Dr. Donald Corenman (http://neckandback.com 970.479.5895) is a spine surgeon and spinal cord expert practicing at the Steadman Clinic in Vail, CO. He created this Power Point presentation on cervical spine injury and the evaluation of the cervical spine with an injury. The cervical spine (C spine) represents the neck area of the upper spine.
This presentation--clearing the cervical spine--offers an in-depth look at cervical spine injury of the neck (C spine) including fractures, cervical nonskeletal injuries, and also offers a 3-view radiograph approach into the exam.
Dr. Corenman is a spine expert and treats nonskeletal injuries such as ligamentous instability, sciwora and central cord injury. He is an expert in myelopathy, sciatica, degenerative disc disease, scoliosis and slipped disc.
Dr. Donald Corenman (http://neckandback.com 970.479.5895) is a spine surgeon and spinal cord expert practicing at the Steadman Clinic in Vail, CO. He created this Power Point presentation on cervical spine injury and the evaluation of the cervical spine with an injury. The cervical spine (C spine) represents the neck area of the upper spine.
This presentation--clearing the cervical spine--offers an in-depth look at cervical spine injury of the neck (C spine) including fractures, cervical nonskeletal injuries, and also offers a 3-view radiograph approach into the exam.
Dr. Corenman is a spine expert and treats nonskeletal injuries such as ligamentous instability, sciwora and central cord injury. He is an expert in myelopathy, sciatica, degenerative disc disease, scoliosis and slipped disc.
Instability of the cranio-vertebral junction (CVJ)Felice D'Arco
Radiological assessment of CVJ in children. 2nd European Society for Pediatric Neurosurgery (ESPN) Hands-on Workshop on Craniovertebral Junction Surgery, Lyon, France
Instability of the cranio-vertebral junction (CVJ)Felice D'Arco
Radiological assessment of CVJ in children. 2nd European Society for Pediatric Neurosurgery (ESPN) Hands-on Workshop on Craniovertebral Junction Surgery, Lyon, France
Spinal Cord Injuries are uncommon, but they are a leading cause of high cost disability, and with ageing population, the incidence is expected to increase. This presentation looks at the many facets of spinal cord injuries.
Spinal cord injuries complete topic about it and how to make good rehabilitation for the patient with spinal cord injuries .
wish it help people
my pleasure :)
Mostafa shakshak
Dr.MD.Monsur Rahman,PT
MPT-Musculoskeletal Disorders
Maharishi Markandeshwar Institute Of Physiotherapy And Rehabilitation, Maharishi Markandeshwar (Deemed to be University), Mullana - Ambala,133-207 (Haryana)
spinal injury
Goal of spine trauma care
Pre-hospital management
Clinical and neurologic assessment
Acute spinal cord injury
Term, type and clinical characteristic
Common cervical spine fracture and dislocation
Similar to CERVICAL SPINE INJURY SURAIN edited.pptx (20)
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.
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
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
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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
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
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8. FLEXION INJURY
• Common injuries associated
with a flexion mechanism
include the following:
-Simple wedge compression
fracture without posterior
disruption
-Flexion fracture
-Anterior subluxation
-Bilateral facet dislocation
-Anterior atlantoaxial dislocation
9. ANTERIOR SUBLUXATION
• Occurs when posterior ligamentous
complexes rupture. The anterior
longitudinal ligament remains intact.
No bony injury is seen.
• The lateral view Xray shows widening
of interspinous process. Since the
anterior columns remain intact, this
fracture is considered mechanically
stable.
10. BILATERAL FACET DISLOCATION
• Extreme form of anterior
subluxation that occurs
when a significant degree
of flexion and anterior
subluxation causes
ligamentous disruption to
extend anteriorly
11. FLEXION-ROTATION INJURY
• Unilateral facet dislocation
• stable fracture.
• Anterior displacement of
spine is less than one half
diameter of vertebral body
12. EXTENSION INJURY : HANGMAN
FRACTURE
• commonly caused by
motor vehicle collisions
• bilateral fractures pedicles
of C2 due to
hyperextension.
• Potentially unstable
15. SPINAL CORD INJURIES
• Insult to spinal cord resulting in a change in the
normal motor, sensory or autonomic function. This
change is either temporary or permanent.
• All spinal cord injuries are divided into two
categories: incomplete and complete.
16. TYPES OF SPINAL CORD INJURIES
Incomplete
the cord is only partially
severed, allowing the
injured person to retain
some function
With incomplete injuries,. In
these cases, the degree of
function depends on the
extent of the injuries
Complete
fully severed
with treatment and physical
therapy, it may be possible
to regain some function.
17.
18. TYPES OF INCOMPLETE OR PARTIAL
SPINAL CORD INJURIES INCLUDE
Anterior cord syndrome
•This type of injury, to the
front of the spinal cord
•Motor paralysis, loss of
pain and temperature below
level of lesion.
Proprioception and vibration
intact.
Central cord syndrome
• injury to the center of the
cord
• Loss of fine motor skills,
paralysis of the arms, and
partial impairment, usually
less pronounced in the
legs are common. Some
survivors also suffer a loss
of bowel or bladder control
19. Brown-Sequard syndrome
•Result in paralysis and loss
of proprioception on
ipsilateral side of body and
loss of sensation(pain and
temperature) in the
contralateral side
Posterior cord syndrome
•affecting posterior column
(fine touch, vibration,
proprioception, pressure)
20. HIGH-CERVICAL NERVES (C1 – C4)
• Inability to breathe without assistance from a ventilator
• Inability or reduced ability to speak
• Loss of feeling or sensation below the level of injury
• Paralysis in the arms, hands, trunk, and legs
• Limited neck and/or head movement
21. LOWER CERVICAL NERVES C5-C8
• Corresponding nerves control arms and hands.
• A person with this level of injury may be able to breathe
on their own and speak normally
22. NEUROGENIC SHOCK
• Temporary loss of autonomic function of the cord at the
level of injury
• results from cervical or high thoracic injury
• Presentation
• Flaccid paralysis distal to injury site
• Loss of autonomic function
• hypotension
• vasodilatation
• loss of bladder and bowel control
• loss of thermoregulation
• warm, pink, dry below injury site
• bradycardia
23. TRIAD FOR NEUROGENIC SHOCK
• Triad
i) hypotension
ii) bradycardia
ii) Hypothermia
• More commonly in injuries above T6
• Secondary to disruption of sympathetic outflow from T1 –
L2
24. TREATMENT
Airway management
Cervical spine immobilization
Hemodynamic stabilization
• 1st line – intravenous fluid resuscitation
• 2nd line – Vasopressor ( noradrenaline)
• Recommnd to keep MAP 85-90 to to improve spinal perfusion
• For bradycardia- atropine
• Use of steroid (methylprednisolone, corticosteroid) Controversial-risk of
infection,GI bleed
25. SPINAL SHOCK
• The direct force applied to the spinal cord results in a
physiologic block to conduction (called spinal shock),
which is recognized clinically as complete cessation of
all neurologic function—motor, sensory, and
autonomic—below the level of the injury (complete or
incomplete spinal cord injury).
• a spinal cord injury which usually involves 24-72 hours
period of immediate temporary loss of total power,
sensation and reflexes below the level of injury
• Spinal shock refers to the In slight injuries, this phase
lasts only minutes, but in more severe injuries, it may last
weeks.
26. CHARACTERISTIC OF SPINAL
SHOCK
• Motor Effects – Paraplegia or Quadriplegia
• Loss of tone -Muscles become flaccid
• Areflexia - All superficial and deep reflexes are lost
• Sensory Effects -All Sensations are lost below the
level of transection
27. FEATURES OF SPINAL SHOCK
• Hypotension
• Hypothermia
• Bradycardia
• Flaccid paralysis
• Loss of sensation
• Areflexia or depressed reflexes
• Urinary and bladder incontinence
• Sweating
• Sometimes priapism
28. • Assessment of the end of spinal shock is
based on the return of reflexes, with the
bulbocavernosus reflex typically being the
first to return.
• The diagnosis of complete or incomplete
spinal cord injury cannot be made until the
period of spinal shock is over.
29. PROGNOSTIC FACTORS OF
NEUROLOGICAL RECOVERY
Good prognostic factor
• 1.Spinal shock of <24 hours and
• 2.Early appearance of deep tendon reflexes
Poor prognostic factor
• 1.Complete lesion
• 2.Spinal shock for >1 week,
• 3.Flexor spasms within three weeks
• 4. Bedsore within one week
30. SPINAL V/S NEUROGENIC SHOCK
Spinal shock Neurogenic shock
Definition Immediate temporary loss of
total power, sensation and
reflexes below the level of
injury
Sudden loss of the
sympathetic nervous system
signals
BP Hypotension Hypotension
Pulse Bradycardia Bradycardia
Bulbocavernosu
s reflex
Absent Variable
Motor Flaccid paralysis Variable
Time 48-72 hrs immediate after SCI
Mechanism Peripheral neurons become
temporarily unresponsive to
brain stimuli
Disruption of autonomic
pathways → loss of
sympathetic tone and
vasodilation
31. CERVICAL SPINE EXAMINATION
• Inspection and palpation
• Occiput to Cervical
• Soft tissue swelling and bruising
• Point of spinal tenderness
• Gap or Step-off
• Spasm of associated muscles
• Neurological assessment
• Motor, sensation and reflexes
• Cranial nerve examination should always be
performed.
• PR
32.
33. RADIOGRAPHIC IMAGING
✓NEXUS -The National Emergency X- Radiograph
Utilization Study
• Prospective study to validate a rule for the decision to obtain cervical
spine x- ray in trauma patients
• Hoffman, N Engl J Med 2000; 343:94-99
✓Canadian C-Spine rules
• Prospective study whereby patients were evaluated for 20
standardized clinical findings as a basis for formulating a decision as to
the need for subsequent cervical spine radiography
• Stiell I. JAMA. 2001; 286:1841-1846
34. NEXUS
• NEXUS Criteria:
1. Absence of tenderness in the posterior midline
2. Absence of a neurological deficit
3. Normal level of alertness (GCS score = 15)
4. No evidence of intoxication (drugs or alcohol)
5. No distracting injury/pain
35. NEXUS
• Patient who fulfilled all 5 of the criteria were
considered low risk for C-spine injury
→ No need C-spine X-ray
• For patients who had any of the 5 criteria
→ radiographic imaging was indicated
( AP, lateral and open mouth views)
36. THE CANADIAN C-SPINE RULE FOR ALERT AND STABLE TRAUMA PATIENTS
WHERE CERVICAL SPINE INJURY IS A CONCERN.
• Any high-risk factor that mandates radiography?
• Age>65yrs or
• Dangerous mechanism or
• Paresthesia in extremities
Any low-risk factor that allows safe
assessment of range of motion?
• Ambulatory at any time, or
• Delayed onset of neck pain, or
• Absence of midline C-spine tenderness
Able to actively rotate neck?
• 45 degrees left and right
No Radiography
Radiography
NO
YES
ABLE
YES
NO
UNABLE
37. CERVICAL SPINE IMAGING OPTIONS
• Plain films
• AP, lateral and open mouth view
• Optional: Oblique and Swimmer’s , odontoid
• CT
• Better for occult fractures
• MRI
• Very good for spinal cord, soft tissue and
ligamentous injuries
• Flexion-Extension Plain Films
• to determine stability
39. ADEQUACY
• Must visualize entire C-spine
• A film that does not show the upper
border of T1 is inadequate
• Caudal traction on the arms may
help
• If can not, get swimmer’s view or
CT
41. ALIGNMENT
• The anterior vertebral
line, posterior vertebral
line, and spinolaminar
line should have a
smooth curve with no
steps or discontinuities
• Malalignment of the
posterior vertebral
bodies is more
significant than that
anteriorly, which may
be due to rotation
• A step-off of >3.5mm is
significant anywhere
42. DISC
• Disc Spaces
• Should be uniform
• Assess spaces
between the spinous
processes
43. LATERAL CERVICAL SPINE X-
RAY
• Anterior subluxation of one vertebra
on another indicates facet dislocation
• < 50% of the width of a vertebral body
→ unilateral facet dislocation
• > 50% → bilateral facet dislocation
45. SOFT TISSUE
• Nasopharyngeal space
(C1)
• 10 mm (adult)
• Retropharyngeal space
(C2-C4)
• 5-7 mm
• Retrotracheal space
(C5-C7)
• 14 mm (children)
• 22 mm (adults)
46. AP C-SPINE FILMS
• Spinous processes should
line up
• Disc space should be
uniform
• Vertebral body height
should be uniform. Check
for oblique fractures.
47. OPEN MOUTH VIEW
• Adequacy: all of the
dens and lateral
borders of C1 & C2
• Alignment: lateral
masses of C1 and C2
• Bone: Inspect dens for
lucent fracture lines
48. CT SCAN
• Thin cut CT scan should be
used to evaluate abnormal,
suspicious or poorly
visualized areas on plain film
• The combination of plain film
and directed CT scan
provides a false negative rate
of less than 0.1%
49. MRI
• Ideally all patients with
abnormal neurological
examination should be
evaluated with MRI scan