. Spinal intrathecal baclofen suppresses central pain after a stroke. J Neurol Neurosurg Psychiatry 1994;57(3):381-2. PMID 8158194
178: Tanei T, Kajita Y, Noda H, et al. Efficacy of motor cortex stimulation for intractable central neuropathic pain: comparison of stimulation parameters between post-stroke pain and other central pain. Neurol Med Chir (Tokyo) 2011;51(1):8-14. PMID 21273738
179: Tanei T, Kajita Y, Takebayashi S, Aoki K, Nakahara N, Wakabayashi T. Predictive factors associated with pain relief of spinal cord stimulation for central post-stroke pain. Neurol Med Chir (Tokyo) 2019;59(6):213-21. PMID 31061256
180: Thieme H, Mehrholz J, Pohl M, Behrens J, Dohle C. Mirror therapy for improving motor function after stroke. Cochrane Database Syst Rev 2012;(3):CD008449. PMID 22419334
181: Thomas LH, Barrett J, Cross S, et al. Prevention and treatment of urinary incontinence after stroke in adults. Cochrane Database Syst Rev 2005;(3):CD004462. PMID 16034933
182: Thomas LH, Coupe J, Cross LD, Tan AL, Watkins CL. Interventions for treating urinary incontinence after stroke in adults. Cochrane Database Syst Rev 2019;2:CD004462. PMID 30706461
183: Tondel BG, Morelli VM, Hansen JB, Braekkan SK. Risk factors and predictors for venous thromboembolism in people with ischemic stroke: a systematic review. J Thromb Haemost 2022;20(10):2173-86. PMID 35815351
184: Turkstra F, Kuijer PM, van Beek EJ, Brandjes DP, ten Cate JW, Buller HR. Diagnostic utility of ultrasonography of leg veins in patients suspected of having pulmonary embolism. Ann Intern Med 1997;126(10):775-81. PMID 9148650
185: Turner-Stokes L, Jackson D. Shoulder pain after stroke: a review of the evidence base to inform the development of an integrated care pathway. Clin Rehabil 2002;16(3):276-98. PMID 12017515
186: Valeriani E, Potere N, Candeloro M, et al. Extended venous thromboprophylaxis in patients hospitalized for acute ischemic stroke: a systematic review and meta-analysis. Eur J Intern Med 2022;95:80-6. PMID 34649783
187: Van Bladel A, Lambrecht G, Oostra KM, Vanderstraeten G, Cambier D. A randomized controlled trial on the immediate and long-term effects of arm slings on shoulder subluxation in stroke patients. Eur J Phys Rehabil Med 2017;53(3):400-9. PMID 28145396
188: Velasco F, Argüelles C, Carrillo-Ruiz JD, et al. Efficacy of motor cortex stimulation in the treatment of neuropathic pain: a randomized double-blind trial. J Neurosurg 2008; 108(4):698-706. PMID 18377249
189: Vestergaard K, Andersen G, Gottrup H, Kristensen BT, Jensen TS. Lamotrigine for central poststroke pain: a randomized controlled trial. Neurology 2001;56(2):184-90. PMID 11160953
190: Vestergaard P. New strategies for osteoporosis patients previously managed with strontium ranelate. Ther Adv Musculoskelet Dis 2014;6(6):217-25. PMID 25435924
191: Vranken JH, Dijkgraaf MG, Kruis MR, van der Vegt MH, Hollmann MW, Heesen M. Pregabalin in patients with central neuropathic pain: a randomized, double-blind, placebo-controlled trial of a flexible-dose regimen. Pain 2008;136(1-2):150-7. PMID 17703885
192: Vranken JH, Hollmann MW, van der Vegt MH, et al. Duloxetine in patients with central neuropathic pain caused by spinal cord injury or stroke: a randomized, double-blind, placebo-controlled trial. Pain 2011;152(2):267-73. PMID 21078545
193: Wanklyn P, Forster A, Young J. Hemiplegic shoulder pain (HSP): natural history and investigation of associated features. Disabil Rehabil 1996;18(10):497-501. PMID 8902421
194: Wells PS, Anderson DR, Bormanis J. Value of assessment of pretest probability of deep-vein thrombosis in clinical management. Lancet 1997;350(9094):1795-8. PMID 9428249
195: Wells PS, Owen C, Doucette S, Fergusson D, Tran H. Does this patient have deep vein thrombosis? JAMA 2006;295(2):199-207. PMID 16403932
196: Wicki J, Perneger TV, Junod AF, Bounameaux H, Perrier A. Assessing clinical probability of pulmonary embolism in the emergency ward: a simple score. Arch Intern Med 2001;161(1):92-7. PMID 11146703
197: Wiffen P, Collins S, McQuay H, Carroll D, Jadad A, Moore A. Anticonvulsant drugs for acute and chronic pain. Cochrane Database Syst Rev 2005;20(3):CD001133. PMID 16034857
198: Wiffen PJ, Derry S, Moore RA. Lamotrigine for chronic neuropathic pain and fibromyalgia in adults. Cochrane Database Syst Rev 2013;12:CD006044. PMID 24297457
199: Wiffen PJ, Derry S, Moore RA, Kalso EA. Carbamazepine for chronic neuropathic pain and fibromyalgia in adults. Cochrane Database Syst Rev 2014a;4:CD005451. PMID 24719027
200: Wiffen PJ, Derry S, Moore RA, Lunn MP. Levetiracetam for neuropathic pain in adults. Cochrane Database Syst Rev 2014b;7:CD010943. PMID 25000215
201: Wijdicks EF, Scott JP. Pulmonary embolism associated with acute stroke. Mayo Clin Proc 1997;72(4):297-300. PMID 9121173
202: Wilson RD, Bennett ME, Nguyen VQC, et al. Fully implantable peripheral nerve stimulation for hemiplegic shoulder pain: a multi-site case series with two-year follow-up. Neuromodulation 2018;21(3):290-5. PMID 29164745
203: Wissel J, Camões-Barbosa A, Comes G, Althaus M, Scheschonka A, Simpson DM. Pain reduction in adults with limb spasticity following treatment with incobotulinumtoxinA: a pooled analysis. Toxins (Basel) 2021;13(12):887. PMID 34941725
204: Yelnik AP, Colle FM, Bonan IV, Vicaut E. Treatment of shoulder pain in spastic hemiplegia by reducing spasticity of the subscapular muscle: a randomised, double blind, placebo controlled study of botulinum toxin A. J Neurol Neurosurg Psychiatry 2007;78(8):845-8. PMID 17088333

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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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Medical complications of stroke

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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

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Ischemic stroke

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Hormonal contraception and stroke

Antiphospholipid antibody syndrome

Sleep, stroke, and vascular dementia

Vein of Galen malformations

Patent foramen ovale

Neuroimaging in acute stroke

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

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Editor

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Ischemic stroke

Cerebral embolism

Hormonal contraception and stroke

Antiphospholipid antibody syndrome

Sleep, stroke, and vascular dementia

Vein of Galen malformations

Patent foramen ovale

Neuroimaging in acute stroke

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