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57. Progressive sporadic adult onset cerebellar ataxia from superficial hemosiderosis
Abstracts / Journal of Clinical Neuroscience 16 (2009) 1514–1546
56. Effects of hypoglycaemia on the brain in children with Type 1 Diabetes Mellitus: Changes in EEG and Quantitative EEG Ghosh S 1, Nagarajan L 1,2, Bulsara M 1,2, Davis EA 2, Carne CL 2, Jones TW 2 1 Centre for Neuromuscular and Neurological Disorders, 3School of Population Health, University of Western Australia 2 Princess Margaret Hospital for Children, Subiaco, Perth, Western Australia
Introduction: Neurophysiological, neuroanatomical, neuroimaging, neurocognitive and neurochemical studies suggest that children and adolescents with Type 1 Diabetes Mellitus (TIDM) may be at risk for neurological impairment. The aetiopathogenesis of this increased risk is not well understood. Intensive and aggressive treatment regimes for TIDM have resulted in an increase in hypoglycaemic episodes. This has raised concerns regarding impact of hypoglycaemia on the developing brain. There is conflicting evidence on the short and long term effects on brain function. In order to further investigate the effect of hypoglycaemia we performed visual and quantatitave analysis of EEG (qEEG) in children with TIDM. Methods: Children with onset of TIDM < 6 years of age, were included in the study approved by the Princess Margaret Ho spital ethics committee. They were 6-15 yrs (mean 10.1 ± 2.4yr) at the time of EEG. Frequency of symptomatic hypoglycaemia was prospectively monitored every 3 months along with HbA1c and other parameters. Eighty five EEGs (international 10 – 20 system) were recorded using Compumedics Digital EEG System in the wake state (BSLs >4.2 mmols/L at recording) and analyzed visually. qEEGs was analyzed in 78 using Neuroscan software. The absolute and relative power spectra in the frequency bands of delta, theta, alpha, beta and gamma were analysed for six left, six right and three midline electrodes. Children were divided into three groups – severe hypoglycaemia (associated with coma or convulsion), moderate hypoglycemia (requiring assistance to manage symptoms) and no hypoglycaemia. There was no significant difference in the age of the children in these three groups. Results: On visual analysis 84% had normal or near normal EEG backgrounds and 16% had definite abnormalities. There was no significant difference in the severity of the hypoglycemias in those with an abnormal background compared to those with a normal one. Children with abnormalities on visual analysis appeared to be of a younger age. On qEEG there were statistically significant differences in the power spectra from some leads in the theta and gamma frequency range in the moderate and severe hypoglycemia groups compared to the no hypoglycemia group. Theta power was increased in F3, P3, F4 T4 and T6 leads, and gamma power was reduced in O1 lead. Comparison of visual and quantitative analysis of EEG showed that in the EEGs that were abnormal on visual analysis the relative power in the alpha range was significantly lower and in the delta and theta ranges significantly higher in many leads. Conclusions: Children with TIDM and hypoglycemic episodes have abnormal EEG background which can be detected by qEEG analysis. These abnormalities include increase in slow activity in frontal regions in both hemispheres, and left parietal and right temporal regions. The clinical significance of these findings needs to be elucidated by further study. doi:10.1016/j.jocn.2009.07.081
57. Progressive sporadic adult onset cerebellar ataxia from superficial hemosiderosis Aggarwal A 1,2, Sandy Patel 3,4, Thompson PD 1,2
1545
1
Department of Neurology, Royal Adelaide Hospital, Adelaide, Australia University Department of Medicine, University of Adelaide, Adelaide, Australia 3 Department of Neuroradiology, Royal Adelaide Hospital, Adelaide, Australia 4 Department of Neuroradiology, Women’s and Children’s Hospital, Adelaide, Australia 2
Sporadic and genetic cerebellar degenerations are most frequent causes of adult onset cerebellar ataxias but in a majority of patients the etiology remains unexplained. Superficial hemosiderosis is an uncommon and often unrecognized cause of cerebellar ataxia in adults. It results from hemosiderin deposit in the subplia layers of the brain and spinal cord following chronic or intermittent extravasation of blood into the cerebrospinal fluid. We report two patients with superficial hemosiderosis to highlight the clinical and radiological features of the disorder. Both developed a progressive sporadic adult onset cerebellar ataxia accompanied by anosmia, hearing loss and pyramidal signs. Hearing impairment and anosmia were important clues and brain MRI confirmed superficial hemosiderosis. Neither patient had an identifiable source of active bleeding into the CSF though the second patient did recall a neck injury. MRI in both patients showed cerebellar atrophy with rim of T2W hypointensity (representing hemosiderin deposits) along the cerebellar folia, cortical gyri, brainstem and cord. The changes were best appreciated on T2* (gradient echo images) and most marked in the cerebellum. This report indicates that superficial hemosiderosis should be considered in the differential diagnosis of sporadic onset progressive cerebellar ataxia. doi:10.1016/j.jocn.2009.07.082
58. Management of transient ischaemic attacks; a retrospective analysis of inpatient versus outpatient care Chen Ming Sheng 1,2, Ahmad Omar 1, Ahmad Kate 1, Hughes Andrew 1, Lueck Christian 1 1 Department of Neurology, The Canberra Hospital and ANU Medical School, Canberra, Australia 2 Department of Neurology, No 1 Municipal Hospital, Longyan City, Fujian Province, China
Background & Aims: The management of transient ischaemic attacks (TIAs) involves rapid evaluation and early treatment of patients in order to reduce the risk of subsequent stroke. It is often presumed that hospital admission is a more efficient way of ensuring optimum management, but this is not necessarily the case, and hospital admission is expensive. In this study we attempted to compare the investigation and management of TIAs in those patients who had been admitted to hospital and in those who were evaluated on an outpatient basis. Methods: We retrospectively reviewed the records of all patients presenting to the emergency department (ED) of the Canberra Hospital over a 2 1/2 yr period with a diagnosis of TIA. Patients that were discharged directly from ED to be managed on an outpatient basis were compared to those that were admitted for further evaluation. Clinical characteristics including ABCD2 score and other stroke risk factors were evaluated for all patients. Data on essential investigations, management and outcome were also collected. In terms of investigations, the time intervals between presentation and neuroimaging, carotid ultrasonography, cardiac investigations and blood tests (including lipids & blood sugar) were determined for all patients. Regarding management, patients were assessed as to whether
56. Effects of hypoglycaemia on the brain in children with Type 1 Diabetes Mellitus: Changes in EEG and Quantitative EEG Ghosh S 1, Nagarajan L 1,2, Bulsara M 1,2, Davis EA 2, Carne CL 2, Jones TW 2 1 Centre for Neuromuscular and Neurological Disorders, 3School of Population Health, University of Western Australia 2 Princess Margaret Hospital for Children, Subiaco, Perth, Western Australia
Introduction: Neurophysiological, neuroanatomical, neuroimaging, neurocognitive and neurochemical studies suggest that children and adolescents with Type 1 Diabetes Mellitus (TIDM) may be at risk for neurological impairment. The aetiopathogenesis of this increased risk is not well understood. Intensive and aggressive treatment regimes for TIDM have resulted in an increase in hypoglycaemic episodes. This has raised concerns regarding impact of hypoglycaemia on the developing brain. There is conflicting evidence on the short and long term effects on brain function. In order to further investigate the effect of hypoglycaemia we performed visual and quantatitave analysis of EEG (qEEG) in children with TIDM. Methods: Children with onset of TIDM < 6 years of age, were included in the study approved by the Princess Margaret Ho spital ethics committee. They were 6-15 yrs (mean 10.1 ± 2.4yr) at the time of EEG. Frequency of symptomatic hypoglycaemia was prospectively monitored every 3 months along with HbA1c and other parameters. Eighty five EEGs (international 10 – 20 system) were recorded using Compumedics Digital EEG System in the wake state (BSLs >4.2 mmols/L at recording) and analyzed visually. qEEGs was analyzed in 78 using Neuroscan software. The absolute and relative power spectra in the frequency bands of delta, theta, alpha, beta and gamma were analysed for six left, six right and three midline electrodes. Children were divided into three groups – severe hypoglycaemia (associated with coma or convulsion), moderate hypoglycemia (requiring assistance to manage symptoms) and no hypoglycaemia. There was no significant difference in the age of the children in these three groups. Results: On visual analysis 84% had normal or near normal EEG backgrounds and 16% had definite abnormalities. There was no significant difference in the severity of the hypoglycemias in those with an abnormal background compared to those with a normal one. Children with abnormalities on visual analysis appeared to be of a younger age. On qEEG there were statistically significant differences in the power spectra from some leads in the theta and gamma frequency range in the moderate and severe hypoglycemia groups compared to the no hypoglycemia group. Theta power was increased in F3, P3, F4 T4 and T6 leads, and gamma power was reduced in O1 lead. Comparison of visual and quantitative analysis of EEG showed that in the EEGs that were abnormal on visual analysis the relative power in the alpha range was significantly lower and in the delta and theta ranges significantly higher in many leads. Conclusions: Children with TIDM and hypoglycemic episodes have abnormal EEG background which can be detected by qEEG analysis. These abnormalities include increase in slow activity in frontal regions in both hemispheres, and left parietal and right temporal regions. The clinical significance of these findings needs to be elucidated by further study. doi:10.1016/j.jocn.2009.07.081
57. Progressive sporadic adult onset cerebellar ataxia from superficial hemosiderosis Aggarwal A 1,2, Sandy Patel 3,4, Thompson PD 1,2
1545
1
Department of Neurology, Royal Adelaide Hospital, Adelaide, Australia University Department of Medicine, University of Adelaide, Adelaide, Australia 3 Department of Neuroradiology, Royal Adelaide Hospital, Adelaide, Australia 4 Department of Neuroradiology, Women’s and Children’s Hospital, Adelaide, Australia 2
Sporadic and genetic cerebellar degenerations are most frequent causes of adult onset cerebellar ataxias but in a majority of patients the etiology remains unexplained. Superficial hemosiderosis is an uncommon and often unrecognized cause of cerebellar ataxia in adults. It results from hemosiderin deposit in the subplia layers of the brain and spinal cord following chronic or intermittent extravasation of blood into the cerebrospinal fluid. We report two patients with superficial hemosiderosis to highlight the clinical and radiological features of the disorder. Both developed a progressive sporadic adult onset cerebellar ataxia accompanied by anosmia, hearing loss and pyramidal signs. Hearing impairment and anosmia were important clues and brain MRI confirmed superficial hemosiderosis. Neither patient had an identifiable source of active bleeding into the CSF though the second patient did recall a neck injury. MRI in both patients showed cerebellar atrophy with rim of T2W hypointensity (representing hemosiderin deposits) along the cerebellar folia, cortical gyri, brainstem and cord. The changes were best appreciated on T2* (gradient echo images) and most marked in the cerebellum. This report indicates that superficial hemosiderosis should be considered in the differential diagnosis of sporadic onset progressive cerebellar ataxia. doi:10.1016/j.jocn.2009.07.082
58. Management of transient ischaemic attacks; a retrospective analysis of inpatient versus outpatient care Chen Ming Sheng 1,2, Ahmad Omar 1, Ahmad Kate 1, Hughes Andrew 1, Lueck Christian 1 1 Department of Neurology, The Canberra Hospital and ANU Medical School, Canberra, Australia 2 Department of Neurology, No 1 Municipal Hospital, Longyan City, Fujian Province, China
Background & Aims: The management of transient ischaemic attacks (TIAs) involves rapid evaluation and early treatment of patients in order to reduce the risk of subsequent stroke. It is often presumed that hospital admission is a more efficient way of ensuring optimum management, but this is not necessarily the case, and hospital admission is expensive. In this study we attempted to compare the investigation and management of TIAs in those patients who had been admitted to hospital and in those who were evaluated on an outpatient basis. Methods: We retrospectively reviewed the records of all patients presenting to the emergency department (ED) of the Canberra Hospital over a 2 1/2 yr period with a diagnosis of TIA. Patients that were discharged directly from ED to be managed on an outpatient basis were compared to those that were admitted for further evaluation. Clinical characteristics including ABCD2 score and other stroke risk factors were evaluated for all patients. Data on essential investigations, management and outcome were also collected. In terms of investigations, the time intervals between presentation and neuroimaging, carotid ultrasonography, cardiac investigations and blood tests (including lipids & blood sugar) were determined for all patients. Regarding management, patients were assessed as to whether