The procedure involves applying small metal discs called electrodes to the surface of the scalp using a dab of special gel. The length of the recording varies, but is usually minutes. Applying and removing the electrodes takes longer, though, so the entire process is over an hour. During the actual recording, all the patient has to do is sit in a recliner and relax. It is helpful if you doze off during the recording, since abnormalities often show up during the transition between sleep and wakefulness.
A normal EEG does not rule out the possibility of epilepsy. The sensitivity of the EEG—that is, the likelihood that the test will pick up abnormality—increases each time the test is run. Sometimes patients need a second or third EEG or more over the course of evaluation. For such a simple test, the EEG or "brain wave test" is surrounded by many myths! Here are a few. The EEG has little to do with what a person is thinking, and certainly cannot allow your doctor to "read your mind.
Because many abnormalities tend to show up during the transition between sleep and wakefulness, your neurologist may ask you to have a "sleep deprived EEG. Ideally, you should get only 3 or 4 hours of sleep and should avoid caffeine for 24 hours before the EEG.
You do not have to stay up all night, but just as late as you can so that you are tired during the test the next day. Not all seizures require treatment.
The decision is made on a case-by-case basis after discussion with your neurologist. For example, a single seizure that occurs during hospitalization for a major illness might not require long-term treatment with medications. In such cases we often say that the seizure was provoked by some other medical problem.
When the other medical problem is treated, the chance of the seizure recurring is usually low. A wide variety of medications is available when treatment is required.
Like all drugs, each of these medications has pros and cons. Choosing the right medication for you requires discussion with your neurologist. More information on medications is available from the Epilepsy Foundation. Some common-sense lifestyle modifications can also reduce the risk of seizures in susceptible individuals. Remaining artefacts were annotated and removed. Measures of spectral shape included spectral power, spectral flatness a measure of spectral entropy and spectral difference a measure of difference in spectral shape over time.
This filtered and time-compressed representative of EEG is similar to the aEEG but has a unique definition, which therefore allows for standard quantitative measures. Artefacts were annotated and removed. Quantitative HRV features were extracted from the R-R interval 39 including both time-domain and frequency-domain features. These features are consistent with previous neonatal studies. Continuous variables were described using the mean and standard deviation SD or the median and interquartile range IQR and categorical variables using frequency and percentage.
Sixteen healthy term infants were included in the non-HIE group. Fifty-eight infants with mild HIE were included. Qualitative analysis of the EEG was divided into three main categories as described above: temporal organisation, abnormal waves, and abnormal features.
The main results are displayed in Table 3. Infants in the non-HIE group demonstrated normal SWC with continuous mixed-frequency activity with absence of abnormal waves and features. The most striking difference visually was the high frequency of slow and sharp waves, periods of excessive discontinuity and lower amplitude.
Epochs were analysed at a median time of 0. Quantitative analysis revealed significant differences in spectral features between infants with mild HIE and those without Table 4. Both spectral flatness and spectral difference were significantly lower in the delta and theta frequency bands for the mild HIE group compared with the non-HIE group. There were no differences between groups in quantitative measures of amplitude which included rEEG measures , and no differences in measures of inter-hemispheric coherence.
SWC should be present from birth 40 and the absence of SWC is associated with poor neurodevelopmental outcome. It is important to consider the effect that interventions in the neonatal unit may have on SWC; however, it is our practice to only perform necessary procedures and cares on admission and nurse these infants in incubators with minimal handling thereafter.
We have also previously shown that normal continuous SWC activity is present from birth in healthy control infants without perinatal asphyxia.
Qualitative analysis demonstrated excessive slow waves in infants with mild HIE, which was also confirmed on quantitative analysis. There is a growing body of evidence that infants with mild HIE have significant levels of disability at follow-up, yet no current evidence or guidance exists regarding potential therapeutic interventions in this group.
This, coupled with the medico-legal implications of not offering TH to infants who may have benefitted, leads to unease and difficulty for clinicians in objective decision-making regarding treatment. In addition, there is therapeutic creep and many centres are now cooling infants with mild HIE. Although TH has a wide margin of safety, it is not without consequences.
Inappropriate TH has a number of potential adverse consequences. Animal studies have suggested that induced hypothermia in a normal brain may lead to apoptosis. Concerns have been raised about commonly used drugs such as morphine as it may contribute to neuronal and microglial apoptosis.
Tolerance has also been described requiring increased doses and problems with withdrawal on discontinuation. Improved identification and selection of infants who may potentially benefit from TH would limit the numbers required to power such a study.
Our current methods of identifying infants are flawed as the primary and most widely available assessment is based on clinical examination, which is highly subjective. Initially developed as a quick and easy tool to assess infants with encephalopathy, it was also developed to examine infants on a daily basis and is most predictive of outcome on days 3—4.
For quantitative analysis, we used rEEG, which has a standard definition. While continuous multichannel EEG may not be available in all the neonatal units, most aEEG devices allow visualisation of at least some raw EEG channels that can provide richer information and a more enhanced aEEG interpretation. It also has the potential to detect more subtle differences, which may not be easily identified on visual assessment alone. In this cohort, quantitative analysis demonstrated significant differences in all measures of spectral shape at the lower frequency bands when compared to the non-HIE group.
These features of the EEG would be very difficult, if not impossible, to detect visually. Quantitative EEG features provides a scalable, continuous and objective assessment of the EEG that may be useful in the future to improve our identification of at-risk infants.
It is also easily applied to a smaller number of EEG channels. Our study is limited by the fact that it was a retrospective analysis of data; however, EEGs of infants with HIE were collected over different cohorts in both the TH and pre-TH era capturing the clinical variability in presentation.
In addition, it was not possible to completely blind the neurophysiologists conducting the qualitative analysis to study group; however, their findings were remarkably consistent with the objective quantitative analysis. Outcome data is currently unavailable for the entire population; however, neurodevelopmental follow-up is underway.
We plan to clinically follow these infants to 5 years of age to determine which, if any, of these abnormal features correlate with outcome.
We do know from previous studies that a proportion of infants with mild HIE will have cognitive or behavioural disability on follow-up; however, these difficulties may not be evident until 5 years of age or later. Quantitative analysis of the EEG reveals significant differences in spectral measures of the lower frequency bands.
The challenge now is to correlate these features with outcome and determine the importance of each feature.
Incorporation of early quantitative EEG features could be useful for future trials of TH in infants with mild HIE to aid in the early and objective identification of cases. Kurinczuk, J. Epidemiology of neonatal encephalopathy and hypoxic-ischaemic encephalopathy. Early Hum. Sarnat, H. Neonatal encephalopathy following fetal distress. A clinical and electroencephalographic study. Thompson, C. The value of a scoring system for hypoxic ischaemic encephalopathy in predicting neurodevelopmental outcome.
Acta Paediatr. Mendler, M. Predictive value of Thompson-score for long-term neurological and cognitive outcome in term newborns with perinatal asphyxia and hypoxic-ischemic encephalopathy undergoing controlled hypothermia treatment. Neonatology , — Robertson, C. Child Neurol. Jacobs, S. Cooling for newborns with hypoxic ischaemic encephalopathy. Cochrane Database Syst. CD Sabir, H. Stroke 43 , — Gunn, A. Cerebral hypothermia is not neuroprotective when started after postischemic seizures in fetal sheep.
Laptook, A. JAMA , — Whole-body hypothermia for term and near-term newborns with hypoxic-ischemic encephalopathy: a randomized controlled trial. Gluckman, P. Selective head cooling with mild systemic hypothermia after neonatal encephalopathy: multicentre randomised trial. Lancet , — Finer, N. Factors affecting outcome in hypoxic-ischemic encephalopathy in term infants.
Long-term follow-up of term neonates with perinatal asphyxia. Serial MRI and neurodevelopmental outcome in 9- to year-old children with neonatal encephalopathy. Murray, D. Early EEG grade and outcome at 5 years after mild neonatal hypoxic ischemic encephalopathy. Pediatrics , e Finder, M.
Two-year neurodevelopmental outcomes after mild hypoxic ischemic encephalopathy in the era of therapeutic hypothermia. JAMA Pediatr. Chalak, L. Prospective research in infants with mild encephalopathy identified in the first six hours of life: neurodevelopmental outcomes at 18—22 months. Therefore, an EEG may be useful only when there is no response to treatment.
The authors concluded that EEG screening may be of limited value in children with behavioral problems who had no clinical evidence of a neurological disorder. Frank 24 reported significantly higher rates of abnormalities.
Patients with rapid cycling bipolar disorder may exhibit isolated epileptic discharges on an EEG. Levy and associates 26 compared the EEGs of patients with rapid cycling with those of non-rapid cycling patients. The EEGs of 3 of the 5 rapid cycling patients had isolated epileptic discharges, compared with none of the controls.
Subictal mood disorders. Note that the EEG does not contribute to the diagnosis of schizophrenia or bipolar disorders except that it helps the clinician rule out a neurological cause for the symptoms when a patient presents with an atypical picture eg, unusual age of onset.
Dementia versus pseudodementia. Because patients with advanced dementia rarely have a normal EEG, a normal EEG can play an important role in diagnosing cases of pseudodementia dementia secondary to depression or psychosis.
When dementia and depression coexist, it becomes important to have some idea about the relative contribution of each disorder to the overall clinical presentation. Brenner and associates 28 compared the EEGs of patients with depression, dementia, pseudodementia, and dementia plus depression with the EEGs of age-matched healthy controls.
Their findings indicate that the more abnormal the EEG is, the less likely it is that a patient will respond favorably to an antidepressant. This is particularly important because aging increases the likelihood of experiencing adverse effects from antidepressants.
A year-old woman with Alzheimer disease who has been in a nursing home for 4 years stopped eating and was admitted to the neuropsychiatry ward of a psychiatric hospital. In reviewing her history, a complete workup for possible reversible causes of dementia had never been done. There was nothing significantly abnormal on any test; the EEG was normal.
A normal EEG was incompatible with advanced stage Alzheimer disease. A trial of antidepressant therapy was therefore initiated. Nothing happened for 2 weeks. During the third week, the patient started speaking. Her speech was completely disorganized with severe psychotic content.
Haloperidol was added, and the patient was ambulatory and able to leave the hospital within 2 weeks. Possible focal problem. Patients with a history of head injury or an early brain insult during infancy or childhood may have developed behavior that helps them compensate for the deficit resulting from the injury. Such behavior could be deemed aberrant.
An EEG may detect focal slowing most commonly frontal or temporal , which indicates a disordered brain region. Knowledge of the focal deficit followed by detailed neuropsychological evaluation could shed much light on the particular case and help guide treatment and rehabilitation efforts. The differential diagnosis of acutely disorganized and disoriented patients often includes delirium. In acutely agitated delirious patients, the EEG often helps determine the cause of altered consciousness: a diffuse encephalopathic process, a focal brain lesion, or continuous epileptic activity without motor manifestations ambulatory nonconvulsive status epilepticus.
Most often, patients with delirium have a toxic-metabolic encephalopathy. In general, as encephalopathy progresses, there is diffuse slowing of the background rhythms, including alpha 8 to 13 Hz to theta 4 to 7. Delta less than 3. The major exception to the above rule is seen during withdrawal from alcohol and during delirium tremens DTs.
Excessive fast activity rather than slowing dominates the EEG beta activity: 13 to 30 Hz in patients with alcohol withdrawal delirium. A year-old man with a long history of alcohol dependence presented to the emergency department with a blood alcohol level of 0. He was admitted for detoxification. As his alcohol level started coming down, he became progressively more confused. The benzodiazepine dosage was increased. He progressively became agitated and was placed in 4-point restraints.
A neurology consultation was called. The consultant diagnosed DTs and suggested increasing the benzodiazepine dose. Symptoms continued to escalate despite increasing doses of the benzodiazepine. Later that day, the patient had a medical consultation. It was suggested that the patient was in iatrogenic delirium and that all medications should be stopped.
An abbreviated 8 leads EEG was obtained and revealed a moderate degree of diffuse slowing, consistent with encephalopathy and not the fast low-voltage picture expected with DTs. Medications were rapidly tapered and the patient recovered. Electroencephalography is burdened by several constraints that place limitations on the information provided. These constraints have been extensively discussed elsewhere 30 and include:.
A number of problems make detection of isolated epileptic discharges in nonepileptic psychiatric patients difficult and likely an expensive process. Standard neurological training in EEG interpretation strongly emphasizes under-interpretation to avoid stigmatizing the patient with the diagnosis of seizure disorder.
In psychiatric EEGs, abnormalities, when present, tend to be infrequent in the record and require full vigilance on the part of the interpreter. The chance of a false negative can be lessened by repeating the EEG or by doing the EEG testing for extended periods eg, 1 to 3 days , which increases the chances of recording the EEG signal when the patient is actually in a panic attack or a rage episode.
Additional problems may arise because the patient does not understand the special needs associated with obtaining an accurate recording-eg, staying still, activating procedures such as hyperventilating or staying up all night before the procedure sleep deprivation improves the detection of isolated epileptic discharges , or relaxing and falling asleep during the test.
Furthermore, a patient may behave inappropriately during the test. These factors necessitate that the laboratory be placed in a psychiatrically oriented space with psychiatrically trained technicians who can help the patient particularly children relax and cooperate. The contents presented herein are largely derived from the textbook Standard Electroencephalography in Clinical Psychiatry: A Practical Handbook.
Portions of it may have since been updated. Behavior and symptoms of psychiatric patients and the electroencephalogram. Arch Gen Psychiatry.
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