Physical Medicine Final Slides & Notes PDF

INDEX PAGE LEC 1 Neck pain & Cervical spines 2 LEC 2 Rheumatoid Arthritis 17 LEC 3 Ankylosing Spondylitis 25 LEC 4 Electromyography & Nerve conduction Studies 38 Special thanks : • Reem El-Nagar • Bahaa Muhammed • Alaa Akram • Muhamed Aziza • Yumna Ghareeb • Abdelrahman Ahmed •...

INDEX PAGE LEC 1 Neck pain & Cervical spines 2 LEC 2 Rheumatoid Arthritis 17 LEC 3 Ankylosing Spondylitis 25 LEC 4 Electromyography & Nerve conduction Studies 38 Special thanks : • Reem El-Nagar • Bahaa Muhammed • Alaa Akram • Muhamed Aziza • Yumna Ghareeb • Abdelrahman Ahmed • Ghadeer Reda • Asmaa Malak • Ola Reda • Kamar Muhammed Wishing you all the best with your endeavors "Life is not about finding yourself. Life is about creating yourself". 🌔💫 Cervical spine NB: all the pictures are IMP. Normal curvature of vertebral column: - Cervical lordosis Dorsal kyphosis Lumbar lordosis Sacral kyphosis Abnormal situations: ● longstanding muscle strain (ex: ankylosing spondylitis) leads to straightening of lumbar curvature. ● exaggeration of lumbar lordosis in: Pregnancy and pendulous abdomen (fat). ● exaggeration of dorsal kyphosis in: Osteoporosis. General consideration of Vertebrae: - Transitional vertebrae: is the point between parts of the column ex: vertebrae from cervical to dorsal, dorsal to lumber, lumbar to sacral. It takes character from both parts (transitional vertebrae from cervical to dorsal have features from both cervical & dorsal). - Spinous process, transverse process, and features of the canal are parts that can differentiate between vertebrae along the vertebral column. - Foramen transversarium passes in it the vascular elements and roots of the nerves. 2 Osseous structures: 3 Cervical vertebrae: - Comprised of seven cervical vertebrae C1-C7 - The 1st two vertebrae are different from the other C3-C7. - C1 (Atlas) & C2 (Axis) have no disk in between & have vertebral foramen which allow the vertebral arteries to reach through to the brain and supply it with blood. - The body of the vertebrae gets bigger as we go down in the spine so it can bear the weight of the body. - There is special movement to examine C1 & C2 different than movement for all the cervical spine: a. Atlas (C1) allows head nodding “yes”; due to its upper articular facet articulates with occiput in skull and lower articular facet articulates with lower segment. b. Axis (C2) allows head rotation “No”. c. Flexion, extension, lateral flexion, and rotation are for all of cervical spines. { all these movement must be done during examination } - Axis (C2) is characterized by an odontoid process. The odontoid process is articulated with atlas that is stabilized and fixated by ligaments. - Upward migration of the odontoid process will compress the spinal cord leading to shocking, respiratory problems …etc. - Atlanto-axial joint (AAJ): is a synovial joint between the atlas and odontoid process of the axis, which may be affected in inflammatory diseases, as juvenile idiopathic arthritis (JIA) and Rheumatoid Arthritis (RA). - Affection of atlantoaxial joint → erosions → subluxation of ligaments → upward migration of the odontoid process (critical situation) leading to quadriplegia, or mediolateral instability. 4 - For these reasons, Neck pain or headache complaints in a patient with rheumatoid arthritis should never be neglected. Full clinical examination, neurological examination, and investigations with special views in imaging should be done to detect affection of AAJ. Planes of movement: The uncovertebral joint: (reading) - are small joints that sit on each side of the cervical discs. They are not present at birth. They develop as a person grows. The uncovertebral joints allow for flexibility, movement, and stability within the neck and limit sideways movement. - also called Luschka's joint, is located on each side of the four cervical discs between levels C3 and C7 in the spine. - Related pathology ● ● ● The vertebral artery and spinal nerve roots may be compromised due to osteophyte formation. Resection of the uncovertebral joint and associated osteophytes may decompress acquired impingement. when edematous, may precipitate torticollis. bilateral resection may be performed if an artificial cervical disc is inserted. 5 Soft tissue structures - Composition of the disc: 80% water, annulus fibrosus “outer”, nucleus pulposus “inner”. - The water content is decreased with aging. so, It’s not logical to disc herniation at old age (50-60 decades) because the cartilage will be fibrotic. - Age of disc herniation: middle age. - Old age characterized by osseous changes: narrowing of spinal canal, spondylosis, osteophyte formation may occur. - if osteophyte occurs post. will affect the spinal cord, and if occurs post. lateral or medial will affect nerves. (as same as disc herniation in young age) Ligaments: - Anterior longitudinal ligament - Posterior longitudinal ligament { NB } Decussation ligaments that are defective posteriorly → weak point → disc herniation of nucleus pulposus posteriorly → encroachment of spinal cord, if herniation is posterolateral or posteromedial → compress the nerves. 6 Neck muscles 1. 2. 3. 4. Rectus capitis major & minor. Obliques muscles Scalenus muscles Sternomastoid 7 { NB } - The origin of the sternocleidomastoid is at the sternum and clavicle, and the insertion is at the mastoid process of the skull, which lies just behind the ear. - Sternomastoid tumor: not an actual tumor. It’s a benign mass that appears in a newborn after delivery due to trauma of sternomastoid by traction during delivery, If neglected it will end up with hematoma then calcification. The baby will present with torticollis ”shortening of cervical muscles”. - other delivery complications due to traction is Erb's palsy. injury to the brachial plexus nerves which formed by the lower four cervical nerves and first thoracic nerve (C5-T1). Neural structures 8 Neural Structures 9 Dermatomes & myotomes: { IMP } - Dermatome: superficial sensation (skin). - Myotome: supply muscles of a specific area. { both aiming to detect a level of affection } - Regimental area = exclusive for C5. - T1, T2, T3:inner arm, forearm, and axilla. - The charts are very important. ** Esp. Cervical supply ** - 10 DERMATOMES MYOTOMES 11 Pain generators I - important structures in the neck producing pain, there are bone muscles and ligaments, LN, Thyroid and parathyroid, vascular bundle, carotid, esophagus, trachea, larynx, and cervical plexus (c1-T1), and Referred pain to neck as: myocardial infarction ,biliary colic. ** Pain generators II 12 ● Non musculoskeletal neck pain: - Lymph nodes infection (draining LN) as in Tonsillitis/impetigo, they infect the lymph nodes. - LN also as a part of generalized lymphadenopathy will involve neck LN → pain. - Odynophagia (painful swallowing = neck pain ) and pharyngeal dysphagia (there are other levels of dysphagia). - Chondromalacia of the thyroid cartilage of the larynx (softening of the cartilage induces pain). - Tumors of the apical part of the lung (Pancoast tumor) may compress neck structure causing pain. - Others: thyroid, carotid aneurysm, recurrent laryngeal nerve (neuritis ”neurological pain”), any diaphragmatic irritation will cause neck pain. 13 History taking: { IMP } Features of pain be elicited from clinical history : ● mode and time of onset ● site of pain ● radiating or referred pain , as in radicular pain: pt. complaint of ● ● ● ● ● ● ● shoulder pain but it actually radicular from the cervical spine . quality of pain frequency and duration of episodes of pain; mechanical pain (late in the day), inflammatory (early morning ass. with stiffness) , pain suggesting malignancy (at night) etc. pattern of episodes (see table 18.7) if periodic, mode of onset and time of onset aggravating factors relieving factors associated features. { NB } Osteoporosis is a silent disease, there is a defect in trabeculation. OP is NEVER painful unless fracture occurs. microfractures → wedge fracture that compress the nerves → Pain. 14 { NB } - Why is the tumor painful at night? Pain is affected with the circadian rhythm and hormones, such as endogenous endorphins response to stress or pain → potent analgesic, and steroids have anti-inflammatory and analgesic effects. - Circadian rhythm starts at dawn 4am and declines up to 10pm. So, any patient with pain may become better during the morning as an endogenous anti-inflammatory & analgesic. - Circadian Rhythm of steroids is also the cause behind quotidian fever of juvenile idiopathic arthritis patients, which start at 6 AM, peak at 10 AM, and go down at 2 PM. Cervical local clinical examination: Provocative tests: ● Spurling’s test ● Adson’s test ● Lhermitte’s sign ● Swallowing test 15 Diagnostic studies: { History taking & physical examination is a must before imaging, to specify what you need to investigate } Radiographs CT & myelography MRI Discography Scintigraphy Electrodiagnostic studies = Electromyography (EMG) and nerve conduction studies. ● Thermography ● Musculoskeletal ultrasonography. ● Sonography (US used for thyroid) ● ● ● ● ● ● Cervical sprain & strain 16 Rheumatoid arthritis • ✓ ✓ ✓ ✓ ✓ ✓ Definition Epidemiology Pathophysiology Clinical picture Investigations TTT Definition • Chronic [ more than 6 weeks to differentiate it from viral infection ] autoimmune systemic inflammatory disorder. • Of unknown etiology • Characterized by primary affection of synovial joints, [ so usually no fatal complications ]. Epidemiology • Age: [ middle aged but may first presented at any age with poor prognosis if old age → malignancy must be excluded (Para malignant) ]. • Sex more common in females. { NB } rheumatic diseases that are more common in males: Gout, Ankylosing spondylitis and for lesser extent polyarteritis nodosa. • Race: all races (less in Chinese more in European & Caucasian). Pathophysiology The cause is unknown but may be : ● Genetic component [ incidence increases with first degree relative history ]. { NB } - any HLA class I , one polypeptide chain (A ,B,C ) stimulates CD8 cytotoxic T cells e.g., HLA B27 common in ankylosing spondylitis. - HLA class II , 2 polypeptide chains (DP, DQ, DR) stimulate CD4 Helper. - HLA DR4 is associated with rheumatoid **, lupus is associated with DR2 & DR3 - R.F. & Autoantibodies ( Igg and IgM) which are non-specific. - Anti-cyclic citrullinated peptide antibody (ACPA) as CCP. ● Environmental components [ trigger as viral infection , and smoking increases the sacculation process (CCP Antibody) ]. ● Autoimmune disease 17 Relative incidence of joint involvement in RA [ Small joints affection mainly ]. • MCP and PIP joints of hands & MTP of feet 90% • Knees, ankles & wrists- 80% • Shoulders- 60% • 50% Elbows- • TMJ, ACJ 30% { NB } any rheumatoid U/S protocol → wrist and small joint examination is a must. - Deformities: the most common deformities are swan neck( flexion of DIP joint and hyper extension in proximal ) to and boutonniere. - In rheumatoid DIP joints are spared, clinically false affection to DIP joints with NO X-RAY findings due to subluxation of tendons only mechanical, if there is radiological finding suspect psoriatic affection or osteoarthritis. 18 Ulnar Deviation, MCP Swelling, Left Wrist Swelling 19 IMP { NB } - its aim is to pick up the patient early , these criteria are put to detect early cases score 6 or more is needed for diagnosis . - IMPORTANT : There is no rheumatoid diagnosis without arthritis - in serology if RF or ACPA are positive , you should say if it is high or low positive , they are considered high positive if they are more than 3 folds the upper limit . Extra Articular Involvement • Rheumatoid nodules (30%) [ especially with +ve RF ]. • Rheumatoid vasculitis [ ccc by skin ulceration ] - mononeuritis multiplex [ means one limb has more than one nerve affection → suspect vasculitis ] , cutaneous ulceration, digital gangrene, visceral infarction. • CNS- peripheral neuropathy, atlantoaxial/mid cervical spine subluxation, entrapment neuropathies. • EYE- keratoconjunctivitis sicca, episcleritis, scleritis. • CVS- pericarditis , pericardial effusion. • Respiratory- pleural effusion, pneumonitis , pleuro-pulmonary nodules, ILD. • Hematological - normocytic normochromic anemia - leukocytosis /leukopenia ( rare , in case of felty syndrome , or suppressed by immunosuppressive therapy e.g., MTX ) NB: if rheumatoid with leukopenia suspect it's lupus - thrombocytosis • Felty’s syndrome- Chronic nodular Rheumatoid Arthritis - Splenomegaly - Neutropenia 20 - leucopenia - leg ulcers 21 Investigations: • Acute phase reactants [ high with activity ] • CBC [ normocytic normochromic anemia, leukocytosis & thrombocytosis with activity ] • Immune profile [ ACPA / RF ] • Other (LFT , KFT, etc.) )‫ حاجات عنه على األقل‬3 ‫(كل دواء الزم تبقى عارف‬ Treatment • Dose • Form • Side effect • NSAIDS ( side effects : gastritis ( if need to give for a longer period , add a PPI to protect against gastritis ) , renal impairment , never give to pt who is on anticoagulant , never give to old age pt before you do a KFT ) ( dose : short term only for 1 week or 5 days then if needed) • Corticosteroids ( its role in lupus is more important than in rheumatoid) dose : 10 mg oral , we give it early in ttt as it has a rapid effect (bridge therapy) then stop it gradually in 6 months. side effects : peptic ulcer (most common SE ) , hypertension , diabetes , osteoporosis (so in long term give vit D & ca ), avascular necrosis (very serious ) (any pt on corticosteroid therapy complains from hip pain , you should do MRI immediately) 22 • DMARDS (Disease-modifying antirheumatic drugs ): a. Methotrexate (MTX): most common and important one in this group o cheap o Dose : 12.5 ml (¼ ampoule),parenteral ,every week ( if taken daily it may lead to bone marrow suppression & MTX toxicity which is fatal ). o Side effects: ▪ GIT disturbances nausea and vomiting (common) , ▪ hepatotoxicity (commonest ), if liver enzymes increased 3 folds ,stop the drug , before you start this medication ask for hepatitis markers and LFT. ▪ ▪ Follow up every 2-3 months, by CBC as it may lead to BM suppression. Mouth ulcers ▪ Methotrexate pneumonitis (allergic reaction) , before giving this medication you should ask for an X-ray on the chest, because if the patient has a preexisting lung disease ,this allergic reaction will be ▪ more serious. Teratogenic ( before 3 months of pregnancy you should stop the drug). b. Leflunomide (ideal alternative for MTX) - Dose : 20 mg daily oral - Side effects: ▪ hepatotoxicity ▪ Hypertension ▪ Teratogenic but it is more serious than MTX as it stays in tissues for 2 years so in females who are in childbearing period try not to give this medication, if she is already on this medication and she will be pregnant, give her cholestyramine for 11 days 66 bags )‫(كأنك بتعلمها غسيل‬. c. Salazopyrin - oral - triple therapy ( MTX , salazopyrin , hydroxychloroquine) d. Antimalarial ‫ → اه يا عيني‬hydroxychloroquine - may be given in association with MTX. - Side effects: Retinopathy and sometimes maculopathy may occur , if discovered early it is reversible , but if not, it may lead to blindness, so you Should do fundus examination before administering the drug and every 6 months after start of the medication. 23 Biological treatment ▪ Anti-TNF [ (most common ) we should do tuberculin test ]. ▪ Anti-IL 6 [ Tocilizumab (Actemra) in cytokine storm (was used in covid) ] ▪ Rituximab [ in very severe cases , anti B-lymphocyte , can be used in SLE ] ▪ JAK inhibitors [ oral drug ]. { NB } these drugs may lead to thromboembolism (DVT) , Herpes zoster, malignancy. Quick recap of RA - Middle-aged female Caucasian with “arthritis involving PIP”. - C/O of joint pain & morning stiffness. - Pathology: synovitis of mainly peripheral joints. - Ex. sub-cutaneous nodules on extensors & deformities (swan neck ,boutonniere, z-shape). - Extra articular: hematological→ vasculitis (mononeuritis multiplex), CNS, Chest→ ILD “Caplan’s $”... - investigations ▪ for diagnosis: 1-CRP,ESR, 2-Immune profile (HLA DR4, ACPA ”CCP”, RF), 3-U/S ▪ for treatment FU 4-LFTs,KFTs 5-CBC 6-chest x-ray. ▪ 6 marks of the criteria are needed (onset of symptoms, Number of joints affected, CPR & ESR, RF & ACPA) - Treatment: 4 1. NSAIDs 2. Corticosteroids 3. DMARDs: MTX 4. Biological agents 24 Ankylosing Spondylitis ● ● ● ● ● Is a chronic systemic inflammatory disorder of undetermined etiology? Usually beginning in early adulthood. Primarily affecting the axial skeleton. Generally, begins in the sacroiliac joint. Often with enthesopathy [ entheses are the connective tissues between bones and tendons ]. ● Extra articular features can also exhibit. ● The disease prevalence in adult population is close to 0.2%. ● Male to female ratio is 2 : 1. { NB } - Symptoms may include: Dull back pain and stiffness in the lower back and hips, especially in the morning, which improve with exercise or NSAID. - It can cause fusing parts of the spine → lose flexibility (patient moves as a one unit). - One of the earliest x-ray abnormalities is pseudo-widening of SI joint spaces. AS is a disease associated with 3 compartments: ❖ Axial. ❖ Non- axial rheumatoid disease. ❖ Extra-articular manifestations. • Axial joint involvement – Axial arthritis can progress from the sacroiliac joints1. – Spine can be affected at any site2. – Arthritis in the shoulders and hips1,3 • Non-axial rheumatic involvement – – – – – – Peripheral arthritis occurs in 22%–30% of patients with AS5,6 Predictor of poor outcomes and rapid progression of disease1 Predominantly of lower limbs1 Swollen knee joints are common4. Dactylitis occurs in ~10% of patients with AS7. Enthesitis occurs in 20%–60% of patients with AS7. 25 • AS is primarily a disease of the axial skeleton and over time, axial arthritis can progress from the sacroiliac joints.1,2 However, the spine can be affected at any site and inflammation is most often found in the thoracic spine.3 Some patients frequently develop arthritis in the hips and shoulders early in the course of AS and it occurs more often than involvement of distal joints.1,2 • Peripheral joint involvement occurs in as many as 70% of patients, 4 with full-blown peripheral arthritis present in an estimated 22% to 30% of patients.5,6 It should be noted that the appearance of peripheral arthritis early in the course of the disease generally predicts poor outcome and rapid progression.1 Most commonly, there is asymmetrical distribution of arthritis predominantly in the lower limbs1; the knee joints are most often affected.4 Enthesitis, an inflammation of tendon-to-bone insertion sites, occurs often in AS patients (20%–60%) and usually involves the Achilles tendon and plantar fascia. 7 Dactylitis associated with sspondylarthritis, also referred to as 'sausage-like' digit, is a diffuse painful swelling of the fingers and toes.8 The relative frequency of dactylitis is approximately 10% in AS patients.7 Extra-Articular Manifestations and Comorbid Conditions of AS: • Due to the central role of immune-mediated inflammation in AS, a wide variety of inflammatory extra-articular manifestations and comorbid conditions are associated with the disease. Psoriasis is common; it is found in approximately 10% to 20% of AS patients.1 IBD appears in 5% to 10% of cases,2 and subclinical inflammation of the gut is reported in 40% to 60% of AS patients.1 Anterior uveitis is a very common ophthalmic disorder occurring in 20% to 40% of AS cases.3 26 • Cardiac abnormalities such as conduction disturbances and aortic insufficiency are not uncommon, but prevalence estimates vary widely, ranging from 1% to 33% for conduction disturbances and from 1% to 10% for aortic insufficiency.4 Associated pulmonary conditions are also documented including fibrosis, cauda equine syndrome and, in late disease, amyloidosis.4 Inflammatory Back Pain according to experts: [ to be considered in diagnosis ]. - Insidious onset Pain at night (with improvement upon getting up) Age at onset <40 years Improvement with exercise [ daily exercises help to improve the condition ]. - No improvement with rest • In fact, the confirmation of IBP* is the most widely accepted starting point for assessing the potential presence of an axial spondylarthritis such as AS.* [ Inflammatory back pain ]. Inflammatory vs Mechanical Back Pain: 27 Signs: → painful Sacro-iliac tests * limited spinal movements 28 Spinal mobility – Modified Schober: ● ● ● ● ● ● Patient standing erect. Mark an imaginary line connecting both posterior superior iliac spines (close to the dimples of Venus) (1) A next mark is placed 10 cm above (2) The patient bends forward maximally. measure the difference between the marks (3) Report the increase (in cm to the nearest 0.1 cm) The best of tries is recorded. Spinal mobility – Chest Expansion: ● ● ● ● Hands resting on or behind the head. Measure at 4th intercostal level anteriorly Difference between maximal inspiration (1) and expiration (2) in cm (e.g., 4,3 cm) is recorded. Report the best of two tries. 29 Disease Course (radiographic): ● ● ● ● Progression of sacroiliac disease to fusion of sacroiliac joints Syndesmophyte formation along the spine Typically ascends from lumbar to cervical. “Bamboo spine”- total fusion of the spine { NB } X-Ray features may take around 2 years to appear, clinical examination and MRI are used for early diagnosis. Age of Onset and Diagnosis in AS - Ankylosing Spondylitis is a disease characterized by early onset & delayed diagnosis. - Clearly there is a significant gap between onset and diagnosis (8-9 years). • Early diagnosis may be more important now due to the availability of new, more effective treatments that have the potential to prevent damage if treatment is initiated early. Efforts to diagnose earlier may help to provide more information about early stages of ankylosing spondylitis (AS) disease and to identify prognostic factors and patients at risk of AS. Also, the development of improved diagnostic methods, such as MRI, and advances in DNA technology and genetic screening to determine disease susceptibility will help in early confirmation of AS disease. 30 Why is Early Diagnosis of AS Important? - Spinal damage is cumulative, irreversible & independent of symptoms. - 81% of AS patients lose spinal mobility in the first 10 years of disease. • Improved diagnostic tools (MRI) and advances in genetic screening make early diagnosis, more reliable. • Effective treatments are available anti-TNF agents & IL 17 inhibitor. Enthesitis is different from synovitis: In the spine, enthesitis occurs at capsular and ligamentous attachments at disco vertebral, costovertebral, costotransverse, & facet joints. { Unlike rheumatoid arthritis the pathology starts at entheses not the synovial membrane } Genetics of AS: - HLA-B27 is the primary disease susceptibility gene for AS but is not a prerequisite for AS, as the disease also affects individuals who do not possess this gene. However, how this gene led to disease is not known. - Only 1 to 5% of subjects possessing HLA-B27 carriers AS. Over 90% of people that have been diagnosed with AS are HLA-B27 positive. - However, 20% of HLA-B27(+) relatives of AS patients will develop AS/SpA. [ Psoriatic Arthritis / Spondylarthritis ]. - [ Ask about family history as AS can run in families ]. 31 Blood parameters - During acute inflammatory periods, increase in the blood concentration of C-reactive protein (CRP) and an increase in the erythrocyte sedimentation rate (ESR), - But some people with AS have normal levels of CRP and ESR, despite experiencing a significant amount of inflammation. Modified New York Criteria for AS (1984):  Clinical criteria: • Low back pain and stiffness for more than 3 months that improves with exercise but is not relieved by rest. • Limitation of motion of the lumbar spine in both the sagittal and frontal planes • Limitation of chest expansion relative to normal values correlated for age and sex.  Radiological criterion: • Sacroiliitis grade ≥ 2 bilaterally or grade 3-4 unilaterally  Definite AS: • If the radiological criterion is associated with at least 1 clinical criterion. 32 IMP AS Measures of Disease Outcome Bath Ankylosing Spondylitis Scales: • BASDAI - Disease Activity Index • BASFI - Functional Index • BASMI - Metrology Index • BASRI - Radiographic Index 33 { NB } - Nonpharmacological therapy is very effective. - Half of patients usually respond to NSAID with non-pharmacological therapy. - Give local corticosteroids for knee joint effusion. - Systemic corticosteroids are contraindicated for joint affection. - Hydrotherapy is very effective. • The ASsessment in AS (ASAS) working group together with the European League Against Rheumatism (EULAR) have developed evidence-based recommendations for the management of AS. With disease progression moving vertically from top to bottom, this figure emphasises the importance of nonpharmacological treatments throughout the course of the disease, early introduction of NSAIDs and options for refractory disease and alternatives for concomitant peripheral disease including TNF inhibitors. 34 • Lying prone for 15 to 30 minutes once or several times a day is useful to reverse the tendency toward kyphosis , and flexion contractures of the hip joints. • Use your back properly: 35 { Start with NSAIDs } Efficacy of NSAIDs in AS: Cornerstone of Pharmacological Treatment for Symptomatic Relief • NSAIDs are the cornerstone of treatment for AS patients when focusing on symptoms. However, there is no apparent disease-altering effect seen with NSAIDs. This can be seen when comparing the percentage of patients with AS responding to NSAIDs versus the percent of patients with mechanical back pain responding to NSAIDs. • 20-50% of AS patients still have active [ 4 weeks ] disease despite treatment with NSAIDs. • For those patients, Anti-TNF have meant a breakthrough in treatment. The five TNF blockers approved by the Food & Drug Administration to treat ankylosing spondylitis are: 1. 2. 3. 4. 5. Adalimumab (Humira) Certolizumab pegol (Cimzia) Etanercept (Enbrel) Golimumab (Simponi; Simponi Aria) Infliximab (Remicade) 36 - middle-aged male with +HLA-B27 (associated with IBS). - c/o insidious onset back pain worse at morning or rest relive with activity or NSAIDs (DD mechanical pain). - Ex: eye→ iritis SpA features (criteria for diagnosis). - Investigation: • HLA-B27, RF -ev ”seronegative”, ESR >100. • X-Ray lumber spine : straightening of lumber curvature, syndesmophytes, bamboo spine. - Treatment: non-pharmacological is most importat→15 min exercise daily, hydrotherapy. - Pharmacological: NSAIDs , local steroids , sulfasalazine. - If no respond to NSAIDs → biologic treatment. 37 Quick recap of AS Electromyography & Nerve conduction Studies  An electromyogram (EMG) measures the electrical activity of muscles at rest and during contraction.  Nerve conduction studies measure how well and how fast the nerves can send electrical signals. The normal neurophysiologic function of the nervous system - Electrical signals are generated in the brain. pass through the spinal cord. and travel into the peripheral nervous system. These signals are carried down the nerve to the synaptic cleft, where a chemical release of acetylcholine crosses the synaptic cleft to create an electrical discharge in the muscle. This electrical signal causes the muscle to contract.  Why Is It Done? To help in the diagnosis [ NOT diagnostic ] & assessment of the diseases that damage muscle [ as myopathy ] tissue, nerves [ as neuropathy ], or the junctions [ as myasthenia gravis ] between nerve and muscle.  Electromyography and nerve conduction studies is an important & helpful Extension of the physical examination and can detect minor abnormalities when physical examination cannot In the assessment of the peripheral nervous system injuries. 38 Key steps: - Review of referral materials. Eliciting the patient’s history. Performing a physical examination. Developing a differential diagnosis. Putting together a plan for electrodiagnostic evaluation.  Electromyography: This procedure involves the placement of a needle into various muscles to record different stages of muscle activity, including: Rest, minimal contraction, & maximal activity. [ There are also surface electrodes, used as references, and to evaluate sensory response ]. - At rest, normal muscle is electrically silent. - Damaged muscle tissue may result in spontaneous depolarization of individual muscle fibers. Needle Insertion - Activity at rest [ Insertional activity; normally there’s No rigidity (fibrosis) & No records (waves) = silent → deprivation occur in case of denervation ]. [ Insertional activity is useful for follow-up ] 39 Main electromyographic criteria: - Activity at rest - Motor unit potentials analysis - Pattern of recruitment Muscular Contraction: Motor Unit Potential (MUP) 40 EMG - Recruitment Interference Pattern [ each disease has its own patter → e.g., Myopathy is characterized by Early Recruitment; prevent the muscle to reach maximum contraction ] EMG of normal muscle: • At rest: no activity. • On minimal volition: MUAPs are of average amplitude and duration. The polyphasic potentials are less than 10%. • On maximum volition: contraction). full interference pattern (maximum • The normal MUAP is usually biphasic or triphasic with amplitude range of 0.5 to 3 mV, and a duration between 2 and 10 ms. { NB } - - The motor unit action potential (MUAP) is the sum of the extracellular potentials of muscle fiber action potentials of a motor unit. Waves under the baseline are the +ve waves. EMG device is also translating waves into characteristic sound for each potential for each disease “muscles talking”. 41 Pathologies in Striated Muscle: Anatomical sites of involvement including possible Etiology: Site Etiology AHC - Poliomyelitis - Motor neuron disease - Spinal muscular dystrophy Nerve Root - Prolapsed IVD - Traction injury Plexus - Penetrating Wounds - Traction injury Peripheral nerve - Neuropathies including Compression neuropathies- Neuromuscular junction - Myasthenia Gravis - Myasthenic syndrome Muscle fiber - Myopathies - Polymyositis - Myotonias [ EMG helps in detection of the site of the lesion & the type of the injury ( e.g., nerve concussion as in Neuropraxia or degenerative as in axion or myelinated sheet affection) ] 42 Nerve Conduction Studies  Measuring the electrical activity in muscles and nerves can help detect the presence, location& extent of diseases.  that can damage muscle tissue (such as muscular dystrophy) or nerves (such as entrapment neuropathy).  In the case of nerve injury, the actual site of nerve damage can be located.  EMG and nerve conduction studies can be done together to provide more complete information. Motor Response Pathologic Responses 43 Stimulation Points: a. Upper Extremities - entrapment neuropathy → median nerve b. Lower Extremities c. Head & Trunk 44 Motor Conduction: Median Nerve - The Term Entrapment describes the mechanical irritation by which a specific peripheral nerve becomes locally injured in a vulnerable anatomic site. - Familiarity with the anatomy of the peripheral Nerves is essential. - Nerve compression can occur at any point where a peripheral nerve passes through An opening In fibrous tissue or through An Osseo fibrous Canal. - In addition to a neurologic examination, the evaluation of every patient with an entrapment neuropathy should include electromyography (EMG) motor and sensory nerve conduction velocity studies, and appropriate radiographs. - EMG and nerve conduction velocity measurements provide localizing information often necessary in the early diagnosis of a compressive neuropathy and reliably document the severity and extent of nerve entrapment. - [ latency : Onset latency is the time it takes for the stimulus to initiate an evoked potential and reflects the conduction along the fastest fibers ]. MCQ Classification of nerve injuries • Neurapraxia: It is a comparatively. • Mild injury with motor and sensory loss with no evidence of Wallerian degeneration. • The nerve distally conducts normally. Focal demyelination and/or ischemia are thought to be the aetiology of the conduction block. • Recovery may occur within hours, days, weeks, or up to a few months. 45  Axonotmesis: - It is commonly seen in crush injuries The axon and their myelin sheaths are broken, yet the surrounding stroma remains partially or fully intact. - Wallerian degeneration occurs, but subsequent axonal regrowth may proceed along the intact endoneurial tubes.  Neurotmesis: - It describes a nerve that has been either completely served or is so markedly disorganized by scar tissue that axonal regrowth is impossible. - Prognosis for spontaneous recovery is extremely poor without surgical intervention. Characteristic features associated with Various nerve compressions: 46 What Is Carpal Tunnel Syndrome? Causes: - - Trauma R.A Pregnancy Teno-synovitis Hypothyroidism Gout Acromegaly Amyloidosis Ganglion - Mixed sensor motor N. - Sensory - paresthesia - Motor - weakness and atrophy of the thenar muscles • The discomfort worsens at night and often awakens her from sleep. • Frequently bilateral. • If sever , the CTS may produce retro grade pain to the forearm and less commonly to the shoulder and neck regions. { NB } Provocative test (carpal compression test): - Apply pressure over the wrist for 30sec pt. will feel numbness & tingling. - Other clinical tests: ▪ Phalen's test ▪ ▪ Reversed Phalen’s. Tinel’s test 47 Double crush syndrome of the MEDIAN nerve: Treatment: A. Nonoperative: Splint the wrist in the neutral position that maximize space for the entrapped nerve. Maintain good blood flow to the limb and reduce swellings and oedema in order to prevent the compression. Rest the Wrist: Wrist rests help to avoid carpal tunnel syndrome by keeping the wrists elevated above the keyboard. An Ergonomic Glove: IMAK Products' Smart Glove uses a removable splint (upper cutout) to keep the wrist in the proper position. The ergo Beads (bottom cutout) massage the area to increase blood circulation and promote healthy muscle tissue. 48 - Modify activity and avoid positions that can be a source of trauma. - Reduce inflammation and consider the use of ice, NSAIDs and corticosteroid injection in structures around the nerves that may be inflamed. B. Operative: If despite of nonoperative treatment, there is evidence of continuing axonal degeneration in the entrapped nerve, surgical decompression of the nerve is considered. 49