maintain constant intracranial pressure. Symptoms of CHS may occur up to several weeks after revascularization but usually occur within the first few days. Clinically, patients with CHS present with an ipsilateral headache, convulsion, a neurological deficit (hemiparesis, hemiplegia, dysarthria or visual disturbance) or a facial oedema. The most catastrophic event of CHS is intracerebral haemorrhage. In patients who are undergoing carotid endarterectomy, longstanding hypertension, diabetes mellitus and severe brain ischaemia are known as risk factors of CHS.23 To prevent CHS, preand post-operative BP control is extremely important. According to Tada et al.,19 there was a lower incidence of cerebral hyperperfusion syndrome after using autogenous pantaloon vein grafts. [Q8: A]

As late complications, anastomotic restenosis, graft thrombosis, anastomotic false aneurysms and graft infections can occur. [Q8: B, C] Among these, an anastomotic aneurysm is one of the well-known complications after surgical treatment of patients with TA. Miyata et al.24 reported that anastomotic aneurysms can occur at any time after operations for TA. Theyreportedthatthemeantimebeforedevelopingananastomoticaneurysmwas9.8years (range1.6–30years)andthatthecumulativeincidencewas6%,12%and19%at10,20and 30 years after various forms of bypass surgery among patients with TA, respectively. They found that the only risk factor for the development of anastomotic aneurysms was the presence of an aneurismal lesion at the time of surgery. They recommended life-long follow-up for patients with TA who undergoarterial surgery. However,most (18/22)of the aneurysms occurred in an early series in which silk suturing was used for the arterial anastomosis. In recent series, anastomotic false aneurysms developed in only 1.8% and 3.5% of patients at 10 and 20 years, respectively. To prevent this complication, some authors have recommendedreinforcementoftheanastomoticsuturelinewiththeuseofaTeflonfeltstrip.25 We do not use any adjuvant surgical procedure to prevent anastomotic aneurysms. However, we consider that the post-operative monitoring of disease activity and pharmacologic treatment of active disease are very important for all patients with TA who undergo surgical intervention. [Q8: C]

References

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 2. Liang P, Hoffman GS. Advances in the medical and surgical treatment of Takayasu arteritis.

Curr Opin Rheumatol. 2005;17:16-24.

 3. Matsuura K, Ogino H, Kobayashi J, et al. Surgical treatment of aortic regurgitation due to Takayasu arteritis: long-term morbidity and mortality. Circulation. 2005;112:3707-3712.

 4. Park JH, Chung JW, Im JG, Kim SK, Park YB, Han MC. Takayasu arteritis: evaluation of mural changes in the aorta and pulmonary artery with CT angiography. Radiology. 1995;196: 89-93.

 5. Choe YH, Kim DK, Koh EM, Do YS, Lee WR. Takayasu arteritis: diagnosis with MR imaging and MR angiography in acute and chronic active stages. J Magn Reson Imaging. 1999;10:751-757.

 6. Kissin EY, Merkel PA. Diagnostic imaging in Takayasu arteritis. Curr Opin Rheumatol. 2004;16:31-37.

 7. Andrews J, Mason JC. Takayasu’s arteritis – recent advances in imaging offer promise.

Rheumatology (Oxford). 2007;46:6-15.

 8. Maksimowicz-McKinnon K, Hoffman GS. Takayasu arteritis: what is the long-term prognosis? Rheum Dis Clin North Am. 2007;33:777-786. vi.

 9. Fields CE, Bower TC, Cooper LT, et al. Takayasu’s arteritis: operative results and influence of disease activity. J Vasc Surg. 2006;43:64-71.

10.Park MC, Lee SW, Park YB, Lee SK, Choi D, Shim WH. Post-interventional immunosuppressive treatment and vascular restenosis in Takayasu’s arteritis. Rheumatology (Oxford). 2006;45:600-605.

11.Kerr GS, Hallahan CW, Giordano J, et al. Takayasu arteritis. Ann Intern Med. 1994;120: 919-929.

12.ParkJH,ChungJW,ImJG,KimSK,ParkYB,HanMC.Takayasuarteritis:evaluationofmural changes in the aorta and pulmonary artery with CT angiography. Radiology. 1995;196:89-93.

13.Park JH, Chung JW, Lee KW, Park YB, Han MC. CT angiography of Takayasu arteritis: comparison with conventional angiography. J Vasc Interv Radiol. 1997;8:393-400.

14.Choe YH, Han BK, Koh EM, Kim DK, Do YS, Lee WR. Takayasu’s arteritis: assessment of disease activity with contrast-enhanced MR imaging. AJR Am J Roentgenol. 2000;175: 505-511.

15.Tso E, Flamm SD, White RD, Schvartzman PR, Mascha E, Hoffman GS. Takayasu arteritis: utility and limitations of magnetic resonance imaging in diagnosis and treatment. Arthritis Rheum. 2002;46:1634-1642.

16.Andrews J, Al-Nahhas A, Pennell DJ, et al. Non-invasive imaging in the diagnosis and management of Takayasu’s arteritis. Ann Rheum Dis. 2004;63:995-1000.

17.Kobayashi Y, Ishii K, Oda K, et al. Aortic wall inflammation due to Takayasu arteritis imaged with 18F-FDG PET coregistered with enhanced CT. J Nucl Med. 2005;46:917-922.

18.Shiiya N, Matsuzaki K, Watanabe T, Kuroda S, Yasuda K. Descending aorta to carotid bypass for takayasu arteritis as a redo operation. Ann Thorac Surg. 2003;76:283-285.

19.Tada Y, Sato O, Ohshima A, Miyata T, Shindo S. Surgical treatment of Takayasu arteritis. Heart Vessels. 1992;7:159-167.

20.Tada Y, Kamiya K, Shindo S, et al. Carotid artery reconstruction for Takayasu’s arteritis the necessity of all-autogenous-vein graft policy and development of a new operation. Int Angiol. 2000;19:242-249.

21.Tann OR, Tulloh RM, Hamilton MC. Takayasu’s disease: a review. Cardiol Young. 2008;18:250-259.

22.Rockman CB, Riles TS, Landis R, et al. Redo carotid surgery: An analysis of materials and configurations used in carotid reoperations and their influence on perioperative stroke and subsequent recurrent stenosis. J Vasc Surg. 1999;29:72-80. discussion 80–81.

23.Moulakakis KG, Mylonas SN, Sfyroeras GS, Andrikopoulos V. Hyperperfusion syndrome after carotid revascularization. J Vasc Surg. 2009;49:1060-1068.

24.Miyata T, Sato O, Deguchi J, et al. Anastomotic aneurysms after surgical treatment of Takayasu’s arteritis: a 40-year experience. J Vasc Surg. 1998;27:438-445.

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26.IshikawaK.DiagnosticapproachandproposedcriteriafortheclinicaldiagnosisofTakayasu’s arteriopathy. J Am Coll Cardiol. 1988;12:964-972.

Part VII

Neurovascular Conditions

of the Upper Extremity

Richard J. Sanders

A 30-year-old woman presented with complaints of pain in her neck, right shoulder, right trapezius, right anterior chest wall, right axilla, right arm, elbow, and forearm; occipital headaches every other day; numbness and tingling in all fingers of the right hand, worse in the fourth and fifth fingers; aggravation of her symptoms when elevating her arms, especially to comb or blow dry her hair or drive a car; weakness of her righthandanddroppingcoffeecups;andcoldnessandcolorchangesinherrighthand. The symptoms had been present for 1 year and began following a rear-end collision.

Her history began 1 year ago when her automobile was sitting still at a traffic light and another vehicle hit her from the rear. She wore a seat belt and recalled going forward and backward, but did not recall what happened to her neck at the time of the accident. She had no immediate symptoms. On the next day she awoke with a sore neck and pain above her shoulder blades. A few days later, she began noticing headaches in the back of her head that radiated forward to behind her eyes, and the neck soreness became progressively painful. Two or 3 weeks later, pain developed in the right shoulder area and down the right arm. Several weeks later, numbness and tingling developed in the fingers of the right hand, more noticeable in the ring and baby fingers. Because of severe, persistent right shoulder pain, arthroscopic repair of the right shoulder had been performed 6 months ago with partial improvement of her shoulder pain, but no change in any of her other symptoms.

Her occupation was a legal secretary. Since the accident, although she had been able to return to work, she was now able to work only 4 h a day. She could not type for more than 10 min, because the pain and numbness in her right hand was too uncomfortable. At home she could do light housework only. She could not vacuum, wash windows or floors, or lift heavy laundry baskets. Diagnostic studies to date included cervical spine X-rays, which were normal, and an electromyography/nerve conduction velocity (EMG/NCV) study, which revealed very mild nonspecific changes in the ulnar nerve distribution, but was close to normal.

Treatment to date included 6 months of physical therapy with the following modalities: heat, massage, ultrasound, neck stretching exercises, and posture.

R.J. Sanders

Department of Surgery, University of Colorado Health Science Center, Aurora, CO, USA