Inpatient Management of Encephalopathy.

Pramod Reddy,Kaleb Culpepper

doi:10.7759/cureus.22102

Abstract

Unexplained encephalopathy is a common occurrence in tertiary care centers and neurologic disorders should be considered after ruling out the infectious, toxic and metabolic etiologies. Neuroimaging combined with a thorough history and examination is often helpful in ruling out stroke and fulminant demyelinating encephalopathies. Autoimmune encephalopathy should be suspected in any patient with unexplained acute or subacute onset encephalopathy or rapidly progressing dementia. Anti-N-methyl-D-aspartate receptor (NMDA-R) encephalitis is the most studied form and Hashimoto encephalitis is the most controversial form of autoimmune encephalopathies. Obtaining a combined serum and Cerebrospinal fluid (CSF) autoantibody testing will increase the diagnostic yield of autoimmune and paraneoplastic encephalitis. When diagnosing NMDA receptor antibodies CSF is always more sensitive than serum and in contrast, voltage-gated potassium channel (VGKC) complex antibodies are more readily detectable in serum than in CSF. Neural-specific antibody tests frequently result after several weeks and treatment should be administered without a significant delay to prevent brain damage. Autoimmune encephalitis is often treatment responsive when immunotherapy (glucocorticoids, intravenous immune globulin, plasma exchange) is used in various combinations. The absence of inflammatory markers and autoantibodies in the serum or CSF may not rule out the possibility of paraneoplastic encephalopathies.

Highlights

BackgroundAltered mental status (AMS) is a common occurrence in both hospitalized and patients visiting the emergency department
While minor focal deficits may be present on the neurologic examination in patients with metabolic encephalopathies, the finding of prominent focal signs should suggest the possibility of a structural lesion
While these markers are useful in the diagnosis of multiple sclerosis (MS), their utility is limited in autoimmune encephalopathies, where nonspecific elevations are seen due to central nervous system (CNS) inflammation

Summary

Introduction

Severe encephalopathy results in AMS due to global brain dysfunction and manifests with headache, nausea, vomiting, visual disturbances, confusion, seizures followed by stupor and coma in advanced cases. Acute encephalopathy can occur from both systemic and neurological processes and patients require rapid evaluation and intervention in order to limit the brain injury. Examples of systemic causes include drug overdose, drug withdrawal, electrolyte disturbances, thyroid disorders, hypoxia, hypoglycemia, hypotension, severe hypertension and organ (renal/hepatic) failure. Focal central nervous system (CNS) derangements include tumors, edema with mass effect, seizures, stroke, bleeding, infectious meningoencephalitis and various forms of demyelinating, vasculitis and autoimmune encephalopathies. While minor focal deficits may be present on the neurologic examination in patients with metabolic encephalopathies, the finding of prominent focal signs should suggest the possibility of a structural lesion

Background

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Disclosures