Pre-Learning Dizziness v3 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  Understand the subtypes of dizziness  Understand common conditions that can provoke dizziness  Refine testing for common conditions and be able to screen out red flags  Understand key questions that help you to evaluate a patient with dizziness and what conditions they may relate to 3  Huge variety of causes – neurological, traumatic, cardiovascular, cerebrovascular, vestibular, psychogenic…  Huge impact on society ◦ 80% of people 65+ will experience at some time ◦ 85% of people 85+ have some vestibular dysfunction ◦ By age 75, most people have an expected loss of 35% to accurate encode faster head movement due to age related change  Light-headed ◦ Implies systemic – e.g endocrine/cardiovascular  Unsteadiness ◦ Implies proprioceptive ◦ Related to movement disorder (cerebellum, basal ganglia) ◦ Low level dysfunction of vestibular centre  Vertigo ◦ High level dysfunction of vestibular centres ◦ Can be related to posterior blood supply strokes  Need to confirm if triggered by: ◦ Movement of head  Different to worsened by movement of head ◦ By visual stimulation ◦ Occuring at rest without provocation  How acutely it came on ◦ Can be, but is not always, a red flag  How long does it last ◦ If in peripheral nervous system  Severe vertigo, positional aggravators, episodic occurrence  “Dizzy” is a layman’s term  No meaning clinically  When trying to differential diagnose, KEY question is  What does your dizziness feel like to you?  3 major divisions for a “dizzy patient” ◦ Wobbly  Disequilibrium ◦ Whirling  Vertigo ◦ Weak  pre-syncope  light-headedness  BPPV  Meniere’s disease  Labyrinthitis  Vestibular neuritis  Vestibular migraine  PICA occlusion  VBAI  Acoustic neuroma Vertigo  Illusion of rotatory movement (self or surround)  If vertigo is present, nausea and vomiting are always expected  Vertigo will affect vision – like being on a carousel ◦ Does not cause blurring or vision loss  Key question towards diagnosis: does head movement TRIGGER this or does it merely AGGRAVATE this ◦ BPPV – triggers ◦ Labyrinthitis - aggravates  Free floating otoliths in the semi-circular canals inappropriately stimulate the vestibular nerve ◦ Typically formed from calcium crystals  Aggravated by head movement ◦ Typically unilateral rotation or extension  Triggers severe vertigo  Vertigo should resolve within 2 minutes max ◦ Typically in approx. 30 seconds  May have feeling of unsteadiness in between vertigo if have had for a while because nerve has been over-stimulated  Slow range of motion tests should not trigger ◦ Faster head movements will trigger  CAD testing always done FIRST to exclude arterial red flags  Dix-Hallpike test ◦ Positive: delayed onset of rotatory nystagmus and vertigo which fatigues out within 2 minutes  Treatment – Epley Manoeuvre  Auto-immune condition leading to over-production of endolymph in 1 ear which compresses both the vestibular and cochlear aspects of the nerve ◦ Typical onset in 50’s ◦ Caucasian female highest incidence  May be hours or days with constant symptoms (episodic)  Typically 12 minutes – 12 hours per episode, but may be daily  Simultaneous occurrence: severe vertigo, aural fullness, tinnitus, balance difficulty ◦ Nausea and vomiting due to vertigo ◦ May have a history of hearing loss – usually early subtle sign  Highly significant impact to all ADLs when in episode ◦ No symptoms or ADL impact when not in episode  Fluctuating pattern typically will last 10 years  Nerve progressively damaged with each flare  Progressive hearing loss and tinnitus in between flares ◦ Hearing aids often required  Progressive balance difficulty in between flares ◦ Rehab needed for balance training progressing to walking aids  Quiescent period but in later years Meniere’s develops in opposite ear and pattern begins again  Balance testing – depending on stage of disease  Weber’s and Rinne’s (nerve damage)  Negative testing for exclusion: ◦ CAD testing ◦ Sensory/proprioceptive testing  Rx: symptomatic relief via ↓salt intake, diuretics, vasodilators, anti-emetics/nausea. Surgery last resort  “Itis” = inflammation  Inflammation of the semi-circular canals ◦ Will typically affect cochlea also due to proximity  Multiple causes: ◦ Viral infection - typically following upper respiratory tract infection ◦ Bacterial infection - following otitis media or meningitis ◦ Medications (benzodiazepine, beta blockers, certain types of antibiotics…) ◦ Auto-immune disease ◦ Ear surgery, trauma, other  May have an acute onset or come on over several hours  Ear pain and headache – unilateral typically ◦ Aural fullness and possible discharge  Severe, constant vertigo whilst inflammation present ◦ Aggravated by head movement as stimulating the nerve  Fever  Hearing loss and tinnitus  Typically true symptomatic period will last for approximately a week ◦ Symptoms constant during this time period ◦ Important to advise patients to mobilise even if worsens vertigo as important for vestibular healing  After inflammation reduces, vertigo and ear pain will resolve  Patient will still experience unsteadiness, or even brief periods of vertigo, as nerve heals ◦ May take 6-8 weeks to fully resolve ◦ May be aggravated by movement of the head/neck  Temperature  Weber and Rinne – sensorineural  Cervical ARoM – may trigger some unsteadiness  Balance may be somewhat affected  Sensory/proprioception - normal  Treatment cause dependent ◦ Anti-emetics, anti-viral, antibiotics or steroids (cause dependent)  Inflammation of the vestibular portion of the nerve only ◦ Not affecting cochlea or cochlear branch of nerve ◦ Less common than labyrinthitis  Typical onset 40+  Can last for weeks and have a longer resolution  Same symptomatic presentation as labyrinthitis but NO: ◦ hearing loss ◦ ear pain, discharge  A new type of migraine which leads to vertigo as a prolonged aura ◦ Vertigo may be simultaneous to or separate from headache ◦ Migraine headache must be in history for textbook cases  Is most common cause of spontaneous vertigo  High female incidence  Typical onset in late 30s onwards ◦ Migraine history likely to be from teens/early 20s Topic reference: Tsang et al (2015) Diagnosis and Management of Vestibular Migraine. Journal of Clinical Outcomes Management. 22(10)  Variable dizziness ◦ 50-60% report vertigo ◦ May also present less typically as disequilibrium  May also have head-motion vertigo (like motion sickness) lasting seconds  Busy visual stimulus may aggravate  Episodes will last from 5 minutes - 3 days  Migraine headache/symptoms ◦ Some never have HA and vertigo simultaneously – difficult to diagnose  First must rule out other conditions ◦ TIA PICA – abrupt onset and quicker resolution, not recurrent ◦ Dissection vertebral artery – CAD testing ◦ VBAI (atheroma) – CAD testing ◦ Tumour – slow growth, progressive, focal neuro signs ◦ BPPV – EG Dix Hallpike ◦ Meniere’s - hearing loss, aural fullness in/during attacks ◦ Cervicogenic – Fitzritson’s and cervical screen, neck pain  Clinical Presentation is key (diagnosis of exclusion): ◦ ≥5 episodes of vestibular symptoms of moderate/ severe intensity lasting 5 minutes to 72 hours ◦ Current or previous Hx migraines with/without aura ◦ One or more migraine features with at least 50% of vestibular episodes:  Headache with ≥ 2 of the following characteristics  One-sided location, pulsating quality, moderate or severe pain intensity; photophobia or phonophobia  Visual aura  Because this is a new symptom in headache referral is warranted to GP  Especially in over 50s or children  However, if seeing typical migraine type symptoms and other red flags are excluded reassure patient likely benign  Migraine precursor in children = benign paroxysmal vertigo of childhood  Dx requires 5 episodes of severe vertigo  Occur w/out warning and resolve minutes to hours  In between episodes: neurological examination, audiometry, vestibular functions and EEG - normal  A unilateral throbbing headache may occur during attacks  This requires referral because it’s a child!  Management ◦ Lifestyle – avoid caffeine & rich food excess, eat regular meals ◦ Triptans – migraine relief ◦ Anti-emetics ◦ Pain relief – NSAIDS, paracetamol ◦ Vestibular rehabilitation therapy ◦ Chiropractic care – migraine prevention ◦ Medical care prevention – beta blockers, tricyclic antidepressants, calcium channel blockers, seratonin antagonists, anti-eleptics  ≥50% reduction is considered excellent outcome  Most common type of posterior circulatory occlusion ◦ AKA Wallenburg’s syndrome  TIA – must fully resolve within 24 hours, typically lasts 1 hour  Stroke – permanent damage to neurons  Incidence: Males, 55+  Links with diabetes and smoking  Sudden onset of vertigo most common sign  Nausea and vomiting  Ipsilateral hemi-ataxia  Difficulty with unconscious postural control  Horner syndrome – ptosis, meiosis  Ipsilateral facial pain and loss pin prick/temperature  Contralateral body loss of pin prick and temperature  Why the variety of symptoms? ◦ PICA feeds cerebellum and lateral medulla ◦ CL loss pain/temp sensation due to LST location in medulla ◦ Cranial nerve palsy from medulla location ◦ Ataxia from cerebellar disruption – ipsilateral to side effected  Atheroma in vertebral  Tear in layers of the artery vertebral artery  Most common creating a 2nd lumen occurrence Atheroma (VBAI) Vertebral dissection  For the purposes of this class, when referring to VBAI we are implying atheroma  Dissection will be considered a separate diagnosis  You need to confirm WHICH ONE YOU MEAN if given a case history to get full marks ◦ Stable atheroma may only be monitored (stage 1) ◦ Dissection will typically require medical management and may be more of an emergency  Atherosclerosis  Trauma  Smoking ◦ Seatbelt blow ◦ Cervical distortion in  Obesity trauma  Abnormal blood ◦ Blow to neck properties – e.g.  Instability Factor 5 Liden ◦ Collagen disease ◦ Makes blood more (Marfans/EDS) viscous ◦ Down’s syndrome/RA Atheroma (VBAI) Dissection  3 stage progression: 1. Vertigo or light-headedness on ipsilateral head turn lasting as long as head put into that position ◦ Possible visual disturbance as well 2. Experience light-headedness or vertigo in neutral 3. Severe insufficiency in neutral → advanced neurological signs ◦ Ataxia, 5 Ds, 3 Ns  Neck ◦ Stiffness (from arterial inflammation) with normal range of motion ◦ Ripping or tearing pain in posterior neck  Headache referring sub-occipitally and forward ◦ New quality, worst ever  Vertigo (or light-headedness) on ipsilateral head rotation  Larger tears – same as above in neutral  Visual changes ◦ Ataxia ◦ 3 N’s  Nausea, Numbness, Nystagmus ◦ 5 D’s  Dizziness (vertigo or light-headedness)  Dysarthria  Dysphagia  Diplopia (or other visual abnormalities)  Drop attacks – loss of muscle tone leading to fall to floor without loss of consciousness  If blood loss sufficient may pass out  Blood pressure  Slow cervical range of motion (if not symptomatic in neutral)  CAD testing  Cerebellar tests  Pin prick  Swallow  Listen for stridor  Cranial nerves 3-12  Benign tumour which encircles the vestibulocochlear nerve ◦ Most common type of cerebellar pontine angle tumour  Slow growing over decades ◦ Typically not diagnosed until patient is 50+  Early stage ◦ Looks like repetitive labyrinthitis as irritates the nerve  May be disequilibrium or vertigo ◦ Slow growing so nerve adjusts - symptoms resolve  Later stage ◦ Progressive sub-occipital, unilateral headache ◦ Progressive hearing loss and tinnitus ◦ Progressive disequilibrium moving to vertigo ◦ May lead to cerebellar signs (ataxia) – ipsilateral ◦ May lead to impact on CN5 or CN7  Weber and Rinne – sensorineural loss  Balance testing  Cerebellar testing – ipsilateral affect  CN5  CN7  Cervicogenic disequilibrium  Peripheral neuropathy – covered in peripheral nerve lesions  Parkinson's – covered in movement  Cerebellar disease – covered in movement  Defined as imbalance or unsteadiness related to movements or position of the cervical spine or occurring with a stiff or painful neck ◦ Damage to proprioceptors leads to faulty information being fed to vestibular centre  Proprioceptors heavily located in cervical musculature via muscle spindles  SCM and sub-occipital musculature heavily implicated  May have less significant relationship to receptors in joint capsules ◦ AKA - Cervicogenic vertigo, cervical vertigo, Proprioceptive vertigo Reiley, AS et al (2017) How to diagnose Cervicogenic Dizziness. Archives of Physiotherapy. 7:12  Frequently results from: ◦ Flexion-extension injuries (e.g. whiplash) or contact sports ◦ Pts w/ prior vestibular insults may alter/restrict head motion, altering normal cervical spine mechanics → symptoms of dizziness ◦ Osteoarthritis ◦ Inflammatory processes in cervical spine ◦ Cervical instability  Feeling of unsteadiness or being on a boat rocking triggered by neck movement or sustained position of neck ◦ May last minutes or hours  Neck pain or stiffness – may refer to shoulder/scapula  Reduced or painful RoM cervical spine ◦ May make sleeping difficult/uncomfortable  Cervicogenic headache possible  Considered a diagnosis of exclusion ◦ Look for constellation of signs + clinical history 1. Must exclude red flags if trauma ◦ Canadian C-spine Rule sensitive screen 2. Must exclude VBAI or arterial dissection ◦ Auscultation and palpation of carotid ◦ Cervical arterial dysfunction testing  Use sparingly, slowly and with utmost caution ◦ Neurological testing if any doubt  Lower cranial nerves - vertebral  Motor/sensory, eyes and speech – carotid  Balance, SMR…as required 4. Cervical screen ◦ Observe for postural changes or compensations ◦ Palpate for pain, muscle hypertonicity or joint restrictions ◦ RoM: May see reductions and restrictions  Stiffness without a loss of range of motion – sign of dissection! 5. Vestibular assessment  Fitzritson’s ◦ +ve head stabilised CGD ◦ +ve when head not stabilised CN8 issue  Screen to decide if imaging req’d post-trauma  FIRST: Rule out high-risk factors: 1. Age ≥ 65 years OR 2. Dangerous mechanism of injury  Fall from elevation ≥0.9 m (3 ft)/five stairs  Axial loading to head  Motor vehicle collision at high speed (>100 kmh, 60MpH)  Rollover, ejection, motorized recreational vehicles  Bicycle struck or bicycle collision 3. Paraesthesia in extremities ◦ If YES to any, refer for radiography  Confirm they have indicators that allow safe assessment of range of motion 1. Simple rear-end motor vehicle collision 2. Sitting position in emergency department 3. Ambulatory at any time 4. Delayed (not immediate) onset of neck pain 5. Absence of midline cervical spine tenderness  if YES to any, continue to step 3  If NO to all (high risk factors present) not safe to assess, refer for imaging  Is the patient able to actively rotate neck 45° left and right? ◦ If yes - continue general cervical spine screen ◦ If no - radiography should be performed  IMPORTANT – IF ACCIDENT OCCURRED SOME TIME AGO MUST ASK IF PROGRESSION IN SYMPTOMS! ◦ Would expect neck pain to grow and then plateau ◦ Would not expect new symptoms to develop  Cardiovascular causes  Cerebrovascular causes  Endocrine causes  Mostly covered in CMI  Neurological ◦ Multiple sclerosis (U/LMN lesion), syringomyelia, cerebellar disturbances, Parkinson's, Polyneuropathy  Neoplastic ◦ Acoustic neuroma, CNS tumours (UMN lesion)  Degenerative ◦ Polyneuropathy (LMN lesion e.g. diabetes), central myelopathy (UMN lesions), Dementia  Intoxication ◦ Alcohol/drugs  Primarily covered in your clinical medicine module but…  Vascular ◦ VBAI, cervical arterial disease ◦ Postural/orthostatic hypotension – hypermobility, medication ◦ Cardiac disease – arrhythmia, CHF (low cardiac output) ◦ Subclavian steal syndrome  Rare-leads to reversal of blood flow from vertebral artery to subclavian → VBAI ◦ GI bleeds (ulceration)  Intoxication- all same effect ◦ Diuretics ◦ cardiac meds (beta-blockers, ACE inhibitors…) ◦ muscle relaxants ◦ tricyclic anti-depressants  Metabolic ◦ Hypo/hyperglycaemia  Something else ◦ Anxiety/depression ◦ dementia (meds/orthostatic HT)  Vascular ◦ VBAI, Postural/orthostatic hypotension, arrhythmia, subclavian steal syndrome, GI bleeds (ulceration)  Intoxication ◦ Diuretics, cardiac meds (beta-blockers, ACE inhibitors…), muscle relaxants, tricyclic anti- depressants  Metabolic ◦ Hypo/hyperglycaemia  Something else ◦ Anxiety/depression, dementia (meds/orthostatic HT)  What does the dizziness feel like to you? ◦ Vertigo, disequilibrium, light-headed ◦ Know conditions for each  How long does the dizziness last? ◦ BPPV – under 2 minutes, Meniere's – hours/days/weeks, labyrinthitis – constant during inflammation  When did it come on? ◦ Seconds – TIA/Stroke, BPPV ◦ Hours – inflammation – labyrinthitis, vestibular neuritis ◦ Months – acoustic neuroma  What triggers it? ◦ Head rotation – BPPV, cervicogenic disequilibrium, VBAI/dissection ◦ *any vestibular problem will aggravate with head rotation  Does anything make it better? ◦ Neutral position/rest – BPPV, stable VBAI  What other symptoms do you have? ◦ Neck stiffness and no loss Rom - dissection ◦ Neck pain – dissection, cervicogenic disequilibrium ◦ Hearing loss – menieres, labyrinthitis ◦ Ataxia – acoustic neuroma, PICA, VBAI - progressive  Have you had this before? ◦ Acoustic neuroma – history of repetitive labyrinthitis or BPPV diagnosed ◦ Meniere’s –repetitive early stages but episodic  Have you had any illness or trauma ◦ Cervicogenic disequilibrium, dissection, labyrinthitis  Do you have any other medical conditions ◦ Dissection, VBAI atheroma,  Practice full examination of cranial nerves  Prepare notes on involved anatomy, interpretation of examination findings and possible causes of abnormalities