EEG in metabolic disorders

EEG in Metabolic Diseases

Dr.Roopchand.PSSenior Resident AcademicDepartment of Neurology

TDMC, Alappuzha.

Introduction:

• Diffuse brain dysfunction due to impaired nutrition to glia and neurons.

• EEG changes have progressive alterations.

– Parallels the severity of encephalopathy.

• Help in prognostication.

• Helps in differentiating between seizure and psychogenic cause of altered sensorium.

Sequence of EEG changes:

• Early stage: patient alert – α slowing mixed with regular theta waves. Bisynchronous generalized frontal theta-delta activity attenuated by eye opening.

• Paradoxical arousal response: frontal slowing may become apparent on eye opening.

• Stage 2: generalized theta activity with less reactivity to eye opening.

• Stage 3: variable delta slowing with increase in voltage.

• Stage 4: severe encephalopathy – low voltage continuous or intermittent delta activity or burst suppression pattern.

Hepatic Encephaloopathy:

• Pathology due to increased ammonia.

– Enhances GABA transmission.

• Octopamine, manganese.

• Degree of slowing parallels the rise in ammonia.EEG changes are sensitive and accurate indicator of CNS involvement.

• Triphasic waves are seen.

– Initial low voltage negative wave followed by a prominent positive sharp wave and broad negative wave.

– 2-4Hz, anterior location, slowed back ground.

– Not pathognomonic

EEG changes according to level of consiousness:

Stage Consciousness EEG

1 Alert Normal

2 Drowsy Slow alpha, poorly developed k complexes, sleep spindles

3 Stupor Theta activity with occasional FIRDA, absence of sleep pattern.

4 Coma Triphasic waves

5 Deep coma Delta waves, triphasicdisappear.

6 Deep coma Flat EEG

Reye’s Syndrome:

• EEG may correlate with prognosis

• Grade 1&2: Slow background of theta-delta activity – patients often survives.

• Grade 3: intermediate changes – 50% survival

• Grade 4 &5: low voltage non reactive delta activity or burst suppression – either dies or survives with major sequel.

Wilson’s Disease:

• EEG is normal in majority.

• May show pronounced slowing.

• Decreased sleep spindles and occasional spike discharges.

• Changes do not correlate

Renal Diseases:

Uremic encephalopathy:

• Changes depends more on acuteness.

• Seizure can be focal or generalized.

– Due to water and electrolyte imbalance.

• EEG changes parallels level on consciousness.

• Early stage: slowing of alpha mixed with diffuse or bitemporal theta activity.

• Alternating pattern: normal frontal delta.

• Severe encephalopathy: diffuse slowing

• Paradoxical arousal response may be seen.

• IPS : photomyoclonic or photoparoxysmalresponse.

• Triphasic waves also may be sen.

Dialysis Disequilibrium syndrome:

• Occurs during or immediately after dialysis.

• Head ache, nausea, fatigue, confusion, fasciculation's, convulsions, coma

• Sudden transient osmotic changes and electrolyte changes.

• EEG reflects the uremia prior to dialysis.

• Bursts of delta, rhythmic delta activity, rhythmic theta activity with normal background activity.

Dialysis Dementia:

• Occur to patients on c/c dialysis.

• Progressive dementia after 3-4 yrs.

• EEG pattern may appear months before onset of dementia.

• 2-4hz high voltage irregular frontally dominant delta waves– Vertex waves, sharp waves, triphasic waves, spikes

with normal background.

• Slowing of background with clinical disease.

Action myoclonus renal failure syndrome:

• AR disorder manifest in late adolescence.

• Hand tremor, action myoclonus cerebellar signs, generalized seizure, proteinuria and progressive seizures.

• Slowing of background with epileptiform discharges.

• Hv – paroxysmal discharge

• IPS – photoparoxysmal response.

• Hyponatremia: rhythmic delta activity can occur.

– EEG changes can remain for long durations even after correction of hyponatremia.

• Hypoglycemia: slowing of background and epileptiform discharges.

– Changes disappear once hypoglycemia corrected.

– Summation effect: permanent EEG changes in prolonged hypoglycemia.

• Hyperglycemia: if > 400mg% - slowing mixed with fast activity.

• In DKA slowing parallels with depth of coma

• PLEDS may be seen in Epilepsia partialiscontinua.

• Thyrotoxicosis: augmentation of alpha activity with central beta activity.

• Thyroid storm: high amplitude delta spike and sharp waves, burst suppression and triphasicwaves.

• Hashimoto encephalopathy: diffuse slowing, medial temporal lobe focal epileptiform discharges, triphasic waves and periodic activity.

• Myxedema: poor maturation of EEG.

• Adrenal insufficiency: background slowing, poor response to eye closure reduced beta and increased sensitivity to HV.

• Alpha slowing may be seen at the end of pregnancy and 1-3 days prior to menstruation.

• Hypocalcemia: Seizure occur at serum level >5mg%– EEG changes do not correlate with calcium levels.

– Slowing with generalized bursts of spikes.

• Hypercalcemia: background slowing with intermittent rhythmic delta activity.– Prominent photic response > 13mg%

– Focal epileptiform discharges and triphasic waves >16mg%

• Carbon dioxide narcosis: diffuse theta delta activity with occasional triphasic wave.