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Year 3 - NeurologySession Overview Headache ● Primary headaches ● Secondary headaches + intracranial bleeds Transient Loss of Consciousness ● Syncope ● Epilepsy + status epilepticusHeadache Headache is a common neurological condition that can cause a variety of symptoms, most notably pain or discomfort in the face, head, or neck area Headaches can be divided into two categories: * Headache is very high yield in CCAs and progress test1° - Primary Headaches1° - Migraine Migraines are characterised typically by: - A severe, unilateral , throbbing headache - Associated with nausea, photophobia , and phonophobia - Attacks may last up to 72 hours - Patients characteristically go to a darkened, quiet room during an attack 1/3 of migraine patients experience “ classic ” migraines. These are precipitated by an aura - Changes to vision Progressive, lasting 5-60 mins Transient hemianopic disturbance or scintillating scotoma Migraines are commonly associated with triggers - tiredness, stress - alcohol - combined oral contraceptive pill - lack of food or dehydration - cheese, chocolate, red wines, citrus fruits - menstruation - bright lights1° - Migraine Migraine Triggers CHOCOLATES Chocolate + Cheese Oral contraceptive pill + menstruation Caffeine + Citrus Odours Lack of sleep Alcohol Travel Exercise Stress1° - Migraine S Unilateral O Gradual onset / aura / trigger C Severe / throbbing / pounding R +/- A Photophobia / phonophobia / osmophobia Nausea and vomiting *hemiplegia / motor weakness T Last between 4 - 72 hours E Bright light / loud sounds / strong smells / trigger S moderate - severe intensity1° - Migraine Management of an acute migraine attack - Oral or nasal triptan + Simple analgesia [paracetamol/NSAIDs/aspirin] - Antiemetic - Follow up within 2-8 weeks Migraine prophylaxis - Avoid known triggers - Acupuncturetechniques - Try one of: ● Propranolol ● Topiramate * ● Amitriptyline1° - Cluster Headache Cluster headaches are known to be one of the most painful conditions a patient can suffer The name relates to the pattern of the headaches: Typically occur in clusters lasting 4-12 weeks , clusters themselves typically occurring once a year - Intense sharp pain, stabbing around one eye - Pain occurs once or twice a day - Patients are restless and agitated during attacks - Eye redness , lacrimation , lids swelling - Nasal stuffiness - Miosis and ptosis in some Most patients with suspected cluster headaches will have an MRI + gadolinium contrast to check for any brain lesions1° - Cluster Headache S Around/behind the eye O May be triggered by alcohol, smoking, or nocturnal sleep C Intense / sharp / stabbing R +/- A Restlessness / agitation Eye redness / lacrimation/ lid swell Miosis / ptosis T Once or twice a day for 4-12 weeks Roughly once a year E Alcohol / smoking S severe intensity1° - Cluster Headache Refer to neurology Management of an acute cluster headache - Subcutaneous triptanrebreather face mask Cluster headache prophylaxis - Verapamil - Tapering dose of Prednisolone1° - Tension Headache Tension headaches are characterised typically by: - A “tight band ” around the head or pressure sensation - Bilateral Tension headaches may be related to stress Chronic tension-type headache is defined as a tension headache occurring on 15 or more days per month1° - Tension Headache S “Band” around the head / bilateral O May be triggered by stress / gradual C Pressure sensation R +/- A T E Stress Not associated with aggravation by exercise S Lower intensity than migraine1° - Tension Headache Management of an acute tension headache - Aspirin, NSAIDs, or paracetamol Tension headache prophylaxis - Low dose amitriptyline [not supported by NICE but widely used] - Manage any: ● Stress ● Chronic pain ● Sleep disorders2° - Secondary Headaches2° - Medication Overuse Headache Headache present for 15 days or more per month Developed or worsened whilst taking regular symptomatic mediation Using paracetamol or NSAIDS >15 days per month Using triptans or opioids >10 days per month Patients using opioids or triptans are at most risk Management - Opioid analgesics should be withdrawn graduallyawn abruptly Withdrawal symptoms such as vomiting, hypotension, tachycardia, restlessness, sleep disturbances and anxiety may occur when medication is stopped2° - Giant Cell Arteritis GCA or temporal arteritis is a potential medical emergency as it can lead to blindness GCA is caused by chronic large vessel vasculitis [inflammation of big arteries and veins] andis strongly associated with polymyalgia rheumatica [rheumatological proximal limb stiffness] Typically patients are age > 60 years and will present with - Unilateral scalp tendernesshe - Jaw claudication - Visual changes ● Transient loss of vision ● Diplopia Management - High dose oral steroids for 1 year → tapering dose - Patient education and steroid card - Bone protection using bisphosphonates and review patient for osteoporosis2° - Bacterial Meningitis Meningitis is the inflammation of the meninges secondary to infection , autoimmunity , or malignancy Most common causative organisms - Neisseria meningitidis - Streptococcus pneumoniae - Haemophilus influenzae - Listeria monocytogenes Clinical features - Neck stiffness - Fever - Photophobia - Paralysis - sepsis , secondary to abscess formation - Purpuric rash, secondary to development of meningococcal septicaemia - Sensorineural hearing loss - Positive Kernig’s test2° - Bacterial Meningitis Lumbar Puncture A key decision is when/whether to attempt an LP In many cases patients are treated with IV antibiotics immediately if LP cannot be done within the first hour of admission LP should be delayed if: - Signs of severe sepsis or a rapidly evolving rash - Severe respiratory or cardiac compromise - Significant bleeding risk - Signs of raised ICP ● Focal neurology ● Papilledema ● Continuous or uncontrolled seizures ● GCS <122° - Bacterial Meningitis IV antibiotics Aged 3 months - 50 years = cefotaxime [or ceftriaxone] Aged >50 years = cefotaxime [or ceftriaxone] + amoxicillin [or ampicillin] For raised ICP secure airway and give high-flow oxygen + Dexamethasone Fo- seget critical care input - secure airway + high-flow oxygen - IV access → take bloods and blood cultures - IV fluid resuscitation - IV antibiotics as above Raised Intracranial Pressure: Brief review of causes What is in the cranium? Space occupying lesions (Tumours, abscesses, bleeding) ● Brain, CSF, blood ● Intra-axial = brain parenchyma ● Raised ICP = more content than usual against an immovable cranium ● Extra-axial = external to brain Intracranial Bleeding ● Intraparenchymal bleeding ● Subarachnoid haemorrhage ● Subdural haemorrhage ● Extradural/Epidural haemorrhage CSF Flow alteration ● Physical obstruction ● Reduced absorption through arachnoid granulations (think about IIH) Venous sinus thrombosis ● A clot basically ● Backlog causes raised ICP Brain Swelling (cerebral oedema) ● Encephalitis ● Metabolic insult ● Ischaemic stroke causing inflammation Raised ICP: Symptoms Constant Headache Other neurological symptoms ● Worse when bending forward ● Focal signs ○ Think about possible sinusitis ○ Cerebellum affected causes ataxia ● Worse when lying down to sleep at night ○ Focal seizures possible ○ At first headache improves when lying down ● Confusion or behaviour change implies frontal lobe affected ○ Then worsens as pressure rises again ● Reduced GCS ○ Pain can wake up from sleep ○ Think about herniation into brainstem ● Valsalva (coughing, straining) worsens headache Symptoms of papilloedema ● Loss of peripheral vision ● Blurring of central vision ● Transient visual obscuration ○ Vision worsens (grey/black) when bending forwards then improves over seconds or minutes ● Diploplia (double vision) may be possible ○ CN VI Palsy (Abducens) Papilloedema Raised ICP: Signs & Investigations ● Margin blurred ● Elevated disk Signs (vessels crossing ● Fundoscopy shows papilloedema disc appear ● Visual fields elevated) ○ Peripheral vision loss ● Engorged veins ○ Enlarged blindspot ● Haemorrhages ● Ne○ro GCS altered around optic disc ○ UMN signs may be present ● Paton’s lines (folds of retina Investigations: Looking for a secondary cause around disc) 1. Imaging a. CT, MRI (CT if urgent) b. Venography for Venous sinus thrombosis 2. Lumbar puncture a. DO NOT LP SOMEONE WITH RAISED ICP AND MASS EFFECT b. But if CT does not demonstrate this go ahead c. Measure opening pressure and analyse constituents i. Meningitis (chronic meningitis like TB) 3. Once secondary cause found then refer to neurology or neurosurgery to treat the causeBrain Bleeds: Extradural haemorrhage What is it? Diagnosis ● Arterial (usually) bleeding between skull and dura ● Non-contrast CT Causes ○ Biconvex SOL // lens (lentiform) shape ● Usually due to middle meningeal ○ Does not cross skull sutures artery rupture ○ Hyperdense (brighter) ○ This underlies the pterion, which is the weakest and Management thinnest spot of the skull ● No neurological deficit Features ○ Cautious clinical and ● LOC then regain then LOC again radiological observation ○ This is due to the may be appropriate expanding haematoma and ● Neurological deficit(s) present resulting herniation ○ Definitive management ● Uncal Herniation ○ ipsilateral fixed dilated pupil is surgical craniotomy and evacuation (Parasympathetic CN III) ○ contralateral hemiparesis (Corticospinal) Brain Bleeds: Subdural Haematoma What is it? ● Venous bleeding between the dura and arachnoid ● Acute, sub-acute, chronic Features Acute Sub-acute Chronic ● Gradual neurological deficits ● Latency between injury and symptoms can be weeks or even t=0 3d 7d 2w 3w months Causes ● Headache, drowsiness, confusion common in late stages ● Fluctuating levels of consciousness possible as the haematoma ● Usually following head trauma (even minor contracts and expands injuries!) ● More likely to occur with brain atrophy because this places more tension on bridging veins between the SSS and the brain parenchyma ○ Increasing age ○ Alcohol excess ● More likely to occur with increasing falls risk ○ Dementia ○ Delirium ● Think about blood thinners as well Brain Bleeds: Subdural Haematoma Acute Subacute Chronic Acute on chronic T imaging ● Crosses suture lines Management ● Color ● Crescent shaped ○ Acute = hyperdense (White) ● No symptoms, small, chronic ○ Chronic = hypodense (dark ○ CM can be considered grey) ○ Subacute = in between ● Decompressive craniectomy ● Prophylactic antiapilepticsBrain Bleeds: Subarachnoid Haemorrhage What is it? ● Bleeding into subarachnoid space Causes - Traumatic and Spontaneous ● Trauma is most common cause ● Spontaneous ○ Aneurysms ○ Arteriovenous malformation General Risk Factors: HTN, smoking, excess alcohol Particular associations: ● FH Features ● Cocaine use ● Sickle cell anaemia ● Thunderclap headache ● Connective tissue disorders (Marfans, ○ “WORST headache Ehlers-Danlos) (aneurysms) of my life” ● NF (aneurysms) ○ Peaks within 5 mins ● Blood irritates the meninges ● ADPKD (predisposes to aneurysms) ○ Photophobia and vomiting ● Reduced GCS ● Focal neurologyBrain Bleeds: Subarachnoid Haemorrhage If negative CT within 6h, no LP needed If negative CT Investigations after 6h, perform LP ManagementHeadache - CCA stations Unilateral (migraine) S bilateral , band-like (tension) Around eye (cluster) Neck (meningitis) O Gradual onset (SoL, idiopathic intracranial hypertension, GCA) Sudden onset (SAH, meningitis, encephalitis, migraine, cluster headache) C throbbing/pounding (migraine) Pressure (tension) sharp/stabbing (cluster) Down neck (meningitis) R Into eye (cluster)A Neck stiffness/rash/N+V (mening.) Aura/N+V/photophobia (migraine) Unilateral/lacrimation (cluster) Jaw claudication (GCA) Worse bending over/in morning/weight loss/neuro deficit (SoL, malignancy) T Very sudden (SAH) waxing/waning consc. (subdural) alcohol/memory loss/low GCS (extradural) Long history of worsening symptoms (malignancy) E Bright light/loud sounds/strong smells (migraine) S Very severe (SAH, GCA, mening.)Headache - Red Flags Subarachnoid haemorrhage Thunderclap Photophobia/N+V/Fever/neck stiffness/rash Meningitis, meningococcal sep. Seizure, neurological deficit Would majorly affect immediate management Emergency and need hosp. and like bleed or malignancy/SoLther acute thing Jaw claudication/temporal tenderness GCA Loss of consciousness Head injury, bleed, emergency Trauma Can explain aetiology of headache e.g. bleed Worsening headache, wakes up from night, Malignancy worse in morning or on walking, lying down, bending, coughing, straining, FH of cancer, weight loss, older age, worsened by coughing/straining (raised ICP), papilloedemaTransient Loss of ConsciousnessSyncope - Transient Loss of Consciousness Syncope may be defined as a short duration and spontaneous complete recoveryrebral hypoperfusion with rapid onset, Reflex syncope - Orthostatic syncope - Cardiac syncope Reflex syncope is the most common cause in all age groups although orthostatic and cardiac causes become progressively more common in older patients .Syncope - Reflex Vasovagal - triggered by - Emotion - pain - stress Often referred to as 'fainting' Situational - triggered by - cough - micturition - gastrointestinalSyncope - Orthostatic Primary autonomic failure Drug-induced - Diuretics - Parkinson's disease - Alcohol - Lewy body dementia - Vasodilators secondary autonomic failure Volume depletion - Haemorrhage - Diabetic neuropathy - Diarrhoea - UraemiaosisSyncope - Cardiogenic Arrhythmias - Bradycardias (sinus node dysfunction, AV conduction disorders) - Tachycardias (supraventricular, ventricular) Structural - Myocardial infarction - Hypertrophic obstructive cardiomyopathy Others - Pulmonary embolismInvestigation and Differentiation Taking a detailed (+ collateral ) history will allow you to differentiate between the different causes of an episode of transient loss of consciousness If cardiogenic or orthostatic syncope is suspected the following investigations would be indicated - Full cardiovascular examination - Postural blood pressure readings : ● A symptomatic fall in systolic BP > 20 mmHg or diastolic BP > 10 mmHg ● Or a decrease in systolic BP < 90 mmHg is considered diagnostic - ECG for all patientsSeizures Seizures are the result of abnormal electrical activity in the brain Generalised Tonic Clonic Seizure // Focal // Partial Seizures Absence seizures Grand mal Tonic: tone Start in an isolated area of brain Become blank, stare into distance, don’t Clonic: muscle jerking (clonus) (usually temporal lobe) respond to environment Non-epileptic attack disorder (NEAD) Awake during partial seizure Usually in children presents similarly to GTCS but awareness is retainedling right before Divided into focal aware and focal Sometimes disappears by adolescence the seizure unaware Aware in simple focal seizure Unaware in complex focal seizure Tongue biting, incontinence, growning, Deja vu irregular breathing Strange smells, tastes, sight, so und Unusual emotions Abnormal behaviours Post ictal period of confusion, tiredness, Automatisms (lip smacking, plucking Usually lasts a few seconds irritability, low mood fingers) can occur There are many other types of seizures but they tend to be more common in childrenInvestigations following a seizure 1. Everyone with LOC should have an ECG done! 2. Bloods a. FBC, U&E, CRP, glucose b. Lactate is useful to confirm seizure (repeated clonus causes anaerobic respiration) 3. EEG (though it can be normal) 4. Neuroimaging - CT or MRI a. CT if urgent (like suspecting increased ICP, comatose, progressive neurology) 5. LP if suspected meningitis/encephalitisEpilepsy ● Recurrent, unprovoked seizures ○ At least 2 unprovoked seizures at least 24h apart ○ At least 1 unprovoked seizure and high probability of further seizures ○ Diagnosis of an epilepsy syndrome (childhood syndromes) ● Diagnosis made by neurologists based on history and EEG to support diagnosis ● Management differs based on the seizures Epilepsy: management Type of seizure 1st line 2nd line GTCS Sodium valproate Lamotrigine Myoclonic = Levetiracetam (Keppra) Brief jerks Focal Lamotrigine Lamotrigine Tonic = whole Levetiracetam (Keppra) Levetiracetam (Keppra) body stiffens and falls Myoclonic Sodium valproate Levetiracetam (Keppra) backwards Tonic and atonic Sodium valproate Lamotrigine Atonic = drop attacks Absence Ethosuximide Loss of tone resulting in fall A note on sodium valproate: ● DO NOT give to females of childbearing age as it is teratogenic ○ Causing neural tube defects and developmental delaysLifestyle changes for epilepsy ● Cannot drive until a year of being seizure-free (encourage them to inform DVLA ● Taking showers rather than baths (to avoid possibly drowning) ● Caution with ○ Swimming ○ Heights ○ Working with heavy machinery ○ TrafficStatus epilepticus ● This is a medical emergency ● Defined as ○ Seizure lasting >= 5 mins ○ Two or more seizures without regaining consciousness in between ● Management ○ ABCDE to stabilise ○ Lorazepam ○ Lorazepam ○ Keppra & get Anaesthetist to review for possible intubationTLoC - History Taking Timeline is key ! – Will most likely be a TLoC Hx if it comes up in OSCEs BEFORE - Precipitating events (head injury, prolonged standing, fever, recreational drugs) - Aura (vision changes, olfactory hallucinations, etc), - Cardiac symptoms (chest pain, palpitations), focal neurology DURING - What exactly happened (limb movements, incontinence, tongue biting) - How long did it last? AFTER - How long to recover? – post ictal period - Any injuries (did they hit their head?) - weakness, sensory disturbance, systemic features etcTLoC - History Taking PMH - Epilepsy - Neurological disease - Cardiac disease? DH - Seizures: AEDs, clozapine, opioids (tramadol, pethidine), recent Abx - Cardiogenic syncope: Antihypertensives, antiarrhythmics, antidepressants FH - Hx of epilepsy/seizures - Hx of SCD/arrhythmia SH - DRIVING – no driving for 6 months after 1st seizure, 12 months after 2nd - seizure onwards - Alcohol – can cause seizures - Recreational drugs!!! –cocaine, amphetamines, heroin, ecstasyTLoC - Red Flags GTCS lasting > 5 mins = STATUS EPILEPTICUS Fever + seizure Chest pain , palpitations , SOB - ?CNS infection - ?arrhythmia - Encephalitis - Brain abscess Seizure + head injury Focal neurology - ?intracranial bleed - ?ISOL - ?stroke Headache + seizure - ?ISOL (eg: bleed, tumour, etc)Any Questions?