Headache - Red Flag, Part 1 PDF

Chandra Ricks  Practice and Problem Solving Communication Patient Awareness Team Working Professional Knowledge/Skills...

Chandra Ricks  Practice and Problem Solving Communication Patient Awareness Team Working Professional Knowledge/Skills Year 3 CLINICAL NEUROLOGY 2  Learn the presenting features for red flag headache conditions  Recognise risk factors for vascular HA  Understand the difference between cerebrovascular and cervical artery presentations  Understand the presentation of common vascular headaches  Understand what evidence says about chiropractic and arterial dissection 3  Cerebrovascular ◦ Stroke ◦ TIA  Cervical arterial disease ◦ Atheroma ◦ Dissection  Aneurysm  Sub-arachnoid haemorrhage  Temporal arteritis  New headache  Constant duration ◦ Abrupt onset  ICP signs ◦ New 50+ ◦ Worse in AM on waking ◦ New in paeds ◦ Worse after prolonged  WORST headache supine ◦ Agg. by Valsalva  Progression ◦ Constant  Change in features – e.g neuro, fever, rash ◦ Frequent  Post trauma - neuro signs ◦ Duration  Post trauma – suspected ◦ New fracture (C-spine rule) symptoms/location  High cholesterol  Age  Heart disease – a. fib  Abdominal obesity  High red blood cell  Physical inactivity count  Smoking  History of TIAs  Hypertension  Family history  Heavy alcohol use (genetics)  Collagen disease – Marfans/EDS Modifiable Non-modifiable  Occlusion / infarction – blockage of a “tube” in body ◦ In brain = blood vessel  Thrombus – clot forming at site of injury  Embolus – clot formed elsewhere travelling to site of injury  Haematoma – blood collecting outside of a blood vessel  Dissection – tear in the layer of a blood vessel wall often leading to aneurysm  Haemorrhage – rupture of a blood vessel leading to blood loss  Any problem which causes a disruption to blood supply of the brain  2 main divisions ◦ Occlusive (blockage) – 80% ◦ Haemorrhagic (rupture)  Causes of CVD include: ◦ Blood clot, atheroma… ◦ Vascular malformations  aneurysms or arteriovenous malformations ◦ Degenerative disease arteries ◦ Inflammatory disease of arteries ◦ Blood diseases  Some neurons die immediately ◦ Brain has high requirement for energy and O2  No storage of either in brain  For other neurons, ATPase pump malfunctions ◦ Cell membrane becomes depolarised and releases stored neurotransmitters ◦ Calcium floods into the neurons ◦ Calcium activates proteases and lipases which further damage/destroy nearby neurons ◦ Chemical cascade of damage can continue for weeks  Transient blockage to  Blockage to a an already narrowed narrowed blood vessel blood vessel leads to leads to permanent short term neurological neurological symptoms symptoms without ◦ Blockage resolves – NO resolution PERMANENT DAMAGE ◦ Damage and death of ◦ Red flag for stroke neurons occurs development  Biggest risk within 48 hrs  Risk within 3 months TIA (transient ischaemic Stroke attack)  Sudden onset without warning ◦ MCA – contralateral upper body paraesthesia/numbness, spastic weakness and Wernicke, neglect possible ◦ ACA – contralateral lower body paraesthesia/numbness, spastic weakness, Broca dysphasia, B/B control loss ◦ PICA – Ipsilateral loss of coordination, nystagmus, dizziness, visual change, pin prick loss sensation  Pulsatile headache likely - TIA  TIA - Neurological symptoms resolve within 24 hours (commonly 30 minutes)  Stroke – permanent damage of varying severity  TIA and migraine can look similar ◦ Pulsatile, severe, can lead to visual/motor/sensory changes  If this is a new or first onset in a patient, you must always exclude the worst outcome first  Treat as if a potential TIA ◦ Urgent referral to stroke clinic until proven otherwise  Carry on treatment for migraine once all clear is given  Disease effecting carotid or vertebral arteries  2 categories 1. Occlusion – blockage to a blood vessel 2. Dissection – tear in the layers of the blood vessel wall  AKA infarction,  Creates a second atheroma lumen in artery with 2  Leads to a partial outcomes: blockage of an artery 1. Blood may become  May eventually totally trapped and block the block the artery main lumen of the artery over time 2. Wall becomes weakened due to tear and ruptures Occlusion Dissection  General dissection symptoms: ◦ May report an acute tearing pain in artery  May have a minor inciting event or no event at all  May only report stiffness into the neck – due to inflammation ◦ May report a new type of headache  Pulsatile in quality  Progressive – severity, constancy ◦ As time progresses, neuro symptoms progress ◦ Atheroma is totally painless Pain referral common Pain referral common to to Vertebral Artery Internal Carotid Carotid dissectio n most common  Neurological symptoms for dissection and occlusion the same ◦ Specific symptoms are artery dependent  Early stage – neuro symptoms triggered by unilateral head rotation ◦ May lead to dizziness ◦ May lead to visual disturbance ◦ May lead to low level numbness ◦ May lead to low level nausea  Symptoms remain until head turned back to neutral  More on this in dizzy…  Focal spastic Contralateral pain and weakness in extremity temperature loss -body Ipsilateral pain and or half body temperature loss -face  Focal numbness in dysphagia extremity in extremity dysarthria or half body tongue deviation ataxia Vertigo 4 D’s, 3 N’s Carotid Vertebral  Dissection may result from trauma – e.g. blow to the neck whiplash – VBA seat belt injury – carotid Spontaneous arterial dissection - risk factors Collagen disorders - Marfan’s, Ehlers Danlos Hypertension Smoking Hx of cardiovascular disease/stroke migraine (+aura) Manual therapy? Yoga? Gymnastics… May occur in absence of known risk factors  ◦ Blood pressure  CAD testing ◦ Carotid auscultation ◦ attempts to separate out artery influence – but is ◦ Carotid palpation not 100% isolated ◦ General RoM tests ◦ Sensitivity – 0-57%  if aggravates  It will not always pick symptoms, stop! something up!  When in doubt, REFER ◦ Specificity – 87-100% Non-invasive testing first CAD testing  CAD - any position that the patient reports as provocative for symptoms is positive ◦ Nystagmus, dizziness, diplopia ◦ loss of consciousness ◦ Sweating ◦ dysphagia, dysarthria ◦ Nausea ◦ numbness around the lips ◦ other symptoms  If positive, send them to A&E for immediate checks  May not be a true positive, but you are negligent if you do not rule out red flags  Lee KP et al. (1995) Neurology. Neurologic complications following chiropractic manipulation: a survey of California neurologists. investigated number pts over 2 years w/ neurologic complication w/in 24 hours of chiropractic manipulation 177 neurologists saw: 55 strokes, 16 myelopathies, and 30 radiculopathies were reported Patients 21-60 and majority experienced complications following cervical manipulation. Most of the patients continued to have persistent neurologic deficits 3 months after the onset 50% had marked or severe deficits. Conclusion: risks of chiropractic must be discussed with patient – informed consent  Symons BP, Leonard T, Herzog W (2002). Internal forces sustained by vertebral artery during spinal manipulative therapy Used cadavers to test strain forces into vertebral artery comparing VBAI testing and cervical SMT ◦ Results: trained strain values of cervical manipulation are lower than those observed during VBAI screening and neck rotation.  SMT results in strains within the range of strains produced during normal, physiologic motion of the cervical spine.  Conclusion: normal circumstances, a single, typical HVLA thrust is very unlikely to tear or disrupt the vertebral artery ◦ BUT – person must be trained and have appropriate psychomotor skills – take years to develop!  Cassidy et al (2008) Case-control study of chiropractic, GP visits and stroke