Volume 198 - Issue 2
Finding the key: acute locked-in syndrome treated with interventional neuroradiology
Author: Gordon Stuart
Med J Aust 2013; 198 (2): 112-113. || doi: 10.5694/mja12.10992
Published online: 4 February 2013
Published online: 4 February 2013
A neurosurgeon’s personal account of the experience of, treatment for and recovery from a basilar artery occlusion provides a unique "insiders view" into acute locked-in syndrome.
A neurosurgeon’s personal account of recovery from a potentially catastrophic event
On 30 December 2011, I, a 77-year-old, semiretired neurosurgeon with a 16-year history of controlled auricular fibrillation, awoke at 3:00 in the morning with intense vertigo, nausea and vomiting. After vomiting I collapsed on the bathroom floor, with painful spasms in my left leg. I was then unable to move, speak, cough or clear secretions from my mouth. I was still conscious and able to see and feel, but was unable to move any voluntary muscles. In the absence of headache I reasoned that an ischaemic event involving the brainstem was occurring. At that stage I hoped that I would not survive in that state.
My wife, who is not medically trained but is competent in first aid, writes:
I saw Gordon standing at the bathroom holding onto taps. I knew at once that he was having difficulty standing and communicating. Lowered him to the floor and laid him on his side.
Asked him if he was experiencing a similar condition he had had a few years previously. He mumbled agreement and could no longer speak.
My wife rolled me onto my side and called an ambulance, which arrived promptly.
Knew at once I needed help and rang 000. Received wonderful response — was advised to keep him on his side and keep his airway clear — they asked repeatedly about his breathing, which I described as laboured and stertorous.
I recall the ambulance and paramedics asking me to move my limbs and pressing on my chest, but I was unable to respond, although I was able to see them and hear their voices, and understand what was being said. This was my last recollection of events.
Within 10 minutes paramedics arrived, gave injections and monitored him en route to RBWH [Royal Brisbane and Women’s Hospital]. I sent all his medications and prescriptions with him and followed the ambulance.
I was transported by ambulance to the RBWH emergency department. I have been told that I had investigations and treatment for thromboembolism of the basilar artery. The blood clot was successfully removed from the basilar artery with interventional neuroradiology (Box). Endovascular embolectomy was considered a better option than thrombolysis because of the urgency of the situation.1 In the initial postoperative phase, my condition was reportedly precarious, with pinpoint pupils, rigid muscles and myoclonic jerks. At this stage the prognosis was considered poor.
I next saw Gordon in the emergency medicine department, then in the ICU [intensive care unit], when he had been intubated and ventilated. After surgical clot removal he was initially still comatose and areflexic. The prognosis at this stage seemed grim. However, some hours later I received a message that he was moving all limbs. On the next day he was conscious and indicated that he wanted the tube out. An apparent facial asymmetry was noticeable.
Our family are very close and our children and grandchildren all encouraged him and worked continuously at making him laugh and use facial expression. His facial weakness recovered quickly. The staff who had worked alongside him at RBWH encouraged him tirelessly — especially his close colleagues.
My next recollection was on the evening of the day I collapsed, when I became aware that I was in the intensive care unit with an endotracheal tube in situ and was able to move all my limbs. I was extremely pleased to find myself in this state and indicated to the treating staff that I was able to breathe satisfactorily and that I wanted the endotracheal tube removed.
It appeared to me that I had no neurological deficit, but assessors found a mild left hemiparesis, maximal in the face. This resolved after a few days and I then had no overt neurological deficit, but had some intermittent diplopia.
As the event had occurred while I was taking a therapeutic dose of warfarin, it was decided that I should undergo open-heart surgery to prevent further thromboembolism. Knowing the lethal nature of basilar artery thromboembolism, with mortality rates of 80%–95%,2 I eagerly embraced this advice and resolved to go through with this proposal.
Some 2 weeks later, when I was in a good, stable state, open-heart surgery was performed to ligate the left auricular appendage, replace the aortic valve, repair the mitral valve, and resect a portion of the hypertrophied inter-atrial muscular septum. A pacemaker was inserted 4 days later. My postoperative course after open-heart surgery was uncomplicated. On 16 February 2012, I was assessed by the cardiac surgeon as being fit to exercise as I saw fit, to resume driving, and resume work.
Following heart surgery, Gordon made every effort to improve his walking and is now more fit to cope with life in his late seventies. Bike riding and tennis are part of his weekly routine. The family are most appreciative of the excellent outcome.
As of 27 February 2012, I started planning to return to part-time work and to exercise, and possibly to resume playing tennis. I am extremely grateful for my wife’s prompt actions, and for the expert, rapid and successful treatment of my condition — including the prompt response of the ambulance, prompt care in the emergency department, the expertise of the stroke team and, in particular, the urgent response of the neuroradiology team. I am also grateful for the expert care in intensive care and subsequent care in the cardiac units at RBWH and the Prince Charles Hospital.
I had a long personal and professional relationship with the nursing staff, medical consultants and radiographers who provided wonderful treatment and support. My delight at recovering was shared by all concerned. The excellent result was because there was a good system of care in place.
By mid June (almost 6 months after the stroke), I had a partial left 6th nerve gaze palsy, but no other neurological deficit, and resumed working part-time and playing tennis.
I believe that this outcome reflects very well on the acute medical care services that swung into action on a night just before the coming of a new year.
Competing interests
No relevant disclosures.
Acknowledgements
I would like to acknowledge the prompt, expert interventional neuroradiology by John Clouston, Director of Radiology.
References
- Jankowitz BT, Aleu A, Lin R, et al. Endovascular treatment of basilar artery occlusion by manual aspiration thrombectomy. J Neurointerv Surg 2010; 2: 110-114. 0_CHDBFIAH
- Schoen JC, Boysen MM, Warren CR, et al. Vertebrobasilar artery occlusion. West J Emerg Med 2011; 12: 233-239. 0_BICCIJDJ
Provenance: Not commissioned; externally peer reviewed.