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Saturday, 26 July 2025

Clinical Cases in Seizure Localisation

 Recognising seizure types isn't just about memorising lists — it's about observing patterns, interpreting subtle clues, and linking symptoms to functional neuroanatomy. The ability to reason clinically, even from brief descriptions, is one of the most important skills you’ll develop as a future doctor. 

In this post, we’ll walk through a series of realistic case vignettes that should be a challenge for not just first years, but clinical second and third years as well. 

Take your time with each one — some may seem straightforward, others more ambiguous. That’s okay. Clinical reasoning is a skill, not an instinct — and every case you puzzle through builds it.



🧠 Case 1
A 21-year-old university student reports waking abruptly one morning to sudden, uncontrollable jerking in her left arm. The movements lasted less than a minute. She remained alert, remembered the episode clearly, and had no confusion or fatigue afterward.

Step-by-step reasoning:

  • The rhythmic, involuntary jerking suggests seizure activity involving the motor cortex, which controls voluntary movement.
  • The symptom is confined to the left arm, so the affected brain region is likely in the right hemisphere.
  • Why the opposite side? The brain controls movement contralaterally: the right hemisphere governs the left side of the body and vice versa.
  • Her awareness is preserved, which tells us the seizure likely stayed focal and didn’t spread to networks involved in consciousness.
  • The movements involve the arm, pointing us to the lateral part of the right precentral gyrus, or primary motor cortex, where the arm is mapped on the motor homunculus.

Summary:

🧠 Likely localisation: Right frontal lobe, primary motor cortex (arm region)

πŸ” Possible aetiology

    • Focal epilepsy (idiopathic or genetic)
    • Cortical dysplasia (a condition where the brain's outer layer (cerebral cortex) doesn't develop properly during foetal development, leading to abnormal brain cell organization)
    • Structural lesion (tumour, scar, cavernoma)
    • Post-traumatic origin
    • Electrolyte/metabolic derangement (less likely due to isolated focal feature)

🧠 Case 2
A 30-year-old software engineer describes brief episodes of tingling that start in his right foot and slowly move upward through his leg. Each event lasts about 30 seconds. He remains alert, can talk throughout, and feels fine afterward.

Step-by-step reasoning:

  • The symptom is a tingling sensation, often described as “pins and needles” or “electric” → this suggests abnormal activation of sensory pathways, rather than motor ones, suggesting involvement of the sensory cortex.
  • The fact that it starts in the right foot and ascends → gives us a map of which body part is involved and that the seizure activity seems to “march,” which is common in focal sensory seizures.
  • The right side of the body maps to the left hemisphere - because sensory input, like motor control, is processed contralaterally.
  • The foot and leg are represented on the medial surface of the postcentral gyrus (sensory homunculus), - the primary sensory cortex in the parietal lobe.
  • Since he’s fully conscious, the seizure likely remains focal and hasn’t spread to areas involved in awareness.
  • The lack of motor involvement, preserved awareness, and stereotyped nature of the episodes support a diagnosis of focal aware seizures, probably originating from the left parietal cortex.

Summary:

🧠 Likely localisation: Left parietal lobe, primary sensory cortex (leg region of the sensory homunculus)

πŸ” Possible aetiology:

  • Focal epilepsy involving the sensory cortex
  • Structural lesion near the sensory cortex (tumour, small stroke, malformation)
  • Migraine aura (less likely due to short duration and preserved function)
  • Multiple sclerosis (consider if there’s a history of transient sensory episodes anywhere else)
🧠 Case 3
A 25-year-old man describes occasional episodes where he hears a loud buzzing noise that isn’t coming from his environment. This is sometimes followed by faint, distorted voices. He remains still during the events and seems confused for a few minutes afterward, unable to recall the full episode.

Step-by-step reasoning:

  • - Hearing sounds that aren’t really there, especially buzzing and voices, suggests auditory hallucinations.
  • - These types of symptoms typically come from abnormal activity in the auditory cortex, which processes sounds - not your thoughts, but actual noise signals.
  • The auditory cortex is located in the temporal lobe, specifically on the superior temporal gyrus.
  • Since there's no clear left or right sidedness to the sounds, it could arise from either hemisphere.
  • The fact that he becomes confused after the event and can’t remember it well implies the seizure impaired his awareness — this suggests it affected deeper parts of the temporal lobe or spread to networks involved in memory and consciousness.
    • Those deeper structures include the hippocampus and limbic system, which are responsible for memory and emotional processing.

·        Postictal confusion usually means the brain needed time to recover — suggesting wider involvement beyond just the auditory cortex.

Summary

🧠 Likely localisation: Temporal lobe — likely beginning in the auditory cortex with spread to medial limbic structures.

πŸ” Possible aetiology:

  • Focal temporal lobe epilepsy
  • Cortical lesion near the auditory cortex (tumour, encephalitis, trauma)
  • Post-traumatic scarring or encephalitis
🧠 Case 4
A 19-year-old student sees bright flashes of light in her left visual field while reading. Within seconds, she stares blankly and stops responding to others in the room. After about a minute, she regains consciousness but feels exhausted and slightly confused.

Step-by-step reasoning:

  • The flashing lights indicate a problem with visual processing, which points to the visual cortex.
  • Since the lights are in her left visual field, the affected area is the right occipital lobe.
  • Why the opposite side? Like motor and sensory functions, vision is processed contralaterally — each visual field is mapped to the opposite occipital cortex, so your right visual cortex sees the left field of both eyes..
  • Her staring and lack of response tell us her awareness was impaired, meaning the seizure likely spread beyond the visual cortex (occipital lobe) to involve areas responsible for consciousness.
  • This suggests involvement of association areas or deeper networks connected to consciousness.
  • The postictal confusion is another clue that more than just visual processing was disrupted.

Summary:

🧠 Likely localisation: Right occipital lobe (visual cortex) with spread into adjacent areas affecting awareness

πŸ” Possible aetiology:

  • Occipital lobe epilepsy
  • Migraine with aura (consider if there’s associated headache, slower onset)
  • Focal-onset seizure with impaired awareness
  • Cortical malformation, stroke, or tumour in posterior brain
🧠 Case 5
A 22-year-old man suddenly stops talking mid-sentence. He appears alert but cannot say any words, though he gestures that he knows what he wants to say. After about 90 seconds, his speech returns fully.

Step-by-step reasoning:

  • This is a sudden loss of speech production, suggesting a problem with Broca’s area, which controls the motor side of language.
  • Broca’s area is located in the inferior frontal gyrus of the left hemisphere, which controls motor aspects of language.
  • How do we know it’s on the left? For most right-handed people (and many left-handers), language is lateralised to the left hemisphere.
  • His awareness is intact, so the seizure is likely focal and hasn’t spread to networks involved in consciousness.
  • The absence of comprehension issues or confusion suggests Wernicke’s area (responsible for understanding language) and limbic structures were unaffected

Summary

🧠 Likely localisation: Left frontal lobe — Broca’s area (motor language cortex).

πŸ” Possible aetiology:

  • Focal seizure affecting language motor cortex
  • Transient ischemic attack (consider in older or vascular-risk patients)
  • Structural lesion near language areas
  • Speech arrest due to psychogenic non-epileptic attack (PNES — less likely here)
🧠 Case 6
A 24-year-old woman is talking fluently but saying things that don’t make sense. Her sentences are grammatically correct but filled with random words. She seems unaware that her speech lacks meaning and becomes frustrated when people don’t understand her.

Step-by-step reasoning:

  • This sounds like receptive aphasia — the patient can speak clearly but doesn’t understand the problem with their language.
  • That points to Wernicke’s area, located in the posterior superior temporal gyrus on the left side (for most individuals).
  • Since she’s unaware of her speech errors, comprehension is impaired — that’s a hallmark of seizures in this region.
  • No mention of confusion or fatigue afterward → it could be a brief focal seizure limited to Wernicke’s area.

Summary:

🧠 Likely localisation: Left temporal lobe — Wernicke’s area.

πŸ” Possible aetiology:

  • Focal seizure affecting receptive language cortex
  • Stroke in posterior temporal region (less likely in young person without sudden onset)
  • Transient language disturbance from migraine aura
🧠 Case 7
A 35-year-old man is observed during a team meeting to suddenly stare blankly, fumble with his pen, and smack his lips repetitively. The episode lasts about 90 seconds. He doesn’t respond to questions and seems confused afterward, asking what just happened.

Step-by-step reasoning:

  • The automatisms (lip-smacking, fumbling) and impaired awareness are strong indicators of a focal seizure with impaired awareness.
  • These types of episodes are most commonly associated with the temporal lobe, especially the medial and association areas.
  • The temporal lobe contains deep structures like the hippocampus and amygdala that are involved in memory, emotion, and behaviour — which explains the blank stare and repetitive actions.
  • His postictal confusion supports the idea that the seizure disrupted normal network function, requiring recovery time.

Summary:

🧠 Likely localisation: Temporal lobe — association and medial limbic areas.

πŸ” Possible aetiology:

  • Focal temporal lobe epilepsy
  • Mesial temporal sclerosis
  • Complex partial seizure (older terminology)
  • Psychogenic non-epileptic seizure (consider if atypical features or emotional trigger)
🧠 Your Turn
A 20-year-old student describes a strange episode where she suddenly feels intense fear, followed by a wave of dΓ©jΓ  vu. She then begins fiddling with her necklace and smacking her lips unconsciously. Friends say she stared blankly and didn’t respond for about 90 seconds. She was confused afterward and couldn’t remember the event.

What can you tell from this presentation?

  • What kind of symptoms are being described?
  • Is awareness preserved or impaired?
  • Are there automatisms?
  • Which cortical and subcortical structures might be involved?
  • What hemisphere is likely affected?
  • How would you summarise the likely localisation and differential diagnosis?

 Let's reason this one through it together — every symptom is a clue, and your cortex is ready to connect the dots. πŸ§ πŸ•΅️‍♂️

Have a think about it, jot some points down on paper, and when you're ready, reveal the answer. 



Let’s walk through it step by step:

  • The episode begins with intense fear and dΓ©jΓ  vu → These are classic signs of a seizure originating in the temporal lobe, especially the limbic system (amygdala and hippocampus).
  • She then performs automatisms — fiddling with her necklace, lip-smacking — which strongly suggest involvement of association areas in the temporal lobe.
  • Blank staring and lack of response for ~90 seconds → Her awareness is impaired, meaning the seizure isn’t just focal, but likely involves medial temporal structures.
  • Postictal confusion and amnesia strengthen the suspicion of limbic system involvement, particularly the hippocampus (memory) and adjacent networks.

🧠 So what does this tell us?

  • The seizure likely started in the medial temporal lobe, especially near the amygdala or hippocampus, and spread within temporal circuits.
  • The constellation of emotion, memory, automatisms, and impaired awareness points strongly to focal temporal lobe epilepsy.

🧠 Summary:
🧠 Likely localisation: Medial temporal lobe, limbic system (amygdala, hippocampus)

πŸ” Possible aetiology:

  • Temporal lobe epilepsy (most likely)
  • Mesial temporal sclerosis (common underlying cause)
  • Focal seizure with impaired awareness
  • PNES (psychogenic non-epileptic seizure) — less likely, but consider if emotional triggers dominate or EEG is normal


Summary 

Clinical reasoning isn’t about instantly knowing the answer — it’s about making sense of what you see, hear, and know. These vignettes are deliberately brief, just like the fragments of information you’ll get on a busy ward round or in ED handover. 

Learning to ask: What does this suggest? What’s missing? What else could this be? is what turns observation into insight. It’s normal to feel uncertain at times — that’s the space where learning happens. 

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