Electroencephalography of Encephalopathy in Patients With Endocrine and Metabolic Disorders

Abstract

Patients with acute alteration in mental status from encephalopathy due to underlying metabolic-toxic or endocrine abnormalities are frequently seen in the acute hospital setting. A rapid diagnosis and correction of the underlying cause is essential as a prolonged state of encephalopathy portends a poor outcome. Correct diagnosis and management remain challenging because several encephalopathies may present similarly, and further laboratory, imaging or other testing may not always reveal the underlying cause. Electroencephalography (EEG) provides rapid additional information on the encephalopathic patient. It may help establish the diagnosis, and is indispensable for identifying non-convulsive status epilepticus – an important possible complication in this context. The EEG may assist the clinician in gauging the severity of brain dysfunction, and may aid in predicting outcome. This review summarizes the current knowledge on EEG findings in selected metabolic and endocrine causes of encephalopathy, and highlights distinct EEG features associated with particular etiologies.

Population of the ictal-interictal zone: The significance of periodic and rhythmic activity

“…However, TWs are also seen in other scenarios such as hypernatremia, hypothyroidism, sepsis, lithium toxicity, and hypertensive encephalopathy (Faigle et al, 2013, Kaplan and Sutter, 2015). One recent study of GPDs found that those with triphasic morphology were just as likely to be associated with seizures as were GPDs without (Foreman et al, 2016).…”

Reversible central neural hyperexcitability: an electroencephalographic clue to hypocalcaemia

“…Hyperventilation and photic stimulation induced epileptiform discharges have been reported in patients with hypocalcaemia. [1][2][3] In our patient, appearance of epileptiform discharges after eye closure, hyperventilation and photic stimulation may suggest presence of central neural hyperexcitability due to hypocalcaemia. These features may be an equivalent of peripheral neuromuscular hyperexcitability (Chvostek's and Trousseau's signs) that occurs in hypocalcaemia.…”

De novo status epilepticus with isolated aphasia

“…Improve the EEG under benzodiazepine treatment without normalization of the clinical picture may not be helpful in differentiating NCSE, since EEG improvement can also be seen in metabolic encephalopathy [7]. Pure persistent rhythmic delta activity has been reported in NCSE [8]; more often toxic-metabolic encephalopathies and viral or limbic encephalitis [9,10] present with pure rhythmic delta activity. These conditions could more or less be excluded by normal spinal tap, and resolving aphasia under anticonvulsant therapy may support ictal origin.…”