Background and Purpose-Aortic dissection typically presents with severe chest or back pain. Neurological symptoms may occur because of occlusion of supplying vessels or general hypotension. Especially in pain-free dissections diagnosis can be difficult and delayed. The purpose of this study is to analyze the association between type A aortic dissection and neurological symptoms. Methods-Clinical records of 102 consecutive patients with aortic dissection (63% male, median age 58 years) over 7.5 years were analyzed for medical history, preoperative clinical characteristics, treatment and outcome with main emphasis on neurological symptoms. Results-Thirty patients showed initial neurological symptoms (29%). Only two-thirds of them reported chest pain, and most patients without initial neurological symptoms experienced pain (94%). Neurological symptoms were attributable to ischemic stroke (16%), spinal cord ischemia (1%), ischemic neuropathy (11%), and hypoxic encephalopathy (2%).Other frequent symptoms were syncopes (6%) and seizures (3%). In half of the patients, neurological symptoms were transient. Postoperatively, neurological symptoms were found in 48% of all patients encompassing ischemic stroke (14%), spinal cord ischemia (4%), ischemic neuropathy (3%), hypoxic encephalopathy (8%), nerve compression (7%), and postoperative delirium (15%). Overall mortality was 23% and did not significantly differ between patients with and without initial neurological symptoms or complications. Conclusion-Aortic dissections might be missed in patients with neurological symptoms but without pain. Neurological findings in elderly hypertensive patients with asymmetrical pulses or cardiac murmur suggest dissection. Especially in patients considered for thrombolytic therapy in acute stroke further diagnostics is essential. Neurological symptoms are not necessarily associated with increased mortality. (Stroke. 2007;38:292-297.)
Typically, aortic dissection has to be considered in patients with acute thoracic or abdominal pain and accompanying cardiovascular symptoms. Due to these clinical symptoms, neurologists have not been involved in the routine emergency management of aortic dissection. However, transient or permanent neurological symptoms at onset of aortic dissection are not only frequent (17–40% of the patients), but often dramatic and may mask the underlying condition. Especially in pain-free dissection (which occurs in 5–15%) with predominant neurological symptoms diagnosis of aortic dissection can be difficult and delayed. Affecting the outflow of supra-aortal, spinal as well as extremity arteries leads to a variety of neurological symptoms including disturbances of central or peripheral nervous system. Thrombolysis as an emergency stroke therapy without considering aortic dissection may be life-threatening for these patients. Routine chest X-ray and being alert to physical examination findings such as hypotension, asymmetrical pulses or cardiac murmur may reduce risk of delayed diagnosis or misdiagnosis. Neurological symptoms at onset or in the postoperative course of aortic dissection are not necessarily associated with increased mortality.
The outcome of severe CVT is almost equally divided between severe impairment or death and survival with no or only mild handicap. Specifically, space-occupying mass effect and associated neurologic deterioration seem to determine a poor outcome. Therefore, early detection and treatment of mass effect should be the focus of critical care.
Hypoglycemia‐induced peripheral neuropathy due to insulinoma is unusual and, as far as we know, has previously been reported in only 34 patients. In this case report, we describe the clinical features, electrophysiological features, and pathological findings in a 37‐year‐old patient with polyneuropathy from repeated hypoglycemic episodes over a 9‐year period that related to an insulinoma. The literature is discussed. The reported case is of special interest because the peripheral neuropathy led to the correct diagnosis. © 2000 John Wiley & Sons, Inc. Muscle Nerve 23: 1891–1894, 2000
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