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The facial nerve is the seventh cranial nerve, or simply CN VII. It emerges from the pons of the brainstem, controls the muscles of facial expression, and functions in the conveyance of taste sensations from the anterior two-thirds of the tongue.
Anatomy of cavernous sinus, structures passing through the caveernous sinus, spread of infections, clinical features of cavernous sinus thrombosis, investigations and management of cavernous sinus thrombosis.
The facial nerve is the seventh cranial nerve, or simply CN VII. It emerges from the pons of the brainstem, controls the muscles of facial expression, and functions in the conveyance of taste sensations from the anterior two-thirds of the tongue.
Anatomy of cavernous sinus, structures passing through the caveernous sinus, spread of infections, clinical features of cavernous sinus thrombosis, investigations and management of cavernous sinus thrombosis.
Detailed discussion on tumors and other pathologies of paranasal sinus and their management. Surgical anatomy and approaches are also discussed. Complications of PNS surgeries are discussed briefly
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Cerebral Venous anatomy from the neuroradiology point of view. Anatomy of the cerebral veins and venous sinuses. Important for Neuroradiologists and Neurointerventionalists.
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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
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Cavernous sinus
1. “CAVERNOUS SINUS”“CAVERNOUS SINUS”
• Venous sinuses of Dura Mater.
• Cavernous sinus.
Structure.
Location.
Boundaries.
Relations.
Tributaries (Incoming Channels).
Draining Channels (Communications).
Applied Anatomy & Complications.
Cavernous Sinus Thrombosis.
Introduction
Etiology
Mortality/Morbidity rate
History of the patient
Clinical signs & symptoms
-Venous
-Cranial
-Systemic
Differential Diagnosis
Lab Studies
Imaging/Radiographic aids
Treatment protocol
-Emergency department care
-Do’s & Don’ts
-Right time to call the doctor
Damage to the Internal Carotid Artery.
Conclusion.
References.
“CAVERNOUS SINUS”
2. VENOUS SINUS OF DURA MATER:- These are venous spaces the
walls of which are formed by the duramater. They have an inner lining of
endothelium. There is no muscle in their walls. They have no valves.
Venous sinuses receive venous blood from the brain, meninges, and
bones of the skull. Cerebrospinal fluid is poured into some of them.
Cranial venous sinuses communicate with veins outside the skull
through emissary veins. These communications help to keep the pressure of
the blood in the sinuses constant.
There are about 15 venous sinuses, of which some are paired and others are
unpaired.
Paired Venous Sinuses:-
There is one sinus on each side (right or left).
1. Cavernous sinus.
2. Superior petrosal sinus.
3. Inferior petrosal sinus.
4. Transverse sinus.
5. Sigmoid sinus.
6. Sphenoparietal sinus.
7. Petrosquamous sinus.
8. Middle meningeal sinus.
Unpaired venous Sinuses:-
These are median in position.
1. Superior sagittal sinus.
2. Inferior sagittal sinus.
3. Straight sinus.
4. Occipital sinus.
3. 5. Anterior intercavernous sinus.
6. Posterior intercavernous sinus.
7. Basilar plexus of veins.
CAVERNOUS SINUSES:-
Where is it Located?
Each Cavernous sinus (right or left) is a large venous space situated in the
middle cranial fossa, on either side of the body of sphenoid bone. Its interior
is divided into a number of spaces (caverns) by trabeculae. The trabeculae
are much less conspicuous in the living than in the dead.
Structure of cavernous sinus:-
BUTLER (1957):- asserted that a distended adult sinus contains a few
trabeculae, mostly in its periphery near the entry of its tributaries. When the
sinus is collapsed, as in cadavers, its cavity is encroached upon by nerves
and arachnoid granulations in its wall, creating a spurious resemblance to
cavernous tissue; hence called as the Cavernous Sinus.
PARKINSON (1963) & PERNKOPF (1973):- depicted the sinus as a
“venous plexus”.
BROWDER & KAPLAN (1976):- described the sinus as “reticulated”. It
was not clear whether they meant plexiform or cavernous.
4. What are its Boundaries?
The floor of the sinus is formed by endosteal dura mater. The lateral
wall, roof and median wall are formed by the meningeal dura mater.
Anteriorly, the sinus extends up to the medial end of the superior orbital
fissure and posteriorly, up to the apex of the petrous temporal bone. It is
about 2cm long and 1 cm wide.
Relations:-
A. Structures outside the sinus:
• Superiorly:
a) Optic Tract,
b) Internal carotid artery and anterior perforated
substance.
• Inferiorly:
a) Foramen lacerum and the junction of the body
and greater wing of sphenoid bone.
• Medially:
a) Hypophysis cerebri and sphenoidal air sinus.
• Laterally:
a) Temporal bone with uncus.
• Anteriorly:
a) Superior orbital fissure and the apex of the orbit.
B. Structures in the lateral wall of the sinus, form above downwards:
• Occulomotor nerve:- In the anterior part of the sinus it divides
in to superior and inferior divisions which leave the sinus by
passing through the superior orbital fissure.
5. • Trochlear nerve:- In the anterior part of the sinus it crosses
superficial to the 3rd
nerve, and enters the orbit through the
superior orbital fissure.
• Ophthalmic nerve:- In the anterior part of the sinus it divide
into the lacrimal, frontal and nasociliary nerves
• Maxillary nerve:- It leaves the sinus by passing through the
foramen rotundum on its way to the pterygopalatine fossa.
• Trigeminal ganglion:- The ganglion (and its dural cave) project
Ainto the posterior part of the lateral wall of the sinus.
C. Structures passing through the centre of the sinus:-
• Internal carotid artery:- with the venous and sympathetic
plexuses around it.
• Abducent nerve:- inferolateral to the internal carotid artery.
These structures in the lateral wall and in the centre of the sinus are
separated from blood by endothelial lining.
Tributaries (incoming channels):-
A. From the orbit:-
• The superior ophthalmic vein.
• A branch of inferior ophthalmic vein (sometimes the vein
itself)
• The central vein of retina:- may drain either into the
superior ophthalmic vein or into the superior ophthalmic
vein or into the cavernous sinus.
B. From the brain:-
• Superficial middle cerebral vein
6. • Inferior cerebral vein from the temporal lobe.
C. From the meninges:-
• Sphenoparietal sinus
• Frontal trunk of the middle meningeal vein:- may drain
either into the pterygoid plexus (through the foramen
ovale) or into the Sphenoparietal or cavernous sinus.
Draining channels (communications):-
The cavernous sinus drains:-
• Into the transverse sinus through the superior sinus,
• Into the internal jugular vein through the inferior petrosal
sinus and through a plexus around the internal carotid
artery,
• Into the pterygoid plexus of veins through the emissary
veins passing through the foramen ovale, foramen
lacerum and the emissary sphenoidal foramen,
• Into the facial vein through the superior ophthalmic vein.
• The right and the left cavernous sinuses communicate
with each other through the anterior and posterior
intercavernous sinuses and through the basilar plexus of
veins.
All these communications are valve less and blood can flow in either
direction.
Applied Anatomy and Complications of infections of cavernous sinus:-
7. The importance of cavernous sinus arises because of the structures
which lie in and around it. They may be involved with infections which can
spread to it along the many tributaries. Through its communications, it forms
a route of communication between the face, cheek, brain and the internal
jugular vein.
Following are the complications arising from the infection of the
cavernous sinus:-
A). Cavernous sinus thrombosis:-
Cavernous Sinus Thrombosis, as the name states, is the formation of
blood clot (thrombus) in the cavernous sinus.
It is important to know that CST affects cranial nerves III, IV and VI,
which are necessary for eye movement, and cranial nerve V, which gives
sensation to the top and middle portion of the face. Therefore, it is a serious,
life-threatening infection that requires aggressive medical and surgical
intervention.
• Etiology:-
It is not contagious neither infectious. The cause is usually
infections starting in the face, sinuses (esp. sphenoid and ethmoid)
or the ears; as the bloodstream drains back into the cavernous sinus
in the skull, the infection spreads to this area and results in the
disease.
The causative agent is generally Staphylococcus aureus,
although streptococci, pneumococci and fungi may be implicated
in rare cases.
Other sources of infection are:-
8. Source Disease Route
Nose & Danger area
of the face
Furuncle, Septal abscess Pharyngeal Plexus.
Ethmoid sinus Orbital cellilitis or abscess. Ophthalmic veins.
Sphenoid sinus Sinusitis Direct.
Frontal sinus Sinusitis and osteomylitis of
frontal bone
Supraorbital and
ophthalmic veins
Orbit Cellulitis and abscess Ophthalmic veins
Upper eye lid Abscess Angular and
ophthalmic veins
Pharynx Acute tonsillitis or
peritonsillar abscess
Pharyngeal plexus
Ear Petrositis Petrosal venous
sinuses.
• Mortality / Morbidity rates:-
Prior to the advent of effective antimicrobial agents, the
mortality rate from CST was effectively between 80-100%. With
aggressive management, the mortality rate has come down to 20-
30%.
Morbidity, however, remains high, and complete recovery is
rare. Roughly, one-sixth of patients are left with some degree of
visual impairment, and one half has cranial defects.
• History of the patient:-
• Patients generally have sinusitis or a midface infection (most
commonly a furuncle) for 5-19 days.
• Headache, fever and malaise typically precede the development
of ocular findings. As the infection tracts posteriorly, patients
9. complain of orbital pain and fullness accompanied by
periorbital edema and visual disturbances.
• In some patients, periorbital findings do not develop early on,
and the clinical picture is subtle.
• Without effective therapy, signs appear in the contra lateral eye
by spreading through the communicating veins to the contra
lateral cavernous sinus. This is pathognomonic of CST. The
patient rapidly develops mental status changes from CNS
involvement and/or sepsis. Death follows shortly thereafter.
• Clinical featres:-
Clinical picture presents the following systemic,venous and nervous
symptoms:
1) Nervous symptoms:-
• Severe pain in the eye and forehead in the area of distribution of
Ophthalmic nerve.
• Involvement of the third, fourth and sixth cranial nerves individually
and sequentially resulting in the paralysis of the muscles supplied and
eventually total ophthalmoplegia. Paralysis of the V cranial nerve
results in the loss of sensation in the top and the middle portion of the
face.
2) Venous symptoms:-
• Eyelids get swollen with chemosis and proptosis of the eyeball.
• Pupils become dilated and fixed.
• Optic disc shows congestion and oedema with diminution of vision.
10. • Exophthalmos and ophthalmoplegia.
3) Systemic signs indicative of sepsis:-
• Chills, Fever, Shock, Delirium and coma appear as late findings.
• Differential Diagnosis:-
CST needs to be differentiated from…
• Cellulitis
• Epidural Hematoma
• Epidural and subdural infections
• Glaucoma, Acute angle closure cases
• Orbital infections
• Periorbital infections
• Sinusitis
• Subarachnoid hemorrhage
• Subdural hematoma
• Orbital cellulites (most difficult to distuinguish).
Distinguishing between CST and Orbital Cellulitis:-
Orbital Cellulitis Cavernous Sinus
Thrombosis
Source Commonly ethmoid
sinus
Nose, sinus, orbit, ear or
pharynx
Onset Slow Abrupt
Cranial nerve
involvement
Involved concurrently
with complete
Involved individually
and sequentially.
11. ophthalmoplegia.
Laterality Often involves eyes. Involves both eyes.
• Lab Studies:-
CST is a clinical diagnosis and lab studies are seldom specific.
Most patients exhibit a PMN leucocytosis often marked with shift
towards immature form.
Blood cultures are generally positive for the offending
organism.
• Imaging studies:-
Historically, a number of techniques have been used like:-
• Plain Sinus radiography,
• Carotid angiography
• Orbital venography.
In current practice the techniques being used are:-
• CT scan
• MRI
• MR angiography
• Lumber puncture
• Neuroradiology
• Treatment:-
• I.V. broad spectrum antibiotic coverage and attention to
the focus of infection.
Eg:- Penicillin, Sulfadiazine, Chlomphenicol and
metrinidazole.
12. Blood culture should be taken prior to starting
antibiotic therapy.
• Surgery of the cavernous sinus is technically difficult and
never been shown to be helpful. The primary source of
infection should be drained if possible (infected Ethmoid or
Sphenoid sinus or facial abscess).
• Corticosteroids may help to reduce inflammation and
edema and should be considered as an adjunctive therapy
Role of anticoagulants like heparin is not clear but is supported by recent
studies.
• Do’s:-
a) Best treatment is prevention. Recognise the primary
source of infection and treating this primary source
expeditiously is the best way to prevent CST
b) Understand that CST can be a life threatening, rapidly
progressing disease with high mortality rates despite
antibiotic use
• Don’t s:-
a) Don’t forget that CST is a medical emergency and
depending on the location of the primary infection,
the appropriate specialist should be involved. For
Example: an ophthalmologist should be consulted if
the infection is in the eye.
• Right time to call the Doctor:-
• Eye problems:-
Eye pain
13. Loss/difficulty in vision
Bulging of the eyeball or drooping of eyelids.
Difficulty in moving the eye in a certain direction.
• Ear problems:-
Ear pain
Hearing loss
Drainage from ear.
• Fever, headache, nausea, vomiting, stiff neck
• Drainage from the sinus.
B) Damage to the Internal Carotid Artery:-
The Internal Carotid Artery can be damaged by injuries to the base of
the skull, leading to the leakage of the arterial blood into the sinus. This
increases the pressure in the sinus and the veins entering it, so that the
eyeball may protrude and produce a pulsating exophthalmos.
CONCLUSION:-
In our routine practice, we as dentists, would encounter many patients who
would seem to be suffering from otherwise non-threatening and common
infections of the eye, ear and nose. It is of paramount importance on our part
that we assume the patient as a suspected case if he presents with a clinical
picture suggesting that of CST.
Though the occurrence of CST is very rare due to Operative procedures, the
possibility still remains and it is called for that we employ sterilization
procedures properly and consistently; reduce chances of cross-infection; to
keep the threat of CST at bay.