22 results on '"Henning Piilgaard"'
Search Results
2. P65-F EEG evolution in a case of rapidly progressive dementia
- Author
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Henning Piilgaard
- Subjects
Pathology ,medicine.medical_specialty ,medicine.diagnostic_test ,business.industry ,Autopsy ,Disease ,Electroencephalography ,medicine.disease ,Apraxia ,Sensory Systems ,Neurology ,Neuroimaging ,Physiology (medical) ,Biopsy ,medicine ,Dementia ,Neurology (clinical) ,business ,Dominance (genetics) - Abstract
Background Rapidly progressive dementia can be caused by several factors like neurodegenerative, toxic/metabolic, infectious, autoimmune or neoplastic disorders. Here I present a case of this type and the diagnostic process leading to diagnosis. Material and methods This case describes a woman in her sixties admitted to hospital with dementia and anxiety as initial symptoWithin 2 month progression of these symptoms and appearance of apraxia, visual affection and cerebellar gait. The diagnostic process is illustrated. including consecutive EEGs, PET, MRi, CSF markers. Results Initial MRi was considered normal and first EEG with normal posterior dominant rhythm and bi-fronto-temporal 2–3 Hz activity (leftsided dominance) and no paroxystic activity. Repeated tests revealed classic changes seen in sporadic CJD on MRi in the form of cortical ribbon sign and adynamic periodic paroxyms and low frequency activity (2–3 Hz) lateralized in the EEG. CSF with normal count of protein and normal count of White blood cells and elevated count of total tau 1200 (normal range Conclusions Even though a definite diagnosis of Creutzfeldt-Jacob disease (CJD) can only be manifest by brain autopsy or biopsy post mortem a possible or likely diagnosis can be established combining CSF markers, brain imaging and EEG. This case illustrates the importance of EEG and especially consecutive EEGs in the diagnostic process of rapidly progressive dementia.
- Published
- 2019
3. Increased 20-HETE Synthesis Explains Reduced Cerebral Blood Flow But Not Impaired Neurovascular Coupling after Cortical Spreading Depression in Rat Cerebral Cortex
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Brent M. Witgen, Rebecca W.Y. Ko, Henning Piilgaard, Hyun B. Choi, Micael Lønstrup, Brian A. MacVicar, Claus Mathiesen, Kirsten Thomsen, Jonas C. Fordsmann, and Martin Lauritzen
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Male ,medicine.medical_specialty ,Local field potential ,Rats, Sprague-Dawley ,chemistry.chemical_compound ,Organ Culture Techniques ,In vivo ,Internal medicine ,Hydroxyeicosatetraenoic Acids ,medicine ,Animals ,Rats, Wistar ,Cerebral Cortex ,Chemistry ,General Neuroscience ,Cortical Spreading Depression ,Articles ,Laser Doppler velocimetry ,Rats ,medicine.anatomical_structure ,Endocrinology ,Cerebral blood flow ,Cerebral cortex ,Cerebrovascular Circulation ,Cortical spreading depression ,cardiovascular system ,lipids (amino acids, peptides, and proteins) ,Arachidonic acid ,medicine.symptom ,Neuroscience ,Blood Flow Velocity ,Vasoconstriction ,circulatory and respiratory physiology - Abstract
Cortical spreading depression (CSD) is associated with release of arachidonic acid, impaired neurovascular coupling, and reduced cerebral blood flow (CBF), caused by cortical vasoconstriction. We tested the hypothesis that the released arachidonic acid is metabolized by the cytochrome P450 enzyme to produce the vasoconstrictor 20-hydroxyeicosatetraenoic acid (20-HETE), and that this mechanism explains cortical vasoconstriction and vascular dysfunction after CSD. CSD was induced in the frontal cortex of rats and the cortical electrical activity and local field potentials recorded by glass microelectrodes, CBF by laser Doppler flowmetry, and tissue oxygen tension (tpO2) using polarographic microelectrodes. 20-HETE synthesis was measured in parallel experiments in cortical brain slices exposed to CSD. We used the specific inhibitor HET0016 (N-hydroxy-N′-(4-n-butyl-2-methylphenyl)formamidine) to block 20-HETE synthesis. CSD increased 20-HETE synthesis in brain slices for 120 min, and the time course of the increase in 20-HETE paralleled the reduction in CBF after CSDin vivo. HET0016 blocked the CSD-induced increase in 20-HETE synthesis and ameliorated the persistent reduction in CBF, but not the impaired neurovascular coupling after CSD. These findings suggest that CSD-induced increments in 20-HETE cause the reduction in CBF after CSD and that the attenuation of stimulation-induced CBF responses after CSD has a different mechanism. We suggest that blockade of 20-HETE synthesis may be clinically relevant to ameliorate reduced CBF in patients with migraine and acute brain cortex injuries.
- Published
- 2013
4. Multi-modal assessment of neurovascular coupling during cerebral ischaemia and reperfusion using remote middle cerebral artery occlusion
- Author
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Sutherland, Brad A, Fordsmann, Jonas C, Martin, Chris, Neuhaus, Ain A, Witgen, Brent M, Hansen, Henning Piilgaard, Lønstrup, Micael, Couch, Yvonne, Sibson, Nicola R, Lauritzen, Martin, Buchan, Alastair M, Sutherland, Brad A, Fordsmann, Jonas C, Martin, Chris, Neuhaus, Ain A, Witgen, Brent M, Hansen, Henning Piilgaard, Lønstrup, Micael, Couch, Yvonne, Sibson, Nicola R, Lauritzen, Martin, and Buchan, Alastair M
- Abstract
Hyperacute changes in cerebral blood flow during cerebral ischaemia and reperfusion are important determinants of injury. Cerebral blood flow is regulated by neurovascular coupling, and disruption of neurovascular coupling contributes to brain plasticity and repair problems. However, it is unknown how neurovascular coupling is affected hyperacutely during cerebral ischaemia and reperfusion. We have developed a remote middle cerebral artery occlusion model in the rat, which enables multi-modal assessment of neurovascular coupling immediately prior to, during and immediately following reperfusion. Male Wistar rats were subjected to remote middle cerebral artery occlusion, where a long filament was advanced intraluminally through a guide cannula in the common carotid artery. Transcallosal stimulation evoked increases in blood flow, tissue oxygenation and neuronal activity, which were diminished by middle cerebral artery occlusion and partially restored during reperfusion. These evoked responses were not affected by administration of the thrombolytic alteplase at clinically used doses. Evoked cerebral blood flow responses were fully restored at 24 h post-middle cerebral artery occlusion indicating that neurovascular dysfunction was not sustained. These data show for the first time that the rat remote middle cerebral artery occlusion model coupled with transcallosal stimulation provides a novel method for continuous assessment of hyperacute neurovascular coupling changes during ischaemia and reperfusion, and offers unique insight into hyperacute ischaemic pathophysiology.
- Published
- 2017
5. Neocortical gamma oscillations in idiopathic generalized epilepsy
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Martin Lauritzen, Henning Piilgaard, Antal Berényi, Krisztina Benedek, and Péter Gombkötő
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0301 basic medicine ,Male ,Adolescent ,Neocortex ,Electroencephalography ,Brain mapping ,Idiopathic generalized epilepsy ,03 medical and health sciences ,Epilepsy ,0302 clinical medicine ,Gamma Rhythm ,medicine ,Humans ,Ictal ,Generalized epilepsy ,Child ,Retrospective Studies ,Brain Mapping ,medicine.diagnostic_test ,medicine.disease ,030104 developmental biology ,medicine.anatomical_structure ,Neurology ,Case-Control Studies ,Child, Preschool ,Anticonvulsants ,Epilepsy, Generalized ,Female ,Neurology (clinical) ,Psychology ,Neuroscience ,030217 neurology & neurosurgery - Abstract
Summary Objective Absence seizures in patients with idiopathic generalized epilepsy (IGE) may in part be explained by a decrease in phasic GABAA (type-A γ-aminobutyric acid) receptor function, but the mechanisms are only partly understood. Here we studied the relation between ictal and interictal spike-wave discharges (SWDs) and electroencephalography (EEG) gamma oscillatory activity (30–60 Hz) in patients with IGE. Methods EEG recordings were obtained of 14 children with IGE (mean age, 8.5 ± 5 years) and 14 age- and sex-matched controls. Time-frequency analysis of each seizure and seizure-free control epochs was performed and cross-coherences of neocortical gamma oscillations were calculated to describe interictal and ictal characteristics of generalized seizures. Results SWDs were characterized with an abrupt increase of oscillatory activity of 3–4 and 13–60 Hz, peaking at 3–4 and 30–60 Hz, and with a simultaneous decrease in the 8–12 Hz frequency band. The rise in EEG gamma oscillations was short-lasting and decreased before activity declined at lower frequency ranges. Compared to control patients, patients with epilepsy also showed higher interictal values of mean coherence of gamma activity, but this interictal increase was not significant after post hoc analysis. Significance Our data support the hypothesis that gamma oscillatory activity increase concomitantly with rises in activity of lower EEG frequencies during absence seizures and that the activity starts to cease earlier than lower EEG frequencies. The data did not support a change in gamma activity preceding the 3–4 Hz SWDs. SWDs are hypothetically generated by the synchronous interaction between the thalamus and the cortex, whereas the production of gamma activity is the result of activity in local inhibitory networks. Thus, the modification of SWD by gamma activity may be understood in terms of the cellular and synaptic mechanisms involved.
- Published
- 2016
6. Recording, analysis, and interpretation of spreading depolarizations in neurointensive care: Review and recommendations of the COSBID research group
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Erdem Güresir, Sergei A. Kirov, Egill Rostrup, Christoph Drenckhahn, Martyn G. Boutelle, Brian A. MacVicar, Michael Schöll, Andrew I R Maas, Michael Scheel, Daniel Kondziella, Clemens Reiffurth, Johannes Platz, Jason M. Hinzman, Juan Sahuquillo, M. Ross Bullock, Frank Richter, Tomas Watanabe, Ilan Shelef, Kazutaka Sugimoto, Martin Lauritzen, Bart Feyen, Julia S. Bretz, Brandon Foreman, David O. Okonkwo, Eun Jeung Kang, Hartmut Vatter, Markus Dahlem, Anthony J. Strong, Ana I Oliveira-Ferreira, Jens P. Dreier, Nils Hecht, Baptiste Balança, Otto W. Witte, Christina M. Kowoll, Yoash Chassidim, Sharon L. Jewell, Rudolf Graf, Nina Eriksen, Thomas Lieutaud, Gerrit Brinker, Johannes Woitzik, Alon Friedman, Andrew P. Carlson, Nora F. Dengler, Henning Piilgaard, Bente Pakkenberg, Svetlana Lublinsky, Lee S Chung, Maren K.L. Winkler, Gajanan S. Revankar, C. William Shuttleworth, Christian Dohmen, Jan Claassen, Janos Luckl, Delphine Feuerstein, André P. Schulte, Michiyasu Suzuki, Edgar Santos, Michael Reiner, Denny Milakara, Peter Vajkoczy, Jed A. Hartings, Lori Shutter, Sebastian Major, Stéphane Marinesco, Daniel N. Hertle, Martin Fabricius, Michel D. Ferrari, Paul Jahnke, Viktor Horst, Uwe Heinemann, Alois Josef Schiefecker, Oliver W. Sakowitz, Peter Martus, M. Brandon Westover, Cenk Ayata, Renán Sánchez-Porras, Rick M. Dijkhuizen, Kc Brennan, Christian K. Friberg, Norberto Andaluz, R. David Andrew, Karl Schoknecht, Eric Rosenthal, Oscar Herreras, Georg Bohner, Raimund Helbok, Anna Maslarova, Eszter Farkas, and Arn M. J. M. van den Maagdenberg
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0301 basic medicine ,Spreading depolarization ,cerebral blood flow ,Review ,Epileptogenesis ,0302 clinical medicine ,anoxic depolarization ,asphyxial depolarization ,Gray Matter ,Electrocorticography ,Review Articles ,brain edema ,spreading depression ,medicine.diagnostic_test ,spreading ischemia ,Cortical Spreading Depression ,Depolarization ,Stroke ,peri-infarct depolarization ,neurocritical care ,Neurology ,Cerebral blood flow ,Cortical spreading depression ,Cerebrovascular Circulation ,Practice Guidelines as Topic ,brain trauma ,neuroprotection ,Cardiology and Cardiovascular Medicine ,Critical Care ,subarachnoid hemorrhage ,neurovascular coupling ,Ischemia ,Focal ischemia ,03 medical and health sciences ,Journal Article ,medicine ,Humans ,vasospasm ,business.industry ,Neurointensive care ,medicine.disease ,intracerebral hemorrhage ,Neurophysiological Monitoring ,global ischemia ,030104 developmental biology ,Brain Injuries ,focal ischemia ,epilepsy ,epileptogenesis ,Human medicine ,Neurology (clinical) ,business ,Neuroscience ,030217 neurology & neurosurgery - Abstract
Spreading depolarizations (SD) are waves of abrupt, near-complete breakdown of neuronal transmembrane ion gradients, are the largest possible pathophysiologic disruption of viable cerebral gray matter, and are a crucial mechanism of lesion development. Spreading depolarizations are increasingly recorded during multimodal neuromonitoring in neurocritical care as a causal biomarker providing a diagnostic summary measure of metabolic failure and excitotoxic injury. Focal ischemia causes spreading depolarization within minutes. Further spreading depolarizations arise for hours to days due to energy supply-demand mismatch in viable tissue. Spreading depolarizations exacerbate neuronal injury through prolonged ionic breakdown and spreading depolarization-related hypoperfusion (spreading ischemia). Local duration of the depolarization indicates local tissue energy status and risk of injury. Regional electrocorticographic monitoring affords even remote detection of injury because spreading depolarizations propagate widely from ischemic or metabolically stressed zones; characteristic patterns, including temporal clusters of spreading depolarizations and persistent depression of spontaneous cortical activity, can be recognized and quantified. Here, we describe the experimental basis for interpreting these patterns and illustrate their translation to human disease. We further provide consensus recommendations for electrocorticographic methods to record, classify, and score spreading depolarizations and associated spreading depressions. These methods offer distinct advantages over other neuromonitoring modalities and allow for future refinement through less invasive and more automated approaches.
- Published
- 2016
7. Cyclosporine A, FK506, and NIM811 ameliorate prolonged CBF reduction and impaired neurovascular coupling after cortical spreading depression
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Henning Piilgaard, Peter Rasmussen, Brent M. Witgen, and Martin Lauritzen
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Male ,Traumatic brain injury ,NIM811 ,Pharmacology ,Tacrolimus ,chemistry.chemical_compound ,medicine ,Animals ,Vasoconstrictor Agents ,Enzyme Inhibitors ,Rats, Wistar ,Chemistry ,MPTP ,Cortical Spreading Depression ,Brain ,Depolarization ,medicine.disease ,Rats ,Oxygen ,Calcineurin ,nervous system ,Neurology ,Mitochondrial permeability transition pore ,Cerebral blood flow ,15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid ,Brain Injuries ,Cerebrovascular Circulation ,Cortical spreading depression ,Anesthesia ,Cyclosporine ,cardiovascular system ,Original Article ,Neurology (clinical) ,Cardiology and Cardiovascular Medicine ,Immunosuppressive Agents ,circulatory and respiratory physiology - Abstract
Cortical spreading depression (CSD) is associated with mitochondrial depolarization, increasing intracellular Ca2+, and the release of free fatty acids, which favor opening of the mitochondrial permeability transition pore (mPTP) and activation of calcineurin (CaN). Here, we test the hypothesis that cyclosporine A (CsA), which blocks both mPTP and CaN, ameliorates the persistent reduction of cerebral blood flow (CBF), impaired vascular reactivity, and a persistent rise in the cerebral metabolic rate of oxygen (CMRO2) following CSD. In addition to CsA, we used the specific mPTP blocker NIM811 and the specific CaN blocker FK506. Cortical spreading depression was induced in rat frontal cortex. Electrocortical activity was recorded by glass microelectrodes, CBF by laser Doppler flowmetry, and tissue oxygen tension with polarographic microelectrodes. Electrocortical activity, basal CBF, CMRO2, and neurovascular and neurometabolic coupling were unaffected by all three drugs under control conditions. NIM811 augmented the rise in CBF observed during CSD. Cyclosporine A and FK506 ameliorated the persistent decrease in CBF after CSD. All three drugs prevented disruption of neurovascular coupling after CSD; the rise in CMRO2 was unchanged. Our data suggest that blockade of mPTP formation and CaN activation may prevent persistent CBF reduction and vascular dysfunction after CSD.
- Published
- 2011
8. Principal Cell Spiking, Postsynaptic Excitation, and Oxygen Consumption in the Rat Cerebellar Cortex
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Henning Piilgaard, Gilles Bonvento, Martin Lauritzen, Kirsten Thomsen, and Albert Gjedde
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Male ,Physiology ,Biophysics ,Action Potentials ,Tetrodotoxin ,Deoxyglucose ,Bicuculline ,GABA Antagonists ,Neuronal action potential ,Cerebellar Cortex ,Purkinje Cells ,chemistry.chemical_compound ,Nerve Fibers ,Oxygen Consumption ,Postsynaptic potential ,Neural Pathways ,Laser-Doppler Flowmetry ,medicine ,Animals ,Rats, Wistar ,6-Cyano-7-nitroquinoxaline-2,3-dione ,Analysis of Variance ,Carbon Isotopes ,Chemistry ,General Neuroscience ,Excitatory Postsynaptic Potentials ,GABA receptor antagonist ,Electric Stimulation ,Rats ,Regional Blood Flow ,Cerebellar cortex ,CNQX ,Excitatory postsynaptic potential ,Dizocilpine Maleate ,Excitatory Amino Acid Antagonists ,Neuroscience ,Sodium Channel Blockers ,medicine.drug - Abstract
One contention within the field of neuroimaging concerns the character of the depicted activity: Does it represent neuronal action potential generation (i.e., spiking) or postsynaptic excitation? This question is related to the metabolic costs of different aspects of neurosignaling. The cerebellar cortex is well suited for addressing this problem because synaptic input to and spiking of the principal cell, the Purkinje cell (PC), are spatially segregated. Also, PCs are pacemakers, able to generate spikes endogenously. We examined the contributions to cerebellar cortical oxygen consumption (CMRO2) of postsynaptic excitation and PC spiking during evoked and ongoing neuronal activity in the rat. By inhibiting excitatory synaptic input using ionotropic glutamate receptor blockers, we found that the increase in CMRO2 evoked by parallel fiber (PF) stimulation depended entirely on postsynaptic excitation. In contrast, PC spiking was largely responsible for the increase in CMRO2 when ongoing neuronal activity was increased by γ-aminobutyric acid type A receptor blockade. In this case, CMRO2 increased equally during PC spiking with excitatory synaptic activity as during PC pacemaker spiking without excitatory synaptic input. Subsequent inhibition of action potential propagation and neurotransmission by blocking voltage-gated Na+-channels eliminated the increases in CMRO2 due to PF stimulation and increased PC spiking, but left a large fraction of CMRO2, i.e., basal CMRO2, intact. In conclusion, whereas basal CMRO2 in anesthetized animals did not seem to be related to neurosignaling, increases in CMRO2 could be induced by all aspects of neurosignaling. Our findings imply that CMRO2 responses cannot a priori be assigned to specific neuronal activities.
- Published
- 2009
9. Contribution of somatosensory cortex to evoked cerebellar blood flow responses
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Martin Lauritzen and Henning Piilgaard
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Male ,Cerebellum ,Neural Conduction ,Action Potentials ,Somatosensory system ,Synaptic Transmission ,Cerebellar Cortex ,Cerebellar hemisphere ,Neural Pathways ,medicine ,Animals ,Trigeminal Nerve ,Rats, Wistar ,Neurons ,Afferent Pathways ,Chemistry ,General Neuroscience ,Cortical Spreading Depression ,Somatosensory Cortex ,Granule cell ,Electric Stimulation ,Rats ,Electrophysiology ,medicine.anatomical_structure ,Somatosensory evoked potential ,Cerebrovascular Circulation ,Cerebellar cortex ,Cortical spreading depression ,Blood Vessels ,Neuroscience - Abstract
Projections from the trigeminocerebellar pathway and the somatosensory cortex coincide spatially in the granule cell layer of Crus I/II of the cerebellar hemisphere. A biphasic field potential was seen: one peak at 10 ms (trigeminal input) and another at 20 ms (somatosensory input). Linear correlation analysis revealed only a weak coupling between somatosensory input and cerebellar blood flow responses to infraorbital nerve stimulation. In separate experiments, cortical spreading depression attenuated the field potential peak at 20 ms while blood flow responses remained unaltered. Thus, trigeminocerebellar activity explained the evoked blood flow responses. Our data provide further evidence that activity-dependent blood flow responses are context-sensitive and that interaction between excitatory neuronal circuits targeting the same cells may occlude vascular responses.
- Published
- 2004
10. P352 Neuromyotonia – A rare but important electrophysiological finding
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Henning Piilgaard, Martin Lauritzen, and Krisztina Benedek
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Pediatrics ,medicine.medical_specialty ,Neuromyotonia ,business.industry ,Involved muscles ,Disease ,medicine.disease ,Sensory Systems ,Surgery ,Electrophysiology ,Neurology ,Physiology (medical) ,medicine ,Sensory symptoms ,Neurology (clinical) ,Myokymia ,Differential diagnosis ,business ,Rare disease - Abstract
Objectives Neuromyotonia is a rare disease with typical electromyographical changes which can easily be overlooked or misdiagnosed. Neuromyotonia is characterized by stiffness; cramps, myokymia, increased sweating and occasionally sensory symptoms may be associated with a variety of inherited and acquired disorders. The diagnosis is based on neurophysiological findings. Though the consequently identified antibodies are supporting but not a requirement of the diagnosis. Here we present a follow up on diagnosis and outcome in patients found with clinical neurophysiological confirmed neuromyotonia. Methods We review retrospectively the reports and neurophysiological investigations performed in our out-patient department in the period from 2000 to present. In cases where neuromyotonia was found we made a follow up on the underlying diagnosis, looked into additional diagnostic markers found and looked at the outcome for the patients. Results We here present a case-series of 11 patients seen in our out-patient department during the period 2001–2016 who all during electrophysiological evaluation showed evidence of neuromyotonia. The most common complaint was stiffness in the involved muscles. We present cases where antibody testing showed antibodies against voltage-gated potassium channels (VGKC) which can be present in Isaacs or Morvans syndrome and one case with anti-GAD antibodies which can be found in cases of for example stiff-man syndrome. Discussion The differential diagnosis in neuromyotonia seen in Isaacs or Morvan syndrome can be paraneoplastic conditions where prognosis depent on the right medication applied in time or motor neuron disease (Amyotrophical lateral sclerosis). The latter condition with extremely pure prognosis. Conclusion/Significance It is important to raise the attention of these Neurophysiology based findings, and find the right cause, since about 50% of patients with neuromyotonia can be treated with the right medication when applied in time.
- Published
- 2017
11. Neurovascular Coupling in Relation to Cortical Spreading Depression
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Henning Piilgaard and Martin Lauritzen
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Subarachnoid hemorrhage ,Traumatic brain injury ,business.industry ,Neurophysiology ,medicine.disease ,Neurovascular bundle ,Migraine with aura ,Electrophysiology ,medicine.anatomical_structure ,Cerebral cortex ,Cortical spreading depression ,medicine ,medicine.symptom ,business ,Neuroscience - Abstract
Cortical spreading depression (SD) has been known for more than 70 years. It has been a unique method investigating basic neurophysiology. A growing body of evidence indicates SD is involved in clinical conditions such as migraine with aura, subarachnoid hemorrhage, and traumatic brain injury. In this chapter we describe the application of SD in studying neurovascular and neurometabolic coupling in rat cerebral cortex. Description of the different techniques (electrophysiology, laser-Doppler flowmetry, and oxygensensitive electrodes) is followed by in depth step-by-step instructions on how to use them. This chapter will also describe the vascular consequences of SD and how to elicit SD experimentally.
- Published
- 2014
12. Persistent increase in oxygen consumption and impaired neurovascular coupling after spreading depression in rat neocortex
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Martin Lauritzen and Henning Piilgaard
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Male ,medicine.medical_specialty ,Inhibitory postsynaptic potential ,Synaptic Transmission ,Oxygen Consumption ,Internal medicine ,medicine ,Animals ,Humans ,Rats, Wistar ,Hypoxia ,Cerebral Cortex ,Neocortex ,Chemistry ,Cortical Spreading Depression ,Neurovascular bundle ,Rats ,Electrophysiology ,medicine.anatomical_structure ,Ion homeostasis ,Endocrinology ,Neurology ,Cerebral blood flow ,Cerebral cortex ,Regional Blood Flow ,Cortical spreading depression ,Anesthesia ,Cerebrovascular Circulation ,Neurology (clinical) ,Cardiology and Cardiovascular Medicine - Abstract
Cortical spreading depression (CSD) is associated with a dramatic failure of brain ion homeostasis and increased energy metabolism. There is strong clinical and experimental evidence to suggest that CSD is the mechanism of migraine, and involved in progressive neuronal injury in stroke and head trauma. Here we tested the hypothesis that single episodes of CSD induced acute hypoxia, and prolonged impairment of neurovascular and neurometabolic coupling. Cortical spreading depression was induced in rat frontal cortex, whereas cortical electrical activity and local field potentials (LFPs) were recorded by glass microelectrodes, cerebral blood flow (CBF) by laser—Doppler flowmetry, and tissue oxygen tension (tpO2) with Polarographic microelectrodes. Cortical spreading depression increased cerebral metabolic rate of oxygen (CMRO2) by 71% ± 6.7% and CBF by 238% ± 48.1% for 1 to 2 mins. For the following 2 h, basal tpO2 and CBF were reduced whereas basal CMRO2 was persistently elevated by 8.1% ± 2.9%. In addition, within first hour after CSD we found impaired neurovascular coupling (LFP versus CBF), whereas neurometabolic coupling (LFP versus CMRO2) remained unaffected. Impaired neurovascular coupling was explained by both reduced vascular reactivity and suppressed function of cortical inhibitory interneurons. The protracted effects of CSD on basal CMRO2 and neurovascular coupling may contribute to cellular dysfunction in patients with migraine and acutely injured cerebral cortex.
- Published
- 2009
13. Pathway-specific variations in neurovascular and neurometabolic coupling in rat primary somatosensory cortex
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Henning Piilgaard, Ara Kocharyan, Pia Enager, Nikolas Offenhauser, Edith Hamel, Martin Lauritzen, and Priscilla Fernandes
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Male ,Interneuron ,Neurotransmission ,Biology ,Inhibitory postsynaptic potential ,Somatosensory system ,Oxygen Consumption ,Interneurons ,Evoked Potentials, Somatosensory ,medicine ,Laser-Doppler Flowmetry ,Premovement neuronal activity ,Animals ,Rats, Wistar ,gamma-Aminobutyric Acid ,Neurons ,Pyramidal Cells ,Glutamate receptor ,Somatosensory Cortex ,Synaptic Potentials ,Immunohistochemistry ,Electric Stimulation ,Oxygen tension ,Rats ,medicine.anatomical_structure ,nervous system ,Neurology ,Cerebral blood flow ,Cerebrovascular Circulation ,Neurology (clinical) ,Cardiology and Cardiovascular Medicine ,Neuroscience - Abstract
Functional neuroimaging signals are generated, in part, by increases in cerebral blood flow (CBF) evoked by mediators, such as nitric oxide and arachidonic acid derivatives that are released in response to increased neurotransmission. However, it is unknown whether the vascular and metabolic responses within a given brain area differ when local neuronal activity is evoked by an activity in the distinct neuronal networks. In this study we assessed, for the first time, the differences in neuronal responses and changes in CBF and oxygen consumption that are evoked after the activation of two different inputs to a single cortical area. We show that, for a given level of glutamatergic synaptic activity, corticocortical and thalamocortical inputs evoked activity in pyramidal cells and different classes of interneurons, and produced different changes in oxygen consumption and CBF. Furthermore, increases in stimulation intensities either turned off or activated additional classes of inhibitory interneurons immunoreactive for different vasoactive molecules, which may contribute to increases in CBF. Our data imply that for a given cortical area, the amplitude of vascular signals will depend critically on the type of input, and that a positive blood oxygen level-dependent (BOLD) signal may be a consequence of the activation of both pyramidal cells and inhibitory interneurons.
- Published
- 2009
14. Øged 20-HETE syntese forklarer reducered cerebral blod gennemstrømning men ikke the nedsatte neurovascular kobling efter kortikal spreading depression i rotte cerebral cortex:20-HETE syntes forklarer reduceret CBF efter CSD
- Author
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Fordsmann, Jonas Christoffer, ko, Rebecca, Choi, Hyun B, Thomsen, Kirsten Joan, Witgen, Brent Marvin, Mathiesen, Claus, Lønstrup, Micael, Hansen, Henning Piilgaard, MacVicar, Brian A, Lauritzen, Martin, Fordsmann, Jonas Christoffer, ko, Rebecca, Choi, Hyun B, Thomsen, Kirsten Joan, Witgen, Brent Marvin, Mathiesen, Claus, Lønstrup, Micael, Hansen, Henning Piilgaard, MacVicar, Brian A, and Lauritzen, Martin
- Abstract
Cortical spreading depression (CSD) is associated with release of arachidonic acid (AA), impaired neurovascular coupling, and reduced cerebral blood flow (CBF), caused by cortical vasoconstriction. We tested the hypothesis that the released AA is metabolized by the cytochrome P450 enzyme to produce the vasoconstrictor 20-hydroxyeicosatetraenoic acid (20-HETE), and that this mechanism explains cortical vasoconstriction and vascular dysfunction after CSD. CSD was induced in the frontal cortex of rats and the cortical electrical activity and local field potentials (LFPs) recorded by glass microelectrodes, CBF by laser Doppler flowmetry, and tissue oxygen tension (tpO2) using polarographic microelectrodes. 20-HETE synthesis was measured in parallel experiments in cortical brain slices exposed to CSD. We used the specific inhibitor HET0016 (N-hydroxy-N'-(4-n-butyl-2-methylphenyl)formamidine) to block 20-HETE synthesis. CSD increased 20-HETE synthesis in brain slices for 120 min, and the time course of the increase in 20-HETE paralleled the reduction in CBF after CSD in vivo. HET0016 blocked the CSD-induced increase in 20-HETE synthesis and ameliorated the persistent reduction in CBF, but not the impaired neurovascular coupling after CSD. These findings suggest that CSD-induced increments in 20-HETE cause the reduction in CBF after CSD, and that the attenuation of stimulation-induced CBF responses after CSD has a different mechanism. We suggest that blockade of 20-HETE synthesis may be clinically relevant to ameliorate reduced CBF in patients with migraine and acute brain cortex injuries.
- Published
- 2013
15. YIA5: Predictor of severity and long distance outcome of patients with critical illness myopathy and polyneuropathy
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A. Jelinek, Anna Horwitz, Krisztina Benedek, Henning Piilgaard, and Martin Lauritzen
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Pediatrics ,medicine.medical_specialty ,Critical Illness Myopathy ,business.industry ,medicine.disease ,Outcome (game theory) ,Sensory Systems ,Neurology ,Physiology (medical) ,Severity of illness ,medicine ,Neurology (clinical) ,business ,Polyneuropathy - Published
- 2014
16. Cyclosporine A, FK506, and NIM811 ameliorate prolonged CBF reduction and impaired neurovascular coupling after cortical spreading depression
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Hansen, Henning Piilgaard, Witgen, Brent Marvin, Rasmussen, Peter, Lauritzen, Martin, Hansen, Henning Piilgaard, Witgen, Brent Marvin, Rasmussen, Peter, and Lauritzen, Martin
- Abstract
Cortical spreading depression (CSD) is associated with mitochondrial depolarization, increasing intracellular Ca(2+), and the release of free fatty acids, which favor opening of the mitochondrial permeability transition pore (mPTP) and activation of calcineurin (CaN). Here, we test the hypothesis that cyclosporine A (CsA), which blocks both mPTP and CaN, ameliorates the persistent reduction of cerebral blood flow (CBF), impaired vascular reactivity, and a persistent rise in the cerebral metabolic rate of oxygen (CMRO(2)) following CSD. In addition to CsA, we used the specific mPTP blocker NIM811 and the specific CaN blocker FK506. Cortical spreading depression was induced in rat frontal cortex. Electrocortical activity was recorded by glass microelectrodes, CBF by laser Doppler flowmetry, and tissue oxygen tension with polarographic microelectrodes. Electrocortical activity, basal CBF, CMRO(2), and neurovascular and neurometabolic coupling were unaffected by all three drugs under control conditions. NIM811 augmented the rise in CBF observed during CSD. Cyclosporine A and FK506 ameliorated the persistent decrease in CBF after CSD. All three drugs prevented disruption of neurovascular coupling after CSD; the rise in CMRO(2) was unchanged. Our data suggest that blockade of mPTP formation and CaN activation may prevent persistent CBF reduction and vascular dysfunction after CSD.
- Published
- 2011
17. Effects of Cortical Spreading Depression on Synaptic Activity, Blood Flow and Oxygen Consumption in Rat Cerebral Cortex
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Hansen, Henning Piilgaard and Hansen, Henning Piilgaard
- Abstract
As the title of this thesis indicates I have during my PhD studied the effects of cortical spreading depression (CSD) on synaptic activity, blood flow and oxygen consumption in rat cerebral cortex. This was performed in vivo using an open cranial window approach in anesthetized rats. I applied Laser-Doppler Flowmetry for measurements of cerebral blood flow, glass microelectrodes for recording of synaptic activity – local field potentials – and ongoing cortical electrical activity and a Clark type electrode for measurements of tissue partial pressure of oxygen (tpO2). Offline calculations of cerebral metabolic rate of oxygen (CMRO2) were performed using a compartment model as described Gjedde1. In the first study we characterized the frequency dependency of evoked responses of the transcallosal fiber network (TC) in the somatosensory cortex concerning: synaptic activity, cerebral blood flow (CBF), tissue partial pressure of oxygen (tpO2) and cerebral metabolic rate of oxygen (CMRO2). Furthermore the subpopulation of inhibitory interneurons activated during TC stimulation was characterized. Once characterized the investigated parameters in the TC network were compared to the equivalent parameters of the whisker/infraorbital nerve etwork (IO) targeting the same cortical area. We tested the hypothesis that the relation between increases in CBF and CMRO2 evoked by stimulation and synaptic activity differed for the two activated networks and that activation of two distinct networks activate two different sets of interneurons. Our data imply that for a given cortical area the amplitude of vascular signals will depend critically on the type of input and hence on the type of neurons activated. In the second study I investigated the effect of cortical spreading depression (CSD) on the evoked responses of synaptic activity (LFP), CBF, tpO2 and CMRO2 in the TC network. Also the impact on neurovascular and neurometabolic coup
- Published
- 2010
18. Pathway-specific variations in neurovascular and neurometabolic coupling in rat primary somatosensory cortex
- Author
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Enager, Pia, Hansen, Henning Piilgaard, Offenhauser, Nikolas, Kocharyan, Ara, Fernandes, Priscilla, Hamel, Edith, Lauritzen, Martin, Enager, Pia, Hansen, Henning Piilgaard, Offenhauser, Nikolas, Kocharyan, Ara, Fernandes, Priscilla, Hamel, Edith, and Lauritzen, Martin
- Abstract
Functional neuroimaging signals are generated, in part, by increases in cerebral blood flow (CBF) evoked by mediators, such as nitric oxide and arachidonic acid derivatives that are released in response to increased neurotransmission. However, it is unknown whether the vascular and metabolic responses within a given brain area differ when local neuronal activity is evoked by an activity in the distinct neuronal networks. In this study we assessed, for the first time, the differences in neuronal responses and changes in CBF and oxygen consumption that are evoked after the activation of two different inputs to a single cortical area. We show that, for a given level of glutamatergic synaptic activity, corticocortical and thalamocortical inputs evoked activity in pyramidal cells and different classes of interneurons, and produced different changes in oxygen consumption and CBF. Furthermore, increases in stimulation intensities either turned off or activated additional classes of inhibitory interneurons immunoreactive for different vasoactive molecules, which may contribute to increases in CBF. Our data imply that for a given cortical area, the amplitude of vascular signals will depend critically on the type of input, and that a positive blood oxygen level-dependent (BOLD) signal may be a consequence of the activation of both pyramidal cells and inhibitory interneurons.
- Published
- 2009
19. Persistent increase in oxygen consumption and impaired neurovascular coupling after spreading depression in rat neocortex
- Author
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Hansen, Henning Piilgaard, Lauritzen, Martin, Hansen, Henning Piilgaard, and Lauritzen, Martin
- Abstract
Cortical spreading depression (CSD) is associated with a dramatic failure of brain ion homeostasis and increased energy metabolism. There is strong clinical and experimental evidence to suggest that CSD is the mechanism of migraine, and involved in progressive neuronal injury in stroke and head trauma. Here we tested the hypothesis that single episodes of CSD induced acute hypoxia, and prolonged impairment of neurovascular and neurometabolic coupling. Cortical spreading depression was induced in rat frontal cortex, whereas cortical electrical activity and local field potentials (LFPs) were recorded by glass microelectrodes, cerebral blood flow (CBF) by laser-Doppler flowmetry, and tissue oxygen tension (tpO(2)) with polarographic microelectrodes. Cortical spreading depression increased cerebral metabolic rate of oxygen (CMRO(2)) by 71%+/-6.7% and CBF by 238%+/-48.1% for 1 to 2 mins. For the following 2 h, basal tpO(2) and CBF were reduced whereas basal CMRO(2) was persistently elevated by 8.1%+/-2.9%. In addition, within first hour after CSD we found impaired neurovascular coupling (LFP versus CBF), whereas neurometabolic coupling (LFP versus CMRO(2)) remained unaffected. Impaired neurovascular coupling was explained by both reduced vascular reactivity and suppressed function of cortical inhibitory interneurons. The protracted effects of CSD on basal CMRO(2) and neurovascular coupling may contribute to cellular dysfunction in patients with migraine and acutely injured cerebral cortex.
- Published
- 2009
20. Principal cell spiking, postsynaptic excitation, and oxygen consumption in the rat cerebellar cortex
- Author
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Thomsen, Kirsten, Piilgaard, Henning, Gjedde, Albert, Bonvento, Gilles, Lauritzen, Martin, Hansen, Henning Piilgaard, Thomsen, Kirsten, Piilgaard, Henning, Gjedde, Albert, Bonvento, Gilles, Lauritzen, Martin, and Hansen, Henning Piilgaard
- Abstract
Udgivelsesdato: 2009-Sep, One contention within the field of neuroimaging concerns the character of the depicted activity: Does it represent neuronal action potential generation (i.e., spiking) or postsynaptic excitation? This question is related to the metabolic costs of different aspects of neurosignaling. The cerebellar cortex is well suited for addressing this problem because synaptic input to and spiking of the principal cell, the Purkinje cell (PC), are spatially segregated. Also, PCs are pacemakers, able to generate spikes endogenously. We examined the contributions to cerebellar cortical oxygen consumption (CMRO2) of postsynaptic excitation and PC spiking during evoked and ongoing neuronal activity in the rat. By inhibiting excitatory synaptic input using ionotropic glutamate receptor blockers, we found that the increase in CMRO2 evoked by parallel fiber (PF) stimulation depended entirely on postsynaptic excitation. In contrast, PC spiking was largely responsible for the increase in CMRO2 when ongoing neuronal activity was increased by gamma-aminobutyric acid type A receptor blockade. In this case, CMRO2 increased equally during PC spiking with excitatory synaptic activity as during PC pacemaker spiking without excitatory synaptic input. Subsequent inhibition of action potential propagation and neurotransmission by blocking voltage-gated Na+-channels eliminated the increases in CMRO2 due to PF stimulation and increased PC spiking, but left a large fraction of CMRO2, i.e., basal CMRO2, intact. In conclusion, whereas basal CMRO2 in anesthetized animals did not seem to be related to neurosignaling, increases in CMRO2 could be induced by all aspects of neurosignaling. Our findings imply that CMRO2 responses cannot a priori be assigned to specific neuronal activities.
- Published
- 2009
21. Hansen, Henning Piilgaard
- Author
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Hansen, Henning Piilgaard and Hansen, Henning Piilgaard
- Published
- 2009
22. Contribution of somatosensory cortex to evoked cerebellar blood flow responses.
- Author
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Henning Piilgaard
- Published
- 2004
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