Metabolic and Diffuse Encephalopathies: Disruption of the Internal Milieu

Chapter 5 examines the broad range of metabolic causes of unconsciousness and the specific treatments they require. The main feature distinguishing diffuse or metabolic impairment of consciousness is that it is normally not associated with focal neurological findings that would suggest a structural lesion of the brain. However, there are some features of the neurological examination of patients with metabolic encephalopathies that can help to pinpoint the cause of the disturbance. In addition, there are some findings on examination that may appear to be due to focal lesions, but which can be due to diffuse or metabolic disease. The chapter first examines the diagnostic features of metabolic encephalopathies. It then looks at the internal metabolic milieu in which the brain functions normally. It also considers specific types of metabolic and diffuse disturbances of that internal milieu that can cause encephalopathy. Finally, it considers various endogenous and exogenous toxins that produce toxic encephalopathies.

DELIRIUM IN ACUTE NEUROLOGICAL CARE DEPARTMENT. CAUSES, PATHOGENESIS AND MANAGEMENT

Defined as an organic decline, often transient, ondulant, mainly of cognitive function, memory, language, delirium is often considered the attribute of patients hospitalized with multiple illnesses. Medical costs, and subsequent psychological implications, prognostic particularities gives him a special social importance. Although with multiple recognized etiology, its pathogenesis is partially known, involving relays and neural networks. In the presence of known predisposing factors and under some precipitating influence like acute metabolic or inflammatory disorders (interleukins 1, 6, caspaze), infections, vascular endothelial dysfunction that cause malfunctions of neurotransmitters (GABA, glutamate, acetylcholine, melatonin) occurs, mainly, an atentionale matrix disruption (attention modulation is done through the collaboration of the neocortex, thalamus and brainstem’s reticular substance) as well as structural changes of neural networks and their interaction with cerebral default network. Its prevalence is estimated at the time of admission between 11-30% of patients. Early identification of patients at risk and multifactorial and multidisciplinary approach represents efficient solution to prevent delirium consequences. Authors performed a synthetic rundown of the main theorical aspects of delirium and exemplify by a retrospective study in “Prof. Dr. N. Oblu” Neurologycal Clinic of Emergencies hospital, Iasi. From 3,707 patients admitted in one year, 32% had impaired language and only 7% have presented confusional syndrome: 58% in ischemic strokes or haemorrhagic (9%), epilepsy (18%), intracerebral tumors (1.8%), metabolic encephalopathies (7%), neurodegenerative disorders (22%), infections (3%). Ages prevailed over 60 years and males (64%), low outcome in 15%, 80% had improvement in evolution and 5% died.

P.077 EEG attenuations in adults: clinical correlates

Background: Intermittent EEG attenuations have relatively clear significance in pediatric populations, but a consistent clinical correlation has not been identified in adults. While generally seen in metabolic encephalopathies, the specific clinical correlates and prognostic value have not been determined. Methods: We prospectively collected 22 consecutive EEGs noted to have intermittent generalized attenuations. Baseline and discharge modified Rankin Scale (mRS), diagnosis at discharge, EEG altering medications, ICU admissions, relevant imaging, mental status, the location the patient was discharged to, and pertinent lab values were assessed. Results: Mean patient age was 73.7 (SD=11.0) at admission. Twelve of the twenty-two patients (55%) died during their course in hospital. Four patients (18.2%) did not have a change in mRS score from baseline to discharge, while most had an increase in their mRS scores reflecting increased disability. Twelve patients (55%) were admitted to the ICU or CCU during their time in hospital. The most common etiologies were metabolic encephalopathies, and often associated with triphasic waves. Conclusions: Intermittent generalized EEG attenuations in adults are associated with severe metabolic encephalopathies and poor outcome including high association with mortality. The physiologic mechanism of generalized attenuations in poorly understood. Patients with this pattern should be suspected of having a severe metabolic encephalopathy and treated accordingly.

Adult EEG

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.

Toxic and metabolic encephalopathies: iconographic essay

Generally, toxic-metabolic diseases affecting the central nervous system can hardly be differentiated just on the basis of their clinical presentation. However, some typical neuroradiological features can guide the correct diagnosis. In this context, magnetic resonance imaging is an important tool which, in association with clinical and laboratory data, can establish an early and specific treatment. The present pictorial essay with selected cases from the archives of the authors' institution describes imaging findings which might help in the etiologic diagnosis of toxic-metabolic diseases.

Possible levetiracetam induced encephalopathy presenting as electrical status epilepticus: An unknown occurrence

Levetiracetam is a novel, broad spectrum anti-epileptic drug with proven efficacy in generalized as well as focal onset seizures. It has renal elimination with no hepatic metabolism. Levetiracetam induced encephalopathy is rarely reported in literature. Triphasic waves in the electroencephalogram are seen in toxic-metabolic encephalopathies of various aetiology like hepatic encephalopathy, uraemia. We report a patient who was on levetiracetam for acute symptomatic seizures and developed encephalopathy with electroencephalogram showing generalised triphasic waves. These triphasic waves disappeared with intravenous lorazepam but without clinical improvement in sensorium. The electroencephalographic abnormality appeared as electrical status epilepticus which got normalised on discontinuation of levetiracetam. This is the first report of levetiracetam induced encephalopathy presenting as electrical status epilepticus and also depicts electroencephalographic correlate of levetiracetam induced encephalopathy.