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  • Neuro: Tension Headaches: Free MSRA Podcast
    2025/06/08

    ⚕️ FREE MSRA PODCAST – Tension Headache

    🎧 A clear, high-yield breakdown of this common,pressure-like primary headache – perfect for exam prep and real-life clinicalscenarios.

    🧠 Key Learning Points

    📌 Definition

    • The most commonprimary headache, characterised by a dull, bilateral, pressure-like sensationaround the head or neck.

    • Typically notassociated with nausea, vomiting, or focal neurological symptoms.

    📌 Causes & Risk Factors

    •Stress and anxiety 😰

    • Poorposture 🪑

    •Fatigue and sleep disturbances 😴

    •Bruxism (teeth grinding) 😬

    •Female gender 🚺

    • Family history

    •Excessive screen time or neck strain 💻

    🧠 Mnemonic: “SLEEP” – Stress, Lifestyle, Emotion,Ergonomics, Posture

    📌 Pathophysiology

    • Multifactorial –involves increased pericranial muscle tension.

    •Central sensitisation may play a role 🧠

    • Potentialserotonin imbalance

    📌 Symptoms

    •Bilateral dull ache or pressure 🔁

    • Feels like a tightband around the head

    • No photophobia,phonophobia or nausea (or only mild)

    • May have scalp orneck tenderness

    🧠 Mnemonic: “BAND” – Bilateral, Aching,Non-throbbing, Dull

    📌 Differential Diagnosis

    • Migraine

    • Cluster headache

    • Cervicogenicheadache

    • Sinus headache

    •Raised ICP or red-flag secondary causes ⚠️

    📌 Diagnosis

    • Clinical diagnosisbased on history

    • No imaging orbloods unless red flags present

    • Red flags:thunderclap onset, focal neurology, altered consciousness, trauma, fever, orimmunosuppression

    📌 Management

    • 🧘 Lifestyle: stress reduction, posture correction, hydration, regularsleep

    • 💊 Medication: Paracetamol or NSAIDs for acute episodes

    • 🧠 Chronic: low-dose amitriptyline may be considered

    • 🧠 CBT, mindfulness, headache diary

    • ❌Avoid codeine or routine opioid use – risk of medication-overuse headaches

    📌 Complications

    • Medication overuseheadaches (rebound)

    •Chronic tension-type headache 😖

    • Reduced quality oflife if unmanaged

    📌 Prognosis

    •Episodic types resolve easily with self-care 🟢

    •Chronic types may impair functioning and require longer-term management 🟠

    • Avoid analgesicoveruse to prevent rebound headaches

    📎 More MSRA Resources for Tension Headache

    📝 Revision Notes: https://www.passthemsra.com/topic/tension-headache-revision-notes/

    🧠 Flashcards: https://www.passthemsra.com/topic/tension-headache-flashcards/

    💬 Accordion Q&A Notes: https://www.passthemsra.com/topic/tension-headache-accordion-qa-notes/

    🚀 Rapid Quiz: https://www.passthemsra.com/topic/tension-headache-rapid-quiz/

    🎓 Full Course: https://www.passthemsra.com/courses/neurology-for-the-msra/

    Hashtags

    #MSRA #MSRARevision#MSRATextbook #MSRAQuiz #MSRAQuestionBank #MSRAFlashcards #MSRAQANotes#MSRAAccordions #MultiSpecialityRecruitmentAssessment #MSRAOnlineRevision#MSRARevisionWebsite #TensionHeadache #Neurology

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    21 分
  • Neuro: Friedreich's Ataxia: Free MSRA Podcast
    2025/06/08

    🧬FREE MSRA PODCAST –Friedreich’s Ataxia: From Genes to Gait and Beyond

    🎧 In this episode, we untangle Friedreich’s Ataxia (FA)—the most common early-onset inherited ataxia.We’ll break down the genetics, the mitochondrial link, clinical features,complications, and management—everything you need for the MSRA and clinical practice. Quick, focused, and high-yield!

    🧠Key Learning Points

    📌 Definition

    Friedreich’s Ataxia is a progressive,hereditary neurodegenerative disorder—caused by autosomalrecessive mutations in the FXN gene(chromosome 9) resulting in deficient frataxinprotein.

    • Hallmarks:Progressive ataxia (loss of coordination), muscle weakness, and reduced/absentreflexes.

    📌 Genetics & Pathophysiology

    Trinucleotide GAA repeat expansion in the FXNgene → reduced frataxin → mitochondrial dysfunction, iron accumulation,oxidative stress, and cell damage (especially nerves & heart).

    • No “anticipation”(unlike some other repeat disorders).

    • Most common inindividuals of European descent.

    • Onset: Usuallyages 10–15.

    📌 Symptoms & Clinical Features

    Progressive limb/gait ataxia (balance/walkingdifficulties)

    Dysarthria (slurred speech)

    Reduced proprioception & vibration sense

    Muscle weakness (limbs)

    Areflexia (absent ankle/knee jerks)

    Babinski sign (upgoing plantars)

    Cerebellar ataxia, optic atrophy

    Scoliosis, pes cavus (high-arched feet), high-archedpalate (may appear early)

    Cardiomyopathy (90%: hypertrophic, often amajor cause of death)

    Diabetes mellitus (10–20%)

    Other: Bladder dysfunction, cold peripheries(cyanosis), respiratory issues in late disease

    📌 Diagnosis

    Genetic testing (GAA repeat in FXN gene = goldstandard)

    Clinical exam: Progressive ataxia, areflexia,cerebellar/cord signs

    Nerve conduction studies: Absent/reducedsensory potentials

    ECG/echo: Cardiac hypertrophy, arrhythmias

    MRI: Spinal cord atrophy

    Bloods: Glucose (diabetes), vitamin E (excludedeficiency)

    📌 Differentials

    • Other inheritedataxias (spinocerebellar ataxias)

    • Vitamin Edeficiency (treatable mimic!)

    • Multiplesclerosis, toxins, metabolic, immune, or structural causes

    • Early cognitiveimpairment or marked cerebellar atrophy suggest alternatives

    📌 Management

    No cure—focus is on symptom & complicationmanagement

    Multidisciplinary care: Neuro, cardio, physio,OT, speech & language, social support

    Physiotherapy: Mobility, manage spasticity

    Speech therapy: Speech & swallow support

    Cardiac management: Standard treatment forcardiomyopathy/arrhythmias

    Diabetes: Standard diabetic management

    Orthopaedics: Surgery for scoliosis/footdeformity if needed

    Genetic counselling is essential forpatients/families

    Research ongoing: Antioxidants, ironchelation, gene therapy (none proven effective yet)

    📌 Complications & Prognosis

    Progressive disability: Wheelchair use ~15years post-diagnosis

    Cardiac complications: Main cause of mortality(mean life expectancy 40–50 years, some live longer)

    Diabetes & respiratory complications alsoreduce quality & length of life

    📎More MSRA Resourcesfor Friedreich’s Ataxia:

    📝 Revision Notes: https://www.passthemsra.com/topic/friedreichs-ataxia-revision-notes/

    🧠 Flashcards: https://www.passthemsra.com/topic/friedreichs-ataxia-flashcards/

    💬 Accordion Q&A: https://www.passthemsra.com/topic/friedreichs-ataxia-accordion-qa-notes/

    🚀 Rapid Quiz: https://www.passthemsra.com/topic/friedreichs-ataxia-rapid-quiz/

    🎓 Neurology Course: https://www.passthemsra.com/courses/neurology-for-the-msra/

    #MSRA #MSRARevision#MSRATextbook #FriedreichsAtaxia #Ataxia #Neurology #MitochondrialDisease#MSRAFlashcards #MSRAQuiz #MSRAAccordions #ExamPrep #PassTheMSRA #Revision

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    15 分
  • Neuro: DVLA Neurological Conditions and Driving Guidelines: Free MSRA Podcast
    2025/06/08
    ⚕️ FREE MSRA PODCAST – DVLA Guidelines for Neurological Disorders and Driving🎧 A clear, high-yield breakdown of UK driving restrictions for neurological conditions – perfect for MSRA exam prep and safe clinical decision-making.🧠 Key Learning Points📌 Definition• UK DVLA guidelines outline when individuals with neurological conditions can legally and safely drive• Aimed at balancing individual independence with public safety📌 Causes & Risk Factors• Conditions affecting consciousness, coordination, vision, or cognition– Epilepsy, syncope, stroke, MS, Parkinson’s, MND– Brain surgery, narcolepsy, cataplexy– Risks vary by condition, treatment response, and recurrence📌 Pathophysiology• Conditions that impair neural control, awareness, or motor function may affect driving• Guidelines assess functional risk – not just diagnosis📌 Symptoms Affecting Driving• Loss of consciousness (e.g., seizure, faint)• Sleep attacks, cognitive decline, vision or motor impairment• Severity and unpredictability determine restriction length📌 DVLA Timeframes & Conditions🧠 Epilepsy/Seizures• 1st seizure:– 6 months off if normal scan & EEG– 12 months if abnormalities or higher risk• Established epilepsy:– 12 months seizure-free required– 5 years seizure-free (on or off meds) → Till-70 license• Med withdrawal: No driving until 6 months after last dose🧠 Syncope (Fainting)• Explained, treated cause: 4 weeks off• Unexplained cause: 6 months off• 2+ episodes: 12 months off💡 Key message: Diagnosis clarity = shorter restriction🧠 Stroke / TIA• Single TIA/stroke: 1 month off• No DVLA notification needed if no persistent deficit• Multiple TIAs over short period: 3 months + must inform DVLA🧠 Brain Surgery (Craniotomy)• Craniotomy: 12 months• Exception: Benign meningioma without seizures → reconsider at 6 months• Pituitary tumour via craniotomy: 6 months• Transsphenoidal approach: can drive once safely recovered🧠 Narcolepsy / Cataplexy• Stop driving immediately on diagnosis• Resume only when symptoms well controlled, with medical support🧠 Chronic Progressive Conditions• MS, MND, Parkinson’s, dementia:– Must notify DVLA immediately on diagnosis– Complete form PK1 for individual assessment📌 Diagnosis & Reporting• HCPs must assess driving fitness based on guidelines• DVLA must be informed in specific conditions – patients may need support completing forms• Non-disclosure risks: legal consequences + patient/public safety📌 Management Role for HCPs• Provide accurate advice on driving restrictions• Encourage notification to DVLA where needed• Support medication decisions (e.g., AED withdrawal)📌 Complications• Non-adherence → legal consequences, insurance voiding, public safety risk• Delays in return to driving → loss of independence, mental health effects📌 Prognosis• Many patients can return to driving if well controlled• Longer bans if recurrence, poor medication compliance, or high risk• Functional recovery and DVLA reassessment guide outcomes📎 More MSRA Resources📝 Revision Notes: https://www.passthemsra.com/topic/dvla-guidelines-for-neurological-disorders-and-driving-revision-notes/🧠 Flashcards: https://www.passthemsra.com/topic/dvla-guidelines-for-neurological-disorders-and-driving-flashcards/💬 Accordion Q&A Notes: https://www.passthemsra.com/topic/dvla-guidelines-for-neurological-disorders-and-driving-accordion-qa-notes/🚀 Rapid Quiz: https://www.passthemsra.com/topic/dvla-guidelines-for-neurological-disorders-and-driving-rapid-quiz/🎓 Full Course: https://www.passthemsra.com/courses/neurology-for-the-msra/Hashtags#MSRA #MSRARevision #MSRATextbook #MSRAQuiz #MSRAQuestionBank #MSRAFlashcards #MSRAQANotes #MSRAAccordions #MSRAOnlineRevision #MultiSpecialityRecruitmentAssessment #DVLA #DrivingAndNeurology #NeurologyForMSRA #Epilepsy #Stroke #Syncope #DVLAFitnessToDrive #DrivingRestrictionsUK
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    7 分
  • Neuro: Vasovagal Syncope: Free MSRA Podcast
    2025/06/08
    🎧 FREE MSRA PODCAST – Vasovagal Syncope: Mastering the Most Common Cause of FaintingToday we unpack everything you need to know about vasovagal syncope — a surprisingly common, usually benign, but sometimes dramatic reason people collapse in clinic and in life.📝 Key Learning Points📌 Definition• Vasovagal syncope (neurocardiogenic syncope) is the most common cause of fainting.• It’s a temporary loss of consciousness caused by a sudden, brief drop in heart rate (bradycardia) and blood pressure (vasodilation), leading to reduced blood flow to the brain.📌 Pathophysiology & Triggers• Trigger = overstimulation of the vagus nerve, causing both slow heart rate & widened blood vessels.• Common triggers: prolonged standing, emotional distress, pain, heat, dehydration, sight of blood, medical procedures (e.g. injections).• “Vaso” = vessels (vasodilation), “vagal” = vagus nerve (bradycardia) — the name itself is a memory hook!📌 Who Gets It?• More common in younger people and those with a family history.• May be increased with certain autonomic or cardiac conditions.📌 Classic Clinical Features• Prodromal symptoms (“warning signs”): dizziness, lightheadedness, nausea, pallor, sweating, blurred/tunnel vision.• Brief loss of consciousness, rapid recovery when supine.• Episodes are often predictably triggered (standing, heat, anxiety, etc).📌 Differential Diagnosis• Rule out: arrhythmias, orthostatic hypotension, epilepsy, cardiac/structural causes, neurological disease.• Key history points: no tongue biting, no incontinence, no exertional syncope, no cardiac prodrome (palpitations, chest pain).• Family history of sudden cardiac death is a red flag — investigate thoroughly!📌 Diagnosis & Investigations• Clinical diagnosis — classic history & trigger is key!• ECG is essential (to rule out arrhythmia).• Tilt-table test can help confirm diagnosis.• Other tests (bloods, echo, EEG, imaging) only if atypical features or red flags.📌 Management• Education & reassurance — most cases are benign and manageable!• Lifestyle: – Avoid triggers (heat, dehydration, prolonged standing) – Stay hydrated – Use counterpressure manoeuvres (leg crossing, fist clenching, muscle tensing) at first sign of prodrome• Medications: Only for frequent/severe episodes (beta-blockers, fludrocortisone, SSRIs, midodrine in select cases).• Pacemaker rarely needed for severe, refractory cases.📌 Prognosis & Complications• Excellent prognosis — episodes are usually infrequent and self-limiting.• Main risk: Injury from falls during episodes (cuts, fractures, head injury).• Rarely, recurrent syncope may impact quality of life.💡 Mnemonic for Management:ABC = Avoid triggers, Boost hydration, Counterpressure manoeuvres!📎 More Vasovagal Syncope Resources:📝 Revision Notes: https://www.passthemsra.com/topic/vasovagal-syncope-revision-notes/🧠 Flashcards: https://www.passthemsra.com/topic/vasovagal-syncope-flashcards/💬 Accordion Q&A: https://www.passthemsra.com/topic/vasovagal-syncope-accordion-qa-notes/🚀 Rapid Quiz: https://www.passthemsra.com/topic/vasovagal-syncope-rapid-quiz/🧪 Quiz Bank: https://www.passthemsra.com/quizzes/vasovagal-syncope/🎓 Neurology MSRA Course: https://www.passthemsra.com/courses/neurology-for-the-msra/#MSRA #VasovagalSyncope #Fainting #NeurocardiogenicSyncope #MSRARevision #MSRAFlashcards #MSRAQuiz #MSRAAccordions #Syncope #PassTheMSRA
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    18 分
  • Neuro: Syncope: Free MSRA Podcast
    2025/06/08

    ⚕️ FREE MSRA PODCAST – Syncope
    🎧 A high-yield breakdown of this brief loss of consciousness condition – perfect for exams and real-life clinical practice.

    🧠 Key Learning Points

    📌 Definition
    • Syncope is a sudden, short-lived loss of consciousness due to transient cerebral hypoperfusion, with rapid, full recovery.

    📌 Causes & Risk Factors
    • 🧠 Neurally mediated syncope (vasovagal, situational, orthostatic)
    • ❤️ Cardiac causes (arrhythmias, structural heart disease)
    • 🩺 Mixed/other: pulmonary embolism, stroke, hypoglycaemia, drugs
    • 👵 More common in teenagers and older adults
    • 💊 Risk ↑ with diuretics, antihypertensives
    • 💡 Mnemonic: "PUMP, PIPES, or CONTROL" = Cardiac, Vasodilation, Autonomic

    📌 Pathophysiology
    • 🔻 Drop in BP or HR → cerebral hypoperfusion
    • 🔁 Disruption in autonomic regulation or cardiac output
    • 💥 Rapid but reversible ‘power cut’ to the brain

    📌 Symptoms
    • 😵 Dizziness, nausea, sweating, visual blurring
    • 🥴 “Blackout” followed by rapid recovery
    • 🔍 Warning signs (prodrome) help differentiate from seizures
    • 🧠 Duration usually seconds (longer = consider pseudoseizure)

    📌 Differential Diagnosis
    • ⚡ Seizure (postictal confusion, tongue bite)
    • 🧪 Hypoglycaemia
    • 🌪️ Vertigo
    • 🤯 Pseudosyncope
    • 👨‍⚕️ Drop attacks, TIAs, substance misuse

    📌 Diagnosis
    • 📖 History + witness account = 🥇most important
    • 🩺 Orthostatic BP
    • 📉 ECG (arrhythmias, QT changes)
    • 🩸 FBC, glucose
    • 🪑 Tilt table test for suspected NMS
    • 🫀 Echocardiogram, Holter/event monitoring if cardiac cause suspected

    📌 Management
    • 🔁 Depends on the underlying cause
    • 🧘‍♀️ NMS: reassurance, trigger avoidance, hydration, isometric manoeuvres
    • 🧦 Compression stockings, raise bed head, salt intake
    • 💊 Fludrocortisone/midodrine (caution: limited evidence)
    • ❤️ Cardiac: pacemaker, ICD, ablation, surgery as required
    • 🚗 DVLA: 3P rule (Provoked, Prodrome, Posture) determines driving eligibility

    📌 Complications
    • 🤕 Injuries from falls
    • 🧠 Anxiety and impaired QoL from recurrent episodes
    • ⚠️ Red flags: Abnormal ECG, Age >45, Ventricular arrhythmia Hx → ↑ mortality risk

    📌 Prognosis
    • 🟢 NMS often benign
    • 🔴 Cardiac syncope → high risk → prompt treatment essential
    • 📈 Risk stratification vital to guide workup and management

    📎 More MSRA Resources for Syncope
    📝 Revision Notes: https://www.passthemsra.com/topic/syncope-revision-notes/
    🧠 Flashcards: https://www.passthemsra.com/topic/syncope-flashcards/
    💬 Accordion Q&A Notes: https://www.passthemsra.com/topic/syncope-accordion-qa-notes/
    🚀 Rapid Quiz: https://www.passthemsra.com/topic/syncope-rapid-quiz/
    🎓 Full Course: https://www.passthemsra.com/courses/neurology-for-the-msra/

    Hashtags
    #MSRA #MSRARevision #MSRATextbook #MSRAQuiz #MSRAQuestionBank #MSRAFlashcards #MSRAQANotes #MSRAAccordions #MultiSpecialityRecruitmentAssessment #MSRAOnlineRevision #MSRARevisionWebsite #Syncope #NeurologyMSRA

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    19 分
  • Neuro: Tuberous Sclerosis: Free MSRA Podcast
    2025/06/08
    🎧🧠 MSRA DEEP DIVE: Tuberous Sclerosis — High-Yield Made SimpleWelcome back to another focused Deep Dive! Today we’re breaking down Tuberous Sclerosis Complex (TSC) — a complex but HIGH-YIELD multisystem condition. Perfect for your MSRA prep 🚀🔑 Core MSRA Revision Summary📌 Definition• Rare genetic multisystem disorder• Characterised by benign tumours (hamartomas) in multiple organs: brain, skin, kidneys, heart, lungs, eyes• Also called Tuberous Sclerosis Complex (TSC)📌 Genetics & Pathophysiology• Mutations in TSC1 (hamartin) or TSC2 (tuberin) genes• 🧬 Affects the mTOR pathway → uncontrolled cell growth → hamartomas• TSC2 mutations = more severe phenotype• 75–80% = sporadic (de novo); 20–25% = inherited (autosomal dominant, 50% risk if parent affected)📌 Epidemiology• Prevalence: 1 in 10,000• Incidence: ~1 in 5,800 births• Equal sex & ethnic distribution• ⚠️ Huge variability in presentation & severity📌 Clinical Features🩺 Skin (early & key clue):• Ash-leaf spots (hypomelanotic macules, fluoresce under Wood’s lamp)• Shagreen patches (lower back, leathery texture)• Facial angiofibromas (adenoma sebaceum – butterfly pattern)• Forehead plaques• Subungual fibromas (nails)• Cafe-au-lait spots may occur but NOT diagnostic🧠 Neurology:• Seizures (infantile spasms, focal, GTC seizures)• Developmental delay, intellectual disability• Autism, ADHD, behavioural issues• Cortical tubers, subependymal nodules (SENs), subependymal giant cell astrocytomas (SEGAs)👁 Ophthalmology:• Retinal hamartomas (phacomata)❤️ Cardiology:• Cardiac rhabdomyomas (may regress spontaneously)• Rarely arrhythmias (WPW)🩺 Renal:• Angiomyolipomas (AMLs)• Polycystic kidney disease• Risk of haemorrhage, hypertension, renal failure🫁 Pulmonary:• Lymphangioleiomyomatosis (LAM) — more common in females• Multifocal micronodular pneumocyte hyperplasia (MMPH)📌 Differential Diagnosis• Neurofibromatosis• Sturge-Weber syndrome• Neurocutaneous melanosis• von Hippel-Lindau syndrome• MEN1📌 Investigations• Full clinical history & exam• 🧬 Genetic testing (TSC1/TSC2)• MRI brain (tubers, SENs, SEGAs – urgent if SEGA suspected)• Renal MRI/CT → AMLs, cysts• Fundoscopy → retinal hamartomas• Wood’s lamp → ash-leaf spots• EEG → epilepsy workup• ECG → arrhythmias, WPW• Echocardiography → rhabdomyomas• Yearly renal function, BP, and urinalysis• HRCT chest if respiratory symptoms (LAM)📌 Management• 🔑 Multidisciplinary approach: neurology, dermatology, nephrology, cardiology, pulmonology, genetics, developmental paediatrics• Anti-epileptic drugs for seizures• Vagal nerve stimulation (VNS) or epilepsy surgery for refractory epilepsy• Behavioural support, tailored education plans• mTOR inhibitors (e.g. everolimus) for SEGAs, AMLs, and sometimes LAM• Surgery: AML bleeding, SEGA growth, skin lesion removal• Yearly surveillance for all organ systems• Genetic counselling for family planning📌 Complications• Intractable epilepsy• Intellectual disability• Renal haemorrhage or failure• SEGAs causing hydrocephalus• Respiratory failure (LAM)📌 Prognosis• Lifelong condition; highly variable course• Early diagnosis & regular monitoring = better outcomes• Good prognosis for SEGA if monitored & treated early• Ongoing research into targeted MTOR therapy 💊📚 Extra MSRA Revision Resources📝 Revision Notes:https://www.passthemsra.com/topic/tuberous-sclerosis-revision-notes/🧠 Flashcards:https://www.passthemsra.com/topic/tuberous-sclerosis-flashcards/💬 Accordion Q&A:https://www.passthemsra.com/topic/tuberous-sclerosis-accordion-qa-notes/🚀 Rapid Quiz:https://www.passthemsra.com/topic/tuberous-sclerosis-rapid-quiz/🎓 MSRA Neurology Course:https://www.passthemsra.com/courses/neurology-for-the-msra/#MSRA #MSRARevision #TuberousSclerosis #NeurologyMSRA #MSRAFlashcards #MSRAQuiz #HighYieldMSRA #NeurologyRevision #PassTheMSRA
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    21 分
  • Neuro: Trigeminal Neuralgia: Free MSRA Podcast
    2025/06/08

    ⚕️ FREE MSRA PODCAST – Trigeminal Neuralgia
    🎧 A clear, high-yield breakdown of this chronic facial nerve pain disorder – perfect for exam prep and real-life clinical scenarios.

    🧠 Key Learning Points

    📌 Definition
    • A chronic pain condition affecting the trigeminal nerve (CN V), causing severe, electric shock-like facial pain.

    📌 Causes & Risk Factors
    • Vascular compression (most common – e.g., superior cerebellar artery)
    • Multiple sclerosis (especially in younger patients)
    • Tumours or cysts compressing the nerve
    • Risk ↑ with age >50, female sex, MS, family history
    💡 Mnemonic: “COMPress” – Compression, Old age, MS, Pseudotumour (mass)

    📌 Pathophysiology
    • Demyelination or irritation of trigeminal nerve → ectopic firing → paroxysmal neuropathic pain
    • Often linked to abnormal sodium channel activity

    📌 Symptoms
    • Unilateral, sudden, sharp/stabbing or electric-shock pain
    • Lasts seconds to minutes
    • Triggered by touch, chewing, talking, brushing teeth
    💡 Mnemonic: “UP STAIRs” – Unilateral, Paroxysmal, Shock-like, Triggered, Activities, Intense, Recurrent

    📌 Differential Diagnosis
    • Cluster headache
    • Migraine
    • Dental pain
    • Glossopharyngeal neuralgia
    • Temporal arteritis
    • Tumours or demyelination (e.g., MS)

    📌 Diagnosis
    • Clinical diagnosis based on classic presentation
    • MRI if red flags: age <40, bilateral pain, forehead-only pain, sensory loss, optic neuritis
    💡 MRI rules out secondary causes like tumours, MS plaques, or vascular loops

    📌 Management
    • 🥇 First-line: Carbamazepine
    • Alternatives: gabapentin, lamotrigine, phenytoin, baclofen
    • Refractory: Microvascular decompression (MVD), radiofrequency ablation, gamma knife
    • Support: Multidisciplinary input, psychosocial care
    ❌ Paracetamol, NSAIDs, opioids are not effective

    📌 Complications
    • Side effects from antiepileptics (e.g., dizziness, hyponatraemia)
    • Surgical risks (e.g., facial numbness, deafness)
    • Severe impact on quality of life and mental health

    📌 Prognosis
    • Often chronic and recurrent
    • Good symptom control with early and appropriate treatment
    • Some achieve long-term relief, especially post-surgery

    📎 More MSRA Resources for Trigeminal Neuralgia

    📝 Revision Notes: https://www.passthemsra.com/topic/trigeminal-neuralgia-revision-notes/
    🧠 Flashcards: https://www.passthemsra.com/topic/trigeminal-neuralgia-flashcards/
    💬 Accordion Q&A Notes: https://www.passthemsra.com/topic/trigeminal-neuralgia-accordion-qa-notes-2/
    🚀 Rapid Quiz: https://www.passthemsra.com/topic/trigeminal-neuralgia-rapid-quiz/
    🎓 Full Course: https://www.passthemsra.com/courses/neurology-for-the-msra/

    🔖 Hashtags
    #MSRA #MSRARevision #MSRATextbook #MSRAQuiz #MSRAQuestionBank #MSRAFlashcards #MSRAQ&ANotes #MSRAAccordions #MultiSpecialityRecruitmentAssessment #MSRAOnlineRevision #MSRARevisionWebsite #TrigeminalNeuralgia #Neurology


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    18 分
  • Neuro: Tremors: Free MSRA Podcast
    2025/06/08
    ⚕️ FREE MSRA PODCAST – Tremor🎧 A clear, high-yield breakdown of this neurological movement disorder with diverse causes – perfect for exam prep and real-life clinical scenarios.🧠 Key Learning Points📌 Definition• Involuntary, rhythmic shaking or oscillation of a body part• Can occur at rest or during movement – classification is key📌 Causes & Risk Factors• Essential tremor (ET) – most common; often familial; worsens with age• Parkinson’s disease – rest tremor hallmark• Medication-induced – e.g., SSRIs, antipsychotics, withdrawal• Physiological tremor – enhanced by anxiety, fever, caffeine, hyperthyroidism• Cerebellar tremor – intention tremor; suggests cerebellar pathology• Neurological conditions – MS, Parkinsonism, dystonia, stroke• Metabolic – thyroid dysfunction, liver/kidney failure, electrolyte imbalance• Toxins – arsenic, heavy metals, B1 deficiency• Psychogenic tremor – worsens with stress, improves with distraction💡 Mnemonic for causes: “VAMP CAPPERS” – Vitamin deficiency, Anxiety, Meds, Parkinson's, Cerebellum, Alcohol, Physiological, Psychogenic, Electrolytes, Rare diseases, Stroke📌 Pathophysiology• Caused by abnormal oscillations in the motor control circuits of the brain• Type and location of these faulty signals determine the tremor type• Cerebellum and basal ganglia play central roles📌 Symptoms• Tremor may affect hands, head, voice• Rest tremor → Parkinson’s (e.g. "pill-rolling")• Postural tremor → ET, physiological tremor• Kinetic/intention tremor → cerebellar disease• Psychogenic tremor → variable, abrupt, distractible💡 ET = 8–10 Hz, bilateral, worsens with stress, improves with alcohol📌 Differential Diagnosis• Essential tremor vs Parkinson's• Dystonia, Wilson's disease, drug-induced, psychogenic• History + exam crucial to differentiate between overlapping patterns📌 Diagnosis• Primarily clinical – based on type, history, neuro exam• Investigations only if atypical or cause unclear:– TFTs (thyroid), Copper/ceruloplasmin (Wilson’s)– MRI/CT (lesion, stroke), LFTs, U&Es, FBC for systemic causes• Avoid scattergun testing – tailor to clinical suspicion📌 Management• Essential Tremor:– Mild: may need no treatment– Moderate: Propranolol or Primidone (1st-line)– Severe: DBS, botulinum toxin, MR-guided ultrasound• Physiological tremor:– Usually non-progressive, may improve with CBT if anxiety-driven• Secondary tremor:– Treat underlying cause – e.g., Parkinson’s, hyperthyroidism– Always review medications first• Occupational therapy for functional support💡 Clinical pearl: Trial med reduction before adding tremor meds📌 Complications• Can significantly impact daily functioning and quality of life• Progressive disability in some cases (esp. ET, Parkinson’s)• Emotional toll – anxiety, social withdrawal📌 Prognosis• ET: progressive, neurodegenerative, worsens 3–5% yearly• Physiological tremor: non-progressive• Drug-induced: may persist post-withdrawal• Secondary tremors: follow course of the parent condition📎 More MSRA Resources for Tremor📝 Revision Notes: https://www.passthemsra.com/topic/tremor-revision-notes/🧠 Flashcards: https://www.passthemsra.com/topic/tremor-flashcards/💬 Accordion Q&A Notes: https://www.passthemsra.com/topic/tremor-accordion-qa-notes/🚀 Rapid Quiz: https://www.passthemsra.com/topic/tremor-rapid-quiz/🧪 Quiz Bank: https://www.passthemsra.com/quizzes/tremor/🎓 Full Course: https://www.passthemsra.com/courses/neurology-for-the-msra/Hashtags#MSRA #MSRARevision #MSRATextbook #MSRAQuiz #MSRAQuestionBank #MSRAFlashcards #MSRAQANotes #MSRAAccordions #MSRAOnlineRevision #MultiSpecialityRecruitmentAssessment #Tremor #EssentialTremor #NeurologyForMSRA #MovementDisorders #Parkinsons #WilsonDisease
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