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
Which retinal fibres are present in the left optic tract?
- Left temporal and left nasal
- Left temporal and right nasal
- Right temporal and right nasal
- Right temporal and left nasal
Left temporal and right nasal
- The nasal fibres cross over in the optic chiasm, so the right nasal fibres and left temporal fibres form the left optic tract. They carry information from the left nasal and right temporal visual fields.
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.
Where do the fibres of the oculomotor nerve originate?
- Primary visual cortex
- Midbrain
- Hypothalamus
- Basal ganglia
Midbrain
The oculomotor nerve originates from the oculomotor nucleus – located within the midbrain of the brainstem
A 85-year-old man attends his primary care physician with headache and diplopia.
Which of the clinical presentations is most consistent with a diagnosis of oculomotor nerve palsy?
- Ipsilateral anhidrosis
- Abducted and depressed eye at rest
- Adducted eye at rest
- Constricted pupil
Abducted and depressed eye at rest
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).
Common presentation of a CN IV palsy (trochlear nerve palsy)?
Vertical diplopia, exacerbated by looking downwards (eg. walking down the stairs or reading a book), pts may also develop a head tilt away from the affected side
What is the function of the trochlear nerve?
- Somatic sensory
- Somatic motor
- Visceral sensory
- Visceral motor
Somatic motor
Trochlear nerve palsy would result in the denervation of which extraocular muscle?
- Superior oblique
- Inferior oblique
- Superior rectus
- Orbicularis oculi
Superior oblique
A fracture involving which bony foramina would be most likely to affect the trochear nerve?
- Optic canal
- Superior orbital fissure
- Inferior orbital fissure
- Supraorbital foramen
Superior orbital fissure
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).
The trigeminal nerve gives rise to three main divisions. Which branch is the only one to contain motor fibres?
- Ophthalmic
- Maxillary
- Mandibular
- All of the above
Mandibular
- It innervates the muscles of mastication and several other muscles within the head and and neck.
Which of the following cranial foramina transmits the maxillary nerve?
- Foramen ovale
- Foramen spinosum
- Superior orbital fissure
- Foramen rotundum
Foramen rotundum
- The maxillary nerve arises from the trigeminal ganglion, travels along the lateral wall of the cavernous sinus and then exits the cranium via the foramen rotundum (sphenoid bone).
What is the course and nuclei of CN VI (Abducens nerve)?
- Nucleus: Abducens nucleus (pons).
- Course: Pons → Cavernous sinus → Superior orbital fissure → Lateral rectus muscle.
- Function: Eye abduction.
Where in the brainstem is the abducens nucleus located?
- Midbrain
- Medulla
- Cerebellum
- Pons
Pons
What is the general somatic motor function of the abducens nerve?
- Inferior rectus
- Lateral rectus
- Medial rectus
- Superior rectus
Lateral rectus
What action does the lateral rectus muscle have on the eyeball?
- Abduction
- Elevation
- Depression
- Adduction
Abduction
What is the course and nuclei of CN VII (Facial nerve)?
- Nuclei:
- Motor nucleus (pons).
- Parasympathetic nuclei: Superior salivatory and lacrimal nuclei.
- Sensory: Nucleus solitarius. - Course: Pons → Internal acoustic meatus → Facial canal → Stylomastoid foramen → Face muscles.
- Function:
- Motor: Facial expression.
- Sensory: Taste (anterior 2/3 of tongue).
- Parasympathetic: Lacrimation, salivation.
What are the 5 main branches of the facial nerve (CV VII) ?
*marginal mandibular
What is the course and nuclei of CN VIII (Vestibulocochlear nerve)?
- Nuclei: Vestibular and cochlear nuclei (pons/medulla).
- Course: Inner ear → Internal acoustic meatus → Pons.
- Function: Hearing and balance (special sensory).
Which bony structure permits the passage of the vestibulocochlear nerve to exit the cranium?
- Hypoglossal canal
- Foramen rotundum
- Jugular foramen
- Internal acoustic meatus
Internal acoustic meatus
Where are the cochlear hair cells located?
- Utricule
- Organ of Corti
- Saccule
- Semicircular canals
Organ of Corti
- The hair cells of the organ of Corti detect the magnitude and frequency of sound waves
Which of the following symptoms is least associated with damage to the vestibular component of the eight cranial nerve?
- Vertigo
- Hearing loss
- Nystagmus
- Nausea
Hearing loss
- The vestibular component of the vestibulocochlear nerve is responsible for balance. The cochlear nerve component is responsible for hearing.
What is the course and nuclei of CN IX (Glossopharyngeal nerve)?
- Nuclei:
- Motor: Nucleus ambiguus.
- Sensory: Nucleus solitarius.
- Parasympathetic: Inferior salivatory nucleus. - Course: Medulla → Jugular foramen → Pharynx and tongue.
- Function:
- Motor: Swallowing (stylopharyngeus).
- Sensory: Taste (posterior 1/3 of tongue), carotid body/sinus.
- Parasympathetic: Parotid gland secretion.
Glossopharyngeal nerve palsy can occur as a result of multiple sclerosis.
In such a case, what would be the expected finding on examination of the tongue?
- Absent taste sensation in anterior two-thirds with preserved general sensation
- Absent taste sensation in posterior third with preserved general sensation
- Intrinsic tongue muscle paralysis
- Absent taste and general sensation in posterior third
Absent taste and general sensation in posterior third
- The glossopharyngeal nerve provides taste and general sensation to the posterior third of the tongue.
Which muscle of the pharynx is innervated by the glossopharyngeal nerve?
- Inferior pharyngeal constrictor
- Stylopharyngeus
- Palatopharyngeus
- Salpingopharyngeus
Stylopharyngeus (swallowing)
Where in the brainstem does the glossopharyngeal nerve arise?
- Pons
- Medulla oblongata
- Midbrain
- Cerebellum
Medulla oblongata
What is the course and nuclei of CN X (Vagus nerve)?
- Nuclei:
- Motor: Nucleus ambiguus.
- Sensory: Nucleus solitarius.
- Parasympathetic: Dorsal motor nucleus. - Course: Medulla → Jugular foramen → Thorax and abdomen.
- Function:
- Motor: Swallowing, phonation.
- Parasympathetic: Heart, lungs, GI tract.
- Sensory: Thoracic and abdominal viscera.
What are the modalities of the vagus nerve?
- Motor
- Sensory
- Parasympathetic
- All of the above
All of the above
What is the course and nuclei of CN XI (Accessory nerve)?
- Nucleus: Spinal accessory nucleus (C1–C5).
- Course: Spinal cord → Foramen magnum → Jugular foramen → Neck muscles.
- Function: Motor to sternocleidomastoid and trapezius
Which cranial foramina allows the spinal component of the accessory nerve to enter the cranial cavity?
- Jugular foramen
- Foramen magnum
- Foramen ovale
- Foramen spinosum
Foramen magnum
Which of the following muscles receives somatic motor innveration from the accessory nerve?
- Anterior belly of digastric
- Cricopharyngeus
- Latissimus dorsi
- Trapezius
Trapezius
- The spinal accessory nerve innervates two muscles – the sternocleidomastoid and trapezius.
The spinal part of the accessory nerve arises from which spinal segments?
- C2-C3
- C1-C4
- C1-C7
- C1-C5/C6
C1-C5/C6
What is the course and nuclei of CN XII (Hypoglossal nerve)?
- Nucleus: Hypoglossal nucleus (medulla)
- Course: Medulla → Hypoglossal canal → Tongue muscles
- Function: Motor to tongue muscles (except palatoglossus which is innervated by vagus nerve)
Where in the brainstem is the hypoglossal nucleus located?
- Medulla oblongata
- Pons
- Midbrain
- Cerebellum
Medulla oblongata
In broad terms, what is the function of the hypoglossal nerve?
- Somatic sensory
- Visceral sensory
- Parasympathetic
- Somatic motor
Somatic motor
- The hypoglossal nerve has a somatic motor function, innervating the majority of muscles in the tongue
What is the general rule for cranial nerve nuclei localisation in the brainstem?
- Midbrain: CN III, IV.
- Pons: CN V, VI, VII, VIII.
- Medulla: CN IX, X, XI, XII.
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)
Complete the sentence: The frontal fontanelle represents the junction of the ____________ and ___________ sutures
- Frontal and parietal
- Sagittal and lambdoid
- Coronal and lambdoid
- Coronal and sagittal
Coronal and sagittal
Which of the following bones contributes to the calvarium of the skull?
- Sphenoid
- Ethmoid
- Parietal
- Lacrimal
Parietal
- The calvarium forms the roof of the skull and is comprised of the frontal, occipital and two parietal bones.
Label the 3 parts of the brainstem
Which cranial nerves are associated with the midbrain?
- CN III (oculomotor)
- CN IV (trochlear)
Which cranial nerves originate from the ventral surface of the pons?
- CN V (trigeminal)
- CN VI (abducens)
- CN VII (facial)
- CN VIII (vestibulocochlear)
The pons develops from which part of the primitive brain?
- Telencephalon
- Diencephalon
- Mesencephalon
- Metencephalon
Metencephalon
Which of the following structures lies posteriorly to the pons?
- Cerebrum
- Midbrain
- Cerebellum
- Medulla
Cerebellum
Which of the following cranial nerves does NOT originate from the pons?
- CN IV - Trochlear
- CN V - Trigeminal
- CN VI - Abducens
-CN VII - Facial
Trochlear
- The trochlear nerve arises from the posterior midbrain
Label the layers of the brain
3 layers of meninges:
- dura mater
- arachnoid mater
- pia mater
What are the 2 layers of the dura mater?
- Periosteal layer
- Meningeal layer
The dural venous sinuses are located between the two layers of dura mater, what are they responsible for?
venous drainage of the cranium and empty into the internal jugular veins
What are dural reflections?
- where the meningeal layer of the dura mater folds inwards on itself to form four dural reflections
1. Falx cerebria - separates left and right cerebral hemispheres
2. Tentorium cerebelli - separates occipital lobes from cerebellum
3. Flax cerebelli - separates left and right cerebellar hemispheres
4. Diaphagma sellae
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
Is the arachnoid space vascularised or avascular?
avascular
Meningitis - what is it + aetiology + complications
- Meningitis = inflammation of the meninges
- usually caused by pathogens, but can be drug-induced
- bacteria are most common infective cause - Neisseria meningitidis and Streptococcus pneumonia
- complication - cranial herniation (if ICP increases too much then part of the brain is forced out of the cranial cavity)
Which of the following cranial nerves provides sensory innervation to the dura mater?
- Abducens nerve
- Accessory nerve
- Olfactory nerve
- Trigeminal nerve
Trigeminal nerve
Where does blood accumulate in an extradural haematoma?
- Between the dura mater and arachnoid mater
- Between the periosteal and meningeal layers of the dura mater
- Between the arachnoid mater and pia mater
- Between the skull and periosteal layer of the dura mater
Between the skull and periosteal layer of the dura mate
- In an extradural haematoma, arterial blood collects between the skull and the periosteal layer of the dura mater
What is contained within the sub-arachnoid space?
- Skull periosteum
- Dural venous sinuses
- Cerebrospinal fluid
- Emissary veins
Cerebrospinal fluid
- The sub-arachnoid space contains cerebrospinal fluid that acts to cushion the brai
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 are Broca’s and Wernicke’s areas within the cerebrum?
- Broca’s (speech production and articulation) - Frontal lobe in dominant hemisphere (left hemisphere for most ppl)
- Wernicke’s (language comprehension and understanding spoken/written language) - Temporal lobe in dominant hemisphere (left hemisphere for most ppl)
From which structure is the cerebrum embryonically derived?
- Mesencephalon
- Myelencephalon
- Diencephalon
- Prosencephalon
Prosencephalon
Which arteries supply the most lateral portions of the cerebrum?
- Anterior cerebral arteries
- Middle cerebral arteries
- Posterior cerebral arteries
- Basilar artery
Middle cerebral arteries
If a patient experiences damage to the temporal lobe, which symptom are they most likely to present with?
- Visual field defects
- Recognition deficits
- Personality changes
- Attention deficits
Recognition deficits
- Damage to the temporal lobe usually presents with recognition deficits, for example, the patient may not recognise basic sounds or be unable to recognise faces
During embryonic development, the anterior portion of the neural tube forms three parts that give rise to the brain and associated structures - what are these three parts?
- Forebrain (cerebrum, thalamus, and hypothalamus) - prosencephalon
- Midbrain - mesencephalon
- Hindbrain - rhombencephalon
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
When considering the development of the central nervous system, what is the embryonic origin of the cerebellum?
- Myelencephalon
- Metencephalon
- Telencephalon
- Diencephalon
Metencephalon
- the hindbrain divides into the metencephalon (superior) and the myelencephalon (inferior) - the cerebellum develops from the metencephalon divison
What structure separates the cerebellum from the occipital and temporal lobes?
- Tentorium cerebelli
- Longitudinal fissure
- Falx cerebri
- Fourth ventricle
Tentorium cerebelli
Which functional division of the cerebellum is responsible for balance?
- Cerebrocerebellum
- Spinocerebellum
- Vestibulocerebellum
- None of the above
Vestibulocerebellum
Which of these substances is produced by the pineal gland?
- Melatonin
- Calcitonin
- Serotonin
- Thyrotropin-releasing hormone
Melatonin
- The pineal gland produces melatonin, which regulates the circadian rhythm of the body.
What does the ascending tracts refer to + what are the conscious and unconscious tracts comprised of?
- Ascending tracts - refer to the neural pathways by which sensory information from the peripheral nerves is transmitted to the cerebral cortex
.
1. Conscious tracts - comprised of the dorsal column-medial lemniscal pathway and the anterolateral system
2. Unconscious tracts - comprised of the spinocerebellar tracts
Dorsal column-medial lemniscal pathway (DCML) - what sensory modalities does this carry?
- fine touch (tactile sensation)
- vibration
- proprioception
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
The anterolateral system can be split into the anterior spinothalamic tract and the lateral spinothalamic tract - what sensory modalities are carried in each?
- Anterior spinothalamic tract – carries the sensory modalities of crude touch and pressure
- Lateral spinothalamic tract – carries the sensory modalities of pain and temperature
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
Which of the following sensory modalities is transmitted by the dorsal column-medial lemniscus pathway?
- Crude touch
- Temperature
- Pain
- Proprioception
Proprioception
- The DCML transmits touch (tactile sensation), vibration and proprioception
Which tracts carry unconscious proprioceptive information?
- DCML
- Spinocerebellar tracts
- Anterior spinothalmic tract
- Lateral spinothalmic tract
Spinocerebellar tracts
Complete the sentence: The third order neurones of the DCML ascend from the ___________ and synapse in the sensory cortex
- Cuneate nucleus
- Gracile nucleus
- Thalamus
- Medulla oblongata
Thalamus
- The 3rd order neurones of the DCML ascend from the ventral posterolateral nucleus of the thalamus, travel through the internal capsule and terminate at the sensory cortex.
Ascending tracts VS Descending tracts
- Ascending tracts - refer to the neural pathways by which sensory information from the peripheral nerves is transmitted to the cerebral cortex
- Descending tracts - pathways by which motor signals are sent from the brain to lower motor neurones, the lower motor neurones then directly innervate muscles to produce movement
Descending tracts - the motor tracts can be divided into 2 major groups…
- Pyramidal tracts - originate in the cerebral cortex, carrying motor fibres to the spinal cord and brainstem (responsible for voluntary control of the musculature of the body and face)
- Extrapyramidal tracts - originate in the brainstem, carrying motor fibres to the spinal cord (responsible for involuntary and automatic control of all musculature - eg. muscle tone, balance, posture, and locomotion)
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
Extrapyramidal tracts - there are 4 tracts, name the function + origin within the brainstem of each
- Vestibulospinal tracts
- Reticulospinal tracts
- Rubrospinal tracts
- Tectospinal tracts
(they all originate in the brainstem, carrying motor fibres to the spinal cord)
- Vestibulospinal (arises from vestibular nuclei) - balance and posture
- Reticulospinal tracts - medial (arises from the pons - facilitates voluntary movements + increases muscle tone), lateral (arises from the medulla - inhibits voluntary movements + reduces muscle tone)
- Rubrospinal tracts (arises from red nucleus) - thought to play role in fine control of hand movements
- Tectospinal tracts (arises from superior colliculus) - coordinates movements of head in relation to visual stimuli
The corticobulbar tracts provide innervation to the musculature of which region of the body?
- Head and neck
- Upper limbs
- Lower limbs
- Neck
Head and neck
Which of the following statements most accurately describes the function of the tectospinal tracts?
- Increase muscle tone and facilitate voluntary movements
- Coordinate movements of the head
- Decrease muscle tone and inhibit voluntary movements
- Fine control of hand movements
Coordinate movements of the head
- The tectospinal tract coordinates movements of the head in relation to visual stimuli.
The medial reticulospinal tract is an extrapyramidal tract, responsible for involuntary and automatic control of all musculature. Which region of the brainstem does it originates from?
- Cerebellum
- Pons
- Medulla
- Midbrain
Pons
What is a dermatome?
a strip of skin that is innervated by a single spinal nerve
Dermatomal distribution diagram
What is a myotome?
a group of muscles innervated by a single spinal nerve root
Myotomes table
A 45 year old man is brought to hospital following a motorcycle accident. He is suspected to have a C5 root avulsion injury.
Which action is most associated with the C5 myotome?
- Elbow flexion
- Finger abduction
- Shoulder abduction
- Hip flexion
Shoulder abduction
Where do the 12 pairs of cranial nerves arise from? (generally)
- Olfactory (CN I) and Optic (CN II) nerves - originate from the cerebrum
- CN III - CN XII - arise from the brainstem
Which of the following cranial nerves arise from the pons of the brainstem?
- Trochlear
- Trigeminal
- Vagus
- Hypoglossal
Trigeminal
- The trigeminal nerve arises from the pons. The trochlear nerve emerges from the midbrain, whilst the vagus and hypoglossal nerves both arise from the medulla
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
Which vertebral level marks the bifurcation of the common carotid artery?
- C1
- C2
- C4
- C7
C4
- The common carotid artery typically bifurcates at the upper border of the thyroid cartilage – the level of the C4 vertebrae
Which of the following is NOT a branch of the internal carotid artery?
- Anterior cerebral artery
- Posterior communicating artery
- Superior thyroid artery
- Ophthalmic artery
Superior thyroid artery
- The superior thyroid artery is a branch of the external carotid artery
The vertebral arteries arise from which artery?
- External carotid
- Thyrocervical
- Subclavian
- Common carotid
Subclavian
Between which layers of the brain do the dural venous sinuses lie?
between the periosteal and meningeal layers of the dura mater
What vein do all of the dural venous sinuses ultimately drain into?
internal jugular vein
Do the dural venous sinuses have valves?
NO (the only veins in the body to not have valves)
Label this diagram of the dural venous sinuses
Note: the great cerebral vein
What is a cerebral venous sinus thrombosis (CVST) + treatment
presence of a thrombus within one of the dural venous sinuses
- treatment –> anticoagulation
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
The superior cerebral veins drain to which dural venous sinus?
- Inferior sagittal
- Superior sagittal
- Transverse sagittal sinus
- Sigmoid sinus
Superior sagittal
- The superior cerebral veins drain the superior surface of the cerebrum and empty into the superior sagittal sinus
The great cerebral vein empties into which dural venous sinus?
- Transverse
- Sigmoid sinus
- Straight sinus
- Inferior sagittal sinus
Straight sinus
- The great cerebral vein combines with the inferior sagittal sinus to form the straight sinus
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)
Which structure of the ventricular system is chiefly involved in the synthesis of cerebrospinal fluid?
- Cerebral aqueduct
- Arachnoid granulations
- Choroid plexus
- Subarachnoid cisterns
Choroid plexus
Which type of epithelial cells are present in the choroid plexus of the ventricular system?
- Cuboidal
- Columnar
- Transverse
- Squamous
Cuboidal
- The choroid plexus consists of capillaries and loose connective tissue surrounded by cuboidal epithelial cells.
In the ventricular system of the brain, the foramen of Munro connects which structures?
- Lateral ventricles - 3rd ventricle
- 3rd ventricle - 4th ventricle
- Lateral ventricle - lateral ventricle
- 4th ventricle - lateral ventricle
Lateral ventricles - 3rd ventricle
What key aspects of history should be explored when assessing neuropathy?
- Occupational history: Exposure to toxins (e.g., heavy metals, solvents)
- Nutritional history: Deficiencies in vitamins (e.g., B1, B6, B12, E)
- Social history: Alcohol use, recreational drugs, socioeconomic status
- Family history: Inherited neuropathies (e.g., Charcot-Marie-Tooth disease)
- Medical history: Diabetes, infections, autoimmune diseases, malignancies
What symptoms help determine the type of neuropathy?
- peripheral
- sensory
- motor
- autonomic
- Peripheral: Numbness, tingling, burning, or weakness in extremities
- Sensory: Loss of vibration, proprioception, or pain sensation
- Motor: Weakness or atrophy of muscles
- Autonomic: Postural hypotension, gastrointestinal issues, or sweating abnormalities
What initial investigations are useful in diagnosing neuropathy?
- Blood tests: HbA1c, B12, folate, TFTs, U&E, liver function, autoantibodies
- Nerve conduction studies: Differentiate axonal vs. demyelinating neuropathy
- Electromyography (EMG): Evaluate muscle and nerve function
- Consider further tests: Serum electrophoresis (e.g., myeloma), genetic testing, lumbar puncture if Guillain-Barré syndrome is suspected
What are common causes of neuropathy based on history and investigation?
- Metabolic: Diabetes, hypothyroidism
- Nutritional: Vitamin B12 or thiamine deficiency
- Toxic: Alcohol, chemotherapy, heavy metals
- Inherited: Charcot-Marie-Tooth disease
- Infective: HIV, Lyme disease
- Immune-mediated: Guillain-Barré syndrome, CIDP
What clinical examination findings help define the cause of a generalised neuropathy?
- Distribution: Symmetrical (metabolic/toxic) vs. asymmetrical (vasculitis, infections)
- Motor: Distal weakness (axonal) or proximal weakness (demyelinating/inflammatory)
- Sensory: Vibration/proprioception loss (demyelination, e.g., B12 deficiency) vs. pain/temperature loss (axonal, e.g., diabetes)
- Autonomic: Postural hypotension, abnormal sweating → diabetes, amyloidosis
- Reflexes: Reduced/absent reflexes in most neuropathies
What investigations help define the cause of generalised neuropathy?
- Blood tests: HbA1c (diabetes), B12, folate, U&E, TFTs, ANA/ENA, serum electrophoresis
- Nerve conduction studies: Axonal (low amplitude), Demyelinating (slowed velocity)
- Lumbar puncture: Raised protein (Guillain-Barré or CIDP); inflammatory cells (infection)
- Genetic testing: For hereditary neuropathies (e.g., Charcot-Marie-Tooth)
Which causes of neuropathy are treatable?
- Metabolic: Diabetes (glycaemic control), hypothyroidism (hormone replacement)
- Nutritional: Supplement B12, B1, folate
- Toxic: Alcohol cessation; stop neurotoxic drugs
- Immune-mediated: Guillain-Barré (IVIG/plasma exchange), CIDP (Steroids, IVIG, immunosuppressants)
- Infective: Treat infections (e.g., HIV, Lyme disease)
- Paraneoplastic: Treat underlying cancer
What findings suggest specific causes of neuropathy?
- Diabetes: Stocking-glove sensory loss, abnormal HbA1c
- Alcohol: Mixed sensory-motor neuropathy, chronic alcohol use
- B12 deficiency: Sensory ataxia, macrocytic anaemia
- Guillain-Barré: Rapid weakness, areflexia, raised CSF protein
- Vasculitis: Painful asymmetrical neuropathy, systemic signs (e.g., rash)
What red flags suggest urgent causes of neuropathy?
- Guillain-Barré: Rapid progression, respiratory compromise
- Vasculitis: Painful, multifocal neuropathy with systemic inflammation
- Paraneoplastic: Subacute neuropathy, malignancy symptoms
- Critical illness: ICU patients with sepsis or organ failure
What key aspects of history should be explored when assessing a headache in primary care?
- SOCRATES: Site, Onset, Character, Radiation, Associated symptoms, Timing, Exacerbating/relieving factors, Severity
.
Red flags (SNOOP): - Systemic symptoms (fever, weight loss)
- Neurological symptoms (weakness, vision changes)
- Onset sudden/thunderclap
- Older age of onset (>50)
- Pattern change (progressive or unresponsive to treatment)
. - Triggers: Stress, sleep, caffeine, dehydration, medications.
- Hx of migraines, family history, medication use (e.g., analgesic overuse)
What are the most common causes of headache seen in primary care?
Primary headaches:
- Tension-type headache: Bilateral, pressure-like, no nausea/photophobia
- Migraine: Unilateral, pulsating, associated with nausea, photophobia, aura
- Cluster headache: Severe, unilateral, orbital/temporal, autonomic symptoms (e.g., tearing, nasal congestion)
.
Secondary headaches:
- Medication overuse headache
- Sinusitis: Frontal/maxillary pain, worse with bending forward
- TMJ dysfunction: Jaw pain, worse with chewing
What are the red flag conditions to consider in headache assessment?
- Subarachnoid haemorrhage: Sudden, thunderclap headache, neck stiffness
- Meningitis/encephalitis: Fever, photophobia, neck stiffness, altered consciousness
- Raised intracranial pressure (ICP): Worsening with lying down, morning vomiting, visual disturbances, papilloedema
- Temporal arteritis: New headache in >50s, scalp tenderness, jaw claudication, visual changes
- Brain tumour: Progressive, focal neurological symptoms
- Acute angle-closure glaucoma: Severe eye pain, nausea, vision loss, red eye, fixed mid-dilated pupil
What should the clinical examination focus on when assessing headache?
- General appearance: Signs of distress, fever, weight loss
- Neurological exam: Cranial nerves, fundoscopy (papilloedema), motor/sensory deficits, coordination
- Head/neck: Scalp tenderness (temporal arteritis), sinus tenderness, neck stiffness (meningitis)
- Eye exam: Visual acuity, visual fields, pupil response, signs of acute angle-closure glaucoma (red eye, mid-dilated pupil, corneal oedema)
- Blood pressure: Hypertensive crisis
What are the key differential diagnoses for headache in primary care?
- Primary headaches
- Secondary headaches (benign and serious)
- Primary headaches: Tension, migraine, cluster
- Secondary headaches:
- Benign: Sinusitis, TMJ dysfunction, medication overuse.
- Serious: SAH, meningitis, raised ICP, temporal arteritis, brain tumour, acute angle-closure glaucoma
What key questions can help differentiate headache types in primary care?
- Migraine: Do you experience nausea, vomiting, or sensitivity to light/noise?
- Cluster: Is the pain severe, around one eye, with tearing or nasal congestion?
- Tension: Is the headache bilateral, dull, or pressure-like?
- Red flags: Was the onset sudden and severe, or are there neurological or systemic changes?
What are the common headache features associated with raised intracranial pressure (ICP)?
- Worsening headache: Typically worse in the morning or on awakening
- Dull, constant pain: Often described as a pressure-like headache
- Exacerbated by: Coughing, sneezing, bending over, or straining (Valsalva manoeuvre)
- Position-dependent: Worse when lying down or on awakening
- Nausea and vomiting: Often occur in the morning or after a headache episode
- Visual changes: Blurred vision, double vision due to papilloedema or cranial nerve compression
What associated features may suggest raised intracranial pressure?
eg. examination findings
- Papilloedema: Swelling of the optic disc seen on fundoscopy due to increased pressure on the optic nerve
- Neurological signs: Focal deficits (e.g., hemiparesis, cranial nerve palsies)
- Altered mental status: Confusion, drowsiness, or agitation due to compression of the brainstem
- Cushing’s triad: Bradycardia, hypertension, irregular respirations (late signs)
- Hyperreflexia: Increased reflexes due to pressure on the brainstem
What are the main causes of raised intracranial pressure?
- Mass effect: Brain tumour, abscess, or haemorrhage causing displacement of brain tissue
- Hydrocephalus: Accumulation of cerebrospinal fluid (CSF) due to blockage or impaired absorption
- Cerebral oedema: Swelling of the brain, often seen in trauma, stroke, or infections (e.g., encephalitis)
- Increased blood volume: Venous sinus thrombosis, cerebral venous hypertension
- Infection: Meningitis or encephalitis causing inflammation and increased ICP
- Increased CSF production: Rare causes, e.g., choroid plexus tumour
What red flag features in a headache presentation suggest raised ICP?
- Severe, sudden onset headache: Often referred to as a “thunderclap headache.”
- Progressive headache: Increasing frequency or intensity over time
- Morning headaches: Particularly if associated with vomiting or nausea
- Neurological deficits: New or worsening focal neurological symptoms, such as weakness or vision changes
- Papilloedema: Detected on fundoscopy
How is raised intracranial pressure managed?
- Medical management:
- Osmotic diuretics (e.g., mannitol) to reduce cerebral oedema
- Corticosteroids (e.g., dexamethasone) for tumour-induced ICP
- Hyperventilation (in emergency settings) to decrease CO2 and vasoconstrict cerebral vessels - Surgical management:
- Decompression surgery for mass lesions
- Ventriculostomy for hydrocephalus - Monitoring: ICP monitoring for severe cases (e.g., head trauma, intracranial surgery)
How are anxiety and headache commonly related?
- Anxiety disorders (e.g., generalized anxiety disorder, panic disorder) are often linked to chronic headaches (e.g., tension-type headaches, migraines)
- Headaches can exacerbate anxiety, creating a cycle of pain and distress
- Individuals with anxiety are more likely to experience both episodic and chronic headaches
What mechanisms link anxiety to headache development?
- Muscle tension: Anxiety increases muscle tension, particularly in the head, neck, and shoulders, which can trigger or worsen tension-type headaches
- Autonomic nervous system: Anxiety activates the sympathetic nervous system, potentially triggering vascular changes that contribute to migraines
- Stress hormones: Anxiety raises cortisol levels, which can increase pain sensitivity and contribute to headache onset or intensification
How can headaches contribute to anxiety?
- Chronic headaches can lead to anticipatory anxiety, especially if the person fears frequent pain or disability
- Health anxiety may develop, where headaches are misinterpreted as a sign of a serious condition, exacerbating anxiety
How are both anxiety and headaches treated together?
- Medications: Tricyclic antidepressants (e.g., amitriptyline), SSRIs, and SNRIs can treat both conditions.
- Cognitive Behavioral Therapy (CBT): Addresses cognitive patterns that exacerbate both anxiety and headaches.
- Biofeedback and relaxation techniques: Help reduce muscle tension and anxiety, alleviating tension-type headaches.
How does anxiety specifically relate to migraines?
- People with migraines are at higher risk for anxiety disorders
- Anxiety can increase the frequency and intensity of migraines, making patients more sensitive to common triggers such as stress, poor sleep, or hormonal fluctuations
How do chronic headaches and anxiety interact to impact mental health?
- Chronic pain from headaches can reduce quality of life, leading to social withdrawal and increased anxiety
- Managing one condition often leads to improvements in the other, helping to break the cycle of pain and anxiety
What are chronic daily headaches and what types exist?
- Headaches occurring on 15 or more days per month for at least 3 months
- Types: Chronic Tension-Type Headache, Chronic Migraine, Medication Overuse Headache (MOH), and Chronic Cluster Headache
What are the key risk factors for chronic daily headaches?
- Previous episodic headaches (migraine, tension-type)
- Chronic stress, poor sleep hygiene, and medication overuse
- Psychological factors like anxiety and depression
- Genetic predisposition to headache disorders
Which medications are commonly associated with medication overuse headache?
- Simple analgesics: Paracetamol, ibuprofen
- Triptans: E.g., sumatriptan
- Opioids: Codeine, tramadol
- Combination analgesics: Containing caffeine, codeine, or other additives
How is medication overuse headache treated?
- Discontinue the overused medication, preferably gradually
- Pain management with alternative treatments (e.g., NSAIDs, antiemetics)
- Preventive treatments like tricyclic antidepressants, anticonvulsants, or botulinum toxin for chronic migraine or tension-type headache
What is the initial assessment approach for a patient with headache?
- Thorough history (onset, duration, frequency, type, associated symptoms, family history)
- Neurological examination to check for focal deficits, papilloedema, and signs of raised ICP
What are red flags in a headache history that warrant urgent referral?
- Sudden onset (thunderclap headache)
- Neurological deficits (weakness, speech issues)
- Signs of raised ICP (vomiting, papilloedema)
- New headache in patients over 50
- Headache with systemic symptoms (fever, weight loss)
What is the first-line treatment for non-severe headaches in primary care?
- For mild tension-type headaches: Paracetamol, ibuprofen, or aspirin
- For acute migraine: Triptans (e.g., sumatriptan)
- For chronic headaches: Consider prophylactic medications (e.g., amitriptyline, topiramate)
When should a headache patient be urgently referred to neurology or emergency care?
- Sudden onset or atypical headache with red flags (e.g., thunderclap, neurological signs)
- Headaches with signs of secondary causes (e.g., subarachnoid haemorrhage, brain tumour)
- Progressive headache pattern or increasing severity
When should a patient with chronic headaches be referred to a specialist?
- If headaches are severe, frequent (15+ days/month), or refractory to first-line treatments
- Referral to a headache clinic for advanced treatments like botulinum toxin or CGRP inhibitors
What are the key components in the general management of migraine?
- Identify and avoid triggers (e.g., stress, certain foods)
- Maintain regular sleep hygiene and exercise
- Educate patients and encourage keeping a headache diary
When should a patient with migraine be referred to a specialist?
- For frequent or severe migraines unresponsive to treatment
- For chronic migraine (15+ headache days/month)
- If there are atypical features or suspicion of secondary causes
What are the key differential diagnoses for headache, neck stiffness, photophobia, and pyrexia?
- Meningitis (Bacterial & Viral)
- Subarachnoid Hemorrhage (SAH)
- Cerebral Venous Sinus Thrombosis (CVST)
- Encephalitis
- Post-infectious Meningitis
What tests would you use to distinguish between the differential diagnoses of headache, neck stiffness, photophobia, and pyrexia?
- Meningitis (Bacterial & Viral)
- Lumbar Puncture (LP): Bacterial (low glucose, high protein, neutrophils), Viral (normal glucose/protein, lymphocytes)
- PCR testing (for viral causes like HSV or enteroviruses) - Subarachnoid Hemorrhage (SAH)
- CT Brain: Initial test to detect blood in the subarachnoid space
- LP: If CT is negative, look for xanthochromia (yellow color of CSF due to blood breakdown - at least 12hrs after onset) - Cerebral Venous Sinus Thrombosis (CVST)
- MRI Brain with Venography: Gold standard for detecting clot in the cerebral venous sinuses - Encephalitis
- MRI Brain: To identify inflammation in the brain parenchyma
- LP: CSF PCR testing to identify viral causes (e.g. HSV, enteroviruses) - Post-infectious Meningitis
- LP: CSF analysis shows mild pleocytosis (slightly elevated WBC), normal glucose, slightly elevated protein
- History: Recent viral infection history helps guide the diagnosis
What is the role of medical management in spinal cord injury (SCI) or chronic neurological diseases?
- Neurological Rehabilitation: Physical therapy, occupational therapy, and speech therapy
- Pain Management: Medications like gabapentin, amitriptyline for neuropathic pain
- Bladder/Bowel Management: Catheterisation, bowel training
- Pressure Ulcer Prevention: Skin checks, pressure-relieving cushions, regular repositioning
What psychosocial support is essential for patients with SCI or chronic neurological diseases?
- Mental Health: Counselling, cognitive-behavioural therapy (CBT), antidepressants (SSRIs, SNRIs)
- Support Groups: Connecting patients with peers who have similar conditions
- Social Services: Home adaptations, disability benefits, patient advocacy
What is the role of different agencies and healthcare providers in managing SCI or chronic neurological diseases?
- Multidisciplinary Team: Neurologists, physiatrists, physical/occupational therapists, nurses, psychiatrists, dietitians, social workers
- Specialist Clinics: Spinal cord injury clinics, neurorehabilitation centres, pain management clinics
What secondary prevention strategies are used in SCI or chronic neurological diseases?
- DVT/PE Prevention: Compression stockings, anticoagulation, early mobilisation
- Osteoporosis: Bone density screening, bisphosphonates, vitamin D
- Cardiovascular Health: Monitoring blood pressure, cholesterol, and blood sugar
- Respiratory Complications: Respiratory physiotherapy, monitoring lung function
How is depression and mental health managed in patients with SCI or chronic neurological diseases?
- Screening for Depression: Regular mental health screening
- Psychotherapy: Cognitive-behavioural therapy (CBT)
- Pharmacotherapy: Antidepressants (SSRIs like sertraline, fluoxetine, SNRIs like duloxetine)
What support is provided for patients and their families in SCI or chronic neurological diseases?
- Long-Term Support Networks: Ongoing follow-up with healthcare providers, community resources
- Empowerment: Involvement in decision-making regarding care plans, treatment options
- Education: Information on the condition, treatment options, and lifestyle changes
How do you assess a patient with impaired consciousness and a potential head injury?
- Initial Assessment (ABCDE Approach)
- Airway: Ensure the airway is patent
- Breathing: Assess respiratory rate and effort
- Circulation: Check heart rate, blood pressure, and signs of shock
- Disability: Neurological status, including GCS (Glasgow Coma Scale)
- Exposure: Expose to check for injuries, avoiding hypothermia. - History:
- Mechanism of injury (e.g., fall, trauma)
- Loss of consciousness, duration, and any post-traumatic amnesia
- Any seizures, vomiting, or focal neurological signs
What is the Glasgow Coma Scale (GCS) and how is it used in assessing impaired consciousness?
The GCS assesses the level of consciousness based on three components:
- Eye Opening (E):
4 = Spontaneous
3 = To speech
2 = To pain
1 = None - Verbal Response (V):
5 = Oriented
4 = Confused conversation
3 = Inappropriate words
2 = Incomprehensible sounds
1 = None - Motor Response (M):
6 = Obeys commands
5 = Localises pain
4 = Withdraws from pain
3 = Abnormal flexion (decorticate posture)
2 = Abnormal extension (decerebrate posture)
1 = None
What is the acute diagnostic approach for a patient with a head injury and impaired consciousness?
- Initial Screening:
- Glasgow Coma Scale: Establish baseline consciousness
- Clinical Examination: Look for signs of focal neurological deficits, hemotympanum, Battle’s sign (bruising behind ears), raccoon eyes, or cervical spine injury - Imaging:
- CT Head: First-line imaging in patients with significant trauma or GCS <15, focal neurological signs, or worsening symptoms
- MRI Head: Used in some cases for more detailed assessment, especially for diffuse axonal injury (DAI), but not first-line - Other Tests:
- Cervical Spine X-ray or CT if cervical spine injury is suspected
- Blood tests (e.g., glucose, electrolytes, blood alcohol level) for any metabolic causes or intoxication
What are the indications for neurosurgical intervention in a patient with a head injury?
- Surgical Decompression:
- Epidural hematoma (if significant mass effect, typically after arterial bleeding).
- Subdural hematoma (if there is deterioration in GCS or significant brain compression).
- Intracerebral hemorrhage (if there is significant brain compression or herniation).
- Diffuse Axonal Injury (DAI): Surgical intervention is rarely required, but medical management for raised ICP may be necessary. - Craniotomy: If there is significant brain swelling or hematoma that requires drainage.
What is involved in the secondary prevention and follow-up care of a patient with a head injury?
- Monitor for Post-Concussion Syndrome:
- Symptoms like headaches, dizziness, fatigue, and mood disturbances may last for weeks to months after a mild head injury
- Psychological support for anxiety or depression related to recovery.
. - Rehabilitation:
- Physical therapy for balance and coordination
- Cognitive therapy for memory and attention deficits
- Speech therapy if there are communication difficulties
. - Return-to-Play/Work:
- Gradual return to activity is recommended, particularly for athletes, with careful monitoring for any worsening symptoms
- Follow return-to-work guidelines for patients in high-risk professions, depending on the severity of the injury
What is the acute management of a patient with a head injury and impaired consciousness?
- Airway and Breathing:
- Ensure airway patency (intubate if GCS ≤8)
- Monitor for respiratory distress - Circulation: Maintain SBP >90 mmHg; fluid resuscitation if necessary
- ICP Control: Elevate head of the bed (30°), use mannitol or hypertonic saline to reduce swelling
- Neuroimaging: Perform CT if condition deteriorates (worsening GCS, new deficits)
- Monitor for Seizures: Treat with phenytoin or levetiracetam if seizures occur
What are the key features in the presentation of a patient with decreased or loss of consciousness?
- Loss of Consciousness (LOC): Sudden or gradual onset, with complete or partial unresponsiveness to external stimuli.
- Duration: Transient (syncope) vs. prolonged (coma).
.
Associated Features: - Preceding Symptoms: Dizziness, nausea, visual disturbances (e.g., lightheadedness in syncope).
- Post-Event Symptoms: Confusion, headache, amnesia (common in seizures or post-ictal state).
- Signs of Seizure: Tongue biting, incontinence, jerky movements.
- Trauma: Head injury or neck injury if LOC follows trauma.
- Autonomic Symptoms: Pallor, sweating, bradycardia in syncope; signs of raised intracranial pressure (e.g., vomiting, headache).
What are the initial investigations for a patient with decreased or loss of consciousness?
- History and Physical Exam:
Thorough history (e.g., triggers, duration, associated symptoms).
Neurological exam: Assess GCS, cranial nerve function, and motor/sensory status. - Basic Investigations:
- Blood Glucose: Rule out hypoglycemia.
- ECG: To check for arrhythmias (e.g., bradycardia, prolonged QT).
- FBC: To assess for anaemia or infection.
- Electrolytes: Check for electrolyte imbalances (e.g., hyponatremia, hyperkalemia).
- Cardiac Enzymes: If considering myocardial infarction (e.g., troponins). - Imaging:
- CT/MRI of Brain: If suspecting intracranial causes (e.g., stroke, hemorrhage).
- Carotid Doppler/ECG: If syncope is suspected to be of cardiovascular origin.
What are the key differential diagnoses for decreased or loss of consciousness?
- Syncope: Sudden, transient LOC due to decreased cerebral perfusion, often associated with a drop in blood pressure (e.g., vasovagal, orthostatic hypotension)
- Seizures: Sudden LOC with jerking movements, tongue biting, and post-ictal confusion
- Stroke: LOC or altered consciousness due to acute cerebrovascular event (e.g., ischemic or hemorrhagic)
- Hypoglycemia: Sudden LOC due to low blood glucose
- Cardiac Arrhythmias: LOC due to transient loss of cardiac output (e.g., bradycardia, tachycardia, or conduction disturbances)
- Trauma: LOC following head injury; consider concussions, contusions, or more severe brain injury
- Intoxication/Overdose: LOC due to drugs, alcohol, or toxins (e.g., opioids, sedatives)
- Metabolic/Endocrine Causes: Hyponatremia, hypercalcemia, thyroid disorders
- Infections: Sepsis, meningitis, or encephalitis may lead to altered mental status and LOC
What is the initial management for a patient with decreased or loss of consciousness?
- Airway: Ensure airway is clear; consider intubation if GCS ≤8.
- Breathing: Monitor oxygen saturation and provide supplemental oxygen if needed.
- Circulation: Monitor vitals (e.g., blood pressure, heart rate), manage hypotension or arrhythmias (e.g., IV fluids, medications).
- Monitor for Seizures: Administer benzodiazepines (e.g., lorazepam, diazepam) if seizures are observed.
- Investigate Underlying Cause:
- If syncope: Elevate legs, assess for orthostatic hypotension, or cardiovascular triggers (ECG).
- If seizures: Consider anticonvulsants (e.g., phenytoin or levetiracetam).
- If stroke or intracranial pathology: Perform neuroimaging (CT/MRI), manage ICP if indicated. - Glucose: If hypoglycemia is suspected, administer glucose (oral or IV).
How would you manage a patient with decreased consciousness based on the suspected cause?
A:
- Syncope:
- Seizure:
- Stroke:
- Cardiac Arrhythmia:
- Hypoglycemia:
- Syncope:
- Position patient supine with legs elevated.
- Identify and treat underlying cause (e.g., arrhythmias, dehydration).
- Educate on lifestyle changes to prevent recurrent episodes. - Seizure:
- Benzodiazepines (e.g., lorazepam or diazepam) to terminate seizure activity.
- Post-ictal monitoring and evaluation with EEG and possible MRI for structural abnormalities. - Stroke:
- CT brain to rule out hemorrhagic stroke.
- Thrombolysis (if ischemic stroke, within 4.5 hours).
- Supportive care for stroke complications (e.g., ICP management, rehabilitation). - Cardiac Arrhythmia:
- ECG to identify arrhythmias; pacemaker or defibrillation if indicated.
- Long-term arrhythmia management with medications (e.g., beta-blockers, anticoagulants) or device therapy. - Hypoglycemia:
- Administer IV glucose or glucagon if severe hypoglycemia is confirmed.
- Long-term management with blood sugar control and dietary adjustments.
Multiple Sclerosis - more common in men or women?
WOMEN
What are the different types of Multiple Sclerosis (MS) and their clinical presentations?
- Relapsing-Remitting MS (RRMS):
- Presentation: Episodic flare-ups of neurological symptoms followed by partial or complete recovery (remissions).
- Symptoms: Includes fatigue, optic neuritis, sensory changes, muscle weakness, and ataxia.
- Course: Most common type (85% of patients); relapses are unpredictable but symptoms often improve during remission. - Primary Progressive MS (PPMS):
- Presentation: Gradual progression of symptoms from the onset, without distinct relapses or remissions.
- Symptoms: Slow and steady worsening of motor and sensory function, often with walking difficulties and spasticity.
- Course: Affects about 10-15% of patients; generally has a poorer prognosis due to continuous progression without improvement. - Secondary Progressive MS (SPMS):
- Presentation: Initially relapsing-remitting course (like RRMS), but later transitions to a phase of steady progression with or without relapses.
- Symptoms: Similar to RRMS but with more severe long-term disability.
- Course: Typically develops 10-20 years after the onset of RRMS. - Progressive-Relapsing MS (PRMS):
- Presentation: Steady progression of disability from the onset, with superimposed acute relapses.
- Symptoms: Continuous deterioration in neurological function, along with occasional exacerbations.
- Course: Rare and severe form, associated with a poor prognosis.
Q: What are the risk factors for developing Multiple Sclerosis (MS)?
- Age: Most commonly diagnosed between ages 20-40 years
- Gender: Women are more likely to develop MS (2-3 times higher than men)
- Genetics: Family history of MS increases risk; specific genetic markers (e.g., HLA-DRB1 locus) are linked to susceptibility
- Geography: Higher prevalence in regions farther from the equator (e.g., Northern Europe, North America, and Australasia)
- Vitamin D Deficiency: Low levels of vitamin D are associated with an increased risk of MS
- Infections: Certain viral infections, particularly Epstein-Barr virus (EBV), have been linked to the development of MS
- Smoking: Increases risk and may accelerate disease progression
- Ethnicity: More common in individuals of Caucasian descent, less common in Asian and Native American populations
- Obesity: Particularly in adolescence, obesity has been associated with a higher risk of developing MS
What is myelopathy?
Myelopathy refers to functional or pathological disturbance of the spinal cord, which can result from intrinsic or extrinsic causes.
What is intrinsic myelopathy?
Myelopathy caused by conditions within the spinal cord, such as tumours, syringomyelia, or inflammatory diseases (e.g., multiple sclerosis).
What is extrinsic (compressive) myelopathy?
Myelopathy caused by external compression of the spinal cord, often due to herniated discs, tumours, trauma, or spinal stenosis
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.
What are the features of anterior horn cell involvement in myelopathy?
- Flaccid paralysis at the level of the lesion
- Muscle atrophy.
- Fasciculations.
How can meningeal pathology contribute to myelopathy?
Compression or infiltration of the spinal cord by meningeal tumours, infections (e.g., meningitis, TB), or subdural/epidural haematomas.
What vascular structures supply the spinal cord?
- Anterior spinal artery (supplies anterior two-thirds of the cord)
- Paired posterior spinal arteries (supply the posterior one-third).
- Radicular arteries (e.g., artery of Adamkiewicz).
What are the clinical features of anterior spinal artery syndrome?
- Bilateral weakness (corticospinal tract involvement).
- Loss of pain and temperature sensation (spinothalamic tract involvement).
- Preserved proprioception and vibration sense (dorsal columns spared).
What symptoms arise from posterior spinal artery ischaemia?
- Loss of proprioception and vibration sense.
- Sensory ataxia.
What are the clinical signs of cervical myelopathy?
- Weakness in upper and/or lower limbs.
- Spasticity in the legs.
- Loss of hand dexterity.
- Hyperreflexia and positive Hoffman’s sign.
What are the features of thoracic myelopathy?
- Spastic paraparesis.
- Sensory level on the trunk (e.g., loss of sensation below a specific dermatome).
- Bowel and bladder dysfunction in advanced cases.
What clinical signs indicate lumbar myelopathy?
- Lower motor neuron signs at the level of the lesion.
- Spasticity and upper motor neuron signs in the legs (if the lesion extends to the thoracic cord).
- Cauda equina syndrome if compression affects nerve roots.
What is a blackout?
A transient loss of consciousness (TLOC) or awareness caused by various conditions, including seizures, syncope, or psychogenic events
What are the main causes of blackouts?
- Seizures (e.g., epilepsy).
- Syncope (e.g., vasovagal, cardiac).
- Psychogenic (e.g., psychogenic non-epileptic seizures, anxiety).
- Rare causes (e.g., hypoglycaemia, hypoxia).
What are key historical features of seizures?
- Sudden onset.
- Preceded by an aura (in some cases).
- May have a stereotypical pattern.
- Postictal confusion or drowsiness.
How does the duration of a seizure typically compare to other causes of blackouts?
Seizures often last 1–2 minutes, whereas syncope is usually much shorter (seconds).
What are key historical features of vasovagal syncope?
- Triggered by prolonged standing, pain, or emotional stress.
- Preceded by prodromal symptoms (e.g., dizziness, nausea, sweating).
- Rapid recovery without confusion.
What distinguishes cardiac syncope from other blackouts?
- Sudden onset without warning.
- Often exertional or associated with palpitations.
- Rapid recovery without postictal confusion.
What features suggest psychogenic non-epileptic seizures (PNES)?
- Asynchronous or irregular movements.
- Prolonged duration without postictal phase.
- Triggered by stress or emotional events.
- Eye closure during the event.
How can hyperventilation-induced blackouts present?
- Associated with anxiety or panic attacks.
- Lightheadedness, tingling in extremities, and chest tightness before TLOC.
Seizures vs Syncope
- Onset
- Duration
- Recovery
What are the functions and symptoms of frontal lobe damage?
- Functions: Motor control, planning, decision-making, behaviour, and speech (Broca’s area)
- Symptoms: Weakness or paralysis (opposite side), personality changes, poor planning, speech problems (e.g., Broca’s aphasia), and shuffling gait
Focal VS Generalised seizures
What are the functions and symptoms of temporal lobe damage?
- Functions: Hearing, memory, language comprehension (Wernicke’s area), and emotion regulation
- Symptoms: Hearing issues, memory problems, nonsensical speech (Wernicke’s aphasia), emotional changes (fear, aggression), and seizures with automatisms like lip-smacking
What are the functions and symptoms of parietal lobe damage?
- Functions: Sensation, spatial awareness, and visual-sensory integration
- Symptoms: Numbness (opposite side), difficulty recognising objects, spatial neglect (ignoring one side), trouble with maths or writing (dominant side), and movement coordination problems (apraxia)
What are the functions and symptoms of occipital lobe damage?
- Functions: Visual processing
- Symptoms: Vision loss on one side, inability to recognise objects or faces, and visual hallucinations (e.g., flashes of light)
What are the functions and symptoms of cerebellum damage?
- Functions: Coordination, balance, and fine motor control
- Symptoms: Unsteady movements (ataxia), tremors during action, and trouble judging distances (dysmetria)
What are the functions and symptoms of brainstem damage?
- Functions: Autonomic control (breathing, heart rate), cranial nerve functions, and motor/sensory pathways
- Symptoms: Difficulty breathing, irregular heart rate, trouble swallowing or speaking, and weakness in arms/legs
What is the prevalence of epilepsy in children?
- Prevalence: Around 1 in 100 children.
- Higher in younger children (under 5 years) and those with neurodevelopmental disorders
How is a history of seizures and blackouts investigated?
- Medical history: Onset, duration, frequency, triggers, aura, and post-episode symptoms (e.g., confusion, tongue biting).
- Witness accounts: Observations of the episode (e.g., jerking, loss of consciousness, incontinence).
- Patient history: Head injury, strokes, epilepsy, substance use, or family history of neurological conditions.
What is assessed in the physical examination during the investigation?
- Neurological exam: Check for focal deficits, reflexes, and gait abnormalities.
- Signs of injury: Tongue biting, bruises, incontinence.
- Systemic signs: Fever, rashes (suggesting infection).
What tests are commonly used to investigate seizures and blackouts?
- EEG: Brain wave patterns to identify epilepsy.
- MRI/CT brain: Structural abnormalities like brain lesions or tumours.
- Blood tests: To rule out metabolic disturbances, infections, or electrolyte imbalances.
- ECG: If cardiac cause of blackout is suspected (e.g., arrhythmias).
How can seizures be differentiated from other causes of blackouts?
- Syncope: Triggered by lightheadedness, rapid recovery.
- Psychogenic non-epileptic seizures (PNES): Emotional triggers, no postictal confusion.
- TIA: Brief focal neurological symptoms, resolving quickly.
- Sleep disorders: Abnormal movements during sleep, no loss of consciousness
What should be ruled out in the investigation of blackouts or seizures?
- Cardiac causes: Arrhythmias or structural heart problems.
- Metabolic causes: Hypoglycaemia or electrolyte imbalances.
- Psychogenic causes: Non-epileptic seizures (PNES).
- Neurological causes: TIAs, strokes, or structural brain abnormalities.
hat is the key difference in presentation between epilepsy and Non-Epileptic Attack Disorder (NEAD)?
Epilepsy:
- Seizures often triggered by identifiable factors (e.g., sleep deprivation, flashing lights).
- May involve jerking movements, loss of consciousness, and postictal confusion.
- Aura or warning signs may precede the event.
.
NEAD:
- No clear trigger or identifiable neurological cause.
- Events may appear similar to seizures but often have psychogenic features (e.g., atypical movements, no postictal confusion).
- Often associated with stress, trauma, or psychological factors.
- No LOC in some cases.
How do investigations differ between epilepsy and NEAD?
(EEG, MRI/CT, bloods, psychological assessment)
Epilepsy:
- EEG: Shows abnormal brain activity during seizures (e.g., epileptiform discharges).
- MRI/CT brain: Can show structural abnormalities such as lesions or tumours.
- Blood tests: To rule out metabolic or infectious causes.
.
NEAD:
- EEG: Usually normal during the attack or shows no epileptiform activity.
- Video-EEG monitoring: May be used to differentiate NEAD from epilepsy (no seizure activity on EEG).
- MRI/CT brain: Typically normal, unless there’s another underlying condition.
- Psychological assessment: Key to diagnosis, often revealing underlying stress or trauma.
How does the response to treatment differ between epilepsy and NEAD?
Epilepsy:
- Antiepileptic drugs (AEDs): Typically effective in controlling seizures.
- Treatment may also involve lifestyle changes (e.g., avoiding triggers, improving sleep).
.
NEAD:
- Psychological therapies: Cognitive-behavioural therapy (CBT) or other psychotherapies are most effective.
- Antiepileptic drugs: Not effective in controlling NEAD episodes.
- Focus on addressing psychological triggers such as trauma or stress.
What are the key clinical features to differentiate epilepsy from NEAD?
Epilepsy:
- Loss of consciousness and jerking movements.
- Postictal confusion and disorientation.
- Consistent seizure patterns and triggers.
.
NEAD:
- No postictal confusion or confusion that resolves quickly.
- More variable attack features, including emotional or psychological triggers.
- Symptoms often involve atypical movements, which are not consistent with typical seizures.
What are the psychological associations seen in NEAD?
- Psychological triggers: Stress, trauma, or emotional factors are often associated with NEAD.
- Coexisting psychiatric conditions: Anxiety, depression, or post-traumatic stress disorder (PTSD) are common in NEAD patients.
- History of trauma: Many patients with NEAD have a history of psychological trauma, abuse, or emotional distress.
What are the DVLA guidelines regarding fitness to drive for individuals with epilepsy?
- Seizure-free period: Individuals must be seizure-free for 12 months (without medication or after the last seizure) before being allowed to drive.
- Medically controlled seizures: If seizures are well-controlled, the DVLA may grant a short-term driving license (1 to 3 years) with regular reviews.
- Sudden seizures: If a patient experiences a sudden or unprovoked seizure, they must inform the DVLA and refrain from driving until cleared.
- Driving restrictions: In some cases, driving restrictions may be placed (e.g., not allowed to drive large vehicles or public transport).
- Doctor’s obligation: Doctors must report a patient’s fitness to drive if seizures are not well-controlled, in the interest of public safety.
How can teenage behaviour impact seizure control and management?
- Medication non-compliance: Teenagers may be more likely to skip doses or not take medication consistently, especially if they feel well or experience side effects.
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Lifestyle factors: - Sleep deprivation due to irregular sleep patterns or late nights can trigger seizures.
- Stress from school, peer pressure, or emotional issues may increase seizure frequency.
- Substance use (alcohol, recreational drugs) can interfere with AEDs and increase seizure risk.
- Dietary habits (e.g., skipping meals) may affect seizure threshold or AED absorption.
What strategies can help address teenage behaviour to improve seizure management?
- Education: Provide age-appropriate education about the importance of medication adherence and seizure triggers.
- Family involvement: Encourage open communication between the teenager, family, and healthcare providers to ensure support and understanding.
- Routine establishment: Help establish a consistent sleep schedule and stress-reduction techniques.
- Psychological support: Offer counselling or mental health support to manage stress, anxiety, and peer-related issues.
- Monitor lifestyle: Encourage healthy habits, including regular meals, limited alcohol use, and avoidance of recreational drugs.
What is SUDEP (Sudden Unexpected Death in Epilepsy), and what are the key risk factors?
- SUDEP: The sudden, unexplained death of an individual with epilepsy, often occurring during or after a seizure.
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Key risk factors: - Frequent tonic-clonic seizures (especially if uncontrolled).
- Nocturnal seizures (seizures during sleep).
- Young adulthood (most common in 20-40 years).
- Severe epilepsy or poorly controlled seizures.
- Polytherapy (use of multiple AEDs).
- Non-adherence to medication and inadequate seizure control.
How can SUDEP be prevented and managed?
- Improved seizure control: Optimising treatment and achieving better seizure control reduces the risk of SUDEP.
- Monitoring: Consider video-EEG and other monitoring tools to track seizure activity, especially during sleep.
- Seizure avoidance strategies: Night-time monitoring, supervision during high-risk activities (e.g., swimming).
- Patient and family education: Inform patients and families about the risk of SUDEP, and encourage regular follow-ups with healthcare providers.
- Psychosocial support: Address psychological aspects of living with epilepsy, including coping strategies for anxiety around SUDEP.
What are the health economics of epilepsy, and how do they impact healthcare systems?
- Direct costs: Hospital admissions, outpatient visits, diagnostic tests, AEDs, and emergency care for seizures.
- Indirect costs: Loss of productivity due to work absenteeism, disability, and the impact of seizures on daily functioning.
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Cost-effectiveness: - Optimising seizure control reduces overall costs by preventing hospital admissions and complications.
- Early diagnosis and appropriate management can reduce long-term healthcare costs.
- Investment in education and support services for people with epilepsy may improve quality of life and reduce healthcare burden.
- Epidemiological data on epilepsy helps policymakers allocate resources effectively.
What is the presentation of altered sensation and weakness?
- Altered sensation: Includes numbness, tingling, or a “pins and needles” feeling, which may be localized or widespread.
- May be associated with pain or temperature changes.
- Can affect light touch, proprioception, or vibration.
- Weakness: Loss of muscle strength, resulting in difficulty with activities such as walking, gripping objects, or lifting.
- May be proximal (affecting limbs close to the body) or distal (affecting limbs further from the body).
- Can be gradual or acute onset, potentially associated with fatigue or muscle wasting.
What are the initial investigations for altered sensation and weakness?
- Clinical assessment: Full neurological exam, including sensory testing (light touch, pinprick, vibration) and muscle strength testing (power, tone).
- Blood tests: Look for signs of infection, inflammation, metabolic disorders, or vitamin deficiencies (e.g., B12, thyroid function).
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Imaging: - MRI of the brain or spine: To assess for lesions, spinal cord issues, or brain abnormalities.
- CT scan: If MRI is not available or in acute settings (e.g., acute stroke).
. - Nerve conduction studies: To evaluate peripheral nerve function.
- Electromyography (EMG): To assess muscle activity and differentiate between nerve and muscle pathology.
What are the key differential diagnoses for altered sensation and weakness?
Neurological causes:
- Stroke, transient ischemic attack (TIA), or brain tumors.
- Multiple sclerosis (MS), Guillain-Barré syndrome, or myasthenia gravis.
- Peripheral neuropathy (e.g., diabetes, alcohol use, vitamin deficiencies).
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Muscle disorders:
- Myopathy (e.g., inflammatory myopathies, muscular dystrophy).
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Spinal cord disorders:
- Spinal cord compression or herniated discs (leading to radiculopathy).
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Metabolic or toxic causes:
- Electrolyte imbalances, hypothyroidism, or drug-induced neuropathies.
What is the autonomic nervous system (ANS), and what are its main divisions? (3 divisions)
- The ANS controls involuntary bodily functions like heart rate, blood pressure, digestion, and respiration
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It is divided into: - Sympathetic nervous system: Mediates “fight or flight” responses, preparing the body for stress by increasing heart rate, dilating pupils, and inhibiting digestion.
- Parasympathetic nervous system: Promotes “rest and digest” functions, slowing heart rate, constricting pupils, and stimulating digestion.
- Enteric nervous system: Often referred to as the “second brain,” it controls the gastrointestinal system independently of the brain and spinal cord.
What are the key neurotransmitters and receptors involved in the ANS pathways?
- Sympathetic system:
- Neurotransmitters: Noradrenaline (NA) and adrenaline (epinephrine) (from adrenal medulla).
- Adrenergic receptors: α (alpha) and β (beta) receptors respond to NA and adrenaline.
. - Parasympathetic system:
- Neurotransmitters: Acetylcholine (ACh).
- Cholinergic receptors: Muscarinic receptors (on target organs, mediate parasympathetic effects) + Nicotinic receptors (on post-ganglionic neurons in both sympathetic and parasympathetic systems)
What are the key functions of the sympathetic and parasympathetic nervous systems?
Sympathetic nervous system:
- Fight or flight response: Increases heart rate, dilates pupils, dilates bronchial tubes, inhibits digestion, and redirects blood flow to muscles.
- Stress response: Mobilizes energy and prepares the body for quick action.
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Parasympathetic nervous system:
- Rest and digest response: Decreases heart rate, constricts pupils, stimulates digestion, and promotes energy conservation.
- Homeostasis: Maintains and restores normal bodily functions during periods of rest and recovery.
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
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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
Which neurotransmitter is released by pre-ganglionic neurones of the parasympathetic nervous system?
- Noradrenaline
- Serotonin
- Glutamine
- Acetylcholine
Acetylcholine
- Acetylcholine is released by both pre-ganglionic and post-ganglionic neurones of the parasympathetic nervous system.
- Acetylcholine released by pre-ganglionic neurones acts on nicotinic receptors, whilst acetylcholine from post-ganglionic neurones acts on muscarinic receptors.
Which nerve roots from the spinal cord contribute to the parasympathetic nervous system?
- C1-S5
- T1-L2
- S2-4
- T6-S5
S2-4
- Parasympathetic nervous innervation comes from the paired cranial nerves III, VII, IX and X, and sacral segments S2-S4
Which nerve roots from the spinal cord contribute to the SYMPATHETIC nervous system?
- C1-S5
- T1-L2
- S2-4
- T6-S5
T1-L2
Damage to the vagus nerve (CN X) is likely to lead to which of the following effects on the body?
- Increased insulin secretion from the pancreas
- Urinary retention
- Increased gastrointestinal activity
- Increased heart rate
Increased heart rate
- Parasympathetic activity from the vagus nerve acts on the sinoatrial and atrioventricular nodes of the heart to reduce heart rate.
- Damage to the vagus would decrease gastrointestinal motility, an effect that is seen as a result of a truncal vagotomy.
