Key Neuroimaging Concepts For Rehab Experts

Bridging brain imaging and rehabilitation practice

Beginner · 12 chapters · 144 MCQs · 144 flashcards

This course equips rehabilitation professionals with essential knowledge of neuroimaging techniques, including MRI, CT, and fMRI. Participants will learn to interpret common findings and apply imaging insights to optimize patient assessment and treatment planning. Ideal for physiotherapists and occupational therapists seeking to enhance their clinical reasoning.

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What you'll learn

  1. Chapter 1: Imaging Sequences and Staged Stroke Rehabilitation

    This chapter explains how CT and MRI generate image contrast, how key MRI sequences, particularly diffusion-weighted imaging (DWI), are read in stroke, hemorrhage and traumatic brain injury (TBI), and how those findings shape safe, staged…

  2. Chapter 2: TBI Staging, Stroke Perfusion and Cord Compression

    This chapter links the imaging findings seen in traumatic brain injury, stroke, subarachnoid haemorrhage, multiple sclerosis and spinal cord compression to the pathophysiology, assessment and graded physiotherapy decisions that follow from…

  3. Chapter 3: DWI-ADC Pitfalls, DTI Tractography and MS Diagnosis

    This chapter links core neuroimaging principles (diffusion-based MRI, vascular imaging, and spinal cord imaging) to the clinical reasoning physiotherapists need when treating stroke, traumatic brain injury, subarachnoid haemorrhage,…

  4. Chapter 4: Stroke, ICH, MS Activity and Functional MRI Mapping

    This chapter links the imaging findings physiotherapists meet most often (acute stroke, intracerebral haemorrhage, multiple sclerosis, spinal cord injury, spinal metastases and functional MRI) to the clinical reasoning that guides safe…

  5. Chapter 5: DTI White Matter Damage, Tumour Patterns and Lacunar Stroke

    Neuroimaging findings, from conventional MRI to diffusion tensor imaging (DTI) and molecular PET, tell the physiotherapist what is damaged, how fast it is changing and what is safe to load, and so shape both prognosis and graded…

  6. Chapter 6: Tumour PET, Epilepsy SPECT, NMOSD and Parkinson DaTscan

    This chapter links the imaging findings in brain tumor, epilepsy, demyelinating disease, neuromyelitis optica, Alzheimer's disease and Parkinson's disease to the physiotherapy decisions they inform: safety, prognosis, outcome measure…

  7. Chapter 7: Spinal Cord Injury Prognosis, Hydrocephalus Gait and Migraine SPECT

    This chapter links imaging findings in spinal cord injury, hydrocephalus, migraine, Alzheimer's disease and lesion-mapping research to what a physiotherapist should examine, prioritise and avoid.

  8. Chapter 8: Abscess Versus Tumour, Carotid Doppler and Cerebral Palsy Patterns

    This chapter links structural and diffusion neuroimaging findings (traumatic brain injury, infection, tumour, metastases, carotid disease, cerebral palsy and spinal cord injury) to the clinical reasoning, outcome measurement and graded…

  9. Chapter 9: Cryptogenic Stroke, fNIRS Neurofeedback and Disorders of Consciousness

    A neuroimaging-informed approach to rehabilitation links what the scan shows (infarct, contusion, venous stenosis, nerve injury, network disruption) to what the patient can safely do and how they should be assessed, progressed and…

  10. Chapter 10: Perfusion Mismatch, MR Spectroscopy and Vestibular Imaging

    This chapter links advanced neuroimaging (perfusion MRI, spectroscopy, vascular imaging, spinal and vestibular imaging) to the clinical reasoning and safe, graded physiotherapy decisions needed for patients with aneurysmal subarachnoid…

  11. Chapter 11: Concussion Return to Play, Posterior Fossa Tumours and Wernicke

    Neuroimaging findings, from a normal conventional MRI after concussion to a perfusion mismatch on CT, define the pathophysiology, the safe exercise ceiling and the prognosis that a physiotherapist must plan around.

  12. Chapter 12: MR Spectroscopy, Cerebral Venous Thrombosis and Prion Disease

    This chapter links the neuroimaging modalities that rehabilitation clinicians meet most often (functional imaging, MR spectroscopy, diffusion tensor imaging, vascular imaging and neurodegenerative imaging) to bedside reasoning, outcome…

Free chapter

Chapter 1: Imaging Sequences and Staged Stroke Rehabilitation

This chapter explains how CT and MRI generate image contrast, how key MRI sequences, particularly diffusion-weighted imaging (DWI), are read in stroke, hemorrhage and traumatic brain injury (TBI), and how those findings shape safe, staged physiotherapy.

1. Imaging Fundamentals: CT versus MRI

CT measures X-ray attenuation, reported in Hounsfield units (HU). Air is black (about −1000 HU), CSF is dark (0–15 HU), white matter is darker grey (25–30 HU), gray matter is lighter (35–40 HU), acute blood is bright (about 50–80 HU), and bone is white. Non-contrast CT (NCCT) takes minutes, is widely available, is tolerant of patient movement and monitoring equipment, and is highly sensitive for acute blood. It is therefore the first-line study for suspected hemorrhage, acute stroke before thrombolysis, and acute head trauma.

MRI uses a strong magnetic field (1.5 T or 3 T) and radiofrequency pulses to excite hydrogen protons. Contrast depends on proton density and on relaxation times (T1, T2). MRI offers superior soft-tissue contrast, so it distinguishes gray from white matter and shows small brainstem, cerebellar and cortical lesions that CT misses. It is slower, more motion-sensitive and costlier.

MRI safety: Screen for non-conditional pacemakers or defibrillators, cochlear implants, ferromagnetic aneurysm clips, and orbital metal fragments. Gadolinium requires renal function checks. These are absolute screening issues, not rehab concerns, but therapists should know why a patient may have CT rather than MRI.

2. Core MRI Sequences

SequenceAppearanceMain use
T1Fat bright, CSF dark, gray darker than whiteAnatomy; subacute blood; contrast studies
T2CSF and edema brightGeneral pathology, chronic infarcts
FLAIRT2 with CSF suppressed; edema bright against dark CSFPeriventricular and cortical lesions, subacute infarct, SAH
DWI/ADCRestricted diffusion bright on DWI, dark on ADCAcute ischemia
GRE/SWIBlood products and calcium appear as signal voids ("blooming")Microbleeds, hemorrhage, diffuse axonal injury (DAI)
DTIFractional anisotropy (FA, 0–1) maps directional water diffusionWhite matter tract integrity

In DTI, water diffuses preferentially along intact axons (high FA). Axonal injury lowers FA. The corticospinal tract FA asymmetry is a research marker of motor recovery potential after stroke.

3. Pathophysiology of Stroke and What Imaging Shows

Ischemic stroke follows arterial occlusion, usually embolic (atrial fibrillation) or atherothrombotic (hypertension, diabetes). Energy failure causes Na⁺/K⁺-pump failure and cytotoxic edema, in which water shifts into cells and diffusion of water becomes restricted. The tissue consists of an infarct core and a salvageable penumbra. Hemorrhagic stroke (intracerebral hemorrhage, ICH; subarachnoid hemorrhage, SAH) follows vessel rupture, often related to chronic hypertension, anticoagulation, or aneurysm.

DWI shows restricted diffusion within minutes, as bright signal with a matching dark ADC. This distinguishes true acute infarct from T2 shine-through. ADC pseudonormalizes at around 1 week, while DWI may stay bright for 1–2 weeks. T2/FLAIR hyperintensity appears only after roughly 4–6 hours as net water uptake (vasogenic edema) develops. Therefore a DWI-positive, FLAIR-negative mismatch suggests onset within about 4.5 hours and supports thrombolysis in unwitnessed or wake-up stroke (WAKE-UP trial).

4. Acute Stroke Imaging Pathway

  1. NCCT head first: exclude hemorrhage, identify early ischemic signs (loss of gray–white differentiation, insular ribbon loss, sulcal effacement) and the hyperdense vessel sign (e.g., hyperdense MCA from intraluminal thrombus). NCCT may be normal in the first hours of ischemia.
  2. ASPECTS (Alberta Stroke Program Early CT Score): 10 points for MCA territory, one point deducted per region with early change. Scores of 6 or above generally identify patients with a smaller core suitable for thrombectomy.
  3. CT angiography identifies large-vessel occlusion (LVO). Suspect LVO with NIHSS ≥ 6–10 and cortical signs such as aphasia or neglect.
  4. CT perfusion or MRI DWI/perfusion selects patients beyond 6 hours. Thrombectomy may be considered up to 24 hours when a small core with a large penumbra is present (DAWN and DEFUSE-3 criteria).

Treatment windows: IV thrombolysis (alteplase or tenecteplase) is given within 4.5 hours of onset or last known well. Contraindications include any hemorrhage on CT, BP above 185/110 mmHg before treatment, glucose below 50 mg/dL, and therapeutic anticoagulation (for example, a DOAC within 48 hours).

A 72-year-old with atrial fibrillation, not anticoagulated, with right hemiparesis, aphasia and NIHSS 14 at 2 hours, is a thrombolysis candidate after a hemorrhage-negative NCCT. A hyperdense left MCA sign suggests LVO and warrants urgent CTA for thrombectomy.

5. Hemorrhage Imaging and Its Evolution

CT is the first-line study because acute blood is bright, rapid to detect, and the scan is fast. Blood becomes isodense in about 1–2 weeks and hypodense later. NCCT is close to 100% sensitive for SAH within 6 hours of onset on modern scanners, but sensitivity falls with time and with low hematocrit. In a 72-year-old on anticoagulants with thunderclap headache, vomiting and left weakness, a negative CT does not end the work-up. Next steps include CTA, repeat imaging, MRI with FLAIR/SWI, or lumbar puncture, according to local protocols.

MRI signal of blood by age:

  • Hyperacute (<24 h): oxyhemoglobin; T1 iso, T2 bright
  • Acute (1–3 days): deoxyhemoglobin; T1 iso/dark, T2 dark
  • Early subacute (3–7 days): intracellular methemoglobin; T1 bright, T2 dark
  • Late subacute (about 1 week to 1 month): extracellular methemoglobin; T1 bright, T2 bright
  • Chronic: hemosiderin rim; dark on T1 and T2, with blooming on GRE/SWI

GRE and SWI are the most sensitive sequences for chronic and microscopic blood, including cerebral microbleeds indicating amyloid angiopathy or hypertensive vasculopathy.

6. Traumatic Brain Injury: Pathophysiology and Imaging

TBI includes primary injury (focal contusion, epidural or subdural hematoma, DAI from rotational shear at the gray–white junction, corpus callosum and dorsolateral brainstem) and secondary injury (edema, raised intracranial pressure, ischemia, excitotoxicity). Severity is graded using the Glasgow Coma Scale: 13–15 mild, 9–12 moderate, 3–8 severe.

NCCT is the acute study for skull fracture, hematoma, contusion, midline shift and herniation. MRI is more sensitive for DAI and brainstem injury, where CT is often normal despite poor function. SWI shows punctate hemorrhages, and DTI shows reduced FA in affected tracts. Frontal and temporal contusions are common because of the skull's bony contours.

A 45-year-old woman 3 months after a motor vehicle collision with balance deficits and left-sided neglect should have imaging reviewed for right parietal or frontal contusion, right-hemisphere encephalomalacia, or DAI. A negative CT does not exclude diffuse injury.

7. Clinical Presentation and Localization

  • Left MCA: right hemiparesis (face and arm more than leg), right facial droop, expressive (Broca) aphasia with non-fluent speech and preserved comprehension.
  • Right MCA: left hemiparesis, left hemispatial neglect, anosognosia, visuospatial deficits.
  • ACA: leg-predominant weakness, abulia.
  • Posterior circulation: ataxia, vertigo, diplopia, crossed signs.
  • Hemorrhage: sudden severe headache, vomiting, rapid decline in consciousness. This presentation cannot be reliably separated from ischemia clinically, which is why imaging comes first.

Red flags during therapy: new headache, drop in GCS or alertness, new pupil asymmetry, vomiting, seizure, rising BP, or sudden neurological worsening should prompt immediate cessation of activity and medical review.

8. Assessment and Outcome Measures

  • NIHSS (0–42): 1–4 minor, 5–15 moderate, 16–20 moderate–severe, 21–42 severe.
  • Modified Rankin Scale (0–6): 0–2 functional independence.
  • Fugl-Meyer Assessment: upper limb 0–66, lower limb 0–34.
  • Muscle strength: MRC/Oxford 0–5. Spasticity: Modified Ashworth Scale 0–4.
  • Berg Balance Scale (0–56): below 45 indicates increased fall risk. TUG: above about 14 s suggests fall risk.
  • 10-Meter Walk Test: under 0.4 m/s indicates household ambulation, 0.4–0.8 m/s limited community, above 0.8 m/s community ambulation. 6MWT: the minimal clinically important difference after stroke is about 34 m.
  • Neglect: line bisection, star cancellation, Behavioural Inattention Test.
  • TBI: Rancho Los Amigos levels I–X; posttraumatic amnesia measured with the Galveston Orientation and Amnesia Test (GOAT; ≥75 indicates emergence).
  • Barthel Index (0–100) for ADLs.

9. Physiotherapy Management: Staged Approach

Acute phase (0–72 hours). Confirm imaging diagnosis, BP limits and mobilization orders. After thrombolysis, mobilization is generally deferred until about 24 hours and follow-up imaging exclude hemorrhagic transformation. After ICH, follow neurosurgical or stroke team BP limits and avoid Valsalva. Interventions include positioning, respiratory care, passive and active-assisted range of motion, and early sitting. The AVERT trial showed that very early, high-dose mobilization (out of bed within 24 hours, frequent and intensive) worsened 3-month outcomes (favorable mRS 0–2: 46% vs 50%). Therefore mobilize early but with modest, frequent sessions.

Subacute phase (days to 3 months). Highest neuroplastic potential.

  • Task-specific training: sit-to-stand 3 sets of 10 repetitions, step-ups, and overground gait training. Aim for 30–60 minutes, 5 days per week.
  • Body-weight-supported or high-intensity treadmill training, progressing speed toward 70–80% of maximum safe speed.
  • Constraint-induced movement therapy where the patient has at least 10° finger extension and 20° wrist extension: restraint of the less affected hand for up to 90% of waking hours, with intensive practice of 3–6 hours/day for 2 weeks.
  • Neglect: visual scanning training, limb activation, prism adaptation (about 10° rightward prisms, 2 sessions daily over 2 weeks), and environmental cueing from the neglected side.
  • Balance: progress from sitting reach to standing narrow-base, dual-task and perturbation training, 3 times weekly, targeting a Berg score of 45 or above.

Chronic phase (>3–6 months). Aerobic training: 20–60 minutes, 3–5 days per week, 40–70% heart-rate reserve (RPE 11–14), plus resistance training of 1–3 sets of 8–12 repetitions on 2 days per week. Monitor BP and use cardiac screening in patients with atrial fibrillation.

TBI-specific: In early recovery (Rancho IV–V), use structured, low-stimulation environments and short, repetitive sessions. Watch for heterotopic ossification, fatigue, and vestibular and oculomotor dysfunction. Avoid high-impact or contact exertion until medical clearance after concussion.

10. Evidence and Clinical Pearls

  • Imaging colors management: ask what the scan shows (infarct vs hemorrhage, territory, size, midline shift) before planning loading, positioning and BP-sensitive activities.
  • A normal early NCCT does not exclude stroke. A positive DWI with a matching ADC confirms acute infarction.
  • A bright DWI lesion with dark ADC is acute; bright DWI with bright ADC suggests T2 shine-through and not acute ischemia.
  • Dark signal on SWI/GRE signals blood or calcification. Many microbleeds raise concern about intensity of exertion and anticoagulation.
  • Lesion location predicts deficits: corticospinal tract involvement in the posterior limb of the internal capsule predicts poor hand recovery; right parietal lesions predict neglect.
  • Rehabilitation intensity and task specificity matter more than a single named technique (Winstein 2016).

11. Summary

CT is the fast first-line study for hemorrhage, acute stroke triage and TBI; MRI offers superior soft-tissue detail through T1, T2, FLAIR, DWI/ADC, SWI/GRE and DTI. DWI identifies acute ischemia within minutes, while SWI and DTI reveal hemorrhagic and axonal injury that CT misses. Physiotherapists who read imaging reports can anticipate deficits, recognize red flags, choose valid outcome measures, and apply staged, intensity-appropriate rehabilitation.

References

  1. Powers WJ, Rabinstein AA, Ackerson T, et al. Guidelines for the early management of patients with acute ischemic stroke: 2019 update. Stroke. 2019;50(12):e344–e418.
  2. Winstein CJ, Stein J, Arena R, et al. Guidelines for adult stroke rehabilitation and recovery. Stroke. 2016;47(6):e98–e169.
  3. AVERT Trial Collaboration Group. Efficacy and safety of very early mobilisation within 24 h of stroke onset (AVERT): a randomised controlled trial. Lancet. 2015;386(9988):46–55.
  4. Thomalla G, Simonsen CZ, Boutitie F, et al. MRI-guided thrombolysis for stroke with unknown time of onset (WAKE-UP). N Engl J Med. 2018;379:611–622.
  5. Nogueira RG, Jadhav AP, Haussen DC, et al. Thrombectomy 6 to 24 hours after stroke with a mismatch between deficit and infarct (DAWN). N Engl J Med. 2018;378:11–21.
  6. Greenberg SM, Ziai WC, Cordonnier C, et al. 2022 guideline for the management of patients with spontaneous intracerebral hemorrhage. Stroke. 2022;53(7):e282–e361.
  7. Carney N, Totten AM, O'Reilly C, et al. Guidelines for the management of severe traumatic brain injury, fourth edition. Neurosurgery. 2017;80(1):6–15.
  8. Billinger SA, Arena R, Bernhardt J, et al. Physical activity and exercise recommendations for stroke survivors. Stroke. 2014;45(8):2532–2553.

The other 11 chapters, all 144 MCQs and the flashcards are in the PhysioAI app.

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Practice questions

5 sample MCQs from this course. Tap a question to see the answer.

  1. A 72-year-old male with a history of hypertension and atrial fibrillation presents with sudden onset right-sided weakness and aphasia. Onset was 2 hours ago. NIHSS score is 14. He is not on anticoagulation. Vital signs are stable.

    1. What is the most appropriate initial neuroimaging study for this patient?

    • A. CT head without contrast
    • B. MRI brain with diffusion-weighted imaging
    • C. CT angiography with perfusion
    • D. MRI brain with contrast
    Show answer

    Answer: A. CT head without contrast is the first-line imaging for acute stroke to rule out hemorrhage before thrombolysis. While MRI DWI is more sensitive for early ischemia, it takes longer and may not be available emergently. CTA with perfusion is useful for thrombectomy evaluation but not initial. Contrast is not needed initially.

  2. A 25-year-old male involved in a high-speed motor vehicle collision arrives with a Glasgow Coma Scale of 10. He has a scalp contusion and was briefly unconscious. A CT head is ordered.

    2. What is the most likely finding on CT head in this patient?

    • A. Subdural hematoma
    • B. Epidural hematoma
    • C. Diffuse axonal injury
    • D. Cerebral contusion
    Show answer

    Answer: A. Subdural hematoma is common after acceleration-deceleration injuries, often from bridging vein rupture. It appears as a crescent-shaped hyperdensity along the convexity. Epidural hematoma is lentiform and usually from arterial injury, often with a lucid interval. DAI is not typically seen on CT; it requires MRI. Contusions are focal cortical hemorrhages.

  3. A 35-year-old female presents with intermittent numbness in her left leg and blurred vision in her right eye. She reports previous episodes of transient symptoms. MRI brain with contrast is performed.

    3. What is the most characteristic imaging finding for this patient's condition?

    • A. Single large ring-enhancing lesion in the frontal lobe
    • B. Multiple periventricular ovoid T2 hyperintensities with contrast enhancement
    • C. Diffuse leptomeningeal enhancement
    • D. Cortical ribboning on DWI
    Show answer

    Answer: B. Multiple periventricular ovoid T2 hyperintensities (Dawson fingers) with contrast enhancement are classic for multiple sclerosis. They represent demyelinating lesions. A single ring-enhancing lesion could be an abscess or tumor. Leptomeningeal enhancement suggests meningitis. Cortical ribboning is seen in Creutzfeldt-Jakob disease.

  4. A 22-year-old male sustained a fall from height and presents with paraplegia and loss of sensation below T10. MRI of the thoracic spine is performed 2 hours after injury.

    4. Which MRI finding is most indicative of a complete spinal cord injury?

    • A. Cord edema without hemorrhage
    • B. Cord hemorrhage with cord transection
    • C. Normal cord signal
    • D. Anterior cord syndrome pattern
    Show answer

    Answer: B. Cord hemorrhage and transection on MRI indicate a complete injury (ASIA A). Cord edema alone may be incomplete. Normal signal suggests no structural injury. Anterior cord syndrome is a clinical syndrome with preserved dorsal columns, not a specific MRI finding.

  5. A 65-year-old male presents with new-onset seizures and progressive left-sided weakness. MRI brain with contrast shows a lesion in the right temporal lobe.

    5. Which imaging feature is most suggestive of a glioblastoma multiforme?

    • A. Well-circumscribed, homogeneously enhancing mass
    • B. Irregular rim-enhancing mass with central necrosis and surrounding edema
    • C. Non-enhancing T2 hyperintense lesion in the cortex
    • D. Extra-axial enhancing mass with dural tail
    Show answer

    Answer: B. Glioblastoma typically appears as an irregular rim-enhancing mass with central necrosis and extensive vasogenic edema. Well-circumscribed homogeneous enhancement suggests meningioma. Non-enhancing T2 lesion could be low-grade glioma. Extra-axial mass with dural tail is typical for meningioma.

Flashcards

  • What is the primary advantage of MRI over CT for visualizing soft tissue pathology in the brain?

    MRI provides superior contrast resolution for soft tissues, allowing better delineation of white matter, gray matter, and lesions such as tumors or demyelination. CT is faster and better for acute hemorrhage or bony detail.

  • How does a T1-weighted MRI sequence differ from a T2-weighted sequence in appearance of CSF?

    On T1-weighted images, CSF appears dark (low signal) because it has long T1 relaxation time. On T2-weighted images, CSF appears bright (high signal) due to long T2 relaxation time.

  • What does restricted diffusion on DWI indicate in the setting of acute stroke?

    Restricted diffusion appears as bright signal on DWI with corresponding low ADC values, indicating cytotoxic edema from acute ischemia. This can be seen within minutes to hours of symptom onset.

  • What is the principle behind fMRI and how is it used for preoperative motor mapping?

    fMRI measures blood oxygen level-dependent (BOLD) signal changes related to neural activity. During motor tasks, activated motor cortex shows increased blood flow and oxygen consumption, allowing identification of eloquent cortex near lesions.

  • What does fractional anisotropy (FA) measure in diffusion tensor imaging (DTI)?

    FA quantifies the directionality of water diffusion, ranging from 0 (isotropic, random) to 1 (anisotropic, highly directional). Higher FA indicates more coherent white matter tracts, while lower FA suggests disruption.

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