Transcript Slide 1
Nick Pendleton What are the causes of Headache? What worries you about dealing with patients with headache? Tension Type Headache Referred pain from the neck or teeth Medication overuse Sinusitis, Migraine Carbon Monoxide Poisoning Temporal Arteritis, Meningitis Subarachnoid Haemorrhage and CVA Subdural Haematoma Raised intracranial pressure Brain Tumours (1o or 2o) • • • • • • • • • • Take a proper history! Review established diagnoses Make sure you understand the story Has an existing headache changed? Grade severity What is the effect on their normal activities Consider- age, smoking, PMH, Medication Examine the patient Explain your diagnosis & plan Safety-netting ‘So it’s not a brain tumour then?’ What is a proper examination? • Be thorough and careful and document what you have done • This reassures both yourself and the patient • Cranial nerve examination and fundoscopy • Blood pressure/cardiovascular system • ENT/Dental/Opticians eye test • Neck & Head/Scalp examination Conditions affecting cranial nerves • • • • • • • • • Diabetes mellitus Multiple Sclerosis, Tumours, Sarcoid Vasculitis (e.g. Polyarteritis nodosa) Aneurysms Injury, raised ICP, infections eg Zoster Systemic Lupus Erythematosus Syphilis Chronic meningitis – (TB, fungal, malignant) • • • • I Olfactory smell II Optic vision III Oculomotor eyelid and eyeball movement IV Trochlear innervates superior oblique turns eye downward and laterally • V Trigeminal chewing face & mouth touch & pain • VI Abducens turns eye laterally (lateral rectus) • VII Facial controls most facial expressions secretion of tears & saliva, taste SHE IS TRYING TO LOOK TO HER LEFT LEFT VI CRANIAL NERVE PALSY RIGHT III NERVE PALSY RIGHT FACIAL (VII) NERVE BELLS PALSY OPHTHALMIC SHINGLES (branch of V trigeminal) • VIII Vestibulocochlear (auditory) hearing, equillibrium sensation • IX Glossopharyngeal taste senses carotid blood pressure • X Vagus senses aortic blood pressure slows heart rate, stimulates digestive organs,taste • XI Spinal Accessory controls trapezius & sternocleidomastoid, controls swallowing movements • XII Hypoglossal controls tongue movements HEADACHE RED FLAGS • • • • • • • • Onset of new or different headache Nausea or vomiting Worst headache ever experienced Progressive visual or neurological changes Paralysis Weakness, ataxia or loss of coordination Drowsiness, confusion, memory impairment or loss of consciousness Onset of headache after age of 50 years RED FLAGS • Papilloedema • Stiff neck • Onset of headache with exertion, sexual activity or coughing • Systemic illness • Numbness • Asymmetry of pupillary response • Sensory loss • Signs of meningeal irritation British Journal of Radiology 2003 BMJ Clinical Review 2008 Tension-Type Headache • Episodic or Chronic • Episodic type headache is most common cause of headache in the general population and is usually self managed • Chronic tension-type headache may be highly disabling and often prompts medical consultation • Diagnosis is clinical, based on widely accepted and validated criteria (A)At least 10 episodes fulfilling the criteria B-D: (B) Headache lasting from 30 minutes to 7 days (C) Headache has at least two of the following characteristics: Bilateral location Pressing/tightening (non-pulsating) quality Mild or moderate intensity Not aggravated by routine physical activity such as walking or climbing stairs (D) Both of the following: No nausea or vomiting (anorexia may occur) No more than one episode of photophobia or phonophobia (E) Not attributable to another disorder Infrequent episodic tension-type headache Diagnosed if headaches meeting the above criteria occur <1 day a month (<12 days a year) on average Frequent episodic tension-type headache Diagnosed if headaches occur >1 and <15 days a month (>12 and <180 days a year). Chronic tension-type headache Diagnosed if headaches occur ≥15 days a month (180 or more days a year). What causes TTH? • The underlying cause is uncertain • Activation of hyperexcitable peripheral afferent neurons from head and neck muscles is the most likely explanation for episodes of infrequent TTH • Muscle tenderness and psychological tension are associated with and aggravate TTH but are not clearly its cause. What causes TTH? • Abnormalities in central pain processing and generalised increased pain sensitivity are present in some patients with tension-type headache. • Susceptibility to tension-type headache is influenced by genetic factors Tension-Type Headache • Peripheral factors are implicated in episodic tension-type headache, whereas central factors probably underlie chronic tension-type headache • Simple analgesics, especially aspirin/nsaids, are used for acute treatment • Amitriptyline and biofeedback assisted relaxation training have the best evidence of effectiveness for headache prevention Patient with Tension-Type Headache indicating location of his headache pain. Loder E , Rizzoli P BMJ 2008;336:88-92 ©2008 by British Medical Journal Publishing Group Medication Overuse Headache • May present as a chronic daily or near daily pattern of relatively non-descript headache. • The amount, type, duration, and frequency of medication use needed to cause overuse headache is not clearly established. • Consider this in patients taking opioid or combination analgesics for an average of 10 or more days a month, or simple analgesics for an average of 15 or more days a month BMJ Clinical Review 2006 MIGRAINE • The World Health Organization considers that severe migraine can be as disabling as quadriplegia! • 15% adults in N America & W Europe • A brain disorder involving abnormal sensory processing (not vascular) • Can often be well managed by a combination of acute and preventive treatment MIGRAINE Simplified Diagnostic Criteria • Repeated attacks of headache lasting 4–72 hours that have these features : • A: Normal physical examination • B: No other reasonable cause for the headache • C: At least two of: Unilateral pain • Throbbing pain, Aggravation of pain by movement, Moderate or severe intensity of pain • D: At least one of Nausea or Vomiting • Photophobia and phonophobia Migraine with Aura • 20–30% experience migraine with aura, • Focal neurological phenomena that precede or accompany the attack. • Appear gradually over 5 to 20 minutes and generally last fewer than 60 minutes. • Headache phase usually begins within 60 minutes of the end of the aura phase. • Symptoms of migraine aura can be visual, sensory, or motor in nature. Aura? • Common aura symptoms include: • Visual disturbances (such as flashing/flickering lights, zigzag lines and even temporary blindness) • Numbness, tingling sensations and slurred speech. • Other aura symptoms include a stiff neck, weakness on one side, partial paralysis, confusion or fainting Migraine Vs TTH 1. Migraine is essentially head pain with associated features whereas tension-type headache is featureless head pain’ 2. Migraine has biological signatures that tension-type headache does not seem to, namely the inherited tendency to headache when confronted with particular triggers Migraine Triggers • • • • • • • • Altered sleep patterns (too little or too much) Skipping meals Overexertion Change in stress level (too much or relaxation) Excess afferent stimuli (such as bright lights) Weather change Chemical (delayed headache after alcohol or GTN) Menstruation MIGRAINE TREATMENT • Triptans, selective 5-HT1B/1D receptor agonists –various formulations & types • Ergot derivatives (older treatment, not commonly used) • Antiemetics & nsaids Preventive : 2/3 will have 50% reduction • But all have significant side effects: • Pizotifen – weight gain, drowsiness • B- Blockers – tiredness • Tricyclics – drowsiness • Anticonvulsants – valproate, topiramate, gapapentin – significant s/e • Many people find their migraines so disabling that they are prepared to accept side-effects from the preventive treatments Migraine & risk of stroke/CVD risk • Iceland 2010 – Increased risk of CVD/CHD & mortality (migraine with aura only) • France 2010 – Women. Migraine with aura might be a risk factor for haemorrhagic stroke • Harvard meta-analysis 2009 – Migraine with aura is associated with a two-fold increase in ischaemic stroke, higher in women, < 45, smokers, on OCP • OCP contraindicated in focal (ie.with aura) migraine Sinister Headaches • Raised ICP & Brain Tumours • Subarachnoid Haemorrhage • Subdural Haematoma Causes of Raised ICP • Mass effect – tumours, abscesses • Generalised brain swelling eg anoxia • Increase in venous pressure - Heart failure • Obstruction to CSF flow absorptionhydrocephalus, arnold-chiari malformation • Increased CSF production – meningitis, choroid plexus tumours • Idiopathic • Cerebral venous sinus thrombosis • Acute liver failure Signs & Symptoms of Raised ICP • Headache, vomiting without nausea, ocular palsies, altered level of consciousness, back pain • Papilloedema – visual disturbances, optic atrophy • If mass effect present & brain tissue displacement: pupillary dilatation, abducens nerve palsies, Cushing’s triad – increased Systolic BP, widened pulse pressure/bradycardia & abnormal resp pattern. Normal Papilloedema T1 Weighted MR Scan Subacute L Subdural Haematoma & Cerebellar Tonsillar Herniation • Simple classification! • Primary – arising from the tissues which make up the brain & spinal cord – neurons & glia (glioma, astrocytoma), meninges (menigioma) • Behaviour – Malignant (glioblastoma multiforme) or Benign (often meningiomas) • Agressive, slow-growing, invasive, metastatic (rarely) • Secondary – Metastatic arising from other organs Lung, Breast, Malignant Melanoma, Kidney, Colon Van Gijn & Rinkel BRAIN, 2000 Subarachnoid Haemorrhage • Most caused by aneurysmal rupture • • • • 80% congenital eg Berry aneurysm Peak age 40-50 years 10-15% other acquired aneurysms 5% arteriovenous malformations (20-40y) • < 5% bleeding disorder, anticoagulants, tumours Berry Aneurysms and the Circle of Willis The Patient with SAH • Risk factors similar to stroke eg. Smoking, hypertension • Family History in 5-20% • Incidence 6 cases per 100,000 patient yrs • 50% fatality, 1/3 remain dependent • Sudden explosive headache is the cardinal feature. • If related to sexual intercourse ?SAH • CT scanning is mandatory in all, to be followed by (delayed) lumbar puncture if CT is negative SAH Symptoms & Signs • A period of unresponsiveness of >1 h occurs in almost half the patients and focal signs develop at the same time as the headache or soon afterwards in one third of patients • Classically, the headache from aneurysmal rupture develops in seconds, but can be minutes • Vomiting occurs in 70% of patients • Neck stiffness is a common sign in SAH of any cause, but takes hours to develop and therefore cannot be used to exclude the diagnosis if a patient is seen soon after the sudden-onset headache • If thunderclap headache is the only symptom then 10% only will have SAH, but all need investigation! Subdural Haematomas • Usually occurs because of injury • Occasionally spontaneous • Clotting blood collects in subdural space between dura mater & arachnoid mater • Acute – symptoms develop in hours: Signs of increased ICP • Chronic – 2-3 weeks after (forgotten about injury!), asymptomatic & then general deterioration, confusion, drowsiness, nausea, vomiting, gradual limb weakness, speech disturbance, personality change, seizures • An emergency – refer for surgical evacuation EPILEPSY EPILEPSY • • • • • • Nearly 500,000 in UK, Incidence 24-50/100,000 (Europe) Often begins in childhood 1/3 grow out of it by adulthood Generalised seizures affect the whole brain Partial seizures affect only part of the brain Symptoms of partial seizures depend on which part of the brain is affected. Simple or complex • A person is considered to have epilepsy if they have had two or more unprovoked seizures • EEG - PRIMARY GENERALISED EPILEPSY Generalised Seizures • • • • • Affect the whole brain Loss of consciousness Tonic-clonic (grand-mal) most common Tonic phase Lose consciousness, stiff muscles, fall over! Cry out, bite tongue or cheek • Clonic phase • Jerking muscles, loss of bladder or bowel control, pallor • Post-ictal – drowsy & confused Generalised Seizures • Also classified as generalised seizures are : • Atonic (drop attack) - sudden loss of muscle tone • Myoclonic – jerking of legs, arms or whole body often just after waking • Absence (petit- mal) – mainly in children, no stiffness or jerking, loss of awareness, daydreaming • Secondary Generalised – start as partial, become general Partial Seizures • • • • • • Fully conscious, only part of brain affected SIMPLE PARTIAL SEIZURES A sense of ‘déjà vu’ A feeling of fear or joy An unusual taste or smell Numbness, tingling or 'pins and needles' in part of the body • Involuntary, jerky movements or twitching in part of the body • Seeing flashing or coloured lights • Hallucinations Complex Partial Seizures • Affect a larger part of the brain and last longer • • • • • • May only be partly conscious, often amnesic Lip-smacking or chewing movements Repetitive movements such as fiddling with the clothes Wandering around in a confused way Making kicking movements of arms or legs Talking nonsense, muttering or mumbling Epilepsy Consider – • How important the history is in diagnosis • Any witnesses, any injuries? • Status epilepticus - seizure or group of seizures lasting > 30 minutes, without regaining consciousness • Tonic-clonic status epilepticus is a medical emergency • SUDEP – sudden unexpected death in epilepsy, 1:1000 people with epilepsy, usually severe • How a diagnosis of epilepsy affects life – driving, anxiety about fitting, side effects from anticonvulsants Causes of Syncope Vasovagal Situational – eg sneezing, micturition Orthostatic hypotension – autonomic failure, iatrogenic Hypoglycaemia? Cardiac arrhythmias – sick sinus, SVT, drug induced Structural Cardiac or Cardiopulmonary - HOCM, PE, ACS Cerebrovascular – subclavian steal syndrome, TIA Substance abuse, alcohol intoxication Psychogenic – factitious, anxiety, panic attacks, hypoventilation Is it syncope or is it a seizure? What causes Epilepsy? • Genetics – 1 in 5 people have family history • Neurological damage caused by – Perinatal brain injury/hypoxia, Head injury, Stroke, Brain Surgery, Alcohol, Drugs, other toxins • Febrile convulsions? • Infections eg meningitis, encephalitis • Brain Tumours • Degenerative disease • Demyelinating Disease Prognosis • 60% of untreated people have no further seizures during the 2 years after their first seizure. • Prognosis is good for most people with epilepsy. About 70% go into remission, defined as being seizure free for 5 years on or off treatment. • This leaves 20% to 30% who develop chronic epilepsy, which is often treated with multiple antiepileptic drugs Management • If a patient presents with an unexplained loss of consciousness including a seizure, they need urgent investigation which may include neurological opinion • Take a thorough history • Perform a neurological & cardiovascular examination • Investigations may include - Blood tests including fasting glucose, ECG, Brain imaging, EEG • Tell them not to drive and that includes driving from the surgery back home! Aims of Treatment • To reduce the risk of subsequent seizures • To improve the prognosis of the seizure disorder • To improve quality of life • In people in remission, to withdraw antiepileptic drugs without causing seizure recurrence • To minimise adverse effects of treatment. Self-help: avoid triggers • • • • • • Lack of sleep Missing a dose of anti-epileptic medicine Missing meals, alcohol or illegal drugs Flashing or flickering lights - photosensitive epilepsy Stress Hormonal changes, eg. at certain times of the menstrual cycle - catamenial epilepsy • Feverish illness • Certain medicines Anti-Epileptic Drugs (AEDs) • 1st line : Carbemazapine, Lamotrigine, Phenytoin, Topiramate, Sodium valproate • 2nd line examples: Clonazepam, Gabapentin, Levetiracetam, Oxcarbazepine • Combinations can be used, overlapping of weaning off & weaning on, all have individual s/e profile • Anticonvulsants can affect OCP & require increased doses– check the BNF & consult with family planning/gynae if needed • Unresponsive to AEDs & combinations, very severe epilepsy - Vagus nerve stimulators, neurosurgery ie resection of the focus & palliative surgery, deep brain stimulation • MS is the most common disabling neurological disease in young adults • MS is a clinical diagnosis made on the basis of two episodes involving two or more areas of the central nervous system over time, with MRI evidence of multiple areas of involvement & change with time (McDonald Criteria) BMJ Clinical Review 2006 • About 85% present with relapsing-remitting form, comprising episodic relapses and remissions that may be partial or complete. • After many years they will enter a progressive phase – Secondary Progressive MS • 15% present without relapses/remissions: Primary Progressive MS • Benign MS – 15% of relapsing-remitting have minimal disability after 15 years • Multiple sclerosis was thought to be an intermittent disease with inflammatory breakdown of myelin in patches in the white matter • It is now evident that the disease is more continuous, with diffuse changes in the white and grey matter, breakdown of myelin, and damage to axons • The first attack is known as a clinically isolated syndrome, by definition it cannot be called MS • • • • • A wide variety of symptoms : Visual - optic neuritis (pain & loss of vision) Muscle spasms & spasticity Neuropathic & musculoskeletal pain Fatigue, Emotional problems & Depression • Numbness or tingling in parts of the skin. This is the most common symptom of a first relapse. • Weakness or paralysis of some muscles, tremor, Mobility may be affected. • Balance and co-ordination problems • Problems with concentration and attention • Dizziness • Problems with passing urine • Erectile dysfunction • Speech difficulties • In addition to early symptoms becoming permanent rather than transient: Contractures, urine infections, osteoporosis, muscle wasting and reduced mobility • The degree of disability a person experiences five years after the onset on their MS is, on average, about three-quarters of the expected disability at 10-15 years • Autoimmune (T-cell mediated, Antibodies, Cytokines) • Inflammation of nerve fibres and subsequent damage (scarring = sclerosis) & BBB breakdown • Damaged nerves & atrophy of brain leads to loss of function • Viral trigger, Environmental trigger, Genetics? • Early is Late in MS as when symptoms appear the disease has already been present for a long time (evidence seen on MRI at diagnosis) • Treatment is of acute attacks, prevention of relapses and progression, management of symptoms, and rehabilitation • Acute attack – IV methylprednisolone 1000mg daily for 3 days, or large doses of oral steroids • Preventing relapse – Beta-interferon (Immunomodulator), 1 in 4 develop neutralising antibodies, Glatiramer acetate sc (4 AAs in myelin, Mechanism of action unknown), linoleic acid (sunflower, corn, soya) NICE GUIDELINE 8 2003 • Treatment of symptoms eg anticholinergic for bladder spasm, baclofen for muscle spasticity, may need PEG for swallowing difficulty • Cognitive deficits may raise capacity issues • Emotional support & treatment of depression • Access to physiotherapy & OT, mobility aids, adaptations • Vaccination against influenza • Treatment of ED. Complementary therapies? NICE GUIDELINE 8 2003 G.B.S ???