This document discusses ptosis, or drooping of the eyelid. It begins by describing the functional anatomy of the levator palpebrae superioris muscle and other muscles involved in eyelid elevation. It then defines ptosis and classifies it as congenital or acquired, with the acquired category further divided into neurogenic, myogenic, aponeurotic, mechanical, and neurotoxic causes. Several types of congenital ptosis are described in detail, including blepharophimosis syndrome and Marcus Gunn jaw-winking syndrome. Evaluation of ptosis involves assessing history, appearance of eyelids at rest, levator function testing, and identifying associated signs. Investigations may include imaging or blood tests depending on
visual field- its assessment, defects, diseases associated. Types of visual field defects. visual field defects in glaucoma in detail. Humphrey's visual field analyser chart.
visual field- its assessment, defects, diseases associated. Types of visual field defects. visual field defects in glaucoma in detail. Humphrey's visual field analyser chart.
Neurological examination lec 1 vision and ocular systemLobna A.Mohamed
functional anatomy of the ocular system including ON,EOM and 3,4,6 CN
examination and signs of affection
differential diagnosis of poly CN and Optic neuropathy
you will get knowledge about the ptosis, its different types, its examination, its measurement, its treatment in detail.
different eyelid muscles such as LPS, Orbicularis oculi and frontalis are also explained.
The oculomotor nucleus complex present in the midbrain, at the level of the superior colliculus
Contains Main motor nucleus and Accessory parasympathetic nucleus (Edinger-Westphal nucleus)
Fibers pass between the posterior cerebral artery and the superior cerebellar artery to reach the cavernous sinus.
During this course, the oculomotor nerve lies lateral to the posterior communicating artery.
The nerve then divides into a superior and inferior division and enters the orbit through the superior orbital fissure
Third nerve palsy results from dysfunction of the nerve along its pathway from the midbrain to the extraocular muscles it innervates.
Third nerve palsies can cause dysfunction of the somatic muscles (SR ,IR,MR,IO, levator palpebral superioris) and autonomic muscles (the pupillary sphincter and ciliary muscle.)
classification
1. Complete or incomplete palsy
Complete: Involves both superior and inferior divisions of the nerve.
Incomplete: Involves superior division, inferior division (rarely), or an isolated muscle
2. Total palsy or partial paresis
● Total: Full restriction of extraocular muscles is present.
● Partial: Restriction of extraocular muscles is limited.
3. Pupil-involving or pupil-sparing palsy
● Pupil involving: Pupil is dilated, with an accommodative insufficiency.
● Pupil sparing: Pupil and accommodative function are normal.
Ocular nerve palsies are tricky to understand and are confusing. Learning the features by correlating with the anatomy make it easy.
These are both congenital and acquired.
With differential diagnosis and by proper stepwise ocular evaluation takes us to final diagnosis.
Ephaptic transmission of impulses between neighbouring neurons (i.e. coupling of adjacent nerve fibres due to local exchange of ions or local electric fields) leading to excessive or abnormal firing.
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
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
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
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.
- 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
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
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.
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.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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.
Follow us on: Pinterest
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
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
2. Functional anatomy
• Levator palpebrae superioris (LPS):
– is the primary muscle responsible for lid elevation.
– It arises from the back of the orbit and extends forwards
over the cone of eye muscles.
– It inserts into the eyelid and the tarsal plate, a fibrous
semicircular structure which gives the upper eyelid its
shape.
– The LPS is supplied by the superior division of the
oculomotor nerve.
• Muller’s muscles:
– The way that the LPS attaches to the tarsal plate is modified
by the underlying Müller's muscle.
– This involuntary muscle, comprising sympathetically
innervated smooth muscle,
– has the capacity to 'tighten' the attachment and so raise the
lid a few millimetres.
3.
4. • Frontalis & orbicularis oculi:
– frontalis muscle and the orbicularis oculi, both supplied
by the facial nerve.
– Frontalis contraction helps to elevate the lid by acting
indirectly on the surrounding soft tissues,
– while orbicularis oculi contraction depresses the eyelid.
5. DEFINITION
• Ptosis (from Greek Ptosis -to "fall") is a
drooping or falling of the upper or lower
eyelid.
6. CLASSIFICATION OF PTOSIS
A. Congenital
B. Acquired
1.
2.
3.
4.
5.
Neurogenic
Myogenic
Aponeurotic
Mechanical
Neurotoxic
C. Pseudotosis
7. Congenital ptosis
• It is associated with congenital weakness (maldevelopment)
of the levator palpebrae superioris (LPS).
1. Simple congenital ptosis
– not associated with any other anomaly.
2. Congenital ptosis with associated weakness of superior
rectus muscle.
3. Blepharophimosis syndrome,
– which comprises congenital ptosis, blepharophimosis,
telecanthus and epicanthus inversus .
4. Congenital synkinetic ptosis
– (Marcus Gunn jaw winking ptosis).
– In this condition there occurs retraction of the ptotic lid with jaw
movements i.e., with stimulation of ipsilateral pterygoid muscle.
9. Blepharophimosis syndrome
•
Rare congenital disorder
•
Dominant inheritance
•
•
•
•
•
•
Moderate to severe symmetrical ptos
Short horizontal palpebral aperture
Telecanthus (lateral displacement
of medial canthus)
Epicanthus inversus (lower lid
fold larger than upper)
Lateral inferior ectropion
Poorly developed nasal bridge
and hypoplasia of superior orbital
rims
10. Congenital synkinetic ptosis
• This condition is characterized as a synkinesis:
when two or more muscles that are
independently innervated have either
simultaneous or coordinated movements.
• In MARCUS GUNN PHENOMENON
– The stimulation of the trigeminal nerve by
contraction of the pterygoid muscles of jaw results in
the excitation of the branch of the oculomotor nerve
that innervates the LPS ipsilaterally, so the patient
will have rhythmic upward jerking of their upper
eyelid.
11. • There are two major groups of trigeminooculomotor synkineses:
1) External pterygoid-levator synkinesis:
– is when the eyelid raises upon Jaw thrust to opposite
side (homolateral external pterygoid) Jaw is projected
forward (bilateral external pterygoid) Mouth is opened
widely
2) Internal pterygoid-levator synkinesis
– is when the eyelid raises upon teeth clenching
• External pterygoid-levator synkinesis is the more
common group.
12. Marcus Gunn jaw-winking syndrome
• Accounts for about 5% of all cases of congenital ptosis
• Retraction or ‘wink’ of ptotic lid in conjunction with
stimulation of ipsilateral pterygoid muscles
Opening of mouth
Contralateral movement of jaw
13. • Inverse Marcus Gunn phenomenon:
– Synkinesia between CN V and the levator more rarely causes ptosis on
mouth opening .
• Marin Amat syndrome:
– is a facial nerve aberrant innervation syndrome with levator inhibition
with mouth opening.
• Ptosis in Lambert-Eaton syndrome :
– may temporarily improve after a brief period of upgaze.
• Eyelid myotonia :
– may cause transient difficulty opening the eyes after a forceful
contraction or transient lid retraction after looking up.
• Blepharospasm :
– is a focal dystonia causing involuntary eye closure;
– levator function is normal.
• In apraxia of lid opening,
– the patient has difficulty in voluntarily initiating lid elevation although
there is no levator impairment or blepharospasm.
• Rosenbach's sign:
– A fine tremor of the lid may occur in hyperthyroidism
15. A. Neurogenic ptosis
• It is caused by innervational defects such as
third nerve palsy,
• 3rd nerve misdirection
• Horner’s syndrome,
• Ophthalmoplegic migraine
• Cerebral ptosis
• Multiple sclerosis.
16. Right third nerve misdirection
• Rare, unilateral
• Aberrant regeneration following acquired third nerve palsy
• Pupil is occasionally involved
• Bizarre movements of upper lid accompany eye movements
Right ptosis in primary
position
Worse on right gaze
Normal on left gaze
17. Horner syndrome
Central
(first order neurone)
Posterior hypothalamus
•
•
Brainstem disease
(vascular, demyelination)
Spinal cord disease
(syringomyelia, tumours)
Pre-ganglionic
(second order neurone)
Superior cervical
ganglion
Intrathoracic lesions
(Pancoast tumour, aneurysm)
•
•
Neck lesions
(glands, trauma)
Post-ganglionic
(third order neurone)
Ciliospinal centre of
Budge( C8 - T2 )
Internal carotid artery disease
• Cavernous sinus mass
•
18. Phenyl ephrine test
• Patients with minimal ptosis (2 mm or less) should
have a phenylephrine test performed in the involved
eye or eyes
• Either 2.5 or 10% phenylephrine is instilled in the
affected eye or eyes. Usually two drops are placed
and the patient is reexamined 5 minutes later.
• The MRD1 is rechecked in the affected and
unaffected eyes .
• A rise in the MRDl of 1.5 mm or greater is
considered a positive test. This indicates that
Müller's muscle is viable
19. Ophthalmoplegic migraine
• Ophthalmoplegic Migraine is a rare eye disorder, previously
called a “complicated migraine”, which is also recognized as
cranial neuralgia by the International Classification of
Headache Disorders (HIS II) .
• This disorder most commonly presents itself in early childhood
or infancy.
• To date, there is no conclusive hypothesis as to the etiology of
this disorder (3, 4).
• Ophthalmoplegic migraines are characterized by
– Severe headaches
– weakening of muscles around the eye.
– these headaches commonly precede episodes of partial paralysis of
one or more ocular nerve (most commonly the third cranial nerve),
– drooping of the eyelid,
– double vision,
– dilation of pupils
20. IHS diagnostic criteria:
• At least 2 attacks fulfilling criterion B
• Migraine-like headache accompanied or
followed within 4 days of its onset by paresis
of one or more of the third, fourth and/or
sixth cranial nerves
• Parasellar, orbital fissure and posterior fossa
lesions ruled out by appropriate investigations
21. Cerebral ptosis
• is due to supranuclear lesions.
• Unilateral cerebral ptosis occurs with lesions,
usually ischemic, of the opposite hemisphere, and
is more common with right hemisphere lesions.
• Bilateral supranuclear ptosis may occur with
unilateral or bilateral hemispheric lesions.
• Ptosis has been reported in as many as 37.5% of
patients with hemispheric strokes.
22. B. MYOGENIC PTOSIS
• It is due to acquired disorders of the LPS
muscle or of the myoneural junction.
1. Myasthenia gravis
2. Myotonic dystrophy
3. Ocular myopathies
4. oculo-pharyngeal muscular dystrophy
5. following trauma to the LPS muscle.
23. Myasthenia Gravis
• The ptosis in MG is frequently asymmetric and may
be unilateral, though it will tend to shift from side
to side
• It characteristically fluctuates from moment to
moment and is worsened by prolonged upgaze
(fatiguable ptosis).
• Cogan's lid twitch sign,
– characteristic of myasthenia, consists of a brief
overshoot twitch of lid retraction following sudden
return of the eyes to primary position after a period of
downgaze.
24. • Curtain sign, seesaw ptosis:
– When the ptosis is asymmetric, the driving discharges
attempting to keep the more ptotic eyelid open are also
transmitted, per Hering's law, to the less ptotic eyelid.
– Manually raising the more ptotic lid causes relaxation
and the eye with less ptosis, sometimes even no ptosis,
may suddenly crash.
25. Myasthenia Gravis
2. Investigations
•
Edrophonium (Camiston) test
•
Electromyography to confirm fatigue
•
Antibodies to acetylcholine receptors
•
CT or MRI for presence of thymoma
3. Treatment options
•
Medical - anticholinesterases, steroids and azathioprine
•
Thymectomy
27. Edrophonium (Tensilon) Test:
• Edrophonium chloride inhibits acetylcholinesterase,
• thereby prolonging the presence of acetylcholine at the neuromuscular
junction.
• This results in enhanced muscle strength.
• In ptosis, a positive test is the elevation of eyelids in 2-5 minutes post
adminstration of Tensilon.
• A negative response is no improvement within 3 minutes.
• the Tensilon test has a relatively low sensitivity, approximately 60% for
MG.
• False positive results occur in patients with
– Lambert-Eaton Myasthenic Syndrome (LEMS),
– Amyothrophic Lateral Sclerosis (ALS), and
– localized intracranial mass lesions.
• Edrophonium chloride can cause overactivation of the parasympathetic
system, and cause unwanted side effects like fainting, dizziness,
involuntary defecation, severe bradycardia, apnea, and even cardiac
arrest. It is important to always have atropine at hand if such side
effects should occur
28. Edrophonium test
Before injection
•
•
Measure amount of ptosis or
diplopia before injection
Inject i.v. atropine 0.3 mg
Positive result
•
•
Inject i.v. test dose of edrophonium
(0.2 ml-2 mg)
Inject remaining (0.8 ml-8 mg) if no
hypersensitivity
29. Myotonic dystrophy
Facial weakness and
ptosis
Release of grip difficult
Hypogonadism
• Frontal baldness in males
• Involvement of tongue and pharyngeal muscles
• Intellectual deterioration
• Ophthalmoplegia - uncommon
• Presenile stellate cataracts
•
Muscle wasting
•
30. Ocular myopathies
Ocular features
Clinical types
•
•
•
Isolated
Ptosis - slowly progressive
and symmetrical
Oculopharyngeal dystrophy
• Ophthalmoplegia - slowly
Kearns-Sayre syndrome
progressive and symmetrical
(pigmentary retinopathy)
(no diplopia)
•
31. C. APONEUROTIC PTOSIS
• It develops due to defects of the levator
aponeurosis in the presence of a normal
functioning muscle.
• It includes
– involutional (senile) ptosis,
– postoperative ptosis
• Ptosis due to aponeurotic weakness associated with
blepharochalasis (Blepharochalasis is an inflammation of the eyelid that is
characterized by exacerbations and remissions of eyelid edema, which results in a
stretching and subsequent atrophy of the eyelid tissue resulting in redundant folds
over the lid margins)
– Posttraumatic dehiscence or disinsertion of the
aponeurosis.
32. Aponeurotic ptosis
Weakness of levator aponeurosis
• Causes - involutional, postoperative and blepharochalasis
•
Mild
High upper lid crease
Good levator function
Severe
Absent upper lid crease
Deep sulcus
33. Senile ptosis
• Senile or involutional ptosis is very common.
Asymmetric lids and redundant lid tissue in the
elderly.
• The levator aponeurosis attaches the levator muscle
to the tarsal plate, which forms the eyelid.
• Aging may cause levator dehiscencedisinsertion
(LDD)—with stretching, thinning, or detachment of
the aponeurosis.
• Normally, with the eyelids gently closed, the upper
lid margin lies 5 mm to 7 mm below the upper lid
fold (the skin fold at the upper part of the lid).
• An increase in this distance suggests LDD.
34.
35. D. Mechanical ptosis
• Due to excessive weight on the upper lid
– lid tumours,
– multiple chalazia
– lid oedema.
• Cicatricial Ptosis
– ocular pemphigoid
– trachoma.
37. E. NEUROTOXIC PTOSIS
• Envenomation by elapids such as cobras, or
kraits.
– Bilateral ptosis is usually accompanied by diplopia,
dysphagia and/or progressive muscular paralysis.
– Regardless, neurotoxic ptosis is a precursor to
respiratory failure and eventual suffocation
caused by complete paralysis of the thoracic
diaphragm.
– It is therefore a medical emergency and
immediate treatment is required.
38. PSEUDOPTOSIS
• Pseudoptosis is the appearance of ptosis in the
absence of levator abnormality.
• Exclude pseudoptosis (simulated ptosis) on
inspection.
• Its common causes are:
– microphthalmos,
– anophthalmos,
– enophthalmos
– Phthisis bulbi.
– Double elevator palsy
– Blepharospasm
– Contralateral proptosis
39. • Blepharochalasis (dermatochalasis)
– refers to age-related lax, baggy skin around the
eyelids;
– it can also simulate ptosis but levator function is
normal
• Duane's syndrome
– the palpebral fissure narrows on ocular adduction
because of globe retraction causing dynamic
enophthalmos.
40. Causes of pseudoptosis
Lack of lid support
Ipsilateral hypotropia
Contralateral lid retraction
Brow ptosis - excessive
eyebrow skin
Dermatochalasis - excessive
eyelid skin
44. HISTORY
• Ptosis
– Age of onset
– Duration
– One/both eye
– Diurnal variability
• Associated history :
– Diplopia
– Dysphagia
– Muscle weakness
• Vision
45. • Association with
– Jaw movements
– Abnormal ocular movements
– Abnormal head posture
• History of
– Trauma or previous surgery
– Poisoning
– Use of steroid drops
– Any reaction with anesthesia
– Bleeding tendency
• Previous photographs may prove to be of great
help.
• Is there a family history of ptosis or of other muscle
weakness?
46. Ocular Examination:
NORMAL POSITION OF EYELIDS
• The normal upper eyelid in primary position
– crosses the iris between the limbus (junction of the iris
and sclera) and the pupil,
– usually 1 mm to 2 mm below the limbus;
– the lower lid touches or crosses slightly above the
limbus.
– Normally there is no sclera showing above the iris.
• The palpebral fissures:
– are normally 9 mm to 12 mm from upper to lower lid
margin.
47. Ptosis
• U/L or B/L
• Complete /incomplete
• Total unilateral ptosis
– complete third nerve palsy.
• Mild to moderate unilateral ptosis
– Horner's syndrome,
– partial third nerve palsy.
• Mild to moderate bilateral ptosis
– neuromuscular disorders, such as MG,
– muscular dystrophy,
– Ocular myopathy.
48. • Head Posture:
– chin elevation as the ptosis is minimum in downgaze in a
patient with congenital ptosis is also one of the indications
for surgery especially in the pediatric age group.
– In ptosis there will be superior altitudinal defect which is
corrected by elevating the eyelids
• Ocular Motility:
– Importance in myogenic ptosis,
– To R/O 3rd nerve palsy
– presence of strabismus, especially vertical strabismus entails
that it be corrected prior to the correction of the ptosis.
• Visual acuity
– Best-corrected visual acuity should be assessed to record any
amblyopia if present, especially in cases of congenital ptosis.
• Pupillary Examination:
– TO diagnosis Horner’s syndrome
– Involvement in a case of third nerve palsy
50. 1. MARGIN REFLEX DISTANCE
• Margin-to-reflex distance 1 (MRD1) :
– When light is thrown on the cornea a reflection occurrs
.the distance from the central pupillary light reflex to the
upper eyelid margin with the eye in primary gaze.
• NORMAL : 4 - 5 mm.
• If the margin is above the light reflex the MRD 1 is a
+ve value.
• If the lid margin is below the corneal reflex in cases
of very severe ptosis the MRD 1 would be a –ve
value.
51.
52. Marginal reflex distance
• Distance between upper lid
margin and cornal light reflex
(MRD)
• Mild ptosis (2 mm of droop)
• Moderate ptosis (3 mm)
• Severe ptosis (4 mm or more)
53. 2. Vertical fissure height
• The distance between the upper and lower
eyelid in vertical alignment with the center of
the pupil in primary gaze, with the patient’s
brow relaxed.
• Normal – 9-10mm in primary gaze
• Should be seen in up gaze, down gaze and
primary gaze
• Amount of ptosis = difference in palpebral
apertures in unilateral ptosis or Difference
from normal in bilateral ptosis
54.
55. Grading of severity of ptosis
< or = 2mm : mild ptosis
= 3 mm : moderate ptosis
= or > 4 mm : severe ptosis
56. 3. Levator function assesment
• It is determined by the lid excursion caused by LPS
muscle (Burke’s method).
– Patient is asked to look down, and thumb of one hand is
placed firmly against the eyebrow of the patient (to block
the action of frontalis muscle) by the examiner.
– Then the patient is asked to look up and the amount of
upper lid excursion is measured with a ruler held in the
other hand by the examiner.
– Levator function is graded as follows:
•
•
•
•
Normal 15 mm
Good 8 mm or more
Fair 5-7 mm
Poor 4 mm or less
57. Upper lid excursion- burke’s ,method
•
Reflects levator function
•
Normal (15 mm or more)
•
Good (8 mm or more)
•
Fair (5-7 mm)
•
Poor (4 mm or less)
58. Upper lid crease
Pretarsal show
fold
crease
•
•
•
•
Distance between lid margin and lid
crease in down-gaze
Normals - females 10 mm; males 8 mm
Absence in congenital ptosis indicates
poor levator function
High crease suggests an aponeurotic
defect
•
Distance between lash line and skin
fold in primary position of gaze