Learning for professional autonomy Candidate Number: …



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Contents

Congenital (occurred prior to birth) 4

Spina Bifida Occulta 4

Spondylolisthesis 4

Facet direction anomalies, L/S anomalies 5

Scoliosis 6

Klipperfeil 7

Acquired - Traumatic 8

Muscle tear 8

Ligament injury 8

Fractures e.g. Vertebral 9

Facet Dysfunction 9

Herniated Disc 10

Acquired - Infective 11

Osteomyelitis 11

Tuberculosis TB 11

Discitis 12

Acquired - Inflammatory 13

Ankylosing Spondylitis 13

Rheumatoid disease of joints RA 14

Acquired - Neoplastic 15

Bone Metastasis 15

Osteosarcoma, Fibrosarcoma, Chondrosarcoma 15

Acquired - Degenerative 16

Osteoarthritis, Spondylosis, Spondyloarthrosis 16

Disc lesion 16

Facet problems 17

Lumbar spine stenosis 17

Acquired - Metabolic 19

Osteoporosis 19

Osteomalacia / Rickets 19

Acquired - Endocrine 21

Cushings 21

Acquired - Idiopathic 22

Padget’s disease 22

Scheuermann’s disease aka Osteochondrosis or Osteochondritis 22

Piriformis syndrome 23

|Congenital |Acquired |

|Spina Bifida |Traumatic |

| |Muscle tear |

| |Ligament damage |

| |Joint strain |

| |Fracture |

| |Disc injury |

|Block vertebrae |Infective |

| |Osteomyelitis |

| |TB |

|Lumbarisation |Inflammatory |

| |AS |

| |RA |

|Sacralisation |Neoplastic |

|Scoliosis |Degenerative |

| |OA |

| |Disc |

| |Metabolic |

| |Osteoporosis |

| |Osteomalacia |

|Klipperfeil |Endocrine |

| |Cushings |

|Facet Anomalies |Idiopathic |

| |Padgets |

| |Schermanns |

|Low riding, High riding L5 |Psychogenic |

| |Visceral |

| |Vascular |

| |Gynae |

| |Renal |

Red Flags

• Unexplained weight loss

• Hxx of malignancy

• Infection

• Symptoms unrelated to movement

• Cauda Equina

Anatomy:

Congenital (occurred prior to birth)

|Spina Bifida Occulta |

|Definition |Failure to unite/develop the posterior arch leaving the spinal canal exposed reducing the attachment site of ligaments and|

| |muscles |

|Who gets it |Estimated that 25% of LBP population |

| |Folic acid defect in diet prior to conception and during pregnancy (folic acid is found in breakfast cereal, baked beans, |

| |green leafy veg, peas and chickpeas, oranges) |

| |Suspected link to LDL gene error |

| |Taking epilepsy and bipolar medication whilst pregnant (valproate, carbamazepine, lamotrigine) |

|Signs |Dimple in low back |

| |Hairy patch in low back |

| |Pigmented area in low back |

| |Haemangioma |

|Symptoms |Low back ache |

| |Stiff low back |

| |Poor gait |

|Medical Tests |X-ray |

|Complications |Congenital neoplasm |

| |Mid-line spur splitting the spinal canal |

| |Tightened shortened filum terminale causing a low lying spinal cord |

| |Spina cord can be tethered which can cause paralysis as the child grows |

| |Poor bladder control |

| |Carvo varus – heel inverted, increased arch, clawed toes and adducted foot |

|What can we do |Advise on diet prior to and during pregnancy |

| |Advise to discuss medications with the doctor prior to and during pregnancy |

| |Avoid HVT of the low l.sp considering the possible instability in that area |

|Spondylolisthesis |

|Definition |Anterior movement of the vertebral body with or without Spondylolytic (a fracture of the pars interarticularis in the |

| |lumbar spine) |

| |Retro lythesis is a backward movement of the vertebral body |

|Who gets it |Young: spondylolytic spondylolisthesis (commonly L5/S1 with step at L4/5) |

| |Elderly: non-spondylotytic spondylolithesis (commonly L3/4 with a step at L3/4) due to degenerative changes |

| | |

| |Predisposed by: congenital anomaly, bony weakness, fibrosis union only, increased lumbar lordosis, increased functional |

| |demands, growth spurts with participation in active sports, pregnancy, visceralptosis and a loss of abdominal tone. |

|Symptoms |Odd gait |

| |Acute back pain eased by rest, worse on standing, agg by increased hamstring tone |

| |Groin strains, Hamstring strains that won’t resolve |

| |C/T pain or H/A |

| |Wide ranging from no symptoms (incidental finding, esp. in children) to severe back & leg pain with nerve damage esp. on |

| |hyperextension of the back. Beware of Cauda Equina syndrome |

| | |

| |Young child 6-7 YOA – acute back pain, agg by weight bearing and eased by bed rest. Poor range of l.sp flexion |

| |Older child – excessive sports >24 hours per week with hard landings and falls, stress from hyperlordotic activities |

| |Young adult – hxx of contact sports with an injury that is failing to resolve. |

|Signs |Palpable step |

| |Reduced flexion |

| |Increased tension in hamstrings |

|tests you can do |Vibration test with tuning form to establish whether there is a # |

| |Palpate for a palpable step |

|medical tests |X-Ray (most visible from an oblique view), looking for the scotty dog with an increased neck length (degenerative) or a |

| |collar (fracture) at worst decapitated! |

| |CT scan |

| |Grading according to the amount of slippage (grade 1 M by 2:1 esp. in hands and knees. Risk factors incl: age >45 YOA, wt,|

| |Hxx of trauma, infection & arthritis, post menopausal, total hysterectomy |

|Pathology |1.Breakdown of the articular surface |

| |2.Synovial irritation |

| |3.Remodelling |

| |4.Eburnation and cyst formation |

| |5.Disorganisation |

|Symptoms |Transient pain (aching, burning) , Clicking Crepitus |

| |Worse after activity (rel by rest) & end of day, Stiffness (short-lived); |

| |Night pain; |

| |Weakness due to disuse (no systemic (s) |

|Signs |Swelling (poss. bony enlargements) & deformity; Crepitus on movement; Jt. line tenderness; Muscle weakness & wasting; Alt wt |

| |bearing; ( ROM, Synovitis |

|Tests |Fixed flexion test for Hip OA but principally clinical based on Hxx & examination |

|Medical tests |X-rays (blood tests are normal with OA) showing joint space narrowing, osteophytes, sub-chondral sclerosis, sub-chondral |

| |cysts; loose bodies |

|Medical treatments |Conservative (reassurance, life-style changes (wt, exx, diet); Medication (NSAIDs, corticosteroids) for pain control, manual |

| |therapy. Surgery incl: |

| |Debridement, Joint replacement; Joint fusion; Joint realignment, Arthroscopy |

|Contraindications to OMT |Strong techniques; HVT |

|Disc lesion |

|Definition |Cracks and fissures |

| |Herniation |

| |Prolapse |

|Who gets it |20-45 YOA more commonly get NRI following annulus material in the spinal canal |

| |People with a Hxx of acute LBP and NRP |

|Symptoms |Disc injury with no NRI – LBP central, Unilateral, Bilateral. With or without referred pain into buttock, post/lat thigh, |

| |rarely post calf. |

| | |

| |Disc injury with NRI – LBP or Pain into buttock, thigh and calf. Possibly tingling, numbness, cold, heavy sensation in the |

| |distal dermatome |

| | |

| |Initially intense muscular spasm and inflammation can confuse diagnosis of the structural cause. Facets symptoms settle within|

| |10 days |

| | |

| |Cauda Equina symptoms: Urinary retention, Faecal incontinence and bilateral sensory loss in the saddle area |

|Onset |Slight twinge then pain builds over hours/overnight |

| |Sudden acute pain on trivial movement often following flexion with rotation or awkward lifting |

|Daily pattern |Worse on rising in AM for 1-3 hours with stiffness and pain on movement. |

| |Difficulty flexing |

| |Pain eases during the day but stays |

| |Possibly difficulty laying down initially |

|Aggravating factors |Flexion postures: sitting, bending as it increases intra-discal pressure. |

| |Pain increases with sitting |

| |Valsalve aggravates leg pain |

| |NRP pain be aggravated on standing, walking and weight bearing on side. |

|Relieving factors |Pain may be relieved by moving about |

|Facet problems |

|Definition |Facet lock – no joint movement. |

| |Intracapsular – Inflammation In the capsule. Subchondral bruising |

| |Extracapsular – The tissues surrounding the capsule |

|Who gets it |Anyone |

| |Particularly vulnerable are hypermobile segments due to degenerative changes |

|Symptoms |Unilateral or Bilateral pain |

| |Referral to Buttock, thigh, calf, (shoulder, arm, Ant-Lat chest wall) |

| | |

| |Intense pain 3-4 days which tends to resolve in 7-10 days |

| |Pain lasting for longer may be from a degenerative facet lasting months |

| | |

| |Agg: changing position standing from sitting, initially ache on resting and acute pain on movement. Stiffness following |

| |sedentary position |

| | |

| |Initially stiffness in AM which reduces after a few days |

| |Initially rest relieves symptoms, eventually movement reduces symptoms |

|Onset |Facet joint strain |

| |Commonly with a torsion injury at End or Mid range e.g. FLEX & ROT. Pain usually felt immediately but it may increase later |

| |with inflammation |

| | |

| |Apophysitis |

| |Woke with a painful and stiff neck – Apophysitis (trapping a synovial fold causing pain and restriction) |

| | |

| |Facet Lock – trivial movement, reaching, flexing, pushing at mid range. No movement available |

|Signs |Tender to palpate the facet joint |

| |Swelling of the joint capsule may be palpated |

|Test |Quadrant tests |

| |Intracapsular endochondral bruising – pain on opposition of the facets |

| |Intracapsular inflammation – pain of flexion, stretching the capsule. Pain on sidebending away from the inflamed capsule. |

|OMT |Apophysitis – NO HVT |

| |Facet Lock - HVT |

|Lumbar spine stenosis |

|Definition |Narrowing of the spinal canal either |

| |Congenital or |

| |Secondary to Spondylosis, herniation, facet invasion or spondylolythesis, Padgets, venous congestion |

| |Space occupying lesion (epiconus, arachnoiditis) |

| | |

| |If the spinal canal is < 14mm = spinal stenosis |

|Pathophysiology |L1 = 23mm |

| |L2 = 22mm |

| |L3 = 21mm |

| |L4 = 22mm |

| |L5 = 23mm |

Acquired - Metabolic

|Osteoporosis |

|Definition |Progressive metabolic bone disease that ( bone density leading to skeletal weakness and #s with minor trauma esp. in |

| |T.sp, L.sp, Wrist & hip |

|Who gets it |Post-menopausal women (due to lack of Oestrogen) but also 2( due to cancer, COPD, renal failure, drugs (steroids), |

| |endocrine disease, immobilization etc |

|Risk Factors |>50 YOA, Female>Male, Post menopausal, Family Hxx, Long term Glucocorticosteriod use, Race, Hypogonadism in men, RA |

| |Low BMI, Poor nutrition, Low calcium, Alcohol, Smoking, Low exx, immobile |

|Symptoms |Asymptomatic until #s occur in which case acute chronic back pain is common. |

| |Common #: Hip, Vertebrae, Wrist |

| |Eventually muscle pain. Agg by wt bearing. |

| |Loss of height, Stooped posture |

|Signs |Local tenderness, dorsal Kyphosis & exaggerated CSp lordosis (due to multiple T.sp compression #s); loss of height; |

|Tests you can do |Non conclusive but checking for #s with tuning forks and local palpation |

|Medical tests |Dual energy x-ray absorptiometry (DEXA) measuring bone density T score -2.5 |

| |X-rays only show ( density until 30% of bone is lost) |

|Medical treatments (and side |Medication Bisphosophonates (alendronatehen, risedronate ) to preserve bone mass reducing Osteoblastic activity |

|effects) |Calcium, Calcitonin and Vit D supplements |

| |Exx to max bone & muscle strength & minimize risk of falls; |

|Contraindications to OMT |No strong techniques that can cause #s, HVT |

|Osteomalacia / Rickets |

|Definition |Softening of bones due to defective bone matrix mineralisation, ultimately as a result of vitamin D deficiency |

| |Osteomalacia: Adult form of the disease – after growth plates have closed |

| |Rickets:Childhood form of the disease – before growth plates have closed |

|Who Gets It |Primarily as a result of insufficient nutrition. |

| |Secondary to disorders of gut e.g. celiac, pancreas, liver and kidney. |

| |Others include people who have insufficient sunlight exposure, are pregnant, |

|Risk Factors |Poor Vitamin D intake (little exposure to sunlight, housebound or hospitalised |

|Symptoms |Bone pain, esp. Lower spine, pelvis, Hips, leg bone, ribs or dental pain |

| |Muscle weakness + fatigue possibly a waddling gait |

|Signs |Weak bones with increased risk of # |

| |Compressed vertebrae / pelvic flattening / bone softening and waddling gait. |

| |Osteomalacia: Bony deformity – vertebral bodies + skull |

| |Rickets: Bony deformity – bowed legs, knock knees |

| |Hypocalcaemia – Perioral P+N, Tetany |

|Tests I can Do |Case history, Tuning fork to oscillate cracks in bone to generate pain. Unreliable! |

|Medical Tests |Blood/Urine test: Low Vitamin D, Low Phosphosus, Low Calcium |

| |X-ray – slight cracks may be seen in bones, Bone density scan, Bone biopsy! |

|Medical Treatments |Exposure to Sunlight |

| |Diet modification to increase intake of Vitamin D, Calcium, Phosphates. Sources:  cod liver oil, viosterol, fortified foods or |

| |supplements. |

|Contraindications to OMT |Diagnosis or suspicion of Rickets or Osteomalacia is an absolute contraindication to HVT or robust articulation. |

|Calcium metabolism |Calcium is absorbed in the small intestine via Vitamin D dependant active ion transport. Primarily in the duodenum dependant on |

| |Vit D, If calcium intake levels are high it can be absorbed in the Jejunum and the Ileum passively |

| |The kidney processes Vit D into Calcitrol which enables absorption of calcium, stimulated by parathyroid hormone |

| |Calcitonin helps store calcium in bone (reducing it from blood) |

| |Parathyroid hormone releases calcium from bone (increasing blood calcium levels) |

Acquired - Endocrine

|Cushings |

|Definition |Cushing’s disease is a condition in which the pituitary gland releases too much adrenocorticotropic hormone |

| |(ACTH). |

| |A tumour or hyperplasia of the Pituitary gland |

| |ACTH stimulates the release of Cortisol (controls carb, fat, protein metabolism and inflammatory response) |

|Who gets it |People taking glucocorticoid drugs |

| |Tumour that produces ACTH e.g. in pituitary |

|Symptoms |Rapid weight gain |

| |Hyperhydrosis |

| |Skin thinning and easy bruising |

| |Insomnia |

| |Amennhorea/Oligomenorrhea, infertility |

|Signs |Back ache |

| |Bone pain and tenderness |

| | |

| |Central obesity, thin limbs, Moon face, Buffalo hump, Acne |

| |Purple strae ½ an inch wide |

| |Hirsuitism |

| |Decreased fertility, impotence |

| |Mental changes: fatigue, poor mood, depression, anxiety |

|Medical Tests |24 hour urine cortisol |

| |Blood ACTH level |

| |Brain MRI |

|Medical TTT |Surgery to remove tumour or Radiation to the Pituitary |

| |Removal of Adrenal Glands |

| |Medication to control Cortisol production |

|OMT | |

Acquired - Idiopathic

|Padget’s disease |

|Definition |Normal cycle of bone renewal and repair is disrupted, can cause bone weakening |

| |Second most common bone disease to Osteoporosis |

|Who gets it? |1-2% >55 YOA increasing to 7% >80 YOA |

| |White British decent more widespread in the north of the country. Also in countries with high levels of migration from the UK |

|Symptoms |Often none |

| |Bone pain, worse at night or laying down |

| |Hypercalcaemia: Malaise, Depression, Drowsiness, Constipation (linked to kidney stones) |

| | |

| |Other Complications include: |

| |# to bone |

| |Bone deformity |

| |Deafness |

| |Vertigo |

| |Headaches |

| |Tinnitus |

| |Neurological symptoms where the bone has reduced nerve passage |

| |OA |

| |Heart failure, vessels become damaged in bone and require increased effort to pump the blood (SOB, Tired, Peripheral Oedema) |

| |Cancer – 1 in 1000 Padget’s get sarcoma (bone pain, swelling around the affected bone, lump on the bone) |

|Signs | |

|Medical Tests |X-Ray signs of increased bone remodelling |

|Medical TTT |Pain relief |

| |Bisphosphonates –reduces Osteoclastic activity, tablet taken 1* day and stand up for 30 mins to avoid heartburn if taken orally |

| |Calcitonin – where calcium in blood is low, injection 1* day |

| |Physio – following # |

| |Surgery – following # or OA changes to replace a joint |

|Scheuermann’s disease aka Osteochondrosis or Osteochondritis |

|Definition |Adolescent osteochondritis usually in T.sp (T6 – T10). |

| | |

| |A defect in the secondary ossification centre in the vertebral body causes an irregularity in the ossification of the vertebral |

| |body epiphyses. Cartilaginous end-plates may be weaker than normal and damaged by pressure from adjacent IV discs, sometimes |

| |associated with small herniations of disc material into vertebral body (Schmorl’s nodes). With ( growth and mm activity, |

| |affected vertebrae become wedge-shaped as ant bodies are subjected to greatest stress. |

|Who gets it? |Adolescents (13 – 16yoa), boys>girls |

| |Possibly due to collagen defects |

| |Can be associated with mental and physical shocks |

|Symptoms |Active stage (1-2 years during puberty): Pain in T.sp, fatigue, after some months pain (, parents may comment that their |

| |teenager is “round shouldered” or has poor posture. |

| | |

| |Later life: LBP from compensatory L.sp ext, pain above and below the hypomobile segment |

|Signs |Flexed hypomobile segment does not improve with a change in posture |

| |Round back/round shoulders |

| |Compensatory lumbar lordosis |

| |Active stage: Pain agg by activity or long periods standing. |

| |Later in life: pain from OA, pain above and below segment |

|Effects on the body |Hypomobile segment leads to early degenerative change to disc through reduced tissue health results in Spondylosis |

| |Change in neural health in the area affected |

| |Reduced force transmission |

| |Can restrict rib movement, increasing upper rib breathing and increased chance of RTI |

| |Can affect the thoracic pump affecting venous drainage from LEX |

|Tests you can do |Does the Hypomobile segment flexed segment improve with a change in posture? |

|Medical tests |X-ray signs: |

| |Vertebral end plates appear irregular or fragmented |

| |Radioluscent defects in subchondral bone (Schmorl’s nodes). |

| |Bodies become wedge-shaped |

| |Claw osteophytes |

| |Detached epiphyseal ring |

|Medical treatments (and|60o: Fusion using a hook-rod system |

|OMT |Work to improve ROM of hypomobile segment |

| |Look at rib, diaphragm movement |

| |Advise at the hyper vascular stage during puberty to modify activities avoiding high impact |

|Contraindications to |Avoid extreme flexion |

|OMT |Be aware of possibility of anterior spurs on vertebral bodies |

|Piriformis syndrome |

|Definition |Sciatic neuritis (L5-S3)due to Piriformis contracture or spasm leading to mechanical or chemical infiltration of the|

| |nociceptors of the nevi nevorum of the epineurium causing pain and paraesthesia in the sciatic nerve distribution. |

|Who gets it |Anatomic anomaly - In 75% of people the sciatic and posterior cutaneous nerve pass beneath Piriformis. In 5% of |

| |people the sciatic nerve or branches of it (common peroneal, tibial) pass through Piriformis |

| |Injury to gleutei |

| |Biomechanical overuse (LLD) |

| |Tight external rotators |

|Symptoms |Can cause minot low back ache |

|Signs |Aggrevated by neck flexion and SLRT |

|Tests |SLRT +ve |

| |Hibb’s +ve which stretches piriformis |

|TTT |Massage |

| |Mobilise with MET |

| |Look at the pelvis and LLD |

| |Stretching exx |

Acquired - Psychogenic

o Psychosomatic

Acquired - Visceral

o IBS

o Crohns

o Peptic ulcer

o Carcinoma GIT

Acquired - Vascular

o AAA

o Dissecting

Acquired – Renal conditions

o Calculus

o Carcinoma

o Inflammatory disease

Acquired – Gynaecological conditions

o PID

o Endometriosis

o Neoplasm

o Batsons Plexus can influence LBP before or after periods

Pain

Nociceptor stimulation:

Nociceptors are found in all tissues of the body which a nerve supply (Skin, Muscle, Ligaments, Fascia, Tendons, Joint capsules, Synovium, Outer disc, Dura, Blood vessels, Viscera)

Nociceptors sample the environment to report disturbance from normal: Chemical irritation, Mechanical deformation, Temperature changes

Information enters the dorsal horn and is transmitted to higher centres where it may be modulated

Central neurogenic

Peripheral neurogenic

Pain referral patterns

Pain felt other than at the source of pain. No actual damage to the region of pain. Results from central processing of pain sensation. Extent of referral is proportional to the intensity of the stimulation. Referred pain usually presents with local pain. Non dermatomal pattern and can vary in a subject from moment to moment. Usually aggravated by movement of the inflamed tissue, not movement at the location of referral

• Nerve root pain – Motor loss of muscles supplied by the nerve, Sensation loss in a dermatomal pattern

NRI – Leg pain

NRC - objective neurological signs, sensory loss, muscle power loss. More serious!

NRP –

o unpleasant,

o More intense in the limb than spine,

o in a nerve root distribution, tingling in a dermatome

o Pain exacerbated by movement

o Unpleasant tingling, numbness

o Shooting lancinating pain in a line into the leg

Causes:

o Disc commonly ................
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