scholarly journals Migraine with Prolonged Aura: Correlation of Clinical and EEG Features

1995 ◽  
Vol 8 (2) ◽  
pp. 109-114 ◽  
Author(s):  
A. O. Ogunyemi
Keyword(s):  
Cerebral Cortex ◽  
Migraine With Aura ◽  
Slow Waves ◽  
Spreading Cortical Depression ◽  
Eeg Abnormalities ◽  
Cortical Depression ◽  
Eeg Changes ◽  
Eeg Recordings ◽  
The Brain

Migraine with prolonged aura has rarely been examined with regard to the sequence of the neurological symptoms and the associated EEG changes. This report describes five patients who underwent clinical assessment and EEG recordings during attacks of migraine with prolonged aura. CT scan of the brain was obtained in four of them. Follow-up EEG was also obtained. The aura symptoms either preceded the headache or were coincident with it. The aura symptoms evolved in a manner consistent with posterior-to-anterior dysfunction of the cerebral cortex. The EEG abnormalities were non-epileptiform and consisted of focal delta slow waves or theta slow waves. The EEG abnormalities showed good correlation with the patients' aura symptoms and resolved when the patients became symptom free. The posterior-to-anterior sequence of the aura symptoms is in accord with the findings during cerebral blood flow studies in patients having migraine with aura. Also the symptoms and EEG changes in our patients indicate dysfunction of the cerebral cortex, consistent with the notion that spreading cortical depression may be the underlying pathophysiological event in migraine with aura.

Adult EEG

2016 ◽  
pp. 110-126
Author(s):  
Joseph I. Sirven ◽  
Barbara F. Westmoreland
Keyword(s):  
Cerebral Cortex ◽  
Brain Death ◽  
Underlying Process ◽  
Medication Effects ◽  
Eeg Abnormalities ◽  
Brain Death Determination ◽  
Death Determination ◽  
The Brain ◽  
Metabolic Encephalopathies ◽  
Disease Specific

The EEG can be helpful in evaluating patients with focal or diffuse disorders, altered consciousness, or who are comatose. The occurrence of certain patterns and the presence of variability and reactivity of the EEG can help ascertain their prognosis or potential for improvement. Sequential recordings are very helpful in determining whether the patient is improving or deteriorating, or developing other complications such as seizures, metabolic encephalopathies, or toxic or medication effects Specific EEG patterns, when present, can give clues to what the underlying process is. This chapter discusses the group of abnormal non-epileptic EEG findings that can occur in an adult, including common abnormal non-epileptiform EEG abnormalities, EEG in disease-specific focal processes affecting the cerebral cortex, and EEG findings of disorders that affect the brain in a diffuse manner. The current evaluation and EEG standards in brain-death determination is reviewed.

scholarly journals Calcified cephalohematoma as an unusual cause of EEG anomalies: case report

2017 ◽  
Vol 19 (1) ◽  
pp. 46-50 ◽  
Author(s):  
Vera Vigo ◽  
Domenica Immacolata Battaglia ◽  
Paolo Frassanito ◽  
Gianpiero Tamburrini ◽  
Massimo Caldarelli ◽  
...  
Keyword(s):  
Head Injuries ◽  
Surgical Removal ◽  
Long Term Effects ◽  
Indication For Surgery ◽  
Eeg Abnormalities ◽  
Skull Deformity ◽  
First Time ◽  
The Brain

Cephalohematoma, one of the most common neonatal head injuries, generally undergoes spontaneous resorption. When calcified, it may cause cranial vault distortion and depression of the inner skull layer, although it remains asymptomatic. Surgery, indeed, is usually performed for cosmetic purposes. For these reasons, the long-term effects of calcified cephalohematoma (CC) are widely unknown. The authors report the case of an 11-year-old girl with a persistent calcified CC causing skull deformity and delayed electroencephalography (EEG) anomalies. These anomalies were detected during routine control EEG and were not clinically evident. The young girl underwent surgical removal of the CC for cosmetic purpose. The EEG abnormalities disappeared after surgery, thus reinforcing the hypothesis of a correlation with the brain “compression” resulting from the CC. To the best of the authors' knowledge this is the first time that CC-associated EEG anomalies have been described: even though these anomalies cannot be considered an indication for surgery, they merit late follow-up in case of skull deformity.

scholarly journals Rapid Efflux of Lactate from Cerebral Cortex during K+-Induced Spreading Cortical Depression

1999 ◽  
Vol 19 (4) ◽  
pp. 380-392 ◽  
Author(s):  
Nancy F. Cruz ◽  
Keiji Adachi ◽  
Gerald A. Dienel
Keyword(s):  
Cerebral Cortex ◽  
Steady State ◽  
Brain Structures ◽  
Brain Regions ◽  
Uniform Pattern ◽  
Spreading Cortical Depression ◽  
Cortical Depression ◽  
Rapid Transport ◽  
Glucose Metabolites ◽  
Derivatives Of

Rapid transport of lactate from activated brain regions to blood, perhaps reflecting enhanced metabolite trafficking, would prevent local trapping of labeled metabolites of [6-14C]glucose and cause underestimation of calculated CMRglc. Because the identities of glucose metabolites lost from activated structures and major routes of their removal are not known, arteriovenous differences across brains of conscious normoxic rats for derivatives of [6-14C]glucose were determined under steady-state conditions in blood during K+-induced spreading cortical depression. Lactate was identified as the major labeled product lost from brain. Its entry to blood was detected within 2 minutes after a pulse of [6-14C]glucose, and it accounted for 96% of the 14C lost from brain within approximately 8 minutes. Lactate efflux corresponded to 20% of glucose influx, but accounted for only half the magnitude of underestimation of CMRglc when [14C]glucose is the tracer, suggesting extensive [14C]lactate trafficking within brain. [14C]Lactate spreading within brain is consistent with (1) relatively uniform pattern labeling of K+-treated cerebral cortex by [6-14C]glucose contrasting heterogeneous labeling by [14C]deoxyglucose, and (2) transport of 14C-labeled lactate and inulin up to 1.5 and 2.4 mm, respectively, within 10 minutes. Thus, newly synthesized lactate exported from activated cells rapidly flows to blood and probably other brain structures.

scholarly journals Electroclinical Features of Epilepsy in Mucopolysaccharidosis III: Outcome Description in a Cohort of 15 Italian Patients

2021 ◽  
Vol 12 ◽  
Author(s):  
Rita Barone ◽  
Agata Fiumara ◽  
Mariangela Gulisano ◽  
Lara Cirnigliaro ◽  
Maria Donatella Cocuzza ◽  
...  
Keyword(s):  
Early Recognition ◽  
Age At Onset ◽  
Lysosomal Storage ◽  
Epileptiform Discharges ◽  
Appropriate Care ◽  
Behavioral Abnormalities ◽  
Eeg Abnormalities ◽  
Eeg Changes ◽  
Mps Iii

Mucopolysaccharidosis III (Sanfilippo syndromes) types A–D are rare lysosomal storage disorders characterized by heparan sulfate accumulation and neurodegeneration. Patients with MPS III present with developmental stagnation and/or regression, sleep disturbance, and behavioral abnormalities usually in the first years of life. Epilepsy may occur in a proportion of patients during the disease course. However, the progression of epilepsy and EEG changes in MPS III have not been systematically investigated. We report electroclinical features in a cohort of patients with MPS III over a follow-up period ranging from 6.5 to 22 years. Participants include 15 patients (11 females; aged 7–31 years) with MPS III A (n = 7, 47%), MPS III B (n = 5, 34%), MPS III C (n = 2, 13%), and MPS III D (n = 1, 6%). At the time of this study, 8 out of 15 patients (53%) had epilepsy. Epilepsy occurred in patients with advanced disease even in the first decade of life (mean age at onset: 12.1 ± 6.7 years). However, seizure onset may also be associated with abrupt worsening of the neurobehavioral phenotype. The main epilepsy types observed were generalized (four out of eight, 50%), followed by focal (three out of eight, 37%) and combined (two out of eight, 25%) epilepsy and status epilepticus (one out of eight, 12.5%). Seizures were generally controlled by one antiepileptic drug (AED) and most patients (seven out of eight, 87%) were still on therapy after a median follow-up period of 5 years (range: 1–9 years). A total of 66 EEGs were analyzed with a median EEG follow-up duration of 7 years (range: 6 months−14 years). Slowing of the background activity occurred in 7 (46%) patients aged 4–19 years. Epileptiform EEG abnormalities were observed in 10 patients at a mean age of 9.6 ± 2.9 years. EEG epileptiform discharges were not unavoidably linked to epilepsy. Early recognition and careful monitoring of electroclinical features in MPS III is necessary for appropriate care and for the detection of disease progression.

Electroencephalogram indices in patients undergoing cardiac arrest

2020 ◽  
Vol 1 (14) ◽  
pp. 32-38
Author(s):  
I. Yu. Berezina ◽  
L. I. Sumsky ◽  
A. Yu. Mikhailov ◽  
Yu. L. Arzumanov
Keyword(s):  
Cardiac Arrest ◽  
Electrical Activity ◽  
Paroxysmal Activity ◽  
Equivalent Dipole ◽  
Neurophysiological Mechanisms ◽  
Eeg Changes ◽  
Eeg Recordings ◽  
The Moment ◽  
Electroencephalogram Eeg ◽  
The Brain

Objective: to assess the safety of indicators of electrical activity of the brain for the approach to the analysis of the basic neurophysiological mechanisms of the brain in patients after cardiac arrest.Materials and methods: 52 patients were examined (age — 54,68 ± 19,33) after cardiac arrest. At the time of recording the electroencephalogram (EEG), the level of wakefulness of the examined patients on the Glasgow coma scale was in the range of 3 to 13 points. In 35 patients, EEG recording was performed starting from the first three days from the moment of cardiac arrest, in 17 patients — from the fourth to the 18th day. EEG was registered on electroencephalographs ‘Encephalan–EEGR–19/26’ by ‘Medikom MTD’, ‘Neuron-Spectrum–5/EP’ and ‘Neuron-Spectrum–65’ by ‘Neurosoft’ in accordance with the recommendations of the International Federation of Clinical Neurophysiologists (IFCN). The duration of a single EEG recordings lasted at least 30 min. To localize equivalent dipole sources of pathological activity we used the program ‘BrainLoc 6.0’, (Russia). In 19 patients EEG was recorded in dynamics from 2 to 8 times.Results: all patients showed EEG changes of varying severity, which can be divided into three groups (according to the severity of changes in the EEG: moderate, severe and rough). In the group of patients with gross changes in EEG can be identified 4 variants: the first variant — absence of the alpha rhythm and the dominance of slow-wave fluctuations of the frequency spectrum; variant II — continuous generalized paroxysmal activity; variant III — phenomenon of ‘burst-suppression’; variant IV — a marked decrease in the amplitude of electrical activity of the brain to the level of 2–4 microvolt.Conclusions: based on the dynamics of the EEG pattern in patients after cardiac arrest, it is possible to assume with a certain degree of probability the level of violations in the basic mechanisms of the brain.

On the Possible Relation of Spreading Cortical Depression to Classical Migraine

Cephalalgia ◽  
1985 ◽  
Vol 5 (2_suppl) ◽  
pp. 47-51 ◽  
Author(s):  
Martin Lauritzen
Keyword(s):  
Spreading Depression ◽  
Posterior Part ◽  
Low Flow ◽  
Neuronal Function ◽  
Pathogenetic Mechanism ◽  
Paper Briefly ◽  
Spreading Cortical Depression ◽  
Cortical Depression ◽  
The Brain ◽  
Lasting Influence

During the first 1 to 2 h of the classical migraine attack a hypoperfusion develops which starts in the posterior part of the brain and progresses anteriorly at a rate of 2-3mm/min. The hypoperfusion stops at primary sulci outlining major cortical macro-and microstructural changes, but seems not to be inhibited by other changes of the cortical architecture. The low flow regions are cortical and the low flow persists for 4–6 h, until the attack abates. Regions of hyperperfusion are either minor or non-existent. A similar behavior characterizes the velocity and mode of evolution of a cortical spreading depression, a transient perturbation of cortical neuronal function which has profound and long-lasting influence on the cortical blood flow. This paper briefly summarizes the arguments which have been put forward in recent years suggesting that spreading depression is a pathogenetic mechanism of migraine.

Migraine with aura with onset in childhood and adolescence: Long-term natural history and prognostic factors

Cephalalgia ◽  
2010 ◽  
Vol 30 (6) ◽  
pp. 674-681 ◽  
Author(s):  
C Termine ◽  
M Ferri ◽  
G Livetti ◽  
E Beghi ◽  
S Salini ◽  
...  
Keyword(s):  
Prognostic Factors ◽  
Natural History ◽  
Migraine With Aura ◽  
Remission Rate ◽  
Childhood And Adolescence ◽  
Visual Aura ◽  
Eeg Abnormalities ◽  
Headache Diagnosis

The long-term course of migraine with aura (MA) has been poorly explored. The present 11-year follow-up study assessed the long-term natural history and possible prognostic factors of MA with onset in childhood or adolescence. Patients were recruited from the original case records of our department, which are specifically designed to report all headache characteristics, aura symptoms and electroencephalogram (EEG) findings. A total of 77 patients (47 females; 30 males) whose records contained detailed descriptions of both headache and aura symptoms apparently meeting the International Classification of Headache Disorders (ICHD)-II criteria for MA (i.e., 1.2.1, 1.2.2, 1.2.6) underwent structured face-to-face follow-up headache interviews, all of which were conducted by the same neurologist, who has particular expertise in this field. A multivariate model (logistic regression analysis) was used to investigate the association between possible prognostic factors and the remission of both aura and headache at follow-up. The results of our study showed that 23.4% of the MA patients were headache-free at follow-up, 44.1% still had MA and 32.5% had a transformed headache diagnosis (i.e., fulfilling the criteria for ICHD-II 1.1. or 2). Patients with basilar-type migraine (1.2.6) showed the highest headache remission rate (38.5%). Our study seems to show that migraine with typical aura (1.2.1–1.2.2) is associated with a favourable evolution of aura symptoms over time (remission of aura in 54.1% of patients). Subjects experiencing only visual aura had a lower remission rate compared with those with visual ± sensory ± aphasic aura symptoms (36.8% vs. 61.5%, p = 0.054). A short headache duration (<12 hrs) and the presence of EEG abnormalities at baseline were the only significant predictors of aura remission at follow-up (odds ratio [OR] = 9.12, 95% confidence interval [CI]: 1.79 ± 46.51, and OR = 4.76, 95% CI: 1.18 ± 19.15, respectively). No significant predictors of headache remission were found. In conclusion, our results suggest that MA shows a favourable course. Further prospective studies with detailed EEG analysis both at baseline and at follow-up are needed in order to confirm the possible prognostic role of EEG abnormalities in MA. That said, it would, in our opinion, be highly premature at present to submit children with MA to EEG examinations for prognostication purposes.

Changes in Cortical pH and Blood Flow Accompanying Spreading Cortical Depression and Convulsion

1957 ◽  
Vol 190 (3) ◽  
pp. 557-562 ◽  
Author(s):  
Robert D. Tschirgi ◽  
Kazutoyo Inanaga ◽  
J. Langdon Taylor ◽  
Robert M. Walker ◽  
Ralph R. Sonnenschein
Keyword(s):  
Blood Flow ◽  
Cerebral Cortex ◽  
Spreading Depression ◽  
Potential Difference ◽  
Ion Concentration ◽  
Ph Change ◽  
Hydrogen Ion Concentration ◽  
Neuronal Membranes ◽  
Spreading Cortical Depression ◽  
Cortical Depression

Local changes in cerebral cortex hydrogen ion concentration of as much as 0.5 ph units were observed to accompany the waves of cortical spreading depression or convulsion in cats and rabbits. A diphasic wave consisting of an initial alkaline followed by a more prolonged acid shift was observed in most cases. No significant differences were found between the ph changes accompanying spreading depression and those accompanying spreading convulsion. These ph shifts, like the abnormal ECG activity and the slowly changing potential wave which accompanied them, spread over the surface of the cerebral cortex with a velocity of 1–3 mm/min. The curve of cortical ph change is coincident with, and similar in shape to, the slowly changing potential difference measured between a point on the cortical surface and the jugular blood. For every unit change in ph, the cortex-blood P.D. is shifted approximately 30 mv. It is suggested that the slowly changing potential difference arises across the blood-brain barrier rather than as a result of depolarization of neuronal membranes. A significant but variable change in local blood flow accompanied the spreading depression.

Clinical Predictive Factors of Pathological EEG in Children with Febrile Seizures and Their Association with Subsequent Epileptic Seizures

2021 ◽  
Author(s):  
Khouloud Kchaou ◽  
Ines Kammoun ◽  
Sahar Chakroun ◽  
Asma Haddar ◽  
Kaouthar Masmoudi
Keyword(s):  
Febrile Seizure ◽  
Epileptic Seizures ◽  
Febrile Seizures ◽  
Psychomotor Retardation ◽  
Only Children ◽  
Psychomotor Delay ◽  
Eeg Abnormalities ◽  
Eeg Data ◽  
Eeg Recordings

AbstractThe objective of this study was to identify clinical parameters predicting either a pathological EEG or a subsequent epileptic seizure (SES), based on the relation between paroxysmal EEG abnormalities and clinical features in children who presented at least one febrile seizure (FS). We collected data of children who presented to our department during the period 2013 to 2018 for EEG recording as part of their febrile seizure assessment. Only children aged between 1 month to 5 years were included. Both the clinical and EEG data were retrospectively collected and statistically studied. We performed a detailed analysis of the EEG recordings. SES was identified for patients with sufficient follow-up. A total of 120 children were included in the study, of whom 48% had EEG abnormalities. Psychomotor retardation (p = 0.002), completion of an EEG within 7 days of the last FS (p = 0.046), and late age (> 3 years) of the first FS onset (p = 0.021) were significantly associated with a pathological EEG. In multivariate analysis, performing early EEG (< 7 days from the last FS) (odds ratio [OR]: 2.35; p = 0.043; confidence interval [CI]: 1.028–5.375) and psychomotor retardation (OR: 4.19; p = 0.008; CI: 1.46–12) were independent predictors of a pathological EEG. Of 120 patients, 45 had a follow-up. However, only 10 (22.22%) had SES. Children with SES tended more to have a psychomotor delay, compared with children without SES (50% vs. 14.28%, p = 0.029). Moreover, the percentage of initial abnormal EEG in patients with SES was significantly higher than those without SES (70% vs. 34.28%, p = 0.05). Even though some FS characteristics predict EEG abnormalities, they are not always associated with SES. We highlight the importance of performing an EEG in the group of children who had both FS and psychomotor retardation. This is most likely the group at the highest risk of developing epilepsy.

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