This instructive session, led by experts Holly Haines and Bruce Dickson, will guide medical professionals in neurology history taking, offering advice and explaining methodologies. You will master the structure of a neurological history and understand the crucial questions to ask your patients. The session also includes an in-depth review of conditions like depression, anxiety, stroke/TIA, epilepsy, headaches and fatigue and the role these conditions play in patient dialogues. Comprising of two major parts - History Taking and Explanation & Advice, the program will also explore the importance of clear communication in medical consultations and how to devise a plan with your patient. This session is an invaluable opportunity for medical professionals to enhance their neurology sidelights and patient interaction skills.
By the end of the session, learners will be able to describe the process and key elements of conducting a neurological patient history.
Learners will understand how to navigate through a patient history with a neurology focus, including questions regarding presenting complaints, past medical history, drug history, family history, and social history.
Learners will interpret and demonstrate the knowledge to advise patients on neurological disorders such as depression, anxiety, stroke/TIA, epilepsy, headache, and tiredness.
Learners will demonstrate their understanding of the sequence and flow of a neurological patient-centric ‘Explanation & Advice’ station.
Learners will be able to recognize common neurological symptoms and relate them to potential diagnoses during history taking, demonstrating this through sample patient scenarios.
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The following transcript was generated automatically from the content and has not been checked or corrected manually.
Neurology History Taking, Explanation, and Advice Holly Haines; Bruce DicksonLearning Outcomes ▶ Outline the general structure of a neurological history ▶ Understand key questions to ask in a neurological history in relation to common presenting complaints ▶ Outline the general structure of an ‘Explanation & Advice’ station ▶ Know how to apply knowledge of depression, anxiety, stroke/TIA, epilepsy, headache, and tiredness when speaking to patientsSession Structure ▶ Part 1: History Taking ▶ Part 2: Explanation & Advice ▶ QuestionsPart 1: History TakingHistory Taking Structure 1. Introduction 2. Presenting Complaint 3. History of Presenting Complaint 4. Past Medical History 5. Drug History 6. Family History 7. Social History 8. Systems Enquiry1. Introduction ▶Introduce yourself ▶Confirm patient details ▶Explain conversation ▶Gain consent2. Presenting Complaint ▶Open question ▶ ‘What brings you in today?’ ▶ ‘Tell me about what you’ve been experiencing’ ▶Quick summary of issue ▶Ideally record in patient’s own words (e.g. dizzy)Neuro PC Examples ▶Headache ▶Seizures ▶Syncope ▶Muscular symptoms – weakness/tremor/spasms ▶Sensory symptoms – numbness, paraesthesia ▶Vertigo, dizziness ▶Instability, loss of coordination ▶Visual changes – blurring, diplopia ▶Hearing changes – hearing loss, tinnitus3. History of Presenting Complaint ▶Expand with follow-up questions ▶Symptom duration ▶Speed of onset – acute vs. chronic ▶Location ▶Variation ▶IntensityPain ▶ SOCRATES ▶ Site ▶ Onset ▶ Character ▶ Radiation ▶ Associated symptoms ▶ Timing ▶ Exacerbators/relievers ▶ Severity (1-10)Headache - SOCRATES ▶Site ▶Unilateral – migraine ▶Bilateral – tension headache ▶Onset ▶Sudden – subarachnoid haemorrhage ▶Character ▶Aching, throbbing, pounding, stabbing ▶‘Thunderclap’ – subarachnoid haemorrhageHeadache - SOCRATES ▶Radiation ▶Neck – meningitis ▶Face – trigeminal neuralgia ▶Eye – acute angle-closure glaucoma ▶Associated Symptoms ▶Nausea – raised ICP ▶Visual disturbance – migraine aura ▶Photophobia – migraine, meningitis ▶Neck stiffness – meningitis ▶Fever – infection ▶Non-blanching rash - meningitisHeadache - SOCRATES ▶Exacerbators ▶Caffeine, excessive codeine, stress ▶Coughing, lying flat – raised ICP ▶Standing – low ICP ▶Relievers ▶Hydration ▶Lying flat – low ICP ▶Standing – raised ICP ▶Severity ▶‘Worst pain ever felt, 10/10’ – subarachnoid haemorrhageHeadache – RED FLAGS ▶ Sudden onset, extreme pain – subarachnoid haemorrhage ▶ Worsening headache with fever, neck stiffness, altered mental state – meningitis ▶ New onset focal neuro deficit – haemorrhage, lesion, encephalitis, meningitis ▶ Decreased consciousness, posture dependant – raised ICP ▶ Severe eye pan, reduced vision, nausea – acute angle- closure glaucomaStroke & TIA ▶ Weakness ▶ Distribution, severity, onset, duration, course ▶ Sensory Disturbance ▶ Arms, legs, face ▶ Distribution, severity, onset, duration ▶ Visual Disturbance ▶ Area of visual field, severity, onset, duration ▶ Speech ▶ Slurring, issues speaking, issues understandingStroke & TIA ▶ Ataxia ▶ Balance, coordination ▶ Dysphagia ▶ Difficultyswallowing – solids, liquids ▶ Consciousness ▶ Collaterals can be helpful ▶ Pain ▶ SOCRATESStroke & TIA – Risk Factors ▶ Heart disease ▶ Hypertension ▶ AF ▶ Hyperlipidaemia ▶ Diabetes ▶ Previous stroke/TIA ▶ Prosthetic valves ▶ Smoking/alcohol ▶ COCP ▶ Family historyDizziness – Neuro Context ▶ Central Vertigo ▶ Hyperacute, continuous – PACS ▶ Episodic – vertebrobasilar insufficiency (atherosclerosis) ▶ Unilateral hearing loss/tinnitus - tumour ▶ Migraine associations – vestibular migraine ▶ Peripheral Vertigo ▶ Hyperacute, short bursts – BPPV ▶ Ear fullness, tinnitus, sensorineural hearing loss – Meniere’s disease ▶ Gradual, recent illness – vestibular neuronitis/labyrinthitisLoss of Consciousness ▶ Reflex syncope ▶Decrease in BP/HR in response to trigger ▶ CV syncope ▶Decreased CO from arrythmias, heart disease, orthostatic hypotension ▶ Seizures ▶ Ask about prodromal symptoms, auras, motor symptoms, time to full recovery, relieving factors ▶ PMH ▶Epilepsy, Parkinson’s, diabetes, CVDMotor Disturbances ▶ Weakness ▶ Chronic, fatigue, specific muscles? ▶ Nerve vs. muscular issue ▶ Proximal vs. distal muscle weakness ▶ Issues with walking ▶ Abnormal Movements ▶ Slowing, jerking, stiffness ▶ Parkinson’s?Sensory Disturbances ▶ Numbness ▶ Abnormal sensations ▶ Abnormal pain perception ▶ Loss proprioception ▶ Dermatome pattern? ▶ Diabetic neuropathy? ▶ ‘Glove & stocking’4. Past Medical History ▶Common neuro conditions: ▶ Stroke (ischaemic & haemorrhagic) ▶ Epilepsy ▶ Migraines ▶ MS ▶ Alzheimer’s disease ▶ Parkinson’s disease ▶ Motor neuron disease4. Past Medical History ▶ Other chronic conditions: ▶ Diabetes (peripheral neuropathy) ▶ Hypertension ▶ Hyperlipidaemia5. Drug History ▶Prescription medications ▶OTC medications ▶Supplements ▶Compliance ▶Allergies6. Family History ▶Inherited neuro conditions: ▶ Dementia ▶ Ataxia ▶ Hereditary neuropathies ▶ Muscular dystrophies ▶ Huntington’s disease ▶ Neurofibromatosis7. Social History ▶Living situation ▶Occupation ▶Mobility ▶Performing activities of daily life ▶Diet ▶Exercise7. Social History ▶Smoking ▶ Pack years ▶ (# of packs/day) x (# of years smoked) ▶A lcohol ▶ Units per week ▶ 14 recommended max8. Systems Enquiry ▶CVS – palpitations, chest pain ▶RS – cough, SOB ▶GI – change in bowels, abdo pain ▶GU – urinary changes ▶MS – aches/stiffness joints/muscles/back ▶General – weight loss, infection/fevers8. Systems Enquiry ▶Cranial nerve screening ▶ Smell ▶ Vision, double vision ▶ Dry eyes/mouth ▶ Taste ▶ Hearing, dizziness ▶ Voice, articulation8. Systems Enquiry ▶Psychological ▶ Mood ▶ Depression ▶ AnxietyPart 2: Explanation & AdviceWhat is ‘Explanation and Advice’? ▶Clinical scenario ▶Involves explaining a condition to someone who may never have heard of it before ▶Addressing patient concerns or questions ▶Coming up with a plan together ▶As much about information giving as information gatheringCOMMUNICATION AND STRUCTURE IN E&AIntroduction ▶ Proper introductions are key ▶ Wash hands ▶ Who you are - name, role ▶ Confirming patient identity ▶ Clarifying purpose of consultation ▶ Check patient understanding of today’s meeting ▶ Explain agenda ▶ ConsentThroughout the consultation ▶ Avoid jargon and complicated language ▶ Always check patient understanding before giving information ▶Non-verbal communication and cues ▶ICEClosing ▶Chunk and check ▶Always give the opportunity for questions ▶Resources and safety-netting ▶Thank patient for timeStructuring an E&A consultationDepression E&A Definition: ▶ Absence of a positive affect (a loss of interest and enjoyment in ordinary things and experiences), low mood, and a range of associatedemotional, cognitive, physical, and behavioural symptoms Pathophysiology: ▶ Cause unknown ▶ Hypothesised to be due to depletion of serotonin/noradrenaline/dopamine in the CNS ▶ Also associatedwith genetic factorDepression E&A continued Non-Pharmacological Management: ▶ CBT ▶ Mindfulness ▶ Increasing exercise + improving diet ▶ Counselling ▶ Psychotherapy Pharmacological Management ▶ Antidepressants e.g. SSRI’s such as Sertraline, SNRI’s such as duloxetine, TCA’s such as amitriptyline, MAOI’s such as tranylcypromineAnxiety E&A Definition: ▶ Excessive worry about everyday issues that is disproportionate to any inherent risk. There are multiple types of anxiety including generalised anxiety disorder, social anxiety, PTSD, phobias, panic attacks Pathophysiology: ▶ Not fully understood ▶ CNS mediators e.g. noradrenaline, serotonin, dopamine and GABA are thought to be involved as well as the autonomic and sympathetic nervous system ▶ Amygdala plays a role in heightened fear responses to anxiety cues ▶ Stressful/traumaticexperiences eg domestic violence, child abuse or bullying, chronic health condition ▶ Also research suggesting role of drug/alcohol misuseAnxiety E&A continued Non-Pharmacological Management: ▶ CBT ▶ Self-help ▶ Psychotherapy ▶ Counselling Pharmacological Management: ▶ SSRI’s e.g. sertraline ▶ SNRI’s e.g. venlafaxine ▶ Buspirone for GAD ▶ Benzodiazepines in short term anxiety, avoided long term due to addictive properties ▶ Beta-blockers to help with side effects e.g. palpitations.Stroke/TIA E&A Definition: ▶ Stroke - Ischaemic infarction of part of brain (usually atheroma or thromboembolism) or from intracerebral haemorrhage ▶ TIA - Temporary inadequacy of the circulation in part of the brain, similar to a stroke except it's transient and reversible. Duration no more than 24h (most >30min) Pathophysiology: ▶ Strokes + TIA’s same pathophysiology ▶ Strokes can be ischaemic (85%) or haemorrhagic. Ischaemic stroke = abrupt deficiency in blood supply to a certain area of the brain Haemorrhagic stroke = bleeding/leaky blood vessels in an area of the brain ▶ Strokes can be caused by thrombus formation in blood vessels or embolisms travelling to brain vessels. Atherosclerosis builds up plaque in vessels and can rupture creating embolisms.Stroke/TIA E&A Non-Pharmacological Management (preventing future strokes): ▶ Increasing physical activity ▶ Reduction/cessation of smoking ▶ Improved diet ▶ Reduced alcohol consumption Pharmacological Management: ▶ Stroke – thrombolytic, anti-coagulant and anti-platelet treatment once a haemorrhagic stroke has been excluded. ▶ TIA – Immediate referral to a stroke clinic. Aspirin is offered if TIA thought to be within past 7 days, then referral to specialist. ▶ Medications such as anti-platelet therapy eg clopidogrel, statins eg atorvastatin,anti-HTN medications eg lisinopril can be used to prevent future strokesEpilepsy E&A Definition: ▶ Epilepsy is the tendency to recurrent spontaneous seizures unprovoked by an acute systemic or neurologic insult ▶ Epilepsy is defined by any of • > 2 unprovoked seizures occurring >24h apart • One unprovoked seizure and a probability of further seizures similar to the general recurrence risk after 2 unprovoked seizures, occurring over the next 10 years • Diagnosis of a epilepsy syndrome Seizures is the manifestation of abnormal paroxysmal neuronal discharges in part(s) of the brainEpilepsy E&A continued Pathophysiology: ▶ Variety of factors including structural, genetic, infectious, metabolic, and immune including hypoglycaemia, electrolyte imbalance, acute head injury, drug abuse, alcohol withdrawal ▶ Seizure initiation is characterised by high frequency bursts of action potential and hyper synchronization of a neuronal population with manifestations in varying parts of the brain which can relate to symptoms experienced Epilepsy and driving: ▶ Patient must be 6 months without seizure (awake + LOC seizure) ▶ Or 12 months if seizure has not affected consciousness ▶ If seizures have only been whilst asleep for the past 3Y, you can still apply for a license.Epilepsy E&A continued ▶ Immediate Management: ▶ Protecting the person from injury, checking airway, placing in recovery position after seizure ▶ Prolonged tonic-clonic seizures can have emergency buccal midazolam first line in the community. ▶ Non-Pharmacological Management: ▶ Reduction of exposure to provoking factors such as stress/anxiety, sleep deprivation, strobe lighting, alcohol + drugs ▶ Pharmacological Management: ▶ Anti-epilepsy drugs such as phenytoin, carbamazepine, valproate, lamotrigine ▶ 70% of patients will be seizure free on 1 AED, 80% on 2, 85% on 3, 15% classed as medically refractory ▶ Single seizures likely don’t need pharmacological managementTension Headache E&A Definition: ▶ Tension type headache is the most common primary headache disorder and involves a band pain across the forehead, worse through the day, not worsened by exercise Pathophysiology: ▶ Exact mechanism unknown ▶ Thought to be due to peripheral pain mechanisms in episodic tension headaches and central pain mechanisms and heightened sensitivity in chronic tension headaches ▶ No measurable features and no biomarkers and are not associatedwith a structural or metabolic abnormality ▶ Involvement of peri-cranial muscle tenderness and pain sensitivity ▶ May be exacerbated by triggers such as stress, caffeine, disturbed sleep, genetic predisposition.Tension Headache E&A continued Non-Pharmacological Management: ▶ CBT has been seen to be helpful in some patients ▶ Identify, monitor and reduce triggers such as stress, poor posture, poor diet, sleep ▶ For chronic tension type headaches, avoid excessive use of analgesics (can lead to medication overuse headaches). Pharmacological Management: ▶ Simple analgesics e.g. paracetamol ▶ Aspirin ▶ NSAIDs for acute attacks ▶ If MOH, reduce use of painkillers ▶ Prophylactic amitriptyline may be used too instead of acute pain relief. Recommend patients to keep a headache diary to monitor symptoms, triggers, frequency, durationMigraine E&A Definition: ▶ Common, chronic, episodic, primary headache disorder, not associated with an underlying condition ▶ Migraines are characterised by headache attacks (moderate to severe), commonly unilateral, being described as throbbing/pulsating. Migraines can present with/without aura (transient focal neurological symptoms/sensory symptoms). Migraines may be worsened by light, movement, physical activity, disturbed sleep, caffeine intake and stress and relieved by remaining still, avoiding light and reducing triggers Pathophysiology: ▶ Not fully understood ▶ One theory is relating to pain receptors in blood vessels of the brain.Migraine E&A continued Management: ▶ Reduce triggers eg caffeine intake, inadequate sleep, improved weight and treat any exacerbating co-morbidities eg insomnia, depression ▶ Recommended patients to keep headache diaries which can be used to track triggers, time of onset, patterns etc ▶ Avoid the excessive use of painkillers, restricted to up to 2 times a week ▶ For acute migraine attacks, analgesics e.g. aspirin or ibuprofen recommended ▶ If analgesics not helping migraine relief, triptans eg sumatriptan may be used in combination with NSAIDs/paracetamol at the start of the headache, not the aura ▶ Preventative treatment may be used in those in which migraines are having a significant impact on QoL, and alter daily function ▶ Examples of preventative medications for migraines are amitriptyline, propranolol and topiramate. These can be given to patients when they are experiencing >/=2 a month.Tiredness E&A Definition: ▶ A sensation of exhaustion during or after usual activities, or a feeling of inadequate energy to begin these activities Pathophysiology: ▶ Multitude of factors, including physiological causes eg pregnancy, inadequate sleep and excessive exercise, physical causes eg anaemia, diabetes, malignancy or psychological/psychosocialcauses eg depression, anxiety, loss and stress ▶ Pathophysiology of chronic fatigue syndrome still unknown but is usually accompanied by other symptoms which suggest a combination of inflammatory, endocrine, immune, cardiac, neurological and viral dysfunctionTiredness E&A continued Management: ▶ Sinister underlying cause referred to secondary care ▶ Routine screening of bloods for those presenting with ‘tiredness' ▶ For general tiredness, assess triggers and precipitating factors and aim to minimise ▶ E.g. reduced alcohol intake, reduced caffeine intake, treatment of underlying causes e.g. anaemia, depression ▶ Advice should be offered on sleep hygiene e.g. avoiding excessive sleep, daytime sleep, caffeine before bed. ▶ Psychological support eg CBT, counselling may be beneficial in some individuals.QUESTIONS?Feedback Please take a minute now before you leave to fill in a quick feedback form! https://app.medall.org/feedback/feedback- flow?keyword=8eaaaed0dea295a60ace610c&organisation=accessibility- in-medicineThank you for coming! ▶ If you have any more questions, feel free to email s2031151@ed.ac.uk (Holly), s2145627@ed.ac.uk (Bruce), or accessibilityinmedicine@gmail.com ▶ Give our Facebook page a like for updates and opportunities, just search @AIMEdinburghSign up to the mailing list ▶ Sign up to the AIM mailing list to be the first to hear about tutorials, discounts, and opportunities! ▶https://forms.gle/q JNyeoFzA9B5urND7Thank you to our sponsors
