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Headaches & Cerebral Inflammation By Hana Machnouk Imperial College London School Of Medicine 16/11/2023 and 18:00 @ BRITISHINDIANMEDICASSOCIATION @BINDIANMEDICS BRITISH INDIAN MEDICAL @BIMA ASSOCIATION BIMA Preclinical series WHO AM I Hana Machnouk 5 Year Medic at Imperial Just finished my BSc in Pharmacology 7569 2002TOPICS COVERED I. Haemorrhages II. Infections III. General Headaches IV. Others Symptom Differential Altered consciousness SAH Subdural haematoma - Fluctuating Headache History consciousness Extradural haematoma- altered consciousness following a lucid interval Meningitis Encephalitis Opening PC HPC ICE Conclusion N&V Raised intracranial pressure Posture-dependent (worse on lying and coughing) Visual disturbance Migraine aura Neural compression due to SOL or hemorrhage What’s brought you in Temporal arteritis today? Site Onset Photophobia Migraine Character Meningitis Can you tell me more Radiation Neck stiffness Meningitis about that? Associated Symptoms Time Exacerbating/Relieiving Fever Bacterial/viral/fungal infection Severity Rash Meningococcal sepsis Weight loss Malignancy Temporal region tenderness Temporal arteritis Neurological tenderness Migraine SOL Head trauma in last 3 months Subdural haemorrhage Sudden onset Subarachnoid haemorrhage 7569 2002SBA1 A 67-year-old male attends the Emergency department with a sudden-onset severe headache. He describes it as feeling as if he has been hit in the head with a baseball bat. This has present for the past 2 hours. He has a background of hypertension and hypercholesterolaemia for which he takes ramipril and simvastatin. What is the most appropriate next step in this patient's management? A)Sumatriptan 50mg PO B)Urgent CT head C)Urgent referral to surgery D)IV Antibiotics E)Paracetamol 7569 2002Haemorrhages A collection of blood in Subarachnoid Haemorrhage the subarachnoid Aetiology: space (between pia mater and arachnoid • Ruptured aneurysm (80%) anterior half of Circle of Willis • Traumatic Brain Injury (TBI) space) RF: Mx: • Hypertension • ABCDE/ Supportive • Smoking • Endovascular coiling(preferred) or • Family History surgical clipping • ADPKD (autosomal dominant polycystic kidney disease) • Oral Nimodipine to prevent vasospasm Symptoms/Signs: • Severe sudden-onset headache "thunderclap” • Loss of consciousness • Neck Stiffness • Photophobia • Nausea/vomiting • Confusion Ix: • URGENT non-contrast CT HEAD • CT head <6 hours of symptom onset and is normal: NO Lumbar Puncture (LP) • CT head >6 hours after symptom onset and is normal: YES LP • LP must be performed within 12 hours of symptom onset: xanthochromia (yellow discolouration) a collection of blood between the dura and arachnoid coverings of Subdural Haemorrhage the brain. Pathophysiology/Aetiology: • Rupture of the bridging veins by trauma RF: • Recent Trauma • Coagulopathy/Anticoagulant use • Advanced age>65 Mx: • Surgery: Craniotomy Symptoms/Signs: • Prophylactic antiepileptics • History: accident • Correction of coagulopathy • Headache • Loss of consciousness • Confusion Ix: • URGENT non-contrast CT HEAD: “Crescent shaped”. CAN cross suture lines • Acute: hyperdense (white) • Chronic: hypodense (dark) a collection of blood between the skull and the dura Extradural Haemorrhage Aetiology: • Low impact trauma: skull is thin around the pterion and middle meningeal artery lies below it. Symptoms/Signs: • Loss of consciousness, followed by ‘lucid interval’, followed by a LOC • Dilated pupils • Signs of herniation Ix: • URGENT non-contrast CT HEAD: “Biconvex/lentiform” hyperdense shape . Can NOT cross suture lines • Acute: hyperdense (white) • Chronic: hypodense (dark) Mx: • CraniotomySBA1 A 67-year-old male attends the Emergency department with a sudden-onset severe headache. He describes it as feeling as if he has been hit in the head with a baseball bat. This has present for the past 2 hours. He has a background of hypertension and hypercholesterolaemia for which he takes ramipril and simvastatin. What is the most appropriate next step in this patient's management? A)Sumatriptan 50mg PO B)Urgent CT head Likely diagnosis is subarachnoid hemorrhage. Must be urgently referred to get a CT. C)Urgent referral to surgery D)IV Antibiotics E)ParacetamolSBA 2 A 19-year-old male university student has currently been feeling unwell after his fresher’s week, with a fever and headache. He is very nervous about his upcoming assignments. He has been taking caffeine pills to help him with revision, however this has affected his sleep. Over the last night he has started to develop a stiff neck and has noticed that the light makes his headache worse. What is the most likely diagnosis? A.Encephalitis B.Medication overuse headache C.Migraine D.Meningitis E.Anxiety 7569 2002 Inflammation of the leptomeningeal (pia mater and arachnoid) coverings of the brain, most commonly caused by infection. Meningitis Pathophysiology: Symptoms/Signs: • Direct extension: pathogens in nose, ears etc. • Headache • Haematogenous Dissemination • Neck Stiffness • Photophobia Aetiology: Bacteria: • Fever • Neisseria meningitidis • N&V • Streptococcus pneumoniae • Non-blanching rash: N.meningitidis • Haemophilus influenzae type b (Hib) • Viral: Prodrome flu–like symptoms Viral: • Kernig's sign • Enteroviruses • Herpes simplex virus (HSV) • Brudzinski Sign RF: •<5/>65 Years old •Crowding: University halls •ImmunocompromisedMeningitis Pre-Investigation: • Pre-hospital setting and meningococcal disease is suspected :IM benzylpenicillin • If suspected: empirical antibiotics should be given if suspected and LP cannot be done within the first hour Ix: • Bloods: FBC ( raised CRP , WCC) • Blood culture • Lumbar puncture (delay if signs of sepsis, severe cardio/resp compromise, significant bleeding risk. Must do CT first if suspecting raised ICP) Mx: • ABCDE approach • IV access → take bloods and blood cultures • IV antibiotics: 3 months - 50 yrs: cefotaxime (or ceftriaxone). <3 months or >50 yrs: Intravenous cefotaxime + amoxicillin • IV dexamethasone: >3 months Inflammation of the brain parenchyma associated with Encephalitis neurological dysfunction such as altered state of consciousness, seizures, personality changes, cranial nerve palsies, speech Aetiology: problems, and motor and sensory deficits • HSV-1 Symptoms/Signs: Tip! : Suspect encephalitis whenever odd behaviour, • Fever consciousness, focal neurology or • Headache seizure is preceded by an infectious prodrome • Altered mental status/conciousness • Seizures • Vomiting • Focal features e.g. aphasia Ix: • CSF fluid: lymphocytosis, elevated protein, PCR for HSV, VZV and enteroviruses • Neuroimaging • MRI: medial temporal and inferior frontal changes (e.g. petechial haemorrhages) • normal in one-third of patients • CT is normal. •EEG • lateralised periodic discharges at 2 Hz Mx: • IV AciclovirMeningitis VS Encephalitis MENINGITIS ENCEPHALITIS Location Meninges Brain Parenchyma Aetiology Bacterial, Viral, TUsually viral Consciousness Usually unimpaired Usually alteredSBA 2 A 19-year-old male university student has currently been feeling unwell after his fresher’s week, with a fever and headache. He is very nervous about his upcoming assignments. He has been taking caffeine pills to help him with revision, however this has affected his sleep. Over the last night he has started to develop a stiff neck and has noticed that the light makes his headache worse. What is the most likely diagnosis? A.Encephalitis B.Medication overuse headache C.Migraine Crowded setting, Fever (likely infectious), Stiff neck, photophobia D.Meningitis E.AnxietySBA 3 A 41-year-old man complains of terrible headache. It started without warning, while sleeping. It affects the right side of his head. He scores it ‘11/10’ in severity. He had a similar episode six months ago, experiencing very similar headaches at the same time of the day over 2 weeks which resolved spontaneously. On observation, he right eye is red and he also has ptosis on the right side. What is the most likely diagnosis? A)Subarachnoid haemorrhage B)Tension headache C)Subdural haemorrhage D)Migraine E)Cluster headache 7569 2002 Tight Band-like, Dull, bilateral, non-pulsatile Tension Headaches headache ± scalp muscle tenderness (pericranial musculature) Aetiology: • Unknown Known Triggers: Ix: • Psychological Stress • Clinical Diagnosis • Disturbed Sleep Pattern • Fatigue Mx: • Dehydration • Simple Analgesia (Paracetamol, NSAID) Symptoms/Signs: S Generalised Bilateral O Gradual or acute C Dull (non-pulsatile) ”tight band” (constricting) Pressure-like R Neck/shoulders A N/A T Episodic Chronic E Exacerbating: eye strain from screens, as day goes on Relieving: analgesics S Moderate Severe, unilateral primary headache lasting from 15 minutes to 3 hours, occurring in clusters of Cluster Headaches weeks and associated with lacrimation. Aetiology: • Unknown Known Triggers: Ix: • Alcohol • Clinical Diagnosis • Smokers More common in Men Mx: Symptoms/Signs: Acute: • 100% oxygen (80% response rate within 15 minutes) • Severe, sharp, stabbing pain around one eye • Subcutaneous triptan (75% response rate within 15 minutes) S Unilateral, behind eye Prophylaxis: O Acute and sudden onset • Verapamil (CCB) Usually at night C Sharp, piercing, burning, worst pain ever A Red and swollen eyes Lacrimation Patient is restless and agitated T 15 minutes – 3 hours Cyclical pattern (4-23 weeks) monthsime each day, for a period of weeks, every few E Triggered by alcohol, strong smells S Excruciating – can be completely disabling Migraine is characterized by recurrent episodes of typically unilateral, throbbing, localized headaches that are Migraine frequently accompanied by nausea, vomiting, and sensitivity Aetiology: to light and sound • Vascular dysregulation: generalized vasospasms? Symptoms/Signs: Name 3 triggers for migraines. S Unilateral • Decreased ability of function O Paroxysmal, comes on gradually• Preceding Aura (10-30%): Known Triggers: C Pulsating, throbbing Visual Changes: Seeing bright lights, • Lack of sleep R / A Aura Zigzag lines or hallucinations Chocolate N&V Neurological Symptoms: Tinnitus, Hangovers T 4 – 72 hours Confusion, tingling/paraesthesia, Orgasms E Exacerbating: activity, stress, phonophobia,photophobia Numbness Cheese/caffeine Relieving: quiet, dark room Motor: Dysarthria and Ataxia, Oral contraceptives S Moderate to severe ophthalmoplegia or hemiparesis Lights Alcohol Travel ExerciseMigraine Ix: • Clinical Diagnosis Mx: Conservative: • Headache diary: Acute: • Triptans e.g.Sumatriptan. they cause vasoconstriction and improve migraines • Analgesia (NSAID/Paracetamol) • Antiemetic (metoclopramide) Prophylaxis: 1st line: • Beta Blocker ( Propanolol) • Anti-convulsant (Topiramate - teratogenic) 2nd: line: • Tricyclic Antidepressant (Amitriptyline)SBA 3 A 41-year-old man complains of terrible headache. It started without warning, while sleeping. It affects the right side of his head. He scores it ‘11/10’ in severity. He had a similar episode six months ago, experiencing very similar headaches at the same time of the day over 2 weeks which resolved spontaneously. On observation, he right eye is red and leaky. What is the most likely diagnosis? A)Subarachnoid haemorrhage B)Tension headache C)Subdural haemorrhage D)Migraine E)Cluster headache lacrimation and rednessche which is cyclical in nature, showing associated symptomsSBA 4 A 40-year-old woman with a history of multiple sclerosis presents with headache and weight loss. On direct questioning she reveals that she has stopped eating as this leads to a headache which whilst lasting only for a couple of seconds, is very sharp and intense, feeling like an electric shock in her cheek. Her neurological examination is normal. Which is the most appropriate first-line medication? A.Carbamazepine B.Gabapentin C.Lamotrigine D.Sumatriptan E.Topiramate 7569 2002 a facial pain syndrome in the distribution of ≥1 divisions of Trigeminal Neuralgia the trigeminal nerve Aetiology: • Compression of Trigeminal Nerve Root (typically by the Superior Cerebellar Artery) • Demyelinating disease • SOL Ix: RF: • Clinical Diagnosis • Increased age • MRI can be done • Female • Multiple Sclerosis Mx: • Anticonvulsants (Carbamazepine) Symptoms/Signs: Long term: S Unilateral, along trigeminal division • Microvascular decompression O Paroxysmal, lasting seconds, recurrent • Ablative surgery episodes C Stabbing, shooting, “electric-shock” A Numbness E Triggered by innocuous stimuli: Brushing teeth, Speaking, Shaving, Talking a granulomatous (hence 'giant cell') vasculitis(inflammation) of Temporal Arteritis / GCA large (and medium-sized) arteries. Aetiology/Pathophysiology: • Unknown • Thought to be due to a cell-mediated immune response to endothelial injury leading to inflammation • Primarily affects branches of the external carotid artery • Associated with polymyalgia rheumatica Ix: RF: • ↑↑ ESR, specifically > 50 mm/h. if high, start • Age>50 years treatment immediately • Female • Temporal artery biopsy (gold standard) Symptoms/Signs: Mx: • Temporal Headache • IMMEDIATE high-dose oral prednisolone • Jaw claudication • Tocilizumab (IL-6 receptor inhibitor) for • Visual loss: Sudden blindness in one or both eyes. • Scalp Tenderness severe/relapsing disease • Symptoms of polymyalgia rheumatica Abnormal growth of cells in the brain that can lead to headaches and behavioural changes. Malignancy Commonly spread to the brain: Mx: • Lung (most common) • High dose corticosteroids(dexamethasone-reduces • Breast swelling) • Bowel • Anti-seizure: sodium valproate • Skin (namely melanoma) • Surgery • Kidney Symptoms/Signs: • Seizure • Headache • Nausea/vomiting • Focal neurological deficit-weakness • Mental changes-memory problems • Drowsiness • Weight loss Ix: • MRI • BiopsySBA 4 A 40-year-old woman with a history of multiple sclerosis presents with headache and weight loss. On direct questioning she reveals that she has stopped eating as this leads to a headache which whilst lasting only for a couple of seconds, is very sharp and intense, feeling like an electric shock in her cheek. Her neurological examination is normal. Which is the most appropriate first-line medication? A.Carbamazepine neuralgia.t PMH, short-lived and sharp pain, avoiding innocuous stimuli: patient has trigeminal B.Gabapentin C.Lamotrigine D.Sumatriptan E.TopiramateTHANK YOU FOR LISTENING ANY QUESTIONS INSERT QR CODE FOR FEEDBACK FORM BIMA Preclinical seriesSubarachnoid Haemorrahage PATHOPHYSIOLOGY INVESTIGATIONS Cerebral aneurysms arise at the • URGENT non-contrast CT HEAD bifurcation of major arteries that form the • CT head <6 hours of symptom onset and is normal: NO Lumbar circle of Willis. The majority are located Puncture (LP) at the anterior communicating/anterior • CT head >6 hours after symptom onset and is normal: YES LP cerebral artery junction, distal internal • LP must be performed within 12 hours of symptom carotid artery/posterior communicating artery junction and middle cerebral onset: xanthochromia (yellow discolouration) artery bifurcation (MCA). MANAGEMENT • ABCDE/ Supportive • Endovascular coiling(preferred) or surgical clipping • Oral Nimodipine to prevent vasospasm • Stop anticoagulants PROGNOSIS + COMPLICATIONS EPIDEMIOLOGY • Poor Prognosis • At 6 months after SAH, more than 25% of patients are dead and up to half of the survivors are • SAH accounts for about 5% of all moderately to severely disabled. • Complications: Neuropsychiatric symptoms- Over 50% of survivors report problems with memory, strokes mood, and other cognitive impairment. This results in negative impact on functional status, • Worldwide= almost 500,000 individuals emotional health, and quality of life.Subdural Haemorrahage PATHOPHYSIOLOGY INVESTIGATIONS Subdural space-> venous blood • URGENT non-contrast CT HEAD drainage. Rupture of the bridging veins Hyperdense Crescent shape. Can cross suture lines that carry blood from subarachnoid space to the sinuses in between the two layers of dura. MANAGEMENT • ABCDE/ Supportive • <10mm size: midline shift <5mm non-expansile without significant neurological dysfunction: observation and motoring and follow up image. GCS, ICP monitoring. prophylactic antiepileptics. e.g. Phenytoin. Correction of coagulopathy. • >10mm size: midline shift >5mm or expansile or significant neurological dysfunction: Burr hole craniotomy, correction of coagulopathy, prophylactic antiepileptics. PROGNOSIS + COMPLICATIONS EPIDEMIOLOGY • Variable Prognosis • Poorer outcome associated with older age, lower GCS, greater severity, raised ICP, • age>65 midline shift, early need for surgery. • Patients on anticoagulants • Complications: Epilepsy, Neurological deficits. • Found in 11% to 20% of patients admitted to hospital with mild to severe traumatic brain injuryExtradural Haemorrahage PATHOPHYSIOLOGY INVESTIGATIONS Low impact trauma, commonly by hitting • URGENT non-contrast CT HEAD the pterion. The middle meningeal artery Hyperdense Biconvex/Lentiform shape. Can NOT cross suture lines lies below it. MANAGEMENT • ABCDE/ Supportive • Craniotomy PROGNOSIS + COMPLICATIONS EPIDEMIOLOGY • Early decompression is associated with good neurological outcomes • Complications include herniation of the brain, permanent coma, • Occurs in approx. 10% of patients with moderate to severe traumatic brain injury neurological deficits. • mostly seen in 20-30 year oldsMeningitis PATHOPHYSIOLOGY INVESTIGATIONS • Direct extension: pathogens in nose, ears • Bloods: FBC ( raised CRP , WCC) etc. • Haematogenous Dissemination • Blood culture • Lumbar puncture (delay if signs of sepsis, severe cardio/resp Aetiology: compromise, significant bleeding risk. Must do CT first if suspecting Bacteria: raised ICP) • Neisseria meningitidis • Streptococcus pneumoniae • Refer to slides to see the table with LP results. • Haemophilus influenzae type b (Hib) Viral: MANAGEMENT • Enteroviruses • ABCDE approach • Herpes simplex virus (HSV) • IV access → take bloods and blood cultures • IV antibiotics: 3 months - 50 yrs: cefotaxime (or ceftriaxone). <3 months or >50 yrs: Intravenous cefotaxime + amoxicillin • IV dexamethasone: >3 months PROGNOSIS + COMPLICATIONS EPIDEMIOLOGY • Prognosis: Viral: Self-limiting. Bacterial: mortality rate of community-acquired • Incidence of bacterial meningitis in Western countries is 0.7al meningitis is approximately 20%. Mortality rate of meningococcal to 0.9 per 100,000 persons per year • Viruses are the most commonly identified cause of infections is 10% to 15%. meningitis in UK adults • Complications: Septicaemia, Waterhouse-Friderichsen Syndrome, Neurological • Affcets extremes of age (impaired immunity) complications (hearing loss, limb weakness, seizures)Encephalitis PATHOPHYSIOLOGY INVESTIGATIONS • In viral encephalitis the virus initially gains entry and replicates in local or regional • CSF fluid: lymphocytosis, elevated protein, PCR for HSV, VZV and enteroviruses tissue, such as the gastrointestinal tract, • Neuroimaging skin, urogenital system, or respiratory • MRI: medial temporal and inferior frontal changes (e.g. petechial haemorrhages) system. Subsequent dissemination to the • normal in one-third of patients central nervous system occurs • CT is normal. by haematogenous routes (enterovirus, • EEG arboviruses, HSV, HIV, mumps) or • lateralised periodic discharges at 2 Hz via retrograde axonal transport as with the herpes virus). MANAGEMENT • ABCDE/Supportive • IV Aciclovir (main one for HSV) PROGNOSIS + COMPLICATIONS EPIDEMIOLOGY • Poor prognosis • High mortality if untreated. Treated mortality is 20%. Survivors may have epilepsy • 2500 cases in England each year • Highest incidence in those under one or cognitive impairment. year and over 65 years • Complications: Death, seizures, SIADH, neurological sequelae: cognitive impairment.Tension Headache PATHOPHYSIOLOGY INVESTIGATIONS • The release and activation of inflammatory • Clinical diagnosis agents leads to sensitisation of peripheral trigeminal afferents and ultimately in central hypersensitivity. It has been speculated that in tension-type headache, the major nociceptor is the peri- cranial musculature, whereas in migraine, it is blood vessels and meningeal nociceptors. MANAGEMENT • Simple Analgesics (Paracetamol/NSAIDs) PROGNOSIS + COMPLICATIONS EPIDEMIOLOGY • Good prognosis • Most patients respond to analgesics • Mean global prevalence is 42% • Very low % of patients present to their physicians withComplications: peptic Ulcer → secondary to NSAID use. tension-type headache (3% compared to 94% in migraine - due to successful self-treatment)Migraine PATHOPHYSIOLOGY INVESTIGATIONS • Exact underlying pathophysiology is UNKNOWN. • Clinical diagnosis Different aspects contribute to the development and severity of migraine, such as: • The headache of a migraine results from neurogenic inflammation of first-division trigeminal sensory neurons that innervate the large vessels and meninges of the brain. • Vascular dysregulation: vasodilation MANAGEMENT appears to play a role and there is an association between migraine and disorders Conservative: with generalized vasospasms • Headache diary: Acute: • Triptans e.g.Sumatriptan. they cause vasoconstriction and improve migraines • Analgesia (NSAID/Paracetamol) • Antiemetic (metoclopramide) Prophylaxis: • Beta Blocker ( Propranolol) PROGNOSIS + COMPLICATIONS EPIDEMIOLOGY • Chronic illness • Most patients with episodic migraine do well with treatment. • Most common in WOMEN (by 3x) • Before puberty, migraine prevalence is higher i• Frequency of migraine headaches decreases with age • Prevalence declines with age in both sexes. • Complications: Medication overuse headache, disruption of every day activities, status migrainous, depression, chronic migraine, Migrainous InfarctionMigraine PATHOPHYSIOLOGY INVESTIGATIONS • Exact underlying pathophysiology is UNKNOWN. • Clinical diagnosis Different aspects contribute to the development and severity of migraine, such as: • The headache of a migraine results from neurogenic inflammation of first-division trigeminal sensory neurons that innervate the large vessels and meninges of the brain. • Vascular dysregulation: vasodilation MANAGEMENT appears to play a role and there is an association between migraine and disorders Conservative: with generalized vasospasms • Headache diary: Acute: • Triptans e.g.Sumatriptan. they cause vasoconstriction and improve migraines • Analgesia (NSAID/Paracetamol) • Antiemetic (metoclopramide) Prophylaxis: • Beta Blocker ( Propranolol) PROGNOSIS + COMPLICATIONS EPIDEMIOLOGY • Chronic illness • Most patients with episodic migraine do well with treatment. • Most common in WOMEN (by 3x) • Before puberty, migraine prevalence is higher i• Frequency of migraine headaches decreases with age • Prevalence declines with age in both sexes. • Complications: Medication overuse headache, disruption of every day activities, status migrainous, depression, chronic migraine, Migrainous InfarctionCluster Headaches PATHOPHYSIOLOGY INVESTIGATIONS The pathogenesis is complex and not understood completely. • Clinical diagnosis The 3 cardinal features of the disorder are: 1. Trigeminal distribution of the pain 2. Ipsilateral cranial autonomic symptoms 3. Circadian/circannual pattern of attacks. happens at the same time each day MANAGEMENT Acute: • 100% oxygen (80% response rate within 15 minutes) • Subcutaneous triptan (75% response rate within 15 minutes) Prophylaxis: • Verapamil (CCB) PROGNOSIS + COMPLICATIONS EPIDEMIOLOGY • Long-term prognosis is unclear. Epidemiological studies have suggested that • More common in men. M > F ( 3.5 : 1 ratio - unliketoms tend to improve with increasing age, with less frequent cluster periods migraine which primarily affects female) and more prolonged remissions between cluster periods. • The age of onset is usually between 20 and • Complications: short-term depression/anxiety • Commoner in smokersTrigeminal Neuralgia PATHOPHYSIOLOGY INVESTIGATIONS Compression of the trigeminal nerve • Clinical diagnosis root by anomalous (superior cerebellar• MRI can be done artery) or aneurysmal intracranial vessels. Secondary Causes: • MS • Brainstem lesions/tumour MANAGEMENT Short-term: • Anticonvulsants (Carbamazepine) Long term: • Microvascular decompression • Ablative surgery PROGNOSIS + COMPLICATIONS EPIDEMIOLOGY • Prognosis: Chronic condition. Most patients find partial relief with medical therapies, vascular decompression, or ablative procedures, although patients • Rates increase with age typically become less responsive or relapse over time • Female > male • Complications: Post-operative complications-hearing loss, facial hypaesthesia, • Peak 60-70 trigeminal motor weakness.Temporal Arteritis/GCA PATHOPHYSIOLOGY INVESTIGATIONS • Unknown • ↑↑ ESR, specifically > 50 mm/h. if high, start treatment • Thought to be due to a cell-mediated immune response to endothelial immediately injury leading to inflammation • Temporal artery biopsy (gold standard) • Primarily affects branches of the external carotid artery • Associated with polymyalgia rheumatica MANAGEMENT • IMMEDIATE high-dose oral prednisolone • T ocilizumab (IL-6 receptor inhibitor) for severe/relapsing disease PROGNOSIS + COMPLICATIONS EPIDEMIOLOGY • Risk of developing aortic aneurysms is markedly increased in patients with Temporal arteritis. A treatment course of 1 to 2 years with glucocorticoids is often • Rates increase with age necessary. • Female > male • Complications: Permanent vision loss, cerebral ischaemia, aortic • Peak 60-70 aneurysm/dissection.Malignancy PATHOPHYSIOLOGY INVESTIGATIONS Abnormal growth occurring in any tissu• MRI contained within the cranium, due to • Biopsy mutations in cellular growth pathways. MANAGEMENT • High dose corticosteroids(dexamethasone-reduces swelling) • Anti-seizure: sodium valproate • Surgery • Radiotherapy PROGNOSIS + COMPLICATIONS EPIDEMIOLOGY • Prognosis: The 5-year relative survival rate for people younger than age 15 is about 75%. For people age 15 to 39, the 5-year relative survival rate nears 72%. • Age>50 years The 5-year relative survival rate for people age 40 and older is 21%. • Female sex • Complications: Seizures, fatigue, neurological sequelae(e.g. cognitive dysfunction)