Triphasic waves: clinical correlates and morphology.

Cephalosporin-related neurotoxicity: Metabolic encephalopathy or non-convulsive status epilepticus?

Normal brain function depends on normal neuronal metabolism, which is closely related to systemic homeostasis of metabolites, such as glucose, electrolytes, amino acids and ammonia. "Metabolic encephalopathy" indicates diffuse brain dysfunction caused by various systemic derangements. Electroencephalogram (EEG) is widely used to evaluate metabolic encephalopathy since 1937, when Berger first observed slow brain activity induced by hypoglycemia. EEG is most useful in differentiating organic from psychiatric conditions, identifying epileptogenicity, and providing information about the degree of cortical or subcortical dysfunction. In metabolic encephalopathy, EEG evolution generally correlates well with the severity of encephalopathy. However, EEG has little specificity in differentiating etiologies in metabolic encephalopathy. For example, though triphasic waves are most frequently mentioned in hepatic encephalopathy, they can also be seen in uremic encephalopathy, or even in aged psychiatric patients treated with lithium. Spike-and-waves may appear in hyper- or hypo-glycemia, uremic encephalopathy, or vitamin deficiencies, etc. Common principles of EEG changes in metabolic encephalopathy are (1) varied degrees of slowing, (2) assorted mixtures of epileptic discharge, (3) high incidence of triphasic waves, and (4), as a rule, reversibility after treatment of underlying causes. There are some exceptions to the above descriptions in specific metabolic disorders and EEG manifestations are highly individualized.

Electrolytes Disturbances and Seizures

Electroencephalographic patterns in unresponsive pediatric patients

Generalized periodic patterns with triphasic wave morphology, long referred to as triphasic waves [TWs], had been associated with metabolic encephalopathies, although other neurologic and systemic causes have since been identified. In a recent classification of periodic patterns, TWs were formally grouped with the generalized periodic discharges, which are often associated with ictal activity. The interpretation of generalized periodic patterns with TWs as nonictal can have significant implications in the management of comatose patients in nonconvulsive status epilepticus. Electrographic characteristics that help distinguish nonictal periodic patterns with TWs from generalized periodic discharge ictal patterns include (1) TWs in long runs of periodic bilaterally synchronous and symmetric discharges, maximal in frontocentral or posterior head regions with and without a frontal-to-occipital lag or posterior-to-anterior lag, respectively; (2) recurrent spontaneous and/or low-dose benzodiazepine-induced attenuation and/or suppression of the periodic pattern and replacement with a diffuse slow wave activity throughout a prolonged EEG recording; and (3) stimulation-induced activation and/or increase in frequency and/or organization of TWs. We coined the term of status triphasicus to describe the electrographic periodic pattern of TWs with these three distinct characteristics. In this article, we discuss the advantages and limitations of keeping the status triphasicus pattern as a distinct electrographic entity different from periodic ictal generalized periodic discharge patterns. We discuss the circumstances in which a status triphasicus pattern can be associated with ictal activity and propose a simple pragmatic classification of status triphasicus that encompasses the different clinical scenarios it can be associated with.

Pyridoxine-dependent epilepsy (PDE) is a rare disease, of which the EEG manifestations are only partially characterised. We report our observations of EEG recordings in four patients with PDE. EEG tracings from four patients fulfilling the clinical criteria for PDE were reviewed. Relative to the time of treatment with pyridoxine, EEG recordings were available before treatment in two patients (at ages four and 10 months), immediately after treatment in two patients and during long-term follow-up with treatment in all four patients. Pre-pyridoxine interictal EEG findings included: diffuse slowing, bilateral independent multifocal epileptiform discharges, generalized bursts of polyspike slow waves and focal or generalized sharp waves. In addition, the EEG was often asymmetrical and included: generalized semi-rhythmic sharp and slow waves, a burst suppression pattern and continuous generalized spike and slow waves. In one patient, who was followed subsequently, a decrease in multifocal spikes and sharp waves and permanent cessation of clinical seizures, within 10 minutes of concurrent reduction of spikes in the pre-existing generalized spike slow wave pattern, was observed immediately after pyridoxine treatment. However, despite the clinical response in this patient we observed persistent generalized burst suppression for four days, and fluctuation of the EEG with diffuse slowing on day four and transient exacerbation of discharges with continuous spike slow waves on day 22. This was followed by intermittent sharp waves at eight and 20 months, mild slowing at 31 months and normal EEG at 43 months. Long-term EEG findings in the other three patients receiving pyridoxine ranged between normal and intermittent multifocal sharp waves. Our data confirm previous observations and provide the following new findings: (1) the presence of burst suppression pattern after cessation of seizures can occur for up to five days after initiation of pyridoxine and should not exclude the diagnosis of PDE, (2) possible fluctuation and even transient worsening of electrographic discharges were observed for up to three weeks after initiation of pyridoxine and (3) the abnormal EEG can persist for up to 43 months before normalizing (range 1-43 months) and in other cases in which it continues to be abnormal it may still improve after increasing the dose of pyridoxine.

Baclofen has been reported to cause both a metabolic encephalopathy and nonconvulsive status epilepticus. Baclofen is typically used in the management of muscle spasticity but is being increasingly used to manage alcohol withdrawal and opiate dependency. Given the increasing use of baclofen we describe the clinical and electrographical features of baclofen neurotoxicity seen at our institution. The clinical and EEG features of patients with an encephalopathy in the setting of baclofen therapy were analyzed. Patients were identified via our hospital EEG database. Fourteen patients were identified having presented with an acute confusional state without identifiable cause other than baclofen use. Five patients took a deliberate overdose, three of whom were baclofen naive, two patients presented after medication prescription error, and seven patients were on stable doses (30-140 mg daily). All patients presented with an encephalopathy, one patient was reported to have clinical seizures, and seven had multifocal myoclonus. EEGs were abnormal in all patients and showed moderate to severe generalized slowing. Generalized triphasic waves occurring at 1 to 2 Hz, sometimes with an anterior to posterior phase lag, were present in 10 patients (71%), and intermittent generalized suppression of the background was seen in three patients. Three patients received small doses of intravenous benzodiazepines, resulting in a marked depression of consciousness and respiration. All patients recovered within 48 hours of baclofen discontinuation. Baclofen toxicity can produce an acute encephalopathy even at modest doses, with the EEG showing generalized slowing and triphasic waves consistent with a toxic encephalopathy. Management consists of supportive care and cessation of baclofen. Patients with baclofen neurotoxicity exhibit a marked vulnerability to the depressant effects of benzodiazepines.

This chapter focuses on the principles of conventional Electroencephalography (EEG) recording and interpretation and the typical applications of EEG to the assessment of persons with neurological and psychiatric conditions. The electrical activity measured at the scalp with EEG is generated by cerebral cortical neurons underlying the scalp where the recording electrodes are placed. The electrical activity recorded during EEG by pairs of electrodes (channels) is displayed by arranging those channels into specific sets. The two main categories of EEG abnormalities are: slowing or the presence of slower frequency waveforms than what should be present, and epileptiform discharges, or specific EEG waveforms that signify cortical hyper-irritability and an increased risk for clinical seizures. The EEG is commonly used in clinical assessment of Behavioral Neurology & Neuropsychiatry (BN&NP) patients. Triphasic waves usually arise from a diffusely abnormally slow background, and are a classic EEG abnormality associated with metabolic encephalopathy.

Triphasic waves (TWs) are defined as high-amplitude positive waveforms with preceding and after-going negative waves, typically seen in medically ill patients. TWs manifest in similar clinical presentations as other EEG encephalopathies; however, electrographically, they appear different. To better understand the difference, the authors used two different source localization software programs to find a reproducible and unique signature for TW. EEGs performed at Johns Hopkins Hospital and Duke University Hospital were retrospectively analyzed. EEG samples of TW, Delta, Theta-Delta, and Frontal Intermittent Rhythmic Delta Activity were selected. The authors did source localization via Commercial Curry 8 and open-source Brainstorm software. A minimum of 10 stereotypical waveforms per subject were selected. The authors used the Boundary Element Method for the head model, which was derived from the Montreal Neurological Institute averaged imaging data set. Dipole and current density analyses were performed. Twenty-eight patients were selected (10 TW, 4 Frontal Intermittent Rhythmic Delta Activity, 6 Theta-Delta, and 8 Delta). The findings suggest the activation of anterior frontal and midline structures for TW. Frontal Intermittent Rhythmic Delta Activity had a similar localization but without a moving dipole. In comparison, the Delta and Delta-Theta appeared to have a more diffuse origin. Source analysis of TW via two different software suggests the anterior midline location of TW with anterior to posterior propagation. These findings correlate with the previous hypotheses of TW origin. Retrospective analysis, low number of recording electrodes, and difficult analysis of slow waves limit the interpretation of these results. Nonetheless, this article opens the prospect of future studies in this field.

WS1.11. EEG in the ICU: Status Epilepticus and the Ictal-Interictal Continuum

Stimulus-induced reflex epileptic spasms in 5p− syndrome

Objective. The present study aimed to determine the clinical and radiological correlates of different electroencephalographic (EEG) patterns in hospitalized patients. Subjects and Methods. In this retrospective study performed at the Neurology Department, King Fahd University Hospital, Kingdom of Saudi Arabia (KSA), data of 374 patients who underwent EEG were reviewed and analyzed. Results. Presence of focal spike and wave or sharp wave (SW) (P = .00), generalized theta activity (P = .00), generalized delta activity (P = .04), persistent focal slow wave activity (SWA) (P = .003) and asymmetric background (P = .01) in the EEG record was significantly associated with abnormal imaging findings. Specifically, generalized theta delta activity (P = .01) and markedly attenuated EEG activity (P = .007) were associated with presence of cortical lesions; whereas, triphasic waves (TWs) (P = .009), and generalized theta activity (P = .001) were found to be related with presence of subcortical lesions. While, generalized delta activity (P = .01) was the only correlate with extra-axial lesions. Conclusion. At present, certain EEG patterns cannot be precisely correlated with imaging findings, suggesting that intercurrent metabolic, infectious, and/or toxic contributors could be the confounding factors. Nonetheless, when EEG patterns are examined alongside magnetic resonance imaging findings and other clinically relevant data, these might be indicative of a group of diseases in some pertinent situations. Thus, further larger prospective clinical studies that incorporate continuous EEG monitoring, advanced radiology techniques, and laboratory analyses would be beneficial to elucidate their interplay for better firm up the correlations.

6. Ceftriaxone and nonconvulsive status epilepticus (NCSE)

Creutzfeldt-Jakob disease (CJD) is aspongiform encephalopathy with the fatal outcome, caused by the accumulation of pathological prion protein in the central nervous system (CNS). CJD is classified into four types: sporadic (sCJD), familial or genetic (fCJD), iatrogenic (iCJD) and variant form (vCJD). The recognition of CJD is based on the clinical presentation, neuroimaging, electroencephalography and biochemical tests. The hyperintense signals in basal ganglia on brain magnetic resonance imaging (MRI), periodic sharp and slow wave complexes (PSWCs) in the electroencephalogram as well as presence of neuronal proteins such as protein 14-3-3 in the cerebrospinal fluid (CSF) support the diagnosis. The definite diagnosis of CJD still demands neuropathological confirmation. We report the case of a56-year-old woman with the rapidly progressive cognitive impairment, motor dysfunctions and the fulminant neurological deterioration to akinetic mutism during the five weeks' hospitalisation. The probable diagnosis of sCJD was based on medical history and characteristic findings in MRI. The positive result of the real-time quaking-induced conversion (RT-QuIC) test and presence of protein 14-3-3 were obtained post-mortem and definite diagnosis was confirmed by neuropathological examination. In this paper we would like to emphasize the difficulties in reaching the diagnosis and the need for aseries of diagnostic examinations in different points of time to obtain the confirming results.

Forced normalization of Lennox-Gastaut syndrome using lacosamide: A case report