A presentation to understand peripheral nerve injuries assessment, evaluation and management. Includes principles of tendon transfer and techniques of tendon transfer for radial nerve palsy. Also, post operative rehabilitation is included.
Hoffa's Fracture: Diagnosis, management & New Classification System by BAGARI...Vaibhav Bagaria
Hoffa's Fracture - coronal split fracture of distal femur, its diagnosis, management strategy, a new classification and tips and tricks of management. First described Hoffa, a new classification system by Bagaria et al helps plan the surgery for these tricky fracture. The most crucial step is not to miss these fractures in ER.
PNI with Relevant Anatomy, Etiology, Mechanism of Degenration and Regenration, Saddon's and Sunderland Classifications, Clinical symptoms and Examination (Tests) of Brachial Plexus, Radial & Median Nerve.
Hoffa's Fracture: Diagnosis, management & New Classification System by BAGARI...Vaibhav Bagaria
Hoffa's Fracture - coronal split fracture of distal femur, its diagnosis, management strategy, a new classification and tips and tricks of management. First described Hoffa, a new classification system by Bagaria et al helps plan the surgery for these tricky fracture. The most crucial step is not to miss these fractures in ER.
PNI with Relevant Anatomy, Etiology, Mechanism of Degenration and Regenration, Saddon's and Sunderland Classifications, Clinical symptoms and Examination (Tests) of Brachial Plexus, Radial & Median Nerve.
about nerve fibers
It is the structural and the functional unit of nervous system.
The human nervous system contains approximate 1012 neurons.
A nerve fiber is a thread like extension of a nerve cell and consists of an axon and myelin sheath (if present) in the nervous system.
In peripheral nervous system it is formed by
schwann’s cell. While in case of central nervous system it is formed by oligodendroglia.
The places ,where myelin sheath is absent are called node of ranvier(2-3µm) and these are present once about 1-3 mm distance along the myelin sheath.
IT PREVENTS LEAKAGE OF IONS BY 5000 FOLDS.
IT INCREASES VELOCITY OF CONDUCTION BY 5-50 FOLDS DUE TO
SALTATORY CONDUCTION i.e. ABOUT 100 m/s IN CASE OF
MYELINATED NERVE FIBERS WHILE IN NONMYELINATED
IT IS ABOUT 0.25 m/s.
SALTATORY CONDUCTION CONSERVES ENERGY BECAUSE ONLY NODES OF RANVIER GET DEPOLARISED.
These are α type motor nerve fibers.
The neurotransmitter released at the neuron endings is acetylcholine(Ach).
It always leads to muscles excitation . Inhibition takes place centrally due to participation of interneurons.
they innervate smooth muscles , cardiac muscles and glands.
Their main work is to maintain homeostasis with the help of autonomic nervous system.
they can lead to either excitation or inhibition of effector organs
Erlanger and Grasser studied the action potential of mixed nerve trunk by means of cathode ray oscilloscope and they obtained the compounded spike. So they divided nerve fibers into 3 groups. They observed that the main cause of difference in nerve fibers is diameter
AS Diameter increases
Velocity of conduction increases.
Magnitude of electrical response increases.
Threshold of excitation decreases.
Duration of response decreases.
Refractory period decreases.
This is the ppt that describes about organization of nerve in central nervous system. It also classify the nerves in various ways. Functions of different nerves and its characteristics are also described in this ppt.
The nervous system is made up of the central nervous system and the peripheral nervous system. The central nervous system (CNS) is made up of the brain and spinal cord. The brain controls most body functions, including awareness, movements, sensations, thoughts, speech and memory.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Peripheral nerve injuries-ASSESSMENT AND TENDON TRANSFERS IN RADIAL NERVE PALSY
1. PERIPHERAL NERVE INJURY
ASSESSMENT AND TENDON
TRANSFERS IN RADIAL NERVE PALSY
MODERATOR: DR.G.RAMESH
ASSOCIATE PROFESSOR ORTHOPAEDICS, GANDHI HOSPITAL
PRESENTER: DR.G.SAI.SUCHITRA
PG 3RD YEAR, GANDHI MEDICAL COLLEGE
2. PERIPHERAL NERVE
• “Peripheral nerve” is a term used synonymously to describe the
peripheral nervous system.
• The peripheral nervous system is a network of 43 pairs of motor and
sensory nerves that connect the brain and spinal cord (the central
nervous system) to the entire human body.
• These nerves control the functions of sensation, movement and
motor coordination.
3. STRUCTURE OF A PERIPHERAL NERVE
• The peripheral nerve is composed of the axons enclosed in Schwann’s
sheaths and their supporting endoneural tissues.
• Groups of axons are arranged in bundles called fascicles.
• The intraneural tissue around the microscopic Schwann’s tubes is
called the endoneurium, and a fibrous sheath of each fascicle is
called the perineurium.
• The perineurium is only four or five cell layers thick and therefore is
visible only with the aid of a microscope.
• The abundant macroscopic fibrous tissues incorporating all of the
fascicles of well- defined bundles constitute the epineurium.
4. • FASCICLES(AXONS)
• EACH FASCICLE
WRAPPED BY
ENDONEURIUM
• GROUP OF FASCICLES
BY PERINEURIUM
• INNER EPINEURIUM
LOOSELY WRAPPING
AROUND INNER
FASCICULAR GROUPS
AND OUTER
EPINEURIUM CLOSELY
APPOSED TO
PERIPHERAL NERVE
SHEATH CALLED
“ADVENTITIA”
5.
6. • A certain amount of gliding motion occurs between the elastic
adventitia and the epineurium, which gives the nerve mobility for
crossing joints without suffering stretch injuries
7. • Nerve cells are called neurones.
• A neurone consists of a cell body (with a nucleus and cytoplasm), dendrites
that carry electrical impulses to the cell, and a long axon that carries the
impulses away from the cell
• Generation of a nerve impulse (action potential) of a sensory neurone
occurs as a result of a stimulus such as light, a particular chemical, or
stretching of a cell membrane by sound.
• Conduction of an impulse along a neurone occurs from the dendrites to the
cell body to the axon.
• Transmission of a signal to another neuron across a synapse occurs via
chemical transmitter. This substance causes the next neurone to be
electrically stimulated and keeps the signal going along a nerve.
8.
9. ANATOMY:
Neuron:
Cell body:
Motor: anterior horn of spinal cord
Sensory: dorsal root ganglion
Axon:
• Myelinated: wrapped in double basement membrane of Schwann cell
• Non myelinated
Transport of intracellular components[vesicles]: 410 mm/day
• Structural proteins : 1-6 mm /day, limiting factor in nerve regeneration
10. • Individual nerve fibers vary widely in diameter and may also be
myelinated or unmyelinated.
• Myelin in the peripheral nervous system derives from Schwann cells,
and the distance between nodes of Ranvier determines the
conduction rate.
11. • A ganglion is a cluster of neuron cell bodies enveloped in an
epineurium continuous with that of a nerve. A ganglion appears as a
swelling along the course of a nerve.
• The spinal ganglia or posterior or dorsal root ganglia associated with
the spinal nerves contain the unipolar neurons of the sensory nerve
fibers that carry signals to the cord. The fiber passes through the
ganglion without synapsing.
• However, in the autonomic nervous system, a preganglionic fiber
enters the ganglion and in many cases synapses with another neuron.
The axon of the second neuron leaves the ganglion as the
postganglionic fiber.
12.
13. PATHOPHYSIOLOGY OF NERVE INJURY
• All the functions distal to the point of severance are interrupted
• At the end of proximal nerve segment axons multiply and attempt to grow
distally
• A connective tissue growth envelopes the end of the nerve and obstructs
the path of these fibrils
• This connective tissue and fibrillar growth is called neuroma
• Distal nerve segment swells to double its original size and undergoes
Wallerian degeneration.
• This process is complete in about one month
• Occasionally the connective tissue growths at the end of each segment
may successfully penetrate the mass and grow distally restoring partial
functions
14.
15. TINEL’S SIGN
Rate of nerve regeneration: 1-4.5 mm/day
• Tinels rate : 1-2 mm/day.[ 2-3 times in children]
“When percussion is lightly applied to the injured nerve tissue , we find the cutaneous
region of the nerve, a creeping sensation usually compared by the patient to that
caused by electricity”
Reserve only for traumatic neuropathy
Strongly positive Tinels over lesion after injury indicated severance or rupture
Centrifugally moving Tinels sign persistently stronger than at the suture line-repair
that is going to be successful
Tinels at the suture line stronger than at the growing end- repair that is going to fail
Failure of distal progression of Tinels in a closed lesion – rupture or lesion impeding
regeneration
16. CLASSIFICATION OF NERVE INJURIES
• Classification of nerve injuries is useful in understanding their
pathological basis, making decisions on management, and predicting
the prognosis for recovery.
• Seddon described a classification of localized injuries to peripheral
nerves after study of large numbers of casualties during the second
world war, which is still widely used.
• Neurapraxia-
• Axonotmesis
• Neurotmesis
17.
18. • LIMITATIONS OF SEDDON’S CLASSIFICATION-
• Seddon’s classification doesn’t distinguish between all grades of intraneural
damage.
• Lesions classified as axonotmesis have been observed to have variable
recovery. This is because variable degrees of damage to the connective
tissue layers of the nerve, including the endoneurium and perineurium, as
well as disruption of the axons are possible without loss of continuity of
the nerve trunk.
•
20. Sixth degree [ Mac kinnon]:
combination or several degrees with various pattern of injury and
recovery.
Nerve trunk is partially severed, and the remaining part of the trunk
sustains fourth-degree, third-degree, second-degree, or rarely even first-
degree injury
21. ASSESSMENT OF NERVE INJURY
• CLINICALLY-
• SYMPTOMS FOLLOWING COMPLETE NERVE INJURY-
• Loss of stereognosis
• Loss of superficial pain, touch and temperature
• Loss of deep sensation to muscle and joint movements, position,
deep pressure and vibration
• Loss of motor supply to muscle results in muscle atrophy and fibrous
degeneration
• Deep tendon reflexes are diminished or absent
22. • Electrical stimulation of the nerve no longer causes the muscle to
contract but muscle can be individually stimulated by Faradic current
until two weeks after which even Faradism doesn’t elicit any response
• But the muscle continues to respond to Galvanic current with slow
contraction , greater in amplitude followed by slow relaxation
• This phenomenon is known as ”REACTION OF DEGENERATION” and
is characteristic feature of peripheral nerve injury
• Trophic influence is lost
23.
24. • Neurophysiological studies form a relevant and well-established part in the
diagnosis and work-up of nerve injuries
• Does a nerve lesion exist?
• Where precisely is the lesion located?
• Are other nerves involved, which may explain patient’s signs and symptoms?
• What type of lesion is it –axonal or a demyelinating?
• Is there a generalized lesion of peripheral nerves, e.g. polyneuropathy?
• Is the lesion acute, subacute or chronic?
• What is the severity of the lesion?
• Additional questions, which can only partially be answered, are:
• What is the prognosis of untreated nerve injury or entrapment syndrome?
• What treatment modality is necessary –surgery or conservative treatment?
• Was the treatment effective?
25. GENERAL PRINCIPLES OF NCS
• Motor and sensory nerve conduction studies (NCS) are performed .
• The type of study depends on the nerve studied (motor, sensory or
mixed nerve) and on the site of recording
• In NCS the nerve is electrically stimulated by a bipolar surface
stimulator.
• As a general rule, only myelinated nerve fibres can be investigated.
• Skin temperature should be measured and the extremity be warmed
if the temperature is <32°C.
• Nerve conduction gets slightly slower at ages above 75 ys.
26. • Motor nerve conduction studies (mNCS)
• In mNCS compound motor action potentials (CMAP) are recorded
from a muscle innervated by the nerve under investigation. Surface
electrodes are used and the “active” (recording) electrode is placed
over the muscle belly, the other (reference) electrode over the
tendon at the insertion of the muscle (belly-tendon electrode
placement).
27. Figure 1: Median nerve motor nerve conduction study.
Standard electrode placement over the abductor pollicis
brevis muscle and stimulation of the median nerve at the
wrist are displayed.
28. • Sensory nerve conduction studies (sNCS)
• Orthodromic or antidromic nerve conduction studies are performed
to study sensory nerves.
• In antidromic studies amplitudes are usually higher than in
orthodromic studies, otherwise both methods are comparable.
• In antidromic studies of e.g. the median or ulnar nerves, the sensory
nerve action potential (SNAP) may be recorded using ring electrodes
placed around a finger, and the nerves are stimulated at the wrist.
• In orthodromic studies, surface electrodes are placed over the nerve
at the wrist, and finger nerves are stimulated by ring electrodes
29. Standard electrode placement for A) antidromic and B)
orthodromic median nerve sensory nerve conduction
studies. In A) stimulation is at the wrist, in B) at the index
finger.
30.
31.
32.
33.
34.
35. • An NCV test shows the condition of the best surviving nerve fibers,
so in some cases the results may be normal even if there is nerve
damage
36. GENERAL PRINCIPLES OF NEEDLE
ELECTROMYOGRAPHY (EMG)
• Electric potentials produced by muscle fibres can also be recorded
using intramuscular needle electrodes
• Pathologic EMG findings are only seen in axonal nerve lesions.
• Typically, EMG is recorded when the muscle is at rest, during a weak
contraction and during a strong contraction.
• With the muscle at rest, spontaneous activity is assessed.
• In a healthy muscle there is only a brief burst of EMG signal when the
needle is moved within the muscle. This is called insertional activity.
37. • Following an axonal injury, several forms of pathological spontaneous
activity may be found.
• Fibrillation potentials (fibs) and positive sharp waves (psw) are seen
14-21 days following an axonal nerve lesion.
• They usually persist for 6-12 month, although some spontaneous
activity may persist for many years. Complex repetitive discharges and
myokymic discharges are sometimes seen in chronic lesions.
• However, all types of spontaneous activity can occur in other
disorders of nerve or muscle as well
38. • In general the neurophysiology tests can distinguish between injuries
where axons have not degenerated (neurapraxia) and those where
axons have degenerated distally (axonotmesis and neurotmesis)
• If axonotmesis has affected all the fibres in a nerve then the findings
will be indistinguishable neurotmesis.
• If there is a mixed lesion with some fibres intact detection of these
will imply the nerve trunk has not been disrupted.
39.
40. MAGNETIC RESONANCE IMAGING (MRI)
• Normal nerves can be visualised on MRI although their signal
characteristics are not distinct from other tissues.
• A technique called magnetic resonance neurography, which enhances
neural tissue on images, was reported by Filler.
• In the zone of injury signals are affected by oedema and haemorrhage
in the surrounding tissues.
• MRI has proved effective in imaging peripheral nerve tumours.
• It is also useful in assessment of brachial plexus injuries where
avulsion of nerve roots can be defined
41. • In addition to imaging the nerves themselves, information may be
obtained from MRI of muscle innervated by damaged nerves.
• On T2 and STIR images changes may be seen in denervated muscle as
early as two weeks after injury.
• The exact relationship between severity of nerve injury and the early
signal changes in muscles seen on MRI is not clear.
• More prolonged denervation of muscle leads to wasting and fatty
infiltration which can be seen on T1 waited MR images
42. Sagittal T2 weighted magnetic resonance image of the
shoulder showing increased signal in deltoid and teres
minor as a result of axillary nerve injury
43. ULTRASOUND
• Modern ultrasound scanners have improved to the extent that resolution is
now greater than MRI.
• Ultrasound is being used increasingly to examine nerves damaged by
closed trauma.
• It may be able to confirm continuity of a nerve, or diagnose rupture or
entrapment, for example, in a fracture.
• Fascicular disruption within a nerve trunk may be visualised.
• Use of ultrasound to examine the radial nerve injured in an association
with fractures of the humerus been reported and for diagnosis of median
nerve entrapment in the forearm.
• However, ultrasound is operator dependent and requires experience for
optimal interpretation
44. PRINCIPLES OF MANAGEMENT OF NERVE INJURY
• While the classifications of nerve injury provide a basis for prognosis
and management, in reality it can be difficult to diagnose the grade of
injury to a nerve in the early stages.
• The situation may only become clear in retrospect.
• Therefore a practical approach to management is recommended.
• It is useful to divide injuries into those which are open and closed.
45. OPEN NERVE INJURIES
• When there is evidence of loss of function in a nerve associated with a
wound, then in most circumstances exploration of the wound and the
affected nerve should be carried out.
• The only exception to this would be, if expert assessment indicates that the
patient is unlikely to benefit from repair of the nerve or if the patient is
unfit for operation.
• Uncertainty can occur when a nerve is partly divided since some function
will be preserved.
• Therefore lacerations associated with any neurological deficit should be
explored on the assumption that affected nerves are either partly or
completely divided rather than assuming than there is some form of lesion
in-continuity.
46. • Usually nerve repair should be carried out early at the same time as
other injured structures.
• Therefore fracture fixation, tendon repairs and skin closure is carried
out simultaneously, providing adequate vascularised skin and cover
can be provided.
• Full thickness vascularised skin cover is necessary over a nerve repair
rather than split skin graft.
47.
48.
49. CLOSED INJURIES-
• When a nerve has been injured as a result of blunt trauma there is likely to
be more uncertainly regarding the grade of injury.
• In general an assessment should be made of the probability that a nerve
has been disrupted or is under continuing compression.
• If the injury has been caused by high energy trauma then the chance of
disruption of the nerve is higher and early exploration should be
considered. If operation is required in any case, for example, for fracture
fixation, then the opportunity should not be missed to explore damaged
nerves and confirm continuity.
• Early exploration is best carried out within the first 2 weeks following
injury.
• If there has been lower energy trauma and a lesion in-continuity seems
likely then expectant management may be pursued.
50. • However, progress of nerve recovery should be monitored carefully
looking for return of muscle function and an advancing Tinel’s sign.
• If there is no improvement by 2 to 3 months from injury then surgical
exploration should be considered.
• Urgent neurophysiology assessment and imaging may help at this
stage
51. ACUTE NERVE COMPRESSION
• Nerves may be compressed by displaced fragments of fractures, dislocation of joints, or
expanding hematoma.
• The onset of loss of nerve function may be delayed after the injury although this may be
difficult to ascertain.
• Typically there is severe pain associated with the nerve palsy.
• This situation requires urgent management with reduction of fractures and dislocations.
• If closed reduction does not relieve the situation then open reduction with exploration of
the affected nerves should be performed.
• If there is suspicion of arterial injury, for example, false aneurysm, then angiography
should be arranged.
• Haematoma with sufficient pressure to cause nerve compression is likely to have been
caused by arterial haemorrhage.
• Drainage of the haematoma and vessel repair is required as an emergency.
52. A NERVE PALSY OCCURRING AFTER A
MEDICAL OR SURGICAL PROCEDURE
• This is an unfortunate and sometimes disastrous complication of
treatment.
• It is important to examine the function of nerves related to a surgical
procedure and document the findings before and afterwards.
• If a patient is found to have a new loss of nerve function after a
procedure then a prompt, careful and objective assessment needs to
be made.
• Since the clinician who has performed the procedure may have an
emotional attachment to the situation, it is often best to involve
another clinician
53. EXPLORING THE DAMAGED NERVE AT AN EARLY
STAGE TAKING INTO ACCOUNT THE FOLLOWING
FACTORS
• The events during the procedure should be reviewed to check whether the
nerve was identified and what the likely mechanism of injury is, including
laceration or compression.
• Whether the nerve palsy was present immediately after the procedure or
developed after a delay.
• If there is a possibility that the nerve is being subjected to continuing
compression, by haematoma or an implant then urgent re-operation
should be carried out
• Urgent investigations, including ultrasound, MRI, and neurophysiology may
be helpful
• The risks and benefits of carrying out a second procedure, including the
patient’s general condition, the risk of infection, and whether repair of the
affected nerve is likely to lead to useful functional recovery.
56. PREREQUISITES TO TENDON TRANSFER-
• OPEN WOUNDS
• A patient is not a candidate for a tendon transfer if he or she has
open wounds that could predispose to a disastrous postoperative
infection
• SOFT TISSUE COVERAGE
• Tendon transfers will glide only if transplanted through mobile,
unscarred, healthy tissues.
• Meeting this requirement usually entails subcutaneous rerouting of
the tendon out of contact with scar and fixed structures.
57. • MAXIMUM JOINT MOBILIZATION ESTABLISHED
• One never gains more active range of motion from tendon transfers
than the preoperative passive range of motion.
• Therefore, it is important that good joint mobility precede tendon
transfers. With disrupted motor nerves or muscle–tendon losses, the
imbalance of forces acting across the joints occurs immediately (with
the exception of total paralysis, in which there is no imbalance).
• In contrast, joint stiffening and deformity develop as the result of the
imbalance. Attention to joint stiffening and deformity with
appropriate therapy and splinting can substantially prevent these
complications.
58. • SKELETAL STABILIZATION
• RESTORED SENSIBILITY
• When possible, restoration of at least protective sensibility should
precede tendon transfers.
• Skin sensibility is not absolutely required for tendon transfers to be
useful, but it is always desirable
59. • POWER AND CONTROL
• To be a candidate for tendon transfer, a muscle must have adequate
power for the new function, be nonspastic, and be under good
volitional control.
• It also needs to be an independently functioning muscle unit, such as
a finger superficial flexor or the EIP, in contrast to the flexor digitorum
communis (FDC), whose four tendons originate from a common
muscle.
• In general, only muscles having a power grade of 4 or 5 (on the 0 to 5
scale) are suitable candidates for transfer.
60. • AMPLITUDE OF EXCURSION
• The muscle to be transferred must have an adequate amplitude of
excursion for its new function or be so situated that its effective
amplitude can be enhanced by tenodesis as it crosses an actively
controlled joint. Most often this joint will be the wrist
• ANATOMICALLY FAESIBLE LOCATION OF THE MUSCLE
• The surgical rerouting of a muscle and tendon should be in as direct a
line of pull as possible between the muscle’s origin and its new
insertion. Otherwise, as it begins to function, it will work into a
straight line of pull and become too slack.
61. • SYNERGISM
• Muscles that simultaneously and automatically contract to work
together are referred to as synergistic. An example is wrist extension
with finger flexion, as has already been discussed.
• Synergism was once considered important in selecting muscles for
transfer, but it is much less important today
• EXPENDABILITY
• Obviously, if a muscle is to be transferred for a new duty, the surgeon
must be certain that this will be of more benefit to the patient than
the muscle is in its normal situation.
62. • POTENTIAL PIP JOINT COMPLICATIONS
• The surgeon should be constantly aware of the possibilities of creating
secondary problems.
• If the proximal interphalangeal (PIP) joint of the finger from which the
flexor digitorum superficialis (FDS) is to be taken is hyperextensible from an
incompetent or ruptured volar plate, taking its FDS tendon can cause a
distressing recurvatum deformity.
• If the hyperextensibility is slight, simply leaving one slip of the FDS long so
it can adhere proximally in the tendon sheath is all that is necessary.
However, with gross hyperextensibility of the PIP joint, suturing a long
distally attached slip of the FDS to its proximal sheath is necessary for
tenodesis control of the joint.
63. • If any two of the three nerves are irreparably lost, a major functional
impairment is inevitable, and reconstruction must entail a substantial
simplification of the hand’s mechanical design if useful function is to
be restored.
• At the same time, wrist extension–flexion, as emphasized by White
(1960), is of such fundamental importance that its arthrodesis should
be done only as a last resort
74. • PROTECTIVE PHASE (SURGERY – 3-5 WEEKS)
• OBJECTIVES- Edema control, protective splinting, mobilise uninvolved joints
• MOBILISATION PHASE
• Begun when tendon healing is adequate for mobilisation
• OBJECTIVES-
• Mobilise transferred tendons
• Immobilise soft tissue
• Continue mobilisation of uninvolved joints
• Reinforce pre operative teaching and patient education
• Begin home rehabilitation
• Day time dynamic splinting and night time static splinting
75. • INTERMEDIATE PHASE(5-8 WEEKS POST OP)
• Gradually increase hand activities and passive ROM
• Limited functional movements permitted
• RESISTIVE PHASE (8-12 WEEKS POST OP)
• Resistance exercises started
• Therapeutic objective is increasing endurance and strength
• Work related tasks are begun
76.
77. BIBLIOGRAPHY
• TUREK’S TEXT BOOK OF ORTHOPAEDICS
• BEASLEY’S TEXT BOOK OF HAND SURGERY
• LIVING TEXT BOOK OF HAND SURGERY
• TEXT BOOK OF PLASTIC SURGERY
• CAMPBELL’S 12TH EDITION
• JOHN HOPKIN’S NEUROLOGY AND NEUROSURGERY
Editor's Notes
NEUROPRAXIA -caused by transient compression or stretch. Loss of nerve function results from conduction block. Paralysis of muscles innervated by the nerve is complete but some sensation may be preserved. Autonomic function may also be preserved. This type of injury will recover completely providing the cause, for example, ongoing compression, is removed. Recovery does not follow a proximal to distal progression as occurs with axon regeneration. As long as there is no ongoing insult cases of neurapraxia can be managed without operation.
Axonotmesis results from a more severe blunt injury to a nerve. This is sufficient to cause axon degeneration but the connective tissue layers of the nerve including the endoneurial tubes remain intact. Radial nerve injury associated with fracture of the humeral shaft is often an axonotmesis. Clinical examination reveals complete loss of motor, sensory, and autonomic function. Since axons distal to the site of injury have undergone Wallerian degeneration conduction is lost both at and distal to the site of injury. Providing the cause is removed, uncomplicated regeneration of axons occurs along the same pathway will occur, with recovery of function progressing from proximal to distal. Tinel’s sign can be elicited initially at the site of the injury and will advance distally over time. There is usually near normal recovery.
Neurotmesis is the situation where a nerve is completely divided or so badly disorganized that recovery cannot occur. All the connective tissue layers of the nerve as well as the axons are disrupted. There is axon degeneration distal to the injury. Neurotmesis may be caused by laceration or high energy traction injuries sufficient to rupture the nerve. In addition injection of noxious drugs or ischaemia can destroy a nerve. Recovery can only occur after appropriate surgical repair of the nerve and relies on axonal regeneration. Because disruption and mixing of fibres at the site of the repair results in failure of correct distal connections, recovery is never perfect. In general the outcome is worse after repair of a nerve ruptured by severe traction rather than direct repair of a clean laceration.It should be emphasized that the findings on clinical examination and neurophysiology assessment may be the same for axonotmesis and neurotmesis, yet there is a clear difference in prognosis and management.
Normally muscle contracts strongly to faradic current and twitches to galvanic current