Brief introduction to anatomy of sixth and seventh cranial nerves.
Brief introduction to some disorders in the nerve course and its related clinical features.
Few management for the problem.
#neuro-ophthalmology
Anatomy of Lateral Rectus, Anatomy of Abducens Nerve, Palsy of Abducens Nerve | by Optometrist Hasnain Pasha | Presented at Isra School of Optometry - Al-Ibrahim Eye Hospital
Anatomy of Lateral Rectus, Anatomy of Abducens Nerve, Palsy of Abducens Nerve | by Optometrist Hasnain Pasha | Presented at Isra School of Optometry - Al-Ibrahim Eye Hospital
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.
Cranial_Nerves_examination Cranial nerve examination frequently appears in OS...Zachm5
Cranial nerve examination frequently appears in OSCEs. You’ll be expected to assess a subset of the twelve cranial nerves and identify abnormalities using your clinical skills
Similar to Sixth and seventh cranial nerves: anatomy and disorders (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.
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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
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.
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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
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.
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
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4. Functional components
• Somatic efferent: for lateral movement of the eye
• General somatic afferent: for proprioceptive
impulses from the lateral rectus muscle
5. Nucleus
• Situated in the lower part of the pons, close to the midline,
beneath the floor of the 4th ventricle
• Consists of two types of multipolar cells:
a. Large
b. Small
• Large multipolar cells give rise to fibres of the abducent nerve
• Fibres of the small multipolar cells relay in the oculomotor
nucleus via the medial longitudinal fasciculus (MLF)
6. Connections of the nucleus
1. Cerebral cortex:
• Motor cortex (precentral gyrus) through the afferent
corticonuclear fibres from both cerebral hemispheres
(principally contralateral )
• Visual cortex: through the
superior colliculus and
tectobulbar tract
• Frontal cortex (FEF)
7. 2. Nuclei of 3rd, 4th and 8th cranial nerves through the medial
longitudinal bundle
3. Pretectal nucleus of both sides through the tectobulbar tract
4. Horizontal gaze center (paramedian pontine reticular
formation – PPRF) through the medial longitudinal bundle
5. Cerebellum through vestibular nuclei
8.
9. Course and distribution
A. The fascicular part:
• Consists of efferent fibres which start from the nucleus , pass
forward traversing the medial leminiscus and pyramidal tract.
• These then emerge by some 7 to 8 rootlets from the junction
of pons and medulla just lateral to the pyramidal prominence
(of medulla) .
• Rootlets join to form one nerve, at varying distance from the
origin .
10. B. The basilar part :
• The nerve then runs through the cisterna pontis between the
pons and the occipital bone.
• The nerve runs upwards on the back of the petrous temporal
bone near its apex
• At the sharp upper border of the petrous bone, the nerve
bends forward at right angle under petrosphenoidal ligament
and enters the cavernous sinus
11. C. The intracavernous part :
• In the cavernous sinus, the nerve runs below and lateral to
internal carotid artery
• The internal carotid artery is surrounded by sympathetic plexus
• It then leaves the cavernous sinus to enter the orbit through the
middle part of superior orbital fissure within the annulus of Zinn
• In the superior orbital fissure, the abducent nerve lies
inferolateral to the oculomotor and nasociliary nerves
12. D. The intraorbital part:
• In the orbit, the nerve runs forward and enters the ocular
surface of the lateral rectus muscle just behind its middle
portion after dividing into three or four branches.
13. Features and causes of sixth nerve
lesions at various levels
A. Supranuclear lesions:
• cause loss of conjugate movements of eyeball
B. Nuclear lesions:
• Ipsilateral sixth nerve palsy
• Ipsilateral seventh nerve palsy of upper motor neuron type due
to concomitant involvement of facial fasciculus
• Loss of conjugate movements to the same side resulting from
involvement of horizontal gaze center in the PPRF
14. C. Fascicular lesions:
Foville’s syndrome results due to lesions
of dorsal pons involving sixth nerve
fasciculus as it passes through PPRF and is
characterized by the following:
• Ipsilateral sixth nerve palsy
• Loss of conjugate movements of the same
side
• Ipsilateral facial nerve palsy
• Facial analgesia from involvement of the
sensory portion of the fifth nerve
• Deafness
15. Millard gubler syndrome : results due to
lesions of the ventral pons involving
fasciculus and is characterized by the
following :
o Ipsilateral sixth nerve palsy
o Contralateral hemiplegia
o Variable number of signs of dorsal
pontine lesions
oIpsilateral facial paralysis may or may not
be present
Raymond’s syndrome: same as above
except for facial involvement
16. D. Lesions of the basilar part of sixth nerve:
• Cause may include acoustic neuroma, nasopharyngeal tumors
and fracture base of the skull
• The involvement of petrous bone from otitis media may cause
Gradenigo syndrome, characterized by the following :
oIpsilateral sixth nerve palsy
oDeafness
oNeuralgia in the distribution of first division of trigeminal nerve
oFacial weakness
17. • Involvement in raised intracranial pressure :
6th nerve paralysis is commonest false localizing sign in raised ICP
Its susceptibility to such damage is due to its long course in the
cisterna pontis, to its sharp bend over the superior border of the
petrous temporal bone and the downward shift of the brainstem
(towards foramen magnum) produced by raised ICP
18.
19. E. Lesions of the intracavernous part of sixth nerve
• Lesions such as aneurysms, meningioma, carotid cavernous
fistulae and Tolosa-Hunt syndrome
• In contrast to 3rd nerve, aneurysms rarely cause a sixth nerve
palsy
• Vascular causes such as diabetes and hypertension are however
common causes of sixth nerve palsy
• Occasionally may be accompanied by Horner’s syndrome.
20.
21. F. Lesions of the intraorbital part of sixth nerve:
• Uncommon
• Involved in the lesions producing orbital apex syndrome and
superior orbital fissure syndrome
22.
23. Clinical features of sixth nerve palsy:
Deviation : esodeviation
Ocular movements: limited abduction
Diplopia: uncrossed horizontal diplopia
Head posture: face turn toward defective side
24.
25. Investigation
• History
• Observation (clinical presentation)
• Clinical investigation:
₋ Visual acuity at near and distance
₋ Cover test at near and distance (with or without AHP)
₋ Version, duction and vergence movements (EOM)
₋ Measurement of deviation at near and distance
₋ Past pointing
₋ FDT (to exclude mechanical restriction)
₋ Maddox rod
₋ Diplopia chart and Hess chart
27. Past-Pointing
• Anomalies of egocentric/spatial localization, referred to as past-
pointing or false orientation
• If a patient is asked to point at an object in the field of action of a
paretic muscle while the paretic eye is fixating, the patient's
finger will point beyond the object toward the field of action of
the paretic muscle
28. FIGURE 20–6. Past-pointing in a patient with left sixth nerve
paresis. A, Normal egocentric localization in dextroversion. B,
Past-pointing to the left when viewing an object in the median
plane, and C, in the paretic field of gaze.
29. • Egocentric localization of objects in space is approximately
correct as long as there is no discrepancy between innervational
effort to move the eye and the amplitude of the executed eye
movement.
• With left abducens paralysis, for instance, excessive innervation
is required to counteract the unopposed antagonistic medial
rectus muscle when the patient is holding the paralyzed eye in
primary position or moving it toward abduction. As a result, the
subjective impression created by excessive abduction
innervation is that the object to be fixated lies to the left of the
median plane in primary position and even farther to the left on
attempted.
• Also a/w comitant deviations
30. Forced duction test
• Assesses PASSIVE movement of the globe
• Assist in differentiating neurogenic and mechanical restrictions
• Method :
Local anesthetic applied
Pt. looks in direction of restricted gaze
if performed with pt. awake
The eye is then assisted to move in
direction of restricted gaze with forceps
31. Forced Duction Test
The forced duction test. A, Conjunctiva and episclera are
grasped near the limbus with two fixation forceps. The eye is
moved temporally and (C), nasally to test for mechanical
restriction of ocular motility. Note that the eye must not be
depressed into the orbit during the test to avoid false positives.
32. Interpretation
No resistance encountered
• Deviation : neurogenic in origin
• Negative FDT
Resistance is encountered
• A mechanical restriction must be considered
• Positive FDT
33. Diplopia chart
• Provides a record of separation of diplopic
images in the nine position of gaze
• Can be performed in any co operative patient experiencing
diplopia
• Assists in determining which direction of gaze diplopia is worst in
34. Method
• Pt. wears red/green goggles
• Examiner presents a white light source at 50 cm in primary
position
A linear light is best to use.
• Pt. asked to indicate position of diplopic image. Ask about
Horizontal displacement
• The light is then moved into nine positions of gaze
Pt. is questioned about diplopia in each position
36. Hess chart
Principle: Based on
• Foveal projection
• Hering’s and Sherrington’s laws of innervation
• Dissociation of eyes by complementary colors
37.
38. Differentiating between a total and
a partial sixth nerve palsy
• Presence of abduction past the midline, which indicates residual
LR function and identifies a partial palsy
• Failure to abduct past the midline indicates a total palsy or can be
due to mechanical restriction
• The identification of residual LR function in this situation depends
on:
1. Forced generation test
2. Botulinum toxin injection
3. Saccadic velocity analysis
39. Force generation test
• Method:
• Forceps used to stabilize the eye
Eye placed in the opposite direction to limitation
E.g.: limited RE abduction ; eye stabilized in left gaze
• Pt. asked to look in direction of limitation
• Assess the amount of tug/pull felt
Interpretation
• Muscle force can be estimated by
• Noting the tug/ pull felt which is caused by the contraction of the
muscle
• A tug/ pull indicates that muscle has potential function
40. Estimation of generated muscle force.
A, A patient with a left lateral rectus paresis shows movement of the left eye from
adduction toward primary position on levoversion and slightly beyond. This movement
may be active (residual lateral rectus innervation) or passive (medial rectus
relaxation)..
B, The examiner senses a tug on the forceps as the paretic eye moves from adduction
toward primary position. The tug is a sign of residual innervation of the lateral rectus
muscle and incomplete paralysis. Absence of the tug is a sign of complete paralysis.
41. Management
I. Treatment of the cause
II. Conservative measures
Wait and watch for minimum of 6-8 mths
Measures to expedite recovery from palsy (vit B complex,
steroids if non specific inflammation, etc.)
Measures to prevent amblyopia and relieve diplopia (alternate
patching, botulinum toxin injection, Fresnel prism)
III. Surgical treatment
Recess-resect operation : large recession of antagonist MR with
resection of LR
44. Functional components
1. Branchial efferent for facial expressions and elevation of hyoid
bone
2. General visceral efferent component is concerned with
parasympathetic supply of the lacrimal gland, submandibular
and sublingual salivary glands and the nasal, palatine and
pharyngeal glands
3. Special visceral afferent for taste sensations from presulcal
area of the tongue and the palate
4. General somatic afferent for sensations from the concha of
the auricle (clinically irrelevant)
45. Nuclei
A. Main motor nucleus
Lies deep in the reticular formation of the lower part of the
pons, in the column of other branchial efferent nuclei
The part of the nucleus that supplies the muscles of the upper
part of the face receives corticonuclear fibres from both cerebral
hemispheres
The part of the nucleus that supplies the muscles of lower part
of the face receives corticonuclear fibres from the opposite
cerebral hemisphere only
46. B. Parasympathetic nuclei:
• Situated posterolateral to the main motor nucleus in the column
of general visceral efferent nuclei
• Includes :
i. Superior salvatory nuclei
ii. Lacrimator nucleus
47. i. Superior salvatory nucleus:
Receives afferent fibres from the hypothalamus through the
descending autonomic pathway
Sends preganglionic fibres which innervate the submaxillary and
sublingual salivary glands
48. ii) Lacrimatory nucleus:
Receives afferent fibres from:
- the hypothalamus for emotional responses
- the sensory nuclei of the trigeminal nerve for reflex
lacrimation secondary to irritation of the cornea or conjunctiva
Sends preganglionic fibres for innervation of the lacrimal gland
49. C) Sensory nucleus
The upper part of nucleus tractus solitarius constitutes the
sensory nucleus of the facial nerve
Belongs to special visceral afferent nuclei
Situated in upper part of medulla oblongata in line with other
nuclei of its group
Receives afferent fibres (central processes of neurons of the
geniculate ganglion of the facial nerve) and also afferents from
the concha of the auricle
50. The efferent fibres from the nucleus tractus solitarius ascend to
the ventral posterior medial nucleus of the opposite thalamus
and also a number of hypothalamic nuclei
From the thalamus, the axons of the thalamic cells pass through
the internal capsule and corona radiata to end in the taste area
of the cortex in the lower part of the post central gyrus.
51.
52. Course and distribution
Consists of motor and sensory root
Fibres of the motor root, travel posteriorly from the medial
side of the abducent nucleus and then pass around this nucleus
beneath facial colliculus, and finally pass anteriorly to emerge
from the brain stem
The sensory root (nervous intermedius) consists of central
processes of the unipolar cells of geniculate ganglion. Also
contains the preganglionic parasympathetic fibres from the
parasympathetic nuclei
53. The two roots of the facial nerve emerge from the junction of
pons and medulla just medial to 8th cranial nerve
Then the two roots run laterally and forwards (with the 8th
nerve) to reach the internal acoustic meatus.
Here the 7th and 8th nerves are accompanied by the labyrinthine
vessels.
At the bottom of the meatus, the two roots (sensory and motor)
fuse to form a single trunk, which lies in the petrous temporal
bone.
54. Within the canal, in the petrous part of temporal bone, the
course of the nerve can be divided in 3 parts by two bends.
The facial nerve leaves the skull by passing through the
stylomastoid foramen
The first part is directed laterally above the vestibule
The second part runs backwards in relation to the medial
wall of the middle ear above the promontory
The third part is directed vertically downwards behind the
promontory
55. In the extracranial course
Crosses the lateral side of the base of styloid
process
Enters the posteromedial surface of the
parotid gland
Runs forward through the gland crossing the
retromandibular vein and external carotid
artery
Behind the neck of the mandible, it divides into its five terminal
branches which emerge along the anterior border of the
parotid gland.
56. Branches
A. Branches within the facial canal
1. Greater petrosal nerve:
Contains mainly taste fibres
Relayed to the lacrimal gland
Relayed to nasal and palatine mucosal glands
2. Nerve to stapedius:
Supplies the stapedius muscle
3. Chorda tympani:
It carries:
-a preganglionic secretomotor fibres to the submandibular ganglion for
supply of the submandibular and sublingual salivary glands
- Taste fibres from anterior two-thirds of the tongue
57. B. Branches at its exit from the stylomastoid foramen:
1. Posterior auricular nerve
2. Digastric branch
3. Stylohoid branch
C. Terminal branches within the parotid gland:
1. Temporal branch:
Auricularis anterior and superior
Intrinsic muscles on the lateral side of ear
Frontalis
Orbicularis oculi
Corrugator supercilli
58. 2. Zygomatic branch : supplies orbicularis oculi
3. Buccal branch : supplies to area around parotid duct
4. Mandibular branch: supplies to muscles of lower lip and chin
5. Cervical branch: platysma
D. Communicating branches
The motor nerves of the 1st, 2nd and 3rd branchial arches
communicate with each other
59. Ganglia
1. Geniculate ganglion :
• Located on the first bend of the facial nerve in relation to medial
wall od middle ear
• Sensory ganglion
• Taste fibres
2. The submandibular ganglion:
• Parasympathetic ganglion
• Relay of secretomotor fibres from submandibular and sublingual
glands
60. 3. Pterygopalatine ganglion or sphenopalatine ganglion:
• Largest parasympathetic peripheral ganglion
•
• Serves as relay station for secretomotor fibres to the lacrimal
gland and to mucous glands of nose, the paranasal sinuses, the
palate and the pharynx.
• Functionally related to facial nerve even though topographically
related to maxillary nerve
61. Clinical features of patient with facial nerv
palsy
• Motor function of the upper face is examined by having the
patient raise their eyebrows to wrinkle their forehead (frontalis).
62. • The most important test of facial nerve function is checking eye
closure (orbicularis oculi).
• Using a cotton wisp to check the corneal reflex also evaluates
efferent innervation of the orbicularis muscle through the
corneal blink reflex arc.
• Lower facial muscle function is tested by having the patient smile
and show their teeth.
63. • The practitioner should evaluate any asymmetry of the patient’s
smile and check for flattening of the nasolabial fold on the
involved side.
64. Ocular examination
1. Motility evaluation
2. Corneal sensitivity
3. Tear film (basal Schirmer testing)
4. Corneal integrity
5. Lower eyelid Ectropian
Patient may complain of epiphora and spilling over of tears onto
cheek.
This is usually result of reflex lacrimation.
6. After assessing orbicularis oculi, Bell’s phenomena should also
be checked.
65.
66. Applied aspects
• In supranuclear lesions of the facial nerve (usually a part of the
hemiplegia), only the lower part of the contralateral face is
paralyzed.
• Upper part (frontalis and part of orbicularis oculi) escapes due
to its bilateral representation in the cerebral cortex.
• At this level, cerebrovascular accidents and tumors are the most
likely causes.
67. • In infranuclear lesions of the facial nerve, the whole of the face
of the ipsilateral side is paralyzed, abolishing both voluntary
and emotional movements.
• The face becomes asymmetrical and is drawn up to the normal
side.
• Wrinkles disappear from the forehead
• The eyes cannot be closed (lagophthalmos)
• Any attempt to smile draws the mouth to the normal side.
During mastication, food accumulates between the teeth and
the cheek.
68. The common causes of infranuclear facial nerve palsy are:
1. Bell’s palsy
2. Diseases of the brainstem
3. Acoustic neuromas
69. • The lesions found distal to the chorda tympani produce isolated
facial palsy.
• Ramsay – Hunt syndrome occurs due to herpes zoster infection
of geniculate ganglion of facial nerve. Characterized by lower
motor neuron type of facial palsy associated with severe pain in
the ear and vesicles near the ear.
70. • Lesions at the level of pons result in the involvement of both
the abducent and facial nerve
• Lesions at the cerebellopontine angle result in the
involvement of both the facial and auditory nerve.
71. Mobius syndrome:
• Bilateral congenital syndrome in which
both CN VI and CN VII palsy combine causing an esotropia and an
inability to form facial expression.
• Aetiology : primary developmental defects of CNS with aphasia
of the motor nuclei of VI and VII nerves and denervation atrophy
of facial and EOMs
72.
73. • Aberrant regeneration is common.
• When fibres originally designed for orbicularis oculi reinnervate
lower facial muscles, each blink may cause twitch of the corner
of mouth or a dimpling of the chin.
• Conversely, movement of lower face, such as pursing lips, smiling
or chewing with the mouth closed may produce involuntary lid
closure.
74. • Other disorders of aberrant facial innervation include
lacrimation caused by chewing (crocodile tears), in which fibers
originally supplying mandibular and sublingual glands
reinnervate the lacrimal gland.
• This syndrome usually follows severe proximal seventh nerve
injury and may be accompanied by decreased reflex tearing and
decreased taste from the anterior two thirds of the tongue.
75. Management
• In cases of orbicularis oculi involvement:
⁻ Artificial tear supplements
⁻ Taping the eyelid shut
⁻ Moisture chamber to be used at night
⁻ Avoid dusty or windy environment
⁻ BCL can be used in superficial punctate keratopathy
⁻ Breakdown of corneal epithelium indicates need for punctal
plugs, tarsorraphy, or injection of botulinum toxin to induce
ptosis.
⁻ In some cases, corticosteroids are used.
76.
77. Disorders of over activity of 7th nerve
1. Essential blepharospasm:
• Episodic contraction of orbicularis oculi
• Between 40-60 yrs. of age
• Facial grimacing and other movements may be associated
(Meige syndrome)
• Unknown cause maybe basal ganglia dysfunction
• Should first exclude other causes (severely dry eyes, intraocular
inflammation, and meningeal irritation)
• Type A botulinum toxin can be used or surgical therapy
78. 2. Hemifacial spasm:
• Characterized by unilateral episodic spasm that involves facial
musculature
• Typically lasts from a few seconds to minutes
• Pathogenesis: compression of seventh nerve root exit zone by an
aberrant vessel
• Abnormal firing in the motor nucleus or ephaptic transmission of
nerve impulses causes innervation directed toward one muscle
group to excite adjacent nerve fibres directed to another muscle
group
• Botulinum toxin A injection and facial myectomy
79.
80. 3. Facial myokymia:
• Characterized by continuous unilateral fibrillary or undulating
contraction of facial muscle bundles
• When confined to eyelid, commonly a self limited, benign
condition
• Occasionally, these rippling movements begin within a portion of
orbicularis oculi and may spread to involve most facial muscles
• Typically signifies intramedullary disease of pons involving the
seventh nerve nucleus or fascicle
• Usually a result of pontine glioma in children and multiple
sclerosis in adults
• May be relieved by carbamazepine, or botulinum toxin injection
81. Summary
• Any clinical signs such as limited abduction, abnormal head
posture, lagophthalmos, facial asymmetry, etc. are to be
carefully examined to rule out possible neurological causes.
• Possible management should be given and be referred as
needed.
82. References
• Anatomy and physiology of eye -A. K. Khurana
• Wolff’s anatomy
• Theory and practice of squint and orthoptics- A.K. Khurana
• Diagnosis and management of ocular motility disorders-
Alec M Ansons
• AAO section5 Neuro-ophthalmology
• Principles and practice of ophthalmology – Albert &
Jackobiec (volume 3)
• CET articles
• Internet
Editor's Notes
Good morning everyone. I am Urusha Maharjan. Here in front of you all to present on topic …
Gsa: these impulses ultimately reach the mesencephalic nucleus of the trigeminal nerve
Closely related to the fasciculus of the facial nerve
The small multipolar cells are believed to form the para abducent nucleus
Since the abducent nucleus belongs to the group of somatic efferent nuclei, it lies in the line with nuclei of fourth and third nerves above and within the nucleus of hypoglossal nerve below.
FEF: frontal eye fields
Nuclei of 3rd, 4th and 8th cranial nerves through the medial longitudinal bundle
Pretectal nucleus of both sides through the tectobulbar tract
Horizontal gaze center (paramedian pontine reticular formation – PPRF) through the medial longitudinal bundle
Cerebellum through vestibular nuclei
FEF: frontal eye fields
Nuclei of 3rd, 4th and 8th cranial nerves through the medial longitudinal bundle
Pretectal nucleus of both sides through the tectobulbar tract
Horizontal gaze center (paramedian pontine reticular formation – PPRF) through the medial longitudinal bundle
Cerebellum through vestibular nuclei
For the purpose of description, the course of the abducent nerve can be divided into fascicular, basilar, intracavernous and intraorbital parts.
by piercing its wall at a point lateral to the dorsum sellae and superior to the apex of petrous temporal bone
In short, the sixth nerve nucleus is located in pons whose fibres run along the brainstem to the lateral rectus muscle through the superior orbital fissure and into the orbit through middle part of superior orbital fissure and to lateral rectus muscle
Sixth nerve has the longest sub arachnoid course which makes it vulnerable to injury at many levels
Due to close association between sixth and seventh nerve (facial) in the brainstem, there maybe involvement of seventh nerve also in some cases
Congenital sixth nerve palsy is due to hypoplasia of its nucleus. 6th paresis occurring shortly after birth usually resolves spontaneously and may be caused by increased ICP associated with labor and delivery.
Congenital bilateral abducent paralysis associated with facial diplegia and microglossia constitutes the Mobius syndrome.
In
addition, the lesions in Wernicke–Korsakoff syndrome are
believed to involve the sixth-nerve nucleus.
The first symptom of acoustic neuroma is hearing loss and first sign is diminished corneal sensations. Therefore, hearing and corneal sensations should be tested in all patients with sixth nerve palsy
“false localizing” if they reflect dysfunction distant or remote from the expected anatomical locus of pathology, hence challenging the traditional clinicoanatomical correlation paradigm on which neurological examination is based.
Since the sixth nerve runs through the middle of the cavernous sinus, it is most prone to damage than the other nerves from the intracavernous lesions such as aneurysms, meningioma…
Horner Syndrome can be caused by damage to the sympathetic pathway at any location of its route from the hypothalamus to the eye.
Since, in its intracavernous part, the sixth nerve is joined by the sympathetic branch from paracarotid plexus, so occasionally sixth nerve palsy may be accompanied by Horner's syndrome
In primary position, eyeball is converged due to unopposed action of the medial rectus muscle. Secondary deviation is greater than primary
Weakness of lateral rectus muscle . If RLR palsy, OA of RMR. OA of LMR. UA of LLR
Diplopia worsens toward the action of paralyzed muscle. Maximum image separation at distance and to side of involvement
Face turn toward the action of paralyzed muscle to minimize diplopia. eye takes its position opposite to its action
For eg,in LR palsy, eye in adducted position. Face turn to same side.
In primary position, eyeball is converged due to unopposed action of the medial rectus muscle. Secondary deviation is greater than primary
Weakness of lateral rectus muscle . If RLR palsy, OA of RMR. OA of LMR. UA of LLR
Diplopia worsens toward the action of paralyzed muscle. Maximum image separation at distance and to side of involvement
Face turn toward the action of paralyzed muscle to minimize diplopia
Deviation greater at distance
Measurement in expected relevant defective gaze (lateroversion in 6th palsy)
More revealing is the examination of versions : show marked over action of the yoke muscle of the paretic muscle in the contralateral eye (secondary deviation) when fixating with the paretic eye.
However, since past-pointing occurs
only with paralysis of the extraocular muscles of
recent onset and tends to disappear gradually, this
sign continues to be of clinical value in distinguishing between congenital and acquired paralysis.
to avoid visual correction of the error of localization while the hand is still moving toward the
One explanation is that the image of the target lies in an abnormal location relative to the fovea so that the patient incorrectly localizes the object into that field. past-pointing that is observed when the image of the target lies on the fovea of the paretic eye
an argument has raged over the relative role of efferent command to the eye muscles versus proprioceptive afferent information from the eye muscles. In support of the efferent command theory, Helmholtz argued that past-pointing depends on the intensity of the effort of will that is sent to the paretic muscle
Can be performed
In clinic on a co-operative pt. with LA
In theatre under GA or LA
In all directions of gaze
Right abduction restriction
Ask to Look into right gaze but eye wont move past midline
Clinician attempt to assist movement into abduction using cotton tip or forceps 6- and 12-o’clock
Wat u feel is either freedom of movement or resistance
most useful method for diagnosing the presence
Occasionally, a
reverse leash effect caused by retroequatorial
adhesion of a rectus muscle may restrict passive
duction It is important not to press the globe
into the orbit during the test since it may become
negative and thus lead to wrong conclusions in the
presence of mechanical restriction
avoid the use
of succinylcholine chloride since generalized
tightness of the extraocular muscles caused by
this drug may simulate mechanical restriction of
the globe.
Deviation confirmed as
Red infront of right eye and green infront of left eye
The use of complementary colored filters, one over each eye, produces maximum dissociation of images, since there is no part of the visible spectrum common to both eyes
R/G gog not necessary. You can ma diplopia without and determine which image belongs to which eye by covering one eye & asking the pt. which image disappears or remains
The contralateral synergist of the primarily affected eye will show the greatest over action in the non affected eye
The ipsilateral antagonist of palsied muscle will show the next greatest over action
Underaction of RLR
Overaction of LMR
2’ inhibitional palsy of LLR
The contralateral synergist of the primarily affected eye will show the greatest over action in the non affected eye
The ipsilateral antagonist of palsied muscle will show the next greatest over action
Imp in surgical plan
1.A local anesthetic is instilled and the conjunctiva is grasped at the nasal limbus with eye adducted. The patient is instructed to abduct the eye, if there is residual lateral rectus function, examiner can feel tug on the forceps. The test can also be performed in a less invasive fashion by placing a cotton tip bud on temporal limbus and instructing the patient to abduct the eye.
2. Botulinum injection into a contracted medial rectus will reduce the contracture in most instances: abduction beyond the midline should then be possible in a partial palsy.
Looking into active movement since
Asking pt. to move their eyes and assessing them
Gaiining an understanding of the potential function of muscle hv noted restriction but nt sure of if d muscle still has some potential function
E.g. RE abduction deficit: lr palsy or mr restriction( contracture)
Push or place d eye opposite to limitation look in to left gaze as limitation in rt gaze
Now Pt. asked into drxn where limitation exist..clinician feel amt of tug
In the first instance, maximal recession of the medial rectus and resection of the paretic lateral rectus may be indicated. In the second situation, a muscle transposition procedure may be considered
A or v pattern seen because of secondary and tertiary actions of other muscles.
Injection into antagonist medial rectus
Prism to correct diplopia in primary position
1.. retraction of globe is seen in DRS.There is often only small esotropia in spite of obvious limitation of abduction
2.. Pseudoabducens paralysis
4. facial diplegia is associated with
abnormalities of horizontal gaze, usually complete absence of
horizontal motility.196–198 Head movements and convergence (if
preserved) are substituted. Other neurologic and musculoskeletal
abnormalities are common. Etiologies are heterogeneous,
including maldevelopment, intrauterine insults such
as infections or hypoxia, and trauma
These pathways explain the voluntary control of facial muscles.
Origin and course of the upper motor neuron pathway is unknown.
Information concerning taste also is received from the nucleus of the solitary tract from the mouth cavity
In the meatus, the motor root lies in the groove on the 8th nerve , with the sensory root intervening.
The firat bend (at the junction of the first and second parts) is sharp. It lies over the anterosuperior part of the promonotory, and ias alos called genu. The geniculate ganglion of the nerve is so called because it lies on that genu.
The second bend is gradual , and lies between the ptomonotory and the aditus to the mastoid antrum.
Relayed to lacrimal through zygomatic and lacrimal nerves
Relayed to nasal through nasal and palatine mucosal glands
The stapedius muscle dampens excessive vibrations of the stapes caused by high pitched sounds. In paralysis, even normal sounds appear too loud (hyperacusis)
supplies auricularis posterior, occipitalis and intrinsic muscles on the back of the auricle
supplies posterior belly of digastric
supplies stylohyoid muscle
). Instruct the patient to close their eyes tightly so that the eyelashes are buried; note the degree to which the eyelashes can become buried on either side. To check the muscle strength further, the practitioner can attempt to open forcibly closed eyelids while noting any weakness between the two eyes. Any asymmetry in eyelid strength or incomplete eyelid closure (lagophthalmos) indicates facial nerve abnormality.
The normal response should be a brisk blink when the non-anaesthetized cornea is touched with the tip of the cotton wisp. Patients with Bell’s palsy will feel the cotton wisp touch their cornea, but will be unable to blink in response.
3.. Absence/ severe diminution of lacrimation generally indicates poor prognosis and potential serious corneal compromise
The affected side is motionless
Articulation of labialis is impaired.
Bells palsy: which should be labelled when other pathology has been excluded since it is synonymous with the term idiopathic palsy.
rare
But may be caused by autoimmune or viral induced inflammatory or ischemic injury with swelling of the peripheral nerve
Loss of corneal sensation (5th nerve) with facial palsy is difficult
Steroid in 7-10 day course without specific systemic contraindications
Disorder in the nerve, nucleus, or the pyramidal and extrapyramidal pathway may produce hyper excitable states
Meige syndrome is a rare neurological movement disorder characterized by involuntary and often forceful contractions of the muscles of the jaw and tongue (or mandibular dystonia) and involuntary muscle spasms and contractions of the muscles around the eyes (blepharospasm)
Starts as intermittent twitching of orbicularis oculi but over years, spreads to involve all facial muscles on 1 side