Paces online support

08/10/2026

06/10/2026

Station 3 – Neurology: Stroke / Hemiplegia

PACES Online Support | Dr. Waleed Zeid

1. Case Scenario

This patient has presented with weakness affecting one side of the body. Please examine their neurological system, focusing on the relevant findings, and present your findings to the examiner.

Task given to candidate:

Perform a focused neurological examination (tone, power, reflexes, coordination, often face/speech) in the time allowed
Localise the lesion and characterise the pattern of weakness
Present findings and discuss differential diagnosis and management with the examiner

Note: Station 3 is examination-led. Ask brief, targeted questions during the examination (e.g., onset, speech, swallowing) rather than taking a full history.

2. History Taking

(Brief, targeted points to weave into the examination)

Key symptoms to ask about

Onset: sudden (vascular) vs. gradual (consider alternative causes — tumour, demyelination)
Time of onset/last known well (critical for acute stroke management decisions, even in a chronic stable case being examined for PACES)
Associated symptoms at onset: headache, loss of consciousness, seizure
Speech disturbance: expressive/receptive difficulty, slurred speech
Swallowing difficulty
Visual disturbance: loss of part of visual field, diplopia

Vascular risk factor screen

Hypertension, diabetes, hyperlipidaemia
Smoking, atrial fibrillation/palpitations history
Previous TIA/stroke history
Family history of stroke/cardiovascular disease

Functional/recovery history

Time since event (if this is a chronic/stable deficit being examined)
Degree of recovery, current function, rehabilitation received
Mobility aids, falls

ICE (Ideas, Concerns, Expectations)

Understanding of diagnosis and cause
Concerns about recurrence, recovery, independence
Questions about driving, return to work
3. Clinical Signs and Symptoms

General inspection

Facial asymmetry: unilateral facial droop (note whether forehead sparing — upper motor neuron pattern — or forehead involved — lower motor neuron pattern)
Posture: flexed arm, extended leg pattern typical of chronic upper motor neuron hemiparesis
Walking aids, orthoses (e.g., ankle-foot orthosis for foot drop)

Tone

Increased tone (spasticity) on the affected side — classically more pronounced in arm flexors and leg extensors ("pyramidal pattern")
Clasp-knife quality to spasticity

Power

Pyramidal pattern weakness: typically weaker in arm extensors/shoulder abductors and leg flexors on the affected side (extensors preferentially weak in arms, flexors preferentially weak in legs)
Test all major muscle groups systematically, grading with MRC scale

Reflexes

Hyperreflexia on the affected side
Extensor plantar response (positive Babinski sign) on the affected side
Clonus may be present

Coordination and gait

Circumducting gait (swinging the affected leg outward) if significant lower limb spasticity/weakness
Arm may be held flexed, not swinging normally

Cranial nerve/face assessment

Facial droop pattern: forehead sparing with UMN lesion (e.g., stroke — due to bilateral cortical innervation of the forehead) vs. forehead involvement with LMN lesion (e.g., Bell's palsy)
Speech assessment: dysarthria vs. dysphasia (expressive/receptive) — important to distinguish, and to localise (dysphasia suggests dominant hemisphere cortical involvement)
Visual fields: check for homonymous hemianopia or other field defects

Sensory examination

May show reduced sensation on the affected side if sensory pathways involved (parietal lobe or thalamic involvement)
Sensory/visual inattention or neglect (parietal lobe signs) — test with simultaneous bilateral stimulation
4. Differential Diagnosis

While "stroke" is often the underlying context for this examination pattern, the differential for a unilateral UMN pattern weakness includes:

Category Diagnosis Distinguishing Features
Most likely Ischaemic stroke Sudden onset, vascular risk factors, pyramidal pattern weakness, cortical signs (dysphasia, neglect) if cortical involvement
Vascular Haemorrhagic stroke May have more prominent headache, reduced consciousness at onset, often more acute deterioration
Vascular Lacunar stroke Pure motor or pure sensory deficit, no cortical signs (no dysphasia/neglect), small vessel disease risk factors
Structural Space-occupying lesion (tumour, abscess) More gradual onset, may have signs of raised ICP (headache, papilloedema), possible seizures
Demyelinating Multiple sclerosis Younger patient, other lesions/history of discrete episodes, relapsing-remitting pattern
Other Todd's paresis (post-ictal) Transient weakness after a seizure, resolves over hours
Functional Functional neurological disorder Inconsistent findings, positive signs of functional weakness (e.g., Hoover's sign)
5. Examiner Discussion

Q: How would you localise this lesion based on the examination findings?

Unilateral UMN pattern weakness with sparing of the forehead and presence of cortical signs (dysphasia, neglect, cortical sensory loss) localises to the contralateral cerebral cortex/subcortical region; a pure motor/sensory deficit without cortical signs suggests a lacunar (subcortical) stroke; brainstem involvement would typically show crossed signs (ipsilateral cranial nerve findings with contralateral limb weakness).

Q: What is the significance of forehead-sparing facial weakness?

The forehead receives bilateral cortical innervation, so a unilateral upper motor neuron lesion (e.g., stroke) spares forehead movement (patient can still wrinkle the forehead/close eyes on the affected side), while a lower motor neuron facial nerve lesion (e.g., Bell's palsy) affects the entire face including the forehead on the affected side — a classic localising distinction.

Q: What investigations would you request in acute stroke?

Urgent non-contrast CT brain (to exclude haemorrhage and guide thrombolysis/thrombectomy eligibility), blood glucose (exclude hypoglycaemia as a stroke mimic), ECG (screen for atrial fibrillation), bloods including clotting profile; further workup once stable includes carotid Doppler, echocardiogram, 24-hour ECG monitoring, and HbA1c/lipid profile to establish aetiology and guide secondary prevention.

Q: Outline your management approach for acute ischaemic stroke.

Hyperacute: IV thrombolysis (alteplase/tenecteplase) if within the appropriate time window and no contraindications; mechanical thrombectomy for large vessel occlusion within extended time windows in appropriate candidates
Acute supportive care: admission to a specialist stroke unit, monitor and manage blood pressure per protocol, maintain euglycaemia, swallow assessment before oral intake (aspiration risk), early mobilisation where appropriate
Secondary prevention: antiplatelet therapy (aspirin initially, often followed by clopidogrel) if not thrombolysed/no haemorrhage, statin therapy, blood pressure and diabetes control, anticoagulation if atrial fibrillation identified (after excluding haemorrhage and considering timing)
Rehabilitation: multidisciplinary input — physiotherapy, occupational therapy, speech and language therapy (for dysphasia/dysphagia), early supported discharge planning

Q: How would you distinguish dysphasia from dysarthria, and why does this distinction matter?

Dysarthria is a problem with the mechanical production of speech (articulation) with normal language content and comprehension, whereas dysphasia is a disorder of language itself (word-finding, comprehension, or both), reflecting dominant hemisphere cortical involvement — this distinction has important localising value and differing implications for the underlying lesion and rehabilitation approach.

Q: What is the significance of sensory/visual neglect in this examination?

Neglect (inattention to one side of space or body, often more pronounced for the left side with right parietal lesions) is a cortical sign indicating parietal lobe involvement, carries implications for rehabilitation and safety (e.g., falls, self-care), and should be actively tested for with tasks like simultaneous bilateral sensory stimulation.
6. Pearls
Know the pyramidal pattern of weakness (arm extensors/leg flexors preferentially weak) and the flexed arm, extended leg chronic posture — classic signs to describe confidently.
Forehead-sparing facial weakness is a key localising sign distinguishing UMN (central) facial weakness from LMN (peripheral) facial nerve palsy — a very frequently tested point.
Always distinguish dysphasia from dysarthria — this has real localising value and is a common area of confusion to clarify confidently.
Actively test for neglect/inattention — a cortical sign that is easy to miss but highly relevant to overall assessment and safety.
Remember that a pure motor or sensory deficit without cortical signs suggests a lacunar stroke, while cortical signs (dysphasia, neglect) suggest cortical/large vessel involvement — a key localising concept.
Know the time-critical nature of acute stroke management (thrombolysis/thrombectomy windows) even when discussing a chronic, stable deficit in the exam setting.
Emphasise the multidisciplinary rehabilitation approach (physiotherapy, OT, SALT) — stroke management extends well beyond the acute phase.
Close your presentation with a clear anatomical synthesis ("This patient has a right-sided spastic hemiparesis with forehead-sparing facial weakness and expressive dysphasia, consistent with a left cortical/subcortical lesion, most likely a previous ischaemic stroke") — precise localisation and synthesis are highly rewarded in Station 3

24/09/2026

Introduction
Imagine a disease that acts like a hacker, selectively stripping the insulation off the wiring in your brain and spinal cord, causing glitchy signals at random times and in completely different parts of the body. Multiple Sclerosis (MS) is the ultimate diagnostic puzzle in neurology. For clinical exams like PACES, mastering this topic requires you to act as a detective: finding evidence of lesions scattered across both space and time.
By completing this lesson, you will be able to:
Conduct a high-yield, targeted history to establish "dissemination in time."
Recognize key physical exam signs, including internuclear ophthalmoplegia (INO) and pyramidal weakness.
Synthesize clinical findings into a precise anatomical diagnosis.
Differentiate MS from its clinical mimics.
Outline the diagnostic criteria (McDonald criteria) and state-of-the-art management strategies.
The Art of Targeted History Taking
In PACES Station 3, time is your scarcest resource. Because this is an examination-led station, you must weave brief, high-yield questions directly into your physical exam rather than taking a traditional full history. Your primary goal during these quick questions is to uncover evidence of historical neurological events—proving "dissemination in time."
Make sure to ask about these classic MS historical clues:
Previous Discrete Episodes: Ask about prior self-limiting episodes of unilateral vision loss, limb weakness, numbness, or balance problems that resolved spontaneously.
Optic Neuritis: Have they ever experienced painful, one-sided vision loss or noticed that colors (especially bright red) looked washed out or faded?
Uhthoff's Phenomenon: Do their symptoms temporarily worsen when they get hot, such as after a hot shower, during exercise, or when running a fever?
Lhermitte's Sign: Do they experience an electric shock-like sensation running down their spine or limbs when they bend their neck forward?
Other Red Flags: Enquire briefly about bladder/bowel urgency or frequency, profound fatigue, and any mobility issues or cognitive processing delays.

Mapping the Lesions: Clinical Signs
When examining the patient, you are systematically hunting for signs that point to more than one anatomical location. This allows you to prove "dissemination in space" right at the bedside.
Keep a sharp eye out for these localized findings:
Cranial Nerves and Eyes
Relative Afferent Pupillary Defect (RAPD): Suggests optic nerve damage from previous or active optic neuritis.
Optic Disc Pallor (Optic Atrophy): Visible on fundoscopy as a pale disc, indicating historical optic nerve damage.
Internuclear Ophthalmoplegia (INO): A hallmark MS sign indicating a lesion in the brainstem's medial longitudinal fasciculus (MLF). On lateral gaze, the eye on the side of the lesion cannot pull inward (impaired adduction), while the opposite eye experiences rapid, involuntary shaking (nystagmus on abduction).
Limbs and Motor Systems
Pyramidal Weakness (Upper Motor Neuron Pattern): Look for increased muscle tone (spasticity), weakness that preferentially affects limb extensors in the arms and flexors in the legs, overactive reflexes (hyperreflexia), and an upward-pointing big toe (extensor plantar or positive Babinski response).
Cerebellar Signs: Remember the mnemonic DANISH:
Dysdiadochokinesia (impaired rapid alternating movements)
Ataxia (gait instability or limb clumsiness)
Nystagmus
Intention tremor (tremor that worsens as the hand approaches a target)
Speech pathology (scanning or slurred dysarthria)
Hypotonia
To wrap up your physical exam presentation to the examiner, synthesize your findings into a clear anatomical summary: "This patient has an internuclear ophthalmoplegia and pyramidal weakness in the legs, suggesting lesions at two separate anatomical sites (brainstem and spinal cord), which is highly consistent with multiple sclerosis."

Bedside Signs of Multiple Sclerosis
An anatomical infographic mapping the typical clinical signs of MS, including optic neuritis, INO in the brainstem, cerebellar 'DANISH' signs, and pyramidal weakness in the limbs.

Confirming the Suspicions: Diagnostics
To confirm a diagnosis of Multiple Sclerosis, we rely on the McDonald criteria. The core concept is simple: we must prove dissemination in space (lesions in at least two different typical central nervous system locations) and dissemination in time (lesions occurring at different times), while ruling out all alternative explanations.
When the examiner asks what investigations you would order, present your diagnostic plan logically:
MRI of the Brain and Spinal Cord (with Contrast): This is the gold standard. We look for characteristic demyelinating plaques in periventricular, juxtacortical, infratentorial, and spinal cord regions. Active lesions will light up with contrast injection.
Lumbar Puncture (CSF Analysis): We analyze the cerebrospinal fluid to look for oligoclonal bands. Finding these bands in the CSF, but not in the patient's blood serum, indicates localized immune activity in the central nervous system.
Visual Evoked Potentials (VEPs): This test measures how fast electrical signals travel along the optic nerve. A delayed response suggests silent, historical demyelination, even if the patient has never noticed visual symptoms.
Screening Bloods: Order blood tests to rule out mimics. These should include Vitamin B12 levels, inflammatory markers, an autoimmune/vasculitis screen, and NMOSD antibodies (AQP4) if atypical clinical features are present.
Recommended · Slide Deck

The MS Diagnostic Toolkit
A slide deck illustrating the McDonald criteria, characteristic MRI findings (periventricular and spinal lesions), CSF oligoclonal bands, and visual evoked potentials.

Differentiating MS from its Mimics
MS is a great mimic, but it has mimics of its own. It is vital to recognize the red flags that point toward alternative diagnoses during your clinical discussion:
Neuromyelitis Optica Spectrum Disorder (NMOSD): Characterized by severe, often bilateral optic neuritis and extensive spinal cord lesions (longitudinally extensive transverse myelitis). These patients test positive for the AQP4 antibody.
Acute Disseminated Encephalomyelitis (ADEM): A rapid, monophasic inflammatory attack that often follows an infection. It is significantly more common in children than adults.
Spinal Cord Compression: Unlike MS, spinal cord compression is a structural lesion. It presents with a clear, sharp sensory level on the abdomen or chest and completely lacks cranial nerve or visual involvement.
Multiple Small Vessel Strokes: Seen in older patients with cardiovascular risk factors (like high blood pressure or diabetes). The progression is typically stepwise rather than the classic relapsing-remitting spikes of MS.
Vitamin B12 Deficiency: Causes subacute combined degeneration of the spinal cord, affecting both the dorsal columns and corticospinal tracts, often accompanied by peripheral neuropathy and macrocytic anemia.
Functional Neurological Disorder: Characterized by inconsistent exam findings and positive signs of functional weakness, such as Hoover's sign (where weak hip extension normalizes when flexing the opposite hip against resistance).

Differential Diagnosis of Demyelinating Disorders
A mind map organizing the key clinical differences between MS, NMOSD, ADEM, B12 deficiency, and structural spinal lesions.

Managing the Journey
Managing Multiple Sclerosis requires a highly organized, multi-pronged approach that balances acute treatments, long-term disease modification, and symptom control.
Acute Relapses When a patient experiences a sudden, severe flare-up, the first-line treatment is high-dose corticosteroids (such as intravenous methylprednisolone). It is crucial to explain to the patient that while steroids speed up recovery from the current flare-up, they do not alter the long-term progression of the disease.
Disease-Modifying Therapies (DMTs) To prevent future relapses and slow down disability progression, we select DMTs based on how active the disease is:
First-line agents (moderate efficacy): Injectable or oral medications such as interferon-beta, glatiramer acetate, dimethyl fumarate, or teriflunomide.
High-efficacy therapies: Reserved for highly active disease, including monoclonal antibodies like natalizumab, ocrelizumab, alemtuzumab, or oral fingolimod. These require careful monitoring due to their complex side-effect profiles.
Symptomatic & Multidisciplinary Care Treating the daily impact of MS is just as vital as treating the disease itself:
Spasticity: Managed with muscle-relaxing medications like baclofen alongside intensive physiotherapy.
Fatigue: A common and disabling symptom that requires lifestyle adaptations and support.
Bladder Dysfunction: Managed using anticholinergic medications or training in clean intermittent self-catheterization.
Multidisciplinary Team (MDT): Involve MS specialist nurses, occupational therapists, physiotherapists, speech therapists, and psychological support professionals early in the process.

MS Management and Escalation Therapy
An audio overview discussing how clinicians manage acute relapses, select first-line versus high-efficacy disease-modifying therapies, and organize multidisciplinary care

Summary
Let's review the core clinical concepts for Multiple Sclerosis:
Dissemination in Time & Space: The foundation of MS diagnosis. History taking focuses on past discrete neurological episodes (time), while the exam looks for lesions in different parts of the central nervous system (space).
Classic Bedside Clues: Master the recognition of INO (MLF lesion), Uhthoff's phenomenon (heat sensitivity), Lhermitte's sign (neck flexion shock), and pyramidal signs (UMN weakness pattern).
Investigative Pillars: Use brain/spine MRI with contrast to visualize plaques, lumbar puncture to find CSF-restricted oligoclonal bands, and VEPs to identify subclinical optic nerve damage.
Strategic Management: Use high-dose steroids to accelerate recovery from acute relapses, escalate disease-modifying therapies (DMTs) based on disease severity, and coordinate a multidisciplinary team to manage symptoms like spasticity, fatigue, and bladder issues.