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.

When caring for critically ill patients needing central venous catheterization, nursing staff and physicians should be aware of this potentially lethal complication.

Cervical dystonia is a disabling basal ganglia disorder characterized by an involuntary head deviation to one side. A typical but also mysterious feature is the impressive improvement of muscle spasms and involuntary head posture by application of a sensory facial stimulus (sensory trick). Here, we report the effect of a sensory trick on cortical activation patterns in 7 patients with cervical dystonia by using H2(15)O positron emission tomography. The application of the sensory trick stimulus, resulting in a near-neutral head position, led to an increased activation mainly of the superior and inferior parietal lobule (ipsilateral to the original head turn) and bilateral occipital cortex and to a decreased activity of the supplementary motor area and the primary sensorimotor cortex (contralateral to the head turn). We propose that a perceptual dysbalance induced by a sensory trick maneuver leads to a relative displacement of the egocentric midvertical reference to the opposite side and a decrease in motor cortex activity. This modulation of motor programming gives novel insights into the mechanisms involved in sensorimotor integration in movement disorders.

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