This document discusses Ardita Vata (facial palsy) according to Ayurveda and modern medicine. It defines Ardita Vata as a deviation leading to deformity of one side of the face or half of the body. The causes, symptoms and types are described according to Ayurvedic texts like Charaka Samhita. Bell's palsy, the most common type of facial palsy, is also discussed in detail including causes like infection, trauma and tumors. The document compares unilateral lower motor neuron lesions in Bell's palsy versus bilateral upper motor neuron lesions. Various treatment approaches are summarized including nerve grafts, slings and weights to correct facial paralysis.
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Sandhigata Vata is the type of pathogenesis involved in various disease conditions affecting the joints, e.g. osteoarthritis, rheumatoid arthritis, etc. and causing pain in affected joints.
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BELL'S PALSY IS AN IDIOPATHIC LMN TYPE FACIAL PALSY..THE SEMINAR TELLS YOU OF COURSE OF NERVE..FACIAL MUSCLES THEIR ACTION..HOW TO EXAMINE..THE SEQUELAE OF FACIAL PALSY...LOOK AT IT..
BELL'S PALSY IS AN IDIOPATHIC LMN TYPE FACIAL PALSY..THE SEMINAR TELLS YOU OF COURSE OF NERVE..FACIAL MUSCLES THEIR ACTION..HOW TO EXAMINE..THE SEQUELAE OF FACIAL PALSY...LOOK AT IT..
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Bell's palsy is a form of temporary facial paralysis resulting from damage or trauma to the facial nerves. The facial nerve-also called the 7th cranial nerve-travels through a narrow, bony canal (called the Fallopian canal) in the skull, beneath the ear, to the muscles on each side of the face. For most of its journey, the nerve is encased in this bony shell.
Each facial nerve directs the muscles on one side of the face, including those that control eye blinking and closing, and facial expressions such as smiling and frowning. Additionally, the facial nerves carries nerve impulses to the lacrimal or tear glands, the saliva glands, and the muscles of a small bone in the middle of the ear called the stapes. The facial nerve also transmits taste sensations from the tongue.
When Bell's palsy occurs, the function of the facial nerve is disrupted; causing an interruption in the messages the brain sends to the facial muscles. This interruption results in facial weakness or paralysis.
Bell's palsy is named for Sir Charles Bell, a 19th century Scottish surgeon who was the first to describe the condition. The disorder, which is not related to stroke, is the most common cause of facial paralysis. Generally, Bell's palsy affects only one of the paired facial nerves and one side of the face, however, in rare cases, it can affect both sides.
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The term facial palsy generally refers to weakness of the facial muscles, mainly resulting from temporary or permanent damage to the facial nerve
Facial palsy not only cause a paresis of the target muscles, but as the nerve is responsible for a range of facial expressions, it causes serious disturbances in social life, facial expression being so important in transferring emotion.
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
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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2. INDEX:
Definition-Ardita vata
Introduction
Nidanam
Samprapti
Poorva rupa
Rupa
Types
Treatment
3. DEFINITION:
It is a disease in which there is a
deviation leading to deformity of one
side of face alone or along with half side
of the body.
4. INTRODUCTION:
Acc to Charaka & Vagbhata ardita vata
is included in the group of Vataja
Nanatmaja Vyadhis.
Acc to Charaka he also included the
same ardita vata under Samanya siro
rogas.
5. NIDANA:
Carrying heavy weights on head
Excessive yawning,laughing
Pregnant woman
Shouting loudly
Eating hard foods
Old persons
Children
Fear
Grief
6. SAMPRAPTI:
Vata gets aggravated
Localised in
head,nose,lips,chin,forehead,eyes
Causes sankocha of organs&produces
pain and causes ardita vata.
7. POORVA RUPA:
Horripulations
Tremors
Belching
Loss of sensation&pain in skin
Catching pain in shoulders
8. RUPA:
Absence of nasolabial fold on affected
side
Absence of wrinkles on head
Drooping of eyelid
Deviation of mouth to healthy side
Difficult in chewing
Slurred speech
Tremors of neck
10. According to charaka 2 types
Ardita vata
Ardita
Visista
ardanga
vata
11. According to bhavamisra and
yogaratnakara 3 types based on dosas
1)vata ardita -pain,excessive
salivation,oedema of lips.
2)pitta ardita - trsna,jwara,daha.
3)kapha ardita - oedema in
neck&stiffness.
12. ASADYA LAKSHANAS:
According to susruta
1)ksheena-weak person
2)Inability to close eyes
3)Disturbed or slurred speech
4)Excessive nasal secretions
5)Excesive tear drops
6)excessive oral secretions
13. TREATMENT:
According to charaka& Susrutha.
1)nasya - shadbindu taila or anutaila
2)nadi swedana
3)upanaha - meat of animals of marshy
lands(anoopa prani)
4)moordha taila - application of oil on head
as
• Pichu
• Sirovasti
• Sirodhara with ksheera bala or
nirgundi taila
14. According to vagbhata
- 1)nasya
- 2)karna poorana
- 3)akshi tarpana
- 4)emesis
- 5)venesection
According to bhavamishra
Ksheera prepared with DMQ or
BMQ
16. DEFINITION:
Paralysis of any structures innervated by
facial nerve is known as facial palsy.
Facial
paralysis
Supra nuclear
lesions
Caused due to
lacunar infarct
affecting fibres
in internal
capsule
Infra nuclear
lesions
Majority of
causes of facial
palsy is due to
this lesions
17. SUPRA NUCLEAR &INFRA
NUCLEAR LESIONS:
The facial motor
nucleus have two
divisions.
1)dorsal division
2)ventral division
Dorsal division
contains UMN’S
which recieves
bilateral input from
brain.
Ventral division
contains LMN’S which
receives only contra
lateral input.
19. BRANCHES OF FACIAL
NERVE:
Temporal branch –
supplies to frontalis
&orbicularis oculi.
Zygomatic branch –
supplies to orbicularis
oculi.
Buccal branch –
supplies to upper lip
&cheek.
Mandibular branch –
supplies to lower lip.
Cervical branch –
supplies to neck
muscles.
20. SYMPTOMS:
Unilateral facial weakness.
Loss of taste.
Hyperacusis-A heightened sensitivity to
some sounds.
Decreased salivation & tear secretion.
21. TYPES OF FACIAL PALSY:
Different types of facial palsy according to
the point at which the nerve is affected.
1)lesion in pons - taste&hearing not effected
2)Lesion in petrous bone – palsy of facial
muscles+loss of taste
3)Lesion in chorda tympani – no salivary
secretions
4)Lesion in stonpedius – sense of hearing is
loss
22. Difference between UMN&LMN
Lesions
UMN LESIONS LMN LESIONS
Only lower 2/3 rd of the
facial muscles are
affected.
Mid face is paralysed.
Eye brow’s can move
normally.
Totally half side of the is
affected.
Half of the Mid face is
only paralysed.
Eye brow’s can’t move
normally.
23. BELL’S PALSY:
It is the commonest type of facial palsy.
It is the major cause of the acute facial
nerve paralysis.
It affects totally half side of the face due to
the LMN Lesion.
Here the palsy is due to the inflammation of
the facial nerve.
The inflammation prevents nerve from
sending correct signals to brain &facial
muscles.
26. INFECTION:
Herpes zoster virus - reactivation of virus
within dorsal root ganglion of facial nerve
is assosiated with vesicles affecting ear
canal.
Symptoms -1)ear pain
2)vesicles
3)hearing loss
4)vertigo
o Treatment –1)anti viral
2)steroids(corticosteroids)
27. Otitis media –inflammation of the middle
ear due to infections can spread to facial
nerve &inflame it causing compression.
Symptoms -1)ottorrhoea(discharge).
2)otalgia(no ear pain).
Treatment –myringotomy(incision to
tympanic membrane).
29. TRAUMA:
1)fractures of temporal bone due to
injury in accidents.
2)birth injury to the facial nerve at the
time of delivery due to application of fore
ceps.
reason :it remains unprotected after
its exit through stylomastoid foramen.
investigation –CT Scan
31. TUMOUR:
The bells palsy may be due to tumour’s
which compress the the nerve along its
course.
investigation -1)Tomography.
2)MRI(to locate tumour)
3)CT Scan
34. Diabetes milletus –the person with DM is more
susceptible for otitis inflammation.
Sarcoidosis –abnormal collections of
inflammatory cells which transform as nodules
is known as sarcoidosis.As it occurs in facial
nerve it is known as nervus sarcoidosis.
investigations –angiotensin converting
enzyme levels.
treatment -1) Ibuprofen or aspirin.
2)if it progress-prednisolone.
35. Moebius syndrome –This can be taken as
congenital malformity.
under development of 7th&6th cranial nerves is
known as moebius syndrome.
symptoms -1)cannot close eye.
2)no facial expression.
3)complete facial palsy.
treatment -1)tarsorraphy-(eye).
2)smile surgery-for fascial
expressions(grafting of muscles from thigh to
corners of mouth).
36. DIFFERENCE BETWEEN
FACIAL PALSY&BELL’S
PALSY
FACIAL PALSY BELL’S PALSY
1)Cause can be known
(infection,trauma,
tumour).
2)Permanent(lasts for
years to life).
3)need surgical
treatment.
4)Site of affection
depends upon
UMN&LMN Lesions.
1)It is idiopathic(may de
velop suddenly).
2)Temporary(permanent
cure with in 3 months in
90% of cases).
3)Without treatment or
surgery regains facial
function.
4)It is mainly due to
LMN Lesions.half side
of the face is totally
affected.
37. Tests for facial palsy:
Ask the patient to show his teeth.
Ask the patient to puff his cheeks.
Ask the patient to close his eyes against
resistance.
Ask the patient to lift his eyebrows.
39. TREATMENT:
Brow ptosis correction – direct brow lift,endoscopic
brow lift.
Eye lid weight placement – occuloplastic
management for lagopthalmus.
Static facial suspension – by using facial slings from
zygomatic/temporalis arch to nasolabial fold & oral
commisure.
Extra nasal valve repair – facia lata sling from alar
base to temporalis facia to open extra nasal valve.
Cross Face Nerve Transplant(CFNT) – It is most
advanced.
It is making continuity between paralysed&normal
facial nerves by means of bridge grafts.