Cerebral cortex and lobes

What it normally does

• The cortex is a map, and so is its blood supply. Motor cortex runs down the front lip of the central sulcus (precentral gyrus), sensory cortex down the back lip (postcentral gyrus), with the body laid out upside down and badly out of proportion — face and hand occupy more strip than the whole trunk (the homunculus). Draped over that map: the middle cerebral artery (MCA) feeds the lateral convexity — face, hand, arm and the language cortex; the anterior cerebral artery (ACA) feeds the medial strip where the leg and foot sit; the posterior cerebral artery feeds the occipital lobe and visual cortex. The frontal eye field, in the caudal middle frontal gyrus, drives the eyes to the opposite side and sits in MCA territory too.

  Explains why a stroke deficit reads backwards to a single artery — face and arm weak with the leg spared is MCA, leg alone is ACA, a hemianopia with no weakness is PCA — why the eyes deviate, and why a seizure that starts in the thumb marches to the face rather than the foot, because hand and face are neighbours on the strip.

• Language lives in one hemisphere: the left in about 95% of right-handed people and around 70% of left-handers (dominance). Two nodes and a cable. The inferior frontal gyrus (Broca) assembles the output and sits immediately next to the motor strip for face and hand. The posterior superior temporal gyrus (Wernicke) decodes what is heard and sits next to auditory cortex. The arcuate fasciculus joins them. All of it is MCA territory.

  Explains why aphasia nearly always means a left hemisphere lesion, why the type of aphasia tells you front or back of the sylvian fissure, and why Broca aphasia comes with a weak right face and arm while Wernicke aphasia often comes with no weakness at all.

• Attention to space is not shared evenly between the hemispheres. The left hemisphere attends mainly to the right half of the world; the right parietal cortex, especially the temporoparietal junction, attends to both halves. Together they give you a seamless field you never have to think about.

  Explains why a right parietal stroke leaves a patient behaving as though the left half of the world does not exist — and unaware anything is missing (neglect, anosognosia) — while the mirror-image left parietal stroke usually does not, because the intact right hemisphere still covers the right side. Note this is inattention, not blindness: the primary visual pathway can be entirely intact.

• Every cortical neuron sits between two opposing streams: glutamate excitation onto AMPA and NMDA receptors, and GABA inhibition — fast, through the chloride-permeable GABA-A receptor, and slower, through G-protein-coupled GABA-B. The pattern and rate of firing are set by voltage-gated sodium, potassium and calcium channels and by the vesicle machinery that releases transmitter. Healthy cortex holds that balance and fires in patterns — but the dense local connectivity that lets it fire in patterns also lets a patch fire all at once.

  Explains a seizure as a patch of cortex firing synchronously, so what the patient does depends on where the patch is and where the discharge spreads, and explains why most anti-seizure medicines are named by which part of that balance they touch: voltage-gated sodium channels (carbamazepine, lamotrigine, lacosamide), calcium channels (ethosuximide, gabapentinoids), GABA transmission (benzodiazepines, phenobarbitone, vigabatrin), the release machinery (levetiracetam at SV2A), or glutamate receptors (perampanel at AMPA) — with mixed-mechanism drugs such as valproate and topiramate that do several at once.

What goes wrong

• Cortical stroke — reading the artery off the patient← from “The cortex is a map, and so is its blood suppl…”

  An artery is blocked, usually by embolus from the heart in atrial fibrillation or from a carotid plaque. The cortex it feeds loses oxygen and the map goes dark in that vessel's shape. A cortical infarct removes functions, not just power: MCA takes the face and arm plus language on the left or spatial attention on the right, and takes the frontal eye field with it, so the eyes stop being driven across the midline and drift towards the damaged side. ACA takes the leg.

  Face and arm worse than leg = MCA. Leg worse than arm = ACA. The eyes look towards a destructive frontal lesion. Cortical signs (aphasia, neglect, field loss) mean cortex; a pure motor hemiparesis with face, arm and leg equally weak and no cortical signs suggests a small-vessel lacune in the internal capsule.

  You would find: Sudden, and maximal at onset. Right face and arm weak with the leg comparatively spared, eyes deviated to the left, no speech — left MCA. Leg weak with a near-normal arm — ACA. Non-contrast CT comes first, and its job is to exclude haemorrhage; it is often normal early in ischaemia, so a normal CT never excludes stroke. Stroke is common — the Stroke Foundation estimates tens of thousands of stroke events in Australia each year (of the order of 40,000–45,000). Aboriginal and Torres Strait Islander people have stroke at roughly 1.5–2 times the rate and at younger ages, driven by earlier hypertension and diabetes and by rheumatic heart disease and atrial fibrillation — so a 40-year-old with a sudden hemiparesis is not too young.

• Aphasia — Broca, Wernicke, conduction, global← from “Language lives in one hemisphere: the left in …”

  Damage to the dominant hemisphere language network, almost always left MCA. In front of the sylvian fissure (Broca) the output is broken: the patient knows what they want to say and cannot assemble it. Behind it (Wernicke) the input is broken: the machinery that produces fluent speech is intact and running, but nothing is checking it against meaning. Cut the cable between them (arcuate fasciculus) and both ends work but repetition fails. Lose the whole territory and you lose all of it (global aphasia).

  Fluent or not tells you front or back. Comprehension tells you whether Wernicke survived. Repetition tests the arcuate. A fluent patient talking rubbish who cannot follow a command has had a stroke until proven otherwise, not a delirium — and no drug treats the aphasia once the infarct is set.

  You would find: Test three things: fluency, comprehension, repetition. Broca — halting, effortful, telegraphic, comprehension relatively preserved (though complex grammar is often affected), patient visibly frustrated, and a weak right face and arm because the motor strip is next door. Wernicke — fluent, well-articulated nonsense with word substitutions, poor comprehension, patient untroubled, and often no weakness at all, which is why they get labelled confused or psychotic in the emergency department. Conduction — fluent and comprehends, but cannot repeat 'no ifs, ands or buts'. Then separate aphasia from dysarthria: an aphasic patient writes badly too, a dysarthric patient writes normally.

• Hemispatial neglect and anosognosia← from “Attention to space is not shared evenly betwee…”

  Right parietal and temporoparietal cortex, MCA territory. The right hemisphere's map of both halves of space is destroyed and the surviving left hemisphere only attends to the right. The left half of the world is not dark — it is not represented, so there is nothing missing for the patient to notice. The same right hemisphere damage frequently removes insight into the deficit itself (anosognosia).

  Neglect means right parietal until proven otherwise. Anosognosia is why they will not do the exercises and why they fall. Test it before discharge and before signing anything about driving. Sedating and anticholinergic drugs — antipsychotics, benzodiazepines, oxybutynin and the like — are associated with poorer post-stroke recovery and are best avoided where there is any alternative: the treatment here is rehabilitation, not a script.

  You would find: Eats only from the right of the plate, shaves half the face, catches the left doorframe with the wheelchair, crushes all twelve numbers into the right half of a drawn clock, bisects a line well to the right of centre. Extinction is the subtle form: each hand felt when touched alone, only the right when both are touched together. Check the visual fields separately — a left homonymous hemianopia is a different lesion, and that patient usually knows something is wrong and turns their head to compensate (the two can coexist). Neglect is one of the strongest predictors of poor rehabilitation outcome and of failing a driving assessment.

• Focal seizure from cortex, with or without spread to bilateral tonic-clonic← from “Every cortical neuron sits between two opposin…”

  A patch of cortex loses the balance between excitation and inhibition and fires synchronously. What you see is only the job that patch normally does; if the discharge spreads along the homuncular map, or across the corpus callosum to the other hemisphere, the semiology spreads with it. In adults the usual substrate is a cortical scar — old stroke, trauma, tumour, previous infection — which makes cortical stroke a leading cause of new epilepsy after the age of 60.

  Semiology is localisation. The aura tells you where it started; the postictal deficit tells you where it has been. Positive symptoms building over seconds is a seizure; negative symptoms maximal at onset is a stroke.

  You would find: Stereotyped, brief, positive symptoms that build over seconds. Temporal lobe — a rising sensation in the stomach, deja vu or an unpleasant smell, then a blank stare with lip-smacking and fumbling, then minutes of confusion; if it is the dominant temporal lobe the patient cannot speak properly afterwards. Motor strip — jerking that starts in the thumb and marches to the face (Jacksonian march), following the homunculus. Frontal — brief, violent, often nocturnal, bizarre enough to be dismissed as non-epileptic, but with fast recovery. Occipital — coloured circles, not the black-and-white zigzag of migraine aura. A first seizure in an adult earns imaging and an EEG, not just a label.

• Todd paresis — the seizure that looks like a stroke← from “Every cortical neuron sits between two opposin…”

  After a focal motor seizure the cortex that was firing is suppressed and hypoperfused, so the limb it controls is weak — the same map running in reverse. The weakness follows the homunculus and typically lasts minutes to hours (usually resolving well within 48 hours). If the seizure arose in the dominant temporal or frontal cortex, the postictal deficit is aphasia rather than weakness, which is even harder to tell from a stroke.

  The three common stroke mimics are seizure with Todd paresis, hypoglycaemia and migraine with aura. It matters because the next decision is thrombolysis. Guidelines still favour treating a disabling deficit that looks like a stroke when the history and imaging fit — thrombolysing a mimic carries a low haemorrhage rate, while missing a real stroke costs brain — but that judgement belongs to the stroke team, and the glucose is checked in every single patient first.

  You would find: Unwitnessed collapse, now a dense right hemiparesis and no speech: on the stroke call this is identical to a left MCA occlusion. The history separates them — a witnessed jerk, a bitten lateral tongue, incontinence, and a deficit that is improving rather than fixed — as does a known seizure focus or old cortical infarct. Check the glucose: hypoglycaemia produces both pictures and costs nothing to fix.

What we give, and how it works

Open a drug to see what it binds, what that does to the cell, and what you then see in the patient.