EEG EXAM NORMAL VS ABNORMAL

Normal Awake EEG Pattern

In a relaxed, awake adult with eyes closed, the expected EEG features include:

• Posterior dominant rhythm (alpha, ~10 Hz) over occipital regions

• Symmetry between left and right hemispheres

• Low-voltage fast activity over frontal regions

• Alpha reactivity: posterior alpha attenuates with eye opening or increased attention

Absence of posterior alpha in an awake adult should prompt further consideration.

Symmetry as a Key Principle

EEG interpretation relies heavily on symmetry.

Always compare:

• Left vs right hemispheres

• Anterior vs posterior regions

Marked asymmetry between equivalent regions often suggests focal cerebral dysfunction.

Symmetry is expected in normal EEG recordings.

Slowing and Brain Dysfunction

Slowing refers to increased theta or delta activity.

• Focal slowing
  Suggests local cortical dysfunction near a structural lesion (e.g. tumour, stroke)

• Generalised slowing
  Suggests diffuse brain dysfunction (e.g. metabolic disturbance, infection, sedation)

Age is critical:

• Slower activity is more normal in children than in adults

Epileptiform Activity

Epileptiform abnormalities are defined by waveform shape, not simply size.

Typical features:

• Sharp contours

• Pointed peaks

• Brief duration

Patterns of concern include:

• Recurrent spikes

• Spike-and-wave complexes

• Rhythmic epileptiform discharges

Single isolated sharp transients are less concerning than repetitive patterns.

EEG Summary

EEG interpretation depends on:

• Understanding that signals are differences between electrodes

• Knowing the reference and montage

• Checking scale before interpretation

• Estimating frequency accurately

• Assessing symmetry and slowing patterns

• Recognising characteristic epileptiform shapes

ABNORMAL EEG

Abnormal EEG: Core Concepts

What is considered abnormal on EEG?

An EEG is considered abnormal when activity:

• Looks irregular, bizarre, or non-rhythmic

• Contains spikes, sharp waves, or spike–wave complexes

• Appears in runs rather than smooth background rhythms

• Is asymmetrical between the two hemispheres

• Is localised to one region or unexpectedly widespread

Loss of symmetry is one of the most reliable signs of abnormality.

Normal EEG (reference pattern)

In an awake, relaxed individual:

• EEG is symmetrical left vs right

• Low-voltage fast activity dominates anteriorly

• Posterior dominant rhythm (~10 Hz alpha) is visible over occipital regions

• Alpha rhythm is blocked by eye opening

• There is a front–to–back gradient in amplitude

Midline Pacemaker Theory

Rhythmic EEG activity is not generated by the cortex alone.

• Deep midline structures, especially the thalamus and reticular nucleus, act as pacemakers

• These structures synchronise activity across large areas of cortex via thalamocortical loops

• This rhythm-generating system is separate from thalamic relay nuclei, which transmit specific sensory information

Because EEG is sensitive to synchronised, widespread activity, rhythms generated by these deep structures are easily detected on the scalp.

large-scale EEG rhythms are strongly shaped by thalamo-cortical synchronisation.

Explaining Abnormal EEG Patterns

Deep or midline dysfunction

Damage or dysfunction affecting:

• Thalamus

• Reticular formation

• Brainstem

→ Produces generalised EEG abnormalities, often widespread slowing

Seen in:

• Metabolic encephalopathy

• Drug effects (e.g. sedatives)

• Reduced consciousness

• Coma

Focal vs Generalised EEG Abnormalities

This distinction is central to EEG interpretation.

General Principles of Abnormal EEG

• Focal lesions usually cause focal EEG abnormalities

• Diffuse pathology (infection, metabolic disease, encephalopathy) causes generalised slowing

• Lesions affecting deep structures can cause widespread EEG changes, even if small

Tumours and Lesions

• Brain tumours are electrically silent

• EEG abnormalities arise from irritated surrounding cortex, especially at tumour edges

• Small or slow-growing lesions may produce little or no EEG change

• Rapidly growing lesions are more likely to produce marked EEG abnormalities

EEG reflects how much the surrounding brain is disturbed, not the size of the lesion.

Speed of Lesion Development

• Rapid lesions → strong EEG abnormalities

• Slow lesions → brain adapts → fewer EEG changes

The rate of change matters more than the size of the lesion.

Consciousness and EEG

The degree of EEG abnormality correlates strongly with level of consciousness:

• Mild impairment → mild EEG changes

• Severe impairment / coma → severe, generalised EEG abnormalities

Diagnostic Caveat

EEG is not diagnostically specific.

• Many different brain insults produce similar EEG patterns

• EEG shows functional disturbance, not disease type

• Structural imaging (e.g. MRI) is required to identify the cause

EEG and MRI are complementary tools, not substitutes.

EEG AND EPILIPSY

EEG is one of the most important tools for investigating epilepsy because seizures arise from abnormal electrical activity in the brain. EEG can show interictal abnormalities, such as spikes and sharp waves, which reflect areas of hyper-excitable cortex that are prone to generating seizures, even when no seizure is occurring. EEG can also record ictal activity during a seizure, helping to confirm that events are epileptic rather than non-epileptic and providing information about seizure onset and spread.

EEG is useful for suggesting seizure localisation, particularly in focal epilepsy, as recurrent abnormalities over the same region indicate a likely seizure focus. EEG also helps classify seizure types, for example distinguishing focal seizures from generalised seizures based on whether abnormalities are localised or widespread across the scalp.

EEG provides information about functional cortical excitability rather than brain structure. It shows where abnormal electrical activity is occurring but does not identify the underlying cause. For this reason, EEG is used to detect epileptic activity and guide localisation, while structural imaging such as MRI is required to identify the cause. EEG and MRI are therefore complementary tools in epilepsy assessment.

What does “hyper-excitable cortex” mean?

It means:

A part of the brain is too easy to activate and fires when it shouldn’t.

Normally, brain cells are picky.
They fire only when they get the right signal.

In a hyper-excitable cortex:

• Neurones fire too easily

• Too many cells fire together

• The brain loses its normal balance between excitation and inhibition

Why is this a problem?

Because the brain depends on balance.

• Excitation = “go”

• Inhibition = “stop”

Hyper-excitability happens when:

• Excitation is too strong

• Inhibition is too weak

• Or both

When that balance tips, you get:

• Spikes on EEG

• Seizures

• Abnormal brain rhythms

What does it look like on EEG?

Hyper-excitable cortex produces:

• Spikes

• Sharp waves

• Spike-and-wave complexes

Important:

• A spike ≠ a seizure

• It means the cortex is capable of producing seizures

Think of it like dry grass:

• Dry grass doesn’t mean a fire is burning

• But it means a fire could start easily

What causes cortex to become hyper-excitable?

Common causes:

• Epilepsy

• Cortical malformations

• Tumours (irritating surrounding cortex)

• Scarring after injury or stroke

• Infection or inflammation

The lesion itself is often silent — it’s the irritated surrounding cortex that becomes hyper-excitable.

Why does this matter clinically?

Because:

• Hyper-excitable cortex explains why seizures recur

• It helps classify epilepsy

• It guides treatment (medication vs surgery)

In EEG interpretation:

• Spikes = hyper-excitability

• Fast evolving rhythms = seizure

• Slow waves = dysfunction or irritation

One-line exam definition (very safe)

Hyper-excitable cortex refers to brain tissue that fires excessively and synchronously due to reduced inhibitory control, predisposing to epileptiform activity.

Focal seizure — what it means

What’s happening in the brain

A focal seizure:

• Starts in one specific spot

• Comes from one side of the brain

• Begins in a particular network (e.g. motor, sensory, language)

That spot is hyper-excitable and misfires.

What it looks like clinically

Depends on where it starts:

• Motor area → twitching of one hand, face, or leg

• Sensory area → tingling, strange smells, visual flashes

• Language area → speech arrest

• Memory/emotion area → déjà vu, fear

The person may:

• Be aware (focal aware seizure)

• Or confused/unresponsive (focal impaired awareness)

What it looks like on EEG

• Abnormal activity starts in one region

• Often asymmetric

• May spread over time

If it spreads to the whole brain → secondary generalisation

What focal seizures usually mean

They suggest:

• A local brain problem

• Examples: tumour, scar, dysplasia, prior injury

That’s why focal seizures often trigger:

• MRI

• Surgical evaluation

• Sometimes SEEG or ECoG

Widespread (generalised) seizure — what it means

What’s happening in the brain

A generalised seizure:

• Involves both hemispheres from the start

• No single starting point

• Comes from brain-wide networks (often thalamo-cortical)

It’s a system-level problem, not a local one.

What it looks like clinically

Typical features:

• Sudden loss of awareness

• Bilateral movements

• No warning

• Very fast recovery (especially in absence seizures)

Examples:

• Absence seizures

• Generalised tonic–clonic seizures

• Myoclonic seizures

What it looks like on EEG

• Symmetrical activity on both sides

• No focal onset

• Classic example: 3 Hz spike–wave in absence epilepsy

What generalised seizures usually mean

They suggest:

• Genetic or developmental epilepsy

• Network-level dysfunction

• Not a single removable lesion

Surgery is usually not helpful.

Why this distinction matters (clinically & for exams)

Because it affects:

• Diagnosis

• Treatment choice

• Prognosis

• Whether surgery is considered

Raised pressure / hydrocephalus (deep system compression)

When pressure rises, deep midline systems get squished and the whole cortex gets “slowed down”:

• hydrocephalus

• diffuse cerebral oedema

• big bleeds / swelling causing global pressure effects

This matches what your lecturer said: deep systems get disrupted → generalised slowing.

How to read abnormal EEG: what these cases teach you

The core idea repeatedly emphasised in the lecture is that EEG shows how the brain is functioning, not what a lesion is called. Interpretation relies on recognising patterns and inferring the likely type and location of pathology from a small number of key features: whether activity is symmetrical or asymmetrical, the frequency of the signal (cycles per second), whether changes are focal or generalised, and whether the activity is rhythmic, irregular, or spiky.

Case 1: Slow wave focus due to glioma (TUMOR)
This EEG shows high-amplitude delta activity (around 1–3 Hz) confined to a single frontal region. The abnormality is focal, clearly asymmetrical, and occurs while the patient is awake, which makes it pathological. Focal slowing in an awake adult strongly suggests a local structural disturbance of cortex. Tumours themselves are electrically silent; the EEG abnormality arises from irritated cortex at the edges of the lesion. A key rule is that focal delta in an awake adult should be assumed to reflect a structural lesion until proven otherwise.

Case 2: Generalised delta due to hydrocephalus
Here the EEG shows delta activity that is symmetrical and maximal frontally on both sides, affecting large areas rather than a single region. This pattern represents generalised slowing and points to deep or diffuse pathology rather than a focal cortical lesion. Hydrocephalus fits this pattern because raised intracranial pressure compresses deep midline structures such as the thalamus and reticular system, disrupting the brain’s pacemaker mechanisms and producing bilateral slowing. Symmetrical frontal delta therefore suggests deep midline involvement rather than a tumour.

Case 3: Irregular slow waves due to encephalitis
This EEG shows slow activity that is irregular, disorganised, and lacks a clear rhythm. The abnormality is diffuse, involving both anterior and posterior regions, with no focal generator. This pattern reflects widespread cortical dysfunction and loss of synchrony. Encephalitis causes inflammation across cortex, subcortex, and white matter, producing chaotic brain activity rather than organised rhythms. Diffuse, irregular slowing is therefore typical of encephalopathy or encephalitis.

Case 4: Bilateral interictal spikes
In this case, sharp, fast transients are seen arising independently from both hemispheres. These are interictal spikes, meaning they occur between seizures rather than during one. Spikes indicate hyper-excitable, epileptogenic cortex but do not mean a seizure is happening at that moment. The presence of two independent spike foci has important clinical implications, as epilepsy with multiple foci is often harder to treat and may produce different seizure types. A key principle is that spikes reflect epileptic tendency, not seizures themselves.

Case 5: Focal seizure beginning on the left
This EEG shows sudden high-frequency activity starting in a single region (left central), evolving over time, spreading, and then slowing, followed by post-ictal slowing. This is an ictal EEG pattern, meaning a seizure is occurring during the recording. The focal onset indicates a focal seizure, with possible secondary generalisation. A left central onset is consistent with motor features involving the face or limbs, and post-ictal slowing reflects the recovery phase. Focal fast activity that evolves in time is characteristic of a focal seizure.

Case 6: Generalised absence seizure
This EEG demonstrates abrupt onset of symmetrical, generalised 3 Hz spike–wave activity, followed by a sudden return to normal. There is no focal onset, no evolution, and no post-ictal confusion. This pattern is classic for absence epilepsy, which presents clinically as brief lapses of awareness. A generalised 3 Hz spike–wave pattern is a hallmark of absence seizures.

Big-picture rules the lecturer wanted you to learn

Symmetry is critical: symmetrical abnormalities usually indicate deep or generalised pathology, while asymmetry points to focal cortical disease. Frequency matters: counting cycles per second helps identify abnormal rhythms, with delta in awake adults indicating pathology and 3 Hz spike–wave indicating absence epilepsy. The distinction between focal and generalised patterns guides interpretation, with focal slowing suggesting tumours or strokes, generalised slowing suggesting metabolic or infectious causes, irregular diffuse slowing suggesting encephalitis, and spikes indicating epileptogenic cortex. Above all, EEG shows brain function, not diagnosis: the same EEG pattern can have many causes, so EEG must always be interpreted alongside clinical findings and imaging.

1. How can the brain be affected even when there is no seizure?

A seizure is the loud, obvious problem.
But an excited cortex causes quiet, constant disruption in the background.

Think of brain activity like traffic on roads.

• Normal brain → cars move smoothly, lights work properly

• Excited cortex → traffic lights flicker randomly

Even if there’s no huge crash (seizure), traffic still doesn’t flow well.

2. Why normal thinking gets interrupted

An excited cortex:

• Fires when it shouldn’t

• Interrupts other signals

• Competes with normal processing

So when the brain tries to:

• Pay attention

• Store information

• Retrieve words

The abnormal activity gets in the way.

This means:

• Thoughts don’t fully form

• Signals are delayed or distorted

• Processing becomes inefficient

Not broken — noisy.

3. Effects on attention, memory, and speech

Attention

Attention needs stable networks.

If one area keeps misfiring:

• The brain keeps “checking” it

• Focus drifts

• Mental effort increases

This can look like:

• Inattention

• Slowness

• Fatigue

• “Zoning out” (even without seizures)

Memory

Memory depends on timing and coordination.

Excited cortex:

• Disrupts encoding (laying memories down)

• Interrupts consolidation (stabilising memories)

• Interferes with retrieval

So children may:

• Learn information

• But not retain it well

• Or recall it inconsistently

This is common in epilepsy even without frequent seizures.

Speech and language

Language relies on very precise timing.

If abnormal firing happens near language networks:

• Word retrieval becomes harder

• Fluency drops

• Comprehension may slow

In children:

• Language development can stall

• Skills may plateau rather than regress

This is why “benign” epilepsies are not always benign.

4. Why this is especially serious in children

Children’s brains are still building networks.

An excited cortex:

• Disrupts normal wiring

• Interrupts learning windows

• Forces the brain to “work around” noise

So instead of developing efficiently:

• Networks develop more slowly

• Or reorganise in less optimal ways

This can lead to:

• Long-term learning difficulties

• Executive function problems

• Language vulnerabilities

Even if seizures later stop.

5. Why excited activity spreads

Now to the spreading part — this is key.

Neurons are connected.
They talk to each other constantly.

When one area becomes over-excited:

• Nearby neurons are repeatedly stimulated

• Inhibitory control gets overwhelmed

• Excitation spreads outward

Think of:

• One person clapping → others join in

• One spark → grass catches fire

6. How excited cortex “pulls in” normal tissue

Normal brain tissue is not diseased, but it is connected.

Repeated abnormal firing:

• Lowers the firing threshold nearby

• Makes normal neurons easier to recruit

• Turns helpers into participants

Over time:

• The abnormal network grows

• More cortex becomes involved

• Seizures spread more easily

7. How focal seizures become generalised

A focal seizure:

• Starts in one area

If excitement spreads:

• It reaches both hemispheres

• Large networks synchronise

• The seizure becomes generalised

This explains why:

• Some patients start with focal symptoms

• Then lose awareness

• Then have whole-body involvement

It’s not sudden — it’s network recruitment.