Clinical Syndromes & Stroke Assessment

1. Clinico-Anatomical Localisation — the Central Skill

Stroke neurology is, at its heart, an exercise in reverse-engineering vascular anatomy from a bedside deficit. A 90-second focused examination — mental status, language, cranial nerves, motor, sensory, coordination, gait — should already place the lesion in one of a dozen recognisable territories before any imaging is obtained. This is not a parlour trick: pre-imaging localisation drives triage (anterior- vs posterior-circulation pathways diverge), explains apparent negative scans (lacunes are often invisible on early CT), and lets the clinician recognise the “stroke chameleons” that mimic non-vascular illness.

Three principles compress most of the syndromology — see Part II for the vascular map:

Memorising this single map — the homuncular layout draped over the MCA/ACA/PCA territories — is the most efficient single investment a clinician can make in stroke neurology. Eighty percent of bedside localisation reduces to reading the deficit off this picture.

2. Cortical Strokes — MCA Syndromes

The middle cerebral artery (MCA) is the largest terminal branch of the internal carotid and supplies most of the lateral hemispheric convexity, the deep grey nuclei via lenticulostriate perforators, and the insula. The MCA bifurcates within the Sylvian fissure into a superior (M2) division (frontal & rolandic cortex) and an inferior (M2) division (temporo-parieto-occipital cortex). Distinguishing these at the bedside has direct treatment implications — proximal M1 occlusion is a thrombectomy target; distal M3/M4 branch occlusions generally are not.

3. ACA Syndrome — the Leg-Predominant Stroke

The anterior cerebral artery supplies the medial frontal and parietal cortex — the homuncular “foot in the interhemispheric fissure.” ACA stroke is uncommon (~3% of ischaemic strokes) because the anterior communicating artery normally provides robust collateral, but when it occurs the syndrome is unmistakable.

• Contralateral leg > arm weakness with foot/hip predominance; face is spared (face is on the lateral convexity, MCA territory).
• Contralateral leg sensory loss in the same distribution.
• Abulia, apathy, akinetic mutism — from medial frontal / cingulate / supplementary motor area damage; the patient is awake but profoundly unmotivated, slow to respond, mute.
• Urinary incontinence — loss of cortical inhibition of the micturition reflex (paracentral lobule).
• Transcortical motor aphasia (dominant) — non-fluent but with preserved repetition; the perisylvian language network is spared.
• Frontal release signs — grasp, palmomental, rooting reflexes; alien hand phenomena if the corpus callosum (genu) is involved.
• Gait apraxia — the “magnetic gait” with feet glued to the floor, especially in bilateral ACA infarcts (e.g., azygous ACA variant or anterior communicating aneurysm rupture).

The recurrent artery of Heubner, a deep perforator from the proximal A1, supplies the head of caudate and anterior limb of internal capsule. Its occlusion produces a small lacune with a characteristic face-and-arm weakness and abulia — a useful counter-example reminding that ACA perforators do not reach the leg (which is supplied by distal cortical branches).

4. PCA Syndrome — the Visual-Cortex Stroke

The posterior cerebral artery is the terminal branch of the basilar; its cortical territory is the occipital lobe and the inferomedial temporal lobe, and its deep perforators (P1) supply the thalamus and midbrain. Hence three distinct PCA presentations:

5. Lacunar Syndromes — Fisher’s Five

C. Miller Fisher, working at the Massachusetts General Hospital in the 1960s, defined the modern concept of the lacune — a small (< 15 mm) deep infarct caused by occlusion of a single penetrating artery, almost always due to lipohyalinosis or microatheroma in chronically hypertensive small vessels. He correlated post-mortem cavities (the “lacunes” of Déjerine) with antemortem clinical syndromes, and from this work emerged the five classical lacunar syndromes that remain the bedrock of clinical neurology today (Fisher 1965, 1969, 1982).

The lacunar pearl: absence of cortical signs (no aphasia, no neglect, no hemianopia, no gaze deviation) in a patient with a focal motor or sensory deficit. The CT is often normal at presentation; DWI MRI reveals the small deep cavity. ~25% of all ischaemic strokes are lacunar.

These five accounts for > 90% of clinically pure lacunar presentations. Fisher additionally recognised many uncommon “atypical” lacunes (e.g., hemichorea-hemiballismus from subthalamic lacune, isolated dysarthria, isolated facial palsy), but the five are the canonical teaching set.

6. Brainstem Syndromes — the Eponym Forest

The brainstem is the most clinically rich tissue per cubic centimetre in the nervous system: a forest of cranial-nerve nuclei, ascending sensory tracts, and descending motor tracts packed into a structure the size of a thumb. Vascular insults produce highly stereotyped — and historically eponymous — syndromes. The unifying feature is the crossed sign: ipsilateral cranial-nerve palsy with contralateral long-tract (corticospinal or spinothalamic) findings localising to the level of the affected cranial nerve nucleus.

The eponym forest can feel arcane, but each label encodes a specific anatomy lesson. Wallenberg in particular is mandatory teaching: it is the most common brainstem stroke, frequently presents only with vertigo and dysphagia and is missed as “BPPV” or oesophageal disease, and the ipsilateral Horner syndrome is often the only quiet clue.

7. Cerebellar Stroke — the Quiet Killer

Cerebellar infarction (~3% of ischaemic strokes) presents with subtle and non-specific symptoms — vertigo, vomiting, headache, gait instability — that mimic peripheral vestibular disease and are often discharged as “labyrinthitis.” Yet cerebellar infarction has a uniquely lethal complication: oedematous expansion in the tight posterior fossa → fourth-ventricle compression, obstructive hydrocephalus, and brainstem herniation, often 24–72 h after onset.

Cerebellar infarcts > 3 cm or those involving the vermis carry the highest herniation risk; serial neuro exams in a stroke unit and early neurosurgical consultation for suboccipital decompression are life-saving. See Part VI for the imaging signs of impending posterior fossa decompensation.

8. Aphasias & Higher-Cortical Syndromes

Language is left-hemisphere dominant in > 95% of right-handers and ~70% of left-handers. The classical Wernicke-Lichtheim model (1885) divides perisylvian language into a posterior comprehension zone (Wernicke, BA 22), an anterior production zone (Broca, BA 44/45), and the connecting arcuate fasciculus. Strokes produce predictable patterns:

Repetition is the discriminator: spared repetition implies the perisylvian arc is intact — therefore the lesion lies outside it (transcortical / watershed). This single test elegantly maps the aphasic taxonomy onto vascular anatomy.

Non-dominant hemisphere syndromes

• Hemispatial neglect — failure to attend to contralateral (usually left) hemispace; right inferior parietal / TPJ. Patients shave half a face, eat half a plate, draw half a clock.
• Anosognosia — denial of deficit (Babinski 1914); the patient with dense left hemiplegia insists they can walk.
• Constructional apraxia — inability to copy a cube or draw a clock face accurately.
• Aprosodia — loss of emotional intonation (Ross 1981); flat speech and impaired emotional comprehension.

Dominant parietal — Gerstmann syndrome (1924)

Lesion of the dominant angular gyrus produces the tetrad of acalculia, agraphia, finger agnosia, right-left disorientation, often with a fluent aphasia or alexia. A neurological curiosity but a useful localiser.

9. The NIH Stroke Scale (NIHSS)

The NIH Stroke Scale (Brott et al., Stroke 1989) is the universal quantitative bedside tool for ischaemic-stroke severity. It comprises 15 items (a-1a, 1b, 1c, 2–11) summing to 0–42 points; higher scores reflect more severe deficit. It is treatment-relevant in three ways:

• LVO triage — NIHSS ≥ 6 has sensitivity ~80% / specificity ~80% for proximal large-vessel occlusion (M1, ICA, basilar) and is the de-facto threshold for transfer to a thrombectomy-capable centre.
• Treatment selection — NIHSS < 4 with non-disabling deficit may have an equivocal benefit-risk balance for IV thrombolysis (PRISMS trial); NIHSS > 25 increases haemorrhagic conversion risk.
• Outcome prediction — baseline NIHSS is the strongest single predictor of 90-day mRS; the “rule of fifths” (NIHSS / 5) loosely approximates 90-day disability category.

10. Pre-Hospital Severity Scales

The full NIHSS takes 6–10 minutes and requires neurological training; it cannot be used in the field by paramedics. A family of simplified pre-hospital scaleshas emerged, each designed to detect probable large-vessel occlusion with a 30-second exam to guide direct triage to thrombectomy-capable centres rather than the nearest emergency department. The trade-off is sensitivity vs simplicity.

All five scales perform broadly similarly — sensitivity 70–85%, specificity 70–90% for LVO — and the choice between them is largely a matter of regional training. The RACE and FAST-ED include a gaze item which improves specificity (forced gaze deviation is a robust cortical sign), at the cost of slightly more cognitive overhead than LAMS.

The downstream cascade — CT, CTA, perfusion, lysis, thrombectomy — is the subject of Part VI and Part VII. The clinical exam stops here, having earned the imaging and pointed it at the right vessel.