The Trendelenburg Gait
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DERMATOLOGY – 15% Acne Vulgaris Inflammatory skin condition assoc. with papules & pustules involving pilosebaceous units Pathophysiology: • 4 main factors – follicular hyperkeratinization with plugging of sebaceous ducts, increased sebum production, Propionibacterium acnes overgrowth within follicles, & inflammatory response • Hormonal activation of pilosebaceous glands which may cause cyclic flares that coincide with menstruation Clinical Manifestations: • In areas with increased sebaceous glands (face, back, chest, upper arms) • Stage I: Comedones: small, inflammatory bumps from clogged pores - Open comedones (blackheads): incomplete blockage - Closed comedones (whiteheads): complete blockage • Stage II: Inflammatory: papules or pustules surrounded by inflammation • Stage III: Nodular or cystic acne: heals with scarring Differential Diagnosis: • Differentiate from rosacea which has no comedones** • Perioral dermatitis based on perioral and periorbital location • CS-induced acne lacks comedones and pustules are in same stage of development Diagnosis: • Mild: comedones, small amounts of papules &/or pustules • Moderate: comedones, larger amounts of papules &/or pustules • Severe: nodular (>5mm) or cystic Management: • Mild: topical – azelaic acid, salicylic acid, benzoyl peroxide, retinoids, Tretinoin topical (Retin A) or topical antibiotics [Clindamycin or Erythromycin with Benzoyl peroxide] • Moderate: above + oral antibiotics [Minocycline 50mg PO qd or Doxycycline 100 mg PO qd], spironolactone • Severe (refractory nodular acne): oral -
Neurologic Outcomes in Friedreich Ataxia: Study of a Single-Site Cohort E415
Volume 6, Number 3, June 2020 Neurology.org/NG A peer-reviewed clinical and translational neurology open access journal ARTICLE Neurologic outcomes in Friedreich ataxia: Study of a single-site cohort e415 ARTICLE Prevalence of RFC1-mediated spinocerebellar ataxia in a North American ataxia cohort e440 ARTICLE Mutations in the m-AAA proteases AFG3L2 and SPG7 are causing isolated dominant optic atrophy e428 ARTICLE Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy revisited: Genotype-phenotype correlations of all published cases e434 Academy Officers Neurology® is a registered trademark of the American Academy of Neurology (registration valid in the United States). James C. Stevens, MD, FAAN, President Neurology® Genetics (eISSN 2376-7839) is an open access journal published Orly Avitzur, MD, MBA, FAAN, President Elect online for the American Academy of Neurology, 201 Chicago Avenue, Ann H. Tilton, MD, FAAN, Vice President Minneapolis, MN 55415, by Wolters Kluwer Health, Inc. at 14700 Citicorp Drive, Bldg. 3, Hagerstown, MD 21742. Business offices are located at Two Carlayne E. Jackson, MD, FAAN, Secretary Commerce Square, 2001 Market Street, Philadelphia, PA 19103. Production offices are located at 351 West Camden Street, Baltimore, MD 21201-2436. Janis M. Miyasaki, MD, MEd, FRCPC, FAAN, Treasurer © 2020 American Academy of Neurology. Ralph L. Sacco, MD, MS, FAAN, Past President Neurology® Genetics is an official journal of the American Academy of Neurology. Journal website: Neurology.org/ng, AAN website: AAN.com CEO, American Academy of Neurology Copyright and Permission Information: Please go to the journal website (www.neurology.org/ng) and click the Permissions tab for the relevant Mary E. -
Tremor, Abnormal Movement and Imbalance Differential
Types of involuntary movements Tremor Dystonia Chorea Myoclonus Tics Tremor Rhythmic shaking of muscles that produces an oscillating movement Parkinsonian tremor Rest tremor > posture > kinetic Re-emergent tremor with posture Usually asymmetric Pronation-supination tremor Distal joints involved primarily Often posturing of the limb Parkinsonian tremor Other parkinsonian features Bradykinesia Rigidity Postural instability Many, many other motor and non- motor features Bradykinesia Rigidity Essential tremor Kinetic > postural > rest Rest in 20%, late feature, only in arms Intentional 50% Bringing spoon to mouth is challenging!! Mildly asymmetric Gait ataxia – typically mild Starts in the arms but can progress to neck, voice and jaw over time Jaw tremor occurs with action, not rest Neck tremor should resolve when patient is lying flat Essential tremor Many other tremor types Physiologic tremor Like ET but faster rate and lower amplitude Drug-induced tremor – Lithium, depakote, stimulants, prednisone, beta agonists, amiodarone Anti-emetics (phenergan, prochlorperazine), anti-psychotics (except clozapine and Nuplazid) Many other tremor types Primary writing tremor only occurs with writing Orthostatic tremor leg tremor with standing, improves with walking and sitting, causes imbalance Many other tremor types Cerebellar tremor slowed action/intention tremor Holmes tremor mid-brain lesion, unilateral Dystonia Dystonia Muscle contractions that cause sustained or intermittent torsion of a body part in a repetitive -
Children with Lower Limb Length Inequality
Children with lower limb length inequality The measurement of inequality. the timing of physiodesis and gait analysis H.I.H. Lampe ISBN 90-9010926-9 Although every effort has been made to accurately acknowledge sources of the photographs, in case of errors or omissions copyright holders arc invited to contact the author. Omslagontwcrp: Harald IH Lampe Druk: Haveka B.V., Alblasserdarn <!) All rights reserved. The publication of Ihis thesis was supported by: Stichling Onderwijs en Ondcrzoek OpJciding Orthopaedic Rotterdam, Stichting Anna-Fonds. Oudshoom B.V., West Meditec B.V., Ortamed B.Y .• Howmedica Nederland. Children with lower limb length inequality The measurement of inequality, the timing of physiodesis and gait analysis Kinderen met een beenlengteverschil Het meten van verschillen, het tijdstip van physiodese en gangbeeldanalyse. Proefschrift ter verkrijging van de graad van doctor aan de Erasmus Universiteit Rotterdam op gezag van de Rector Magnificus Prof. dr P.W.C. Akkermans M.A. en volgens besluit van het College voor Promoties. De openbare verdediging zal plaatsvinden op woen,dag 17 december 1997 om 11.45 uur door Harald Ignatius Hubertus Lampe geboren te Rotterdam. Promotieconmussie: Promotores: Prof. dr B. van Linge Prof. dr ir C.J. Snijders Overige leden: Prof. dr M. Meradji Prof. dr H.J. Starn Prof. dr J.A.N. Verbaar Dr. B.A. Swierstra, tevens co-promotor voor mijn ouders en Jori.nne Contents Chapter 1. Limb length inequality, the problems facing patient and doctor. 9 Review of Ii/era/ure alld aims of /he studies 1.0 Introduction 11 1.1 Etiology, developmental patterns and prediction of LLI 1.1.1 Etiology and developmental pattern 13 I. -
Use of Osteopathic Manipulative Treatment to Manage Compensated Trendelenburg Gait Caused by Sacroiliac Somatic Dysfunction
Editor’s Note: Corrections to this article were published in the March 2010 issue of JAOA—The Journal of the CASE REPORT American Osteopathic Association (2010;110[3]:210). The corrections have been incorporated in this online version of the article, which was posted January 2011. An expla - nation of these changes is available at http://www.jaoa .org/cgi/content /full/110/3/210-a. Use of Osteopathic Manipulative Treatment to Manage Compensated Trendelenburg Gait Caused by Sacroiliac Somatic Dysfunction Adam C. Gilliss, DO; Randel L. Swanson, II, OMS III; Deanna Janora, MD; and Venkat Venkataraman, PhD Gait dysfunctions are commonly encountered in the pri - In the present case report, we provide evidence that com - mary care setting. Compensated Trendelenburg gait is a gait pensated Trendelenburg gait may represent a secondary gait dysfunction that was originally described in patients with dysfunction stemming from somatic dysfunction of the weakness of ipsilateral hip abduction. This condition is sacroiliac joints. We also describe evidence of osteopathic thought to result from neuronal injury or myopathy. No manipulative treatment (OMT) resulting in quantitative treatment modalities currently exist for compensated Tren - improvements in the gait cycle. delenburg gait. The authors present a case in which osteo - pathic manipulative treatment may have improved a Tren - Traditional and Osteopathic Gait Theory delenburg gait dysfunction in a man aged 65 years with The gait cycle is divided into two main phases—stance and multiple sclerosis. Evidence of this improvement was swing, each consisting of numerous subphases. 2,3 Traditionally, obtained with the GaitMat II system for measuring the human gait cycle is considered to have six determinants that numerous gait parameters. -
Hip Arthroscopy PT Protocol
Arthroscopic Hip Surgery Physical Therapy Protocol The intent of this protocol is to provide guidelines for your patient’s therapy progression. It is not intended to serve as a recipe for treatment. We request that the PT/PTA/ATC use appropriate clinical decision- making skills when progressing a patient forward. Please call (833) 872-4477 to obtain the operative report from our office prior to the first post-op visit. Please contact our office if there are any questions about the protocol or your patient’s progression. Please keep in mind common problems that may arise following hip arthroscopy: hip flexor tendonitis, adductor tendonitis, sciatica/piriformis syndrome, ilial upslips and rotations, LB pain from QL hypertonicity and segmental vertebral rotational lesions. If you encounter any of these problems, please evaluate, assess, and treat as you feel appropriate, maintaining American Hip Institute’s precautions and guidelines at all times. Gradual progression is essential to avoid flare-ups. If a flare-up occurs, back off with therapeutic exercises until it subsides. Please reference the exercise progression sheet for timelines and use the following precautions during your treatments. Thank you for progressing all patients appropriately. Successful treatment requires a team approach, and the PT/PTA/ATC is a critical part of the team! Please contact AHI at any time with your input on how to improve the therapy protocol. Please send therapy progress notes and renewal therapy prescription requests with the patient or by fax to (630) 323-5625. Notes by fax must be sent 3 days prior to the patient’s visit to internally process this request. -
The Limping Child Future of Pediatrics June 15, 2016
The Limping Child Future of Pediatrics June 15, 2016 Benjamin D. Martin Division of Orthopaedic Surgery The Limping Child • DDX • Normal Gait • Abnormal Gait Patterns • Common causes 2 HOW OLD IS THE CHILD? IS THE CHILD IN PAIN? PAINLESS PAINFUL Coxa vara Perthes DDH SCFE Leg length difference Discoid meniscus Cerebral palsy Transient synovitis Muscular dystrophy Septic arthritis Osteomyelitis JRA DON’T FORGET TO LOOK AT HIP FOR KNEE PAIN!! Toddler Child Adolescent (1-3) (4-10) (11-15) Transient synovitis Transient synovitis SCFE Septic Arthritis Septic Arthritis Dysplasia Toddler’s fx Perthes Tarsal coalition CP Leg length difference DDH Coxa vara JRA Normal Gait Efficient ?? Gait Analysis Toddler vs. Mature Gait step time cadence walking velocity COMMON GAIT PATTERNS Abnormal Gait Patterns • Antalgic • Trendeleburg • Proximal weakness • Spastic • Short limb Antalgic Gait Antalgic gait = shorten stance phase (amount of time affected limp on the ground) PAINFUL quick, soft steps Trendelenburg Gait Lever Arm Trendelenburg gait = body leans over weak abductors NOT PAINFUL* * Trendelenburg + pain = coxalgic gait Proximal Weakness Gait Weak hamstrings = lordosis Weak abductors = Trendelenburg 1st symptom might be toe walking! Spastic Gait Gross Motor & Functional Classification Delayed walkers? Short Limb Gait • Oblique pelvis • ASIS to medial malleolus • Femur vs. tibia vs. both 15 COMMON CONDITIONS Toxic Synovitis vs. Septic Arthritis Toxic Synovitis Septic Arthritis • 4 – 10 yo • Refusal to bear weight • NOT ALLOW MOTION • Hip pain, limp • Fevers (>38.5°) • Recent illness (URI) • WBC (>12K) • ESR (>40) • Low grade temps • CRP (>2) • Slightly elevated labs • Hematogenous spread • Aspirate • NSAIDs – Gram Stain, WBC>50K • Symptoms 1-2 weeks • Surgical emergency!! MOTRIN CHALLENGE ULTRASOUND (both have effusion) ASPIRATION Osteomyelitis subperiosteal abscess - Bone infection - Hematogenous - S. -
Gait Abnormalities in Functional Problems of the Lower Extremities and in Neurological Diseases
48 Review articles GAIT ABNORMALITIES IN FUNCTIONAL PROBLEMS OF THE LOWER EXTREMITIES AND IN NEUROLOGICAL DISEASES M. Becheva, PhD Medical University- Plovdiv, Medical College, Bulgaria, 120Buxton Bros. 4004 Plovdiv Abstract: Gait is a complex, automated and stereotyped motor activity that allows for movement of the body in an upright position. The investigation of gait is an integral part of the pathokinesiological study of the functional problems in any of the segments of the lower limbs. As the stereotype of walking changes at departure, stopping, turning, walking alongside another one, gait should be examined in different situations. In functional problems of the lower limbs and in some neurological diseases, the follow- ing abnormal gaits are detected: arthrogenic gait in extensional contractures of the hip or knee, walking in flexion contractures, "Gluteus maximus" gait, "Gluteus medius"gait, ataxic gait, hemiparetic (hemiplegic) gait, gait in parkinsonism, gait in paresis of plantar flexor, lameness in spasm of m. psoas major, gait in insufficiency of m. quadriceps femo- ris, gait in shortening of a lower limb, steppage gait and scissor gait. Adjusting abnormal gait is especially important to improve the functional condition of the patients in view of procuring a better quality of life. Keywords: abnormal gait, functional problems, neurological diseases. Introduction ground and allows the body to move forward. Gait is a complex stereotyped and auto- Gait is a conscious and volitional motor activity mated motor activity, which allows for move- [3]. ment of the body in an upright position. It 3. A complex coordination action during consists of several components: body movements, to maintain the center of grav- 1. -
The Clinical Neurophysiology Primer Rutkove Edited By
Blum The Clinical Neurophysiology Primer Rutkove Edited by Andrew S. Blum, MD, PhD The Clinical NeurophysiologyThe Clinical Primer Comprehensive Epilepsy Program, Department of Neurology, Rhode Island Hospital, Brown Medical School, Providence, RI NeurophysiologyThe Clinical Primer and TheThe Seward B. Rutkove, MD Department of Neurology, Beth Israel Deaconess Medical Center, Boston, MA The Clinical Neurophysiology Primer presents a broad yet focused treatment of central topics in the field of clinical Clinical neurophysiology. This volume was inspired by the clinical neurophysiology lecture series at Beth Israel Deaconess Medical Clinical Center and Rhode Island Hospital, where faculty and trainees at these renowned teaching hospitals participate in a lecture series over the course of the academic year. Much like the lecture series, The Clinical Neurophysiology Primer is designed to acquaint trainees with the essential elements of clinical neurophysiology. Each chapter in this four-part volume is written by leading and respected clinical neurophysiologists. Part I presents introduc- tory considerations such as basic electronics, basic CNS physiology, and volume conduction for clinical neurophysiology. Parts NeurophysiologyNeurophysiology II and III attend to all aspects of electroencephalography (EEG) and electromyography (EMG), respectively. In Part IV, topics in fields related to clinical neurophysiology are emphasized, including autonomic testing, evoked potentials, sleep studies, and their applications. Fellows engaged in neurophysiology -
Clinical Gait Analysis Biomechanics & Etiology of Common Walking Disorders
Clinical Gait Analysis Biomechanics & Etiology of Common Walking Disorders Jessica Rose, Ph.D. Assistant Professor, Department of Orthopaedic Surgery Stanford University School of Medicine Motion & Gait Analysis Lab Lucile Packard Children’s Hospital Teaching Points • Phases of the Gait Cycle • Primary Muscle Actions during Gait • Common Gait Disorders 1 Motion Analysis at Stanford Edweard Muybridge & Leland Stanford 1878 Periods 2 Muscle Activity During Gait 3 Toe Walking Diplegic Cerebral Palsy 4 3 Foot & Ankle Rockers Rose J & Gamble JG, Editors. Human Walking 3rd Ed, 2006 5 Calf Muscle Weakness No Fixed Ankle or Heel Rise Spastic Cerebral Palsy Swing Phase Peak knee flexion in initial swing Ankle dorsiflexion to achieve foot clearance 6 Gait Analysis •Video •Kinematics and Kinetics •Dynamic EMG •Postural Balance •Energy Expenditure Musculoskeletal Computer Models of Gait 7 Diplegic Cerebral Palsy Diplegic Cerebral Palsy 8 Kinematics & Kinetics •Kinematics: 3-D Joint Motion 8 Digital Motion Capture Cameras Record Position of Light Reflective Markers • Kinetics: Forces Passing Through the Joints Force Plate Embedded in the Floor Records Ground Reaction Force Vectors Kinematics • Nearly normal hip motion • Increased knee flexion at IC and stance • Reduced peak knee flexion in swing • Increased plantar flexion in terminal stance • Internally rotated foot progression 9 Kinetics Kinetics • Normal ankle plantarflexor moment peaks in terminal stance • Increased plantar flexor moment in loading response “double bump” associated with increased -
Differentiating Hip Pathology from Lumbar Spine Pathology: Key Points of Evaluation and Management
Instructional Course Lecture Differentiating Hip Pathology From Lumbar Spine Pathology: Key Points of Evaluation and Management Abstract Aaron J. Buckland, MBBS, The diagnosis and treatment of patients who have both hip and lumbar FRACS spine pathologies may be a challenge because overlapping Ryan Miyamoto, MD symptoms may delay a correct diagnosis and appropriate treatment. Rakesh D. Patel, MD Common complaints of patients who have both hip and lumbar spine pathologies include low back pain with associated buttock, groin, James Slover, MS, MD thigh, and, possibly, knee pain. A thorough patient history should be Afshin E. Razi, MD obtained and a complete physical examination should be performed in these patients to identify the primary source of pain. Plain and advanced imaging studies and diagnostic injections can be used to further delineate the primary pathology and guide the appropriate sequence of treatment. Both the surgeon and the patient should understand that, although one pathology is managed, the management of the other pathology may be necessary because of persistent pain. The recognition of both entities may help reduce the likelihood of misdiagnosis, and the management of both entities in the appropriate sequence may help reduce the likelihood of persistent symptoms. ip and lumbar spine patholo- symptoms is clear despite coexistent Hgies often occur in combina- hip and lumbar spine pathologies. In tion, which may result in substantial patients with complex hip-spine syn- disability.1-3 Patients with both hip drome, however, no clear source of and lumbar spine pathology com- symptoms is known despite a detailed monly have low back pain (LBP) physical examination. -
Pelvic Support Hip Reconstruction with Internal Devices: an Alternative
ORIGINAL ARTICLE Pelvic Support Hip Reconstruction with Internal Devices: An Alternative to Ilizarov Hip Reconstruction Sreenivasulu Metikala1, Binu T Kurian2, Sanjeev S Madan3, James A Fernandes4 ABSTRACT Aim and objective: Ilizarov hip reconstruction (IHR) is a traditional method of salvaging chronic adolescent problem hips but faces practical issues from external fixators leading to reduced compliance. We present the same reconstruction procedure using only internal devices with a modification in the technique and review early results. Materials and methods: We retrospectively evaluated eight patients between 2014 and 2017 with chronic painful hips treated by two-stage reconstruction; stage I included femoral head resection and pelvic support osteotomy using double plating, whereas stage II comprised distal femoral osteotomy avoiding varus followed by the insertion of a retrograde magnetic nail for postoperative lengthening. Patients continued physiotherapy postoperatively while protecting from early weight-bearing. Results: At a mean follow-up of 19 months (range, 6−36), all osteotomies healed with a bone healing index of 47 days/cm (range, 30−72). Pain improved from 8.3 (range, 7−9) to 2 (range, 0−6) while the limb length discrepancy got corrected from 4.3 cm (range, 3−5) to 1.4 cm (range, 0−2.5) at the final follow-up. Trendelenburg sign was eliminated in three patients and delayed in five patients. No examples of infection or permanent knee stiffness were noted. One patient had plate breakage due to mechanical fall, and another patient had 35 mm of lateral mechanical axis deviation (MAD) requiring corrective osteotomy. Conclusion: Pelvic support hip reconstruction with exclusive internal devices is a technique in evolution with encouraging early results.