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11/22. Case report: diffusion-weighted MRI in anterior spinal artery stroke of the cervical spinal cord.

    The authors present a case of anterior spinal artery stroke demonstrated by diffusion-weighted MRI (DWI) using single-shot echo-planar imaging. DWI clearly demonstrated hyperintensity with a decreased apparent diffusion coefficient (ADC) at 26 hours after onset. At 28 days, there was persistent hyperintensity with an increased ADC, corresponding to T2-weighted hyperintensity in the whole spinal gray matter at the C2-C7 vertebral level. DWI provided satisfactory images and was helpful for diagnosing and evaluating anterior spinal artery stroke. ( info)

12/22. A rare case of aortic tube graft occlusion 35 years after coarctectomy.

    A 52-year-old male with a history of repair of aortic coarctation by prosthetic tube graft replacement 35-years ago developed anterior spinal artery syndrome caused by acute functional occlusion of the aorta at the repair site where pseudoaneurysm formation was observed. The patient was rescued by an emergency axillofemoral bypass, and residual hypertension in upper limbs was improved by elective ascending aorta-descending aorta bypass grafting. ( info)

13/22. anterior spinal artery syndrome after peripheral angiography of the lower limbs.

    STUDY DESIGN: A case report of temporary anterior spinal artery syndrome secondary to peripheral angiography of the lower limbs. OBJECTIVES: To report a rare case of spinal cord ischemia following a straightforward peripheral angiography with femoral access. SETTING: Istanbul, turkey. CASE REPORT: A 70-year-old patient with peripheral vascular disease developed temporary paraplegia after angiography caused by anterior spinal ischemia. His motor weakness improved gradually over a 2 month period. CONCLUSION: Spinal complications are extremely rare after peripheral angiography. The possible mechanisms of spinal cord damage are discussed, and the relevant data regarding the etiology are reviewed. ( info)

14/22. anterior spinal artery syndrome complicated by the ondine curse.

    BACKGROUND: Anterior spinal artery (ASA) syndrome results in motor palsy and dissociated sensory loss below the level of the lesion, accompanied by bladder dysfunction. When the cervical spine is involved, breathing disorders may be observed. OBJECTIVE: To describe the polysomnographic findings in a patient with cervical ASA syndrome complicated by a sleep breathing disorder. SETTING: Unit of neurology at a sleep center.Patient A 30-year-old man had an ischemic lesion that affected the anterior cervical spinal cord (C2-C6) bilaterally because of an ASA thrombosis. He developed ASA syndrome associated with respiratory impairment during sleep. RESULTS: The polysomnographic study during sleep showed a severe sleep disruption caused by continuous central apneas that appeared immediately after falling asleep. Treatment by intermittent positive pressure ventilation normalized the respiratory pattern and sleep architecture. CONCLUSIONS: The sleep breathing pattern was compatible with central alveolar hypoventilation due to automatic breathing control failure caused by a lesion of the reticulospinal pathway, which normally activates ventilatory muscles during sleep. This autonomic sleep breathing impairment resembles that found as a complication in patients who undergo spinothalamic tract cervical cordotomy for intractable pain. This surgical complication is known as the Ondine curse. ( info)

15/22. anterior spinal artery syndrome complicating aortic dissecting aneurysm: case report.

    Spinal Cord ischaemia is rare in the absence of trauma. We report a case of a 45 year old known hypertensive for six years, who presented with features of anterior spinal artery syndrome (ASAS) complicating acute dissection of the descending aorta. He developed sudden onset non-traumatic paraparesis, sphincteric dysfunction and dissociated anaesthesia with a sensory level at T6. This was preceded by a two weeks' history of severe, sharp, lancinating, tearing left parasternal chest pain radiating to the back. He was managed conservatively on pentazocine lactate (fortwin), calcium- and beta-blockers, steroids, anti-platelet and free-radical scavengers. On the 8th day of hospitalisation, he had a sudden abdominal distension, bled from the nose and mouth, went into hypovolaemic shock and died within a time frame of two minutes. He was presumed to have had a progression of the aortic dissection with subsequent rupture. Dissecting aortic aneurysm could run a benign asymptomatic or a lethal course and a high index of suspicion is necessary. The lack of exhaustive diagnostic investigative tools as well as surgical intervention in the management of this patient in a developing country was highlighted as was possible that the patient could have been mismanaged. ( info)

16/22. Acute arm paresis with cervical spondylosis: three case reports.

    BACKGROUND: The mild type of anterior spinal artery syndrome (ASAS) is characterized by motor loss with an absent or insignificant sensory deficit due to a disturbance in the blood supply to the anterior horn of the spinal cord. The clinical symptoms of cervical spondylotic amyotrophy (CSA) are motor loss or atrophy with an absent or insignificant sensory deficit or a long tract sign; however, the pathophysiology has not been clarified. methods: Three patients who suffered from palsy of the deltoid and biceps brachii are presented. magnetic resonance imaging confirmed the intrinsic cord disease as the cause of the paresis. We measured the central motor conduction time (CMCT) and the latencies of the tendon reflex (T waves) of the biceps and triceps and those of the F waves of the abductor pollicis brevis and abductor digiti minimi before, 2 weeks after, and 3 months after starting intravenous injections of prostaglandin E(1) (PGE(1)). RESULTS: In these 3 cases, restoration of muscle strength began after starting injection of PGE(1). The electrophysiologic diagnosis revealed a disturbance of the motor conduction, in the CMCT and the latencies of the T waves, in the paretic muscle, which is more severe than that in other muscles. The radiological diagnosis suggested damage in the spinal cord. Improvements in the disturbance of the motor conduction and those of symptoms were parallel. CONCLUSION: From symptomatologic or radiological viewpoints, it is difficult to differentiate CSA from ASAS with cervical spondylosis. This suggests that there have been patients with ASAS whom we have diagnosed as CSA, and we may add administration of PGE(1) to the treatment for the patients with CSA. The present 3 patients showed improvement of muscle strength after starting injections of PGE(1). Although this improvement was measured by an electrophysiologic method, the mechanisms of PGE(1) require further study. ( info)

17/22. Post-traumatic cervical kyphosis with surgical correction complicated by temporary anterior spinal artery syndrome.

    Post-traumatic undiagnosed disco-ligamentous and osseous lesions of the cervical spine may eventually result in irreducible extreme kyphosis. Correction of such consolidated deformities requires major surgery with a combined posterior and anterior approach, aiming to correct bony impingement on neural and vascular structures, reduce deformity and to attain circumferential instrumentation and fusion in physiological alignment. This can be achieved using either a single-staged or a two-staged procedure. Regardless, this type of major surgery entails considerable neurological risks. Therefore, thorough planning of the intervention and considerable surgical experience is needed. We present an elderly woman with gross restriction of forward gaze and intractable nuchal and radicular pain due to cervical spine deformity. Her cervical kyphosis was corrected using preoperative skeletal axial traction for four days and subsequent operative reduction with circumferential instrumentation and fusion. The post-operative course was complicated by a temporary anterior spinal artery syndrome despite normal intraoperative somatosensory evoked potentials (SSEP) and by a wound infection requiring removal of the implant. Nevertheless, segmental fusion in physiological alignment was successfully achieved and the patient fully recovered from the neurological deficit and infection. quality of life was significantly improved. ( info)

18/22. anterior spinal artery syndrome in two children with genetic thrombotic disorders.

    BACKGROUND: Spinal cord infarction is a well-described, but rare, etiology of myelopathy, especially in children. The most common syndrome, anterior spinal artery syndrome (ASAS), is caused by interruption of blood flow to the anterior spinal artery, producing ischemia in the anterior two-thirds of the cord, with resulting neurologic deficits. Causes of ASAS include aortic disease, thoracolumbar surgery, sepsis, hypotension, and thromboembolic disorders. methods: case reports of 2 patients. RESULTS: Two children developed spinal cord infarctions consistent with ASAS, mostly likely caused by previously undiagnosed thrombotic disorders. A child with prothrombin variant experienced acute bilateral lower limb weakness without any preceding event. magnetic resonance imaging (MRI) revealed increased T2 signal in the anterior cord from midthoracic level to the conus medullaris. A child with protein s deficiency developed lower limb weakness 1 day after a posterior thoracolumbar fusion for idiopathic scoliosis. Computed tomography (CT) myelogram revealed no spinal cord compression. The prothrombin variant mutation is associated with a 2-fold risk of thrombotic events. Individuals with protein s deficiency have an 8-fold increased risk of thrombosis. CONCLUSION: As knowledge of the coagulation pathways grows, it is likely that more patients with spinal cord infarctions will be diagnosed with genetic thrombotic disorders as the etiology of their injury. We review these two disorders, prothrombin variant and protein s deficiency, and the considerations for long-term anticoagulation. ( info)

19/22. Delayed anterior spinal artery syndrome following posterior scoliosis correction.

    The authors report two cases of delayed post-operative anterior spinal artery syndrome (ASAS) following posterior correction with Cotrel Dubousset (CD) instrumentation for adolescent idiopathic scoliosis. Sensory pathways were continuously monitored from skin incision to awakening. In both cases intraoperative SEPs were normal and the wake-up test revealed no neurological deficit. Both patients were presented with incomplete paraplegia (no sensory impairment) three and ten hours after surgery. Without delay, both patients underwent revision surgery, and the CD instrumentation was removed. Immediately after surgery, both patients' motor power in their lower extremities improved rapidly. In cases with delayed ASAS after posterior scoliosis correction, the removal of the instrumentation system was shown to be sufficient to regain full motor recovery caudal to the level of impairment. ( info)

20/22. anterior spinal artery syndrome after thoracic surgery.

    Spinal cord infarction is a rare complication following thoracic surgery. We present a case who developed paraplegia on the first postoperative day of thoracotomy. A 76-year-old man with a history of atherosclerotic cardiovascular disease was operated for bronchial carcinoma. An epidural infusion of ropivacaine and sufentanil was used for postoperative pain. Eight hours after the surgery, he had an episode of hypotension and respiratory depression. One hour later, he described paraplegia and Ischemia of the spinal cord was found on MRI. There was no recovery during the follow-up. ( info)
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