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1. Presentation of myasthenic syndrome after therapeutic botulinum toxin
Clinical Neurophysiology 123 (2012) e69–e76
Contents lists available at SciVerse ScienceDirect
Clinical Neurophysiology journal homepage: www.elsevier.com/locate/clinph
Society Proceedings
Proceedings of the 14th Biennial Clinical Neurophysiology Workshop of the Australian and New Zealand Association of Neurologists, Sheraton Mirage Resort, Gold Coast, Queensland, Australia, 2nd–5th October 2011 ⇑
Matthew Kierman , Ian Maxwell, David Burke Institute of Neurological Sciences, Prince of Wales Hospital, Randwick, NSW 2036, Australia
1. Presentation of myasthenic syndrome after therapeutic botulinum toxin—Marion A. Simpson, Anita Vinton, Timothy J. Day (Cabrini Hospital, Malvern, Victoria, Australia) We describe a 53-year-old male who was receiving therapeutic botulinum toxin to the right lower limb to treat spasticity resulting from a left hemisphere intracerebral haemorrhage 6 years earlier which had resulted in complete right hemiplegia. 2 weeks following injection, he developed proximal weakness of the left upper and lower limb, without ocular, bulbar or sensory symptoms. Clinical examination revealed 4/5 proximal weakness in the left arm and leg with preserved reflexes and normal sensation, together with the old deficits on the right side related to the cerebral haemorrhage. Cranial nerve examination was unremarkable. Electrophysiological evaluation showed normal nerve conduction studies, needle EMG with a myopathic appearance of the proximal muscles but muscle biopsy showed no myopathic changes. Repetitive nerve stimulation of the left deltoid showed changes suggestive of myasthenia. Single fibre EMG in the left arm showed increased jitter with a mean jitter value of 102 ls. Acetylcholine receptor and anti-MUSK antibodies were negative. We discuss the electrophysiological differential of myasthenia from systemic botulism and review the literature regarding the unmasking of myasthenic syndromes by therapeutic botulinum toxin use. doi:10.1016/j.clinph.2011.11.010
2. Neurorehabilitation following neurotization: (radial nerve transfer to axillary nerve). In nerve reconstruction: A case series— Thomas A. Miller a,b, Doug C. Ross a,c, Alex W. Thomas a,d (a The Schulich School of Medicine and Dentistry, The University of Western of Ontario, London, Canada, b Department of Physical Medicine and Rehabilitation, St. Joseph’s Health Care, London, Canada, c Department of Surgery, Division of Plastic Surgery, St. Joseph’s Health Care, London, Canada, d Department of Medical Biophysics and Diagnostic Imaging, London, Canada) Introduction: Nerve transfer may be employed following nerve injury. This procedure relies on the patient’s ability to adapt the acti⇑ Tel.: +65 2 9382 2410. E-mail address: [email protected] (M. Kierman).
vation of a particular nerve to perform a novel motor function via neuroplasticity. We present 2 cases of upper limb nerve transfer (radial nerve triceps branch to axillary) in which the rehabilitation was less than intuitive for the patient, and provided post-rehabilitation challenges. The cases highlight the requirement for brain neuroplasticity post-nerve transfer and emphasize rehabilitation principles in nerve transfers. Case 1: A 24 year old male was involved in a motorcycle accident and suffered a upper trunk brachial plexopathy. The majority of his plexus followed a typical recovery. No recovery of the axillary nerve had occurred by 9 months and as a result he underwent nerve reconstruction with radial nerve branch to long head of triceps transferred to the axillary nerve. At 1.5 year post-neurotization the deltoid had 3/5 strength with shoulder abduction but 4/5 strength, if the patient initiated abduction by first extending the elbow. Case 2: A 26 year old male fell off his dirt bike suffering a fractured clavicle and brachial plexopathy. Due to late recognition, he underwent late nerve transfer some 20 months after the onset of the axillary nerve palsy. Once again the deltoid improved and developed an excellent functional recovery with greater strength generated if the patient first visualized elbow extension before initiating shoulder abduction. This was confirmed using biofeedback and EMG monitoring as part of the rehabilitation. Conclusion: These cases highlight the neurorehabilitation challenges often experienced following nerve transfer. Recovery of function requires more than peripheral nerve re-growth, but also reorganization of the brain to appropriately activate the desired muscle. EMG biofeedback has been useful in re-educating patients to fully utilized nerve transfers. The authors are developing techniques to simultaneously record functional MRI, EEG and EMG after nerve transfer to better understand the timing and rehabilitation implications during the process of neuroplasticity and the initial results will be reviewed. doi:10.1016/j.clinph.2011.11.011
3. Neurogenic thoracic outlet syndrome: A treatable disorder. The natural history and outcome in a case series—Thomas A. Miller a,b, Harpreet Sangha a, Doug C. Ross a,c (a The Schulich School of Medicine and Dentistry, The University of Western of Ontario, London, Canada, b Department of Physical Medicine and
Contents lists available at SciVerse ScienceDirect
Clinical Neurophysiology journal homepage: www.elsevier.com/locate/clinph
Society Proceedings
Proceedings of the 14th Biennial Clinical Neurophysiology Workshop of the Australian and New Zealand Association of Neurologists, Sheraton Mirage Resort, Gold Coast, Queensland, Australia, 2nd–5th October 2011 ⇑
Matthew Kierman , Ian Maxwell, David Burke Institute of Neurological Sciences, Prince of Wales Hospital, Randwick, NSW 2036, Australia
1. Presentation of myasthenic syndrome after therapeutic botulinum toxin—Marion A. Simpson, Anita Vinton, Timothy J. Day (Cabrini Hospital, Malvern, Victoria, Australia) We describe a 53-year-old male who was receiving therapeutic botulinum toxin to the right lower limb to treat spasticity resulting from a left hemisphere intracerebral haemorrhage 6 years earlier which had resulted in complete right hemiplegia. 2 weeks following injection, he developed proximal weakness of the left upper and lower limb, without ocular, bulbar or sensory symptoms. Clinical examination revealed 4/5 proximal weakness in the left arm and leg with preserved reflexes and normal sensation, together with the old deficits on the right side related to the cerebral haemorrhage. Cranial nerve examination was unremarkable. Electrophysiological evaluation showed normal nerve conduction studies, needle EMG with a myopathic appearance of the proximal muscles but muscle biopsy showed no myopathic changes. Repetitive nerve stimulation of the left deltoid showed changes suggestive of myasthenia. Single fibre EMG in the left arm showed increased jitter with a mean jitter value of 102 ls. Acetylcholine receptor and anti-MUSK antibodies were negative. We discuss the electrophysiological differential of myasthenia from systemic botulism and review the literature regarding the unmasking of myasthenic syndromes by therapeutic botulinum toxin use. doi:10.1016/j.clinph.2011.11.010
2. Neurorehabilitation following neurotization: (radial nerve transfer to axillary nerve). In nerve reconstruction: A case series— Thomas A. Miller a,b, Doug C. Ross a,c, Alex W. Thomas a,d (a The Schulich School of Medicine and Dentistry, The University of Western of Ontario, London, Canada, b Department of Physical Medicine and Rehabilitation, St. Joseph’s Health Care, London, Canada, c Department of Surgery, Division of Plastic Surgery, St. Joseph’s Health Care, London, Canada, d Department of Medical Biophysics and Diagnostic Imaging, London, Canada) Introduction: Nerve transfer may be employed following nerve injury. This procedure relies on the patient’s ability to adapt the acti⇑ Tel.: +65 2 9382 2410. E-mail address: [email protected] (M. Kierman).
vation of a particular nerve to perform a novel motor function via neuroplasticity. We present 2 cases of upper limb nerve transfer (radial nerve triceps branch to axillary) in which the rehabilitation was less than intuitive for the patient, and provided post-rehabilitation challenges. The cases highlight the requirement for brain neuroplasticity post-nerve transfer and emphasize rehabilitation principles in nerve transfers. Case 1: A 24 year old male was involved in a motorcycle accident and suffered a upper trunk brachial plexopathy. The majority of his plexus followed a typical recovery. No recovery of the axillary nerve had occurred by 9 months and as a result he underwent nerve reconstruction with radial nerve branch to long head of triceps transferred to the axillary nerve. At 1.5 year post-neurotization the deltoid had 3/5 strength with shoulder abduction but 4/5 strength, if the patient initiated abduction by first extending the elbow. Case 2: A 26 year old male fell off his dirt bike suffering a fractured clavicle and brachial plexopathy. Due to late recognition, he underwent late nerve transfer some 20 months after the onset of the axillary nerve palsy. Once again the deltoid improved and developed an excellent functional recovery with greater strength generated if the patient first visualized elbow extension before initiating shoulder abduction. This was confirmed using biofeedback and EMG monitoring as part of the rehabilitation. Conclusion: These cases highlight the neurorehabilitation challenges often experienced following nerve transfer. Recovery of function requires more than peripheral nerve re-growth, but also reorganization of the brain to appropriately activate the desired muscle. EMG biofeedback has been useful in re-educating patients to fully utilized nerve transfers. The authors are developing techniques to simultaneously record functional MRI, EEG and EMG after nerve transfer to better understand the timing and rehabilitation implications during the process of neuroplasticity and the initial results will be reviewed. doi:10.1016/j.clinph.2011.11.011
3. Neurogenic thoracic outlet syndrome: A treatable disorder. The natural history and outcome in a case series—Thomas A. Miller a,b, Harpreet Sangha a, Doug C. Ross a,c (a The Schulich School of Medicine and Dentistry, The University of Western of Ontario, London, Canada, b Department of Physical Medicine and