Billing and Coding Guidelines for INJ-018 Botulinum Toxin Type A
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Management of Microtropia
Br J Ophthalmol: first published as 10.1136/bjo.58.3.281 on 1 March 1974. Downloaded from Brit. J. Ophthal. (I974) 58, 28 I Management of microtropia J. LANG Zirich, Switzerland Microtropia or microstrabismus may be briefly described as a manifest strabismus of less than 50 with harmonious anomalous correspondence. Three forms can be distinguished: primary constant, primary decompensating, and secondary. There are three situations in which the ophthalmologist may be confronted with micro- tropia: (i) Amblyopia without strabismus; (2) Hereditary and familial strabismus; (3) Residual strabismus after surgery. This may be called secondary microtropia, for everyone will admit that in most cases of convergent strabismus perfect parallelism and bifoveal fixation are not achieved even after expert treatment. Microtropia and similar conditions were not mentioned by such well-known early copyright. practitioners as Javal, Worth, Duane, and Bielschowsky. The views of Maddox (i898), that very small angles were extremely rare, and that the natural tendency to fusion was much too strong to allow small angles to exist, appear to be typical. The first to mention small residual angles was Pugh (I936), who wrote: "A patient with monocular squint who has been trained to have equal vision in each eye and full stereoscopic vision with good amplitude of fusion may in 3 months relapse into a slight deviation http://bjo.bmj.com/ in the weaker eye and the vision retrogresses". Similar observations of small residual angles have been made by Swan, Kirschberg, Jampolsky, Gittoes-Davis, Cashell, Lyle, Broadman, and Gortz. There has been much discussion in both the British Orthoptic Journal and the American Orthoptic journal on the cause of this condition and ways of avoiding it. -
Detrusor Sphincter Dyssynergia: a Review of Physiology, Diagnosis, and Treatment Strategies
Review Article Detrusor sphincter dyssynergia: a review of physiology, diagnosis, and treatment strategies John T. Stoffel Department of Urology, University of Michigan, Ann Arbor, MI, USA Correspondence to: John T. Stoffel, MD. Department of Urology, University of Michigan, Ann Arbor, MI, USA. Email: [email protected]. Abstract: Detrusor sphincter dyssynergia (DSD) is the urodynamic description of bladder outlet obstruction from detrusor muscle contraction with concomitant involuntary urethral sphincter activation. DSD is associated with neurologic conditions such as spinal cord injury, multiple sclerosis, and spina bifida and some of these neurogenic bladder patients with DSD may be at risk for autonomic dysreflexia, recurrent urinary tract infections, or upper tract compromise if the condition is not followed and treated appropriately. It is diagnosed most commonly during the voiding phase of urodynamic studies using EMG recordings and voiding cystourethrograms, although urethral pressure monitoring could also potentially be used. DSD can be sub-classified as either continuous or intermittent, although adoption of this terminology is not widespread. There are few validated oral pharmacologic treatment options for this condition but transurethral botulinum toxin injection have shown temporary efficacy in reducing bladder outlet obstruction. Urinary sphincterotomy has also demonstrated reproducible long term benefits in several studies, but the morbidity associated with this procedure can be high. Keywords: Detrusor sphincter dyssynergia (DSD); neurogenic bladder; urodynamics; external urinary sphincter (EUS) Submitted Nov 30, 2015. Accepted for publication Jan 05, 2016. doi: 10.3978/j.issn.2223-4683.2016.01.08 View this article at: http://dx.doi.org/10.3978/j.issn.2223-4683.2016.01.08 Introduction Physiology The human bladder has two functions—to store and During storage of urine, afferent nerves carry information empty urine. -
Acute Cerebellar Ataxia Associated with Intermittent ECG Pattern Similar to Wellens Syndrome and Transient Prominent QRS Anterior Forces
Acute cerebellar ataxia associated with intermittent ECG pattern similar to Wellens syndrome and transient prominent QRS anterior forces Andrés Ricardo Pérez-Riera, MD, PhD. Post-Graduates Advisor at Design of Studies and Scientific Writing Laboratory in the ABC Faculty of Medicine - ABC Foundation - Santo André – São Paulo – Brazil Raimundo Barbosa-Barros, MD. Specialist in Cardiology by the Brazilian Society of Cardiology (SBC) Specialist in Intensive Care by the Sociedade Brasileira de Terapia Intensiva Chief of the Coronary Center of the Hospital de Messejana Dr. Carlos Alberto Studart Gomes. Fortaleza - Brazil Adrian Baranchuk, MD FACC FRCPC Associate Professor of Medicine and Physiology - Cardiac Electrophysiology and Pacing - Director, EP Training Program - Kingston General Hospital - FAPC 3, 76 Stuart Street K7L 2V7, Kingston ON Queen's University - Canada Male patient, 56 years old, white, uncontrolled hypertension, was admitted to our emergency department (ED) with reports of sudden dizziness, headache of abrupt onset, nausea, vomiting and weakness in the lower limbs. Physical examination drew attention to the presence of manifestations suggestive of cerebellar syndrome: impaired coordination in the trunk or arms and legs, inability to coordinate balance, gait, extremity, uncontrolled or repetitive eye movements, (nystagmus), dyssynergia, dysmetria, dysdiadochokinesia, dysarthria (cerebellar ataxia). Normal myocardial necrosis markers and normal electrolytes ECO 1: anteroseptal-apical akinesis; LVEF = 30% ECO 2 (third day): -
Neurogenic Bowel Dysfunction in Patients with Multiple Sclerosis Open Access to Scientific and Medical Research DOI
Journal name: Degenerative Neurological and Neuromuscular Disease Article Designation: Review Year: 2018 Volume: 8 Degenerative Neurological and Neuromuscular Disease Dovepress Running head verso: Preziosi et al Running head recto: Neurogenic bowel dysfunction in patients with multiple sclerosis open access to scientific and medical research DOI: http://dx.doi.org/10.2147/DNND.S138835 Open Access Full Text Article REVIEW Neurogenic bowel dysfunction in patients with multiple sclerosis: prevalence, impact, and management strategies Giuseppe Preziosi Abstract: Bowel dysfunction in patients with multiple sclerosis (MS) is highly prevalent. Ayeshah Gordon-Dixon Constipation and fecal incontinence can coexist and alternate, impacting on the patient’s quality Anton Emmanuel of life and social interactions, as well as burdening the caregivers. The cost for the health care providers is also significant, with increased number of hospital admissions, treatment-related Gastro-Intestinal Physiology Unit, University College London Hospital, costs, and hospital appointments. The origin is multifactorial, and includes alteration of neu- London, UK rological pathways, polypharmacy, behavioral elements, and ability to access the toilet. Every patient with MS should be sensitively questioned about bowel function, and red flag symptoms should prompt adequate investigations. Manipulation of life style factors and establishment of a bowel regime should be attempted in the first place, and if this fails, other measures such For personal use only. as biofeedback and transanal irrigation should be included. A stoma can improve quality of life, and is not necessarily a last-ditch option. Antegrade colonic enemas can also be an effec- tive option, whilst neuromodulation has not proved its role yet. Effective treatment of bowel dysfunction improves quality of life, reduces incidence of urinary tract infection, and reduces health care costs. -
Pediatric Ophthalmology/Strabismus 2017-2019
Academy MOC Essentials® Practicing Ophthalmologists Curriculum 2017–2019 Pediatric Ophthalmology/Strabismus *** Pediatric Ophthalmology/Strabismus 2 © AAO 2017-2019 Practicing Ophthalmologists Curriculum Disclaimer and Limitation of Liability As a service to its members and American Board of Ophthalmology (ABO) diplomates, the American Academy of Ophthalmology has developed the Practicing Ophthalmologists Curriculum (POC) as a tool for members to prepare for the Maintenance of Certification (MOC) -related examinations. The Academy provides this material for educational purposes only. The POC should not be deemed inclusive of all proper methods of care or exclusive of other methods of care reasonably directed at obtaining the best results. The physician must make the ultimate judgment about the propriety of the care of a particular patient in light of all the circumstances presented by that patient. The Academy specifically disclaims any and all liability for injury or other damages of any kind, from negligence or otherwise, for any and all claims that may arise out of the use of any information contained herein. References to certain drugs, instruments, and other products in the POC are made for illustrative purposes only and are not intended to constitute an endorsement of such. Such material may include information on applications that are not considered community standard, that reflect indications not included in approved FDA labeling, or that are approved for use only in restricted research settings. The FDA has stated that it is the responsibility of the physician to determine the FDA status of each drug or device he or she wishes to use, and to use them with appropriate patient consent in compliance with applicable law. -
Approach to a Patient with Hemiplegia and Monoplegia
CHAPTER Approach to a Patient with Hemiplegia and Monoplegia 27 Sudhir Kumar, Subhash Kaul INTRODUCTION 4. Injury to multiple cervical nerve roots. Monoplegia and hemiplegia are common neurological 5. Functional or psychogenic. symptoms in patients presenting to the emergency department as well as outpatient department. Insidious onset, gradually progressive monoplegia affecting lower limb can be caused by the following Monoplegia refers to weakness of one limb (either arm or conditions: leg) and hemiplegia refers to weakness of one arm and leg on the same side of body (either left or right side). 1. Tumor of the contralateral frontal lobe. There are a variety of underlying causes for monoplegia 2. Tumor of spinal cord at thoracic or lumbar level. and hemiplegia. The causes differ in different age groups. 3. Chronic infection of brain (frontal lobe) or spinal The causes also differ depending on the onset, progression cord (thoracic or lumbar level), such as tuberculous. and duration of weakness. Therefore, one needs to adopt a systematic approach during history taking and 4. Lumbosacral-plexopathy, due to diabetes mellitus. examination in order to arrive at the correct diagnosis. Insidious onset, gradually progressive monoplegia, Appropriate investigations after these would confirm the affecting upper limb, can be caused by one of the following diagnosis. conditions: The aim of this chapter is to systematically look at the 1. Tumor of the contralateral parietal lobe. differential diagnosis of monoplegia and hemiplegia and outline the approach needed to pinpoint the exact 2. Compressive lesion (tumor, large disc, etc) in underlying cause. cervical cord region. 3. Chronic infection of the brain (parietal lobe) or APPROACH TO THE DIAGNOSIS OF MONOPLEGIA spinal cord (cervical region), such as tuberculous. -
Approved and Unapproved Abbreviations and Symbols For
Facility: Illinois College of Optometry and Illinois Eye Institute Policy: Approved And Unapproved Abbreviations and Symbols for Medical Records Manual: Information Management Effective: January 1999 Revised: March 2009 (M.Butz) Review Dates: March 2003 (V.Conrad) March 2008 (M.Butz) APPROVED AND UNAPPROVED ABBREVIATIONS AND SYMBOLS FOR MEDICAL RECORDS PURPOSE: To establish a database of acceptable ocular and medical abbreviations for patient medical records. To list the abbreviations that are NOT approved for use in patient medical records. POLICY: Following is the list of abbreviations that are NOT approved – never to be used – for use in patient medical records, all orders, and all medication-related documentation that is either hand-written (including free-text computer entry) or pre-printed: DO NOT USE POTENTIAL PROBLEM USE INSTEAD U (unit) Mistaken for “0” (zero), the Write “unit” number “4”, or “cc” IU (international unit) Mistaken for “IV” (intravenous) Write “international unit” or the number 10 (ten). Q.D., QD, q.d., qd (daily) Mistaken for each other Write “daily” Q.O.D., QOD, q.o.d., qod Period after the Q mistaken for Write (“every other day”) (every other day) “I” and the “O” mistaken for “I” Trailing zero (X.0 mg) ** Decimal point is missed. Write X mg Lack of leading zero (.X mg) Decimal point is missed. Write 0.X mg MS Can mean morphine sulfate or Write “morphine sulfate” or magnesium sulfate “magnesium sulfate” MSO4 and MgSO4 Confused for one another Write “morphine sulfate” or “magnesium sulfate” ** Exception: A trailing zero may be used only where required to demonstrate the level of precision of the value being reported, such as for laboratory results, imaging studies that report size of lesions, or catheter/tube sizes. -
Myelopathy—Paresis and Paralysis in Cats
Myelopathy—Paresis and Paralysis in Cats (Disorder of the Spinal Cord Leading to Weakness and Paralysis in Cats) Basics OVERVIEW • “Myelopathy”—any disorder or disease affecting the spinal cord; a myelopathy can cause weakness or partial paralysis (known as “paresis”) or complete loss of voluntary movements (known as “paralysis”) • Paresis or paralysis may affect all four limbs (known as “tetraparesis” or “tetraplegia,” respectively), may affect only the rear legs (known as “paraparesis” or “paraplegia,” respectively), the front and rear leg on the same side (known as “hemiparesis” or “hemiplegia,” respectively) or only one limb (known as “monoparesis” or “monoplegia,” respectively) • Paresis and paralysis also can be caused by disorders of the nerves and/or muscles to the legs (known as “peripheral neuromuscular disorders”) • The spine is composed of multiple bones with disks (intervertebral disks) located in between adjacent bones (vertebrae); the disks act as shock absorbers and allow movement of the spine; the vertebrae are named according to their location—cervical vertebrae are located in the neck and are numbered as cervical vertebrae one through seven or C1–C7; thoracic vertebrae are located from the area of the shoulders to the end of the ribs and are numbered as thoracic vertebrae one through thirteen or T1–T13; lumbar vertebrae start at the end of the ribs and continue to the pelvis and are numbered as lumbar vertebrae one through seven or L1–L7; the remaining vertebrae are the sacral and coccygeal (tail) vertebrae • The brain -
Absence of Neurobehavioral Disturbance in a Focal Lesion of the Left Paracentral Lobule
Behavioural Neurology (1992), 5,189-191 ICASE REPORTI Absence of neurobehavioral disturbance in a focal lesion of the left paracentral lobule T. Imamura and K. Tsuburaya Department of Neurology, Tohoku Kohseinenkin Hospital, Sendai, Japan Correspondence to: T. Imamura, Department of Neurology, Institute of Brain Diseases, Tohoku University School of Medicine, 1-1, Seiryo-machi, Aoba-Ku, Sendai 980, Japan The case of a right-handed woman with an infarcation confined to the left paracentral lobule and sparing the supplementary motor area (SMA) is reported. She presented with a right leg monoplegia and displayed no mutism. The absence of any associ ated neurobehavioral disturbances (mutism, forced grasping, reduced spontaneous arm activity or aphasia raises the possi bility that the left SMA has discrete neurobehavioral functions. Keywords: Medial frontal lobe - Precentral gyrus - Supplementary motor area - Transcortical motor aphasia INTRODUCTION Various kinds of neurobehavioral disturbances associated medial part of the left precentral gyrus, which is adjacent with left medial frontal lesions involving the supplemen to the SMA, to evaluate its possible neurobehavioral tary motor area (SMA) have been reported. Aphasia due to functions. damage of the left medial frontal lobe is characterized by an initial period of mutism followed by a stage of CASE REPORT decreased verbal output and spontaneous initiation with normal articulation (Stuss and Benson, 1986). Forced A 73-year-old right-handed woman with a history of grasping, compulsive manipulation of tools and decreased hypertension and diabetes mellitus suddenly developed a spontaneous limb movements have also been described gait disturbance. On examination, 24 h later, she was alert (Wise, 1984; Feinberg et al., 1992). -
ICD9 & ICD10 Neuromuscular Codes
ICD-9-CM and ICD-10-CM NEUROMUSCULAR DIAGNOSIS CODES ICD-9-CM ICD-10-CM Focal Neuropathy Mononeuropathy G56.00 Carpal tunnel syndrome, unspecified Carpal tunnel syndrome 354.00 G56.00 upper limb Other lesions of median nerve, Other median nerve lesion 354.10 G56.10 unspecified upper limb Lesion of ulnar nerve, unspecified Lesion of ulnar nerve 354.20 G56.20 upper limb Lesion of radial nerve, unspecified Lesion of radial nerve 354.30 G56.30 upper limb Lesion of sciatic nerve, unspecified Sciatic nerve lesion (Piriformis syndrome) 355.00 G57.00 lower limb Meralgia paresthetica, unspecified Meralgia paresthetica 355.10 G57.10 lower limb Lesion of lateral popiteal nerve, Peroneal nerve (lesion of lateral popiteal nerve) 355.30 G57.30 unspecified lower limb Tarsal tunnel syndrome, unspecified Tarsal tunnel syndrome 355.50 G57.50 lower limb Plexus Brachial plexus lesion 353.00 Brachial plexus disorders G54.0 Brachial neuralgia (or radiculitis NOS) 723.40 Radiculopathy, cervical region M54.12 Radiculopathy, cervicothoracic region M54.13 Thoracic outlet syndrome (Thoracic root Thoracic root disorders, not elsewhere 353.00 G54.3 lesions, not elsewhere classified) classified Lumbosacral plexus lesion 353.10 Lumbosacral plexus disorders G54.1 Neuralgic amyotrophy 353.50 Neuralgic amyotrophy G54.5 Root Cervical radiculopathy (Intervertebral disc Cervical disc disorder with myelopathy, 722.71 M50.00 disorder with myelopathy, cervical region) unspecified cervical region Lumbosacral root lesions (Degeneration of Other intervertebral disc degeneration, -
Abadie's Sign Abadie's Sign Is the Absence Or Diminution of Pain Sensation When Exerting Deep Pressure on the Achilles Tendo
A.qxd 9/29/05 04:02 PM Page 1 A Abadie’s Sign Abadie’s sign is the absence or diminution of pain sensation when exerting deep pressure on the Achilles tendon by squeezing. This is a frequent finding in the tabes dorsalis variant of neurosyphilis (i.e., with dorsal column disease). Cross References Argyll Robertson pupil Abdominal Paradox - see PARADOXICAL BREATHING Abdominal Reflexes Both superficial and deep abdominal reflexes are described, of which the superficial (cutaneous) reflexes are the more commonly tested in clinical practice. A wooden stick or pin is used to scratch the abdomi- nal wall, from the flank to the midline, parallel to the line of the der- matomal strips, in upper (supraumbilical), middle (umbilical), and lower (infraumbilical) areas. The maneuver is best performed at the end of expiration when the abdominal muscles are relaxed, since the reflexes may be lost with muscle tensing; to avoid this, patients should lie supine with their arms by their sides. Superficial abdominal reflexes are lost in a number of circum- stances: normal old age obesity after abdominal surgery after multiple pregnancies in acute abdominal disorders (Rosenbach’s sign). However, absence of all superficial abdominal reflexes may be of localizing value for corticospinal pathway damage (upper motor neu- rone lesions) above T6. Lesions at or below T10 lead to selective loss of the lower reflexes with the upper and middle reflexes intact, in which case Beevor’s sign may also be present. All abdominal reflexes are preserved with lesions below T12. Abdominal reflexes are said to be lost early in multiple sclerosis, but late in motor neurone disease, an observation of possible clinical use, particularly when differentiating the primary lateral sclerosis vari- ant of motor neurone disease from multiple sclerosis. -
Autosomal Dominant Cerebellar Ataxia Type I: a Review of the Phenotypic and Genotypic Characteristics
Whaley et al. Orphanet Journal of Rare Diseases 2011, 6:33 http://www.ojrd.com/content/6/1/33 REVIEW Open Access Autosomal dominant cerebellar ataxia type I: A review of the phenotypic and genotypic characteristics Nathaniel Robb Whaley1,2, Shinsuke Fujioka2 and Zbigniew K Wszolek2* Abstract Type I autosomal dominant cerebellar ataxia (ADCA) is a type of spinocerebellar ataxia (SCA) characterized by ataxia with other neurological signs, including oculomotor disturbances, cognitive deficits, pyramidal and extrapyramidal dysfunction, bulbar, spinal and peripheral nervous system involvement. The global prevalence of this disease is not known. The most common type I ADCA is SCA3 followed by SCA2, SCA1, and SCA8, in descending order. Founder effects no doubt contribute to the variable prevalence between populations. Onset is usually in adulthood but cases of presentation in childhood have been reported. Clinical features vary depending on the SCA subtype but by definition include ataxia associated with other neurological manifestations. The clinical spectrum ranges from pure cerebellar signs to constellations including spinal cord and peripheral nerve disease, cognitive impairment, cerebellar or supranuclear ophthalmologic signs, psychiatric problems, and seizures. Cerebellar ataxia can affect virtually any body part causing movement abnormalities. Gait, truncal, and limb ataxia are often the most obvious cerebellar findings though nystagmus, saccadic abnormalities, and dysarthria are usually associated. To date, 21 subtypes have been identified: SCA1-SCA4, SCA8, SCA10, SCA12-SCA14, SCA15/16, SCA17-SCA23, SCA25, SCA27, SCA28 and dentatorubral pallidoluysian atrophy (DRPLA). Type I ADCA can be further divided based on the proposed pathogenetic mechanism into 3 subclasses: subclass 1 includes type I ADCA caused by CAG repeat expansions such as SCA1-SCA3, SCA17, and DRPLA, subclass 2 includes trinucleotide repeat expansions that fall outside of the protein-coding regions of the disease gene including SCA8, SCA10 and SCA12.