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284 papers/frontiers_in_neuroscience_oct_2012.bib
@@ -0,0 +1,284 @@
+@Article{Niedermeyer2009,
+author="Niedermeyer, E.",
+title="The burst-suppression electroencephalogram.",
+journal="American journal of electroneurodiagnostic technology",
+year="2009",
+month="Dec",
+volume="49",
+number="4",
+pages="333-341",
+keywords="Diagnosis, Differential",
+keywords="Electroencephalography",
+keywords="Humans",
+keywords="Hypoxia, Brain",
+abstract="The burst suppression (BS) pattern of the EEG was originally described as a response to large dosages of anesthetics and sedatives. It was subsequently found over/in isolated cortex due to surgical procedures or lesions underlying the cortex. Around 1960 with the introduction of modern intensive care treatment (intubation, artificial respiration) the BS pattern has become a typical EEG correlate of cerebral anoxia. These obvious consequences of this therapeutic approach with their impact on the EEG picture are more or less inexplicable. The BS pattern is also typical in two rare and severe central nervous system (CNS) disorders in infants: early infantile myoclonic encephalopathy (EIME) and Ohtahara syndrome.",
+url="http://ukpmc.ac.uk/abstract/MED/20073416"
+}
+@article{Derbyshire31071936,
+author = {Derbyshire, A. J. and Rempel, B. and Forbes, A. and Lambert, E. F.},
+title = {THE EFFECTS OF ANESTHETICS ON ACTION POTENTIALS IN THE CEREBRAL CORTEX OF THE CAT},
+volume = {116},
+number = {3},
+pages = {577-596},
+year = {1936},
+URL = {http://ajplegacy.physiology.org/content/116/3/577.short},
+eprint = {http://ajplegacy.physiology.org/content/116/3/577.full.pdf+html},
+journal = {American Journal of Physiology -- Legacy Content}
+}
+
+@article{Swank01031949,
+author = {Swank, Roy L. and Watson, C. Wesley},
+title = {EFFECTS OF BARBITURATES AND ETHER ON SPONTANEOUS ELECTRICAL ACTIVITY OF DOG BRAIN},
+volume = {12},
+number = {2},
+pages = {137-160},
+year = {1949},
+URL = {http://jn.physiology.org/content/12/2/137.short},
+eprint = {http://jn.physiology.org/content/12/2/137.full.pdf+html},
+journal = {Journal of Neurophysiology}
+}
+
+@article{Henry19521,
+title = "Suppression-burst activity from isolated cerebral cortex in man",
+journal = "Electroencephalography and Clinical Neurophysiology",
+volume = "4",
+number = "1",
+pages = "1 - 22",
+year = "1952",
+note = "",
+issn = "0013-4694",
+doi = "10.1016/0013-4694(52)90027-8",
+url = "http://www.sciencedirect.com/science/article/pii/0013469452900278",
+author = "Charles E. Henry and William B. Scoville"
+}
+
+@article{FischerWilliams1963568,
+title = "Depth recording from the human brain in epilepsy",
+journal = "Electroencephalography and Clinical Neurophysiology",
+volume = "15",
+number = "4",
+pages = "568 - 587",
+year = "1963",
+note = "",
+issn = "0013-4694",
+doi = "10.1016/0013-4694(63)90030-0",
+url = "http://www.sciencedirect.com/science/article/pii/0013469463900300",
+author = "M Fischer-Williams and R.A Cooper"
+}
+
+@article{Treiman199049,
+title = "A progressive sequence of electroencephalographic changes during generalized convulsive status epilepticus",
+journal = "Epilepsy Research",
+volume = "5",
+number = "1",
+pages = "49 - 60",
+year = "1990",
+note = "",
+issn = "0920-1211",
+doi = "10.1016/0920-1211(90)90065-4",
+url = "http://www.sciencedirect.com/science/article/pii/0920121190900654",
+author = "David M. Treiman and Nancy Y. Walton and Carol Kendrick",
+keywords = "Status epilepticus",
+keywords = "EEG",
+keywords = "Monitoring",
+keywords = "Experimental models"
+}
+
+@article{Schwartz1989,
+author = {Schwartz, Arthur E. and Tuttle, Robert H. and Poppers, Paul J.},
+title = {Electroencephalographic Burst Suppression in Elderly and Young Patients Anesthetized with Isoflurane},
+volume = {68},
+number = {1},
+pages = {9-12},
+year = {January 1989},
+abstract ={The electroencephalograms of seven elderly (70–85 years) and seven younger patients (23–31 years) anesthetized with a concentration of isoflurane sufficient to produce burst suppression were studied. Anesthesia in these unpremedicated subjects was induced by inhalation of nitrous oxide, isoflurane, and oxygen. Tracheal intubation was facilitated with succinylcholine and the lungs were next ventilated with oxygen and isoflurane to produce an end-tidal concentration of 1.7%. Isoflurane concentration was determined by infrared analysis of expired gas collected from a Teflon catheter inserted through the endotracheal tube. After 25 minutes at steady state, the EEG was recorded for 5 minutes prior to surgical stimulation. Arterial blood pressure, temperature, and ventilation were maintained at normal values. In elderly patients the EEG had both a greater proportion of total time in electrical silence (76.0 ± 10.8% vs 37.6 ± 15.4%; P < 0.01) and a greater number of isoelectric periods (19.7 ± 8.1 vs 10.7 ± 5.4; P < 0.05). This demonstrates a discrete alteration with age in the central nervous system sensitivity to isoflurane.},
+URL = {http://www.anesthesia-analgesia.org/content/68/1/9.abstract},
+eprint = {http://www.anesthesia-analgesia.org/content/68/1/9.full.pdf+html},
+journal = {Anesthesia and Analgesia}
+}
+
+@Article{Akrawi1996,
+author="Akrawi, W. P.
+and Drummond, J. C.
+and Kalkman, C. J.
+and Patel, P. M.",
+title="A comparison of the electrophysiologic characteristics of EEG burst-suppression as produced by isoflurane, thiopental, etomidate, and propofol.",
+journal="Journal of neurosurgical anesthesiology",
+year="1996",
+month="Jan",
+volume="8",
+number="1",
+pages="40-46",
+keywords="Anesthetics, Inhalation",
+keywords="Anesthetics, Intravenous",
+keywords="Animals",
+keywords="Cerebral Cortex",
+keywords="Electroencephalography",
+keywords="Etomidate",
+keywords="Isoflurane",
+keywords="Propofol",
+keywords="Rats",
+keywords="Rats, Sprague-Dawley",
+keywords="Thiopental",
+keywords="Time Factors",
+abstract="Electroencephalogram (EEG) burst-suppression can be produced with several anesthetic agents. Discussions of burst-suppression suggest that it has been viewed by many as a relatively uniform physiologic state independent of the agent used to produce it. This view may be an oversimplification. In this study, relatively deep EEG burst-suppression (suppression to burst time ratio, 4:1) was induced in rats with isoflurane (I), thiopental (T), etomidate (E), and propofol (P). Burst duration, maximum peak-to-peak voltage, area under the curve, and the ratio of power in high versus low frequencies of EEG recorded in both cortex and subcortex (thalamus) were determined. Analysis of the bursts revealed significant differences in duration [I, 1.4 +/- 0.4 (SD); T, 0.8 +/- 0.5; E, 0.3 +/- 0.1; P, 0.4 +/- 0.1 seconds], peak-to-peak voltage (I, 488 +/- 146; T, 285 +/- 106; E, 310 +/- 87; P, 249 +/- 50 muV), and area under the curve (I, 111 +/- 24; T, 35 +/- 31; E, 17 +/- 7; P, 21 +/- 4 muV-s) for all agent pairs except etomidate and propofol. Suppression phase analysis revealed considerable residual activity with all four agents, although peak-to-peak voltage (I, 129 +/- 29; T, 64 +/- 20; E, 62 +/- 11; P, 40 +/- 15 muV) and area under the curve (I, 73 +/- 17; T, 37 +/- 14; E, 30 +/- 5; P, 22 +/- 10 muV-s) were greatest with isoflurane. The cortical versus subcortical comparison revealed, for all agents, greater peak-to-peak voltage and area under the curve in the subcortex. The data indicate that the electrophysiologic characteristics of burst-suppression vary among the four agents, with the possible exception of etomidate and propofol. The data suggest that the neurophysiologic states associated with burst-suppression produced by various anesthetics should not be assumed to be uniform.",
+note="Comparative Study,",
+url="http://ukpmc.ac.uk/abstract/MED/8719192"
+}
+
+@article{GriggDamberger198984,
+title = "Neonatal burst suppression: Its developmental significance",
+journal = "Pediatric Neurology",
+volume = "5",
+number = "2",
+pages = "84 - 92",
+year = "1989",
+note = "",
+issn = "0887-8994",
+doi = "10.1016/0887-8994(89)90032-5",
+url = "http://www.sciencedirect.com/science/article/pii/0887899489900325",
+author = "Madeleine M. Grigg-Damberger and Steven B. Coker and Carey L. Halsey and Craig L. Anderson"
+}
+
+@article{Geocadin2002193,
+title = "Neurological recovery by EEG bursting after resuscitation from cardiac arrest in rats",
+journal = "Resuscitation",
+volume = "55",
+number = "2",
+pages = "193 - 200",
+year = "2002",
+note = "",
+issn = "0300-9572",
+doi = "10.1016/S0300-9572(02)00196-X",
+url = "http://www.sciencedirect.com/science/article/pii/S030095720200196X",
+author = "Romergryko G Geocadin and David L Sherman and Hans Christian Hansen and Tetsu Kimura and Ernst Niedermeyer and Nitish V Thakor and Daniel F Hanley",
+keywords = "Asphyxia",
+keywords = "Brain ischemia",
+keywords = "Cardiac arrest",
+keywords = "Electroencephalography",
+keywords = "Neurological dysfunction",
+keywords = "Resuscitation",
+keywords = "Asfixia",
+keywords = "Isquemia cerebral",
+keywords = "Paragem cardı́aca",
+keywords = "Electroencefalografia",
+keywords = "Disfunção neurológica e reanimação",
+keywords = "Asfixia",
+keywords = "Isquemia cerebral",
+keywords = "Paro cardı́aco",
+keywords = "Electroencefalografı́a",
+keywords = "Disfunción neurológica",
+keywords = "Resucitación"
+}
+
+@article {Amzica2009,
+author = {Amzica, Florin},
+title = {Basic physiology of burst-suppression},
+journal = {Epilepsia},
+volume = {50},
+publisher = {Blackwell Publishing Ltd},
+issn = {1528-1167},
+url = {http://dx.doi.org/10.1111/j.1528-1167.2009.02345.x},
+doi = {10.1111/j.1528-1167.2009.02345.x},
+pages = {38--39},
+year = {2009},
+}
+
+@article{Voss2008,
+author = {Voss, Logan J. and Sleigh, James W. and Barnard, John P. M. and Kirsch, Heidi E.},
+title = {The Howling Cortex: Seizures and General Anesthetic Drugs},
+volume = {107},
+number = {5},
+pages = {1689-1703},
+year = {November 2008},
+doi = {10.1213/ane.0b013e3181852595},
+abstract ={The true incidence of seizures caused by general anesthetic drugs is unknown. Abnormal movements are common during induction of anesthesia, but they may not be indicative of true seizures. Conversely, epileptiform electrocortical activity is commonly induced by enflurane, etomidate, sevoflurane and, to a lesser extent, propofol, but it rarely progresses to generalized tonic-clonic seizures. Even “nonconvulsant” anesthetic drugs occasionally cause seizures in subjects with preexisting epilepsy. These seizures most commonly occur during induction or emergence from anesthesia, when the anesthetic drug concentration is relatively low. There is no unifying neural mechanism of anesthetic drug-related seizurogenesis. However, there is a growing body of experimental work suggesting that seizures are not caused simply by “too much excitation,” but rather by excitation applied to a mass of neurons which are primed to react to the excitation by going into an oscillatory seizure state. Increased ?-amino-butyric acid (GABA)ergic inhibition can sensitize the cortex so that only a small amount of excitation is required to cause seizures. This has been postulated to occur 1) at the network level by increasing the propensity for reverberation (e.g., by prolongation of the “inhibitory lag”), or 2) via different effects on subpopulations of interneurons (“inhibiting-the-inhibitors”) or 3) at the synaptic level by changing the chloride reversal potential (“excitatory GABA”). On the basis of applied neuropharmacology, prevention of anesthetic-drug related seizures would include 1) avoiding sevoflurane and etomidate, 2) considering prophylaxis with adjunctive benzodiazepines (a-subunit GABAA agonists), or drugs that impair calcium entry into neurons, and 3) using electroencephalogram monitoring to detect early signs of cortical instability and epileptiform activity. Seizures may falsely elevate electroencephalogram indices of depth of anesthesia.},
+URL = {http://www.anesthesia-analgesia.org/content/107/5/1689.abstract},
+eprint = {http://www.anesthesia-analgesia.org/content/107/5/1689.full.pdf+html},
+journal = {Anesthesia and Analgesia}
+}
+
+@Article{GarciaMorales2009,
+author="Garc{\~A}?a-Morales, Irene
+and Garc{\~A}?a, M. Teresa
+and Gal{\~A}{\textexclamdown}n-D{\~A}{\textexclamdown}vila, Lucia
+and G{\~A}mez-Escalonilla, Carlos
+and Saiz-D{\~A}?az, Rosana
+and Mart{\~A}?nez-Salio, Antonio
+and de la Pe{\~A}a, Pilar
+and Tejerina, Julian A.",
+title="Periodic Lateralized Epileptiform Discharges: Etiology, Clinical Aspects, Seizures, and Evolution in 130 Patients",
+journal="Journal of Clinical Neurophysiology",
+year="2002",
+volume="19",
+number="2",
+keywords="Electroencephalography",
+keywords="Epilepsy",
+keywords="Periodic lateralized epileptiform discharges",
+keywords="PLED",
+keywords="Seizure",
+keywords="Stroke",
+abstract="Summary : The purpose of this study was to analyze the clinical aspects in 130 patients presenting periodic lateralized epileptiform discharges (PLEDs) in their EEG and to compare these results with those found in the literature. Etiology, neurologic deficit, seizure occurrence, and evolution were studied in each patient by historical review. The recordings were obtained on 8- or 16-channel EEGs with electrode placement according to the International 10-20 System. Recordings containing PLEDs were selected. PLEDs were defined as repetitive periodic, focal, or hemispheric epileptiform discharges (spikes, spike and waves, polyspikes, sharp waves) usually recurring every 1 to 2 seconds. The statistical study was carried out via the [chi]2 test using the computer program SPSS. The main etiology found in this group of patients was stroke (61 of 130 patients). Other processes found were brain infections, tumors, hematomas, and several other entities grouped together as miscellaneous (anoxic encephalopathy, subarachnoid hemorrhage, craniocerebral trauma, Creutzfeldt-Jacob disease, migraine, multiple sclerosis, and aminophylline intoxication). Half of these patients (65 of 130) developed seizures, mostly partial motor seizures. No significant relation between etiology and seizures was found ([chi]2 = 2.81, P = 0.4222). Seizures recurred in 14 of 130 patients during a follow-up of 14.5 months. PLEDs were not recorded in any EEG at the time of seizure recurrence. PLEDs constitute a distinctive but uncommon EEG phenomenon of repetitive, periodic, and stereotyped lateralized complexes. In agreement with the literature, PLEDs were associated with an acute process and occurred early during the course of the illness in all patients studied and were usually associated with structural lesions, with stroke being the main etiology. Traditionally, seizures occur with PLEDs but it is also accepted that they can exist in patients who never develop epileptic activity, either clinically or electrically, as demonstrated in 50\% of the patients studied. No significant association between seizures and any etiology could be found. It was not demonstrated that the occurrence of seizures may influence the outcome in any way. Copyright (C) 2002 American Clinical Neurophysiology Society",
+issn="0736-0258",
+url="http://journals.lww.com/clinicalneurophys/Fulltext/2002/03000/Periodic_Lateralized_Epileptiform_Discharges_.9.aspx"
+}
+
+@article{Bojak2005,
+ title = {Modeling the effects of anesthesia on the electroencephalogram},
+ author = {Bojak, I. and Liley, D. T. J.},
+ journal = {Phys. Rev. E},
+ volume = {71},
+ issue = {4},
+ pages = {041902},
+ numpages = {22},
+ year = {2005},
+ month = {Apr},
+ doi = {10.1103/PhysRevE.71.041902},
+ url = {http://link.aps.org/doi/10.1103/PhysRevE.71.041902},
+ publisher = {American Physical Society}
+}
+
+@article{SteynRoss1999,
+ title = {Theoretical electroencephalogram stationary spectrum for a white-noise-driven cortex: Evidence for a general anesthetic-induced phase transition},
+ author = {Steyn-Ross, Moira L. and Steyn-Ross, D. A. and Sleigh, J. W. and Liley, D. T. J.},
+ journal = {Phys. Rev. E},
+ volume = {60},
+ issue = {6},
+ pages = {7299--7311},
+ year = {1999},
+ month = {Dec},
+ doi = {10.1103/PhysRevE.60.7299},
+ url = {http://link.aps.org/doi/10.1103/PhysRevE.60.7299},
+ publisher = {American Physical Society}
+}
+
+@Article{Liley2005,
+author="Liley, D. T. J.
+and Bojak, I.",
+title="Understanding the Transition to Seizure by Modeling the Epileptiform Activity of General Anesthetic Agents",
+journal="Journal of Clinical Neurophysiology",
+year="2005",
+volume="22",
+number="5",
+keywords="EEG modeling",
+keywords="Enflurane",
+keywords="Isoflurane",
+keywords="Proconvulsant anesthetic",
+keywords="Benzodiazepine",
+abstract="Summary: A central difficulty in modeling epileptogenesis using biologically plausible computational and mathematical models is not the production of activity characteristic of a seizure, but rather producing it in response to specific and quantifiable physiologic change or pathologic abnormality. This is particularly problematic when it is considered that the pathophysiological genesis of most epilepsies is largely unknown. However, several volatile general anesthetic agents, whose principle targets of action are quantifiably well characterized, are also known to be proconvulsant. The authors describe recent approaches to theoretically describing the electroencephalographic effects of volatile general anesthetic agents that may be able to provide important insights into the physiologic mechanisms that underpin seizure initiation. Copyright (C) 2005 American Clinical Neurophysiology Society",
+issn="0736-0258",
+url="http://journals.lww.com/clinicalneurophys/Fulltext/2005/10000/Understanding_the_Transition_to_Seizure_by.3.aspx"
+}
+
+
+
+
+
+
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View
67 papers/frontiers_in_neuroscience_oct_2012.tex
@@ -6,6 +6,7 @@
\usepackage{caption}
\usepackage{subcaption}
\begin{document}
+\bibliographystyle{plain}
\title{Mesoscopic Modelling of Burst Suppression Under Anaesthesia}
\author{Matthew Walsh\\
\small Brain and Psychological Sciences Research Centre (BPsyC),\\
@@ -45,8 +46,7 @@ \section{Introduction}
1960s, featuring intubation, artificial respiration and comprehensive
physiological monitoring, reports of the electroencephalographic
pattern of burst suppression were confined to animal studies involving
-deep anaesthesia and the odd case of psychosurgery (Niedermeyer,
-2009). Since then the burst suppression pattern is now recognized as
+deep anaesthesia and the odd case of psychosurgery~\cite{Niedermeyer2009}. Since then the burst suppression pattern is now recognized as
a major class of generalised EEG waveform abnormality of diagnostic
and prognostic significance that is encountered in a range of
encephalopathic conditions, in addition to its pharmacological genesis
@@ -57,18 +57,16 @@ \section{Introduction}
features of the bursts, together with their duration and the duration of
suppressed periods show a high degree of variability that reflects its
myriad of initiating causes (see Figure \ref{fig:burst_examples} for examples). First identified
-during deep anaesthesia with tribromoethanol in cats (Derbyshire et al,
-1936), labelled “burst-suppression pattern” by Swank \& Watson (1948) during barbiturate and ether anaesthesia in dogs,
+during deep anaesthesia with tribromoethanol in cats~\cite{Derbyshire31071936}, labelled “burst-suppression pattern” by Swank \& Watson~\cite{Swank01031949} during barbiturate and ether anaesthesia in dogs,
it is now
-associated with cortical deafferentation (Henry \& Scoville, 1952),
-cerebral anoxia and hypoxia, various types of intracortical lesions
-(Fischer-Williams, 1963), deep coma, various infantile
-encephalopathies, the final stages of deteriorated status epilepticus
-(Trieman et al 1990), hypothermia, and high levels of many sedative
-and anaesthetic agents (Schwartz et al, 1989; Akrawi et al 1996).
+associated with cortical deafferentation~\cite{Henry19521},
+cerebral anoxia and hypoxia, various types of intracortical lesions~\cite{FischerWilliams1963568}, deep coma, various infantile
+encephalopathies, the final stages of deteriorated status epilepticus~\cite{Treiman199049}
+, hypothermia, and high levels of many sedative
+and anaesthetic agents~\cite{Schwartz1989}~\cite{Akrawi1996}
Burst suppression in the absence of anaesthesia is in general
-associated with a very poor prognosis. Grigg-Damberger et al (1989)
+associated with a very poor prognosis. Grigg-Damberger et al~\cite{GriggDamberger198984}
found that the neonatal appearance of burst suppression, even if
transient, was a portent of death or severe neurodevelopmental
disability in 93\% of infants who were followed up subsequent to the
@@ -76,15 +74,15 @@ \section{Introduction}
suppression. In adult populations while an anoxic/hypoxic burst
suppression pattern signals a serious pathophysiological event the
outcome is not necessarily fatal and recovery with or without severe
-neurological damage is possible (Niedermeyer, 2009). The results of
+neurological damage is possible~\cite{Niedermeyer2009}. The results of
experimental work with EEG monitoring in rats reveals that animals with
greater rates of high amplitude bursts had a better survival and
neurological outcome compared to those with lower rates of low
-amplitude bursts (Geocadin et al, 2002).
+amplitude bursts~\cite{Geocadin2002193}.
While the electroencephalographic phenomenon and clinical
-implications of burst suppression have been studied extensively
-(Niedermeyer, 2009; Brenner, 1985) the physiological mechanisms
+implications of burst suppression have been studied extensively~\cite{Niedermeyer2009}
+(Brenner, 1985) the physiological mechanisms
underlying its emergence remain unresolved and obscure. However the
phenomenal resemblance of the patterns of burst suppression to
disorders of neuronal hyperexcitability suggests that similar
@@ -98,7 +96,7 @@ \section{Introduction}
the wide synchronisation of neuronal activity. Not surprisingly then, in
clinical practice the boundaries between what constitutes coma
induced burst suppression and what is defined as ictal seizure activity
-is blurred (Amzica, 2009; Hirsch et al, 2004). While such
+is blurred~\cite{Amzica2009} (Hirsch et al, 2004). While such
differentiation may be one of only semantics practically speaking there
nevertheless may be important clinical implications if they respond
differentially to pharmacotherapy and have different prognostic
@@ -107,17 +105,15 @@ \section{Introduction}
Surprisingly many anaesthetic agents, at levels well below that needed
to induce burst suppression, quite commonly induce epileptiform
-activity (Voss et al, 2008). While such epileptiform activity rarely
-progresses to clinically apparent seizures (Garcia-Morales et al, 2002)
+activity~\cite{Voss2008}. While such epileptiform activity rarely
+progresses to clinically apparent seizures~\cite{GarciaMorales2009}
the presence of such activity nevertheless is believed to indicate some
form of incipient cortical hyperexcitability. Indeed a number of
mesoscopic mean field models developed to account for the
-electroencephalographic features of anaesthetic action (Bojak \& Liley,
-2005; Steyn-Ross et al, 1999), based on parameterising empirically
+electroencephalographic features of anaesthetic action~\cite{Bojak2005}~\cite{SteynRoss1999}, based on parameterising empirically
identified sub-cellular and molecular targets, have been able to account
for the pro-convulsant properties of many anaesthetic agents known
-to have seizurogenic potential (Wilson et al, 2006; Liley \& Bojak,
-2005). Given that the majority of anaesthetic agents induce burst
+to have seizurogenic potentia~\cite{Liley2005}l (Wilson et al, 2006;). Given that the majority of anaesthetic agents induce burst
suppression it is therefore natural to inquire whether these mesoscopic
mean field models of electrocortical anaesthetic action are able to
account for the appearance of drug-induced burst suppression, and in
@@ -532,22 +528,18 @@ \subsection{Burst suppression arises in all investigated models}
\begin{figure}
\begin{subfigure}[b]{0.5\textwidth}
\includegraphics[scale=0.35]{chosen-frontiers-2012/00143-1-1-6-he-thal.pdf}
- \label{fig:00143_a}
\caption{$h_e (mV)$}
\end{subfigure}
\begin{subfigure}[b]{0.5\textwidth}
\includegraphics[scale=0.35]{chosen-frontiers-2012/00143-1_2-1-6-he-thal.pdf}
- \label{fig:00143_b}
\caption{$h_e (mV)$}
\end{subfigure}
\begin{subfigure}[b]{0.5\textwidth}
\includegraphics[scale=0.35]{chosen-frontiers-2012/00143-1-0_4-6-he-thal.pdf}
- \label{fig:00143_c}
\caption{$h_e (mV)$}
\end{subfigure}
\begin{subfigure}[b]{0.5\textwidth}
\includegraphics[scale=0.35]{chosen-frontiers-2012/00143-1-1-5-he-thal.pdf}
- \label{fig:00143_d}
\caption{$h_e (mV)$}
\end{subfigure}
\label{fig:00143}
@@ -574,22 +566,18 @@ \subsection{Burst suppression arises in all investigated models}
\begin{figure}
\begin{subfigure}[b]{0.5\textwidth}
\includegraphics[scale=0.35]{chosen-frontiers-2012/00493-1-he-intra.pdf}
- \label{fig:493_a}
\caption{$h_e (mV)$}
\end{subfigure}
\begin{subfigure}[b]{0.5\textwidth}
\includegraphics[scale=0.35]{chosen-frontiers-2012/00493-0_5-he-intra.pdf}
- \label{fig:493_b}
\caption{$h_e (mV)$}
\end{subfigure}
\begin{subfigure}[b]{0.5\textwidth}
\includegraphics[scale=0.35]{chosen-frontiers-2012/00493-0_11-he-intra.pdf}
- \label{fig:493_c}
\caption{$h_e (mV)$}
\end{subfigure}
\begin{subfigure}[b]{0.5\textwidth}
\includegraphics[scale=0.35]{chosen-frontiers-2012/00493-0_1-he-intra.pdf}
- \label{fig:493_d}
\caption{$h_e (mV)$}
\end{subfigure}
@@ -608,22 +596,18 @@ \subsection{Burst suppression arises in all investigated models}
\begin{figure}
\begin{subfigure}[b]{0.5\textwidth}
\includegraphics[scale=0.35]{chosen-frontiers-2012/00460-3-he-intra.pdf}
- \label{fig:460_a}
\caption{$h_e (mV)$}
\end{subfigure}
\begin{subfigure}[b]{0.5\textwidth}
\includegraphics[scale=0.35]{chosen-frontiers-2012/00460-3-slow-intra.pdf}
- \label{fig:460_b}
\caption{$\zeta_e (UNITS)$}
\end{subfigure}
\begin{subfigure}[b]{0.5\textwidth}
\includegraphics[scale=0.35]{chosen-frontiers-2012/00460-0_7-he-intra.pdf}
- \label{fig:460_c}
\caption{$h_e (mV)$}
\end{subfigure}
\begin{subfigure}[b]{0.5\textwidth}
\includegraphics[scale=0.35]{chosen-frontiers-2012/00460-0_7-slow-intra.pdf}
- \label{fig:460_d}
\caption{$\zeta_e (UNITS)$}
\end{subfigure}
\label{fig:emerging_slow_zeta}
@@ -648,21 +632,18 @@ \subsection{Burst suppression arises in all investigated models}
\begin{subfigure}[b]{1\textwidth}
\includegraphics[scale=0.32]{chosen-frontiers-2012/00214-1-0_5-5-0_5-he-phi.pdf}
\includegraphics[scale=0.32]{chosen-frontiers-2012/00214-1-0_5-5-0_5-phi_ei-phi}
- \label{fig:214-1-0_5-5-0_5}
\caption{$h_e (mV)$ and $\phi_{ei}$}
\end{subfigure}
\begin{subfigure}[b]{1\textwidth}
\includegraphics[scale=0.32]{chosen-frontiers-2012/00214-1-0_1-5-0_2-he-phi.pdf}
\includegraphics[scale=0.32]{chosen-frontiers-2012/00214-1-0_1-5-0_2-phi_ei-phi}
- \label{fig:214-1-0_1-5-0_2}
\caption{$h_e (mV)$ and $\phi_{ei}$}
\end{subfigure}
\begin{subfigure}[b]{1\textwidth}
\includegraphics[scale=0.32]{chosen-frontiers-2012/00214-1-0_1-5-0_1-he-phi.pdf}
\includegraphics[scale=0.32]{chosen-frontiers-2012/00214-1-0_1-5-0_1-phi_ei-phi}
- \label{fig:214-1-0_1-5-0_2}
\caption{$h_e (mV)$ and $\phi_{ei}$}
\end{subfigure}
\label{fig:phi_dyn}
@@ -686,17 +667,14 @@ \subsection{Burst suppression arises in all investigated models}
\begin{figure}
\begin{subfigure}[b]{0.3\textwidth}
\includegraphics[scale=0.22]{chosen-frontiers-2012/00416-he-phi.pdf}
- \label{fig:416_phi_a}
\caption{$h_e (mV)$}
\end{subfigure}
\begin{subfigure}[b]{0.3\textwidth}
\includegraphics[scale=0.22]{chosen-frontiers-2012/00416-0_5-2-1-he-phi.pdf}
- \label{fig:416_phi_b}
\caption{$h_e (mV)$}
\end{subfigure}
\begin{subfigure}[b]{0.3\textwidth}
\includegraphics[scale=0.22]{chosen-frontiers-2012/00416-1_1-2-1-he-phi.pdf}
- \label{fig:416_phi_c}
\caption{$h_e (mV)$}
\end{subfigure}
@@ -750,15 +728,8 @@ \subsection{Further investigations}
interactions between the presented emergent slow system in a unified model that covers all the presented augmentations to the cannonical model of Liley et al.
-\begin{thebibliography}{999}
+\bibliography{frontiers_in_neuroscience_oct_2012}
-\bibitem{izikevich2007_1}
- Eugene M. Izhikevich,
- Dynamical Systems in Neuroscience: the geometry of excitability and bursting:329-344,
- 1st Edition,
- 2010.
-
-\end{thebibliography}
\end{document}
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