EEG manifestations in metabolic encephalopathy

Electrolytes Disturbances and Seizures

Twenty-six (41%) of 63 consecutive patients with triphasic waves had various types of metabolic encephalopathies while 37 patients (59%) had non-metabolic encephalopathies, usually senile dementia. Triphasic waves were not found to be specific for any single type of metabolic encephalopathy. Etiology was more closely linked to conscious level at recording than any morphological or distributional feature of the triphasic waves themselves. Thus, all 31 alert patients had non-metabolic encephalopathies while all 13 comatose patients had metabolic encephalopathies. The second, positive, component (Wave II) most often had the highest voltage while equally maximal Waves I and II occurred next most commonly. Triphasic waves were most often maximally expressed anteriorly. Among patients with metabolic encephalopathies, a posterior-anterior delay or lag of the wave II peak occurred more commonly than did the better known anterior-posterior lag. Lags occurred with both metabolic and non-metabolic conditions, but were more common with the former. No difference in quantity or mode of appearance existed between the metabolic and non-metabolic groups when matched for conscious level. Prognosis for patients with either metabolic or non-metabolic encephalopathies was unfavourable. Only 4 of 24 metabolic and one of 35 non-metabolic patients were well at follow-up over 2 years later. Forty percent of EEGs with sharp and slow wave complexes (slow spike waves) had sporadically-appearing triphasic waves. The relative amplitudes of the 3 components differed from triphasic waves in other conditions: equally maximal Waves II and III were the most usual form.

Clinical utility of electroencephalography in encephalopathy

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

Electroencephalographic patterns in unresponsive pediatric patients

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.

Portal-systemic encephalopathy (PSE) is usually a complication of late and advanced liver disease. It may present either as insidious and slow deterioration in mental function or with variable waxing and waning severity. Alternatively acute exacerbations including frank coma may follow complications of cirrhosis or ill-advised therapy. Since several moderately effective methods of treatment are now available, it is important to look for PSE in every patient with advanced chronic liver disease, particularly if precipitating causes may be present. It should be ensured that such patients are adequately cared for. PSE may be diagnosed if a patient has chronic liver disease and a mental disturbance. Hyperammonemia may be regarded as confirmatory. Other causes of cerebral dysfunction, particularly metabolic encephalopathies (Table 1) and neurologic diseases, must be excluded in every case.

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

Hepatic encephalopathy (HE) is thought to be generalized and reversible. Focal signs are unusual and should prompt a search for other causes, such as trauma, hemorrhage, or preexisting lesions (1, 2). The electroencephalogram (EEG) shows generalized changes (3), and focal spikes or paroxysmal activity are unusual. However, hepatic encephalopathy can be asymmetrical. Focal signs include reversible strokelike episodes, ocular deviation and bobbing (4), and unilateral or alternating hemiplegia (5). Magnetic resonance imaging (MRI) can reveal multifocal areas of demyelinat ion (6). Little is known about the utility of single-photon-emission computed tomography (SPECT) and positron-emission tomography (PET) in metabolic encephalopathies, even though these techniques are increasingly used in the localization of epileptic foci. Injection of radiotracer during seizures enables localization of the epileptic focus as regional hyperperfusion/hypermetabolism, while in the interictal (ie, between the seizures) period, localized hypoperfusion/hypometabolism is observed. In the case of temporal lobe epilepsy, the sensitivity is higher than 95% for ictal SPECT, while it is close to 50% during the interictal period (7). To our knowledge, SPECT/PET ® ndings in epilepsy induced by hepatic encephalopathy have never been described. We report a case of hepatic encephalopathy with focal seizures occurring in a cirrhotic patient after positionin g a transjugula r intrahepatic portosystemic shunt (TIPS), with no previous focal brain lesions. We discuss the localization of the epileptic focus and report the results of structural and functional imagery. The one-year follow-up is also described.

Journal of Veterinary Internal MedicineVolume 10, Issue 1 p. 39-41 Open Access Apparent Renal Encephalopathy in a Cow Charlotte Dunigan, Corresponding Author Charlotte Dunigan Departments of Large Animal Clinical Sciences College of Veterinary Medicine, Washington State University, Pullman, WADepartment of Large Animal Clinical Sciences, College of Veterinary Medicine, Michigan State University, Veterinary Medical Center, East Lansing, MI 48824–1314Search for more papers by this authorJeff Tyler, Jeff Tyler Departments of Large Animal Clinical Sciences College of Veterinary Medicine, Washington State University, Pullman, WASearch for more papers by this authorReginald Valdez, Reginald Valdez Departments of Veterinary Pathobiology, College of Veterinary Medicine, Washington State University, Pullman, WASearch for more papers by this authorMonica Messinger, Monica Messinger Departments of Large Animal Clinical Sciences College of Veterinary Medicine, Washington State University, Pullman, WASearch for more papers by this authorHarold Schott, Harold Schott Departments of Large Animal Clinical Sciences College of Veterinary Medicine, Washington State University, Pullman, WASearch for more papers by this authorSteven Parish, Steven Parish Departments of Large Animal Clinical Sciences College of Veterinary Medicine, Washington State University, Pullman, WASearch for more papers by this authorPatricia Talcott, Patricia Talcott Departments of Veterinary Pathobiology, College of Veterinary Medicine, Washington State University, Pullman, WASearch for more papers by this author Charlotte Dunigan, Corresponding Author Charlotte Dunigan Departments of Large Animal Clinical Sciences College of Veterinary Medicine, Washington State University, Pullman, WADepartment of Large Animal Clinical Sciences, College of Veterinary Medicine, Michigan State University, Veterinary Medical Center, East Lansing, MI 48824–1314Search for more papers by this authorJeff Tyler, Jeff Tyler Departments of Large Animal Clinical Sciences College of Veterinary Medicine, Washington State University, Pullman, WASearch for more papers by this authorReginald Valdez, Reginald Valdez Departments of Veterinary Pathobiology, College of Veterinary Medicine, Washington State University, Pullman, WASearch for more papers by this authorMonica Messinger, Monica Messinger Departments of Large Animal Clinical Sciences College of Veterinary Medicine, Washington State University, Pullman, WASearch for more papers by this authorHarold Schott, Harold Schott Departments of Large Animal Clinical Sciences College of Veterinary Medicine, Washington State University, Pullman, WASearch for more papers by this authorSteven Parish, Steven Parish Departments of Large Animal Clinical Sciences College of Veterinary Medicine, Washington State University, Pullman, WASearch for more papers by this authorPatricia Talcott, Patricia Talcott Departments of Veterinary Pathobiology, College of Veterinary Medicine, Washington State University, Pullman, WASearch for more papers by this author First published: January 1996 https://doi.org/10.1111/j.1939-1676.1996.tb02022.xCitations: 8AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL References 1 Welles EG, Tyler JW, Sorjonen DC, et al. Composition and analysis of cerebrospinal fluid in clinically normal adult cattle. Am J Vet Res 1992; 53: 2050– 2057. 2 Divers TJ, Crowell WA, Duncan JR, et al. Acute renal disorders in cattle: A retrospective study of 22 cases. J Am Vet Med Assoc 1982; 181: 694– 700. 3 Duncan JR, Prasse KW. Veterinary Laboratory Medicine. Ames , IA : Iowa State University Press; 1977: 145– 156. 4 Spier SJ, Smith BP, Seawright AA, et al. Oak toxicosis ia cattle in northern California: Clinical and pathologic findings. J Am Vet Med Assoc 1987; 191: 958– 964. 5 Casteel SW, Johnson GC, Miller MA, et al. Amaranthus retro-flexus (redroot pigweed) poisoning in cattle. J Am Vet Med Assoc 1994; 204: 1068– 1070. 6 Fetcher A. Renal disease in cattle. Part 2. Clinical signs, diagnosis, and treatment. Comp Cont Ed 1986; 8: S338– S345. 7 Brobst D., Parish S., Torbeck M., et al. Azotemia in cattle. J Am Vet Med Assoc 1978; 173: 481– 485. 8 Tyler JW, Smith BP, Irvine J. Hydronephrosis and pyelonephritis associated with an anomalous vas deferens in a bull. J Am Vet Med Assoc 1991; 198: 871– 872. 9 Isselbacher KJ, Braunwald E., Wilson JD, et al. Harrison's Principles of Internal Medicine, 13th ed. New York , NY : McGraw Hill; 1994: 2336. 10 Wolf AM. Canine uremic encephalopathy. J Am Anim Hosp Assoc 1980; 16735– 738. 11 Summers BA, Smith CA. Renal encephalopathy in a cow. Cornell Vet 1985; 75: 524– 530. 12 Bouchard PR, Weldon AD, Lewis RM, Summers BA. Uremic encephalopathy in a horse. Vet Pathol 1994; 31: 111– 115. 13 Lockwood AH. Metabolic encephalopathies: Opportunities and challenges. J Cereb Blood Flow Metab 1987; 7: 523– 526. 14 Jeppsson B., Freund HR, Gimmon Z., et al. Blood-brain barrier derangement in uremic encephalopathy. Surgery 1982; 92: 30– 35. Citing Literature Volume10, Issue1January 1996Pages 39-41 ReferencesRelatedInformation

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.

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.

Spinal myoclonus can be classified into spinal segmental myoclonus and propriospinal myoclonus, in which myoclonic activities spread up and down the spinal cord via propriospinal pathways [1], and can be idiopathic or may be associated with spinal cord disorders. It occurs rarely during drug and toxin exposure, or can be associated with malignancy or infection. [2] Spinal myoclonus associated with metabolic encephalopathy is exceptional or even questionable for the etiology. We experienced a patient with fulminant hepatitis A and spinal myoclonus. A 22-year-old woman was referred from the hepatology department with jerky, jackknife truncal movement 1 day in duration. The patient suffered from right upper quadrant abdominal pain, anorexia, and nausea due to fulminant hepatitis A. She was neither exposed to neuroleptics, nor did she have a history of movement disorders. Abnormal physical findings included mild icterus of the sclera and skin, abdominal tenderness, hepatomegaly, and palpable spleen. On neurologic examination, the patient presented with myoclonic movement that involved the trunk. The involuntary movements were forceful, jerky, irregular, large-amplitude movements with a frequency of 1–1.5 Hz, and were aggravated in the supine position (video 1), and caused a lurching gait, but did not occur during sleep. The patient’s mental status was normal and cranial, motor and sensory nerve examinations revealed no other abnormalities. Laboratory testing of hepatic function yielded aspartate aminotransferase and alanine aminotransferase over 1,000 U/L, respectively, and anti HAV-IgM antibody was positive. Magnetic resonance imaging (MRI) of the brain demonstrated high signal intensity on both of the basal ganglia on T1-weighted images without gadolinium enhancement (Fig. 1). Whole-spine MRI and electroencephalogram were normal; somatosensory evoked potential was also normal. The patient was diagnosed with hepatitis A with fulminant hepatic failure and symptomatic myoclonus. On hospital day 10, she began showing symptomatic and laboratory improvement and, without treatment for myoclonus, spinal myoclonus resolved completely. Negative myoclonus of the hands occurs commonly in patients with hepatic encephalopathy, who also present with bilateral pallidal hyperintensities in T1-weighted MRI, which may be accompanied by similar changes in the substantia nigra and the dentate cerebellar nucleus [3]. In our patient, spinal myoclonus appeared during the manifestation of fulminant hepatitis. The occurrence of spinal myoclonus with hepatitis and neither evidence of spinal cord lesion nor a history of neuroleptic medication suggests a possible association between the two conditions. Although we cannot be entirely sure of the role of the basal ganglia lesion in the patient’s neurologic symptoms, the temporal relationship suggests that spinal myoclonus was caused by viral infection with hepatitis A. Transverse Electronic supplementary material The online version of this article (doi:10.1007/s10072-014-1948-5) contains supplementary material, which is available to authorized users.

Hepatic encephalopathy is a complex neuropsychiatric syndrome. A previous study showed that chronic nitric oxide (NO) inhibition aggravated the severity of encephalopathy in thioacetamide (TAA)-treated rats. The present study investigated the relative contribution of NO synthase (NOS) isoforms on the severity of hepatic encephalopathy in TAA-treated rats. Fulminant hepatic failure was induced in male Sprague-Dawley rats by intraperitoneal injection of TAA (350 mg/kg/day) for 3 days. Rats were divided into three groups to receive N(omega)-nitro-L-arginine methyl ester (L-NAME, a non-selective NOS inhibitor, 25 mg/kg/day in tap water), L-canavanine (an inducible NOS inhibitor, 100 mg/kg/day via intraperitoneal injection) or normal saline (N/S) from 2 days prior to TAA administration and lasting for 5 days. Severity of encephalopathy was assessed by the counts of motor activity. Plasma levels of tumor necrosis factor-alpha (TNF- alpha) were determined by enzyme-linked immunosorbent assay (ELISA), and total bilirubin, alanine aminotransferase (ALT) and creatinine were determined by colorimetric assay. Compared with L-canavanine or N/S-treated rats (0% and 4%, respectively), the mortality rate was significantly higher in rats receiving L-NAME administration (29%, P < 0.005). Inhibition of NO created detrimental effects on the counts of motor activities (P < 0.05). Rats treated with L-NAME had significantly higher plasma levels of total bilirubin, ALT, creatinine and TNF- alpha as compared with rats treated with L-canavanine or N/S (P < 0.01). Chronic L-NAME administration, but not L-canavanine, had detrimental effects on the severity of hepatic damage and motor activities in TAA-treated rats. These results suggest that constitutive NOS activities play a major protective role in rats with fulminant hepatic failure.

Transjugular intrahepatic portosystemic shunt (TIPS) is increasingly used in the management of refractory ascites. Controversy exists regarding the predictive factors of unfavorable outcomes, useful for patient selection. The primary aim was to identify predictive factors of 1-year survival or recurrent severe hepatic encephalopathy in patients with cirrhosis undergoing covered TIPS for refractory ascites. The secondary aim was overall survival. Observational, retrospective, multicentric study, that included all cirrhotic patients treated with covered-TIPS for refractory ascites since 2001. Demographic, clinical, laboratory and hemodynamic data were collected at baseline and consecutively until dead, liver transplant or end of follow-up. The Cox model was used to identify predictive factors of overall survival. A Fine-Gray competing risk regression model was used to identify predictive factors of 1-year mortality or recurrent hepatic encephalopathy. A predictive nomogram was created based on those factors. In total 159 patients were included. Predictive factors of survival or recurrent severe encephalopathy were renal dysfunction [hazard ratio, 2.12 (95% CI, 1.11-4.04); P = 0.022], albumin [hazard ratio, 0.58 (95% CI, 0.34-0.97); P = 0.036], serum sodium [hazard ratio, 0.94 (95% CI, 0.89-0.98); P = 0.008] and international normalized ratio [hazard ratio 4.27 (95% CI, 1.41-12.88); P = 0.010]. In the competing risk analysis, predictive factors of 1-year mortality/recurrent severe encephalopathy in multivariate analysis were age [sub-distribution hazard ratio (sHR) 1.05 (95% CI, 1.02-1.09); P = 0.001], creatinine [sHR 1.55 (95% CI, 1.23-1.96); P = 0.001] and serum sodium [sHR 0.94 (95% CI, 0.90-0.99); P = 0.011] at baseline. Age, creatinine and sodium baseline levels strongly influence 1-year survival/recurrent severe hepatic encephalopathy in patients with cirrhosis undergoing covered TIPS for refractory ascites. A simple nomogram accurately and easily identifies those patients with worse prognosis.