Module 3C Neurology and Vision - LOs Flashcards

Question

What neurological conditions can cause misaligned eyes in children?

Answer 1

- Cerebral palsy. - Congenital cranial nerve palsies.

Answer 2

- 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.

Answer 3

- Onset and duration of misalignment. - Associated symptoms (e.g., head tilt, poor vision). - Perinatal and developmental history. - Family history of strabismus or amblyopia.

Answer 4

- 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).

Answer 5

Visual acuity testing. Cover test to identify phoria or tropia. Ocular movement assessment. Binocular vision and stereopsis evaluation. Fundoscopy to rule out intraocular pathology

Answer 6

If neurological or orbital causes are suspected (e.g., tumours, fractures, stroke).

Answer 7

Hess chart to map muscle weakness. Blood tests for systemic conditions (e.g., thyroid function, acetylcholine receptor antibodies).

Answer 8

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.

Answer 9

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

Answer 10

Sudden-onset strabismus in adults with diplopia or neurological symptoms. Suspected tumours, orbital trauma, or stroke. Leukocoria in children (rule out retinoblastoma).

Answer 11

Persistent strabismus or amblyopia in children (to orthoptics). Long-standing strabismus or cosmetic concerns in adults.

Answer 12

Endocrinology for thyroid eye disease. Neurology for cranial nerve palsies or stroke-related causes. Paediatric ophthalmology for complex congenital cases.

Answer 13

- Onset: Sudden or rapid (seconds to days). - Nature: Complete loss, partial field loss, or blurring. - Laterality: Unilateral or bilateral. . Associated Symptoms: - Pain (ocular or periocular) - Photophobia or redness - Neurological symptoms (e.g., weakness, headache, vertigo) - History of trauma or systemic disease.

Answer 14

Retinal causes: - Retinal artery occlusion (RAO) - Retinal vein occlusion (RVO) - Retinal detachment - Vitreous haemorrhage - Macular disease (e.g., wet age-related macular degeneration) . Optic nerve causes: - Ischaemic optic neuropathy (arteritic or non-arteritic) - Optic neuritis (often painful) - Compressive lesions. . Neurological causes: - Stroke (affecting the visual pathways) - Migraine with aura. . Other causes: - Functional vision loss (e.g., conversion disorder) - Severe refractive errors (rare but possible with lens dislocation)

Answer 15

Anterior segment causes: - Acute angle-closure glaucoma - Corneal pathology (e.g., severe keratitis or ulcer) - Uveitis (anterior or posterior). . Trauma-related causes: - Orbital or ocular trauma - Chemical burns . Optic nerve causes: - Optic neuritis

Answer 16

- 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

Answer 17

- 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.

Answer 18

Imaging: - Optical coherence tomography (OCT) for macular/retinal disease. - CT or MRI of the head/orbits for neurological or optic nerve pathology. . Blood Tests: - ESR and CRP to rule out giant cell arteritis (if ischaemic optic neuropathy is suspected). - Glucose and HbA1c for diabetic retinopathy. . Fluorescein angiography: - Assess retinal vasculature in RAO or RVO.

Answer 19

- 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)

Answer 20

- Refer to ophthalmology for retinal evaluation. - Treat underlying conditions (e.g., hypertension, diabetes). - Anti-VEGF therapy for macular oedema.

Answer 21

1. Emergency treatment: - Acetazolamide to reduce IOP. - Topical beta-blockers and alpha agonists. 2. Definitive treatment: - Laser iridotomy. 3. Urgent referral to ophthalmology.

Answer 22

- 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.

Answer 23

1. Start high-dose corticosteroids immediately (e.g., prednisolone or IV methylprednisolone). 2. Arrange temporal artery biopsy to confirm diagnosis. 3. ESR and CRP monitoring

Answer 24

- 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

Answer 25

- 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.

Answer 26

- 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.

Answer 27

Conjunctival causes: - Conjunctivitis (viral, bacterial, allergic). - Subconjunctival haemorrhage. - Dry eye syndrome. . Corneal causes: - Corneal abrasion or ulcer. - Keratitis (bacterial, viral, fungal, or herpetic). - Acanthamoeba keratitis (particularly in contact lens users). . Anterior segment causes: - Acute angle-closure glaucoma. - Uveitis (anterior or posterior). . Other causes: - Trauma (blunt or penetrating injury). - Foreign body in the eye. - Episcleritis or scleritis.

Answer 28

Viral conjunctivitis: - Often associated with cold or respiratory symptoms. - Watery discharge, itching, mild irritation. - Typically bilateral. . Bacterial conjunctivitis: - Purulent, yellow or green discharge. - Often unilateral, with crusting of eyelids in the morning. - More painful than viral conjunctivitis. . Allergic conjunctivitis: - Itching, watery eyes, often with sneezing and nasal congestion. - Bilateral redness and swelling of the conjunctiva.

Answer 29

- 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).

Answer 30

- Uveitis: Inflammation of the uveal tract (iris, ciliary body, choroid). . Presentation: - Pain, photophobia, and blurred vision. - Redness (circumcorneal), often associated with a small, irregular pupil. - Associated with systemic conditions (e.g., autoimmune diseases, infections).

Answer 31

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).

Answer 32

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.

Answer 33

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).

Answer 34

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.

Answer 35

1. Topical antibiotics - eg. chloramphenicol, fusidic acid (consider systemic antibiotics in severe cases) 2. Avoid contact lenses during treatment. 3. Hygiene measures - e.g., handwashing, cleaning eye crusts

Answer 36

1. Antihistamines - oral or topical antihistamines (e.g., olopatadine), topical mast cell stabilizers (e.g., cromolyn sodium) 2. Avoidance of allergens where possible 3. Artificial tears for symptomatic relief.

Answer 37

1. Emergency treatment Acetazolamide to lower intraocular pressure, Topical beta-blockers (e.g., timolol), hyperosmotic agents (e.g., mannitol), Pilocarpine to constrict the pupil. 2. Surgical management: Laser iridotomy or iridectomy to relieve blockage.

Answer 38

- 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.

Answer 39

1. No specific treatment is usually required. 2. Reassurance and monitoring for spontaneous resolution. 3. Evaluate for underlying causes (e.g., blood pressure control or bleeding disorders).

Answer 40

- 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.

Answer 41

- 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.

Answer 42

- 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)

Answer 43

- 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).

Answer 44

Diabetic Retinopathy: - Long-term hyperglycaemia damages retinal blood vessels, causing microaneurysms, haemorrhages, and neovascularisation. - Can progress to diabetic macular oedema, impairing central vision. . - 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.

Answer 45

1. Non-proliferative diabetic retinopathy (NPDR): Microaneurysms, retinal haemorrhages, and hard exudates. 2. Proliferative diabetic retinopathy (PDR): Neovascularisation of the retina or optic disc, risking retinal detachment and vitreous haemorrhage. 3. Diabetic macular oedema (DMO): Fluid accumulation in the macula causing central vision loss.

Answer 46

- 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.

Answer 47

Causes band keratopathy, where calcium deposits in the cornea.

Answer 48

- 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.

Answer 49

- 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.

Answer 50

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.

Answer 51

- 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.

Answer 52

- 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).

Answer 53

- 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.

Answer 54

- 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.

Answer 55

- 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.

Answer 56

- 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

Answer 57

- Reduce intraocular pressure (IOP) to prevent further optic nerve damage. - Preserve vision and maintain quality of life. - Monitor disease progression with regular follow-ups.

Answer 58

- 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).

Answer 59

Laser Therapy: - Laser Trabeculoplasty: Improves drainage through the trabecular meshwork. - Cyclophotocoagulation: Reduces aqueous production by targeting the ciliary body. . 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.

Answer 60

- 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

Answer 61

- 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.

Answer 62

- 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.

Answer 63

- 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.

Answer 64

- 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.

Answer 65

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. . 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.

Answer 66

- 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.

Answer 67

- 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.

Answer 68

- 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.

Answer 69

- 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

Answer 70

- 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.

Answer 71

Optic canal

Answer 72

Superior orbital fissure

Answer 73

Inferior orbital fissure

Answer 74

Facial nerve

Answer 75

Optic nerve - enters the boyn orbit via the optic canal

Answer 76

- Sclera (white part of the eye) - provides attachment to the extraocular muscles - Cornea - light entering the eye is refracted by the cornea

Answer 77

- 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

Answer 78

- Pigmented (outer) layer - attached to choroid - Neural (inner) layer - consists of photoreceptors (light-detecting cells of the retina)

Answer 79

Fovea centralis - a depression within the macular (centre of the retina) - has a high concentration of light-detecting cells (photoreceptors)

Answer 80

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

Answer 81

- Aqueous humor - nourishes and protects the eye - drains via the trabecular meshwork - if drainage of aq humor is obstructed --> glaucoma can result

Answer 82

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

Answer 83

aqueous humor (vitreous humor is ofund in the space between the lens and the retina)

Answer 84

- Palpebral part – gently closes the eyelids - Lacrimal part – involved in the drainage of tears - Orbital part – tightly closes the eyelids

Answer 85

Facial nerve - the orbicularis oculi is a muscle of facial expression

Answer 86

Meibomian glands (type of sebaceous gland) - prevent eyelids from sticking together when closed

Answer 87

- Levator palpebrae superioris - main muscle involved (innervated oculomotor nerve) - Superior tarsal muscle - assists the levator palpebrae superioris

Answer 88

Superior and lateral

Answer 89

Sympathetic fibres to the lacrimal gland travel with the maxillary nerve

Answer 90

Lacrimal nerve - branch of the ophthalmic nerve

Answer 91

- 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

Answer 92

"down and out" - displaced laterally by the lateral rectus and inferiorly by the superior oblique

Answer 93

- 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.

Answer 94

Oculomotor nerve - medial rectus

Answer 95

Oculomotor - this is why in a 3rd nerve palsy there is compete ptosis

Answer 96

1. 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). 2. Trochlear Nerve (CN IV): - Innervates the superior oblique muscle, responsible for downward and inward eye movement. 3. Abducens Nerve (CN VI): - Innervates the lateral rectus muscle, responsible for eye abduction. 4. Trigeminal Nerve (CN V): - Opthalmic branch (V1) provides sensation to the cornea, conjunctiva, and skin of the eyelids. 5. Sympathetic Nervous System: - Innervates the dilator pupillae muscle for pupil dilation and the superior tarsal muscle for eyelid elevation.

Answer 97

1. 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. 2. Veins: - Central retinal vein: Drains blood from the retina. - Superior and inferior ophthalmic veins: Drain the eye and orbit into the cavernous sinus.

Answer 98

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)

Answer 99

1. Retina: Light is detected by rods and cones. 2. Optic Nerve (CN II): Axons from the retinal ganglion cells form the optic nerve. 3. 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. 4. Optic Tract: After the chiasm, fibers from both eyes carry information from the contralateral visual field to the brain. 5. Lateral Geniculate Nucleus (LGN): Located in the thalamus, where visual information is relayed. 6. Optic Radiation: Pathway from the LGN to the visual cortex in the occipital lobe. 7. Visual Cortex: Located in the occipital lobe, where visual perception occurs.

Answer 100

- 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

Answer 101

- 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.

Answer 102

- 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.

Answer 103

- 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.

Answer 104

- 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).

Answer 105

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.

Answer 106

1. Inspect eye alignment: Look for any deviations at rest (strabismus). 2. 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. 3. 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).

Answer 107

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).

Answer 108

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).

Answer 109

- 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.

Answer 110

1. Myopia (short-sightedness): - Light focuses in front of the retina. - Distant objects appear blurry. - Associated with elongated eyeball or excessive corneal curvature. 2. Hyperopia (long-sightedness): - Light focuses behind the retina. - Near objects appear blurry. - Associated with shortened eyeball or insufficient refractive power. 3. Astigmatism: - Irregular corneal or lens curvature causes distorted vision. - Light focuses at multiple points on or near the retina. 4. Presbyopia: - Age-related loss of lens elasticity, reducing accommodation. - Difficulty focusing on near objects.

Answer 111

1. Myopia: - Associated with retinal detachment, glaucoma, and macular degeneration in high myopia. 2. Hyperopia: - Linked to angle-closure glaucoma and amblyopia in children. 3. Astigmatism: - Can occur with myopia or hyperopia. - May contribute to eye strain and blurred vision at all distances. 4. Presbyopia: - Typically occurs after age 40, affecting most individuals.

Answer 112

1. Optical Correction: - Myopia: Concave (negative) lenses. - Hyperopia: Convex (positive) lenses. - Astigmatism: Cylindrical lenses. - Presbyopia: Bifocal, trifocal, or progressive lenses. 2. 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. 4. Orthokeratology: - Specialised contact lenses worn overnight to temporarily reshape the cornea (for myopia). 5. Low Vision Aids: - Magnifiers or telescopic lenses for individuals with uncorrectable vision loss.

Answer 113

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).

Answer 114

1. Inflammation: E.g., meningitis, encephalitis, multiple sclerosis (MS). 2. Degeneration: E.g., Alzheimer’s, Parkinson’s, Huntington’s. 3. Haemorrhage: E.g., subarachnoid, intracerebral, subdural, epidural. 4. Neoplasia: E.g., meningioma, glioblastoma, metastases.

Answer 115

- Bright white (T2 hyperintense) patches in brain or spinal cord. - Often around ventricles ("Dawson’s fingers") - shown in image

Answer 116

Bright enhancement of the brain lining (leptomeninges) on MRI with contrast.

Answer 117

Ring-enhancing lesion with a dark (fluid-filled) centre. The centre restricts diffusion on MRI.

Answer 118

- 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)

Answer 119

Crescent-shaped ("banana-shaped"), located between dura mater and arachnoid mater of the brain. - aetiology - usually trauma again, but more common in older pts

Answer 120

Bright blood in grooves (sulci) or cisterns on CT. - aetiology of spontaneous SAH - most commonly intracranial aneurysms

Answer 121

Bright spot in brain tissue surrounded by darker swelling (oedema). - aetiology - usually related to hypertension

Answer 122

Well-defined mass attached to the brain lining (dura), with a "tail".

Answer 123

- Bright ring (contrast enhancement) with a dark centre (necrosis). - Surrounding swelling (oedema) causes pressure effects

Answer 124

Multiple, round, bright lesions. Often at the grey-white matter junction.

Answer 125

Shrinking (atrophy) of the hippocampus and medial temporal lobes. Enlarged spaces (ventricles).

Answer 126

1. Direct response: Constriction of the pupil in the same eye when light is shone. 2. Consensual response: Constriction of the pupil in the opposite eye when light is shone in one eye. 3. Relative afferent pupillary defect (RAPD): Abnormal response to the swinging flashlight test, showing an issue with the afferent pathway.

Answer 127

1. Light stimulates the retina. 2. Signal travels via the optic nerve (CN II). 3. Fibres pass through the optic chiasm and optic tracts. 4. Fibres synapse in the pretectal nucleus in the midbrain.

Answer 128

1. Signal travels from the pretectal nucleus to both Edinger-Westphal nuclei. 2. Parasympathetic fibres travel via the oculomotor nerve (CN III). 3. Fibres synapse in the ciliary ganglion. 4. Postganglionic fibres innervate the sphincter pupillae muscle, causing pupil constriction.

Answer 129

The afferent signal from one eye splits at the pretectal nucleus and activates both Edinger-Westphal nuclei, allowing a response in both eyes.

Answer 130

- 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.

Answer 131

1. 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. 2. Constricted pupil: - Use 1% tropicamide or phenylephrine to assess pupil reactivity.

Answer 132

- Sympathetic input causes pupil dilation via the dilator pupillae muscle. - Disruption leads to miosis (constricted pupil), e.g., in Horner’s syndrome.

Answer 133

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.

Answer 134

1. Dilated pupil: CN III palsy or parasympathetic damage. 2. Constricted pupil: Sympathetic lesion (e.g., Horner’s syndrome). 3. RAPD: Damage to the retina or optic nerve.

Answer 135

- Course: Olfactory receptors (within the nasal epithelium)→ Cribriform plate of the ethmoid bone → Olfactory bulb → Olfactory tract → Temporal lobe. - Function: Smell

Answer 136

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.*

Answer 137

- Course: Retina → Optic nerve → Optic chiasm (partial crossing) → Optic tract → Lateral geniculate nucleus (LGN) → Visual cortex (occipital lobe). - Function: Vision

Answer 138

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.*

Answer 139

- 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.

Answer 140

Midbrain *The oculomotor nerve originates from the oculomotor nucleus – located within the midbrain of the brainstem*

Answer 141

Abducted and depressed eye at rest

Answer 142

- Nucleus: Trochlear nucleus (midbrain). - Course: Posterior midbrain (trochlear nucleus) → Cavernous sinus → Superior orbital fissure → Superior oblique muscle. - Function: Eye movement (depression and intorsion).

Answer 143

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

Answer 144

Somatic motor

Answer 145

Superior oblique

Answer 146

Superior orbital fissure

Answer 147

1. Nuclei: - Motor nucleus (pons). - Sensory nuclei: Mesencephalic, principal, and spinal trigeminal nuclei. 2. 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. 3. Function: Sensory (face) and motor (chewing).

Answer 148

Mandibular - It innervates the muscles of mastication and several other muscles within the head and and neck.

Answer 149

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).*

Answer 150

- Nucleus: Abducens nucleus (pons). - Course: Pons → Cavernous sinus → Superior orbital fissure → Lateral rectus muscle. - Function: Eye abduction.

Answer 151

Lateral rectus

Answer 152

1. Nuclei: - Motor nucleus (pons). - Parasympathetic nuclei: Superior salivatory and lacrimal nuclei. - Sensory: Nucleus solitarius. 2. Course: Pons → Internal acoustic meatus → Facial canal → Stylomastoid foramen → Face muscles. 3. Function: - Motor: Facial expression. - Sensory: Taste (anterior 2/3 of tongue). - Parasympathetic: Lacrimation, salivation.

Answer 153

*marginal mandibular

Answer 154

- Nuclei: Vestibular and cochlear nuclei (pons/medulla). - Course: Inner ear → Internal acoustic meatus → Pons. - Function: Hearing and balance (special sensory).

Answer 155

Internal acoustic meatus

Answer 156

Organ of Corti - *The hair cells of the organ of Corti detect the magnitude and frequency of sound waves*

Answer 157

Hearing loss - *The vestibular component of the vestibulocochlear nerve is responsible for balance. The cochlear nerve component is responsible for hearing.*

Answer 158

1. Nuclei: - Motor: Nucleus ambiguus. - Sensory: Nucleus solitarius. - Parasympathetic: Inferior salivatory nucleus. 2. Course: Medulla → Jugular foramen → Pharynx and tongue. 3. Function: - Motor: Swallowing (stylopharyngeus). - Sensory: Taste (posterior 1/3 of tongue), carotid body/sinus. - Parasympathetic: Parotid gland secretion.

Answer 159

Absent taste and general sensation in posterior third - *The glossopharyngeal nerve provides taste and general sensation to the posterior third of the tongue.*

Answer 160

Stylopharyngeus (swallowing)

Answer 161

Medulla oblongata

Answer 162

1. Nuclei: - Motor: Nucleus ambiguus. - Sensory: Nucleus solitarius. - Parasympathetic: Dorsal motor nucleus. 2. Course: Medulla → Jugular foramen → Thorax and abdomen. 3. Function: - Motor: Swallowing, phonation. - Parasympathetic: Heart, lungs, GI tract. - Sensory: Thoracic and abdominal viscera.

Answer 163

All of the above

Answer 164

- Nucleus: Spinal accessory nucleus (C1–C5). - Course: Spinal cord → Foramen magnum → Jugular foramen → Neck muscles. - Function: Motor to sternocleidomastoid and trapezius

Answer 165

Foramen magnum

Answer 166

Trapezius - *The spinal accessory nerve innervates two muscles – the sternocleidomastoid and trapezius.*

Answer 167

- Nucleus: Hypoglossal nucleus (medulla) - Course: Medulla → Hypoglossal canal → Tongue muscles - Function: Motor to tongue muscles (except palatoglossus which is innervated by vagus nerve)

Answer 168

Medulla oblongata

Answer 169

Somatic motor - *The hypoglossal nerve has a somatic motor function, innervating the majority of muscles in the tongue*

Answer 170

- Midbrain: CN III, IV. - Pons: CN V, VI, VII, VIII. - Medulla: CN IX, X, XI, XII.

Answer 171

- Cranial roof - frontal, occipital, and 2 parietal bones - Cranial base - frontal, sphenoid, ethmoid, occipital, parietal, and temporal bones

Answer 172

- 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

Answer 173

- 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)

Answer 174

Coronal and sagittal

Answer 175

Parietal - *The calvarium forms the roof of the skull and is comprised of the frontal, occipital and two parietal bones.*

Answer 176

- CN III (oculomotor) - CN IV (trochlear)

Answer 177

- CN V (trigeminal) - CN VI (abducens) - CN VII (facial) - CN VIII (vestibulocochlear)

Answer 178

Metencephalon

Answer 179

Cerebellum

Answer 180

Trochlear - *The trochlear nerve arises from the posterior midbrain*

Answer 181

3 layers of meninges: - dura mater - arachnoid mater - pia mater

Answer 182

- Periosteal layer - Meningeal layer

Answer 183

venous drainage of the cranium and empty into the internal jugular veins

Answer 184

- 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

Answer 185

- 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

Answer 186

- 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)

Answer 187

Trigeminal nerve

Answer 188

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*

Answer 189

Cerebrospinal fluid - *The sub-arachnoid space contains cerebrospinal fluid that acts to cushion the brai*

Answer 190

1. 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 2. Ventral horn (also known as the anterior horn) - largely contains motor neurons that exit the spinal cord to innervate skeletal muscle 3. Lateral horn/intermediate column - contains neurons that innervate visceral and pelvic organs

Answer 191

- Function - reduces excitatory input (prevents excessive and exaggerated movements) + regulates cognitive and emotional responses - Middle cerebral artery - lenticulostriate arteries branch off MCA to supply

Answer 192

- 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

Answer 193

- Sulci - grooves or depressions - Gyri - ridges or elevations

Answer 194

- 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

Answer 195

- 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

Answer 196

- 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)

Answer 197

Prosencephalon

Answer 198

Middle cerebral arteries

Answer 199

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*

Answer 200

- Forebrain (cerebrum, thalamus, and hypothalamus) - prosencephalon - Midbrain - mesencephalon - Hindbrain - rhombencephalon

Answer 201

cerebellum sits posterior to the pons

Answer 202

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

Answer 203

Metencephalon - *the hindbrain divides into the metencephalon (superior) and the myelencephalon (inferior) - the cerebellum develops from the metencephalon divison*

Answer 204

Tentorium cerebelli

Answer 205

Vestibulocerebellum

Answer 206

Melatonin - *The pineal gland produces melatonin, which regulates the circadian rhythm of the body.*

Answer 207

- 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

Answer 208

- fine touch (tactile sensation) - vibration - proprioception

Answer 209

1. 1st order neurones - carry sensory info from peripheral nerves to the medulla oblongata 2. 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) 3. 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)

Answer 210

- 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

Answer 211

- Anterior spinothalamic tract – carries the sensory modalities of crude touch and pressure - Lateral spinothalamic tract – carries the sensory modalities of pain and temperature

Answer 212

1. 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) 2. 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: 1. crude touch and pressure fibres - enter the anterior spinothalamic tract 2. pain and temperature fibres - enter the lateral spinothalamic tract) 3. 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)

Answer 213

- 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)

Answer 214

- impairment of pain and temperature sensation - sensory loss will be contralateral (as spinothalamic tracts decussate within the spinal cord)

Answer 215

- 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 1. DCML pathway - ipsilateral loss of touch, vibration, and proprioception 2. Anterolateral system - contralateral loss of pain and temperature sensation (it will also involve the descending motor tracts, causing an ipsilateral hemiparesis)

Answer 216

Proprioception - *The DCML transmits touch (tactile sensation), vibration and proprioception*

Answer 217

Spinocerebellar tracts

Answer 218

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.*

Answer 219

- 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

Answer 220

1. 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) 2. 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)

Answer 221

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)

Answer 222

- Corticospinal tracts – supplies the musculature of the body. - Corticobulbar tracts – supplies the musculature of the head and neck

Answer 223

(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

Answer 224

Head and neck

Answer 225

Coordinate movements of the head - *The tectospinal tract coordinates movements of the head in relation to visual stimuli.*

Answer 226

a strip of skin that is innervated by a single spinal nerve

Answer 227

a group of muscles innervated by a single spinal nerve root

Answer 228

Shoulder abduction

Answer 229

- Olfactory (CN I) and Optic (CN II) nerves - originate from the cerebrum - CN III - CN XII - arise from the brainstem

Answer 230

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*

Answer 231

- 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)

Answer 232

- 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

Answer 233

C4 - *The common carotid artery typically bifurcates at the upper border of the thyroid cartilage – the level of the C4 vertebrae*

Answer 234

Superior thyroid artery - *The superior thyroid artery is a branch of the external carotid artery*

Answer 235

Subclavian

Answer 236

between the periosteal and meningeal layers of the dura mater

Answer 237

internal jugular vein

Answer 238

NO (the only veins in the body to not have valves)

Answer 239

Note: the great cerebral vein

Answer 240

presence of a thrombus within one of the dural venous sinuses - treatment --> anticoagulation

Answer 241

Subarachnoid - *Upon exiting the cerebral parenchyma, the veins run in the subarachnoid space and pierce the meninges to drain into the dural venous sinuses*

Answer 242

Superior sagittal - *The superior cerebral veins drain the superior surface of the cerebrum and empty into the superior sagittal sinus*

Answer 243

Straight sinus - *The great cerebral vein combines with the inferior sagittal sinus to form the straight sinus*

Answer 244

Cavernous sinus

Answer 245

1. Protection - acts as a cushion for the brain, limiting neural damage in cranial injuries 2. 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 3. Chemical stability - the CSF creates an environment to allow for proper functioning of the brain, e.g. maintaining low extracellular K+ for synaptic transmission

Answer 246

- 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)

Answer 247

- 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

Answer 248

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)

Answer 249

Choroid plexus

Answer 250

Cuboidal - *The choroid plexus consists of capillaries and loose connective tissue surrounded by cuboidal epithelial cells.*

Answer 251

Lateral ventricles - 3rd ventricle

Answer 252

- 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

Answer 253

- 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

Answer 254

- 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

Answer 255

- 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

Answer 256

- 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

Answer 257

- 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)

Answer 258

- 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

Answer 259

- 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)

Answer 260

- 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

Answer 261

- 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)

Answer 262

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

Answer 263

- 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

Answer 264

- 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

Answer 265

1. Primary headaches: Tension, migraine, cluster 2. Secondary headaches: - Benign: Sinusitis, TMJ dysfunction, medication overuse. - Serious: SAH, meningitis, raised ICP, temporal arteritis, brain tumour, acute angle-closure glaucoma

Answer 266

- 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?

Answer 267

- 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

Answer 268

- 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

Answer 269

- 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

Answer 270

- 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

Answer 271

1. 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 2. Surgical management: - Decompression surgery for mass lesions - Ventriculostomy for hydrocephalus 3. Monitoring: ICP monitoring for severe cases (e.g., head trauma, intracranial surgery)

Answer 272

- 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

Answer 273

- 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

Answer 274

- 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

Answer 275

1. Medications: Tricyclic antidepressants (e.g., amitriptyline), SSRIs, and SNRIs can treat both conditions. 2. Cognitive Behavioral Therapy (CBT): Addresses cognitive patterns that exacerbate both anxiety and headaches. 3. Biofeedback and relaxation techniques: Help reduce muscle tension and anxiety, alleviating tension-type headaches.

Answer 276

- 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

Answer 277

- 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

Answer 278

- 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

Answer 279

- 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

Answer 280

- Simple analgesics: Paracetamol, ibuprofen - Triptans: E.g., sumatriptan - Opioids: Codeine, tramadol - Combination analgesics: Containing caffeine, codeine, or other additives

Answer 281

1. Discontinue the overused medication, preferably gradually 2. Pain management with alternative treatments (e.g., NSAIDs, antiemetics) 3. Preventive treatments like tricyclic antidepressants, anticonvulsants, or botulinum toxin for chronic migraine or tension-type headache

Answer 282

- Thorough history (onset, duration, frequency, type, associated symptoms, family history) - Neurological examination to check for focal deficits, papilloedema, and signs of raised ICP

Answer 283

- 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)

Answer 284

- 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)

Answer 285

- 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

Answer 286

- 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

Answer 287

1. Identify and avoid triggers (e.g., stress, certain foods) 2. Maintain regular sleep hygiene and exercise 3. Educate patients and encourage keeping a headache diary

Answer 288

- 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

Answer 289

1. Meningitis (Bacterial & Viral) 2. Subarachnoid Hemorrhage (SAH) 3. Cerebral Venous Sinus Thrombosis (CVST) 4. Encephalitis 5. Post-infectious Meningitis

Answer 290

1. 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) 2. 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) 3. Cerebral Venous Sinus Thrombosis (CVST) - MRI Brain with Venography: Gold standard for detecting clot in the cerebral venous sinuses 4. Encephalitis - MRI Brain: To identify inflammation in the brain parenchyma - LP: CSF PCR testing to identify viral causes (e.g. HSV, enteroviruses) 5. 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

Answer 291

- 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

Answer 292

- 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

Answer 293

- Multidisciplinary Team: Neurologists, physiatrists, physical/occupational therapists, nurses, psychiatrists, dietitians, social workers - Specialist Clinics: Spinal cord injury clinics, neurorehabilitation centres, pain management clinics

Answer 294

- 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

Answer 295

- Screening for Depression: Regular mental health screening - Psychotherapy: Cognitive-behavioural therapy (CBT) - Pharmacotherapy: Antidepressants (SSRIs like sertraline, fluoxetine, SNRIs like duloxetine)

Answer 296

- 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

Answer 297

1. 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. 2. History: - Mechanism of injury (e.g., fall, trauma) - Loss of consciousness, duration, and any post-traumatic amnesia - Any seizures, vomiting, or focal neurological signs

Answer 298

The GCS assesses the level of consciousness based on three components: 1. Eye Opening (E): 4 = Spontaneous 3 = To speech 2 = To pain 1 = None 2. Verbal Response (V): 5 = Oriented 4 = Confused conversation 3 = Inappropriate words 2 = Incomprehensible sounds 1 = None 3. 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

Answer 299

1. 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 2. 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 3. 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

Answer 300

1. 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. 2. Craniotomy: If there is significant brain swelling or hematoma that requires drainage.

Answer 301

1. 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. . 2. Rehabilitation: - Physical therapy for balance and coordination - Cognitive therapy for memory and attention deficits - Speech therapy if there are communication difficulties . 3. 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

Answer 302

1. Airway and Breathing: - Ensure airway patency (intubate if GCS ≤8) - Monitor for respiratory distress 2. Circulation: Maintain SBP >90 mmHg; fluid resuscitation if necessary 3. ICP Control: Elevate head of the bed (30°), use mannitol or hypertonic saline to reduce swelling 4. Neuroimaging: Perform CT if condition deteriorates (worsening GCS, new deficits) 5. Monitor for Seizures: Treat with phenytoin or levetiracetam if seizures occur

Answer 303

- 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).

Answer 304

1. History and Physical Exam: Thorough history (e.g., triggers, duration, associated symptoms). Neurological exam: Assess GCS, cranial nerve function, and motor/sensory status. 2. 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). 3. 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.

Answer 305

- 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

Answer 306

1. Airway: Ensure airway is clear; consider intubation if GCS ≤8. 2. Breathing: Monitor oxygen saturation and provide supplemental oxygen if needed. 3. Circulation: Monitor vitals (e.g., blood pressure, heart rate), manage hypotension or arrhythmias (e.g., IV fluids, medications). 4. Monitor for Seizures: Administer benzodiazepines (e.g., lorazepam, diazepam) if seizures are observed. 5. 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. 6. Glucose: If hypoglycemia is suspected, administer glucose (oral or IV).

Answer 307

1. Syncope: - Position patient supine with legs elevated. - Identify and treat underlying cause (e.g., arrhythmias, dehydration). - Educate on lifestyle changes to prevent recurrent episodes. 2. Seizure: - Benzodiazepines (e.g., lorazepam or diazepam) to terminate seizure activity. - Post-ictal monitoring and evaluation with EEG and possible MRI for structural abnormalities. 3. 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). 4. 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. 5. Hypoglycemia: - Administer IV glucose or glucagon if severe hypoglycemia is confirmed. - Long-term management with blood sugar control and dietary adjustments.

Answer 308

1. 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. 2. 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. 3. 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. 4. 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.

Answer 309

- 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

Answer 310

Myelopathy refers to functional or pathological disturbance of the spinal cord, which can result from intrinsic or extrinsic causes.

Answer 311

Myelopathy caused by conditions within the spinal cord, such as tumours, syringomyelia, or inflammatory diseases (e.g., multiple sclerosis).

Answer 312

Myelopathy caused by external compression of the spinal cord, often due to herniated discs, tumours, trauma, or spinal stenosis

Answer 313

- Weakness (usually spastic in nature) - Hyperreflexia and clonus. - Positive Babinski sign (extensor plantar reflex).

Answer 314

- Loss of vibration sense - Loss of proprioception. - Sensory ataxia (unsteady gait, worsens with eyes closed).

Answer 315

- Loss of pain and temperature sensation - Often follows a "cape-like" distribution if cervical cord is affected.

Answer 316

- Flaccid paralysis at the level of the lesion - Muscle atrophy. - Fasciculations.

Answer 317

Compression or infiltration of the spinal cord by meningeal tumours, infections (e.g., meningitis, TB), or subdural/epidural haematomas.

Answer 318

- 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).

Answer 319

- Bilateral weakness (corticospinal tract involvement). - Loss of pain and temperature sensation (spinothalamic tract involvement). - Preserved proprioception and vibration sense (dorsal columns spared).

Answer 320

- Loss of proprioception and vibration sense. - Sensory ataxia.

Answer 321

- Weakness in upper and/or lower limbs. - Spasticity in the legs. - Loss of hand dexterity. - Hyperreflexia and positive Hoffman's sign.

Answer 322

- Spastic paraparesis. - Sensory level on the trunk (e.g., loss of sensation below a specific dermatome). - Bowel and bladder dysfunction in advanced cases.

Answer 323

- 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.

Answer 324

A transient loss of consciousness (TLOC) or awareness caused by various conditions, including seizures, syncope, or psychogenic events

Answer 325

- Seizures (e.g., epilepsy). - Syncope (e.g., vasovagal, cardiac). - Psychogenic (e.g., psychogenic non-epileptic seizures, anxiety). - Rare causes (e.g., hypoglycaemia, hypoxia).

Answer 326

- Sudden onset. - Preceded by an aura (in some cases). - May have a stereotypical pattern. - Postictal confusion or drowsiness.

Answer 327

Seizures often last 1–2 minutes, whereas syncope is usually much shorter (seconds).

Answer 328

- Triggered by prolonged standing, pain, or emotional stress. - Preceded by prodromal symptoms (e.g., dizziness, nausea, sweating). - Rapid recovery without confusion.

Answer 329

- Sudden onset without warning. - Often exertional or associated with palpitations. - Rapid recovery without postictal confusion.

Answer 330

- Asynchronous or irregular movements. - Prolonged duration without postictal phase. - Triggered by stress or emotional events. - Eye closure during the event.

Answer 331

- Associated with anxiety or panic attacks. - Lightheadedness, tingling in extremities, and chest tightness before TLOC.

Answer 332

- 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

Answer 333

- 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

Answer 334

- 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)

Answer 335

- Functions: Visual processing - Symptoms: Vision loss on one side, inability to recognise objects or faces, and visual hallucinations (e.g., flashes of light)

Answer 336

- Functions: Coordination, balance, and fine motor control - Symptoms: Unsteady movements (ataxia), tremors during action, and trouble judging distances (dysmetria)

Answer 337

- 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

Answer 338

- Prevalence: Around 1 in 100 children. - Higher in younger children (under 5 years) and those with neurodevelopmental disorders

Answer 339

- 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.

Answer 340

- Neurological exam: Check for focal deficits, reflexes, and gait abnormalities. - Signs of injury: Tongue biting, bruises, incontinence. - Systemic signs: Fever, rashes (suggesting infection).

Answer 341

- 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).

Answer 342

- 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

Answer 343

- 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.

Answer 344

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.

Answer 345

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.

Answer 346

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.

Answer 347

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.

Answer 348

- 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.

Answer 349

- 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.

Answer 350

- 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. . 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.

Answer 351

- 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.

Answer 352

- SUDEP: The sudden, unexplained death of an individual with epilepsy, often occurring during or after a seizure. . 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.

Answer 353

- 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.

Answer 354

- 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. . 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.

Answer 355

- 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.

Answer 356

- 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). . 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.

Answer 357

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). . Muscle disorders: - Myopathy (e.g., inflammatory myopathies, muscular dystrophy). . Spinal cord disorders: - Spinal cord compression or herniated discs (leading to radiculopathy). . Metabolic or toxic causes: - Electrolyte imbalances, hypothyroidism, or drug-induced neuropathies.

Answer 358

- The ANS controls involuntary bodily functions like heart rate, blood pressure, digestion, and respiration . 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.

Answer 359

1. Sympathetic system: - Neurotransmitters: Noradrenaline (NA) and adrenaline (epinephrine) (from adrenal medulla). - Adrenergic receptors: α (alpha) and β (beta) receptors respond to NA and adrenaline. . 2. 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)

Answer 360

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. . 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.

Answer 361

The sympathetic chain (also known as the sympathetic trunk) is a bilateral structure of ganglia and nerve fibers that runs alongside the vertebral column from the cervical to the sacral region . Function: - Acts as the primary pathway for sympathetic nerve fibers, transmitting signals from the thoracolumbar spinal cord to various target organs throughout the body. - It consists of sympathetic ganglia (groups of nerve cell bodies) connected by nerve fibers, forming a chain. - Pre-ganglionic fibers originate from the lateral horn of the spinal cord (T1-L2) and synapse in the sympathetic ganglia of the trunk. - Post-ganglionic fibers extend from these ganglia to target organs such as the heart, lungs, and blood vessels. - It also contains fibers that innervate the adrenal medulla, which releases adrenaline and noradrenaline during stress responses.

Answer 362

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.

Answer 363

S2-4 - Parasympathetic nervous innervation comes from the paired cranial nerves III, VII, IX and X, and sacral segments S2-S4

Answer 364

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.