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First seizure in a young woman
Journal of Clinical Neuroscience 18 (2011) 874
Contents lists available at ScienceDirect
Journal of Clinical Neuroscience journal homepage: www.elsevier.com/locate/jocn
Images in Neuroscience: Answer
First seizure in a young woman Andrew D. Nichols a,⇑, Katharine J. Drummond a,b a b
Department of Neurosurgery, The Royal Melbourne Hospital, Grattan Street, Parkville 3050, Victoria, Australia Department of Surgery, The University of Melbourne, Parkville, Victoria, Australia
1. Answer C. Trauma.
2. Discussion The 10-mm hyperdense area on CT scan is consistent with a calcified mass or bony lesion and the overlying skull is irregular and abnormal (Fig. 1). On MRI the mass is associated with a wedgeshaped area of encephalomalacia underlying the irregular, thickened frontal bone. Therefore, the possibility of previous trauma was considered. In addition, the area of thickened frontal bone demonstrating abnormal marrow signal is suggestive of previous trauma. A thin rim of T1-weighted hyperintensity surrounding the area of calcification, which enhances with gadolinium contrast, represents granulation tissue. On direct questioning the patient’s parents remembered a significant fall with a blow to the head in infancy. The patient underwent a right frontal stereotactic craniotomy for excision of the lesion and intra-operative specimens were sent for histopathology. This showed features strongly suggestive of remote penetrating trauma including a segment of full thickness glial scarring of the cerebral cortex and dense astrocytic gliosis of underlying white matter. Additionally, there was mature lamellar bone in multiple specimens. No evidence of tumour was seen in any specimen. The patient had an uneventful post-operative recovery. A follow-up electroencephalogram did not demonstrate seizure activity and MRI brain showed excision of the area of encephalomalacia and the intra-axial area of calcification. The occurrence of seizures following a traumatic brain injury (TBI) is well recognised.1 Late post-traumatic seizures (PTS) are defined as those occurring at least 7 days post-injury and have an incidence from 4.4% to 53%2 depending on the population studied and an overall incidence of around 15% in TBI. The presence of a depressed skull fracture in TBI is a risk factor for the development of late PTS.3,4 Other risk factors for late PTS include early seizures, intracerebral haematoma, brain contusion, loss of consciousness, posttraumatic amnesia >24 hours or age >65 years.2 The use of prophylactic antiepileptic drugs (AED) in TBI has been well studied. Multiple randomised controlled trials have shown a benefit in reducing the occurrence of early PTS; that is, DOI of question: 10.1016/j.jocn.2010.04.001
⇑ Corresponding author. Tel.: +61 3 9342 7000. E-mail address: [email protected] (A.D. Nichols). 0967-5868/$ - see front matter Ó 2010 Elsevier Ltd. All rights reserved. doi:10.1016/j.jocn.2010.04.015
Fig. 1. Axial CT brain (bone window).
seizures occurring less than 7 days following injury. However, the use of AED has not been effective in reducing the rate of late PTS.5,6 This been supported by a Cochrane review and incorporated into multiple sets of guidelines regarding the use of AED in TBI.7–9 References 1. Kaye AH. Essential neurosurgery. 3rd ed. Oxford: Blackwell Publishing; 2005. 50– 1, 271–2. 2. Frey LC. Epidemiology of posttraumatic epilepsy: a critical review. Epilepsia 2003;44(Suppl. 10):11–7. 3. Temkin N. Risk factors for posttraumatic seizures in adults. Epilepsia 2003;44(Suppl. 10):18–20. 4. Asikainen I, Kaste M, Sarna S. Early and late posttraumatic seizures in traumatic brain injury rehabilitation patients: brain injury factors causing late seizures and influence of seizures on long-term outcome. Epilepsia 1999;40:584–9. 5. Beghi E. Overview of studies to prevent posttraumatic epilepsy. Epilepsia 2003;44(Suppl. 10):21–6. 6. D’Ambrosio R, Perucca E. Epilepsy after head injury. Curr Opin Neurol 2004;17:731–5. 7. Bratton SL, Chestnut RM, Ghajar J, et al. Guidelines for the management of severe traumatic brain injury. XIII. Antiseizure prophylaxis. J Neurotrauma 2007;24(Suppl. 1):S83–6. 8. Chang BS, Lowenstein DH. Practice parameter: antiepileptic drug prophylaxis in severe traumatic brain injury: report of the quality standards subcommittee of the American Academy of Neurology. Neurology 2003;60:10–6. 9. Schierhout G, Roberts IG. Antiepileptic drugs for preventing seizures following acute traumatic brain injury. Cochrane Database Syst Rev 2001;4.
Contents lists available at ScienceDirect
Journal of Clinical Neuroscience journal homepage: www.elsevier.com/locate/jocn
Images in Neuroscience: Answer
First seizure in a young woman Andrew D. Nichols a,⇑, Katharine J. Drummond a,b a b
Department of Neurosurgery, The Royal Melbourne Hospital, Grattan Street, Parkville 3050, Victoria, Australia Department of Surgery, The University of Melbourne, Parkville, Victoria, Australia
1. Answer C. Trauma.
2. Discussion The 10-mm hyperdense area on CT scan is consistent with a calcified mass or bony lesion and the overlying skull is irregular and abnormal (Fig. 1). On MRI the mass is associated with a wedgeshaped area of encephalomalacia underlying the irregular, thickened frontal bone. Therefore, the possibility of previous trauma was considered. In addition, the area of thickened frontal bone demonstrating abnormal marrow signal is suggestive of previous trauma. A thin rim of T1-weighted hyperintensity surrounding the area of calcification, which enhances with gadolinium contrast, represents granulation tissue. On direct questioning the patient’s parents remembered a significant fall with a blow to the head in infancy. The patient underwent a right frontal stereotactic craniotomy for excision of the lesion and intra-operative specimens were sent for histopathology. This showed features strongly suggestive of remote penetrating trauma including a segment of full thickness glial scarring of the cerebral cortex and dense astrocytic gliosis of underlying white matter. Additionally, there was mature lamellar bone in multiple specimens. No evidence of tumour was seen in any specimen. The patient had an uneventful post-operative recovery. A follow-up electroencephalogram did not demonstrate seizure activity and MRI brain showed excision of the area of encephalomalacia and the intra-axial area of calcification. The occurrence of seizures following a traumatic brain injury (TBI) is well recognised.1 Late post-traumatic seizures (PTS) are defined as those occurring at least 7 days post-injury and have an incidence from 4.4% to 53%2 depending on the population studied and an overall incidence of around 15% in TBI. The presence of a depressed skull fracture in TBI is a risk factor for the development of late PTS.3,4 Other risk factors for late PTS include early seizures, intracerebral haematoma, brain contusion, loss of consciousness, posttraumatic amnesia >24 hours or age >65 years.2 The use of prophylactic antiepileptic drugs (AED) in TBI has been well studied. Multiple randomised controlled trials have shown a benefit in reducing the occurrence of early PTS; that is, DOI of question: 10.1016/j.jocn.2010.04.001
⇑ Corresponding author. Tel.: +61 3 9342 7000. E-mail address: [email protected] (A.D. Nichols). 0967-5868/$ - see front matter Ó 2010 Elsevier Ltd. All rights reserved. doi:10.1016/j.jocn.2010.04.015
Fig. 1. Axial CT brain (bone window).
seizures occurring less than 7 days following injury. However, the use of AED has not been effective in reducing the rate of late PTS.5,6 This been supported by a Cochrane review and incorporated into multiple sets of guidelines regarding the use of AED in TBI.7–9 References 1. Kaye AH. Essential neurosurgery. 3rd ed. Oxford: Blackwell Publishing; 2005. 50– 1, 271–2. 2. Frey LC. Epidemiology of posttraumatic epilepsy: a critical review. Epilepsia 2003;44(Suppl. 10):11–7. 3. Temkin N. Risk factors for posttraumatic seizures in adults. Epilepsia 2003;44(Suppl. 10):18–20. 4. Asikainen I, Kaste M, Sarna S. Early and late posttraumatic seizures in traumatic brain injury rehabilitation patients: brain injury factors causing late seizures and influence of seizures on long-term outcome. Epilepsia 1999;40:584–9. 5. Beghi E. Overview of studies to prevent posttraumatic epilepsy. Epilepsia 2003;44(Suppl. 10):21–6. 6. D’Ambrosio R, Perucca E. Epilepsy after head injury. Curr Opin Neurol 2004;17:731–5. 7. Bratton SL, Chestnut RM, Ghajar J, et al. Guidelines for the management of severe traumatic brain injury. XIII. Antiseizure prophylaxis. J Neurotrauma 2007;24(Suppl. 1):S83–6. 8. Chang BS, Lowenstein DH. Practice parameter: antiepileptic drug prophylaxis in severe traumatic brain injury: report of the quality standards subcommittee of the American Academy of Neurology. Neurology 2003;60:10–6. 9. Schierhout G, Roberts IG. Antiepileptic drugs for preventing seizures following acute traumatic brain injury. Cochrane Database Syst Rev 2001;4.