Overview
This lecture covers motor lesion patterns and their clinical use in localisation, then moves into Stroke (CVA) as the dominant cause of acute focal neurological deficit: its definition, scale, and the two underlying mechanisms (“block/bleed” — ischaemia and haemorrhage), the pathophysiology and imaging appearance of each, how lesion location produces particular sign patterns (anterior vs posterior circulation, cortical language/parietal signs), why identifying the exact cause matters for management, and the broad structure of stroke care. It closes with a case vignette (“Chris”) whose findings are given for practice localising a relapsing, multi-system neurological presentation from examination and investigation data alone.
Motor Lesion Patterns
Four clinical patterns of motor disturbance, each with a characteristic set of features:
- Lower motor neuron (LMN): weakness, wasting, decreased tone, decreased/absent reflexes.
- Upper motor neuron (UMN, “pyramidal”): weakness, increased tone, increased reflexes, plantar response change.
- Extrapyramidal: akinesia, rigidity, tremor.
- Cerebellar: ataxia, dysmetria, nystagmus.
UMN lesion, in detail: weakness; increased tone (spasticity); increased reflexes; no wasting; upgoing plantar response (positive Babinski sign).
Localising a UMN lesion by its accompanying features:
- Cortical lesion: UMN signs + language/perceptual/frontal abnormalities.
- Brain stem lesion: UMN signs + cranial nerve deficits, +/- sensory involvement.
- Spinal cord lesion: UMN signs + sensory pathway involvement, +/- local nerve root (LMN) signs.
Stroke/CVA: Definition, Burden, and Recognition
Definition: a rapidly developing focal (sometimes global) neurological deficit due to a vascular lesion, lasting longer than 24 hours (if the patient survives).
Mechanism/urgency: acute interruption of arterial supply to the CNS causes cerebral infarction (cell death), which is irreversible; 1.9 million neurons die per minute of lost blood supply — hence stroke is a medical emergency. [The transcript notes slide 9 repeats slide 7’s text verbatim, not a new point.]
Epidemiology:
- ~4.5 million stroke deaths per year worldwide.
- 7,000-10,000 strokes per year in NZ (half occur in people over 70).
- 1/3 of stroke patients die by 6 months (10% within 30 days).
- Most survivors are left with some ongoing disability; ~30% have permanent dependence on others.
- Stroke is therefore an important cause of both death and disability.
Act FAST — call 111. Face (smile: is one side droopy?), Arms (raise both: is one side weak?), Speech (speak a simple sentence: slurred or unable to?), Time (lost time could be lost brain — get to hospital fast). Stroke is a medical emergency.
Transient Ischaemic Attack (TIA)
- Focal neurological deficit, rapid onset, lasting minutes to hours — by definition under 24 hours.
- Complete recovery, with no evidence of infarction.
- Tends to recur, and a stroke occurring after a TIA tends to be more severe.
- Prognostic marker: 1/6 of TIA patients progress to CVA within 5 years; 1/4 are dead within 5 years.
Mechanisms of CVA: “Block / Bleed”
Two principal mechanisms, plus rarer others:
- Ischaemia (~80% of CVAs).
- Haemorrhage (~20%): intracerebral or sub-arachnoid.
- +/- other causes, e.g. infection or profound cerebral hypoperfusion, which can also lead to infarction.
Ischaemic stroke subtypes:
- Thrombosis (2/3 of ischaemic strokes; “brain attack”): occurs in medium-sized arteries, due to atherosclerosis, usually in the presence of plaque rupture.
- Embolism (1/3): originates from a site outside the brain (left atrium, left ventricle, or carotid artery). Atrial fibrillation is a risk factor, risk-stratified using CHADS-VASc. On ECG, AF shows irregular distances between complexes and no obvious P waves.
Ischaemic pathophysiology: neuronal injury results from lack of oxygenation and nutritional support, progressing to damage then death. Damage may be stopped or reversed with early reperfusion, and possibly decreased with neuroprotectants (e.g. antioxidants, free radical scavengers) — the slide marks both of these with ”?”, i.e. as uncertain/investigational rather than established.
Haemorrhagic stroke pathophysiology: direct neuronal injury from decreased perfusion, pressure effects (swelling), vasospasm (causing adjacent ischaemia), and neurotoxicity. Haemorrhage tends to have more global effects, since it is not restricted to a vascular territory, and carries higher early mortality than ischaemic stroke.
Imaging appearance: ischaemic infarcts appear hypodense (dark) on CT — e.g. an acute right middle cerebral artery (RMCA) territory infarct, and a large right ischaemic infarct at day 7 showing more extensive hypodensity/demarcation than the acute image. Haemorrhage appears hyperdense (bright white) on CT.
Transcript flags: slide 10 shows an unlabelled CT with a hypodense area similar to the labelled RMCA image, but with no caption identifying it. Slide 11 shows an unlabelled gross post-mortem brain photograph with no caption; its purpose in the sequence (e.g. normal comparison) is not stated. Slide 31 shows an unlabelled CT with a hyperdense lesion, again without a caption.
Localising Signs and Lateralisation
- Signs/symptoms depend on the location of the lesion; weakness is the most frequent sign, usually presenting as a UMN pattern, +/- localising signs.
- Pathways cross: a right-sided stroke produces left-sided body signs, and a left-sided stroke produces right-sided body signs (contralateral relationship).
- Haemorrhagic infarcts tend to “ignore” vascular boundaries, unlike ischaemic infarcts which respect vascular territories.
Anterior vs posterior circulation stroke features:
| Anterior circulation | Posterior circulation |
|---|---|
| Unilateral weakness | Unilateral weakness/sensory loss |
| Unilateral sensory loss | Cranial nerve signs |
| Dysphasia | Nausea and vomiting |
| Sensory inattention | Incoordination |
| Visual field defect | Diplopia / disconjugate eyes |
Non-specific features that can occur with either: dysphagia, incontinence, and rarely, loss of consciousness.
Cranial nerve level reference, used to localise posterior circulation (brainstem) lesions via cranial nerve signs:
- Midbrain: CN 2, 3, 4.
- Pons: CN 5, 6, 7, 8.
- Medulla: CN 9, 10, 11, 12.
Transcript flag: a labelled visual pathway diagram (slide 25) shows the left/right visual fields projecting via temporal/nasal retina to the optic chiasm, then via the pulvinar nucleus, lateral geniculate nucleus, superior colliculus, and optic radiation to the primary visual cortex — illustrating contralateral visual field representation. It is a stock/textbook diagram; the slide itself does not state its specific clinical link to the stroke topic.
Major Cortical Signs
Language impairment (dysphasia/aphasia), including impaired reading and writing, usually from left cortex lesions:
- Non-fluent/expressive aphasia: Broca’s area, frontal lobe cortex, close to the motor cortex.
- Fluent/receptive aphasia: Wernicke’s area, superior temporal lobe.
Apraxia and agnosia, typically from right parietal cortex lesions:
- Apraxia: inability to process, plan, or sequence motor tasks, not explained by other deficits (e.g. dressing apraxia).
- Agnosia: inability to process sensory information — includes visual and sensory inattention.
Why Precise Diagnosis Matters, and Management
Reasons precise diagnosis matters:
- Identify the cause — anything reversible, or to prevent extension.
Don't anticoagulate a haemorrhage. Also anticipate subsequent problems (e.g. aspiration), and use the diagnosis to inform prognosis.
Care spans:
- Acute: ABC, and (marked uncertain on the slide) thrombolysis.
- Prevent extension: (marked uncertain) antiplatelet/anticoagulation, and blood pressure control.
- Prevent secondary problems: infection, DVT, blood pressure.
- Rehabilitation: mobilise, eat, speak, activities of daily living, mood, life changes — delivered via a multidisciplinary team (nurses, physiotherapy, occupational therapy, speech-language therapy, psychology, social work, doctor, plus family/community).
Transcript flag: slide 34 shows an unlabelled mid-sagittal MRI with no caption or highlighted lesion; it appears to introduce the case study that follows but its specific relevance is not stated on the slide.
Case Vignette: Chris
Chris, 35 years old, female. History and findings as given, for practising localisation:
- Longstanding history: heat intolerance precipitating a stumbling gait and falls; visual acuity that fluctuated periodically over several years.
- Two months ago: became sick with flu, and her neurologic condition worsened — she could not hold objects in her hands, had significant tremors and severe exhaustion, and had several bad falls. She then abruptly developed a right hemisensory deficit.
- Current problems: weak and numb on the right side; impaired bladder function (multiple voids each morning, nocturia x3), now incontinent and pad-dependent during the day; persistent balance problems with a spinning sensation; extreme fatigue; a tendency to aspirate both liquids and solids; continuous tinnitus with hearing loss, more prominent on the left; impaired short-term memory; irritability.
- Motor exam: decreased finger dexterity; bilateral hand weakness; relatively normal strength in the upper extremities; decreased rapid alternating movements in both upper extremities, with dysdiadochokinesia in the left hand; mild paraparesis in both legs without severe spasticity; reflexes brisk at ankles and knees; bilateral extensor toe signs (positive Babinski) present.
- Sensory exam: paresthesia on the right to touch; decreased pain sensation on the right, diffusely; mild vibratory sense loss in the distal lower extremities.
- Gait: tandem gait unstable and slow; at times requires a wheelchair.
- Investigations: MRI revealed multifocal white matter disease — areas of increased T2 signal in both cerebral hemispheres. Spinal tap revealed oligoclonal bands in the CSF. Visual evoked response testing was abnormal, with slowed conduction in the optic nerves. Imaging shown: two axial T2/FLAIR MRI images with multiple bright periventricular/white-matter lesions in both hemispheres, and one sagittal MRI with arrows indicating periventricular/corpus callosum lesions.
Transcript flag: the slide describes these findings (multifocal white-matter lesions, CSF oligoclonal bands, slowed optic nerve conduction) but does not explicitly name the diagnosis. No diagnosis is stated beyond what the slide gives.
Self-test
- List the four motor lesion pattern categories and the clinical features associated with each.
- Define the clinical features of a pure upper motor neuron (UMN) lesion.
- Describe how the accompanying features of a UMN lesion are used to localise it to the cortex, brain stem, or spinal cord.
- Define stroke/CVA.
- Explain why stroke is described as a medical emergency, using the figure given for neuronal loss.
- Describe the FAST mnemonic and what each letter checks for.
- Distinguish a TIA from a stroke, including the time criterion and outcome.
- Why is a TIA considered an important prognostic marker rather than a benign event?
- List the two main mechanisms of CVA and their approximate proportions, and name the two subtypes of haemorrhage.
- Distinguish thrombotic from embolic ischaemic stroke, including the vessels/sources typically involved and the relative proportion of each.
- A patient with known atrial fibrillation has a sudden focal neurological deficit. Explain the likely mechanism, and describe how AF appears on ECG.
- Describe the pathophysiological steps by which ischaemia leads to neuronal death, and name two strategies suggested to reduce or reverse this damage.
- List the mechanisms by which haemorrhage causes direct neuronal injury.
- Explain why haemorrhagic stroke tends to have more global effects and higher early mortality than ischaemic stroke.
- Describe how ischaemic and haemorrhagic lesions differ in appearance on CT.
- Explain the contralateral relationship between the side of a stroke lesion and the side of the body affected.
- Distinguish the typical clinical features of anterior circulation stroke from posterior circulation stroke.
- Which cranial nerves localise to the midbrain, pons, and medulla respectively, and how is this used clinically?
- Distinguish non-fluent (expressive) aphasia from fluent (receptive) aphasia, including the cortical area and lobe involved in each.
- Distinguish apraxia from agnosia, including the cortical area typically responsible.
- List the key clinical reasons why identifying the precise cause of a stroke matters.
- Outline the broad components of stroke care from acute presentation through rehabilitation.
- Chris (35F) has a longstanding relapsing history of heat-intolerant gait disturbance, fluctuating visual acuity, later tremor/weakness, and an abrupt right hemisensory deficit, with exam findings of bilateral cerebellar signs, mild paraparesis with brisk reflexes and bilateral extensor toe signs, and right-sided sensory loss. Explain which components of her presentation localise to the cerebellum, which to the corticospinal (UMN) pathways, and which to sensory pathways.
- What did Chris’s MRI, CSF, and visual evoked response findings show, and why do these findings point to a multifocal rather than single-lesion process (without naming a diagnosis beyond what the slide states)?
Answers
Reveal answers
- LMN: weakness, wasting, decreased tone, decreased/absent reflexes. UMN: weakness, increased tone, increased reflexes, plantar change. Extrapyramidal: akinesia, rigidity, tremor. Cerebellar: ataxia, dysmetria, nystagmus.
- Weakness, increased tone (spasticity), increased reflexes, no wasting, upgoing plantar response (positive Babinski).
- A cortical lesion adds language/perceptual/frontal abnormalities to the UMN signs; a brain stem lesion adds cranial nerve deficits (+/- sensory); a spinal cord lesion adds sensory pathway involvement (+/- local nerve root/LMN signs).
- A rapidly developing focal (sometimes global) neurological deficit due to a vascular lesion, lasting longer than 24 hours (if the patient survives).
- Because the interruption of arterial supply causes irreversible cerebral infarction, and 1.9 million neurons die every minute the blood supply is lost — so delay directly costs brain tissue.
- Face: is one side droopy (ask to smile)? Arms: is one side weak (raise both arms)? Speech: is it slurred or absent (speak a simple sentence)? Time: lost time is lost brain — get to hospital fast/call 111.
- A TIA is a focal neurological deficit with rapid onset lasting minutes to hours, by definition under 24 hours, with complete recovery and no evidence of infarction; a stroke’s deficit lasts longer than 24 hours and reflects infarction.
- Because TIAs tend to recur, and a stroke following a TIA tends to be more severe; about 1/6 of TIA patients progress to CVA within 5 years and 1/4 are dead within 5 years.
- Ischaemia (~80%) and haemorrhage (~20%); haemorrhage subtypes are intracerebral and sub-arachnoid.
- Thrombosis (2/3) occurs in medium-sized arteries due to atherosclerosis, usually with plaque rupture. Embolism (1/3) originates from a site outside the brain (left atrium, left ventricle, or carotid), with AF as a risk factor.
- AF predisposes to clot formation (e.g. in the left atrium) which can embolise to the brain and cause an embolic ischaemic stroke. On ECG, AF shows irregular distances between complexes and no obvious P waves.
- Lack of oxygenation and nutritional support causes neuronal injury, progressing to damage and then death; damage may be stopped/reversed with early reperfusion, or reduced with neuroprotectants such as antioxidants or free radical scavengers (both marked as uncertain/investigational on the slide).
- Decreased perfusion, pressure effects (swelling), vasospasm (causing adjacent ischaemia), and neurotoxicity.
- Because haemorrhage is not restricted to a single vascular territory, its effects are more global, causing higher early mortality than ischaemic stroke.
- Ischaemic infarcts appear hypodense (dark) on CT; haemorrhage appears hyperdense (bright white) on CT.
- Motor and sensory pathways cross, so a right-sided stroke/lesion produces signs on the left side of the body, and a left-sided stroke/lesion produces signs on the right side of the body.
- Anterior circulation: unilateral weakness, unilateral sensory loss, dysphasia, sensory inattention, visual field defect. Posterior circulation: unilateral weakness/sensory loss, cranial nerve signs, nausea and vomiting, incoordination, diplopia/disconjugate eyes.
- Midbrain: CN 2, 3, 4. Pons: CN 5, 6, 7, 8. Medulla: CN 9, 10, 11, 12. Cranial nerve signs help localise a posterior circulation (brainstem) lesion to a specific level.
- Non-fluent/expressive aphasia arises from Broca’s area, frontal lobe cortex close to the motor cortex. Fluent/receptive aphasia arises from Wernicke’s area, superior temporal lobe.
- Apraxia is an inability to process, plan, or sequence motor tasks not explained by other deficits (e.g. dressing); agnosia is an inability to process sensory information (visual and sensory inattention). Both are typically associated with right parietal cortex lesions.
- To identify anything reversible or that could prevent extension; to avoid anticoagulating a haemorrhage; to anticipate subsequent problems (e.g. aspiration); and to inform prognosis.
- Acute care (ABC, possible thrombolysis), preventing extension (possible antiplatelet/anticoagulation, BP control), preventing secondary problems (infection, DVT, BP), and multidisciplinary rehabilitation (mobilise, eat, speak, ADLs, mood, life changes — nurses, physio, OT, SLT, psychology, social work, doctor, family/community).
- Cerebellar: decreased rapid alternating movements bilaterally and dysdiadochokinesia in the left hand, unstable/slow tandem gait, heat-intolerant stumbling gait. Corticospinal (UMN): mild paraparesis in both legs, brisk reflexes at ankles/knees, bilateral extensor toe signs, without severe spasticity. Sensory: right-sided paresthesia to touch, decreased pain sensation on the right, and mild vibratory sense loss in the distal lower extremities.
- MRI showed multifocal white matter disease with increased T2 signal in both cerebral hemispheres; CSF showed oligoclonal bands; visual evoked response testing showed slowed optic nerve conduction. Together these show lesions in multiple, separate white-matter locations (cerebral hemispheres and optic nerves) rather than a single focal lesion, consistent with a multifocal disease process — the slide does not name the diagnosis, so none is given beyond these findings.