Cases reported "Quadriplegia"

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1/20. Tracheocarotid artery fistula infected with methicillin-resistant staphylococcus aureus.

    Massive life-threatening haemorrhage from a fistula between the trachea and a major blood vessel of the neck is a rare complication of the tracheostomy procedure, well-recognized by anaesthetists and otolaryngologists. Although the lesion is likely to be encountered at autopsy, it is not described in histopathological literature. The possible causes are discussed together with the macroscopic and microscopic appearances of the lesion. Suitable procedures for its identification and for obtaining appropriate histopathological blocks are suggested. Presence of methicillin-resistant staphylococcus aureus (MRSA) has not been documented before and might have contributed to the genesis of the fistula in this case.
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2/20. Diverticulosis in an unused colon.

    It has been suggested that diverticulosis is the result of uncoordinated muscle activity of the colon in response to normal physiologic stimuli such as eating, emotions and the urge to defecate. This results in spasm of the longitudinal muscle with the heaping up of circular muscle bundles, creating interhaustral folds along the colonic wall adjacent to the mesentery. Narrowing of the lumen and shortening of the colon results which is enhanced by a low residue diet and prevented by a bulky diet. Segmentation results when muscular contraction approximates these interhaustral folds. Higher intraluminal pressure is produced in the areas of segmentation which enhances the development of diverticulosis in the bowel between interhaustral folds where there is a thinning of the circular muscles and where vessels pierce the colonic wall. The case presented herein supports these hypothesis in that the patient has experienced the extreme in a low residue diet for 50 years.
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3/20. Mini-infarct encephalopathy associated with uncommon microvessel convolute formation presenting with presenile dementia.

    A female patient started to suffer from transient ischemic attacks when she was 47 years of age, followed by increasing predominantly left-side spastic tetraparesis, generalized seizures and progressive dementia over a period of 11 years. She died when she was 58 years of age. On gross examination the brain showed enlarged ventricles and arteriosclerotic changes of large extracerebral vessels of the circulus arteriosus. Microscopic examination of the atrophic brain showed innumerable incomplete microinfarcts in the white and gray matter throughout all parts of the brain. In the white matter these lesions were characterized by small foci of demyelination and loss of oligodendrocytes while occasionally some scavenger cells were seen. axons seemed to be unaffected or displayed irregular axonal regeneratory growth. Any inflammatory reaction failed. In the cerebral cortex and subcortical nuclei the lesions showed loss of neurons and decrease in synaptophysin expression. Intracerebral arteries showed fibrosis or fibrohyalinosis of the entire intracerebral small-vessel network. In addition, numerous uncommon clusters of angioma-like telangiectatic vessels were observed. Medium-sized ischemic infarcts were found in the right putamen and adjacent internal capsule region, left-side dorsolateral brain stem and cerebellar hemisphere as well as a left-side pyramidal tract degeneration. Contralateral pseudohypertrophy of the inferior olivary nucleus was seen. The clinical and the neuropathologic observations made in this patient are compatible with small vessel disease characterized by a multicentric special and not yet described type of incomplete mini-infarcts in cerebral cortex and white matter accompanied by some larger ischemic infarcts of the common type in brain stem and cerebellum.
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4/20. cholesterol emboli neuropathy.

    We report the clinical and pathologic features of a patient with peripheral neuropathy that was the first clinical expression of cholesterol emboli syndrome (CES). biopsy of skeletal muscle and peripheral nerve revealed cholesterol clefts in lumens of small arteries, necrotizing arteritis, and severe degeneration of peripheral and intramuscular nerves. At autopsy, the peripheral nervous system was extensively affected by similar changes. We conclude that (1) peripheral neuropathy may be the initial manifestation of CES. Presumably, deposition of cholesterol leads to arteritis. (2) The underlying pathology of CES neuropathy is chronic axonal degeneration, possibly due to chronic ischemia of epineurial arteries. (3) Muscle biopsy is important in the antemortem diagnosis of CES. Nerve biopsy may show involvement of epineurial vessels. (4) CES may resemble polyarteritis nodosa clinically and pathologically. (5) CES may be under-recognized and should be included in the differential diagnosis of any neuropathy of uncertain cause, particularly when there is a history of vascular catheterization, or severe aortic atherosclerosis.
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5/20. Use of a free jejunal graft for oesophageal reconstruction following perforation after cervical spine surgery: case report and review of the literature.

    STUDY DESIGN:: Single-subject (male, 16 years of age) case. OBJECTIVES: To demonstrate a suitable method for oesophageal repair after perforation as a complication of anterior spinal fusion in an individual with quadriplegia, and to review the literature on oesophageal perforation and repair. SETTING: University hospital, large trauma centre with departments for spinal injuries and reconstructive surgery in germany. methods: A free jejunal graft used for oesophageal reconstruction in a post-traumatic situation after a complicated treatment course in a C6 quadriplegic patient. RESULTS: A protuberant loose screw of the titanium plate after anterior spinal fusion perforated the oesophagus. Imbricating sutures and a fascia lata patch were insufficient to repair the oesophageal leakage. An 8 cm long segment of the cervical oesophagus including a fistula had to be excised, and a free microsurgical jejunal flap was used for restitution of continuity. The jejunal vessels were connected to the superior thyroid artery and external jugular vein. At 1 week after the oesophageal repair, an enteral contrast study showed a small amount of contrast medium leaking at the oesophago-pharyngeal anastomosis. A percutaneous gastric tube was inserted, and oral feeding was limited to tea and still water for 4 weeks. The further course was uneventful. CONCLUSIONS: Oesophageal perforation is a rare but recognized complication after cervical spine surgery, which can mostly be managed using secondary suture techniques. The free jejunal flap is a reliable and innovative tool in the particularly complex situation of a segmental oesophageal loss. It should be considered in similar cases to reconstruct oesophageal continuity or to treat stricture and fistula formations.
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6/20. Anterior spinal cord infarction owing to possible fibrocartilaginous embolism.

    anterior spinal artery syndrome is characterised by acute flaccid quadriparesis or paraparesis, disturbance of pain and temperature sensation, and loss of sphincter control. Fibrocartilaginous embolism is a rarely recognised, but important cause of spinal cord infarction. Fibrocartilaginous embolisation usually occurs after minor trauma without major bony lesions, typically with an intervening symptom-free interval and progressive 'stroke-in-evolution' course. There is evidence that the embolus originates from the intervertebral disc, but the mechanism whereby disc fragments enter the spinal vessels is not well understood. We describe the evolution of MRI findings in a case of anterior spinal artery territory infarction thought to be secondary to fibrocartilaginous embolism.
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7/20. Myelopathy due to spinal epidural abscess without cord compression: a diagnostic pitfall.

    Spinal epidural abscess (SEA) is a neurological emergency that requires urgent diagnosis and treatment. We report 2 patients with SEA, in whom, on neuropathological examination, the neurological signs were found to be caused by spinal cord ischemia due to thrombosis of leptomeningeal vessels and compression of spinal arteries, respectively, while evidence of spinal cord compression was absent. Clinicians and neuropathologists should be aware of the variable mechanisms underlying the neurological involvement in SEA. Absence of spinal cord compression by the abscess may hamper early diagnosis and treatment.
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8/20. Spinal epidural epitheloid hemangioma--case report and review of the literature.

    Epitheloid hemangiomas are benign vascular lesions composed of epitheloid endothelial-cell-lined channels. We report an unusual case of a purely extradural non-osseous spinal epitheloid hemangioma presenting with quadriparesis. A 5-year-old boy presented with neck pain and quadriparesis following a trivial fall. MRI revealed a mixed intensity extradural lesion compressing the cervico-thoracic spinal cord posteriorly. At surgery the lesion consisted of vascular granulation tissue admixed with blood clots without abnormal vessels. Bone was normal. Histopathology revealed it to be an epitheloid hemangioma. The case and relevant literature is reviewed.
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9/20. Gowers intrasyringal hemorrhage. Case report and review of the literature.

    The concept of hemorrhage in a preexisting syringomyelic cavity was first described by Gowers in 1904. Since its first description only 13 cases have been reported. The aims of this report are to describe a new case, bring this entity to wider attention, and summarize the existing literature on the subject. This 36-year-old woman presented with progressive gait disturbance and unsteadiness. physical examination revealed incomplete quadriparesis, predominantly on the left side, and hypesthesia below C-7. magnetic resonance imaging revealed hematomyelia characterized by a heterogeneous hyperintense signal within the central cervical cord. A liquefied well-limited hematoma was evacuated. The postoperative course was uneventful; a near-complete recovery was observed at the 7-year follow-up examination. Most cases of intrasyringal hemorrhage (ISH) have occurred in syringomyelic cavities associated with scoliosis or Chiari malformation Type I. Although there is no specific clinical picture associated with this entity, it can be characterized by three neurological forms: 1) sudden onset or rapid development of signs and symptoms, 2) acute worsening of symptoms that may improve but leaving greater neurological dysfunction than before the previous episode, and 3) ISH may initiate progressive deterioration in a patient with known syringomyelia. Intrasyringal bleeding is most probably caused by a sudden dilation of the syringomyelic cavity, which may provoke rupture of the intrasyringal vessels by an acute distension of the accompanying strands. magnetic resonance imaging is the most accurate diagnostic modality, and recognition of ISH can lead to early, safe, and efficient surgical treatment.
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10/20. Fibrocartilaginous emboli to the spinal cord: a case report.

    Fibrocartilaginous emboli to spinal cord vessels are a rare and fatal cause of spinal cord injury. We reviewed the medical literature and discovered only 24 cases reported, all in the last 28 years. For all previously reported patients, onset of initial symptoms to maximal neurologic deficit was from a few minutes to as much as two days. All 24 of these patients died an average of 9.6 weeks post-onset (range = three hours to 11 months) due to complications related to their spinal cord injury; in all cases, the pathologic diagnosis was made postmortem. We report a 20-year-old man with high-level quadriplegia and respiratory paralysis due to fibrocartilaginous emboli to spinal cord vessels, which occurred after a minor automobile accident. He was the longest-surviving patient reported with this diagnosis. He died six years and seven months after onset, having been on 24-hour ventilatory support. The pathologic diagnosis was not suspected before his death; it was made during postmortem examination.
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