Cervical myelopathy is a neurological impairment caused by compression of the cervical spinal cord, most commonly due to degenerative changes like spondylosis. It presents with neck stiffness, leg weakness, gait abnormalities, and clumsy hands. Physiotherapy management includes electrotherapeutic modalities to reduce pain, cervical stabilization exercises, isometric neck exercises, stretching, and progressive resistance exercises. The goals are to relieve pain, improve function, prevent further neurological deficits, and improve existing deficits. Surgery or immobilization may also be considered depending on severity.
This presentation give an upto date insightful information on balance/postural assessment and key domains of Occupational Therapy during assessment of balance using different scales.
This is the presentation which was delivered to third year Bachelor of Physiotherapy students at Kathmandu University School of Medical Sciences (KUSMS), Dhulikhel, Nepal. Different schools of thoughts in manual therapy are the part of curriculum for the undergraduate students at KUSMS.
At the end of the lecture, the students should be able to:
Discuss the theoretical basis of the neurodevelopmental approaches
Discuss the concepts and principles underlying the Bobath approach
Discuss the concepts and principles underlying the Brunnstrom approach
This presentation give an upto date insightful information on balance/postural assessment and key domains of Occupational Therapy during assessment of balance using different scales.
This is the presentation which was delivered to third year Bachelor of Physiotherapy students at Kathmandu University School of Medical Sciences (KUSMS), Dhulikhel, Nepal. Different schools of thoughts in manual therapy are the part of curriculum for the undergraduate students at KUSMS.
At the end of the lecture, the students should be able to:
Discuss the theoretical basis of the neurodevelopmental approaches
Discuss the concepts and principles underlying the Bobath approach
Discuss the concepts and principles underlying the Brunnstrom approach
Cns case-extramedullary compressive myelopathy, Q&AKurian Joseph
Tracts involved-corticospinal tract
anterior and lat spinothalamic
posterior coloumn
Mostly extramedullary compressive myelopathy at T10 level
Etiology –to consider both intra and extradural causes like neurofibroma/meningioma/av malformation.
extradural-potts spine,ivdp
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)
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
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
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Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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.
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Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
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Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
3. DEFINITION -
A form of neurologic impairment caused by
compression of the cervical spinal cord , most
commonly due to degenerative cervical spondylosis .
EPIDEMIOLOGY -
Most common in men > women
Earlier in men ( 50 years ) than in women ( 60
years )
It causes hospitalization at a rate of 4.04 per
100,000 person-years.
4. ETIOLOGY
STATIC FACTORS:
• A narrowing of the spinal canal size commonly results from
degenerative changes in cervical spine such as disc
degeneration, spondylosis, stenosis, osteophyte formation
at the level of facet joints, segmental ossification of
posterior longitudinal ligament and yellow ligament
hypertrophy, classification or ossification.
DYNAMIC FACTORS:
• Due to mechanical abnormalities of the cervical spine or
instability.
VASCULAR AND CELLUALR FACTORS:
• Spinal cord ischemia affects oligodendrocytes which results
in demyelination exhibiting feature of chronic degenerative
disorders.
5. ETIOLOGY
CONGENITAL
• Myelopathy due to congenital stenosis does not have a
specific lesion but caused by a canal diameter which is
narrower from birth.
SPONDYLOSIS
• Degenerative changes which develop with age, including
ligamentum flavum hypertrophy or buckling, facet joint
hypertrophy and disc protrusion. One or all of these
changes contribute to an overall reduction in canal diameter
which may result in cord compression.
DISC HERNIATION:
• Discogenic disease may cause myelopathy in the acute
setting as a large central soft disc herniation causing cord
compression
6. POST TRAUMATIC MYELOPATHY:
• Trauma may include myelopathy or precipitate symptoms of
stenosis of spinal cord. Smaller diameter canals have an increased
chance of neurological injury in trauma.
MYELOPATHY DUE TO TUMOR EXPANSION:
• Intraspinal tumors may originate in spinal cord or compress from
outside.
OTHER ETIOLOGIES:
• Cervical rheumatoid arthritis especially upper cervical spine and
to a lesser extend the lower cervical spine may present with the
clinical picture of cervical myelopathy.
• Rare neurologic complications which can cause narrowing of
cervical canal such as ankylosing spondylitis, gouty tophi from
posterior joint and paget’s disease.
7. CLINICAL PRESENTATION
• Neck stiffness (early complaint)
• Leg weakness, stiffness (proximal-distal)
• Gait abnormalities
• Difficulty with fine motor movements and tasks with hands “clumsy
myelopathic hands”
• Loss of bowel or bladder control
• Heavy feeling in the legs
• Poor exercise tolerance
• Radiculopathy
• Numbness and tingling in the limbs
• Chronic suboccipital headache : suboccipital may radiate to base of the
neck and vertex of the skull
• L’Hermitte’s phenomenon- intermittent electric shock sensations down
the neck, back and limbs, exacerbated by neck flexion
• Myelopathy’s hand: clumsiness, intrinsic wasting
8. CLINICAL SIGNS AND SYMPTOMS
• Patients may present with pain, paresthesia, weakness
or combination of these symptoms.
• Pain usually is in the cervical region, upper limb,
shoulder and/or intrascapular region, intermittent
shoulder pain.
• >2/3 patients present with unilateral or bilateral
shoulder pain.
• 1/3 patients present with headache
• Radicular signs: often non dermatomal
• Radiculopathy most commonly 6th and 7th roots occurs
from C5-6 or C6-7 spondylosis
• More pain proximally in their limbs, while parasthesias
dominate distally
9. CLUSTER FOR MYELOPATHY -
According to cook et al, selected combinations of the
following clinical findings are effective in ruling out and
ruling in cervical spine myelopathy. Combinations of 3
or 4 or 5 of these tests enable post-test probability of
the condition to 90-99% :
① Gait deviation
② +ve Hoffman's sign
③ Inverted Supinator sign
④ +ve Babinski sign
⑤ Age > 45 years or older
10. PHYSIOTHERAPY ASSESSMENT
• DEMOGRAPHIC DATA
• NAME- AGE- SEX- OCCUPATION-
• CHIEF COMPLAINT:
• HISTORY:
• PRESENT HISTORY: Date of onset of symptoms, mechanism of injury,
mode of onset, condition (Improved, stationary, Deteriorated), muscular
weakness
• PAIN HISTORY: Duration, type, aggravating and relieving factors
• PAST HISTORY: Any history of TB, Bronchial asthma, BP, diabetes, cardiac
problems, enquiry made for any accidental injury)
• FAMILY HISTORY: Hereditary?, consanguinity?
• PERSONAL HISTORY: Cigarettes, Alcohol
• SOCIO-ECONOMIC HISTORY:
• MEDICAL HISTORY: Present medication patient is on
11. • ON OBSERVATION :
• General condition of patient- poor, good, fair built
• Wasting
• Oedema
• Attitude of limbs : supine, sitting, standing
• Types of gait
• Bony contours
• Deformities
12. ON PALPATION:
• Tenderness- grading (1-patient complains of pain,
2-patient complains of pain and winces, 3- patient
winces and withdraws, 4- patient will not allow
palpation of the joint)
• Tissue tension and texture
• Temperature variation of skin
• Spasm
• Type of skin – Dry or excessive moisture
• Scar – adherent/ Non adherent
13. Swelling
• Comes on soon after injury- blood
• Comes on after 8-24 hours- synovial
• Boggy, spongy feeling- synovial
• Harder, tense feeling with warmth- blood
• Tough, dry- callus
• Leathery thickening – chronic
• Soft fluctuating- acute
• Hard- bone
• Thick , slow moving- pitting oedema
14. ON EXAMINATION :
• Patients present with a number of clinical findings which are
predominantly upper motor neuron signs.
• Weakness is more severe in the upper limbs.
• Gait is usually affected with an ataxic broad based gait, usually
spastic and spastic
• Hypertonia- increased resting muscle tone identified by passive
movement
• Hyperreflexia- exaggerated response to normal physiological reflexes
• Exaggerated tendon reflexes (patellar and achilles), presence of
pathological reflexes (e.g. clonus, Babinski and Hoffman’s sign)
• Ankle clonus- forced dorsiflexion at the ankle giving rise to sustained
beats of clonus (more than 3 beats is considered pathological)
15. • Muscular atrophy: supraspinatus, infraspinatus, deltoid,
triceps and the first dorsal interosseus muscle
• Motor weakness, most commonly in the iliopsoas followed
by quadriceps femoris
• Sensory abnormalities: variable pattern
• Loss of vibratory sense or proprioception in the extremities
can occur
• Spinothalamic sensory loss may be asymmetric
• Most commonly sensory symptoms including:
• Upper extremity numbness & pain, paresthesias initially,
followed by lower extremity sensory changes
• Motor dysfunction may be unilateral or bilateral depending
on the extend and location of cord damage
16. • Babinski sign – extension of the great toe on scratching
of the sole of the foot
• Hoffman’s reflex- flicking of the terminal phalanx of the
middle or ring finger causing concurrent flexion at the
terminal phalanx of the thumb and index finger
• Finger escape sign – the small finger spontaneously
abducts due to weak intrinsic muscles
• Spurling’s test
• Distraction test
• Hyper reflexic biceps, quadriceps, achilles
• Romberg test
21. NERVE ROOT INVOLVEMENT SYMPTOMS
C3 Nerve Root ① uncommon
② Rx pain may be present as
neck pain or occipital pain
C4 Nerve Root ① C4 Rx ī pain radiating to post
neck , trapezius and ant. chest.
C5 Nerve Root ① presents with Pain and/or
numbness over lat. aspect of
shoulder & deltoid.
② weakness of biceps,
supraspinatus, infraspinatus
③ Abduction relief sign
C6 Nerve Root ① Weakness of biceps , ECR
② Impaired EF & WE
③ sensation loss over thumb &
lat. portion of index finger.
④ dim. biceps & brachioradialis
reflex
⑤ pain radiates from neck-lateral
arm & forearm into the thumb
22. NERVE ROOT SYMPTOMS
C7 Nerve root ① impaired EE and WF
② dim. Tricep reflex
③ pain & numbnessfrom neck to
arm & digits 2-4
④ Horner's syndrome rarely seen
C8 Nerve root ① Weakness in hands intrinsic
muscles , Wrist extensors , and
flexors
② not sble tofully extend 4th &
5th digits
③ sensory loss- medial forearm &
4th 5th digits
④ pain radiating - neck->medial
forearm-> last 2 digits
⑤ Horner's syndrome-rare
T1 Nerve Root ① weakness- intrinsic muscles
② froment's sign +ve
③ Horner's syndome rare
23. INVESTIGATION
① Radiographs
• Pavlov index – the antero-
posterior diameter of the
spinal canal measured from
the middle of the posterior
vertebral body to the
nearest point of the
spinous process is equal to
or less than the antero-
posterior diameter of the
vertebral body.
• Should be 1.0 with <0.85
indicating stenosis
24. 2 . MRI
• Compression Ratio -
( < 0.4 indicates poor
prognosis )
CR =
smallest AP diameter of
cord
Largest transverse
diameter of cord
25. • A canal diameter of 17mm or greater at the mid
vertebral body level is considered normal.
• < 10-13mm - risk of cervical spondylosis
• DIAMETER OF CERVICAL SPINAL CANAL
C1 22.1mm
C2 18.8mm
C3 16.2mm
C4 15.8mm
C5 15.7mm
C6 15.6mm
C7 15.9mm
32. INITIAL PHASE -
① A. Electrotherapeutics
modalities like , TENS, US ,
IFT ( to reduce pain )
②
B. CERVICAL STABLISATION
EX'S
③ Chin Tuck
④ Chin tuck into towel
⑤ Cervical Extension
⑥ Shoulder Shrugs
⑦ Shoulder Rolls
⑧ Scapular Retraction
33. B. ISOMETRIC NECK EXERCISES -
① Cervical Flexion
② cervical Extension
③ Cervical Side Bending
④ Cervical Rotation
35. SECOND PHASE -
① Dynamic upper & lower limb
ex's with use of PBU on the
neck
② PNF diagonals for both U/L &
L/L
36. FINAL PHASE -
① Core stability ex's
② Balance training
③ Improving posture
④ Aerobic ex's - Treadmill
training ( 20 min )
37. POST - OP MANAGEMENT
PHASE I - ( 0 to 6 WEEKS )
GOALS -
① Diminish
pain/inflammation
and minimize UE
radiating symptoms.
② Postural correction ,
body mechanics ,
tranfers taught.
③ walking ( 30min × 2
times a day )
EDUCATION
①Postural education
②Body Mechanics
③Driving
38. Exercises -
I. Cardio
II. Deep cervical flexors
stabilisation
III. Scapular Retractions
IV. Isometrics
V. Cervical AROM
VI. Light stretching
Dose - one to twice / day
PRECAUTIONS -
①Avoid
bending,twisting,liftin
g , pushing & pulling.
②Cervical movements
with in painfree range
only.
39. PHASE II - (6-12 WEEKS )
GOALS
① pt. to have proper
neuromuscular control
& posture with
stabilisation &
strengthening
② initiate light
strengthening -> long
term home ex's
③ aerobic endurance to
30mins
④ release soft tissue
restrictions .
PRECAUTIONS
①keep spine in neutral
and good posture
②progression as
tolerated.
40. STRENGTH
* only initiate these once pt can
complete phase I ex's
① Postural/scapular
strengthening
② Cervical postural
strengthening
③ Aquatic ex's
41. PHASE III ( +12WEEKS )
Return to work / work conditioning / Return to
sport ( if applicable ).
① No aggressive rotation or side bend range of
motion
②Functional / sport/job drills may begin now with
supervision
③Possible referral to work reconditioning program
