What diseases cause EEG denervation patterns?

EEG Denervation Patterns: Disease Etiologies

The term "EEG denervation" is not standard neurophysiological terminology—you likely mean EEG slowing or desynchronization patterns, which are caused primarily by metabolic encephalopathies (hepatic, uremic, hyponatremia), neurodegenerative diseases (Alzheimer's disease, Lewy body dementia), and infectious encephalitides.

Primary Disease Categories

Metabolic Encephalopathies

Hepatic encephalopathy is the prototypical metabolic cause, showing progressive EEG slowing from frontal alpha predominance to diffuse slowing, then triphasic waves, and ultimately delta waves in coma 1, 2. The severity of EEG changes directly parallels clinical hepatic encephalopathy grade 1.

• Uremic encephalopathy produces similar generalized slowing patterns with triphasic waves 1, 3
• Hyponatremia with CNS involvement causes progressive slowing ranging from mild background slowing to generalized delta waves, with triphasic waves as a notable but non-specific finding 3
• Hypoxic encephalopathy results in diffuse slowing proportional to the severity of oxygen deprivation 2

Neurodegenerative Diseases

Alzheimer's disease demonstrates characteristic "slowing" with reduced alpha rhythm amplitude (tonic background desynchronization) and increased pathological delta (<4 Hz) and theta (4-7 Hz) rhythms 1. This reflects thalamocortical "disconnection mode" from AD neuropathology causing damage to cortico-cortical and cortico-subcortical pathways 1.

• The posterior alpha peak frequency decreases and power shifts to slower frequencies as disease progresses 1, 4
• Lewy body dementia shows similar slowing patterns but can be differentiated from AD with moderate accuracy (AUC 0.61) using data-driven EEG feature extraction 4
• Vascular cognitive impairment produces slowed frequency patterns and disrupted connectivity, though with low specificity between VCI subgroups 5

Infectious Etiologies

Viral encephalitis causes EEG abnormalities in more than 80% of cases, typically showing diffuse slowing with or without focal features 6, 2. Herpes simplex encephalitis may show periodic lateralized epileptiform discharges (PLEDs), though these are not pathognomonic 6.

Critical Diagnostic Distinctions

Pattern Recognition

• Triphasic waves are highly suggestive of hepatic encephalopathy in confused/stuporous patients but can occur in uremic encephalopathy, hyponatremia, and drug intoxications (lithium, valproate, baclofen) 1, 6
• Generalized periodic discharges appear in sporadic Creutzfeldt-Jakob disease 6
• Extreme delta brush suggests anti-NMDA receptor autoimmune encephalitis 6

Severity Grading

The progression of metabolic encephalopathy follows a predictable EEG pattern: initial frontal alpha predominance or beta increase → diffuse slowing → triphasic waves → delta waves in coma → isoelectric EEG 1, 2. This grading has prognostic value for both survival and risk of developing overt encephalopathy 1.

Common Pitfalls to Avoid

Do not assume generalized slowing equals seizure activity—this pattern typically represents diffuse cortical dysfunction from non-epileptic causes, and inappropriate antiepileptic drug escalation may worsen the slowing 2. Approximately 25% of patients have ongoing electrical seizures despite cessation of visible convulsive activity, requiring video-EEG for proper classification 6.

Do not delay metabolic workup including liver function, renal function, electrolytes, ammonia, and toxicology screening when etiology is unclear 2. The EEG changes are non-specific across different metabolic encephalopathies and require clinical-laboratory correlation for definitive diagnosis 3.

Do not rely on PLEDs as pathognomonic for HSV encephalitis—they occur in many conditions including other viral encephalitides and non-infectious disorders 6.

Clinical Application Algorithm

1. Identify the pattern: Diffuse slowing (<8 Hz dominant frequency) indicates encephalopathy 6
2. Check for specific features: Triphasic waves → hepatic/uremic/hyponatremia; periodic discharges → CJD; extreme delta brush → anti-NMDA encephalitis 6, 3
3. Correlate with clinical context: Liver disease + triphasic waves = hepatic encephalopathy; cognitive decline + alpha slowing = neurodegenerative disease 1, 4
4. Obtain targeted laboratory studies: Ammonia, electrolytes, renal function, toxicology based on suspected etiology 2
5. Consider continuous EEG monitoring if altered consciousness persists to exclude nonconvulsive status epilepticus, which occurs in 8% of comatose ICU patients 6