Atlas of Emergency Medicine 5th

Edition Kevin J. Knoop

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 DEDICATION

The authors dedicate this work to Dr. Corey Slovis, long-time mentor,
teacher, and friend. For Emergency Medicine, he is iconic and his
impact immeasurable. Dr. Slovis has led and taught thousands of
emergency care providers and is one of the greatest educators we
know. Through his teachings we have learned how high-quality
education is essential for medical knowledge and clinical expertise.
His “5 Causes, 5 Steps, 5 Reasons” for almost everything in medicine
has resonated worldwide. As “El Jefe” retires, we offer our gratitude
and deep appreciation for his service to our specialty and to Edition
5 of The Atlas of Emergency Medicine. Our patients have been and
will be the ultimate beneficiaries of his magnificent career.
“Giddy Up”

KJK
LBS
ABS
RJT
 CONTENTS

Videos
To access the collection of videos that accompany the text, please
scan the QR code below or visit www.ematlas.com

Foreword
Preface
Acknowledgments
Contributors
Media Credits

Part 1 REGIONAL ANATOMY

Chapter 1
HEAD AND FACIAL TRAUMA
Christopher L. Stark

SCALP LACERATION
DEPRESSED SKULL FRACTURE
FRONTAL SINUS FRACTURE
BASILAR SKULL FRACTURE
HERNIATION SYNDROMES
NASAL INJURIES
ZYGOMA FRACTURES
LEFORT FACIAL FRACTURES
ORBITAL WALL FRACTURES
TRAUMATIC EXOPHTHALMOS
MANDIBULAR FRACTURES
EXTERNAL EAR INJURIES
FACIAL NERVE INJURY
PENETRATING FACIAL TRAUMA

Chapter 2
OPHTHALMIC CONDITIONS
Manpreet Singh ■ Denise Whitfield

PALLOR/ANEMIA
OSTEOGENESIS IMPERFECTA
CONJUNCTIVAL ICTERUS
NEONATAL CONJUNCTIVITIS (OPHTHALMIA NEONATORUM)
BACTERIAL CONJUNCTIVITIS
VIRAL CONJUNCTIVITIS
ALLERGIC CONJUNCTIVITIS
IRRITANT/CHEMICAL CONJUNCTIVITIS
DACRYOCYSTITIS
DACRYOADENITIS
PTERYGIUM/PINGUECULA
CORNEAL HYDROPS
LEUKOCORIA/CATARACT
HORDEOLUM/CHALAZION
SCLERITIS
EPISCLERITIS
ACUTE ANGLE-CLOSURE GLAUCOMA
ANTERIOR UVEITIS (IRITIS)
ENDOPHTHALMITIS
SYMPATHETIC OPHTHALMIA
ANISOCORIA
HERPES ZOSTER OPHTHALMICUS
OCULAR HERPES SIMPLEX
CORNEAL ULCER
AFFERENT PUPILLARY DEFECT
THYROID EYE DISEASE
INTERNUCLEAR OPHTHALMOPLEGIA (INO)
HORNER SYNDROME
MYASTHENIA GRAVIS
THIRD-NERVE PALSY
SIXTH-NERVE PALSY

Chapter 3
FUNDUSCOPIC FINDINGS
David Effron ■ Beverly C. Forcier ■ Richard E. Wyszynski

NORMAL FUNDUS
AGE-RELATED MACULAR DEGENERATION
EXUDATE
ROTH SPOTS
EMBOLI
CENTRAL RETINAL ARTERY OCCLUSION
CENTRAL RETINAL VEIN OCCLUSION
HYPERTENSIVE RETINOPATHY
DIABETIC RETINOPATHY
VITREOUS HEMORRHAGE
RETINAL DETACHMENT
CYTOMEGALOVIRUS RETINITIS
PAPILLEDEMA
OPTIC NEURITIS
ANTERIOR ISCHEMIC OPTIC NEUROPATHY
GLAUCOMA
SUBHYALOID HEMORRHAGE IN SUBARACHNOID HEMORRHAGE

Chapter 4
OPHTHALMIC TRAUMA
Kevin J. Knoop ■ James K. Palma

CORNEAL ABRASION
SUBCONJUNCTIVAL HEMORRHAGE
CORNEAL FOREIGN BODY/RUST RING
HYPHEMA
INTRAOCULAR FOREIGN BODY
IRIDODIALYSIS
LENS DISLOCATION
PENETRATING GLOBE INJURY
GLOBE RUPTURE
TRAUMATIC CATARACT
EYELID LACERATION
IMPALED FOREIGN BODY
CHEMICAL EXPOSURE
Chapter 5
EAR, NOSE, AND THROAT CONDITIONS
Edward C. Jauch ■ Gregory Hall ■ Kevin J. Knoop

OTITIS MEDIA
BULLOUS MYRINGITIS
CHOLESTEATOMA
EXOSTOSIS
TYMPANIC MEMBRANE PERFORATION
OTITIS EXTERNA
PREAURICULAR SINUS ABSCESS
MASTOIDITIS
AURICULAR PERICHONDRITIS
HERPES ZOSTER OTICUS (RAMSAY HUNT SYNDROME)
FACIAL NERVE PALSY
ANGIOEDEMA
PHARYNGITIS
NASAL SEPTAL CONDITIONS
NASAL CELLULITIS
DIPHTHERIA
PERITONSILLAR ABSCESS
EPIGLOTTITIS
UVULITIS
SIALOADENITIS
MUCOCELE
ACUTE SINUSITIS

Chapter 6
ORAL CONDITIONS
Edward C. Jauch ■ J. Amadeo Valdez

TOOTH SUBLUXATION
TOOTH IMPACTION (INTRUSIVE LUXATION)
TOOTH AVULSION
TOOTH FRACTURES
ALVEOLAR RIDGE FRACTURE
TEMPORAL MANDIBULAR JOINT DISLOCATION
TONGUE LACERATION
VERMILION BORDER LIP LACERATION

Odontogenic Infections
GINGIVAL ABSCESS (PERIODONTAL ABSCESS)
PERIAPICAL ABSCESS
PERICORONAL ABSCESS
HARD PALATE ABSCESS
BUCCAL SPACE ABSCESS
CANINE SPACE ABSCESS
LUDWIG ANGINA
PARAPHARYNGEAL SPACE ABSCESS

Oral Conditions
TRENCH MOUTH (ACUTE NECROTIZING ULCERATIVE GINGIVITIS)
ACID TOOTH EROSION (BULIMIA)
THRUSH (ORAL CANDIDIASIS)
ORAL HERPES SIMPLEX VIRUS (COLD SORES)
APHTHOUS ULCERS (CANKER SORES)
STRAWBERRY TONGUE
BLACK HAIRY TONGUE
ORAL EXOSTOSES
GINGIVAL HYPERPLASIA
ORAL MALIGNANCIES
EXTRAVASCULAR (HEMORRHAGIC) ORAL LESIONS
METHAMPHETAMINE-INDUCED CARIES
ORAL CAVITY PIERCING COMPLICATIONS

Chapter 7
CHEST AND ABDOMEN
Kevin S. Barlotta ■ Lawrence B. Stack ■ Kevin J. Knoop

Chest and Abdominal Trauma

TRAUMATIC ASPHYXIA
FLAIL CHEST
LUNG HERNIATION
STERNOCLAVICULAR DISLOCATION
CLAVICLE FRACTURE
TENSION PNEUMOTHORAX WITH NEEDLE THORACENTESIS
CARDIAC TAMPONADE WITH PERICARDIOCENTESIS
EMERGENCY DEPARTMENT THORACOTOMY
SEAT BELT INJURY
GREY TURNER SIGN AND CULLEN SIGN
IMPALED FOREIGN BODY
ABDOMINAL EVISCERATION
TRAUMATIC ABDOMINAL HERNIA
PELVIC FRACTURE

Nontraumatic Chest and Abdominal Conditions

RESPIRATORY RETRACTIONS
SUPERIOR VENA CAVA SYNDROME
SUPRACLAVICULAR ADENOPATHY
JUGULOVENOUS DISTENSION
CAPUT MEDUSAE
ABDOMINAL HERNIAS
UMBILICAL HERNIA
PATENT URACHAL DUCT
SISTER MARY JOSEPH NODE (NODULAR UMBILICUS)
ABDOMINAL DISTENSION
ABDOMINAL WALL HEMATOMA
PECTUS DEFORMITIES
STOMA PROLAPSE
PRUNE BELLY (EAGLE-BARRETT) SYNDROME
STERNOCLAVICULAR JOINT SEPTIC ARTHRITIS
BREAST MASS

Chapter 8
UROLOGIC CONDITIONS
Sarah Moore ■ Ryan Pedigo

TESTICULAR TORSION
TORSION OF A TESTICULAR OR EPIDIDYMAL APPENDIX
ACUTE EPIDIDYMITIS
ORCHITIS
HYDROCELE
PYOCELE
TESTICULAR TUMOR
SCROTAL ABSCESS
FOURNIER GANGRENE
PARAPHIMOSIS
PRIAPISM
URETHRAL RUPTURE
FRACTURE OF THE PENIS
PENILE TOURNIQUET
STRADDLE INJURY
BALANOPOSTHITIS
PENILE ZIPPER INJURY
VARICOCELE
PENILE IMPLANT COMPLICATIONS

Chapter 9
SEXUALLY TRANSMITTED INFECTIONS AND
ANORECTAL CONDITIONS
Suzanne Dooley-Hash ■ Nicholas W.C. Herrman

SYPHILIS
GONORRHEA
CHLAMYDIA
GENITAL HERPES
LYMPHOGRANULOMA VENEREUM
CHANCROID
CONDYLOMA ACUMINATA (GENITAL WARTS)
PEDICULOSIS PUBIS
ANAL FISSURE
ANORECTAL ABSCESS
HEMORRHOIDS
RECTAL PROLAPSE
PILONIDAL ABSCESS
RECTAL FOREIGN BODY
RECTAL CANCER

Chapter 10
GYNECOLOGIC AND OBSTETRIC CONDITIONS
Suzanne Dooley-Hash ■ Kevin J. Knoop

Gynecologic Conditions
VAGINITIS
CERVICAL POLYPS
BARTHOLIN GLAND ABSCESS
SPONTANEOUS ABORTION
GENITAL TRAUMA AND SEXUAL ASSAULT
VULVAR HEMATOMA
LICHEN SCLEROSUS
LICHEN PLANUS
CERVICAL CANCER
VULVAR CANCER
URETHRAL PROLAPSE
UTERINE PROLAPSE
CYSTOCELE
RECTOCELE
IMPERFORATE HYMEN

Obstetric Conditions
ECTOPIC PREGNANCY
MOLAR PREGNANCY (HYDATIDIFORM MOLE)
FAILED INTRAUTERINE PREGNANCY
THIRD-TRIMESTER BLUNT ABDOMINAL TRAUMA
Emergency Vaginal Delivery
EMERGENCY DELIVERY: NORMAL VERTEX DELIVERY SEQUENCE
BREECH DELIVERY
UMBILICAL CORD PROLAPSE IN EMERGENCY DELIVERY
SHOULDER DYSTOCIA IN EMERGENCY DELIVERY
POSTPARTUM PERINEAL LACERATIONS
INTRAUTERINE FETAL DEMISE
POSTOPERATIVE COMPLICATIONS OF CESAREAN SECTION

Chapter 11
EXTREMITY TRAUMA
Meghan Breed ■ Robert Warne Fitch

ACROMIOCLAVICULAR JOINT SEPARATION

SHOULDER DISLOCATION
ELBOW FRACTURES
ELBOW DISLOCATION
BICEPS TENDON RUPTURE
FOREARM FRACTURES
FRACTURES OF THE DISTAL RADIUS
CARPAL AND CARPOMETACARPAL DISLOCATIONS
SCAPHOID FRACTURE
CLENCHED FIST INJURY (FIGHT BITE)
BOXER’S FRACTURE
PERIPHERAL NERVE INJURY
BENNETT AND ROLANDO FRACTURES
BOUTONNIÈRE AND SWAN-NECK DEFORMITIES
GAMEKEEPER’S THUMB (SKIER’S THUMB)
PHALANGEAL DISLOCATIONS
MALLET FINGER AND JERSEY FINGER
COMPARTMENT SYNDROME
HIGH-PRESSURE INJECTION INJURY
SUBUNGUAL HEMATOMA
HIP DISLOCATION
HIP FRACTURE
KNEE EXTENSOR INJURIES
PATELLAR DISLOCATIONS
KNEE DISLOCATION
FEMUR FRACTURE
TIBIAL-FIBULAR FRACTURES
FRACTURE BLISTERS
ACHILLES TENDON RUPTURE
ANKLE DISLOCATION
ANKLE FRACTURE
ANKLE SPRAIN
CALCANEUS FRACTURE
FRACTURES OF THE FIFTH METATARSAL BASE
LISFRANC FRACTURE-DISLOCATION
AMPUTATIONS

Chapter 12
EXTREMITY CONDITIONS
Kathryn Ritter ■ Robert Warne Fitch

CELLULITIS
FELON
GANGRENE
GAS GANGRENE (MYONECROSIS)
NECROTIZING FASCIITIS
INGROWN TOENAIL (ONYCHOCRYPTOSIS)
LYMPHANGITIS
LYMPHEDEMA
OLECRANON AND PREPATELLAR BURSITIS
PALMAR SPACE INFECTION
TENOSYNOVITIS
THROMBOPHLEBITIS
PARONYCHIA
SUBCLAVIAN VEIN THROMBOSIS
CERVICAL RADICULOPATHY
DIGITAL CLUBBING
PHLEGMASIA DOLENS
DEEP VENOUS THROMBOSIS
DUPUYTREN CONTRACTURE
ACHILLES TENDONITIS
GANGLION (SYNOVIAL) CYST
RAYNAUD DISEASE
ARTERIAL EMBOLUS
MOREL-LAVALLÉE LESION
CONTRAST EXTRAVASATION
LEGG-CALVÉ-PERTHES DISEASE
SLIPPED CAPITAL FEMORAL EPIPHYSIS

Chapter 13
CUTANEOUS CONDITIONS
J. Matthew Hardin

STEVENS-JOHNSON SYNDROME/TOXIC EPIDERMAL NECROLYSIS

ERYTHEMA MULTIFORME
DRUG ERUPTIONS
FIXED DRUG ERUPTION
AUTOIMMUNE BULLOUS DISEASES
IMMUNE THROMBOCYTOPENIA
THROMBOTIC THROMBOCYTOPENIC PURPURA
INFECTIVE ENDOCARDITIS
ERYSIPELAS
ERYTHEMA MIGRANS
ROCKY MOUNTAIN SPOTTED FEVER
DISSEMINATED GONOCOCCUS
ECTHYMA GANGRENOSUM
NONGENITAL HERPES SIMPLEX INFECTIONS
HERPES ZOSTER
SCABIES
HIDRADENITIS SUPPURATIVA
DISSECTING CELLULITIS OF THE SCALP
LIVEDO RETICULARIS
CUTANEOUS SMALL-VESSEL VASCULITIS
SWEET SYNDROME
PYODERMA GANGRENOSUM
ERYTHEMA NODOSUM
SQUAMOUS CELL CARCINOMA
BASAL CELL CARCINOMA
MELANOMA
URTICARIA AND DERMATOGRAPHISM
ALLERGIC CONTACT DERMATITIS
ATOPIC DERMATITIS
NUMMULAR/XEROTIC ECZEMA
DYSHIDROTIC ECZEMA
ID REACTION (DISSEMINATED ECZEMA)
LIP LICKER’S DERMATITIS
DERMATOPHYTE INFECTIONS
TINEA (PITYRIASIS) VERSICOLOR
ONYCHOMYCOSIS
INTERTRIGO
HOT TUB FOLLICULITIS/PSEUDOMONAS HOT-FOOT SYNDROME
PYOGENIC GRANULOMA
SEBORRHEIC DERMATITIS
PSORIASIS
PITYRIASIS ROSEA
STASIS DERMATITIS
UREMIC FROST
JAUNDICE
PORPHYRIA CUTANEA TARDA
VITILIGO
MELASMA
ABDOMINAL STRIAE (STRIAE ATROPHICAE)

Part 2 SPECIALTY AREAS

Chapter 14
PEDIATRIC CONDITIONS
Ashish Shah ■ Brad Sobolewski ■ Matthew R. Mittiga

Newborn Conditions
ERYTHEMA TOXICUM NEONATORUM
SALMON PATCHES (NEVUS SIMPLEX)
NEONATAL JAUNDICE
NEONATAL MILK PRODUCTION (WITCH’S MILK)
NEONATAL MASTITIS
UMBILICAL GRANULOMA
HYPERTROPHIC PYLORIC STENOSIS
INTESTINAL MALROTATION WITH VOLVULUS

Rashes and Lesions

ERYTHEMA INFECTIOSUM (FIFTH DISEASE)
ROSEOLA INFANTUM (EXANTHEM SUBITUM)
IMPETIGO
MEASLES
VARICELLA (CHICKENPOX)
HERPES ZOSTER
HAND, FOOT, AND MOUTH SYNDROME
COLD PANNICULITIS (POPSICLE PANNICULITIS)
HERPETIC GINGIVOSTOMATITIS
MENINGOCOCCEMIA
SUMMER PENILE SYNDROME
STAPHYLOCOCCAL SCALDED SKIN SYNDROME
SCARLET FEVER (SCARLATINA)
BLISTERING DISTAL DACTYLITIS
HENOCH-SCHÖNLEIN PURPURA (IGA VASCULITIS)
SERUM SICKNESS–LIKE REACTION
SUPERFICIAL (STRAWBERRY) HEMANGIOMA
ORBITAL AND PRESEPTAL (PERIORBITAL) CELLULITIS
BRANCHIAL CLEFT CYST
THYROGLOSSAL DUCT CYST
CYSTIC HYGROMA
CAT-SCRATCH DISEASE

General Conditions
EPIGLOTTITIS
RETROPHARYNGEAL ABSCESS
BUTTON (DISK) BATTERY INGESTION
NASAL FOREIGN BODY
MEMBRANOUS (BACTERIAL) TRACHEITIS
DACTYLITIS (HAND-FOOT SYNDROME)
HAIR TOURNIQUET
FAILURE TO THRIVE
NURSING BOTTLE CARIES
NURSEMAID’S ELBOW (RADIAL HEAD SUBLUXATION)
ILEOCOLIC INTUSSUSCEPTION
HYDROCELE OF THE TESTIS
INGUINAL HERNIA
PINWORM INFECTION (ENTEROBIASIS)
LICE
ORAL FRENULUM TEAR
OCULOGYRIC CRISIS
SETTING-SUN PHENOMENON (SUNDOWNING)
KAWASAKI DISEASE

Chapter 15
CHILD ABUSE
Daniel M. Lindberg ■ Antonia Chiesa ■ Angie L. Miller

Physical Abuse
EXTERNAL FINDINGS
ABUSIVE HEAD TRAUMA
SKELETAL FINDINGS
VISCERAL FINDINGS

Sexual Abuse
CHILD SEXUAL ABUSE EXAM AND GENITAL FINDINGS
INJURIES AND FINDINGS INDICATIVE OF GENITAL OR ANAL
TRAUMA, ABUSE, OR INFECTION
MIMICS OF ABUSE: ACCIDENTAL TRAUMA
MIMICS OF ABUSE: MEDICAL CONDITIONS

Chapter 16
ENVIRONMENTAL CONDITIONS
Ken Zafren ■ R. Jason Thurman ■ Ian D. Jones

HIGH-ALTITUDE PULMONARY EDEMA

HIGH-ALTITUDE RETINAL HEMORRHAGE
HIGH-ALTITUDE CEREBRAL EDEMA
HYPOTHERMIA
FROSTBITE
PERNIO
IMMERSION INJURY (TRENCH FOOT)
ULTRAVIOLET RADIATION EXPOSURE
LIGHTNING INJURIES
LARGE TERRESTRIAL ANIMAL ATTACKS
CORAL SNAKE ENVENOMATION
PIT VIPER ENVENOMATION
TROPICAL SNAKE ENVENOMATIONS
GILA MONSTER ENVENOMATION
BLACK WIDOW SPIDER ENVENOMATION
BROWN RECLUSE SPIDER ENVENOMATION
SCORPION ENVENOMATION
TICKS
HYMENOPTERA ENVENOMATION
CATERPILLAR, MITE, AND CENTIPEDE ENVENOMATION
SKEETER SYNDROME
MIDDLE EAR SQUEEZE
MASK SQUEEZE
STINGRAY ENVENOMATION
SEA URCHIN ENVENOMATION
COELENTERATE ENVENOMATION
MARINE DERMATITIS
SCORPIONFISH STING
CONE SNAIL ENVENOMATION
SEA SNAKE ENVENOMATION
CEPHALOPOD ENVENOMATION
ERYSIPELOID
TOXICODENDRON AND OTHER PLANT EXPOSURES
SPOROTRICHOSIS

Chapter 17
TOXICOLOGICAL CONDITIONS
Saralyn R. Williams ■ R. Jason Thurman

AMPHETAMINE TOXICITY
DESIGNER DRUGS: “BATH SALTS” AND “SPICE”
COCAINE TOXICITY
LEVAMISOLE-INDUCED VASCULITIS
ANTICHOLINERGIC (ANTIMUSCARINIC) TOXIDROME
CHOLINERGIC TOXIDROME
OPIOID TOXICITY
DESOMORPHINE (KROKODIL)
ACETAMINOPHEN POISONING
SALICYLATE POISONING
TOXIC ALCOHOL INGESTION
TRICYCLIC ANTIDEPRESSANT POISONING
POISONING BY β-BLOCKER AND CALCIUM CHANNEL BLOCKER
AGENTS
INHALANT ABUSE
METHEMOGLOBINEMIA
CELLULAR ASPHYXIANTS
VANCOMYCIN-INDUCED RED MAN SYNDROME
BOTULISM
ANTICOAGULANTS
CAUSTIC INGESTION
HYDROFLUORIC ACID BURNS
ARSENIC POISONING
IRON POISONING
LEAD POISONING
MERCURY POISONING
MUSHROOM INGESTION
CARDIAC GLYCOSIDE PLANT INGESTION
HOUSEPLANTS WITH CALCIUM OXALATE CRYSTALS
PLANTS WITH BELLADONNA ALKALOIDS
PEYOTE INGESTION
TOXALBUMIN INGESTION
POKEWEED
Chapter 18
WOUNDS AND SOFT-TISSUE INJURIES
Chan W. Park ■ Michael L. Juliano ■ Dana Woodhall

WOUND CLEANING AND IRRIGATION

WOUND ASSESSMENT
WOUND FOREIGN BODIES
TRAUMATIC WOUNDS
EAR LACERATIONS
LIP LACERATIONS
TENDON LACERATIONS
ANIMAL BITE WOUNDS
FISHHOOK INJURIES
SIMPLE WOUND CLOSURES
COMPLEX WOUND CLOSURES
WOUND CARE COMPLICATIONS
BURNS
ELECTRICAL INJURY
DECUBITUS ULCERS

Chapter 19
CLINICAL FORENSIC MEDICINE
William S. Smock ■ Lawrence B. Stack

GUNSHOT WOUNDS

Pattern Injuries of Domestic Violence, Assault, and

Abuse
SHARP-FORCE-PATTERN INJURIES
BLUNT-FORCE PATTERN INJURIES
STRANGULATION INJURIES
THERMAL-PATTERN INJURIES

Chapter 20
HIV CONDITIONS
Stephen P. Raffanti ■ Anna K. Person

PRIMARY HIV INFECTION

IMMUNE RECONSTITUTION INFLAMMATORY SYNDROME (IRIS)
ORAL HAIRY LEUKOPLAKIA
CANDIDIASIS ASSOCIATED WITH HIV
KAPOSI SARCOMA
TOXOPLASMA GONDII INFECTION
PNEUMOCYSTIS
CRYPTOCOCCAL INFECTIONS
HISTOPLASMOSIS
CYTOMEGALOVIRUS INFECTIONS
HERPES ZOSTER
EOSINOPHILIC FOLLICULITIS
HERPES SIMPLEX VIRUS
SCABIES
MOLLUSCUM CONTAGIOSUM
DERMATOPHYTE (TINEA) INFECTIONS
THROMBOCYTOPENIA
DRUG REACTIONS
ACUTE NECROTIZING ULCERATIVE GINGIVITIS

Chapter 21
TROPICAL MEDICINE
Shannon M. Langston ■ Brian D. Bales
FREE-LIVING AMEBA INFECTION
ANEMIA IN THE TROPICS
ANTHRAX
ASCARIASIS
CHAGAS DISEASE
CHOLERA
CUTANEOUS LARVA MIGRANS
CYSTICERCOSIS
DENGUE FEVER
DRACUNCULIASIS
ELEPHANTIASIS
EPIDEMIC MENINGITIS
GOITER
HYDATID CYST
LEECH BITES
LEISHMANIASIS
LEPROSY
LEPTOSPIROSIS
MALARIA
MUMPS
MYCETOMA
MYIASIS
NONTUBERCULOSIS MYCOBACTERIA INFECTIONS
PROTEIN-ENERGY MALNUTRITION—KWASHIORKOR AND
MARASMUS
RABIES
SCHISTOSOMIASIS
TETANUS
TRACHOMA
TRADITIONAL MEDICINE IN THE TROPICS
TROPICAL SPOROTRICHOSIS
TUBERCULOSIS
TUNGIASIS
ZIKA VIRUS

Chapter 22
AIRWAY
Steven J. White ■ Kevin High ■ Lawrence B. Stack ■ Richard M. Levitan

AIRWAY MAXIM ONE

AIRWAY MAXIM TWO
AIRWAY MAXIM THREE
AIRWAY MAXIM FOUR
AIRWAY MAXIM FIVE
LARYNGOSCOPIC OROTRACHEAL INTUBATION
OROPHARYNX AND AIRWAY DECONTAMINATION STRATEGIES
BOUGIE-ASSISTED INTUBATION
VIDEO-ASSISTED INTUBATION—STORZ C-MAC
VIDEO-ASSISTED INTUBATION—McGRATH MAC EDL
LARYNGEAL MASK AIRWAY (LMA)
DIGITAL (TACTILE) INTUBATION
INTUBATING LARYNGEAL AIRWAY (ILA)
KING LARYNGEAL TUBE
NASAL FLEXIBLE FIBEROPTIC INTUBATION
CRICOTHYROTOMY (SELDINGER TECHNIQUE)
SCALPEL-FINGER-BOUGIE CRICOTHYROTOMY
Chapter 23
ECG ABNORMALITIES
Maite A. Huis in ‘t Veld ■ Amal Mattu ■ R. Jason Thurman

Part 1: ST-T Abnormalities

ACUTE ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION
ACUTE ANTERIOR MYOCARDIAL INFARCTION
ACUTE INFERIOR MYOCARDIAL INFARCTION
ACUTE RIGHT VENTRICULAR MYOCARDIAL INFARCTION
ACUTE POSTERIOR MYOCARDIAL INFARCTION
LEFT MAIN LESION
SGARBOSSA CRITERIA FOR AMI IN SETTING OF LBBB
SUBENDOCARDIAL ISCHEMIA
HYPERACUTE T WAVES
WELLENS WAVES
EARLY REPOLARIZATION
LEFT VENTRICULAR ANEURYSM
ACUTE PERICARDITIS

Part 2: Conduction Disturbances

FIRST-DEGREE AV BLOCK
TYPE 1 SECOND-DEGREE AV BLOCK (MOBITZ I, WENCKEBACH)
TYPE 2 SECOND-DEGREE AV BLOCK (MOBITZ II)
THIRD-DEGREE (COMPLETE) AV BLOCK
QT INTERVAL ABNORMALITIES
RIGHT BUNDLE BRANCH BLOCK
LEFT BUNDLE BRANCH BLOCK
LEFT ANTERIOR FASCICULAR BLOCK
LEFT POSTERIOR FASCICULAR BLOCK
TRIFASCICULAR BLOCK
ASHMAN PHENOMENON

Part 3: Rhythm Disturbances

JUNCTIONAL ESCAPE RHYTHM
VENTRICULAR ESCAPE RHYTHM
PACED RHYTHM
ATRIAL FIBRILLATION
ATRIAL FLUTTER
MULTIFOCAL ATRIAL TACHYCARDIA
SUPRAVENTRICULAR TACHYCARDIA (SVT)
SVT WITH ABERRANCY
VENTRICULAR TACHYCARDIA
VENTRICULAR FLUTTER
POLYMORPHIC VENTRICULAR TACHYCARDIA
VENTRICULAR FIBRILLATION

Part 4: Structural Abnormalities

DEXTROCARDIA
LEFT VENTRICULAR HYPERTROPHY
RIGHT VENTRICULAR HYPERTROPHY
LEFT ATRIAL HYPERTROPHY
RIGHT ATRIAL HYPERTROPHY
HYPERTROPHIC CARDIOMYOPATHY
BRUGADA SYNDROME
WOLFF-PARKINSON-WHITE SYNDROME

Part 5: ECG Abnormalities of Noncardiac Origin

HYPOTHERMIA
“CEREBRAL” T WAVES
HYPERKALEMIA
HYPOKALEMIA
PULMONARY EMBOLISM
PERICARDIAL EFFUSION
DIGOXIN EFFECT, TOXICITY
TRICYCLIC ANTIDEPRESSANT EFFECT
LIMB LEAD REVERSAL
LOW VOLTAGE

Chapter 24
EMERGENCY ULTRASOUND
Jeremy S. Boyd ■ Myles Melton ■ Jordan D. Rupp ■ Robinson M. Ferre

EMERGENCY ULTRASOUND: INTRODUCTION

TRAUMA ULTRASOUND
PERICARDIAL (SUBXIPHOID VIEW)
RIGHT UPPER QUADRANT (MORISON’S POUCH)
LEFT UPPER QUADRANT (PERISPLENIC VIEW)
SUPRAPUBIC
THORAX (RIGHT AND LEFT)
CARDIAC ULTRASOUND
SUBXIPHOID CARDIAC (SUBCOSTAL VIEW)
PARASTERNAL LONG-AXIS VIEW (PSLA)
PARASTERNAL SHORT-AXIS VIEW (PSSA)
APICAL FOUR-CHAMBER VIEW (AP4)
SUBXIPHOID LONG-AXIS (IVC)
LUNG ULTRASOUND
ABDOMINAL AORTA ULTRASOUND
DEEP VENOUS THROMBOSIS ULTRASOUND
ULTRASOUND-GUIDED RESUSCITATION
GALLBLADDER ULTRASOUND
RENAL AND BLADDER ULTRASOUND
PREGNANCY ULTRASOUND
PROCEDURAL GUIDANCE: ULTRASOUND-GUIDED VENOUS ACCESS
PROCEDURAL GUIDANCE: ULTRASOUND-GUIDED NERVE BLOCKS
PROCEDURAL GUIDANCE: THORACENTESIS/PARACENTESIS
OCULAR ULTRASOUND
SOFT-TISSUE ULTRASOUND

Chapter 25
MICROSCOPIC FINDINGS AND BODILY FLUIDS
Camiron L. Pfennig ■ B. Ethan Brown

URINALYSIS
SYNOVIAL FLUID ANALYSIS
GRAM STAIN
DARK-FIELD EXAMINATION FOR TREPONEMA PALLIDUM
VAGINAL FLUID WET MOUNT
POTASSIUM HYDROXIDE MOUNT FOR CANDIDA ALBICANS
STOOL EXAMINATION FOR FECAL LEUKOCYTES
SKIN SCRAPING FOR DERMATOSES AND INFESTATIONS
CEREBROSPINAL FLUID EXAMINATION—INDIA INK PREPARATION
FOR CRYPTOCOCCUS NEOFORMANS
WRIGHT STAIN—THIN SMEAR FOR MALARIA
FERNING PATTERN FOR AMNIOTIC FLUID
PERIPHERAL BLOOD SMEAR
TAPE TEST FOR ENTEROBIUS VERMICULARIS EGGS
TZANCK PREPARATION FOR HERPES INFECTION
ACID-FAST STAIN FOR MYCOBACTERIUM

Bodily Fluids
STOOL
EMESIS
SPUTUM
URINE
SYNOVIAL FLUID
CEREBRAL SPINAL FLUID
PERITONEAL FLUID
BLOOD

Chapter 26
RHEUMATOLOGIC CONDITIONS
Timothy Bongartz ■ Jodi A. Dingle

GOUT
SYSTEMIC LUPUS ERYTHEMATOSUS
INFLAMMATORY MYOPATHIES
SMALL-VESSEL VASCULITIS AND PURPURA
RHEUMATOID ARTHRITIS
SEPTIC ARTHRITIS
JUVENILE IDIOPATHIC ARTHRITIS
ACUTE RHEUMATIC FEVER
GIANT CELL ARTERITIS

Chapter 27
MENTAL HEALTH CONDITIONS
Brian D. Bales ■ Max Hensel
TRICHOTILLOMANIA
SKIN PICKING DISORDER (NEUROTIC EXCORIATIONS)
SELF-HARM BEHAVIOR (NONSUICIDAL AND SUICIDAL SELF-HARM)
SUBSTANCE USE DISORDERS
ALCOHOL USE DISORDER
NICOTINE USE DISORDER
EATING DISORDERS
DELUSIONAL INFESTATION

INDEX
 FOREWORD

Despite the expanding use of electronic media in current medical

education, The Atlas of Emergency Medicine remains an essential
textbook for any clinician’s library. What makes The Atlas of
Emergency Medicine so invaluable is its ability to comprehensively
capture all of emergency medicine in a timeless way with high-
quality figures, artwork, and videos.
Anyone who evaluates patients or who needs to see what a
disease or clinical finding looks like will find the complete teacher in
this atlas. Medical students, residents in training, educators, and
clinicians will all greatly benefit from using this book. Although its
primary audience are those of us in emergency medicine, the depth
and breadth of the atlas will also be of significant value to residents
and practicing physicians in other specialties, along with those in
nursing, emergency medical services, and allied health. Anyone who
wants to review the classic findings of a disease that might present
to the emergency department or see subtle differences between two
related entities will find them here.
This newest edition expands on its long-standing reputation as
the definitive atlas in emergency care by adding chapters on mental
health conditions and rheumatologic disorders and by expanding its
presentation of microscopic findings and the analysis of body fluids,
along with significantly increasing the number of high-quality videos,
figures, and photographs. The Atlas of Emergency Medicine
continues its long history of being the single most authoritative
collection of clinical images, illustrations, ultrasounds, radiographs,
and electrocardiograms encountered in the emergency department.
I view this book as indispensable in learning and practicing
emergency medicine.
 Corey M. Slovis, MD
Professor of Emergency Medicine and Medicine
Vanderbilt University Medical Center
Nashville, Tennessee
 PREFACE

“He who studies medicine without books sails an uncharted sea, but
he who studies medicine without patients does not go to sea at all.”
William Osler

We have a passion for improving patient care. Our journey with The
Atlas of Emergency Medicine began with superb mentors who
instilled in us a drive to become excellent clinician educators. We
discovered imaging was a powerful tool to take the learner “to the
bedside” in a fashion unlike any other didactic technique. In 1994,
much by chance, collegial networking brought three, then later four,
of us together to pursue an aggressive goal of producing the most
comprehensive source of high-quality emergency care images
available. While there were some initial detractors, our first four
editions received widespread praise, have been translated into
multiple foreign languages, and have been reproduced in alternative
electronic media. We are humbled and honored to present our fifth
iteration.
Emergency care is defined by time and space. The emergency
department is by far the most diverse melting pot of acute
conditions in the hospital. Diagnostic accuracy, risk stratification, and
treatment rely heavily on visual clues. We desire to maximize this
practitioner skill for the benefit of our patients. We also strongly
believe the visual experience, while sometimes downplayed within
the hectic and time-pressured environment of modern medicine, is
critical to education. Images can teach faster and with greater
impact than many pages of text or hours of lecture.
 We continue our pursuit of these goals with a substantially
updated, expanded, and improved fifth edition of The Atlas of
Emergency Medicine. Nearly all our changes and additions come
from reader suggestions and criticisms as well as superb guidance
from our editors at McGraw Hill. All are received with sincere
gratitude.
We have reduced text to essential information to allow for more
images and increasing depth. After extensive review and critique,
new and replacement images and video have been added. While
there have been radical changes in the way we access medical
knowledge over the past two decades, an image in any form
maintains a potent means to teach and learn. New chapters include
Rheumatologic Conditions and Mental Health Conditions.
The audience for this text is all who provide emergency care,
including clinicians, educators, residents, nurses, prehospital
caregivers, medical technicians, and medical students. Many have
also found it extremely useful as a review for written board
examinations containing pictorial questions. Other healthcare
workers, such as internists, family physicians, pediatricians, nurse
practitioners, and physician assistants, will find the Atlas a useful
guide in identifying and treating acute conditions, where visual clues
significantly guide, improve, and expedite diagnosis as well as
treatment.
We thank the many contributors, readers, and editors who have
helped make this edition possible. Lastly, and most importantly, we
express our deepest gratitude to our patients who were willing to be
a “great case” in the Atlas, thus ultimately paving the way for
improved emergency care.

Kevin J. Knoop, md, ms

Lawrence B. Stack, md
Alan B. Storrow, md
R. Jason Thurman, md
 ACKNOWLEDGMENTS

Special thanks to the McGraw Hill editorial team for their superb
guidance and execution of this edition. In particular, Amanda
Fielding, Senior Editor, who got us started, Kay Conerly, Senior
Editor, whose wealth of experience guided us, Christie Naglieri,
Senior Project Development Editor, who kept us all on track with an
aggressive production schedule, and Sarika Gupta, Production
Manager, Cenveo publishing services who was very flexible and
responsive to the smallest request or detail. Additionally, Becky
Hainz-Baxter permissions coordinator for McGraw Hill went above
and beyond and was invaluable in untangling permission issues. An
atlas of this scope and complexity simply would not have reached
such a high level of quality without their efforts.

On a personal level, the editors would like to gratefully acknowledge:

Our patients, for being such willing teachers; Dr. Tomisaku Kawasaki,
a special colleague, for his passion and generosity; MJ, Mimi and
Stephen, for their unending love and inspiration.
KJK

The patients and their families who have allowed us to photograph

their examination findings for the benefit of caring for others, I pray
God’s grace and blessings on you.
LBS

Father Steve Roberts and Jim O’Dowd. Thank you for being part of
my journey.
 ABS

Lauren, Kate, and Ben—the cornerstones of my life. My colleagues

and friends who have been so incredibly supportive at Skyline. My
lifelong friends—the incomparable CHP, especially our beloved
brother Trent (“AXE”) who is sorely missed. All the residents over the
years who have allowed me to share in their journeys—it is an honor
to have learned with you.
RJT
 CONTRIBUTORS

Brian D. Bales, MD
Assistant Professor of Emergency Medicine
Department of Emergency Medicine
Vanderbilt University Medical Center
Nashville, Tennessee
Chapters 21 and 27

Kevin S. Barlotta, MD, FAAEM, FACEP

Associate Professor of Emergency Medicine
Medical Director
Critical Care Transport University of Alabama
Birmingham, Alabama
Chapter 7

Timothy Bongartz, MD
Associate Professor of Emergency Medicine
Vanderbilt University Medical Center
Nashville, Tennessee
Chapter 26

Jeremy S. Boyd, MD, FACEP

Assistant Professor of Emergency Medicine
Division Director, Emergency Ultrasound
Vanderbilt University
Nashville, Tennessee
Chapter 24

Meghan Breed, MD
PGY-3 Resident in Emergency Medicine
Vanderbilt University Medical Center
Nashville, Tennessee
Chapter 11

B. Ethan Brown, MD
Emergency Medicine
Resident Prisma Health–Upstate
University of South Carolina School of Medicine
Greenville Greenville, South Carolina
Chapter 25

Antonia Chiesa, MD
Associate Professor of Pediatrics
The Kempe Center for the Prevention & Treatment of Child Abuse &
Neglect
Children’s Hospital Colorado
The University of Colorado School of Medicine
Aurora, Colorado
Chapter 15

Jodi A. Dingle, MD
Pediatric Rheumatology Fellow
Monroe Carrel Jr. Children’s Hospital at Vanderbilt
Nashville, Tennessee
Chapter 26

Suzanne Dooley-Hash, MD
Another random document with
no related content on Scribd:
current, and it should be used in the way that will produce the
greatest amount of excitation in the cutaneous end-organs. This is
best done by applying the faradic current to the dry skin with the
metallic brush, or by allowing the cathode of the galvanic current to
rest upon it for some time.

The PROGNOSIS in peripheral anæsthesia is in the main favorable, but

it must, of course, depend much on the gravity of the lesion causing
it, as mechanical injury, pressure, neuritis, cold, etc. Rheumatic
anæsthesia, the result of exposure to cold, is in general readily
recovered from. Vaso-motor anæsthesia yields in most cases without
difficulty to treatment. Washerwoman's anæsthesia and allied cases
are intractable, and often resist the patient and well-conducted
application of remedies.

As a concrete picture of peripheral anæsthesia we will give a

description of anæsthesia of the fifth nerve—the rather that in its
consideration we meet with some of the most interesting and
important complications occurring in connection with paralysis of
sensitive nerves. The fifth nerve may have either of its three
branches separately affected, giving rise to anæsthesia limited to the
distribution of that branch, or all of its fibres may be simultaneously
involved, giving rise to complete anæsthesia of the nerve. In the
latter case the lesion of the nerve in all likelihood exists at some
point of its course between the apparent origin from the pons and the
ganglion of Gasser, which rests upon the apex of the petrous portion
of the temporal bone. Beyond this point the nerve divides into its
three branches. Amongst the causes of trigeminal anæsthesia are
injuries, tumors, syphilitic thickening of the dura mater, neuritis, etc.,
affecting the nerve within the cranial cavity. In complete anæsthesia
of the fifth nerve the parts implicated are the skin of the forehead to
the vertex, the nose, the lips, and chin up to the median line, the
cheek and temporal region, including the anterior portion of the ear,
the conjunctiva, the mucous membrane of the nose, the mucous
membrane of the mouth, and partly of the fauces of the same side.
The tongue is deprived not only of common sensation on the
affected side in its anterior two-thirds, but the sense of taste is also
lost over the same region, by reason that the fibres of the chorda
tympani, the nerve of taste for this region of the tongue, are derived
from the fifth nerve. If the whole thickness of the nerve-trunk is
involved, including the small motor root, there is, in connection with
the anæsthesia, paralysis of the muscles of mastication on the side
affected, which may be distinguished by the want of hardening of the
masseter when the jaws are forcibly brought together, and by the
thrusting of the chin over to the paralyzed side when the mouth is
widely opened, caused by the want of action of the external
pterygoid muscle, which allows the condyle on the paralyzed side to
remain in the glenoid fossa, while the condyle of the opposite side is
pulled forward upon the articular eminence by the sound pterygoid.
The face is of a dusky or livid color, and cooler than natural. Ulcers
of a stubborn character in the mucous membrane of the cheek may
be caused by the patient unconsciously biting the insensitive parts.
An inflammation of the conjunctiva is frequently set up, which may
extend to the cornea, causing ulceration, perforation,
panophthalmitis, and destruction of the eye (ophthalmia neuro-
paralytica). This has been regarded by some as caused by trophic
changes in the tissues, the direct result of irritation or destruction of
trophic fibres connected with the ganglion of Gasser. Experiments
made upon animals, however, seem to show that the inflammation of
the eye depends upon the irritation caused by the intrusion of foreign
bodies, which, owing to the loss of sensation, are not appreciated,
and which from loss of reflex action are not removed by winking nor
washed away by an increased lachrymal secretion, as in the healthy
eye. It may be that although the latter is the true explanation of the
origin of the inflammation, nevertheless the tissues may have lost
their normal power of resistance to its invasion by reason of nutritive
changes consequent upon the lesion of trophic fibres running in the
trunk of the nerve. The reflexes ordinarily induced by irritation of the
parts in their normal state are lost. Irritation of the conjunctiva causes
no winking of the lids nor secretion of tears, and titillation of the
nostrils no movements of the muscles of the face nor mucous or
lachrymal secretion. The movements of the face are less lively on
the affected side, not on account of paralysis of the muscles, but
from the loss of that constant play of reflex activity in them which
takes place in the normal condition. The loss of the reflexes
distinguishes peripheral trigeminal anæsthesia from that of cerebral
origin, in which they may still be excited by irritating the anæsthesic
surfaces. In trigeminal anæsthesia, which sometimes occurs from
the effect of cold upon the surface of the face, the mucous surfaces
are not affected.

The SYMPTOMS and DIAGNOSIS of peripheral paralysis having been

already given under the heads of Injuries of Nerves and Neuritis, a
consideration of the distribution of any motor nerve will enable us to
anticipate the distinguishing features of the paralysis dependent
upon it. With each the picture will be modified according to the
position of the muscles paralyzed and the motor functions destroyed.
It now remains to give the symptoms, diagnosis, and treatment of the
paralysis of an individual motor nerve, which may serve as an
example and paradigm, in the consideration of which points of
interest and instruction may be touched upon applicable to all other
cases.

Peripheral Paralysis of the Facial Nerve (Bell's Paralysis).

Of all the peripheral paralyses, probably that of the seventh is the

one we are most frequently called upon to treat and the symptoms of
which are the most complex and interesting. The frequency of its
paralysis is due to the length and peculiarity of its course, enclosed
as it is in a bony canal which permits no increase of its volume
without compression, the run of its terminal branches through parts
liable to inflammation and disease (parotid gland), and their final
distribution to parts exposed to all vicissitudes of heat and cold and
in constant danger of mechanical injury. The complexity and interest
of the symptoms of its paralysis depend in a great measure upon the
intimate connections it forms at different points of its course with the
fibres of other nerves of entirely different functions (acoustic and
fifth).
The seventh nerve is liable not only to intercranial compression from
tumors, inflammation of the meninges, syphilitic processes, etc., but
its long course through the petrous portion of the temporal bone
renders it liable to injury from fracture or caries, and its close
proximity to the middle ear causes it often to suffer from the
diseased conditions of the bony walls or mucous lining membrane of
that chamber, its paralysis being not infrequently the result of simple
aural catarrh. After the exit of the nerve from the stylo-mastoid
foramen it is imbedded in the parotid gland, and sometimes suffers
from compression produced by an inflammation or abscess in that
organ or by enlarged lymphatic glands in the neighborhood. Surgical
operations, so often demanded for disease of the bones or soft parts
of the face, may necessitate the lesion of its trunk or branches. The
exposed position of this nerve is sometimes the occasion of its injury
at the very outset of the life of the individual, when the application of
the forceps to the head has been resorted to in delivery. But the
most frequent cause of facial paralysis appears to be the exposure
of one side of the face directly to cold—as sleeping in a draught of
air, sitting at the open window of a railroad coach, etc. Here the
causal connection appears evident from the rapidity with which the
paralysis usually follows, although cases occur in which an interval
of hours or days elapses after the exposure before the paralysis
declares itself. Although this is usually designated rheumatic
paralysis, there is nothing to connect it with that disease, nor are
rheumatics more liable to it than others. Under such circumstances
the paralysis is probably brought about by the occurrence of a
neuritis of the nerve-trunk, which is compressed by the hyperæmia,
and it may be by an inflammatory exudation against the bony walls
surrounding it, until not only does it lose the power of conduction, but
its fibres undergo the degenerative process. In some cases the
neuritis thus excited by exposure to cold attacks the nerve after it
has issued from the bony canal, and then the resulting injury to the
fibres is much less grave. Although in some cases there are
prodromal symptoms, as stiffness or pain in the face, generally the
paralysis occurs suddenly, very often being first observed upon
awaking. The patient may be first made aware of the paralysis by an
inability to drink without the fluid dribbling from the affected side of
the mouth or by the overflow of tears from the eye of the same side.
When the paralysis is recent and the face in complete repose, there
may be little or no deformity to mark the condition of the muscles.
When, however, the patient speaks or the slightest emotional or
reflex movements of the face are excited, as laughing, frowning, etc.,
it becomes obvious from the bizarre grimace caused by a one-sided
contraction. After the paralysis has existed for some time the
contrast of the two sides of the face is marked. The paralyzed side is
characterized by a vacancy of expression to which the staring,
unwinking eye contributes. From loss of the tonicity of the muscles
the angle of the mouth droops, and the expressive furrows and lines
about the brow, below the eye, and beside the nose are smoothed
out and obliterated. Speech is affected, inasmuch as the paralysis of
the lip interferes with the pronunciation of the labials, and all
attempts to purse up the mouth, as in whistling, is abortive. The eye
not only remains open, the lids motionless, but there is partial
eversion of the lower lid (lagophthalmos), and the tears, no longer
directed to the punctum (paralysis of Horner's muscle), flow over the
cheek. The natural impulse to reflex winking caused by evaporation
from the conjunctiva or by the contact of particles of dust is
answered by a rolling of the eyeball upward to wipe the cornea
beneath the momentarily relaxed and drooping upper lid. Excited
respiration causes no movement of the ala of the nose on the
affected side, but in deep inspiration, in contrast to the normal
elevation of the ala, it is flattened down by the suction of the
inrushing current of air. In masticating, the cheek bulges out from
want of power in the paralyzed buccinator to press the food inward
against the opposing movements of the tongue. In persons who
have the rather unusual power of voluntarily moving the ear we may
detect the paralysis of the muscles concerned in those movements—
a useful point in diagnosis. Moreover, on the sound side of the face
the features have not entirely the natural appearance. The angle of
the mouth is drawn upward and the naso-labial line more deeply
impressed than natural. This results not from excessive contraction,
but from the muscles remaining in the position they have taken
during contraction, the antagonistic tonic traction from the opposite
side, which would have restored them to their normal position, being
wanting. This may be in a measure remedied by mechanical
appliances which will keep up an elastic pull from the paralyzed side,
or by restoring the muscles after contraction to position with the
hand. The tongue rests symmetrically in the floor of the mouth, and
is thrust out straight, although in appearance it is pushed toward the
side paralyzed—a deceptive appearance produced by the
asymmetrical position of the mouth. In some cases there is partial
paralysis of the velum palati, the half arch on the affected side
hanging lowest, and if we cause the patient to make the sound of ah
the opposite side of the palate is alone drawn upward. The uvula
may also participate in the paralysis, but the explanation of its
position, sometimes directed away from, sometimes toward, the side
of the paralysis, cannot be given. In proportion to the amount of the
paralysis of the soft palate will be the prominence of the symptoms
caused by it, such as difficulty in deglutition, a nasal tone in
speaking, and the escape of fluids through the nostril in swallowing.
The sense of hearing is often affected coincidently with facial
paralysis. Thus by reason of their close juxtaposition the same cause
may in common affect the acoustic and the facial, causing imperfect
hearing, subjective noises, etc. The hearing is frequently affected by
diseased conditions of the middle ear, which also cause a facial
paralysis. Still another defect of hearing, however, is caused by the
paralysis of the facial nerve itself. The stapedius muscle, supplied by
a branch of the facial, is the antagonist of the tensor tympani, and
when it is paralyzed the over-tense tympanic membrane vibrates
more readily to sound-waves, and a condition of uncomfortably
exaggerated sensitiveness to sounds is the result (hyperacuisis).
The rarely-occurring symptom of dryness of the mouth on the side of
the paralysis receives its explanation in the well-known fact of the
presence of secretory fibres for the salivary gland in the chorda
tympani, which are derived from the facial. We observe sometimes,
in connection with facial paralysis, that the patient complains of
certain subjective sensations of taste, as sour or metallic, and an
examination will in some cases reveal that the sense of taste is lost
on the anterior two-thirds of the tongue on the side of the paralysis.
The fibres which convey the sense of taste pass centripetally from
the tongue in the chorda tympani nerve, join the facial just within the
stylo-mastoid foramen, and continue united with it to the geniculate
ganglion of the facial, at which point they leave it to pass in the great
superficial petrosal to the spheno-palatine ganglion, and thence to
the trunk of the fifth nerve. Loss of sensation over the face only
occurs in cases where the fifth nerve has been simultaneously
affected with the facial, which may occur from exposure to cold.

It is obviously of importance in cases of facial paralysis to determine

if they are of central or peripheral origin. The most prominent
symptoms which mark a peripheral paralysis are the implication of all
the branches of the nerve, the loss of the reflexes, the development
of the degenerative reaction, and atrophy of the muscles. In facial
paralysis of cerebral origin the frontal and orbital branches are not at
all or but slightly affected, leaving the eye with its natural
appearance, in contrast to the lagophthalmos, and the open eye
which does not close even in sleep. In cerebral paralysis the reflexes
are normal and the muscles retain their natural electric reaction.
Accompanying brain symptoms assure the diagnosis. In facial
paralysis of bulbar origin the electric reactions are diminished, and
we have a complex of symptoms made up in a great measure by the
implication of neighboring nerves. After the diagnosis of a peripheral
facial paralysis has been made, by a careful consideration of the
symptoms we may with more or less accuracy determine at which
point of the nerve the lesion is situated. If there is paralysis of all the
muscles of the face, without alteration of taste or hearing, the electric
reaction of nerve and muscles normal, the nerve is affected outside
of the stylo-mastoid foramen. This is usually the form of slight
rheumatic paralysis. If we discover that the muscles of the external
ear are paralyzed, it shows that the point of lesion is just within the
stylo-mastoid foramen, where the posterior auricular branch is given
off from the facial. If with paralysis of the face there is alteration of
the sense of taste, with dryness of the mouth, without interference
with hearing, the trunk of the nerve is affected within the Fallopian
canal, involving the chorda tympani fibres below the point where the
stapedius nerve is given off. If to the above symptoms there is added
over-sensitiveness to sounds, hyperacuisis, and there is no paralysis
of the palate, we have the nerve affected still higher up, but below
the geniculate ganglion. If the geniculate ganglion is involved, there
is, in addition to the foregoing, symptoms of paralysis of the palate.
If, now, the lesion is above the geniculate ganglion, we will have
eliminated the symptom due to implication of the chorda tympani,
which leaves the trunk of the facial at the geniculate ganglion, and
the sense of taste is unaffected, while there remains paralysis of the
face, dryness of the mouth (the secretory fibres run in the trunk of
the seventh), hyperacuisis, and paralysis of the palate.

It was in facial paralysis that the first observations upon the

degenerative reaction in muscles were made, and it is in that
affection that these electric phenomena have been best studied, and
give us the clearest indications for prognosis and treatment in
peripheral paralysis generally. In rheumatic facial paralysis, the most
common form of peripheral facial paralysis, the electric reactions of
the paralyzed muscles enable us to classify the cases into three
groups, the prognosis and duration of which vary very much. In the
first group are the slight forms of facial paralysis. Here the faradic or
galvanic current, applied to nerve or muscles, causes an ordinary
contraction; the electric reactions are normal. These cases scarcely
require treatment, and recover in two or three weeks. In a second
group are those cases in which within a short time after the invasion
of the paralysis (two weeks) complete degenerative reaction is
observed. This degenerative reaction, with the accompanying
anatomical changes in nerve and muscle, has already been treated
of in this article, and it is sufficient here to say that it is marked by
total loss of electric excitability, both faradic and galvanic, in the
nerve, loss of faradic and increased galvanic excitability in the
paralyzed muscles, with a reversal of the normal reply of the
muscles to the different poles of the galvanic battery. These cases
constitute the severe form of rheumatic facial paralysis, and the
prognosis is grave, recovery takes place only after months, and even
after the lapse of years traces of the disease remain in the imperfect
action of the muscles. A third group of cases are of a gravity
intermediate between these two. In them is present the milder form
of degenerative reaction; that is, there is a diminution, but not a total
loss, of electric excitability in the nerve for both the galvanic and
faradic currents; but in the muscles there is a marked increase of
galvanic excitability, with qualitative change—i.e. greater contraction
upon application to them of the positive than of the negative pole.
These cases may be expected to recover in from four to eight
weeks, the muscles still exhibiting the degenerative reaction after
voluntary motion has returned. Among the symptoms to be
particularly noticed in the progress of the severe forms of facial
paralysis are spasmodic twitchings or spasms of the muscles on the
affected side of the face, about the angle of the mouth, and around
the eye, occurring spontaneously or when voluntary movements are
made. Also a state of tonic contraction and rigidity may develop in
some of the muscles, causing a permanent elevation of the angle of
the mouth, a narrowing of the opening of the eye, or a rigidity of the
cheek. These symptoms have been erroneously attributed to the use
of electricity in the treatment, but they occur as frequently in cases in
which it has not been employed. Traumatic facial paralysis, as from
wounds, surgical operations, use of the forceps in delivery, or
paralysis from compression of the nerve, as from tumors, syphilitic
thickening of the dura mater, etc., do not require a detailed mention
here, as such cases come under the head of nerve-injuries, already
discussed. Paralysis of both facials (diplegia facialis), in so far as it is
caused by peripheral nerve lesion, is an accidental occurrence, and
need not be considered as a separate form of facial paralysis. It is
often the result of central disease.

The TREATMENT of peripheral facial paralysis must begin with the

effort to remove its cause. If syphilis is suspected, mercury and
iodide of potassium must be freely used. If the cause is an affection
of the middle ear, this must be treated. Wounds or traumatic injuries
must receive the necessary surgical attention. In addition, in such
cases electricity must be employed in the manner presently to be
described. In cases of rheumatic facial paralysis the treatment will
vary with their gravity. In the lighter form in which the nerve is
affected outside of the Fallopian canal, recovery takes place in a
comparatively short time, even without treatment, but is hastened by
the use of the faradic or galvanic current daily along the branches of
the nerve. In the severe form we must open the treatment by an
attempt to combat the condition of inflammation—of inflammatory
exudation—which we suppose exists within the Fallopian canal.
Local blood-letting by leeching upon the mastoid process may be
appropriately used in the very first outset of the paralysis. Iodide of
potassium, given persistently in large doses during the earlier period
of the disease, appears to act beneficially independently of any
syphilitic taint. Electricity is the remedy, however, on which most
reliance is to be placed in the treatment of rheumatic facial paralysis,
and the manner of its application may be taken as a model of how it
should be employed in all cases of peripheral paralysis. The galvanic
current, on account of its power of penetrating to the deeper parts
and its catalytic action, is to be preferred for the direct electrical
treatment of the nerve which should be instituted in recent cases. Its
action is best obtained by placing the positive pole behind the ear on
the affected side, the cathode behind the opposite ear, and passing
a moderate current across the base of the skull (the affected nerve
being thus in the course of the current) for one or two minutes.
Occasionally the position of the poles may be reversed. Besides this
direct application of galvanism to the point of lesion, it is necessary
to make a peripheral application of electricity to the branches of the
nerve and to the paralyzed muscles. For this we use both the faradic
and galvanic currents. The galvanic current is used by applying the
positive pole stationary behind the ear, while the negative pole, with
an electrode of suitable size, is stroked over each branch of the
nerve and applied to each muscle, a current being used sufficiently
strong to produce decided contractions. This peripheral application
should be made once daily, the time of application being from two to
five minutes. The application of the faradic current is made by simply
placing one electrode upon an indifferent spot, and moving the other
over the face, with a current strong enough to cause contractions if
the muscles still respond to it, or if they do not of such strength as
the patient can bear without discomfort. Without doubt, one of the
beneficial effects of peripheral electrization is the reflex excitement of
the facial above the point of lesion through the irritation of the
terminations of the fifth nerve in the skin. A certain advantage
derived from it is that it maintains the tone of the paralyzed muscles,
which in the case of the orbicularis palpebrarum is of great
importance in preventing the eversion of the lower lid and the
overflow of the tears. As it is impossible during the first days
succeeding the paralysis to distinguish severe cases from those of
the middle form, it is best to begin the treatment of all cases in the
manner above described. The use of strychnia in rheumatic facial
paralysis, both internally and by hypodermic injection, may be
mentioned on account of the widespread preposession in its favor,
and to point out distinctly its utter futility.

Mechanical appliances and manipulation are used with advantage in

the treatment of facial paralysis to prevent the paralyzed muscles
about the mouth and cheek from being drawn out of place and over-
stretched by the action of the sound ones of the opposite side, thus
having their tonicity and nutrition impaired.

Contractions and rigidity of muscles receive little benefit from the use
of electricity, and must be treated by mechanical procedures, such
as stretching, massage, etc.

Neuromata.

The term neuromata was applied to all tumors involving the nerve-
trunks at a time when their histological differences had not been
studied and they were all supposed to be composed of nerve-tissue;
and even yet the name is conveniently retained, because, although
differing widely histologically, tumors situated upon the nerves have
a very similar clinical history.

Neuromas must be divided into true and false, the true consisting of
nerve-tissue, the false, or pseudo-neuromas, being composed of
many varieties, having this only in common, that they are seated
upon the nerves.

The true neuromas are again subdivided into those in which the
nerve-tissue composing them resembles exactly the fibres of the
peripheral nerves, showing with the microscope the double-
contoured white substance of Schwann surrounding an axis-cylinder,
and those in which the tumor is made up of fibres which Virchow has
shown to be non-medullated nerve-fibres—i.e. the axis-cylinder
without the white substance of Schwann. These two forms have
been distinguished by the names myelinic and non-myelinic. The
true neuromas are non-malignant, although showing the tendency to
recur after extirpation, are of slow growth, and as a rule do not
increase to a very great size. The best type of the myelinic neuromas
is found in the spherical or spindle-shaped enlargements at the cut
ends of nerves, particularly in the stumps of amputated limbs, where
they are found oftenest intimately connected with the cicatricial
tissue, though sometimes lying free. They consist of true medullated
fibres mixed with some fibrous tissue. The fibres composing them
are derived partly from splitting up and proliferation of the fibres of
the nerve itself, partly are of new formation, the appearances
strongly recalling the process of regeneration in nerves. Myelinic
neuromas consist of fibres and nuclei so closely resembling in
microscopic appearance the fibromas that they have hitherto been
confounded with them; and there is a difference among the highest
authorities as to the certainty of their diagnosis, and, in
consequence, of the frequency of their occurrence. The true
neuromas may include in their structure all of the fibres of the nerve-
trunk or only a portion of them (partial neuroma)—a fact of
importance in their symptomatology. Of the false neuromas, the
fibromas are by far the most frequently met with. They appear as
knots, more or less hard, upon the course of the nerve-trunk, which
they may involve completely or partially. They are often excessively
painful to the touch or spontaneously, most of the so-called tubercula
dolorosa belonging to the fibro-neuromas. Fibromas sometimes
occur along the trunk and branches of a nerve, forming a plexus of
knotted cords (plexiform neuroma). Fibro-sarcomas are not an
infrequent form of neuroma.

Myxomas often occur upon the peripheral nerves, and are frequently
multiple, their points of predilection being the larger trunks, as the
sciatic, ulnar, etc. They show their characteristic soft structure, and
are usually spindle-shape, assuming a rounder form as they attain a
large size. The various forms of sarcoma occasionally form tumors
upon the nerves, attacking generally the large trunks. Carcinomatous
tumors beginning upon the nerves sometimes occur, but as a rule
these growths involve the nerve by extension to it from adjacent
parts.

Syphilitic gummata have been found almost exclusively upon the

intracranial portion of the cranial nerves.

Gliomas appear to affect only the optic and acoustic nerves. Lepra
nervorum (lepra anæsthetica) produces usually a spindle-form
thickening upon the nerve-trunks, but sometimes there are more
distinct knots, which may be felt beneath the skin, bead-like, along
the course of the nerves of the extremities.

Like the true neuromas, the false neuromas, developing from the
neurilemma and perineurium, may involve the whole or only a part of
the fibres of a nerve, or the nerve-fibres may run at the side of the
tumor—different conditions, which may alter materially the effects
produced upon the nerve.

Neuromas, both false and true, may occur not only singly, but often
in large numbers, many hundreds having been counted upon an
individual. Sometimes they are numerous upon a single nerve-trunk
and its branches, and again they may appear scattered over nearly
all of the nerves of the body, even to the cauda equina and roots of
the nerves. According to Erb,9 isolated neuromas are more frequent
in females, while multiple neuromas are found almost exclusively in
men. Neuromas vary greatly in size, as we might expect from the
very great difference of their nature and structure; sometimes no
larger than a pea, they may attain the size of a child's head.
9 Ziemssen's Handbuch.

ETIOLOGY.—In cases of multiple neuromata it would seem as if there

was a constitutional condition or diathesis as the foundation of the
affection. This we may the more readily believe as there appears
good evidence to show that the tendency to the formation of these
nerve-tumors is sometimes hereditary, and some of them are
congenital.

Idiots and cretins have been observed to suffer in undue proportion

with multiple neuromas. We find a direct exciting cause of neuromas
in mechanical injuries of nerves, wounds, blows, pressure, etc. Thus,
as has been already seen, true neuromas occur in the divided ends
of the nerves after amputations or otherwise where a nerve-trunk
has been divided (cicatricial neuroma). As such neuromas are in
some degree the result of inflammation, it is probable that they may
sometimes be caused by chronic neuritis.

For a large number of neuromas no cause can be assigned, and we

must at present consider them as originating spontaneously.

SYMPTOMS.—The position and connections of neuromas being so

different, sometimes simply in contact with the nerve; sometimes
situated in the thickness of the nerve-trunk, the fibres being pressed
aside and spread out upon the surface of the tumor; sometimes
involving in their tissue a part or the whole of the nerve-fibres,—we
cannot but expect a very marked difference in their clinical history.
Not a few cases occur in which the presence of neuromas, even in
large numbers, gives rise to no symptoms during life, and their
existence has been revealed only upon a post-mortem examination.

The symptom most common to neuromas, and one to be expected

from their mechanical interference with the nerves, is neuralgic pain
—sometimes extreme, local or shooting along the course of the
nerves, stubborn, and hardly to be alleviated by remedies. It is
paroxysmal, notwithstanding the unvarying character of its cause, in
consonance with the tendency to periodical activity which prevails in
the nervous system. Sometimes the pain is increased notably by
atmospheric changes. The pain may sometimes be arrested by firm
pressure upon the nerve above the seat of the tumor. In some cases
pressure upon the neuroma, or even handling it, causes great pain.
The intensity of the pain does not depend upon the size of the tumor,
some of the smallest having earned the appropriate name of
tubercula dolorosa. The continued irritation of a neuroma sometimes
produces a condition of general nervous excitability, which shows
itself in hysterical and even in true epileptic convulsions.
Occasionally there are abnormal sensations (paræsthesiæ),
formication, numbness, etc., in the distribution of the nerve affected,
and when from pressure or histological changes the fibres are
destroyed anæsthesia results.

The interference with the conductivity of the motor fibres, which

occurs less frequently than alterations of sensation, shows itself in
cramps, tumors, paresis, and paralysis, according to its degree.

Neuromas may destroy life by the continued excessive pain, which

wears down the strength and depresses the vitality. Death may be
caused by their peculiar situation; as, for instance, upon the cauda
equina, where they produce paraplegia, paralysis of the sphincter
and bladder, and trophic changes.

The DIAGNOSIS of neuromas can only be made when they are

sufficiently superficial to be recognized by the touch, and along with
the symptoms above detailed the tumor is situated upon the known
course of a nerve, to which, moreover, its attachment allows a lateral
movement.

The only TREATMENT available for neuromas is extirpation, which must

be conducted with a view to sparing any fibres of the nerve not
involved in the tumor. Where it is necessary to divide the nerve in the
removal of the tumor, as small a portion as possible must be
excised, with the hope of a regeneration and reuniting of the cut
ends. The success of extirpation depends largely upon the nature of
the neuroma. The true neuromas, while they often show a strong
tendency to recur after removal, are benign and show no metastasis.
For the false neuromas the prognosis will be in accordance with their
benign or malignant character.
NEURALGIA.
 BY J. J. PUTNAM, M.D.

DEFINITION.—It is customary to describe as neuralgic those pains for

which no adequate cause can be assigned in any irritation of the
sensory nerves from outside, which recur paroxysmally, are
unattended by fever, and are distributed along the course of one or
more nerves or nerve-branches.

The general use of the term neuralgia further implies the common
belief that there is a disease or neurosis, not covered by any other
designation, of which these pains are the characteristic symptom. Of
the pathological anatomy of such a disease, however, nothing is
known; and if it could be shown for any given group of cases that the
symptoms which they present could be explained by referring them
to pathological conditions with which we are already familiar, these
cases would no longer properly be classified under the head of
neuralgia.

The attempt has frequently been made, and on good grounds, in

obedience to this reasoning, to cut down the list of the neuralgias,
strictly so called, and to account for many of the groups of symptoms
usually classified under that head by referring them to anæmia or
congestion of the sensory nerves, to neuritis, etc.

One of the best and most recent statements of this view is that of
Hallopeau,1 who, although he does not wholly deny the existence of
a neurosis which may manifest itself as neuralgia, goes so far as to
maintain that the gradual onset and decline and more or less
protracted course so common in the superficial neuralgias, such as
sciatica, suggest rather the phases of an inflammatory process than
the transitions of a functional neurotic outbreak, and that, in general
terms, a number of distinct affections are often included under the
name of neuralgia which are really of different origin, one from the
other, and resemble each other only superficially. This subject will be
discussed in the section on Pathology, and until then we shall, for
convenience' sake, treat of the various neuralgic attacks as if they
were modifications of one and the same disease.
1 Nouveau Dict. de Méd. et de Chir. pratiques, art. “Névalgies.”

GENERAL SYMPTOMATOLOGY.—The neuralgias may be conveniently

divided into—1, external or superficial; 2, visceral; 3, migraine and
the migrainoid headaches.

Superficial Neuralgia.

The most prominent symptom of a neuralgic attack of the superficial

nerves is of course the pain, and sometimes, from first to last, no
other sign of disease is present. In an acute attack the pain is usually
ushered in by a sense of discomfort, which the patient vainly tries to
shake off, or by a feeling of weight and pressure or of numbness and
prickling, or of itching. Sometimes, though far less often than in the
case of migraine, there are prodromal signs of a more general
character, such as a feeling of thirst2 or of mental depression or
drowsiness.
2 Spoken of by Mitchell's patient with neuralgia of the stump (see below).

A dart of pain may then be felt, which soon disappears, but again
returns, covering this time a wider area or occupying a new spot as
well as the old. The intensity, extension, and frequency of the
paroxysms then increase with greater or less rapidity, but, as a rule,
certain spots remain as foci of pain, which radiates from them in
various directions, principally up or down in the track of the nerve-
trunk mainly implicated. The pain rarely or never occupies the whole
course and region of distribution of a large nerve or plexus, but only
certain portions, which may be nearly isolated from one another.
In an acute attack the affected parts may at first look pale and feel
chilly, and later they frequently become congested and throb.
Mucous surfaces or glandular organs in the neighborhood often
secrete profusely, sometimes after passing through a preliminary
stage of dryness.

The skin often becomes acutely sensitive to the touch, even though
firm, deep pressure may relieve the suffering. Movement of the
painful parts, whether active or passive, is apt to increase the pain.
When the attack is at its height, the pain is apt to be felt over a larger
area than at an earlier or a later period, and may involve other
nerves than those first attacked. Thus, a brachial becomes a cervico-
brachial neuralgia or involves also the mammary or intercostal
nerves. A peculiarly close relationship exists between the neuralgias
of the trigeminal and of the occipital nerves. It is said that when the
attack is severe the corresponding nerves of the opposite side may
become the seat of pain. This is perhaps remotely analogous to the
complete transference of the pain from one side to the other which is
so characteristic of periodical neuralgic headaches, especially if they
last more than one day.

Some cutaneous neuralgias pass away after a few hours' or a night's

rest, after the manner of a migraine or a headache, and patients in
whom this takes place are, as a rule, constitutionally subject to
neuralgia or other neuroses. Toward the end of such an attack there
is often a copious secretion of pale, limpid urine. In a large class of
cases, on the other hand, the attack is of several days' or weeks', or
even months' or years', duration, with remissions or intermissions
and exacerbations, which may be either periodical or irregular.

The most marked periodicity of recurrence is seen with the

neuralgias of malarial origin, which may take on any one of the
typical forms of that disease.

These malarial neuralgias affect pre-eminently, though not

exclusively, the supraorbital branch of the fifth nerve; but it should
not be forgotten that there is also a typically periodical supraorbital
neuralgia of non-malarial origin, of which the writer has seen several
pronounced examples, the pain usually recurring regularly every
morning at eight or nine o'clock and passing away early in the
afternoon. The same periodicity is seen, though less often, in other
neuralgias. Thus, Trousseau3 speaks of neuralgic attacks from
cancer of the uterus in a young woman, which recurred daily at
exactly the same hour. Some of the traumatic neuralgias show the
same peculiarity to a marked degree.
3 Clin. Méd.

In many neuralgias, on the other hand, the exacerbations are worse

at night, like the pains of neuritis. In the intervals between the attacks
the pain may be wholly absent, or may persist, usually as a dull
aching.

After a neuralgia has lasted a few days—sometimes, indeed, from

the outset if the attack is severe—it is usually found that definite
spots of tenderness have made their appearance at certain limited
points on the course of the nerve. These are the famous points
douloureux which Valleix described with such minute accuracy,
believing them to be invariably present in true neuralgias. This is
certainly not strictly the case, though they are very common. They
are not necessarily coincident with the foci of spontaneous pain, as
Valleix supposed, but do correspond in general to the points at which
the affected nerve emerges from its bony canal or from deep
muscles and fascia, and to portions of its area of distribution in the
skin. The spinous process corresponding to an affected spinal nerve
may also become tender, but this is probably to be looked on, like
the same symptom in so-called spinal irritation, not as a sign of local
disease, but as due to a general reaction on the part of the nervous
system, and as a fact of a different order from the tenderness along
the nerve.

The termination of an acute neuralgic attack is usually gradual, like

its onset, although in some cases of headache, and in other
neuralgias to a less degree, there comes a moment when the patient
suddenly declares that he is free from pain.