Module 3C Neurology and Vision - LOs Flashcards
What are the key types of squint (strabismus)?
- Esotropia: Eye turns inward.
- Exotropia: Eye turns outward.
- Hypertropia: Eye turns upward.
- Hypotropia: Eye turns downward
What are the symptoms of squint (strabismus)?
- Abnormal eye alignment (noticed by the patient or others).
- May be asymptomatic or cause - double vision (in adults) OR reduced visual acuity (amblyopia in children)
What are the two main types of diplopia?
- Monocular diplopia - persists when one eye is closed (caused by refractive errors, cataracts, etc.).
- Binocular diplopia - resolves when either eye is closed (caused by misalignment of the eyes, e.g., cranial nerve palsy or strabismus).
What examination findings are important in squint and diplopia?
- Visual Acuity: Check for reduced vision.
- Ocular Alignment: Use cover-uncover and alternate cover tests to detect tropias or phorias.
- Eye Movements: Assess extraocular muscles in 9 cardinal directions.
- Pupils: Check for anisocoria or afferent pupillary defect.
- Fundoscopy/Slit-Lamp Examination: Look for papilloedema, optic neuritis, or vascular changes.
- Neurological Exam: Identify cranial nerve palsies or systemic signs.
What are the key investigations for squint and diplopia?
- Blood tests: FBC, ESR, CRP (e.g. giant cell arteritis) + TFTs (e.g. thyroid eye disease).
+ glucose and HbA1c (e.g. diabetic cranial neuropathy) - Imaging: CT/MRI Orbit or Brain for trauma, mass, or intracranial pathology.
- Referral - orthoptic assessment to measure strabismus angle and binocular vision
What are the common differentials for squint (strabismus)?
Congenital/Developmental:
- Congenital esotropia or exotropia, craniosynostosis
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Acquired:
- Neurological: Cranial nerve palsy (III, IV, VI).
- Orbital pathology: Tumors, trauma, thyroid eye disease.
- Refractive error: Accommodative esotropia.
What are the common differentials for diplopia (blurred vision)?
Monocular Causes:
- Refractive error (e.g., astigmatism).
- Cataracts.
- Retinal disorders (e.g., macular hole)
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Binocular Causes:
- Cranial nerve palsies (III, IV, VI): Due to diabetes, aneurysm, or trauma.
- Orbital causes: Thyroid eye disease, trauma, or tumor.
- Myopathy: Myasthenia gravis.
- Brainstem lesions: Stroke, MS.
What is the initial management of squint (strabismus) in children?
- Urgent referral to ophthalmology/orthoptics to prevent amblyopia.
- Refractive correction: Glasses for accommodative strabismus.
- Occlusion therapy: Patching the good eye to prevent amblyopia.
- Surgery if non-surgical measures fail
What is the initial management of diplopia?
- Urgent referral if associated with systemic signs (e.g., headache, nausea, or pupil involvement).
- Treat the underlying cause (e.g., steroids for giant cell arteritis, thyroid treatment for thyroid eye disease).
- Temporary relief: Prism glasses or patching to alleviate diplopia.
What is suppression, and why does it occur?
- Suppression occurs when the brain ignores input from the deviating eye to avoid diplopia (double vision) and confusion
- It is a protective mechanism but can lead to amblyopia if prolonged.
What is amblyopia, and what causes it?
- Amblyopia is a reduction in visual acuity due to abnormal visual experiences, such as strabismus, anisometropia, or visual deprivation
- The brain relies on the better eye, weakening the affected eye
- sometimes referred to as a “lazy eye”
What is eccentric fixation?
Eccentric fixation occurs when the brain shifts fixation to a non-foveal retinal point in the amblyopic eye, impairing fine vision.
What is anomalous retinal correspondence (ARC)?
ARC is a sensory adaptation in which the brain remaps input from the deviating eye to align with the non-deviating eye, preventing diplopia but disrupting binocular vision and stereopsis.
How does sensory adaptation affect binocular vision and depth perception?
Suppression or ARC can result in a loss of binocular vision and stereopsis (depth perception).
How are refractive errors corrected in children with amblyopia?
Corrective lenses (glasses or contact lenses) are used to equalize refractive errors, such as myopia, hyperopia, or astigmatism, to reduce the risk of amblyopia.
What is occlusion therapy, and what is it used for?
Occlusion therapy involves patching the stronger eye to force the brain to use the weaker eye, helping to reverse suppression and treat amblyopia.
What is atropine penalisation, and when is it used?
Atropine drops are used in the stronger eye to blur vision, encouraging use of the weaker eye. It is an alternative to patching for amblyopia treatment.
What is the role of surgical correction in strabismus?
Eye muscle surgery is performed to realign the eyes, restoring normal ocular alignment and promoting binocular vision. It is often combined with other therapies.
What is vision therapy, and how is it used?
- Vision therapy involves structured exercises to improve binocular function, strengthen coordination, and reduce suppression
- It is often used alongside other treatments.
Why is early treatment important for amblyopia and strabismus?
- Early treatment is crucial because the plasticity of the visual system is greatest during the critical period (up to 7–8 years)
- After this period, treatment becomes less effective
What are common signs of misaligned eyes in children?
- Misaligned eyes (constant or intermittent).
- Head turning/tilting.
- Squinting or closing one eye in bright light.
- Difficulty focusing or reduced interest in visual tasks.
- Poor depth perception or clumsiness.
- Amblyopia (reduced vision in one eye).
What are common symptoms of misaligned eyes in adults?
- Diplopia (double vision).
- Eye strain or headaches.
- Difficulty with depth perception.
- Cosmetic concerns.
- Loss of visual function in severe cases.
What are some congenital or developmental causes of misaligned eyes in children?
- Infantile esotropia.
- Duane syndrome.
- Craniofacial syndromes (e.g., Down syndrome).
How do refractive errors cause misaligned eyes in children?
Uncorrected hypermetropia can lead to accommodative esotropia.
What neurological conditions can cause misaligned eyes in children?
- Cerebral palsy.
- Congenital cranial nerve palsies.
What are common causes of misaligned eyes in adults?
- Cranial nerve palsies (ischemic, compressive, or traumatic).
- Stroke or brain injury.
- Myasthenia gravis.
- Orbital fractures or thyroid eye disease.
- Decompensated strabismus.
- Tumours affecting the orbit or cranial nerves.
What are key points to focus on in the clinical history of a child with misaligned eyes?
- Onset and duration of misalignment.
- Associated symptoms (e.g., head tilt, poor vision).
- Perinatal and developmental history.
- Family history of strabismus or amblyopia.
What should be evaluated in the clinical history of an adult with misaligned eyes?
- Onset (sudden or gradual).
- Presence of diplopia and variations with gaze.
- Neurological symptoms (e.g., headaches, weakness).
- History of trauma or systemic disease (e.g., diabetes, myasthenia gravis).
What clinical examinations are essential for investigating misaligned eyes?
Visual acuity testing.
Cover test to identify phoria or tropia.
Ocular movement assessment.
Binocular vision and stereopsis evaluation.
Fundoscopy to rule out intraocular pathology
When should imaging be performed for misaligned eyes?
If neurological or orbital causes are suspected (e.g., tumours, fractures, stroke).
What additional tests might be needed for misaligned eyes?
Hess chart to map muscle weakness.
Blood tests for systemic conditions (e.g., thyroid function, acetylcholine receptor antibodies).
How are misaligned eyes managed in children?
Refractive correction: Prescribe glasses for hypermetropia or anisometropia.
Amblyopia treatment: Patching or atropine penalisation of the better eye.
Surgery: For large-angle strabismus or when non-surgical treatments fail.
Vision therapy: To improve binocular vision and coordination.
How are misaligned eyes managed in adults?
Treat underlying causes: E.g., control diabetes for cranial nerve palsies.
Prisms: Relieve diplopia in mild cases.
Surgery: For ocular alignment and symptom relief.
Botulinum toxin: Temporarily weakens overactive muscles in acute cases.
Vision therapy: Improve binocular coordination where possible
When should urgent referral be made for misaligned eyes?
Sudden-onset strabismus in adults with diplopia or neurological symptoms.
Suspected tumours, orbital trauma, or stroke.
Leukocoria in children (rule out retinoblastoma).
When is routine referral indicated for misaligned eyes?
Persistent strabismus or amblyopia in children (to orthoptics).
Long-standing strabismus or cosmetic concerns in adults.
Which specialists may be involved in managing misaligned eyes?
Endocrinology for thyroid eye disease.
Neurology for cranial nerve palsies or stroke-related causes.
Paediatric ophthalmology for complex congenital cases.
What are the key features of acute visual loss?
- Onset: Sudden or rapid (seconds to days).
- Nature: Complete loss, partial field loss, or blurring.
- Laterality: Unilateral or bilateral.
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Associated Symptoms: - Pain (ocular or periocular)
- Photophobia or redness
- Neurological symptoms (e.g., weakness, headache, vertigo)
- History of trauma or systemic disease.
What are painless causes of acute visual loss?
Retinal causes:
- Retinal artery occlusion (RAO)
- Retinal vein occlusion (RVO)
- Retinal detachment
- Vitreous haemorrhage
- Macular disease (e.g., wet age-related macular degeneration)
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Optic nerve causes:
- Ischaemic optic neuropathy (arteritic or non-arteritic)
- Optic neuritis (often painful)
- Compressive lesions.
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Neurological causes:
- Stroke (affecting the visual pathways)
- Migraine with aura.
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Other causes:
- Functional vision loss (e.g., conversion disorder)
- Severe refractive errors (rare but possible with lens dislocation)
What are painful causes of acute visual loss?
Anterior segment causes:
- Acute angle-closure glaucoma
- Corneal pathology (e.g., severe keratitis or ulcer)
- Uveitis (anterior or posterior).
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Trauma-related causes:
- Orbital or ocular trauma
- Chemical burns
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Optic nerve causes:
- Optic neuritis
What history should be taken in cases of acute visual loss?
- Onset: Sudden or gradual, time course.
- Laterality: Unilateral or bilateral.
- Associated symptoms: Pain, headache, photophobia, or neurological signs.
- Past medical history: Diabetes, hypertension, vasculitis, or autoimmune disease.
- Trauma: Recent eye injury or surgery.
- Medication history: Anticoagulants or steroids
What examinations are essential for acute visual loss?
- Visual acuity test: Check each eye separately.
- Pupillary reactions: Assess for a relative afferent pupillary defect (RAPD).
- Fundoscopy: Look for retinal or optic nerve pathology (e.g., cherry-red spot in RAO, swollen optic disc in optic neuritis).
- Slit lamp exam: Evaluate anterior segment (e.g., cornea, anterior chamber, lens).
- Intraocular pressure (IOP): Measure to rule out glaucoma.
- Visual field testing: Identify defects suggestive of stroke or optic neuropathy.
What additional investigations may be required?
Imaging:
- Optical coherence tomography (OCT) for macular/retinal disease.
- CT or MRI of the head/orbits for neurological or optic nerve pathology.
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Blood Tests:
- ESR and CRP to rule out giant cell arteritis (if ischaemic optic neuropathy is suspected).
- Glucose and HbA1c for diabetic retinopathy.
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Fluorescein angiography:
- Assess retinal vasculature in RAO or RVO.
How is retinal artery occlusion (RAO) managed?
- Emergency treatment: Attempt to lower IOP (e.g., acetazolamide).
- Ocular massage: To dislodge embolus.
- Immediate referral: To ophthalmology.
- Systemic workup: Evaluate for embolic source (e.g., carotid Doppler, echocardiography)
What is the management for retinal vein occlusion (RVO)?
- Refer to ophthalmology for retinal evaluation.
- Treat underlying conditions (e.g., hypertension, diabetes).
- Anti-VEGF therapy for macular oedema.
What is the treatment for acute angle-closure glaucoma?
- Emergency treatment:
- Acetazolamide to reduce IOP.
- Topical beta-blockers and alpha agonists. - Definitive treatment:
- Laser iridotomy. - Urgent referral to ophthalmology.
How is optic neuritis managed?
- Referral to ophthalmology or neurology.
- MRI of the brain and orbits to assess for multiple sclerosis (MS).
- High-dose IV steroids may be used to accelerate recovery.
What is the management for suspected giant cell arteritis?
- Start high-dose corticosteroids immediately (e.g., prednisolone or IV methylprednisolone).
- Arrange temporal artery biopsy to confirm diagnosis.
- ESR and CRP monitoring
When should urgent referral be made for acute visual loss?
- Sudden painless visual loss with features of RAO, RVO, or retinal detachment.
- Painful visual loss with raised IOP or optic neuritis.
- Suspected giant cell arteritis.
- Neurological symptoms suggesting stroke
What are common symptoms of a red eye?
- Redness of the eye or surrounding structures.
- Pain or discomfort (may be mild to severe).
- Photophobia or blurred vision.
- Discharge (watery, mucopurulent, or bloody).
- Foreign body sensation.
- Tearing or excessive lacrimation.
What should be considered in the history of a patient presenting with a red eye?
- Onset: Sudden or gradual.
- Pain: Location and severity (e.g., superficial or deep).
- Visual symptoms: Blurred vision, diplopia, or loss of vision.
- Discharge: Watery or purulent.
- Associated symptoms: Photophobia, headache, or systemic signs of infection.
- Recent history: Trauma, contact lens use, or exposure to chemicals.
- Past medical history: Autoimmune diseases, previous eye conditions, or ocular surgery.
What are the main causes of red eye?
Conjunctival causes:
- Conjunctivitis (viral, bacterial, allergic).
- Subconjunctival haemorrhage.
- Dry eye syndrome.
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Corneal causes:
- Corneal abrasion or ulcer.
- Keratitis (bacterial, viral, fungal, or herpetic).
- Acanthamoeba keratitis (particularly in contact lens users).
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Anterior segment causes:
- Acute angle-closure glaucoma.
- Uveitis (anterior or posterior).
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Other causes:
- Trauma (blunt or penetrating injury).
- Foreign body in the eye.
- Episcleritis or scleritis.
What is the difference between viral, bacterial, and allergic conjunctivitis in terms of red eye presentation?
Viral conjunctivitis:
- Often associated with cold or respiratory symptoms.
- Watery discharge, itching, mild irritation.
- Typically bilateral.
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Bacterial conjunctivitis:
- Purulent, yellow or green discharge.
- Often unilateral, with crusting of eyelids in the morning.
- More painful than viral conjunctivitis.
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Allergic conjunctivitis:
- Itching, watery eyes, often with sneezing and nasal congestion.
- Bilateral redness and swelling of the conjunctiva.
What are the distinguishing features of acute angle-closure glaucoma causing red eye?
- Severe eye pain, often with nausea and vomiting.
- Sudden onset of blurred vision, particularly with halos around lights.
- Raised intraocular pressure (IOP).
- A fixed, mid-dilated pupil.
- Corneal oedema (cloudy cornea).
What causes uveitis and how does it present with a red eye?
- Uveitis: Inflammation of the uveal tract (iris, ciliary body, choroid).
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Presentation: - Pain, photophobia, and blurred vision.
- Redness (circumcorneal), often associated with a small, irregular pupil.
- Associated with systemic conditions (e.g., autoimmune diseases, infections).
How does subconjunctival haemorrhage present?
Bright red blood in the white part of the eye.
Typically painless and does not affect vision.
No discharge, and the redness is confined to the conjunctiva.
Often associated with trauma or increased pressure (e.g., coughing, vomiting).
What key elements should be assessed during the clinical examination of a red eye?
Visual acuity: Check for any visual disturbance.
Inspection: Look for signs of discharge, redness, and foreign bodies.
Pupil reactions: Check for a relative afferent pupillary defect (RAPD), anisocoria, or a sluggish reaction (especially in cases of uveitis or acute angle-closure glaucoma).
Slit lamp examination: Assess corneal integrity, anterior chamber, and iris for signs of inflammation or foreign bodies.
Intraocular pressure (IOP): Measure if glaucoma is suspected.
Fluorescein staining: To detect corneal abrasions or ulcers.
What tests are helpful for diagnosing causes of red eye?
Conjunctival swab or culture: For suspected bacterial infection.
Fluorescein staining: To assess for corneal abrasions or ulcers.
Tonometry: To measure intraocular pressure (for suspected glaucoma).
Slit lamp examination: To examine for uveitis, corneal pathology, and anterior chamber reactions.
Blood tests: In cases of suspected systemic disease (e.g., autoimmune diseases or infection).
How is viral conjunctivitis managed?
Supportive treatment:
1. Lubricating eye drops for comfort.
2. Cold compresses for relief of symptoms.
3. Avoid contact with others to prevent spread (contagious).
4. Usually resolves in 1–2 weeks without specific antiviral treatment.
How is bacterial conjunctivitis managed?
- Topical antibiotics - eg. chloramphenicol, fusidic acid (consider systemic antibiotics in severe cases)
- Avoid contact lenses during treatment.
- Hygiene measures - e.g., handwashing, cleaning eye crusts
How is allergic conjunctivitis managed?
- Antihistamines - oral or topical antihistamines (e.g., olopatadine), topical mast cell stabilizers (e.g., cromolyn sodium)
- Avoidance of allergens where possible
- Artificial tears for symptomatic relief.
What is the management for acute angle-closure glaucoma?
- Emergency treatment Acetazolamide to lower intraocular pressure,
Topical beta-blockers (e.g., timolol), hyperosmotic agents (e.g., mannitol), Pilocarpine to constrict the pupil. - Surgical management: Laser iridotomy or iridectomy to relieve blockage.
How is uveitis managed?
- Corticosteroids: Topical or systemic, depending on severity.
- Cycloplegic agents: (e.g., atropine) to relieve pain and prevent synechiae.
- Referral to ophthalmology: For systemic investigation if associated with autoimmune or infectious causes.
How is subconjunctival haemorrhage managed?
- No specific treatment is usually required.
- Reassurance and monitoring for spontaneous resolution.
- Evaluate for underlying causes (e.g., blood pressure control or bleeding disorders).
Who are the key personnel involved in the care of the eye?
- Ophthalmologists: Medical doctors who diagnose, treat, and perform surgery for eye diseases.
- Optometrists: Specialists in vision correction and eye exams, referring complex cases to ophthalmologists.
- Orthoptists: Experts in eye movement and alignment disorders like strabismus.
- Ophthalmic Nurses/Technicians: Support patient care, perform diagnostic tests, assist with procedures, and educate patients.
- General Practitioners (GPs): First contact for eye symptoms, managing minor conditions or referring complex cases.
- Pharmacists: Provide advice on medications and educate patients on their use.
- Low Vision Specialists/Social Workers: Assist visually impaired patients with aids, rehabilitation, and daily living support.
How do cardiovascular diseases affect the eye?
- Hypertension: Causes hypertensive retinopathy (arteriolar narrowing, haemorrhages, papilloedema).
- Hyperlipidaemia: Causes lipid deposits (corneal arcus, xanthelasma) and retinal vein occlusion.
- Atherosclerosis: Can cause retinal artery occlusion or ischaemic optic neuropathy.
How do immune-mediated diseases affect the eye?
- Rheumatoid Arthritis: Causes dry eye, scleritis, or episcleritis.
- SLE: Leads to retinal vasculitis, choroidopathy, or optic neuropathy.
- Ankylosing Spondylitis: Associated with acute anterior uveitis.
- Sarcoidosis: Causes granulomatous uveitis or optic nerve inflammation.
- MS: Presents with optic neuritis (vision loss, pain on eye movement).
- (Thyroid Eye Disease: Causes proptosis, diplopia, and optic nerve compression)
How do endocrine and metabolic disorders affect the eye?
- Thyroid Eye Disease: Causes orbital inflammation, proptosis, and exposure keratopathy.
- Diabetes Mellitus: Leads to diabetic retinopathy, macular oedema, and cataracts.
- Hypercalcaemia: May cause band keratopathy (calcium deposition in the cornea).
How does diabetes mellitus affect the eye?
Diabetic Retinopathy:
- Long-term hyperglycaemia damages retinal blood vessels, causing microaneurysms, haemorrhages, and neovascularisation.
- Can progress to diabetic macular oedema, impairing central vision.
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- Cataracts: Increased oxidative stress leads to early-onset cataracts.
- Glaucoma: Increased intraocular pressure and damage to the optic nerve.
- Refractive Changes: High blood sugar can cause temporary shifts in vision due to lens swelling.
What are the stages of diabetic retinopathy?
- Non-proliferative diabetic retinopathy (NPDR): Microaneurysms, retinal haemorrhages, and hard exudates.
- Proliferative diabetic retinopathy (PDR): Neovascularisation of the retina or optic disc, risking retinal detachment and vitreous haemorrhage.
- Diabetic macular oedema (DMO): Fluid accumulation in the macula causing central vision loss.
What are the key signs of thyroid eye disease?
- Proptosis (bulging eyes).
- Lid retraction and lid lag.
- Redness and swelling of the conjunctiva.
- Restricted eye movement causing double vision.
- Visual loss if optic nerve is compressed.
How can hypercalcaemia affect the eye?
Causes band keratopathy, where calcium deposits in the cornea.
What are common mechanisms by which endocrine diseases affect the eye?
- Vascular Changes: Diabetes damages retinal and choroidal blood vessels.
- Inflammation: Autoimmune diseases like thyroid eye disease cause orbital swelling and inflammation.
- Metabolic Dysfunction: Conditions like hypercalcaemia lead to deposits in ocular tissues (e.g., cornea).
- Pressure Effects: Pituitary adenomas in acromegaly compress the optic chiasm, causing visual field loss.
How are eye complications of endocrine diseases managed?
- Diabetes: Regular retinal screening, glycaemic control, and treatments like laser photocoagulation or anti-VEGF injections for retinopathy.
- Thyroid Eye Disease:
- Lubricating eye drops for dryness.
- Steroids or radiotherapy for inflammation.
- Surgery for severe proptosis or optic neuropathy.
- Hypercalcaemia: Manage underlying cause (e.g., parathyroidectomy).
- Pituitary Adenomas: Neurosurgical resection or medical therapy to relieve optic chiasm compression.
What causes proptosis in thyroid eye disease?
Proptosis occurs due to an autoimmune reaction where:
- TSH receptor antibodies (autoantibodies) target orbital fibroblasts.
- This stimulates the production of glycosaminoglycans (GAGs), which attract water and cause tissue swelling.
- Orbital fat expands, and extraocular muscles become inflamed and swollen.
- The increased orbital tissue volume pushes the eyeball forward, causing proptosis.
What are the common causes of chronic visual loss?
- Refractive Errors: Myopia, hyperopia, astigmatism.
- Cataracts: Gradual clouding of the lens.
- Glaucoma: Progressive optic nerve damage causing peripheral vision loss.
- Age-Related Macular Degeneration (AMD): Central vision loss due to retinal damage.
- Diabetic Retinopathy: Microvascular damage from long-term diabetes.
How does chronic visual loss present?
- Gradual loss of vision (central or peripheral).
- Blurred or distorted vision.
- Glare or difficulty seeing in low light (cataracts).
- Scotomas (AMD or glaucoma).
- Halos or eye pain (advanced glaucoma).
What investigations are used to assess chronic visual loss?
- Visual acuity: Assess severity of vision loss.
- Fundoscopy: Examine retina for signs of AMD, diabetic retinopathy, or optic nerve damage.
- Tonometry: Measure intraocular pressure for glaucoma.
- Optical Coherence Tomography (OCT): Evaluate macula and retinal layers.
- Visual Field Testing: Detect peripheral vision loss in glaucoma.
What is the management for chronic visual loss?
- Refractive Errors: Corrective lenses or refractive surgery.
- Cataracts: Surgery to replace the cloudy lens.
- Glaucoma: Eye drops (reduce intraocular pressure), laser treatment, or surgery.
- AMD: Lifestyle changes, anti-VEGF injections (wet AMD).
- Diabetic Retinopathy: Glycaemic control, laser therapy (photocoagulation), or anti-VEGF.
When should patients with chronic visual loss be referred?
- Urgent referral: Vision-threatening conditions (e.g., advanced glaucoma or wet AMD).
- Routine referral: Gradual progression of cataracts or stable refractive issues.
- Specialist referral: Persistent unexplained vision loss requiring further evaluation.
Why is screening for chronic glaucoma important + which groups are screened?
- Asymptomatic early stages: Vision loss begins peripherally and progresses unnoticed.
- Prevent irreversible damage: Early detection can slow or stop progression.
- High-risk groups: Screening is essential for individuals with a family history, age >40, African or Asian ancestry, or other risk factors like high IOP
What are the goals of glaucoma management?
- Reduce intraocular pressure (IOP) to prevent further optic nerve damage.
- Preserve vision and maintain quality of life.
- Monitor disease progression with regular follow-ups.
What are the pharmacological options for chronic glaucoma?
- Prostaglandin Analogues (e.g., latanoprost): Increase aqueous outflow.
- Beta-Blockers (e.g., timolol): Reduce aqueous production.
- Carbonic Anhydrase Inhibitors (e.g., dorzolamide): Reduce aqueous production.
- Alpha-2 Agonists (e.g., brimonidine): Reduce production and increase outflow.
- Miotics (e.g., pilocarpine): Increase outflow by contracting the ciliary muscle (less commonly used).
What are the surgical options for chronic glaucoma?
Laser Therapy:
- Laser Trabeculoplasty: Improves drainage through the trabecular meshwork.
- Cyclophotocoagulation: Reduces aqueous production by targeting the ciliary body.
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Surgical Procedures:
- Trabeculectomy: Creates a new drainage pathway to lower IOP.
- Drainage Devices (e.g., Ahmed valve): Implant to help drain aqueous humour.
- Minimally Invasive Glaucoma Surgery (MIGS): Safer, less invasive options for mild-moderate cases.
Why is lifelong monitoring essential for glaucoma patients?
- Glaucoma is a chronic condition with potential for progression even after treatment.
- Regular IOP checks, visual field tests, and optic nerve imaging help ensure treatment remains effective.
- Adjustments to therapy may be required over time
What is the psychological impact of visual loss?
- Depression and Anxiety: Feelings of isolation, loss of independence, and fear of the future can lead to depression and anxiety.
- Loss of Self-Esteem: Difficulty with daily activities can cause a sense of diminished self-worth.
- Grief and Adjustment: Individuals may go through stages of grief, including denial, anger, and acceptance.
- Cognitive Decline: Increased risk of cognitive decline due to social isolation and lack of stimulation.
What are the social impacts of visual loss?
- Social Isolation: Reduced ability to engage in social activities or work, leading to loneliness.
- Loss of Independence: Dependence on others for mobility, transportation, and basic tasks.
- Stigma and Misunderstanding: Social stigma or misconceptions may lead to exclusion or mistreatment.
- Family Burden: Caregivers often face emotional and physical stress in providing support.
What are the economic impacts of visual loss?
- Loss of Employment: Individuals may be unable to continue working, leading to reduced income and financial strain.
- Increased Healthcare Costs: Expenses for medical care, assistive devices, and rehabilitation services.
- Caregiver Costs: Families or carers may need to take time off work, reducing household income.
- Societal Costs: Increased demand for healthcare services and disability benefits.
What are the DVLA requirements for individuals with visual loss?
- Vision Standards: Drivers must meet specific visual acuity (at least 6/12 in the better eye) and field of vision requirements.
- Reporting to DVLA: Individuals must inform the DVLA of any visual impairment that affects their ability to drive.
- Driving Restrictions: Some individuals may be restricted to driving only during the day or with corrective lenses.
- License Revocation: In cases of severe vision loss (e.g., legal blindness), individuals may be unable to hold a driver’s license.
What support is available for children, their families/carers, and adults with visual impairment?
Children and Families/Carers:
- Early intervention services: Support for learning, development, and family counselling.
- Educational support: Specialised teaching and adaptive technologies (e.g., Braille, large print).
- Support groups and counselling: For both children and families to cope with the emotional impact.
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Adults with Visual Impairment:
- Rehabilitation services: Training in independent living skills, mobility, and orientation.
- Assistive technology: Devices such as screen readers, magnifiers, and voice-activated technology.
- Social services and financial support: Disability benefits, personal assistants, and transportation services.
- Peer support and advocacy groups: Offering social connection, advice, and advocacy for rights.
What are the main indications for cataract surgery?
- Significant Visual Impairment: Impact on daily activities like reading, driving, or watching TV.
- Glare or Halos: Difficulty seeing in bright light or at night.
- Decreased Quality of Life: Difficulty performing routine tasks due to poor vision.
- Medical Necessity: Cataracts affecting the management or detection of other eye conditions, such as diabetic retinopathy.
- Failed Conservative Treatment: When glasses or other treatments no longer improve vision.
What are the common risks of cataract surgery?
- Infection: Endophthalmitis or other intraocular infections, although rare, can be severe.
- Inflammation: Postoperative inflammation, treated with corticosteroid eye drops.
- Bleeding: Minor bleeding can occur, but major hemorrhage is uncommon.
- Retinal Detachment: A risk in certain individuals, particularly those with high myopia or previous eye surgery.
- Increased Intraocular Pressure: Can lead to glaucoma, particularly if steroid medications are used.
- Vision Disturbances: Issues such as glare, halos, or a clouded visual field may persist temporarily or become permanent in rare cases.
- Capsular Rupture: A tear in the lens capsule that can complicate the procedure and require further surgery.
- Endothelial Cell Loss: Gradual loss of cells from the cornea, potentially affecting clarity of vision.
What are the factors that increase the risk of complications in cataract surgery?
- Advanced Cataracts: More difficult to remove and can increase surgical risk.
- Other Eye Conditions: Conditions like glaucoma, diabetic retinopathy, or macular degeneration can affect outcomes.
- Age: Older patients may have more medical conditions that increase risks.
- Previous Eye Surgery: Prior surgery can make the procedure more complicated.
- Systemic Conditions: Conditions like diabetes, high blood pressure, or autoimmune disorders can influence healing and complicate surgery.
What are the benefits of cataract surgery?
- Restored Vision: Improvement in clarity and quality of vision, allowing individuals to resume normal activities.
- Improved Quality of Life: Enhanced ability to perform daily tasks and drive safely.
- Reduced Risk of Falls: Better vision helps prevent accidents and falls, particularly in elderly patients.
- Potential for Better Night Vision: Reduced glare and improved visibility in low light conditions
When should cataract surgery be performed?
- When Visual Impairment Affects Function: Surgery is typically recommended when cataracts interfere with daily activities or quality of life.
- When Medical Conditions Are Affected: If cataracts hinder the treatment or monitoring of other eye diseases, such as diabetic retinopathy or macular degeneration.
- After Conservative Treatment Fails: If glasses or other interventions no longer help with vision.
Label this diagram
What structure do the optic nerve and ophthalmic artery travel through to enter/leave the orbit?
Optic canal
What structure do the trochlear (CN IV), oculomotor (CN III), nasociliary and abducens (CN VI) nerves, and superior ophthalmic vein travel through to enter/leave the orbit?
Superior orbital fissure
What structure do the zygomatic branch of the maxillary nerve, the inferior ophthalmic vein, and sympathetic nerves travel through to enter/leave the orbit?
Inferior orbital fissure
Which of the following nerves is not found within the orbit?
- Optic nerve
- Oculomotor nerve
- Facial nerve
- Abducens nerve
Facial nerve
Which of the following structures does not pass through the inferior orbital fissure?
- Optic nerve
- Maxillary nerve
- Inferior ophthalmic vein
- Sympathetic branches
Optic nerve - enters the boyn orbit via the optic canal
What 2 structures make up the fibrous layer of the eye (outermost layer)?
- Sclera (white part of the eye) - provides attachment to the extraocular muscles
- Cornea - light entering the eye is refracted by the cornea
What are the 3 structures that make up the vascular layer of the eye?
- Choroid - layer of connective tissue and blood vessels (provides nourishment tot he outer layers of the retina)
- Ciliary body (ciliary muscle and ciliary processes) - the ciliary muscle consists of a collection of smooth muscle fibres (these are attached to the lens of the eye by the ciliary processes), the ciliary body controls the shape of the lens, and contributes to the formation of aqueous humor
- Iris - circular structure with an aperture in the centre (the pupil), the diameter of the pupil is altered by smooth muscle fibres within the iris, which are innervated by the autonomic NS
The inner layer of the eye is formed by the retina, what are the 2 layers that the retina is composed of?
- Pigmented (outer) layer - attached to choroid
- Neural (inner) layer - consists of photoreceptors (light-detecting cells of the retina)
Which area of the retina is responsible for high acuity vision?
Fovea centralis - a depression within the macular (centre of the retina)
- has a high concentration of light-detecting cells (photoreceptors)
3 main functions of the vitreous body
The vitreous body is a transparent gel which fills the posterior segment of the eyeball (the area posterior to the lens):
- Contributes to the magnifying power of the eye
- Supports the lens
- Holds the layers of the retina in place
Anterior and posterior chambers of the eye - what is the fluid called that fills theses areas? + where is this fluid drained + condition that can result if drainage is blocked
- Aqueous humor - nourishes and protects the eye
- drains via the trabecular meshwork
- if drainage of aq humor is obstructed –> glaucoma can result
What is papilloedema?
refers to swelling of the optic disc that occurs secondary to raised intracranial pressure
- optic disc is the area of the retina where the optic nerve enters and can be visualised using an ophthalmoscope
What structure comprises the majority of the fibrous layer of the eyeball?
- cornea
- sclera
- choroid
- retina
sclera
Which structure forms the innermost layer of the eye?
- sclera
- choroid
- retina
- lens
retina
What is the name given to the fluid which fills the anterior and posterior chambers of the eye?
- vitreous humor
- cerebrospinal fluid
- choroid
- aqueous humor
aqueous humor
(vitreous humor is ofund in the space between the lens and the retina)
What are the 3 distinct parts of the orbicularis oculi and what are their functions?
- Palpebral part – gently closes the eyelids
- Lacrimal part – involved in the drainage of tears
- Orbital part – tightly closes the eyelids
Which cranial nerve innervates the orbicularis oculi muscle?
- Optic nerve
- Facial nerve
- Trigeminal nerve
- Oculomotor nerve
Facial nerve - the orbicularis oculi is a muscle of facial expression
The tarsal plates are located deep to the orbicularis oculi muscle, there are two plates; superior tarsus (upper eyelid) and inferior tarsus (lower eyelid). What glands lie in the tarsal plates?
Meibomian glands (type of sebaceous gland) - prevent eyelids from sticking together when closed
What muscles are involved in opening the eyelid?
- Levator palpebrae superioris - main muscle involved (innervated oculomotor nerve)
- Superior tarsal muscle - assists the levator palpebrae superioris
Where is the lacrimal gland located within the bony orbit?
- superior and medial
- inferior and lateral
- superior and lateral
- superior and posterior
Superior and lateral
With regards to the lacrimal gland, which of the following statements is TRUE?
- Sympathetic fibres to the lacrimal gland travel with the maxillary nerve
- Arterial supply to the lacrimal gland is via branches of the external carotid artery
- The lacrimal lake is located in the lateral canthus of the eye
- The orbital septum is located posteriorly to the lacrimal gland
Sympathetic fibres to the lacrimal gland travel with the maxillary nerve
Which nerve provides sensory innervation to the lacrimal gland?
- Zygomatic nerve
- Maxillary nerve
- Lacrimal nerve
- Mandibular nerve
Lacrimal nerve - branch of the ophthalmic nerve
what are the 7 extraocular muscles, their function, and their innervation?
- Levator palpebrae superioris (oculomotor nerve - CN III) - elevates the upper eyelid
- Superior rectus (CN III) - elevation (+ adduction/medial rotation)
- Inferior rectus (CN III) - depression (+ adduction/lateral rotation)
- Medial rectus (CN III) - adducts the eyeball
- Lateral rectus (CN VI) - abducts the eyeball
- Superior oblique (CN IV) - depresses, abducts, and medially rotates the eyeball
- Inferior oblique (CN III) - elevates, abducts, and laterally rotates the eyeball
What position would the eye adopt in an oculomotor nerve (CN III) lesion?
“down and out”
- displaced laterally by the lateral rectus and inferiorly by the superior oblique
Horner’s syndrome - triad of symptoms
- Partial ptosis (drooping of the upper eyelid) – Due to denervation of the superior tarsal muscle.
- Miosis (pupillary constriction) – Due to denervation of the dilator pupillae muscle.
- Anhidrosis (absence of sweating) on the ipsilateral side of the face – Due to denervation of the sweat glands.
What is the innervation of the extraocular muscle which chiefly acts to the adduct the eyeball?
- Optic nerve
- Oculomotor nerve
- Ophthalmic nerve
- Abducens nerve
Oculomotor nerve - medial rectus
Which nerve provides somatic motor innervation to the levator palpebrae superioris?
- Oculomotor
- Facial
- Trigeminal
- Trochlear
Oculomotor - this is why in a 3rd nerve palsy there is compete ptosis
What is the innervation of the eye?
- Oculomotor Nerve (CN III):
- Controls most eye muscles, including the levator palpebrae (raises eyelid) and inferior oblique.
- Parasympathetic fibers innervate the pupil constrictor and ciliary muscles (for accommodation). - Trochlear Nerve (CN IV):
- Innervates the superior oblique muscle, responsible for downward and inward eye movement. - Abducens Nerve (CN VI):
- Innervates the lateral rectus muscle, responsible for eye abduction. - Trigeminal Nerve (CN V):
- Opthalmic branch (V1) provides sensation to the cornea, conjunctiva, and skin of the eyelids. - Sympathetic Nervous System:
- Innervates the dilator pupillae muscle for pupil dilation and the superior tarsal muscle for eyelid elevation.
What is the blood supply of the eye and orbit?
- Ophthalmic Artery: Main blood supply to the eye, originating from the internal carotid artery.
- Branches include the central retinal artery (supplies the retina) and ciliary arteries (supply the cornea and iris).
- Lacrimal artery: Supplies the lacrimal gland and part of the eyelid. - Veins:
- Central retinal vein: Drains blood from the retina.
- Superior and inferior ophthalmic veins: Drain the eye and orbit into the cavernous sinus.
Retina anatomy - rods and cones (function + location)
Rods:
- photoreceptor cells that are highly sensitive to light
- responsible for night vision (scotopic vision) and help detect shapes and movement in low-light conditions
- located mostly in the peripheral retina - contributing to peripheral vision
Cones:
- photoreceptor cells responsible for color vision and central vision
- they function in bright light (photopic vision) and are essential for sharp, detailed vision
- located mostly in the fovea
- 3 types of cones: S-cones - sensitive to short wavelengths (blue light), M-cones - sensitive to medium wavelengths (green light), and L-cones - sensitive to long wavelengths (red light)
What is the visual pathway from the retina to the brain?
- Retina: Light is detected by rods and cones.
- Optic Nerve (CN II): Axons from the retinal ganglion cells form the optic nerve.
- Optic Chiasm: Fibers from the nasal retina (temporal visual field) cross over, while fibers from the temporal retina (nasal visual field) stay on the same side.
- Optic Tract: After the chiasm, fibers from both eyes carry information from the contralateral visual field to the brain.
- Lateral Geniculate Nucleus (LGN): Located in the thalamus, where visual information is relayed.
- Optic Radiation: Pathway from the LGN to the visual cortex in the occipital lobe.
- Visual Cortex: Located in the occipital lobe, where visual perception occurs.
What visual field defects occur with a lesion in the optic nerve?
- Unilateral vision loss: Loss of vision in the entire field of the affected eye (monocular blindness).
- Cause: Damage to the optic nerve disrupts the transmission of visual information from one eye to the brain.
- Example: Optic neuritis (inflammation of the optic nerve) or optic neuropathy
What visual field defects occur with a lesion in the optic chiasm?
- Bitemporal hemianopia: Loss of vision in the outer (temporal) half of both visual fields.
- Cause: Damage to the optic chiasm affects the crossing fibers from the nasal retina of both eyes, which process the temporal visual field.
- Example: Pituitary tumors or cranial aneurysms compressing the optic chiasm.
What visual field defects occur with a lesion in the optic tract?
- Homonymous hemianopia: Loss of vision in the same side (right or left) of the visual field of both eyes.
- Cause: Damage to the optic tract interrupts the pathway from the optic chiasm to the brain, affecting the contralateral visual field (i.e., the right optic tract affects the left visual field and vice versa).
- Example: Stroke or tumors affecting the optic tract.
What visual field defects occur with a lesion in the visual cortex?
- Homonymous hemianopia or quadrantanopia: Loss of vision in the same side (right or left) of both eyes. The location and extent depend on the site of the lesion in the occipital lobe.
- Cause: Damage to the visual cortex or optic radiations interrupts visual processing, leading to a loss of vision in the contralateral visual field.
- Example: Stroke, trauma, or brain tumors affecting the occipital lobe.
Visual fields - draw out + label
Q1: What are the six extraocular muscles responsible for eye movement, and their innervations?
- Medial Rectus: Adduction (CN III - Oculomotor nerve).
- Lateral Rectus: Abduction (CN VI - Abducens nerve).
- Superior Rectus: Elevation (CN III).
- Inferior Rectus: Depression (CN III).
- Superior Oblique: Depression and intorsion (CN IV - Trochlear nerve).
- Inferior Oblique: Elevation and extorsion (CN III).
What are the neurological pathways involved in eye movement?
Cranial Nerves:
- CN III (Oculomotor): Innervates all muscles except lateral rectus and superior oblique.
- CN IV (Trochlear): Innervates the superior oblique muscle.
- CN VI (Abducens): Innervates the lateral rectus muscle.
.
Supranuclear Pathways - coordinate eye movements via signals from the brainstem, including:
- PPRF (Paramedian Pontine Reticular Formation): Horizontal gaze coordination.
- MLF (Medial Longitudinal Fasciculus): Links CN III, IV, and VI for conjugate gaze.
.
Cortical Control:
- Frontal Eye Fields: Voluntary saccadic movements.
- Occipital Lobe: Smooth pursuit movements.
How do you test ocular movement?
- Inspect eye alignment: Look for any deviations at rest (strabismus).
- Cardinal Gaze Testing:
- Ask the patient to follow your finger in an “H” pattern to test the full range of motion of each extraocular muscle.
- Look for limitations or abnormalities in movement. - Convergence Testing:
- Ask the patient to focus on a near object and bring it closer to their nose.
- Tests the medial rectus and accommodation reflex (involves CN III).
.
Cover-Uncover Test (for alignment):
- Cover one eye while observing the uncovered eye for movement.
- Misalignment indicates a phoria (latent strabismus) or tropia (manifest strabismus).
What does ocular misalignment indicate?
Misalignment (strabismus) can result from issues with:
- Cranial nerves (e.g., CN VI palsy → lateral rectus weakness).
- Brainstem or cortical lesions affecting gaze centers.
- Orbital pathologies (e.g., thyroid eye disease).
What are common findings and their associated lesions in ocular movement testing?
CN III Palsy:
- Eye is down and out.
- Ptosis and pupil dilation (if parasympathetic fibers are involved).
.
CN IV Palsy:
- Difficulty with downward and inward gaze.
- Vertical diplopia (worse when looking down).
.
CN VI Palsy:
- Inability to abduct the affected eye (lateral rectus weakness).
.
Internuclear Ophthalmoplegia (INO):
- Impaired adduction of the affected eye (MLF lesion).
What is the optics of the eye, and how does it focus light?
- The eye functions as an optical system to focus light onto the retina.
- The cornea provides ~70% of refractive power, while the lens adjusts focus for near and distant objects (accommodation).
- Refraction ensures light rays converge on the fovea for sharp vision.
What are the main types of refractive errors?
- Myopia (short-sightedness):
- Light focuses in front of the retina.
- Distant objects appear blurry.
- Associated with elongated eyeball or excessive corneal curvature. - Hyperopia (long-sightedness):
- Light focuses behind the retina.
- Near objects appear blurry.
- Associated with shortened eyeball or insufficient refractive power. - Astigmatism:
- Irregular corneal or lens curvature causes distorted vision.
- Light focuses at multiple points on or near the retina. - Presbyopia:
- Age-related loss of lens elasticity, reducing accommodation.
- Difficulty focusing on near objects.
What are the associations of different refractive errors?
- Myopia:
- Associated with retinal detachment, glaucoma, and macular degeneration in high myopia. - Hyperopia:
- Linked to angle-closure glaucoma and amblyopia in children. - Astigmatism:
- Can occur with myopia or hyperopia.
- May contribute to eye strain and blurred vision at all distances. - Presbyopia:
- Typically occurs after age 40, affecting most individuals.
How are refractive errors managed?
- Optical Correction:
- Myopia: Concave (negative) lenses.
- Hyperopia: Convex (positive) lenses.
- Astigmatism: Cylindrical lenses.
- Presbyopia: Bifocal, trifocal, or progressive lenses. - Contact Lenses:
- Alternative to glasses, offering wider fields of view.
3.Surgical Options:
- Laser Refractive Surgery (LASIK/PRK): Reshapes the cornea for myopia, hyperopia, and astigmatism.
- Lens-based Surgery: Intraocular lens implantation for severe refractive errors or presbyopia.
- Orthokeratology:
- Specialised contact lenses worn overnight to temporarily reshape the cornea (for myopia). - Low Vision Aids:
- Magnifiers or telescopic lenses for individuals with uncorrectable vision loss.
Why is early detection of refractive errors important?
In children:
- Prevents amblyopia (lazy eye) and supports normal visual development.
.
In adults:
- Reduces eye strain and risk of accidents.
- Enables timely treatment of associated complications (e.g., glaucoma in hyperopia).
What are the four main mechanisms of neuropathology?
- Inflammation: E.g., meningitis, encephalitis, multiple sclerosis (MS).
- Degeneration: E.g., Alzheimer’s, Parkinson’s, Huntington’s.
- Haemorrhage: E.g., subarachnoid, intracerebral, subdural, epidural.
- Neoplasia: E.g., meningioma, glioblastoma, metastases.
What is seen on imaging in multiple sclerosis (MS)?
- Bright white (T2 hyperintense) patches in brain or spinal cord.
- Often around ventricles (“Dawson’s fingers”) - shown in image
What does meningitis look like on imaging?
Bright enhancement of the brain lining (leptomeninges) on MRI with contrast.
How does a brain abscess appear on scans?
Ring-enhancing lesion with a dark (fluid-filled) centre.
The centre restricts diffusion on MRI.
How does an epidural haematoma appear on CT?
- Biconvex shape (lens/lemon-shaped), located between the skull and dura
- aetiology - usually trauma to the skull in temporoparietal region
(majority caused by rupture of the middle meningeal artery)
How does a subdural haematoma appear on CT?
Crescent-shaped (“banana-shaped”), located between dura mater and arachnoid mater of the brain.
- aetiology - usually trauma again, but more common in older pts
How does a subarachnoid haemorrhage appear?
Bright blood in grooves (sulci) or cisterns on CT.
- aetiology of spontaneous SAH - most commonly intracranial aneurysms
What does an intracerebral haemorrhage look like on imaging?
Bright spot in brain tissue surrounded by darker swelling (oedema).
- aetiology - usually related to hypertension
What does a meningioma look like on imaging?
Well-defined mass attached to the brain lining (dura), with a “tail”.
What does a glioblastoma look like on imaging?
- Bright ring (contrast enhancement) with a dark centre (necrosis).
- Surrounding swelling (oedema) causes pressure effects
How do brain metastases appear on imaging?
Multiple, round, bright lesions.
Often at the grey-white matter junction.
What is seen in Alzheimer’s disease on MRI?
Shrinking (atrophy) of the hippocampus and medial temporal lobes.
Enlarged spaces (ventricles).
What are the types of pupil reactions tested in clinical practice?
- Direct response: Constriction of the pupil in the same eye when light is shone.
- Consensual response: Constriction of the pupil in the opposite eye when light is shone in one eye.
- Relative afferent pupillary defect (RAPD): Abnormal response to the swinging flashlight test, showing an issue with the afferent pathway.
What is the afferent pathway of the pupillary light reflex?
- Light stimulates the retina.
- Signal travels via the optic nerve (CN II).
- Fibres pass through the optic chiasm and optic tracts.
- Fibres synapse in the pretectal nucleus in the midbrain.
What is the efferent pathway of the pupillary light reflex?
- Signal travels from the pretectal nucleus to both Edinger-Westphal nuclei.
- Parasympathetic fibres travel via the oculomotor nerve (CN III).
- Fibres synapse in the ciliary ganglion.
- Postganglionic fibres innervate the sphincter pupillae muscle, causing pupil constriction.
How is the consensual response mediated?
The afferent signal from one eye splits at the pretectal nucleus and activates both Edinger-Westphal nuclei, allowing a response in both eyes.
What is an RAPD (Relative Afferent Pupillary Defect), and how is it tested?
- RAPD occurs due to damage in the afferent pathway (optic nerve or retina).
.
Swinging flashlight test: - Shine light alternately in both eyes.
- An affected eye will show dilation instead of constriction due to reduced afferent input.
How is pharmacological testing used to assess pupil abnormalities?
- Dilated pupil:
- Test for Adie’s pupil (parasympathetic lesion) with low-dose pilocarpine (0.1%): Constriction confirms diagnosis.
- Test for CN III palsy with 1% pilocarpine: Dilated pupil in CN III palsy will constrict. - Constricted pupil:
- Use 1% tropicamide or phenylephrine to assess pupil reactivity.
What is the role of the sympathetic pathway in pupil size?
- Sympathetic input causes pupil dilation via the dilator pupillae muscle.
- Disruption leads to miosis (constricted pupil), e.g., in Horner’s syndrome.
How does Horner’s syndrome affect pupil function, and how is it tested?
Features: Ptosis, miosis, and anhidrosis.
Testing:
- Apraclonidine drops: Causes dilation in the affected eye due to hypersensitivity.
- Cocaine drops: Failure of dilation in the affected eye.
How can pupil size abnormalities help localise lesions?
- Dilated pupil: CN III palsy or parasympathetic damage.
- Constricted pupil: Sympathetic lesion (e.g., Horner’s syndrome).
- RAPD: Damage to the retina or optic nerve.
What is the course and distribution of CN I (Olfactory nerve)?
- Course: Olfactory receptors (within the nasal epithelium)→ Cribriform plate of the ethmoid bone → Olfactory bulb → Olfactory tract → Temporal lobe.
- Function: Smell
Complete the sentence: The olfactory nerve enters/exits the cranium via the ___________.
- Nasopalatine foramen
- Cribiform plate of ethmoid
- Superior orbital fissure
- Optic canal
Cribiform plate of ethmoid
- The sense of smell is detected by olfactory receptors located within the nasal epithelium. Their axons (fila olfactoria) assemble into small bundles of true olfactory nerves, which penetrate the small foramina in the cribriform plate of the ethmoid bone and enter the cranial cavity.
What is the course and distribution of CN II (Optic nerve)?
- Course: Retina → Optic nerve → Optic chiasm (partial crossing) → Optic tract → Lateral geniculate nucleus (LGN) → Visual cortex (occipital lobe).
- Function: Vision
What is the course and nuclei of CN III (Oculomotor nerve)?
- Nuclei: Oculomotor nucleus (motor) and Edinger-Westphal nucleus (parasympathetic).
- Course: Midbrain → Cavernous sinus → Superior orbital fissure → Eye muscles.
.
Function: - Motor: Moves 4 eye muscles (SR, IR, MR, IO) + raises eyelid (levator palpebrae).
- Parasympathetic: Pupil constriction (sphincter pupillae) and accommodation.
What is the course and nuclei of CN IV (Trochlear nerve)?
- Nucleus: Trochlear nucleus (midbrain).
- Course: Posterior midbrain (trochlear nucleus) → Cavernous sinus → Superior orbital fissure → Superior oblique muscle.
- Function: Eye movement (depression and intorsion).
What is the course and nuclei of CN V (Trigeminal nerve)?
- Nuclei:
- Motor nucleus (pons).
- Sensory nuclei: Mesencephalic, principal, and spinal trigeminal nuclei. - Course: Pons → 3 divisions:
- V1 (Ophthalmic): Superior orbital fissure → Forehead, scalp, and eye sensation.
- V2 (Maxillary): Foramen rotundum → Cheek and upper lip sensation.
- V3 (Mandibular): Foramen ovale → Jaw sensation + muscles of mastication. - Function: Sensory (face) and motor (chewing).
What are the 5 main branches of the facial nerve (CV VII) ?
*marginal mandibular
Label this diagram + which bones make up the cranial roof and which bones make up the cranial base?
- Cranial roof - frontal, occipital, and 2 parietal bones
- Cranial base - frontal, sphenoid, ethmoid, occipital, parietal, and temporal bones
Which area of the skull is vulnerable to trauma and which artery is vulnerable to injury?
- Pterion - a H-shaped junction between the temporal, parietal, frontal, and sphenoid bones
- Middle meningeal artery - blood can accumulate between the skull and dura mater –> forming an extradural haematoma
Facial bones anatomy - label
Sutures and fontanelles of the skull
- Coronal suture - fuses frontal bone with two parietal bones
- Sagittal suture - fuses both parietal bones to each other
- Lambdoid suture - fuses occipital bone to two parietal bones
.
(fontanelle - in neonates the incompletely fused suture joints give rise to membranous gaps between the bones)
Label the 3 parts of the brainstem
Label the layers of the brain
3 layers of meninges:
- dura mater
- arachnoid mater
- pia mater
Extradural and subdural haematomas - where anatomically
- Extradural - arterial blood collects between skull and periosteal layer of dura (causative vessel is usually middle meningeal artery)
- Subdural - venous blood collects between dura and arachnoid mater
What are the three horns of the spinal cord grey matter
- Dorsal horn (also known as the posterior horn) - contains neurons that receive somatosensory information from the body, which is then transmitted via the ascending pathways, to the brain
- Ventral horn (also known as the anterior horn) - largely contains motor neurons that exit the spinal cord to innervate skeletal muscle
- Lateral horn/intermediate column - contains neurons that innervate visceral and pelvic organs
Basal ganglia function + which cerebral artery provides arterial supply?
- Function - reduces excitatory input (prevents excessive and exaggerated movements) + regulates cognitive and emotional responses
- Middle cerebral artery - lenticulostriate arteries branch off MCA to supply
What are the two different types of tissue in which the cerebrum is comprised of?
- Grey matter - forms surface of each cerebral hemisphere (cerebral cortex), and is associated with processing and cognition (contains neuronal cell bodies)
- White matter - forms the bulk of the deeper parts of the brain, it consists of glial cells and myelinated axons that connect the various grey matter areas
Sulci VS Gyri
- Sulci - grooves or depressions
- Gyri - ridges or elevations
Lobes of the cerebrum - label diagram + functions of each lobe
- Frontal lobe - higher intellect, personality, mood, social conduct and language (dominant hemisphere side only)
- Parietal lobe - language and calculation on the dominant hemisphere side, and visuospatial functions (e.g. 2-point discrimination) on the non-dominant hemisphere side.
- Temporal lobe - memory and language – this includes hearing as it is the location of the primary auditory cortex
- Occipital lobe - primary visual cortex (V1) is located within the occipital lobe and hence its cortical association area is responsible for vision
Blood supply of cerebrum - 3 distinct pairs of arterial branches
- Anterior Cerebral Arteries – branches of internal carotid arteries, supplying the anteromedial aspect of the cerebrum
- Middle Cerebral Arteries – continuation of internal carotid arteries, supplying most of the lateral portions of the cerebrum
- Posterior Cerebral Arteries – branches of the basilar arteries, supplying both the medial and lateral sides of the cerebrum posteriorly
Where does the cerebellum sit anatomically in relation to the pons?
cerebellum sits posterior to the pons
Cerebellar dysfunction - symptoms of cerebrocerebellum and spinocerebellum + vestibulocerebellum
Damage to cerebrocerebellum and spinocerebellum:
D - Dydiadochokinesia - difficulty in carrying out rapid, alternating movements
A - Ataxia
N - Nystagmus
I - Intention tremor
S - Scanning speech
H - Hypotronia
.
Damage to vestibulocerebellum:
- loss of balance, abnormal gait with a wide stance
What structure separates the cerebellum from the occipital and temporal lobes?
- Tentorium cerebelli
- Longitudinal fissure
- Falx cerebri
- Fourth ventricle
Tentorium cerebelli
DCML pathway - describe the path of the 1st, 2nd, and 3rd order neurones (include the two different pathways which the 1st order neurons take)
- 1st order neurones - carry sensory info from peripheral nerves to the medulla oblongata
- 2nd order neurones - begin in the medulla oblongata (cuneate nucleus or gracilis), fibres receive info from preceding neurones and deliver it to the 3rd order neurones in the thalamus
(within the medulla oblongata, these fibres decussate - they then travel in the contralateral medial lemniscus to reach the thalamus) - 3rd order neurones - transmit sesnosry signals from the thalamus to the ipsilateral primary sensory cortex of the brain
)they ascend from the ventral posterolateral nucleus of the thalamus, travel through the internal capsule, and terminate at the sensory cortex)
DCML pathway - what are the 2 different pathways which the 1st order neurones take?
- Signals from the upper limb (T6 and above) - travel in the fasciculus cuneatus (lateral part of dorsal column), they then synpase in the nucleus cuneatus of the medulla oblongata
- Signals from the lower limb (below T6) - travel in the fasciculus gracilis (medial part of dorsal column), they then synapse in the nucleus gracilis of the medulla oblongata
Anterolateral spinothalamic tracts - describe the path of the 1st, 2nd, and 3rd order neurones
- 1st order neurones - arise from sensory receptors in the periphery, enter the spinal cord, ascend 1-2 vertebral lvls, and synapse at the tip of the dorsal horn (area known as the substantial gelatinosa)
- 2nd order neurones - carry the sensory info from the substantita gelatinosa to the thalamus
(after synapsing with the 1st order neurones, these fibres decussate within the spinal cord, and then form 2 distinct tracts: - crude touch and pressure fibres - enter the anterior spinothalamic tract
- pain and temperature fibres - enter the lateral spinothalamic tract)
- 3rd order neurones - carry sensory signals from thalamus to the ipsilateral primary sensory cortex of the brain
(ascend from he ventral posterolateral nucleus of the thalamus, travel through he internal capsule, and terminate at the sensory cortex)
DCML pathway lesion - symptoms
- loss of proprioception and fine touch
- is lesion occurs in the spinal cord (most common) - sensory loss is ipsilateral (as decussation occurs in the medulla oblongata)
Anterolateral spinothalamic tracts lesion - symptoms
- impairment of pain and temperature sensation
- sensory loss will be contralateral (as spinothalamic tracts decussate within the spinal cord)
Brown-Sequard syndrome - what is it + symptoms
(rare, but important syndrome as it illustrates the decussation of the sensory pathways)
- refers to a hemisection (one-sided lesion) of the spinal cord - most often due to traumatic injury, it involves both the anterolateral system and the DCML pathway
- DCML pathway - ipsilateral loss of touch, vibration, and proprioception
- Anterolateral system - contralateral loss of pain and temperature sensation
(it will also involve the descending motor tracts, causing an ipsilateral hemiparesis)
Diagram showing the location of the ascending tracts, within the spinal cord
Are there synapses within the descending pathways/tracts?
NO
- at the termination of the descending tracts, the neurones synapse with a lower motor neurone
–> thus, all the neurones within the descending motor system are classed as upper motor neurones
(their cell bodies are found in the cerebral cortex or the brain stem, with their axons remaining in the CNS)
The pyramidal tracts are responsible for the voluntary control of the musculature of the body and face - these tracts can be subdivided into two (one tract supplies the body, the other tract supplies the head and neck)
- Corticospinal tracts – supplies the musculature of the body.
- Corticobulbar tracts – supplies the musculature of the head and neck
Dermatomal distribution diagram
Myotomes table
Internal carotid arteries - where do they arise from + what do each of the branches supply (see below) + what do they continue on to form?
- ophthalmic artery
- posterior communicating artery
- anterior choroidal artery
- anterior cerebral artery
- arise from the common carotid arteries (C4)
. - ophthalmic artery - supplies the structures of the orbit
- posterior communicating artery - acts as an anastomotic ‘connecting vessel’ in the Circle of Willis
- anterior choroidal artery - supplies structures in the brain important for motor control and vision
- anterior cerebral artery - supplies part of the cerebrum
. - the internal carotids then continue as the middle cerebral artery (supplies lateral portions of cerebrum)
Vertebral arteries - where do they arise from + what do each of the branches supply (see below) + what do they continue on to form?
- Meningeal branch
- Anterior and posterior spinal arteries
- Posterior inferior cerebellar artery
- arises from the subclavian arteries
. - Meningeal branch – supplies the falx cerebelli, a sheet of dura mater
- Anterior and posterior spinal arteries – supplies the spinal cord, spanning its entire length
- Posterior inferior cerebellar artery – supplies the cerebellum
. - after this, the two vertebral arteries converge to form the basilar artery
Circle of Willis + other arteries of the brain diagram - label
Label this diagram of the dural venous sinuses
Note: the great cerebral vein
In which ‘space’ are the cerebral veins located?
- Epidural
- Subdural
- Subarachnoid
- Intermeningeal
Subarachnoid
- Upon exiting the cerebral parenchyma, the veins run in the subarachnoid space and pierce the meninges to drain into the dural venous sinuses
Where do the ophthalmic (superior and inferior) and central vein of the retina drain into?
Cavernous sinus
3 main functions of cerebrospinal fluid (CSF)
- Protection - acts as a cushion for the brain, limiting neural damage in cranial injuries
- Buoyancy - by being immersed in CSF, the net weight of the brain is reduced to approximately 25 grams. This prevents excessive pressure on the base of the brain
- Chemical stability - the CSF creates an environment to allow for proper functioning of the brain, e.g. maintaining low extracellular K+ for synaptic transmission
Label the diagram showing a bird’s eye view of the ventricles of the brain
Label the diagram + from the 4th ventricle, where does the CSF drain?
- Central spinal canal – bathes the spinal cord
- Subarachnoid cisterns – bathes the brain, between arachnoid mater and pia mater. Here the CSF is reabsorbed back into the circulation
(Foramen of Monro - connects the lateral ventricles to the third ventricle)
Where is CSF produced and where is CSF drained?
- CSF is produced by the choroid plexus (lines the ventricles)
- CSF is drained in the subarachnoid cisterns (or space)
–> arachnoid granulations protrude into the dura mater and allow the fluid to drain into the dural venous sinuses
What does this CT scan show?
Hydrocephalus
- Hydrocephalus = an abnormal collection of cerebrospinal fluid within the ventricles of the brain
(It is a serious condition, with chronic hydrocephalus causing raised intracranial pressure, and consequently cerebral atrophy)
What clinical features result from damage to the corticospinal tract in myelopathy?
- Weakness (usually spastic in nature)
- Hyperreflexia and clonus.
- Positive Babinski sign (extensor plantar reflex).
What symptoms arise from damage to the dorsal columns in myelopathy?
- Loss of vibration sense
- Loss of proprioception.
- Sensory ataxia (unsteady gait, worsens with eyes closed).
What clinical features are associated with spinothalamic tract damage in myelopathy?
- Loss of pain and temperature sensation
- Often follows a “cape-like” distribution if cervical cord is affected.
Seizures vs Syncope
- Onset
- Duration
- Recovery
Focal VS Generalised seizures
The sympathetic and parasympathetic nervous system are comprised of pre-ganglionic neurones, ganglia, and post-ganglionic neurones - diagram
What is the sympathetic chain/trunk, and what is its role in the sympathetic nervous system?symp
The sympathetic chain (also known as the sympathetic trunk) is a bilateral structure of ganglia and nerve fibers that runs alongside the vertebral column from the cervical to the sacral region
.
Function:
- Acts as the primary pathway for sympathetic nerve fibers, transmitting signals from the thoracolumbar spinal cord to various target organs throughout the body.
- It consists of sympathetic ganglia (groups of nerve cell bodies) connected by nerve fibers, forming a chain.
- Pre-ganglionic fibers originate from the lateral horn of the spinal cord (T1-L2) and synapse in the sympathetic ganglia of the trunk.
- Post-ganglionic fibers extend from these ganglia to target organs such as the heart, lungs, and blood vessels.
- It also contains fibers that innervate the adrenal medulla, which releases adrenaline and noradrenaline during stress responses.
Autonomic NS: Sympathetic VS Parasympathetic pre- and post-ganglionic fibres
- Length
- myelination
- neurotransmitter released
