Vertebral & internal carotid arteries and biomechanics

Transcription

1 LECTURE 17- VERTEBRAL BASILAR INSUFFIENCY (VBI) Definition and aetiology o Temporary signs and symptoms arising from insufficiency of blood supply to the posterior brain. o Due to compromise of the vertebral or basilar artery. o Symptoms vary according to the part of brain affected. o Occurs most commonly in older people years. o Commonly caused by atherosclerosis or degenerative disease of the cervical spine. o May be caused by head and neck position. o Manual therapy treatment positions and techniques may place stress on these arteries. Vertebral & internal carotid arteries and biomechanics Vertebral arteries o Intimately related to cervical spine- travelling through transverse foramina. o Potentially compromised by osteophytes from uncovertebral and zygapophyseal joints. o Supplies 20% overall blood supply to the brain: brainstem, cerebellum, cerebrum (including 11% occipital lobe). o Anatomical anomalies common. o Vulnerable to kinking with contralateral rotation, particularly at C1-2. o Kinking can result in VBI- particularly if opposite VA is congenitally narrow or diseased. Internal Carotid o Provides remaining 80% of blood supply to the brain o Passes just anterior to C2 transverse process o Less commonly involved in manipulative trauma

2 Causes of VBI o Sustained extreme rotation or extension of the neck (e.g. yoga, reversing car, star gazing). o 1 st described as beauty parlour syndrome o In older people can be due to sudden changes in BP (e.g. postural changes or exercise) o Prolonged or more forceful extremes of movement may cause stretching or even tearing of the arteries (arterial dissection). Clinical presentation of VBI o The 5 D s; Dizziness Diplopia (double or blurred vision) Dysphagia (difficulty swallowing) Dysarthria/Dysphasia (speech disturbance) Drop attacks (sudden quads weakness- knees buckling- collapse) o Further symptoms may include; Nausea Nystagmus facial numbness/paresthesia tinnitus o Symptoms can last few seconds up to half an hour. o May cause a transient ischaemic attack (TIA) where VBI symptoms persist up to 24 hours. Screening for VBI o Ask patient if they have experienced any unusual symptoms, particularly the 5 D s. o Must be done for all cervical spine patients to identify signs and symptoms of VBI. o Identify patients with possible arterial dissection. Precautions o Manipulation and end range rotation techniques are contra-indicated in the presence of VBI. o Possible indicator of biomechanical stress on artery. o Risk of VA trauma with cervical techniques e.g. tearing of the artery wall arterial dissection, embolism or vasospasm. o Arterial dissection, embolism or vasospasm may lead to vertebrobasilar stroke.

3 Risk of stroke from Cervical manipulation o General agreement stroke is a rare complication but may be more common due to under-reporting and missed diagnosis. o Physiotherapy- 1 per 163, 371 manipulations. Tests for VBI o VAs are tested prior to end-range physical procedures of the cervical spine or manipulation. o Tests involve sustained (10 secs) end-range; Rotation Extension combined rotation/extension o Positive = VBI symptoms or signs (e.g. nystagmus). o Contraindicates vigorous, end-range manual therapy. o Tests are controversial- found to have limited sensitivity and specificity for screening purposes. Standard of care o Currently expected to follow; APA Clinical Guidelines for Assessing VBI in the Management of Cervical Spine Disorders o Involves 3 stages; Questioning for VBI symptoms in history Physical testing for VBI Monitoring for VBI during & after treatment. APA guidelines o Minimal reliance on physical testing. o Minimum screening includes any nominated provocative position/movement AND end-range positions. o Testing only undertaken where VBI symptoms are absent from history or vague. o Simulated manipulation position should also be practiced if manipulation practiced. o Testing should be done on every occasion prior to manipulation of any endrange rotation procedure. o If adverse event; cease treatment, 1 st aid & 000.

4 Cervical artery dissection (CAD) o Tearing of the inner or middle layers of the artery. o Blood under arterial pressure enters tear and may extend it. o Clot forms which may dissect the artery and alter blood flow. o Clot may create an embolus or alteration in blood flow may lead to embolus formation. o Embolus may propagate to the brain causing ischaemia of brain tissue i.e. Stroke. o Can occur spontaneously. o Cause of ischaemic stroke in10-25% young patients (30-40yrs). o Early symptoms are usually moderate to severe headache, neck pain. o May mimic musculo-skeletal pain. o Danger to manual therapists because a patient may present with dissection in progress. o Symptoms; Sudden, severe, unusual, sharp pain Acute ipsilateral postero-superior neck/occipital pain Occipital headache (VA), frontal headache (ICA) (Thomas et al 2008) No past history of similar pain Ask about neurological features eg 5Ds (Be aware these may be subtle). o Risk factors; Underlying arteriopathy Hereditary subclinical connective tissue disorders Genetic predisposition History of recent minor mechanical stress or trauma to the head or neck E.g. sudden jerking movement of neck, blow to head or face, heavy lifting/ activities involving forced expiratory effort, intensive exercise >45mins, neck manipulation. Recent infection respiratory or gastric (coughing/vomiting). Migraine? Smoking? Cardiovascular pathology seems to be less important (e.g. hypertension).

5 LECTURE 18: NEUROLOGICAL EXAMINATION Causes of conduction dysfunction. o Space-occupying lesion intervertebral disc prolapse spinal degenerative changes zygapophyseal joint osteophytes spinal stenosis Tumours, cysts, ganglions

6 Compression of spinal nerve or nerve root. o Radicular pain- pain located into dermatomal pattern, due to neurological structure. o Simple compression of normal nerve roots does not cause pain. o As nerve becomes ischaemic- initially paraesthesia, pain follows as inflammatory process/ intra-neural oedema continues. o Can take nerve 8-24 hours to return to normal after compression eased. o Compressive lesions are not selective to nociceptive axons (must have more than just pain- sensation loss/impairment, reflexes affected). o For diagnostic purposes, radicular pain must be accompanied by other neurological symptoms. o Cord compression symptoms will be bilateral, affecting from lesion down. o Cord compression symptoms; urinary/anal incontinence/retention intermittent electrical shooting pain hyper-reflexia non-dermatomal symptoms Paresthesia in hands/feet Ataxia Examination of the nervous system o Nerve conduction tests (sensation, motor function, reflexes, electrodiagnosis). o Palpation of nerve trunks o Neurodynamic tests (e.g. ULNT) o Central nervous system tests (clonus, Babinski etc.). Neurological history o Many symptoms potentially neurological; Sharp/burning/shooting/aching pain Numbness/tingling/ PnN s Weakness/heaviness Itching o Note vascular changes that may result from sympathetic involvement (examine skin colour, condition, temperature, swelling etc.). o Precautionary questions; General health (e.g. diabetes, MS) Spinal cord involvement (bilateral involvement, PnN s in hands/feet, ataxia) Cauda equine involvement (saddle paraesthesia, bladder/bowel symptoms).

7 Indications for neurological examination. o Aims to; Confirm or clarify symptoms of neurological nature Diagnose SN/NR compromise Determine involvement of other structures e.g. spinal cord, cauda equina Determine origin of peripheral symptoms Act as a baseline for reassessment o Neurological exam indicated when; Limb symptoms where the spine and/or nerve pathways are suspected. Pain from the spine referred past the acromion or buttocks/anterior groin. Altered sensation in the limbs (paresthesia, anesthesia). Pain in a dermatomal distribution. Neurological physical examination Testing of sensation o Light touch and pinprick (use cotton wool or monofilament) o Large diameter Group II afferent fibres Most vulnerable to compression situated on the nerve periphery require more oxygen/nutrients Often first indication of SN/NR compromise o Should work in circle around region to identify boundaries of sensory impairment. o Light touch- if patient reports sensation difference, delineate with pin prick. o Prick should be sharp but not painful. o Map changes on body chart. o Further test vibration, proprioception and two-point discrimination as indicated. o Must test same way everytime to ensure reliability (same equipment, pressure applied, patient positioning). o Reliability affected by variation/overlapping in dermatomal maps (isolate to 2 possible levels). Testing of muscle strength o Firstly look at atrophy/wasting. o Muscle myotomes tested isometrically o Maximum voluntary contraction in midposition (more reliable midrange) o Identification of single SN/NR C5 - T1 L2 - S2 o Be aware that pain may inhibit muscle contraction- need to distinguish between loss of power and pain inhibition. o Myotomes overlap and vary between individuals.

8 o Compensatory mechanism of motor units ( firing frequency, collateral axon sprouting). o Manual muscle tests have low sensitivity. o Affected by examiner/patient hand dominance. o Muscles exhibit length-tension relationship- must be tested in mid-range every time. o Standardisation of test will enhance reliability. Testing of reflexes o Deep tendon reflexes o Tests integrity of stretch reflex arc o or absent indicates compromise SN/NR or peripheral nerve o indicates a CNS lesion o Normally large variation. o Reduction in response magnitude with increasing age o Reflex arc influenced by converging input (CNS and somatic structures e.g. zygapophyseal joint- pain changes reflexes). o Only large discrepancy or asymmetry important o Standardization of test will enhance reliability.

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