Stroke & Vascular Disorders

Updated 01.18.2023
Released 06.17.1996
Expires For CME 01.18.2026

Vascular disorders of the spinal cord

Author: Eric Goldstein MD

Editor: Steven R Levine MD

Introduction

Overview

Spinal cord vascular disorders are rare, though potentially devastating, conditions that require prompt recognition and treatment. These vascular disorders are heterogenous in origin, with pathologies involving both the arterial and venous vessels. Understanding the clinical hallmarks and potential etiologies are necessary to provide effective intervention and timely management. Most treatment strategies are reliant on a multidisciplinary team.

Key points

	• Spinovascular disorders are relatively rare and encompass a wide breadth of etiologic designations.
	• The majority of acute spinovascular processes have back or radicular pain.
	• Classic intramedullary spinal cord disorders follow well-defined neurovascular territories.
	• The etiologies of these conditions are heterogenous, including embolic, iatrogenic, hypotensive, ischemic, hemorrhagic, and congestive pathologies.
	• Treatment requires a multidisciplinary effort and may require an interventional approach.
	• Owing to the rarity of the disease, much is not robustly known on the outcomes of those with a spinovascular condition.

Historical note and terminology

Although the presence of a spinal epidural hematoma (termed “spinal apoplexy”) was possibly first described in 1682 by GJ Duverney, intramedullary spinovascular disease was not readily identified until the 1800s. In 1817 and 1857, early cases reported spinovascular complications ranging from abdominal aortic aneurysm to the development of paraplegia (108). In 1881 and 1882, Polish pathologist Albert Adamkiewicz provided insight into the vascular anatomy of the spinal cord (68). His work allowed for further characterization of spinal cord vascular syndromes, including the first report of an anterior spinal artery syndrome in 1909 (113). In addition to large artery spinovascular complications, more intricate pathologies were identified. In 1912, Marie and Foix described the syndrome of "tephromalacie anterieure," or ischemic lesions in the anterior horn cells due to atherosclerotic disease (70). In 1926, Foix and Alajouanine subsequently described a congestive myelopathy from two cases of spinal dural arteriovenous fistulas (28). Embolization of spinal dural arteriovenous fistula was subsequently reported by Newton and Adams in 1968 (83). With the increasing interest in cardiovascular surgeries in the 1970s, reports emerged of incidences of anterior spinal cord syndrome related to hypoperfusion (109). More recent advances in neuroimaging have more readily identified spinovascular disorders, such as spinal dural arteriovenous fistula and stroke.

Clinical manifestations

Presentation and course

	• The symptoms of a spinovascular syndrome are highly reliant on the location and etiology of the condition.
	• Timing and onset of symptoms are of great importance in delineating etiology.

Ischemic processes

The clinical presentation varies depending on the vascular territory involved. The following vascular syndromes have been identified: anterior spinal artery syndrome, posterior spinal arteries syndrome, transverse infarction of the spinal cord, central cord infarction, venous infarction, transient spinal ischemia, and lacunar infarction.

Anterior spinal artery infarct. This syndrome is classically heralded by pain in approximately a third of individuals. If pain is present, it can be diffuse, radicular, or girdle-like in distribution and with both neuralgiform and throbbing qualities. Symptoms usually occur suddenly but may progress over minutes to hours, peaking at 12 hours (135). Unique to the spinal cord level involved, pain may mimic other conditions, such as cluster headaches in cervical cord infarcts and ischemic heart disease in thoracic cord infarcts (20; 58). Clinical features of an anterior spinal artery infarct are dependent on level and completeness of the infarct. Typically, lower motor neuron flaccid paralysis occurs with hyporeflexia, though over time, spasticity may occur depending on involvement of the anterior horn cells. Pain and temperature sensation may be lost beginning one to two levels below the infarct owing to the anatomy of the anterior fasciculus (133; 88). A “man-in-a-barrel” semiology has also been reported (07). Autonomic symptoms, such as bradycardia and incontinence, are common and depend on the spinal segments involved. Incomplete anterior spinal cord artery infarcts may lead to variable symptoms (115). Due to anatomical variations in spinal vasculature, partial Brown-Sequard syndromes (also known as hemi-cord myelopathy) may occur (53).

Transient spinal cord symptoms similar to a hemispheric transient ischemic attack may be a heralding sign of impending spinal cord infarct (23). Transient ischemia of the cervical cord may cause "drop attacks," whereas spinal cord claudication may occur in the lumbar region, leading to painless weakness of the lower extremities precipitated by effort and relieved by rest (120).

Posterior spinal artery infarct. These lesions are rare and are often difficult to recognize in a timely manner. Like anterior spinal artery infarcts, patients usually have pain along the spine. Due to predominant dorsal column involvement, vibration and proprioception are absent below the level of the lesion. Accompanying the expected dorsal column dysfunction is typically variable weakness and autonomic dysfunction, likely related to anterior anastomoses with the anterior spinal artery (114).

Complete segmental infarct. The syndrome is characterized by a segmental complete spinal infarct analogous to transverse myelitis. Depending on the segment involved, flaccid quadriplegia or quadriparesis and total loss of sensation below the lesion, as well as sphincter dysfunction, may occur.

Central cord infarction. Ischemia in the arterial border zone between anterior spinal and posterior spinal arteries may result in this type of clinical infarct. The picture, however, is believed to be clinically indistinguishable from anterior spinal artery syndrome (112).

Venous infarction. Spinal venous infarcts are rare and often subacute. There may be some degree of motor and sensory loss but without a well-defined pattern. The level of sensory loss may not be as easily delineated as in arterial infarcts (112). Those with symptoms of portal venous hypertension may be more at risk (38).

Lacunar cord infarction. Though perhaps controversial and with some variability in the literature, another potential ischemic myelopathy is of lacunar origin presenting as a subacute progressive weakness referable to the anterior horns. Lacunar cord infarction is also referred to as "vascular myelopathy in old age." The usual findings are wasting and weakness of the small muscles of the hand as well as scattered pyramidal signs, mimicking motor neuron disease (27).

Hemorrhagic processes

Hematomyelia. Nontraumatic hematomyelia can occur spontaneously or as a symptom of a secondary complication, such as hemophilia (16). The most common presentation is excruciating pain in the back of sudden onset, often with radicular radiation. Neurologic symptoms may occur acutely, subacutely or in a stepwise fashion (59).

Spinal epidural or subdural hematomas. Extramedullary hematomas are rare and often of unclear etiology. Clinically, they present with rapid radicular pain and progressive myelopathic symptoms (depending on location) over the course of hours (56).

Spinal subarachnoid hemorrhage. Clinically, spinal subarachnoid hemorrhage is usually manifest by excruciating pain and meningismus, radicular involvement, and variable weakness (116).

Vascular anomalies

Spinal dural arteriovenous fistulas. Spinal dural arteriovenous fistulas are the most common spinal vascular anomaly. The commonest presenting symptom is subacute lower extremity weakness that worsens with exercise and occurs in a subacute or stepwise deteriorative manner. Sensory and autonomic involvement are variable (79; 66).

Intramedullary fistulas. People with intradural fistulas frequently have an acute hemorrhagic presentation, though a progressive syndrome may be present. The arms are usually affected (cervicothoracic location) (100).

Cavernous malformations. These lesions are typically present in the thoracic cord and are present with an acute hemorrhage or as a subacute progressive or recurrent myelopathy (17).

Prognosis and complications

Ischemic infarcts. The outcomes of an ischemic spinal cord infarct depend on location, severity, and etiology. Nearly a quarter of those with an ischemic spinal cord infarct will die, and complete recovery is unfortunately rare (97). Most with motor symptoms will need assistance with ambulation, though again, this depends on the severity of the index event (19; 35). Rehabilitation has been shown to improve functional outcomes (82).

Long-term complications include persistent pain in as many as 90% of patients, independent of motor function recovery. The frequency and intensity of pain after spinal cord infarction seem higher than with other myelopathies and may have an impact on the quality of life (134). Further, a myriad of complications may emerge, such as autonomic dysfunction with urinary and bowel incontinence leading to urinary tract infections or sepsis, autonomic dysreflexia, sexual dysfunction, pressure sores, deep venous thromboses, and pulmonary emboli as a result of immobility, and mental health dysfunction may occur (134; 103; 97).

Hemorrhagic processes. The prognosis of spinal epidural and subdural hematomas mainly depends on the preoperative neurologic status, anticoagulation use, cervical level, and involvement of the bladder autonomics (121). An estimated 5% of those with a subdural spinal hematoma may die, and 30%, if treated in a timely manner, may make a full recovery (21; 121). Surgical and interventional treatments are preferred to conservative measures (137). Rapid interventional treatment is favored for those with intramedullary hemorrhage or symptomatic medullary cavernoma (119).

Vascular anomalies. Unfortunately, spinal dural arteriovenous fistulas are difficult to diagnose, and those with this condition tend to have a long delay in diagnosis. Rapid identification of the fistula is imperative to forestall the progressive congestive myelopathy (48; 99). Outcomes are dependent on the time to treatment and severity of the symptoms.

Clinical vignette

A 57-year-old man with a history of smoking, coronary atherosclerotic disease, chronic obstructive pulmonary disease, and nephrolithiasis underwent emergency Dacron graft replacement of a dissecting abdominal aortic aneurysm between the renal and distal common iliac arteries. Postsurgically, the patient was noted to have flaccid paraplegia with absent reflexes and a pin-prick sensory level below the umbilicus. His vibration sense was intact at the knees and ankles. MRI of the thoracic cord demonstrated an extensive cord infarction.

Thoracic cord infarction (MRI)

This MRI of a 57-year-old man demonstrates an extensive cord infarction. (Contributed by Dr. Enrique Leira.)

Biological basis

• Vascular anatomy may help define a location of the insult but also define the potential etiology. A thorough history and review of events at the time of onset are key.

Etiology and pathogenesis

Segmental vessels. There are approximately 31 pairs of segmental vessels arising from different sources (in craniocaudal order): vertebral arteries, ascending cervical arteries, deep cervical arteries, superior intercostal artery, aorta, iliolumbar artery, and lateral sacral arteries (112). These segmental arteries then divide into anterior and posterior rami. The posterior rami enter the intervertebral foramen and constitute either the anterior or posterior (or both) radicular arteries. Radicular arteries are also known as medullary or radiculomedullary arteries (112).

Anterior radicular (medullary) arteries supply the anterior spinal artery, which acts as an anastomotic channel between them, and are distributed unevenly throughout the cord. The cervical-upper thoracic region is highly vascularized, whereas the midthoracic area (T4 to T8) is poorly perfused because it is supplied by a single small radicular artery known as the "arteria radicularis magna" or artery of Adamkiewicz (usually T5 to T7 level, but variable). Posterior radicular (medullary) arteries are smaller in size. They supplement the posterior spinal arteries.

Longitudinal vessels. There are three longitudinal vessels: one anterior spinal artery and two posterior spinal arteries. The anterior spinal artery is an anastomotic channel that runs anteriorly in the midline. The anterior spinal artery constitutes the caudal continuation of the two vertebral arteries, at the level of the foramen magnum. It extends throughout the length of the cord in the anterior median fissure. The posterior spinal arteries run in the posterior lateral aspect of the cord. They usually originate from the vertebral arteries but occasionally come from the posterior inferior cerebellar arteries (120; 112).

Vasa coronae. These surface vessels originate from the anterior spinal artery and posterior spinal arteries, forming a vascular ring around the cord (112).

Penetrating vessels. They originate from the anterior spinal artery, posterior spinal arteries, and the vasa coronae to perfuse the central portions of the cord (112).

Central (sulcal) arteries. They are branches of the anterior spinal artery entering the cord through the anterior median fissure and give longitudinal branches. There are more than 200 sulcal arteries, which are unevenly distributed throughout the cord. These arteries mainly perfuse anterior horns, deep gray matter of posterior horn, and central white matter (112).

Posterior median septum arteries. These are branches of the posterior spinal arteries that supply the dorsal funiculi and the central gray matter. The remaining posterior one third of the cord is perfused by other penetrating branches of posterior spinal arteries (112).

Extrinsic veins. Spinal venous anatomy is more variable than its arterial counterpart. There are typically one or two anterior spinal veins and usually a single posterior spinal vein. In addition, posterolateral and anterolateral spinal veins form discontinuous channels.

Extrathecally, an internal venous plexus lies in the epidural space, and an external plexus drains the vertebral bodies (112).

Intrinsic veins. There are two anterior central veins (draining central white matter and medial anterior horn), two posterior central veins (median septum white matter and gray commissure), and an intrinsic venous drainage for the rest of the cord (112).

Spinal cord border zones. The lower thoracic and upper lumbar cord (T6 to L3) is considered the area most vulnerable to ischemia due to less vascular anastomoses compared with other levels. The artery of Adamkiewicz, essentially an end artery, is classically responsible for this segment’s perfusion (111).

In a transverse section, the anterior spinal artery territory (anterior two thirds) is believed to be more susceptible to ischemia than the posterior one third of the cord. The explanation may be the existence of more efficient functional anastomoses at the level of the posterior spinal arteries region (112).

The gray matter is considered more susceptible to ischemia than the white matter, probably due to the differences in metabolic demand (117).

Etiology of spinal cord infarcts. Spinal infarcts result from a heterogenous collection of pathologies and may be divided into non-iatrogenic, iatrogenic, venous infarcts, and spinal transient ischemic attack (See Table 1).

Table 1. Etiology of Spinal Cord Infarctions

Noniatrogenic etiologies
• Diabetic arteriopathy (120) • Atherosclerosis (105)
	- Associated renal transplants (12)
• Inflammatory or infectious
	- Syphilis (10) - Tuberculosis (10) - Arachnoiditis (10) - Herpes zoster (105) - HIV/varicella-zoster virus (51) - Pregnancy/varicella zoster virus reactivation (McNamara and Allworth 2016) - Coccidiomycosis (132) - Schistosomiasis (62) - Cryptococcal (10) - Mucormycosis (124) - Sarcoidosis (120)
• Vasculitic
	- Systemic lupus erythematous (105) - Giant cell arteritis (33) - Panarteritis nodosa (112) - Postinfectious/vaccination? (105) - Granulomatous angiitis (34)
• Non-inflammatory arteriopathies dissection (eg, congenital afibrinogenemia) (57) • Cervical spondylosis (anterior spinal artery compression) (41) • Continuous hyperextension (Surfer myelopathy) (107) • Intervertebral foraminal disease (92) • Lumbar artery compression by the diaphragmatic crus (98) • Aortic disease
	- Dissecting aortic aneurysm (105) - Dissecting radicular artery aneurysms (Sato and Roccatagliata 2012) - Aortic occlusion/thrombosis (30) - Trauma (41) - Takayasu disease (81) - Marfan syndrome (131)
• Embolic
	- Nucleus pulposus embolism (43) - Fibrocartilagous embolism (90) - Caisson disease (decompression sickness) (105) - Atheromatous (112) - Paradoxical embolization (78) - Atrial myxoma (105) - Fibroelastoma (87) - Endocarditis (105)
• Hypoperfusional states (111)
	- Cardiac arrest (15) - Cardiac tamponade (63)
• Disc protrusion (10) • Vertebral artery lesions (120)
	- Cervical hyperextension injuries - Fractures with spine dislocation - Vertebral artery dissection (08)
• Tumor (120)
	- Radicular artery compression - Malignant melanotic schwannoma (136) - Vertebral body metastasis & cord compression (13)
• Recreational drugs
	- Heroin (67) - Cocaine (130) - Traumatic needle stick (49)
• Hypercoagulable states
	- Antiphospholipid syndrome (37) - Protein S deficiency (93) - Congenital afibrinogenemia (04)

• Anemia (15) • Sickle cell anemia (102) • Moyamoya disease (arterial fibrosis) (54) • Malignant histiocytosis (infiltrative) (26) • Malignancy (cholangiocarcinoma) (118) • Intravascular malignant lymphomatosis (IML) (65) • CADASIL (47) • Cryptogenic (77)
Iatrogenic causes
• Aortic surgery (risk increases if previous colectomy) (104)
	- Aortic coarctation - Aortic aneurysms
• Endovascular aortic repair (32) • Endovascular iliac artery dissecting aneurysm repair (32) • Gastrectomy (15) • Surgery for mesenteric vascular occlusion (05) • Thoracolumbar sympathectomy (45) • Coronary artery bypass surgery (101) • Retroperitoneal tumor resection (64) • Aortic bifemoral bypass (55) • Pneumonectomy (radicular artery ligation) (18) • Scoliosis surgery (radicular artery ligation) (18) • Thoracoplasty (radicular artery ligation) (18) • Intra-aortic balloon pump (110) • Hepatic transplantation (arterial reconstruction) (36) • Renal artery embolization • Pineal region tumor resection (positional?) (84) • Posterior fossa surgery (71) • Resection thoracic dumbbell neuroblastomas (09) • Anterior cervical fusion (03) • Drugs
	- Neoarsphenamine (112) - Epidural/spinal anesthesia (vasoconstriction?) (112) - Intrathecal phenol (42) - Zolmitriptan (123) - Carmustine and cisplatin (126) - Nitroglycerin (sudden hypotension) (40) - Sildenafil (125)

• Dural fistula embolization/surgery (if common vessels) (80) • Transposition of the great arteries (61) • Embolization of bronchial artery (14) • Endovascular occlusion spinal dural arteriovenous malformation (72) • Epidural catheter placement (hyperlordosis) (01) • Central line placement (hemothorax) (129) • Cerebral angiography (06) • Peripheral angiography (11) • Coronary angiography (02) • Coronary angioplasty (122) • Transcatheter arterial chemoembolization of hepatocellular carcinoma (86) • Endoscopic ultrasound celiac plexus neurolysis (31) • Extracorporeal membrane oxygenation (60)
Venous infarction
• Sepsis (112) • Embolic (112)
	- Fibrocartilaginous (96) - Caisson disease (112)
• Hypercoagulable states (105)
	- Associated to malignancies (112) - Acute pancreatitis (127)
• Intramedullary tumor (105) • Venous thrombosis (96) • Meningitis (73) • Endoscopic sclerotherapy for esophageal varices (38)
Spinal transient ischemic attack
• Paget disease (flow diversion to bone) (89) • Dural arteriovenous malformation (10) • Atherosclerosis (105)

Diagnostic workup

	• Spinal MRI, including T1, T2, hemosiderin sensitive sequences, and DWI, are recommended for noninvasively diagnosing a spinovascular condition.
	• Conventional arteriography remains the gold standard in diagnosing spinovascular anomalies.

The evaluation for an acute spinal cord infarction includes neuroimaging studies to exclude the presence of an acute extrinsic spinal cord compression or an intraspinal mass. An MRI of the spinal cord should provide the needed information.

Spinal cord infarction (MRI)

This MRI is from a 76-year-old man. Short arrows indicate peripheral enhancement of central gray matter. Long arrows indicate peripheral enhancement of cord, probably near watershed zone between sulcal and perforating arteries. (U...

A series on the use of MRI offered a diagnostic high yield; approximately 93% of T2-weighted images detect the ischemic lesion at the time of the onset of symptoms (29). T1-weighted images are less reliable because 70% appear isointense at onset and only 18% are hypointense. Diffusion-weighted MRI may be useful for the detection of early ischemic cord lesions, though the size of the spinal cord may limit robust determination (128). Classic T2 hyperintense findings of an anterior spinal artery distribution infarct include “owl-eyes” and “pencil-like” hyperintensity patterns (133). Signs of vertebral body infarction on MRI are a useful radiological marker of spinal cord infarction associated with fibrocartilaginous embolism (25).

Admitting laboratory tests should include a comprehensive metabolic, infectious, and autoimmune screening. CSF analysis should be completed if concern arises for an alternative diagnostic etiology to ischemia.

Intramedullary mass at cervical cord (MRI)

T2-weighted sagittal image shows a low T2-signal intramedullary mass at cervical cord. Note multiple serpiginous flow-voids on the back of the spinal cord. (Contributed by Dr. Gaurang Shah.)
Ring enhancing nodule (MRI)

Post-contrast T1-weighted sagittal image shows a ring enhancing nodule (clotted aneurysm on angiogram) with a rim of faint T1-signal border situated superior to it, outlining the acute bleed. Note the flow-voids compatible with hy...
Intramedullary bleed (MRI)

T2-weighted axial image shows the area of intramedullary bleed with a string of flow-voids. (Contributed by Dr. Gaurang Shah.)

Spinal dural arteriovenous fistula may be apparent on sagittal MRI T2 sequences due to the presence of flow voids. A T1 hypointense but T2 hyperintense pattern along three to seven vertebral body lengths additionally suggests a spinal dural arteriovenous fistula (46). However, the gold standard in diagnosis remains a conventional arteriogram (80).

Spinal arteriovenous malformation (myelogram)

The malformation is characterized by dilated and tortuous tangles of vessels. (Contributed by Dr. Sherman Stein.)
Spinal arteriovenous malformation (arteriogram)

This study demonstrates the feeding artery (arrow) of this malformation, as well as a large venous aneurysm superiorly. (Contributed by Dr. Sherman Stein.)
Spinal arteriovenous fistula (angiogram)

Digital subtraction angiography images in the AP (A, B) and lateral (C) projection of a selective thyrocervical trunk injection demonstration of an arterial aneurysm (white arrowhead) and multiple dilated arterial afferents that d...
Spinal arteriovenous fistula (MRI)

Sagittal MR images of the cervical cord demonstrates the intramedullary lesion on the T1 precontrast (A), T1 post-contrast (B) and T2 weighted images (C). Angiography confirmed that this lesion was consistent with an aneurysm. Mar...

Management

	• Treatment of an acute spinal infarct depends on the etiology, though the use of antithrombotics, permissive hypertension, and lowering intrathecal pressures may aid in augmenting spinal blood flow.
	• Intravenous thrombolytics may be beneficial in the acute management of an ischemic spinal cord stroke.
	• Collaboration with neurointerventional and neurosurgical teams are important for the treatment of spinovascular anomalies.

Owing to the rarity of spinovascular conditions, there is no specific approved treatment for acute spinal cord infarctions. Intravenous rtPA has been used anecdotally, but the safety and efficacy are not known (24). Additionally, treatment by intravenous thrombolysis is contraindicated in those with aortic dissection or those who have an index major surgical intervention, further limiting the sample size. The use of permissive hypertension and lower intrathecal pressures through a lumbar drain have shown some theoretical success.

Spinal cord infarcts that are referable to conventional cardiovascular risk factors should be optimized medically with the aid of statin therapy, antihyperglycemics, and antithrombotic medications.

Spinal epidural and subdural hematomas should be decompressed emergently. Occasionally, fresh frozen plasma needs to be given to correct underlying coagulopathies.

Spinal dural and intramedullary arteriovenous malformations can be treated by excision, surgically eliminating the transmission of arterial pressure into the venous system of the cord. Surgical interruption of the intradural draining vein can provide a cure due to retrograde thrombosis. Embolization of these lesions is an alternative (80).

Symptomatic cavernous malformations may benefit from surgery, but there are not enough data about the natural history of these lesions (74).

Outcomes

Much is not known on the outcomes of treatment of a spinal cord infarct because the majority of documentation are case reports. Surgical treatment of spinovascular anomalies is well-documented, with a success rate of over 90% in treating spinal arteriovenous malformation via venous disconnection; however, this ultimately depends on the level of disability preoperatively and the experience of the surgeon (22).

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Vascular disorders of the spinal cord

Associated Disorders

familial cerebral cavernous malformation syndrome
hereditary hemorrhagic telangiectasia
Cobb syndrome

Differential Diagnosis

autoimmune conditions
infectious myelitis
Guillain-Barre–related syndromes

Also Relevant

Cavernous malformations
Cerebral arteriopathies
Drug-induced cerebrovascular disease
Neurologic complications of diseases of the aorta

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Stroke & Vascular Disorders

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Nerve disease and bladder control

	• Preventing an ischemic spinal infarct relies on the same strategies as secondary stroke prevention.
	• Intraoperative monitoring and careful monitoring of vital signs are important in preventing iatrogenic spinal cord infarcts during aortic interventions.

Vascular disorders of the spinal cord

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Ischemic processes

Hemorrhagic processes

Vascular anomalies

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Table 1. Etiology of Spinal Cord Infarctions

Epidemiology

Prevention

Differential diagnosis

Confusing conditions

Associated or underlying disorders

Diagnostic workup

Management

Outcomes

Special considerations

Pregnancy

Anesthesia

Media

References

Contributors

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Editor

Former Authors

Patient Profile

ICD & OMIM codes

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Rostral brainstem and thalamic infarctions

Depression after stroke

Pregnancy and stroke

Nontraumatic intracerebral hemorrhage

Stroke associated with myocardial infarction

Traumatic intracerebral hemorrhage

Lobar hemorrhage

CADASIL

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