Anterior Spinal Artery Syndrome

Etiology

Anterior spinal artery syndrome occurs from direct or indirect damage to the ventral spinal cord. A direct injury arises when the spinal cord is mechanically crushed or compressed, as in the case of an enlarging hematoma. Indirect injuries are the primary cause of anterior spinal artery syndrome caused by ischemia secondary to occlusion or hypoperfusion of the anterior spinal artery or its major branches, such as the radiculomedullary arteries.[7] The artery of Adamkiewicz, also known as arteria radicularis magna, is the most common location for occlusion.[8] The occlusion or hypoperfusion can lead to ischemia within the vascular distribution of the anterior spinal artery.[5] 

The integrity of the aorta is critical for the proper perfusion of the ventral aspect of the spinal cord, and knowledge of vascular anatomy is required. The aorta gives rise to subclavian arteries, which in turn give rise to the vertebral arteries. The vertebral arteries give rise to the anterior spinal artery, which supplies the anterior two-thirds of the spinal cord. Therefore, any condition compromising the aorta, such as aortic dissection, may cause indirect injuries to the spinal cord. 

Some risk factors associated with anterior spinal artery syndrome include smoking, hypertension, diabetes mellitus, dyslipidemia, and family or patient history of ischemic cerebrovascular accidents.[6][9] Anterior spinal artery syndrome can also result from iatrogenic damage to the aorta following surgical complications during attempted vascular repairs or with prolonged clamping of the aorta. Other less common causes of infarcts to the ventral cord are intrinsic arterial occlusion due to emboli or atheroma of the anterior spinal artery or the radicular branches.[1]

The anterior aspect of the spinal cord is particularly susceptible to ischemia because the supplying vessels are end arteries and typically have no anastomoses. Anterior spinal artery infarction may also occur due to impairment of perfusion through the arteria radicularis magna, the major contributor to the caudal two-thirds of the anterior spinal artery in the lower thoracic and upper lumbar region, T5 to L2, of the spinal cord. Other causes of disruption of blood flow in the anterior spinal artery are aneurysms, trauma, or syphilitic arteries.[10] Furthermore, hypotensive states, venous infarctions, multiple sclerosis, and cord impingement by fracture fragments are less common causes of vascular damage to the anterior cord.

Occlusive and Hypoperfusion Etiologies of Anterior Spinal Artery Syndrome

Occlusive and hypoperfusion etiologies of anterior spinal artery syndrome refer to the different mechanisms that can lead to reduced blood flow to the anterior spinal artery, resulting in spinal cord ischemia.

• Aortic surgery: Iatrogenic injury is the most common cause of anterior spinal artery syndrome. Factors that may increase the risk for complications are hypotension, prolonged cross-clamping of the aorta, increased spinal cord pressure, and occlusion of radiculomedullary arteries. These factors may decrease blood flow through the anterior spinal artery, leading to ischemia. Other complications may involve direct surgical injury to major radiculomedullary arteries.[2][6][11]

• Atherosclerotic disease: This disease is a common cause of anterior spinal artery syndrome due to the development of a thrombus or emboli that occludes the anterior spinal artery.[12]

• Thoracoabdominal aortic dissection: Dissection of the aorta frequently causes occlusion of radiculomedullary arteries.[9] 

• Cardiac arrest: Cardiac arrest can cause decreased or absent blood flow to the anterior spinal artery.

• Cardiac emboli: This etiology is an infrequent cause of anterior spinal artery syndrome. The category includes infectious endocarditis, which may lead to septic emboli and occlusion of an anterior spinal artery or major radiculomedullary arteries.[13]

• Vasculitis: Vascular inflammation, such as polyarteritis nodosa, may rarely cause anterior spinal artery syndrome.

• Degenerative spine disease: Although a rare cause of anterior spinal artery syndrome, the literature describes patients with cervical spondylosis or thoracic disc herniation who present with anterior spinal artery syndrome. A large disc herniation can compress the anterior spinal artery and cause spinal cord infarction.[5][14]

• Vertebral fracture: This may cause anterior spinal artery syndrome through anterior cord impingement by a fracture fragment.[4]

• Fibrocartilaginous embolic myelopathy: This condition is sometimes known as idiopathic transverse myelitis. Migration of nucleus pulposus material into vessels supplying the anterior spinal artery may result in embolic infarction of the spinal cord and anterior spinal artery syndrome.[15][16][17]

• Hypotensive shock: Hypotension may lead to anterior spinal artery syndrome.

• Luetic aortitis: This condition was common during the syphilitic era but is rarely observed today.[6]

• Minimally invasive spine surgery: Surgical procedures, such as percutaneous balloon kyphoplasty, may cause anterior spinal artery syndrome.[18][19]

• Arteriovenous malformations: Spinal cord arteriovenous malformations may cause anterior spinal artery syndrome.[20]

• Digital subtraction angiography: This diagnostic and embolization procedure is a rare cause of anterior spinal artery syndrome, with an overall incidence of 1.4% to 6.5%.[7]

• Sickle cell disease: Due to thrombosis, sickle cell disease may lead to anterior spinal artery syndrome, among other complications.[21]

• Other hypercoagulable diseases: Other conditions that cause thrombosis may lead to anterior spinal artery syndrome.[22][23]

• Cocaine use: Because of vasospasm, vasculitis, or thrombosis that may occur in patients using cocaine, anterior spinal artery syndrome can develop.[24][25][26][27]

Epidemiology

Anterior spinal artery syndrome is a rare condition; statistical studies evaluating the incidence and prevalence of this condition are scarce.[6] Approximately 5% to 8% of the cases of acute spinal myelopathies are due to vascular causes such as spinal cord infarctions.[4][15] Spinal cord infarction accounts for 1.2% of all strokes and has an incidence of 3.1 per 100,000 persons in the United States.[28] Studies with small groups have described spinal cord infarction in patients with an average age between 50 and 70.[29] Anterior spinal artery syndrome is the most common of all spinal cord infarction syndromes described in some studies in up to 87.2% of the cases.[12][30] No statistical evidence is available for a sex preference in anterior spinal artery syndrome; however, a few studies have reported that older women with anterior spinal artery syndrome have the worst prognosis.[9]Given the lack of available data and the rarity of this syndrome, further studies are required.

Pathophysiology

The underlying pathophysiology of anterior spinal artery syndrome is better understood by having familiarity with the anatomy. The anterior spinal artery supplies the anterior two-thirds of the medulla and spinal cord and is formed at the level of the foramen magnum by 2 arteries branching from their respective vertebral arteries. This artery is uninterrupted within the anterior median sulcus up to the conus medullaris. Although the anterior spinal artery is a continuous artery, multiple anastomotic networks are supplied by the anterior medullar or radiculomedullary arteries. The anterior spinal artery varies in caliber along the course, with the smallest diameter at the thoracic level, making this segment most vulnerable to ischemia. The largest diameter of this artery is at the lumbar level. 

The anterior spinal artery provides small sulcal and penetrating arteries that enter the spinal cord's body at each level to supply blood to the spinal cord. Each spinal cord level contains a radicular artery that enters through the intervertebral foramen, primarily supplying the nerve root and dura. At some levels, they are enlarged and include embryonic connections with the anterior spinal artery, making them radiculomedullary arteries. The anterior spinal artery connections from the radiculomedullary arteries can be variable in the cervical regions. Typically, the cut-off is above the aortic arch, from either the vertebral or subclavian arteries. At the thoracic and lumbar regions, the intercostal arteries give rise to the radiculomedullary arteries, supplying the anterior spinal artery and the spinal cord at and below their entry-level.

On average, the spinal cord has 7 to 8 radiculomedullary arteries. The largest radiculomedullary artery is the great anterior radiculomedullary artery or artery of Adamkiewicz, also known as arteria radicularis magna. The arteria radicularis magna is the largest and most common radiculomedullary artery occluded, resulting in the development of anterior spinal artery syndrome. This artery originates from the intercostal artery, most commonly from the left side in 70% to 80% of patients; however, the origin may vary. The most common site of origin is the T9 to T12 vertebra in 75% of patients, followed by the T5 to T8 vertebra in 15% of patients and the L1 to L2 vertebra in 10%. Digital subtraction angiography describes the arteria radicularis magna as a straight vessel with a hairpin turn and subsequent communication with the anterior spinal artery coursing along the spine's midline.[7]

Understanding the clinical presentation of anterior spinal artery syndrome requires knowledge of the anatomy of the spinal cord to explain the pathophysiology behind this condition. The spinal cord is subdivided into 3 portions—the posterior part, anterolateral portion, and anteromedial portion. The posterior part of the cord contains the fasciculus gracilis and cuneatus, which are responsible for proprioception, vibration sense, and fine touch. This area is supplied by the 2 posterior spinal arteries that run in the spinal cord's posterior lateral sulcus, which explains why these modalities are preserved in anterior spinal artery syndrome. The anterolateral portion of the spinal cord contains the spinothalamic and spinocerebellar tracts responsible for transmitting pain and temperature sensation from the extremities to the brain. These portions are watershed areas in the spine, and the level of dysfunction depends on the level of anterior spinal artery syndrome ischemic insult. The sensory deficits may not be directly related to the exact injury level because spinothalamic tracts slope 2 or 3 levels upwards before crossing at the anterior commissure of the spinal cord. The anteromedial portion contains the corticospinal and corticobulbar tracts responsible for transmitting motor function from the brain to the extremities.[2] The lateral horns exist from the T1 level to the L2 level. They contain the cell bodies of the sympathetic nervous system. The anterior spinal artery is responsible for the vascular supply to these areas. If an infarction occurs, the sympathetic network is affected, and patients may present with neurogenic bladder and impaired bowel and sexual function.[9]

When anterior spinal artery blood flow is reduced or absent, several events occur at the cellular level. The disruption of blood flow initiates a signaling cascade that results in neuronal destruction. The cascade begins with the ischemic insult when blood flow and oxygen to the spinal cord decrease. Subsequently, astrocytes and microglia are promptly activated, leading to tissue edema, inflammation, disruption of the blood-brain barrier, and the influx of neutrophils. The disruption of blood flow leads to ionic pump failure and anoxic depolarization, which leads to an increased concentration of intracellular calcium and glutamate. The ionic pump failure and anoxic depolarization, in part, produce increased activation of the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors and N-methyl-D-aspartate receptor, alteration in the metabolic and mitochondrial activity, which ultimately causes cell death. Furthermore, the increased intracellular calcium produces free radicals, elevates nitric oxide production, and causes cytotoxic edema, further contributing to cell death. A later reperfusion injury occurs during the subacute stage, where cell death occurs secondary to the inflammatory oxidative response with the activation of the apoptotic cascade.[4]

History and Physical

Clinical Features

Due to the ischemic etiology of anterior spinal artery syndrome, patients commonly have an acute onset of motor dysfunction and loss of pain and temperature sensation below the infarction level following the insult (see Image. Clinical Features of Anterior Spinal Artery Syndrome). Typically, the first presenting symptom is acute back pain, whose location most of the time corresponds with the level of the spinal cord injury. Below this level, bilateral loss or dysfunction of motor function and sensation occurs; however, proprioception, vibratory sense, fine touch, and two-point discrimination are preserved.[2][5][6] These symptoms are almost always bilateral because both halves of the anterior spinal cord receive vascular supply from a midline anterior spinal artery. Motor dysfunction severity varies from paraplegia to quadriplegia, depending on the infarction location (see Image. Corticospinal Tract Lesion Locations).

Often, the location of infarction includes the lateral horns within levels T1 to L2 of the spinal cord, causing autonomic dysfunction, which most commonly results in neurogenic bladder and bowel, hypotension, bradycardia, and sexual dysfunction.[4] If the injury is at a high cervical level, dysfunction of the phrenic nerve may lead to respiratory failure.[31][32] Rare cases of anterior cord syndrome with unilateral symptomatology have been reported; this may be due to occlusion of unilateral sulcal arteries or collateralization from a posterior spinal artery.[9][33] As anterior spinal artery syndrome has no acute treatment, late signs and symptoms, including spasticity, hyperreflexia, neurogenic bladder, and sexual dysfunction, are typically present. The following clinical features are findings observed in patients with acute- and late-onset syndromes.

Acute clinical findings: Acute-onset symptoms appear immediately after the ischemic insult.

• Acute back pain at the level of injury
• Bilateral flaccid paraparesis or quadriparesis or plegia
• Loss of pain and temperature
• Preservation of proprioception, vibratory sense, fine touch, and two-point discrimination
• Autonomic dysfunction with hypotension, bradycardia, and impaired temperature regulation
• Respiratory failure
• Spinal shock

 Late clinical findings: Late-onset symptoms develop gradually over days to weeks after the initial injury.

• Continued or permanent motor and sensory dysfunction
• Bilateral spastic paraparesis or quadriparesis or plegia
• Hyperreflexia
• Bilateral Babinski signs
• Neurogenic bladder and bowel
• Sexual dysfunction

Evaluation

Characteristic clinical features and confirmatory neuroimaging diagnostic studies primarily diagnose anterior spinal artery syndrome. 

Diagnostic Imaging Studies

The gold-standard diagnostic study for anterior spinal artery syndrome is magnetic resonance imaging (MRI) of the spine. Although results can be negative in the first 24 hours, MRIs are indicated to confirm the diagnosis. The hallmark finding is a hyperintensity at anterior horns in the T2-weighted image. Characteristic MRI features of acute spinal cord ischemia are a thin pencil-like hyperintense region that extends vertically, involving multiple spinal levels in the sagittal view. Axial MRI studies show a central T2-hyperintense signal on either side of the median fissure because of relative sparing of the peripheral and posterior cords due to collateral vessels from the vascular pial plexus and posterior spinal arteries. Occasionally, a central T2-hyperintense signal resembling snake or owl's eyes appears in the anterior spinal cord on either side of the median fissure. Although this finding is considered specific to spinal cord infarction, the association with compression myelopathy and various infectious or inflammatory spinal conditions is common.[34] Other findings that suggest a spinal cord infarct are a T1-weighted hypointensity at the area of injury, spinal cord expansion at the injury site due to early signs of inflammation or edema where diffusion-weighted images may help distinguish between ischemia and inflammation, and signs of vertebral body infarction that may not always present. Still, when vertebral body infarction signs are present, the specificity for cord infarction is increased.[6] In addition, MRI studies identify possible etiologies behind anterior spinal artery syndrome, such as herniated discs or tumors.

MRI angiography or computed tomography (CT) angiography are appropriate adjunctive modalities for further delineating vascular pathology. MRI angiography may help further delineate and visualize spinal vascular pathology. CT angiography helps identify the anterior spinal artery and provides adequate visualization of bone anatomy. However, CT angiography also exposes the patient to radiation doses and nephrotoxic agents. In addition, this modality may help rule out an aortic or vertebral artery dissection.[4] Digital subtraction angiography can also be used, although it is not preferred. However, it delineates the vascular anatomy, which is necessary if an interventional procedure is required.[35] Digital subtraction angiography is an ideal imaging technique for diagnosing spinal vascular lesions and identifying aortic or vertebral dissections.[5]

Additional Diagnostic Studies

Laboratory studies are performed to screen for conditions that cause ischemic damage to vessels, such as diabetes mellitus, atherosclerosis, substance abuse, and hypercholesterolemia. These tests include a complete blood cell count, erythrocyte sedimentation rate, electrolytes, glucose, creatinine, cholesterol levels, liver enzymes, protein electrophoresis, and coagulation tests. Serological tests, including borreliosis, Lyme disease, syphilis, HIV, human T-cell lymphotropic virus, and herpes virus, are necessary when considering infectious etiologies of infarction. Screening for antinuclear and antineutrophil cytoplasmic antibodies can be considered in patients with potential causes of spinal cord infarction.

Current treatment is primarily supportive and follows the same guidelines as those for cerebral ischemia, atherosclerotic vascular disease, and acute traumatic spinal cord injury. If the underlying cause is treatable, the promptness of treatment is the most important factor for prognosis. No effective treatment is available to stop or revert anterior spinal artery syndrome. The primary focus is to address the underlying cause, including fever and glycemic control, management of anticoagulation, antiplatelet, and thromboprophylaxis therapy.[36] Protecting airways and maintaining blood pressure support in an acute setting is paramount. If the patient is hypotensive, then blood pressure must be raised using phenylephrine, norepinephrine, and high-dose dopamine. For blood pressure reduction, preferred medications include labetalol, esmolol, and nicardipine.[30] 

The use of high-dose corticosteroids for patients with anterior spinal artery syndrome is ineffective, with few reports showing mild improvement and most patients showing no improvement.[2][5] In cases where atherosclerotic or embolic disease is the underlying cause, patients treated with intravenous thrombolysis within 4.5 hours of symptom onset have reported excellent improvement without complications.[18] In theory, spinal cord strokes can be treated similarly to cerebral strokes; however, due to the need for further studies, this approach is not currently considered the standard of care. Supportive treatment focuses on addressing acute and late symptoms or complications, including:

• Neurogenic hypotension is treated with intravenous fluids and vasopressors
• Manage phrenic nerve impairment and dysfunction of the diaphragm in high cervical lesions with mechanical ventilation 
• Neurogenic urinary retention can be managed with bladder catheterization
• Deep venous thrombosis prevention prophylaxis
• Pressure sore prevention
• Gastrointestinal stress ulcer prevention
• Physical, occupational, and psychological therapies

The most common cause of anterior spinal artery syndrome is aortic surgery; therefore, treatment should focus on preventing iatrogenic anterior spinal artery syndrome. A protocol to prevent anterior spinal artery syndrome during aortic surgery has been established. This protocol involves increasing blood flow to the anterior spinal artery by increasing mean arterial pressure and placing a lumbar drain to remove cerebrospinal fluid, thereby decreasing pressure on the spinal cord.[4][9] Furthermore, excluding an arteriovenous malformation or aortic dissection as the underlying cause before thrombolysis is essential due to a thrombolytic contraindication.[6]

Treatment / Management

Current treatment is primarily supportive and follows the same guidelines as those for cerebral ischemia, atherosclerotic vascular disease, and acute traumatic spinal cord injury. If the underlying cause is treatable, the promptness of treatment is the most important factor for prognosis. No effective treatment is available to stop or revert anterior spinal artery syndrome. The primary focus is to address the underlying cause, including fever and glycemic control, management of anticoagulation, antiplatelet, and thromboprophylaxis therapy.[36] Protecting airways and maintaining blood pressure support in an acute setting is paramount. If the patient is hypotensive, then blood pressure must be raised using phenylephrine, norepinephrine, and high-dose dopamine. For blood pressure reduction, preferred medications include labetalol, esmolol, and nicardipine.[30] (B3)

The use of high-dose corticosteroids for patients with anterior spinal artery syndrome is ineffective, with few reports showing mild improvement and most of them showing no improvement.[2][5][5] In cases where atherosclerotic or embolic disease is the underlying cause, patients treated with intravenous thrombolysis within 4.5 hours of symptom onset have reported excellent improvement without complications.[18] In theory, spinal cord strokes can be treated similarly to cerebral strokes; however, due to the need for further studies, this approach is not currently considered the standard of care. Supportive treatment focuses on addressing acute and late symptoms or complications, including:(B3)

• Neurogenic hypotension is treated with intravenous fluids and vasopressors
• Phrenic nerve impairment and dysfunction of the diaphragm in high cervical lesions are typically managed with mechanical ventilation 
• Neurogenic urinary retention can be managed with bladder catheterization
• Deep venous thrombosis prevention prophylaxis
• Pressure sore prevention
• Gastrointestinal stress ulcer prevention
• Physical, occupational, and psychological therapy

The most common cause of anterior spinal artery syndrome is aortic surgery; therefore, treatment should focus on preventing iatrogenic anterior spinal artery syndrome. A protocol to prevent anterior spinal artery syndrome during aortic surgery has been established. This protocol involves increasing blood flow to the anterior spinal artery by increasing mean arterial pressure and placing a lumbar drain to remove cerebrospinal fluid, thereby decreasing pressure at the spinal cord.[4][9] Furthermore, excluding an arteriovenous malformation or aortic dissection as the underlying cause before thrombolysis is essential due to a thrombolytic contraindication.[6](B3)

Differential Diagnosis

Differential diagnoses that should be considered when evaluating a patient with suspected anterior spinal artery syndrome include:

• Transverse myelitis, which has a slower onset
• Multiple sclerosis has similar MRI findings; however, patients show cranial and ocular manifestations
• On imaging, venous congestive myelopathy may demonstrate prominent enlarged pial veins with central, peripheral white matter changes
• Spinal cord neoplasms have a slower onset
• Spinal cord arteriovenous malformations
• Disk herniation
• Epidural hematoma
• Epidural abscess
• Spinal cord compressive pathologies
• Central cord syndrome
• Dorsal cord syndrome
• Brown-Séquard syndrome
• Guillain-Barré syndrome
• Conus medullaris syndrome
• Cauda equina syndrome (see Image. Spinal Cord Syndromes)

Pertinent Studies and Ongoing Trials

Current preclinical research is exploring promising pharmacological agents as a possible treatment for ischemic spinal cord injuries. Neuroprotective therapies limit secondary injury after the initial damage by modulating inflammation, reducing cell death, and guarding against excitotoxicity. Currently, no proven pharmacological therapies for human spinal cord injury provide neuroprotection. Studies use propofol, thymoquinone, minocycline, erythropoietin, and curcumin as possible neuroprotective pharmacologic agents. Antioxidants protect against the oxidative damage caused by secondary neurodegeneration after acute spinal cord injury. These antioxidants also stabilize mitochondrial bioenergetics, protect neurons, and achieve modest neurological recovery.

Emerging research is focusing on measures that could help prevent ischemic spinal cord injury during vascular surgery. Hypothermia preserves tissue integrity during periods of interrupted blood flow; animal studies suggest that hypothermia suppresses excitatory synaptic transmission and reduces injury to neurons. Hyperbaric oxygen increases tissue oxygenation and metabolism in penumbral tissue. Ischemic preconditioning is a way to prepare tissue for the ischemic state to render resistance to a hypoxic insult. Numerous preclinical studies have examined the molecular pathways and potential benefits of pre- and post-ischemic preconditioning with encouraging results. Other studies explore methods to counteract apoptosis, which leads to neuronal cell death. Many of the current treatments for spinal cord infarcts show only modest improvements in the functional outcome if used as monotherapy, which is probably attributable to the development of permanent neurological deficits. Thus, future clinical trials should consider a combined and multimodal treatment approach.[36]

Prognosis

The long-term prognosis of anterior spinal artery syndrome is only briefly described in the literature. In general, the prognosis is poor, but a study mentioned that spinal strokes have a better prognosis compared to cerebral strokes, which also involve cognitive damage.[6] The primary etiology behind anterior spinal artery syndrome is important for prognosis. If treated rapidly and adequately, less common etiologies, such as disc herniation, can completely alleviate symptoms.[5] Spinal cord infarction has an overall mortality rate of 9% to 23% and typically occurs shortly after the injury. A review of patients with spinal cord infarction reported that 24% did not improve, and only 20% improved significantly.[37] Two other studies indicated that only 1% to 5% of patients recovered completely.[32][38]

Most survivors experience varying degrees of functional motor and sensory dysfunction. Patients with more severe presentation and without improvement in the first 24 hours after insult result in a poorer prognosis.[4] In less severe cases, favorable outcomes with improvement in neurological deficits are possible, with a small portion of patients regaining the ability to walk. In others, functional improvement can develop slowly over the years.[9] Multiple factors may affect the prognoses.[39][40][41]

• Etiology: Conditions such as aortic dissection or rupture and high cervical lesions carry a greater risk of death
• Symptom severity at initial presentation: Severe initial presenting symptoms have worse outcomes 
• Improvement in the first 24 hours: No improvement within the first 24 hours has the worst outcomes
• Female sex: Correlates with poorer outcomes
• Older adults: Associated with poorer outcomes

Complications

Patients with anterior spinal artery syndrome develop multiple complications associated with the condition. These complications arise due to the highly incapacitating injury to the spinal cord. The complications and presenting symptoms depend on the level of the spinal cord where the insults occur. The majority of life-threatening complications in anterior spinal artery syndrome present shortly after the ischemic insult or during the hospitalization period, including:

• Hypotension: Involvement of lateral horns T1 to L2 may lead to shock, which can be fatal if not treated or corrected
• Respiratory failure: High cervical-level injury involving the phrenic nerve (C3 to C5) may lead to prolonged mechanical ventilation
• Bradycardia: This can lead to cardiac arrest, for which patients may require atropine or permanent electrical pacing
• Infections such as urinary tract infections, pneumonia, and bacteremia
• Electrolyte imbalances
• Renal failure
• Depression [2]

The prognosis for recovery from anterior spinal artery syndrome is dismal, with poor outcomes. Many complications develop as most patients do not recover their motor and sensory dysfunction and experience prolonged immobilization, including:

• Permanent paraparesis or quadriparesis or plegia
• Deep venous thrombosis
• Pulmonary embolism
• Pressure ulcers with a 50% lifetime risk
• Neurogenic bowel or bladder
• Sexual dysfunction
• Neuropathic pain
• Gastrointestinal stress ulcers
• Gastrointestinal dysmotility
• Chronic pain in 79% of the patients
• Increased risk of osteoporosis due to prolonged immobilization
• Spasticity
• Psychological depression and other conditions
• Economic issues
• Dependency on others in activities of daily living [4][6][9][41][42][43]