601: Respiratory decompensation: An unrecognized potential complication of Botulinum toxin in at...
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463: Neuronal firing patterns of higher order thalamocortical neurons during Inter-ictal absence seizure transition: Poten- tial implications for loss of consciousness Terence J. O’Brien a , Didier Pinault b ; a Unversity of Melbourne, Australia; b Universite ´ Louis Pasteur (Faculte ´ de Me ´decine), France Purpose: Thalamocortical (TC) neurons play a critical role in absence related generalized spike-and-wave dis- charges (SWD) being recruited into a highly synchronised rhythmic firing pattern which blocks the normal function of first order (FO) thalamic nuclei to transmit primary sen- sory information. However, this alone is unlikely to explain the loss of consciousness experienced by patients. Little information exists about the involvement of higher-order (HO) TC neurons, which relay corticocortical signals and play an important role in the integration of sensorimotor information, attention and cognition. Method: Single-cell recordings of TC neurons were made in vivo, under neurolept anaesthesia, along with EEG recording of the related sensorimotor cortex, in adult male Generalised Absence Epilepsy Rats from Strasbourg (GAERS) (n = 13). Firing patterns in the posterior (Po; n = 39) thalamic group were compared with the ventroba- sal (VB; n = 20) thalamus (i.e. the principle somatosensory HO and FO nuclei respectively). Results: Interictally the median percentage of burst firing/ cell was higher in Po cells (15% vs. 5%, p = 0.07), with a higher median maximal number of action potentials per burst (5 vs. 4, p = 0.02). With the ictal transition both neuro- nal types switched early (240 ± 12 vs. 210 ± 8 msecs prior to seizure onset, p = 0.85) to a rhythmic firing pattern that was highly synchronised with the EEG SWDs and had a high fir- ing probability (0.76 ± 0.04 vs. 0.68 ± 0.06, p = 0.31). The firing of the Po cells in relation to each SWD was earlier (19 ± 2 vs. 12 ± 3 msecs, p = 0.01) and showed more burst firing (median/cell 50% vs. 30%, p < 0.001). Conclusions: Somatosensory HO TC neurons are involved in the absence-related firing pattern as early and as extensively as their FO counterparts, with more promi- nent burst firing. These features would be expected to result in a disruption of the function of HO TC neurons to relay and integrate corticocortical information, and therefore may play a mechanistic role in the loss of consciousness. doi:10.1016/j.jocn.2007.07.073 601: Respiratory decompensation: An unrecognized potential complication of Botulinum toxin in at risk patients Andrew Hughes, Rajinder K. Dhamija, Doug Brown; Austin Health, Australia Background: Botulinum toxin is widely used for the treat- ment of dystonia and spasticity. Although relatively safe, transient local weakness and rarely generalized weakness related to systemic spread can be seen. Pulmonary decom- pensation following botulinum toxin has not previously been described. We report a patient developing type 2 respi- ratory failure following treatment with Botulinum toxin. Case report: A 45-year-old man with long standing com- plete T5 paraplegia was treated with increasing doses of bot- ulinum toxin for severe lower limb adductor spasticity. He had no previous history of any other neuromuscular disease. Initial tratment with 1500 mouse units (mu) of Botulinum toxin (Dysport), divided equally into each adductor group, resulted in no improvement. Four months later the dose was increased to 2500 mu with improvement but a still subopti- mal response. After a further 4 months he received a third series of adductor injections totaling 3000 mu. Eight days later he developed gradually increasing upper limb weak- ness, dyspnoea associated with early morning headache and anxiety, mild dysphagia and some difficulty with cough. His neurological examination revealed new mild diffuse upper limb weakness (4/5). There was no objective facial or bulbar muscle weakness. Pulmonary evaluation showed markedly reduced FEV1 (1.4L) and Vital Capacity (1.5L) consistent with a severe restrictive ventilatory defect. Maxi- mal inspiratory and expiratory pressures were severely reduced. Arterial gases showed pCO 2 52 mmHg, pO 2 118 mmHg, pH 7.39, and bicarb 31 mmol/l with Base Excess +5 mmol/ l, consistent with compensated Type 2 respiratory failure. Upper limb NCS and routine EMG were normal. Single fiber EMG showed abnormal jitter and blocking. Repetitive stimulation was normal. The patient was man- aged conservatively and made a full recovery over 4 weeks. Conclusions: Localized lower limb weakness from Botu- linum toxin in paraplegic patients may not always be of functional concern and may encourage the use of larger doses to treat severe spasticity. Our case demonstrates that generalised mild weakness in patients with reduced respira- tory reserve can result in respiratory compromise. doi:10.1016/j.jocn.2007.07.074 602: Progressive supranuclear palsy presenting as classic levodopa-responsive Parkinson’s disease of 20 years duration Andrew Hughes, Rajinder K. Dhamija, Marion Hoffman, Renate Kalnins; Austin Health, Australia Background: Despite established clinical diagnostic cri- teria for Progressive Supranuclear Palsy (PSP) cases resem- bling Parkinson’s disease (PD) are well recognised. Atypical features for PD are however almost always pres- ent late in the clinical course. We report a case of patholog- ically proven PSP with a typical and prolonged clinical course for PD. Case report: In 1985 a 65-year-old man was diagnosed with PD after presenting with rest tremor involving the left Abstracts / Journal of Clinical Neuroscience 15 (2008) 337–369 365
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Transcript of 601: Respiratory decompensation: An unrecognized potential complication of Botulinum toxin in at...
Abstracts / Journal of Clinical Neuroscience 15 (2008) 337–369 365
463: Neuronal firing patterns of higher order thalamocortical
neurons during Inter-ictal absence seizure transition: Poten-
tial implications for loss of consciousness
Terence J. O’Brien a, Didier Pinault b; a Unversity of
Melbourne, Australia; b Universite Louis Pasteur (Faculte
de Medecine), France
Purpose: Thalamocortical (TC) neurons play a criticalrole in absence related generalized spike-and-wave dis-charges (SWD) being recruited into a highly synchronisedrhythmic firing pattern which blocks the normal functionof first order (FO) thalamic nuclei to transmit primary sen-sory information. However, this alone is unlikely to explainthe loss of consciousness experienced by patients. Littleinformation exists about the involvement of higher-order(HO) TC neurons, which relay corticocortical signals andplay an important role in the integration of sensorimotorinformation, attention and cognition.
Method: Single-cell recordings of TC neurons weremade in vivo, under neurolept anaesthesia, along withEEG recording of the related sensorimotor cortex, in adultmale Generalised Absence Epilepsy Rats from Strasbourg(GAERS) (n = 13). Firing patterns in the posterior (Po;n = 39) thalamic group were compared with the ventroba-sal (VB; n = 20) thalamus (i.e. the principle somatosensoryHO and FO nuclei respectively).
Results: Interictally the median percentage of burst firing/cell was higher in Po cells (15% vs. 5%, p = 0.07), with ahigher median maximal number of action potentials perburst (5 vs. 4, p = 0.02). With the ictal transition both neuro-nal types switched early (240 ± 12 vs. 210 ± 8 msecs prior toseizure onset, p = 0.85) to a rhythmic firing pattern that washighly synchronised with the EEG SWDs and had a high fir-ing probability (0.76 ± 0.04 vs. 0.68 ± 0.06, p = 0.31). Thefiring of the Po cells in relation to each SWD was earlier(�19 ± 2 vs. �12 ± 3 msecs, p = 0.01) and showed moreburst firing (median/cell 50% vs. 30%, p < 0.001).
Conclusions: Somatosensory HO TC neurons areinvolved in the absence-related firing pattern as early andas extensively as their FO counterparts, with more promi-nent burst firing. These features would be expected to resultin a disruption of the function of HO TC neurons to relayand integrate corticocortical information, and thereforemay play a mechanistic role in the loss of consciousness.
doi:10.1016/j.jocn.2007.07.073
601: Respiratory decompensation: An unrecognized potential
complication of Botulinum toxin in at risk patients
Andrew Hughes, Rajinder K. Dhamija, Doug Brown;
Austin Health, Australia
Background: Botulinum toxin is widely used for the treat-ment of dystonia and spasticity. Although relatively safe,
transient local weakness and rarely generalized weaknessrelated to systemic spread can be seen. Pulmonary decom-pensation following botulinum toxin has not previouslybeen described. We report a patient developing type 2 respi-ratory failure following treatment with Botulinum toxin.
Case report: A 45-year-old man with long standing com-plete T5 paraplegia was treated with increasing doses of bot-ulinum toxin for severe lower limb adductor spasticity. Hehad no previous history of any other neuromuscular disease.Initial tratment with 1500 mouse units (mu) of Botulinumtoxin (Dysport), divided equally into each adductor group,resulted in no improvement. Four months later the dose wasincreased to 2500 mu with improvement but a still subopti-mal response. After a further 4 months he received a thirdseries of adductor injections totaling 3000 mu. Eight dayslater he developed gradually increasing upper limb weak-ness, dyspnoea associated with early morning headacheand anxiety, mild dysphagia and some difficulty with cough.His neurological examination revealed new mild diffuseupper limb weakness (4/5). There was no objective facialor bulbar muscle weakness. Pulmonary evaluation showedmarkedly reduced FEV1 (1.4L) and Vital Capacity (1.5L)consistent with a severe restrictive ventilatory defect. Maxi-mal inspiratory and expiratory pressures were severelyreduced. Arterial gases showed pCO2 52 mmHg, pO2 118mmHg, pH 7.39, and bicarb 31 mmol/l with Base Excess+5 mmol/ l, consistent with compensated Type 2 respiratoryfailure. Upper limb NCS and routine EMG were normal.Single fiber EMG showed abnormal jitter and blocking.Repetitive stimulation was normal. The patient was man-aged conservatively and made a full recovery over 4 weeks.
Conclusions: Localized lower limb weakness from Botu-linum toxin in paraplegic patients may not always be offunctional concern and may encourage the use of largerdoses to treat severe spasticity. Our case demonstrates thatgeneralised mild weakness in patients with reduced respira-tory reserve can result in respiratory compromise.
doi:10.1016/j.jocn.2007.07.074
602: Progressive supranuclear palsy presenting as classic
levodopa-responsive Parkinson’s disease of 20 years duration
Andrew Hughes, Rajinder K. Dhamija, Marion Hoffman,
Renate Kalnins; Austin Health, Australia
Background: Despite established clinical diagnostic cri-teria for Progressive Supranuclear Palsy (PSP) cases resem-bling Parkinson’s disease (PD) are well recognised.Atypical features for PD are however almost always pres-ent late in the clinical course. We report a case of patholog-ically proven PSP with a typical and prolonged clinicalcourse for PD.
Case report: In 1985 a 65-year-old man was diagnosedwith PD after presenting with rest tremor involving the left
