Hyperhidrosis

Hyperhidrosis or excessive sweating is believed to be secondary to over activity of the sympathetic nerves located in the chest cavity. Surgical treatment of hyperhidrosis involves interrupting the sympathetic nerves.
These nerves have 12 segments in the thoracic cavity from T1 to T12. This procedure is called endoscopic thoracic sympathectomy. In its different variations it is referred to as ETS, ETS-C, or ESB.
Sympathectomy is performed through small keyhole incisions in the underarm area under general anesthesia. The sympathetic nerves are then found in the thoracic cavity and are either cut, clamped or resected.
Sympathectomy can be achieved by various methods:
Sympathectomy by clamping or clipping (ETS-C / ESB)
In this method the sympathetic nerves are interrupted but not physically cut. This is accomplished by applying a titanium clip/clamp to the nerve. The pressure from the clamp interrupts the nerve signals through the sympathetic nerves. The sympathetic ganglia are not destroyed. The advantage of the method is the theoretical possibility of reconstructing the nerves in the future by removing the clamps.
Sympathectomy by cutting
In this method the sympathetic nerves are physically cut with scissors or electrocautery. The disadvantage of this method is that it is extremely difficult to reconstruct the sympathetic nerves in the future.
Sympathectomy by resecting the sympathetic nerves
Some surgeons prefer the removal of a segment of the sympathetic nerves. This method is effective in treating various forms of hyperhidrosis. However again it is extremely to reconstruct the sympathetic chain after this procedure.
The extent of sympathectomy
The extent or level of the endoscopic sympathetic blockade, ESB, varies according to the type of hyperhidrosis or facial blushing:
            Condition                         Level of ESB

            Facial Blushing                      T2
            Facial Sweating                T2 or T3
            Hand Sweating                 T3 or T4
            Underarm Sweating           T4 or T5

       

It is believed that by limiting the level of ESB to a specific segment of the sympathetic chain, compensatory sweating, the most common side effects of surgery, can be reduced.

Cystic Hygroma

A cystic hygroma is a growth that often occurs in the head and neck area. It is a birth defect.
Causes, incidence, and risk factors

A cystic hygroma occurs as the baby grows in the womb. It forms from pieces of material that carry fluid and white blood cells. This material is called embryonic lymphatic tissue.

After birth, a cystic hygroma usually looks like a soft bulge under the skin. The cyst may not be found at birth. It typically grows as the child grows. Sometimes it is not noticed until the child is older.
Symptoms

A common symptom is a neck growth. It may be found at birth, or discovered later in an infant after an upper respiratory tract infection.
Signs and tests

Sometimes, a cystic hygroma is seen when the baby is still in the womb using a pregnancy ultrasound. This can mean that the baby has a chromosomal problem or other birth defects.

The following tests may be done:

Chest x-ray

Ultrasound

CT scan

If the cystic hygroma is detected during a pregnancy ultrasound, other ultrasound tests or amniocentesis may be recommended.
Treatment

Treatment involves removing all of the abnormal tissue. However, cystic hygromas can often spread to other parts of the neck, making it impossible to remove all of the tissue.

Other treatments have been tried with only limited success. These include:

Chemotherapy medications

Injection of sclerosing medications

Radiation therapy

Steroids

Expectations (prognosis)

The outlook is good if surgery can totally remove the abnormal tissue. In cases where complete removal is not possible, the cystic hygroma commonly returns.

The outcome may also depend on what other chromosomal abnormalities or birth defects, if any, are present.
Complications

Complications may include:

Bleeding

Damage to structures in the neck caused by surgery

Infection

Return of the cystic hygroma

Mnemonics of ENT

Nasopharyngeal carcinoma: classic symptoms

NOSE:

Neck mass

Obstructed nasal passage

Serous otitis media externa

Epistaxis or discharge

Ear drops: direction to pull ear when instilling •For an grown UP it is UP.

• For a chilD it is Down.

SEQUELAE OF CSOM-

O-CART

Ossicular necrosis

Cholesterol granuloma

Atrophic tympanic membrane and atelactatic middle ear

Retraction pockets and cholesteatoma

Tympanosclerosis

D/D OF ACUTE TONSILLITIS

MADI LoVe MAT

M-membranous tosillitis

A-agranulocytosis

D-diphtheria

I-infectious mononucleosis

L-ludwig's angina

V-vincent's angina

M-malignancy

A-aphthous ulcer

T-tonsillar cleft

D/D of membrane over the tonsil

We Mainly Discuss At Length About Membrane In Tonsil

We - Vincent's angina

Mainly - Malignancy

Discuss - Diptheria

At - Agranulocytosis

Length - Leukemia

About - Apthous ulcers

Membrane - Membranous Tonsillitis

In - Infectious mononucleosis

Tonsil - Traumatic ulcer

indications of tympanoplasty-

ABCDES

A- age should be above 10yrs when sufficient resistance develops

B- benign (tubotympanic disease) can be corrected

C- conductive deafness can corrected

D- dry perforation gives best results

E- eustachian tube should be functioning properly

S- stapes should be mobile

Mneumonic dor D/D of membrane over tonsillitis:

M2-VIDAAL (form Widal test for Typhoid)

It is:

- Membranous tonsillitis

- Malignancy

- Vincent's angina

- Infectious mononucleosis

- Diptheria

- Apthous ulcers

- Agranulocytosis

- Ludwig's angina

Sequelae of Otitis media

SCALP COST

S-SNHL

C-Cholesteatoma

A-Atelectasis

L-Learning Disability

P-Perforation of TM

C-Conductive HL

O-Ossicular Necrosis

S-Speech Impairment

T-Tympanosclerosis

Treatment of atrophic rhinitis

(RAPE Young GirlS)

r-remove crust

a-antibiotic spray

pe-placental extact

s- supplement vit. A & D

y-youngs operation

g-glucose in glycerine

-girls-(femae more affected)

9 t's of otalgia

tonsil

tube( eustasian tube)

tics (glossopharyngeal)

trachea

thyroid

temporo mandibular joint

throat

tongue

teeth

(lower 4 are reffered causes)

Acute otitis media

Simple Harmonic Motion(SHM)
S-STRPTOCOCCUS PNEUM

H-H. INFLUENGE

M- M. CATARALLIS

Achalasia cardia- clinical features

DWRF-p

Dysphagia> more to liquid than solid (reverse seen in malignancy or stricture)

Weigit loss

Regurgitation of undigested food at ni8

retrosternal or epigastric Fullness after meals

pulmonary Symptoms due to repeated aspiration

ACHOO
A.......Autosomal dominant
C.......Compelling
H........Heli
O........Ophthalmic
O........Outburst

ACHOO ....This is a Autosomal dominant condition where patient involuntrily starts sneezing when he or she is exposed to brightlight and sunlight.




Clinical features of mumps
SOAP-
Salpingitis
Orchitis,Oophritis
Aseptic meningitis
Pancreatitis

Direction to which a ear should be pulled

PUL posterior upward laterally

FESS= INDICATIONS

"MERA FRCP"

M=MUCOCELE OF FRONTOETHMOID/SPHENOID SINUS

E=EPISTAXIS

R=RECURRENT ACUTE BAC. SINUSITIS

A= A C POLYP

F= FUNGAL SINUSITIS

R= REMOVAL OF FOREIGN BODY

C= CHRONIC BAC. SINUSITIS

P=POLYPOID RHINOSINUSITIS

G.E.R.D. diagnosis
24hour BEER
24 hour ambulatory ph monitoring
Bernstein's acid perforation test
Esophageal manometry
Endoscopy
Radionuclide study





Haemoptysis: causes
CAVITATES:
CHF
Airway disease, bronchiectasis
Vasculitis/ Vascular malformations
Infection (eg TB)
Trauma
Anticoagulation
Tumour
Embolism
Stomach




hypopharyngeal pouch




tom kidman cruise- old rated gossips.T of tom is for thyropharygeus,o of tom oblique fibres,k is for killian"s dehisense,c of cruise for cricopharyngeus.old people...da pouch. r of rated for regurgitation at nite,g of gossips for gurglin sound durin swallowin. calld da Boyce sign

Indications of cadwell luc

coffee board

c-chronic maxillary sinusitis

o-oroantral fistula

f-fungal sinusitis

f-foreign body of maxilla

e-ethmoidectomy

e-elevation of floor of orbit in orbital fracture

b-biopsy

o-opening of maxillary sinus for maxillary artery ligation

a-antrchoanal polyp

r-reduction of fracture maxilla

d-dental cyst

INTRA CRANIAL COMPLICATION OF OTITIS MEDIA

ESMOLol

E=EXTRADURAL ABSCESS

S=SUBDURAL ABSCESS

M=MENINGITIS

O=OTOGENIC BRAIN ABSCESS

L=LAT. SINUS THROMBOPHLEBITIS

LARYNX - ALL MUSCLES ACTIONS
A ridiculous story on this :)
{BIG CASE words r the clue}
an aircraft called ''larynx'' takes off wit ABhishek bachchan being the PILOT
[ABductors : Posterior cricoarytenoids] n inside the aircraft for the customers RELAXATION many TVs were put on [RELAX the vocal cords-->
T : Thyroarytenoids
V : Vocalis ] n as they watch the t v they see an AD on TRUE TENDER LOVE n CARE [ADductors-->
TRUE: TRansverse arytenoids
TENDER: Thyroarytenoids
LOVE: Lateral arytenoids
CARE: Cricothyroids ] but suddenly the situation gets TENSE wen they hear a CREAKY sound from outside [TENSE the cords-->
CREAKY: CRicothyroids] n there is an OPEN ANNOUNCEMENT to CLOSE ALL INLETS to the larynx (aircraft) as the TERRORISTS from outside were tryin to OPEN THE INLETS n intrude!
[OPEN: Oblique arytenoids
ANNOUNCEMENT: aryepiglotticus--> both CLOSE THE INLET OF larynx]
[TERRORISTS:Thyroepiglotticus--> OPEN THE INLET of larynx] !!!
n for the rest of story 'ABHISHEK HEIN NA' :)







LETs Sing a Poem (method of communication in laryngectomised patient)

L-lip peech
E-electrolarynx
T-transoral pneumatic device
(S)ing- blom-singer prothesis
(P)oem- panje prosthesis
-pen paper-writen language




nasal cycle is normally influenced by,
C-Climate
R-Respiration
E-Exercise
E-Emotions
P-Posture
E-Endocrine
D-Drugs

Causes of nasal septal perfortation

Lets Walk Through Another MRI

L= Lupus, Leprosy

W=Wegeners granulomatosis

T=Trauma

A=Abscess

M=Myiasis

R=Rhinolith

I=Idiopathic

Naso pharyngeal carcinoma(npc)
n -nitoso amine-salted fish
p-poly cyclic hydrocarbon-burning wood
c-vit c deficency diet
c-china -mc found in china




Direction of nasolacrimal:here is a really wonderful mnemonic 4 it....

LLB

L: Low=downwards

L: Laterally

B: backward





nso pharyngeal carcinoma (NPC)causeing trotters triad
NPC-trotters triad
N-neuralgia ipsilateral temporal(CN-5)
P-palatal paralysis(CN-x)
C-conductive deafeness

Order of paranasal sinuses

My maxillary

Extremely ethmoid

Sweet sphenoid

Friend frontal

HARD better after stapes surgery(selection of patient for stapes surgery)
H-hearing thresold 30 db or worse
A- air - bone gap 15 db
R-rinne negative for 256,512 Hz
D-discriminatoin speech score 60%
ref-dhigara 4th edn-p-88





Stapes surgery contraindication
COW TO MEN
C- young Children
O-Only hearing ear
W-Works in high construction,diving,air travels
T-Tympanic membrane perforation
O-Otitis externa
M-Meniers disease
E-Exostosis
N-works in Noisy surroundings

Symptoms of acute otitis media-

(A Full DPT Course)

A- autophony

Full- fullness sensation in ear

D- deafness

P- pain

T- tinnitus may be present

course- constitutional symptoms

Throat membrane
SUPER VCD (svcd)
s-streptococcus
v-Vincent angina
c-Candida(fungal)
d-diphtheria



types of thyroplasty:
I-medialization
II-lateralization
III-shortening
IV-lengthening

Men Like Short Lengths









TUNING FORK TESTS
THIS IS NOT EXACTLY A NEMONIC BUT A TRICK WHICH IS VERY USEFUL

WEBERS TEST IS LATERALISED TO WORSE SIDE IN CONDUCTIVE DEAFNESS-NO NEED TO MEMORISE IT-JUST CLOSE UR EAR FROM ONE SIDE N SPEAK OUT UR NAME,U WILL NEVER FORGET IT AGAIN.REVERSE IS TRUE FOR SNHL

causes of vertigo is to use the mnemonic AEIOU TIPS:

* A - alcohol

* E - epilepsy or exposure (heat stroke, hypothermia)

* I - insulin (diabetic emergency)

* O - overdose or oxygen deficiency (shortness of breath)

* U - uremia (toxins due to kidney failure)

* T - trauma (shock or head injury)

* I - infection

* P - psychosis or poisoning

* S – stroke

VERY SORRY TO GIRLS..............MY FATHER EAT BEAF N SOUP TO CEREMONIAL QUEEN"S PARTY....MNEMONICS

OTOTOXIC DRUGS MNEMONICS

VESTIBULOTOXIC........

VERY SORRY TO GIRLS

VE......VESTIBULOTOXIC

S.......STREPTOMYCIN

T ......TOBRAMICIN

G......GENTAMICIN

MY FATHER EAT BEAF N SOUP TO CEREMONIAL QUEEN"S PARTY.

M...........MARIJUANA,REST OF -micin drugs

F............FURASAMIDE

E..............ETHACRYNIC ACID

B ..........BUMATANIDE

N ....NITROGEN MUSTURD

S..............SALICYLATE

T.............TOBACCO

C...............CISPATIN,CO-POISONING

Q................QUININE

P................PROPANOLOL,PROPYLTHIOURACIL

Stridor may be-

1. Inspiratory (In case of LARYNX)

2. Biphasic (In case of TRACHEA)

3. Expiratory (In case of BRONCHI)

CHARGE SYNDROME
Coloboma
Heart defects
choanal Atresia
Retarded growth
Genital hypoplasia
Ear anomalies

Types of DNS (Deviated Nasal Septum)

'SCAN your nose'

• S -shaped deformity

• C -shaped deformity

• Anterior dislocation

• Nasal spur

Deviation may involve only the cartilage,bone or both. S -shaped deformity may cause bilateral nasal obstruction.

Recurrent laryngeal nerve injury

Recurrent laryngeal nerve injury can cause 'ABCD' (besides hoarsness of voice)

Aphonia

Bronchopneumonia (due to aspiration)

Cough (ineffective)

Dysphonia

Indications for Tonsillectomy

Tonsillectomy is indicated when a Tonsil 'HARMS'

Hypertrophy with hoarseness

Abscess (Peritonsillar - Quinsy)

Recurrent sore throat

Malignancy is suspected

Seizures (Febrile seizures due to Tonsillitis)

Otogenic Brain Abscess : stages



"INLET"

Stage of INvasion - headache, low grade fever, malaise and drowsiness
Stage of Localisation - formation of a capsule to localise the pus
Stage of Enlargment - zone of edema around the abscess, raised intracranial tension
Stage of Termination - ruptures into the ventricle or subarachnoid space

Tubercular otitis media : clinical features

5 P's

Painless ear discharge

Perforation

Profound hearing loss

Paralysis of face

Pale granulation

Rinne's test

NNN - Normally Rinne's test is Not Negative it's BACkwards test (Bone conduction better than Air Conduction)

Embryology of ear ossicles

Maleus and Incus forms from mesoderm of I arch

Stapes from Second arch.

Fluctuating hearing loss in . . .
"SPAM"
Syphilic labyrinthitis
Perilmph fistula
Autoimmune disorder of inner ear
Meniere's disease

Tonsils: Blood supply

'Love Father And Mother'

• Lingual artery

• Facial artery

• Ascending pharyngeal artery

• Maxillary artery

Little's area: Arteries

" LEGS "

• L - superior Labial artery

• E - anterior Ethmoidal artery

• G - Greater palatine artery

• S - Sphenopalatine artery

The four arteries anastamose at Little's area to form a vascular plexus called Kiesselbach's plexus.

Auditory Pathway

E.COLI-MA'

• Eighth nerve

• Cochlear nuclei

• Olivary complex

• Lateral lemniscus

• Inferior colliculus

• Medial geniculate body

• Auditory cortex

The area of cortex, concerned with hearing is Brodmann's area located in the Superior temporal gyrus.

Each ear is represented in both cerebral hemispheres.

Oropharyngeal cancers: aetiology

6 S's:
Smoking
Spicy food
Syphilis
Spirits [booze]
Sore tooth
Sepsis




causes of SNHL

1.Congenital
-Prenatal factors
-Paranatal factors

2.Acquired

Nakshatra Makes FANSI TOPS

Noise induced HL
Meniere's dz
Familial Prog HL
Ac. Neuroma
Noise Induce HL
Sudden HL
Infections
Trauma to labyrinth/ VIIITH nv
Ototoxic drugs
Presbyacusis
Systemic Dz.
5's' abSolute indications of tonsillectomy.
Sore throat (recurrent).
quinSy.
Suspected malignancy.
Seizure (febrile).
Speech affected due to hypertrophy of tonsil.



Menier's disease - symptoms

F..........fluctuating hearing loss
A ,.......aural fullness
T..........tinnitus
E..........episodic vertigo





skull fracture

tranSVerSe fracture - Seventh palsy Vertigo and Sensorineural hearing loss
lOngitudinal fracture - here O indicates OTORRHEA more common here...




TOWNE'S view is used to demonstrate-
"SIMLA"

Superior semicircular canal



Internal auditory meatus
Mastoid air cells









Laterl semicircular canal

Antrum




contraindications of stapedectomy-(I POD)
I-Infections in ext/middle ear
P-perforation should be closed first
O-only hearing ear is a contraindication
D-deafness (sensorineural)








COMPLICATIONS FOR CANAL WALL DOWN PROCEDURES
3 D's
Discharge
Deafness
Dizziness






Tumors of Cerebellopontine angle
' Angel GAMES'
• Acoustic neuroma (VIII th nerve tumor)
• Glomus tumor
• Arachnoid cyst
• Meningioma
• Epidermoid (cholesteatoma)
• Schwannoma of other Crainial nerves ( V, VII ,IX,X,XI)

Menier's disease

' VAST men'

• Vertigo

• Aural fullness

• Sensorineural hearing loss

• Tinnitus

In Meniere's disease/Endolymphatic hydrops the main pathology is distension of endolymphatic system due to increased volume of endolymph.Thus,there is distension of cochlear duct (scala media) and the saccule and to a lesser extent the utricle and semicircular canals.

Adductors of Vocal cord

Add TALC"

• Thyroarytenoid

• Transverse Arytenoid

• Lateral cricoarytenoid

• Cricothyroid

Think: Add TALC ie., Adductors are TALC.

Gradenigo's triad

"EAR"

• Ear discharge

• Abducens nerve palsy

• Retro-orbital pain (due to 5th nerve involvement)

Voice box: Components
"There are 3 Vs in your Voice box"


The structures as they appear in the sagittal section are
• Vestibular fold
• Ventricle
• Vocal fold

Vogt-Koyanagi-Harada (VKH) syndrome

Vogt-Koyanagi-Harada (VKH) syndrome is a rare systemic disease involving various melanocyte-containing organs. Bilateral panuveitis associated with cutaneous, neurologic, and auditory abnormalities are manifestations of this inflammatory granulomatous disorder. VKH syndrome was first noted in the 10th century by a Persian ophthalmologist, Ali Ibn Isa, who described a case of poliosis associated with ocular inflammation. This association was reported again in 1873 by Schenkl, in 1892 by Hutchinson, and in 1906 by Vogt. In 1926, Haradadescribed a patient with idiopathic uveitis affecting the posterior segment, with retinal detachment and meningeal irritation. Koyanagi reported similar cases in 1929. Babel, in 1932, suggested that symptoms of the disorder described by Vogt, Koyanagi, and Harada were manifestations of the same single entity, referred to as Vogt-Koyanagi-Harada syndrome or uveoencephalitis.

Pathophysiology

The etiologic and pathogenic factors in VKH syndrome remain unclear. The clinical course of VKH syndrome with an influenzalike episode suggests a viral or postinfectious origin. Some studies invoke a possible role of Epstein-Barr virus reactivation in this disease.Although a viral cause has been proposed, no virus has been isolated or cultured from patients with VKH syndrome. Morris and Schlaegel found viruslike inclusion bodies in the subretinal fluid of a patient with VKH syndrome.
Clinical and experimental data continue to support an immunologic etiology. An autoimmune reaction seems to be directed against an antigenic component shared by uveal, dermal, and meningeal melanocytes. The exact target antigen has not been identified, but possible candidates include tyrosinase- or tyrosinase-related proteins, an unidentified 75-kd protein obtained from cultured human melanoma cells (G-361), and S-100 protein. Evidence suggests that Th1 and Th17 subsets of T cells together with cytokines interleukin (IL)–23 and IL-17 are likely involved in the initiation and maintenence of the inflammatory process.
VKH syndrome can be associated with other autoimmune disorders such as autoimmune polyglandular syndrome,hypothyroidism, Hashimoto thyroiditis, diabetes mellitus,Guillain-Barré syndrome, and IgA nephropathy.
Single reports of patients developing VKH syndrome after cutaneous injury have been noted, as well as 2 cases of this condition occurring after BCG therapy for melanoma and 1 case following surgery of metastatic malignant melanoma. Case reports indicate that even an indirect trauma in melanocyte-containing tissue may induce an inflammatory response within the eye, with Vogt-Koyanagi-Harada disease following a closed head trauma. Cases of this syndrome were reported to be linked to malignant lymphoma.
Immunologic analysis of cerebrospinal fluid (CSF) lymphocytes in VKH syndrome and studies of human uveal melanocytes show that uveal pigment can stimulate lymphocyte cultures from patients with VKH syndrome. Lymphocytes of peripheral blood and CSF from these patients may reveal in vitro cytotoxicity against allogenic melanoma cells.
Circulating antibodies against a retinal photoreceptor region have been detected in patients with this disorder.
The possibility that VKH syndrome has an autoimmune pathogenesis is supported by the statistically significant frequency of HLA-DR4, an antigen commonly associated with other autoimmune diseases. VKH syndrome has been closely associated with HLA-B54, HLA-DR4, and HLA-DR53 in Japanese patients ; with HLA-DR4, HLA-DRw53, and HLA-DQw3 in subjects of Native American ancestry; with HLA-DR1 and HLA-DR4 in Hispanic patients living in southern California; and with HLA-DR4 and HLA-DQw7 in Chinese patients.  HLA-DR4 also was found to be significantly related to VKH syndrome in white Europeans, specifically in Italian patients. These findings confirm the possibility of immunogenic predisposition and the decisive role of HLA-DR4 antigen in the development of the disease.
Data indicate that patients with VKH syndrome are sensitized to melanocyte epitopes and display a peptide-specific Th1 cytokine response. Patients bearing HLA-DRB1*0405 recognize a broader melanocyte-derived peptide repertoire, so the presence of this allele increases susceptibility to the development of VKH disease. In a group of French VKH syndrome DRB1*04-positive patients, the HLA-DRB1*0405 subtype was found in 71%^.
A recent study revealed that a decreased vitamin D-3 level has been associated with active intraocular inflammation in VKH syndrome patients.

Epidemiology

Frequency

United States

VKH syndrome is rare. No precise data are available regarding frequency of the disease.

International

VKH syndrome is rare but widely distributed.

Mortality/Morbidity

VKH syndrome is not associated with mortality. Acute disturbances in hearing and vision may occur, and the cutaneous changes may be permanent.

Race

VKH syndrome occurs more frequently in individuals with darker pigmentation (eg, persons of Asian, Native American, Latin American, or black heritage). VKH syndrome is one of the most common forms of uveitis among pigmented races. The manifestations of VKH syndrome in whites resemble those in the Japanese population. However, cutaneous signs are much more rarer.

Sex

Women appear to be affected with VKH syndrome more frequently than men.

Age

The onset of VKH syndrome has been reported to range from 3-89 years, with a maximum frequency in the thirties. Although often unrecognized, VKH syndrome may affect children.

History

VKH syndrome is usually preceded by a prodromal stage of nonspecific symptoms including headache, increased sensitivity to touch of the hair and skin, vertigo, nausea, nuchal rigidity, vomiting, and low-grade fever that may last a few days. Patients usually initially present to an ophthalmologist for ocular problems, including sudden loss of vision, ocular pain, and photophobia. Hearing disturbances and dizziness may be present. After weeks or months, most patients notice cutaneous signs (eg, hair loss, poliosis, vitiligo).

Physical

The American Uveitis Society developed the first diagnostic criteria for VKH Syndrome in 1978. In addition to an absence of prior ocular trauma or surgery, at least 3 of the following 4 criteria should be met to confirm the diagnosis of VKH syndrome:

• Bilateral chronic iridocyclitis
• Posterior uveitis, which may include exudative retinal detachment, optic nerve swelling, or atrophy of the retinal pigment epithelium
• Cerebrospinal fluid pleocytosis or evidence of tinnitus, dysacusis, headache or meningismus, or cranial nerve involvement
• Cutaneous findings of vitiligo, alopecia, or poliosis

Revised diagnostic criteria were established by International Committee of Experts during The First International Workshop on VKH Disease in 1999.^[33] The new criteria allowed for diagnosing VKH Syndrome in different stages of the disease, specifically addressing the early stages during which cutaneous findings are often not present.

Criteria for VKH syndrome (1-5)

1. No history of penetrating ocular trauma or surgery preceding the initial onset of uveitis
2. No clinical or laboratory evidence suggestive of other ocular disease entities
3. Bilateral ocular involvement - (a) or (b) must be met, depending on the stage of disease when the patient is examined, based on early and late manifestations below.
Early manifestations of the disease
(1) There must be evidence of a diffuse choroiditis (with or without anterior uveitis, vitreous inflammatory reaction, or optic disk hyperemia), which may manifest as one of the following: (a) focal areas of subretinal fluid or (b) bullous serous retinal detachments.
(2) With equivocal fundus findings, both of the following must be present as well: (a) focal areas of delay in choroidal perfusion, multifocal areas of pinpoint leakage, large placoid areas of hyperfluorescence, pooling within subretinal fluid, and optic nerve staining (listed in order of sequential appearance) by fluorescein angiography and and (b) diffuse choroidal thickening, without evidence of posterior scleritis by ultrasonography.
Late manifestations of the disease
(1) History suggestive of the prior presence of findings from (3)(a) and either both (2) and (3) below or multiple signs from (3)
(2) Ocular depigmentation: Either (a) sunset glow fundus or (b) Sugiura sign is sufficient.
(3) Other ocular signs may include (a) nummular chorioretinal depigmented scars, (b) retinal pigment epithelium clumping and/or migration, or (c) recurrent or chronic anterior uveitis.
4. Neurological/auditory findings (may have resolved by time of examination) - Meningismus (malaise, fever, headache, nausea, abdominal pain, stiffness of the neck and back, or a combination of these factors; headache alone is not sufficient to meet the definition of meningismus) or Tinnitus, or CSF pleocytosis
5. Integumentary findings (not preceding the onset of CNS or ocular disease) - Alopecia, or Poliosis, or Vitiligo
Complete VKH disease is if criteria 1-5 are present.
Incomplete VKH disease is if criteria 1-3 and either 4 or 5 are present.
Probable VKH disease is isolated ocular disease; criteria 1-3 must be present.
The classic course of VKH syndrome consists of the following 3 phases:

1. In the meningoencephalitis phase, the degree of neurologic symptoms may vary. Generalized muscle weakness, hemiparesis, hemiplegia, dysarthria, and aphasia have been reported. Most of the neurologic symptoms have been directly attributed to changes in CSF (eg, pleocytosis, increased pressure, protein levels), inflammatory arachnoiditis, or resulting subarachnoidal adhesions. Mental changes ranging from mild confusion to psychosis may occur.
2. The ophthalmic-auditory phase is characterized by common features such as decreased visual acuity, eye pain, eye irritation, and loss of vision. Dysacusis (usually bilateral) and tinnitus develop in 50% of patients.
3. The convalescent phase is characterized by cutaneous signs developing after uveitis begins to subside, usually within 3 months from the onset of disease. Although cutaneous signs typically occur several weeks to months after the onset of ocular inflammation, skin changes have sometimes been observed many years before uveitis appeared. Pigmentary changes tend to be permanent. Poliosis, which occurs in 90% of patients, involves the eyebrows and eyelashes and, occasionally, the scalp and body hair. Poliosis affects 50% of patients and usually appears after the onset of alopecia, which may be patchy or diffuse. Vitiligo manifests in 63% of patients and is often symmetric. Most patients have perilimbal vitiligo (Sugiura sign). Atypical variants of vitiligo with inflammatory raised borders and plaque-type inflammatory erythema have also been reported. Halo nevi may be present.

Causes

The cause of VKH syndrome is unknown, but a viral factor has been suggested in the pathogenesis. An autoimmune reaction to melanocytes with the involvement of T-cell–mediated cytotoxicity and apoptosis is postulated. Although almost all instances of VKH syndrome are sporadic, and familial cases are rare, some authors suggest that the condition may be inherited, probably as an autosomal recessive trait. Numerous data demonstrate the association of HLA-DR4 antigen and VKH syndrome in different racial groups. According to some studies, the major factor contributing to susceptibility for the disease is presence of the DRB*0405 allele.

Differentials

• Alezzandrini Syndrome
• Alopecia Areata
• Piebaldism
• Vitiligo

Laboratory Studies

• For quick diagnosis and early treatment, Vogt-Koyanagi-Harada (VKH) syndrome requires a multidisciplinary management strategy involving dermatologists and ophthalmologists.
• Perform neurologic examination with lumbar puncture to detect associated abnormalities.
• Detailed CSF cell analysis is necessary. Changes in the CSF include pleocytosis with the presence of melanin-laden macrophages (specific for the syndrome and helpful in confirming the diagnosis), increased protein levels, and increased pressure.

Imaging Studies

• Standardized A-scan and contact B-scan echography, performed by ophthalmologist
• Orbital MRI
• Brain MRI

Procedures

• Perform fluorescein angiography, which shows multiple hypofluorescent areas in the retina at the level of the retinal pigment epithelium.
• Perform indocyanine green choroidal angiography.
• Audiometry may reveal sensorineural hearing loss.

Histologic Findings

A skin biopsy specimen taken a month after the onset of VKH syndrome ocular symptoms will likely reveal a mononuclear infiltrate concentrated in the area of hair follicles and sweat glands, consisting mostly of T lymphocytes with a small number of B cells. In depigmented skin, the absence of melanin, as anticipated in vitiligo, can be noted. Vasodilatation in the dermis, pigment-laden macrophages, and a lymphocytic infiltrate have also been described.

Medical Care

• For pigmentary changes with Vogt-Koyanagi-Harada (VKH) syndrome, treatment options mirror those for vitiligo.
• For eye inflammatory changes, treatment includes systemic corticosteroids, with an average initial dose of 80-100 mg of oral prednisone per day. Early, aggressive use of systemic corticosteroids and a gradual tapering of drug dosage for 6 months after presentation are recommended to prevent progression and development of complications. Some authors recommend pulse corticosteroid therapy.
• In patients whose conditions fail to respond to high-dose corticosteroid (oral or intravenous) therapy or who develop significant adverse effects, immunosuppression with cyclosporine or other antimetabolites (eg, azathioprine, cyclophosphamide, methotrexate [MTX]) may be required.
• Case reports suggest that intravenous immunoglobulins (IVIGs) and infliximab may be of interest in the treatment for VKH syndrome. Further trials are needed to assess the efficacy of these agents.
• Topical and periocular corticosteroids are used. If systemic medications are not effective,subtenon injections may be considered before intraocular treatment modalities.
• Cycloplegic-mydriatic eye drops are used symptomatically.

Surgical Care

• Surgical therapy for glaucoma is necessary in some patients. Surgical intervention includes laser iridotomy, surgical iridectomy, and trabeculectomy. 
   
   

  Consultations

  Ophthalmologists and neurologists must be consulted.
  
  
  

  Medication Summary

  The goals of pharmacotherapy are to reduce morbidity and to prevent complications.
  
  

  Corticosteroids

  Class Summary

  Have anti-inflammatory properties and cause profound and varied metabolic effects. Modify the body's immune response to diverse stimuli.
  
  

  Prednisone (Deltasone, Orasone)

   

  Synthetic adrenocortical steroid with predominantly glucocorticoid properties. Immunosuppressant for treatment of autoimmune disorders; may decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. Stabilizes lysosomal membranes and suppresses lymphocytes and antibody production.
  
  
  
  

  Immunosuppressive agents

  Class Summary

  Have antiproliferative and immunosuppressive effects.
  
  
  

  Pediatric Dosing & Uses

  Dosing Forms & Strengths

  tablet

  • 50mg

  powder for injection

  • 100mg/vial

  oral suspension

  • 50mg/mL

  Safety and efficacy not established; however used as adults (off label)
  
  
  

  Pregnancy & Lactation

  Pregnancy Category: D
  Lactation: excreted at low levels in breast milk/not recommended
  
  
  

  Pharmacology

  Absorption: good (PO)
  Half-Life: 5 hr
  Duration: variable
  Plasma Concentration: <1 mcg/mL
  Protein Bound: 30%
  Metabolism: liver
  Metabolites: mercaptopurine, 6-thiouric acid
  Dialyzable: partially
  

  Pharmacogenomics

  Azathioprine is a prodrug and extensively metabolized to the active metabolite 6-mercaptopurine
  6-mercaptopurine is activated further by guanine phosphoribosyltransferase (HGPRT) to form thioinosine monophosphate (TIMP) and by kinase enzymatic pathways to form active 6-thioguanine nucleotides
  Thiopurine S-methyltransferase (TPMT) inactivates 6-mercaptopurine
  Although complete TPMT deficiency is rare in the general population (0.3%), TPMT screening should be performed prior to administration in all patients prescribed azathioprine or 6-mercaptopurine
  With TPMT deficiency, a larger proportion of 6-mercaptopurine is converted to the cytotoxic 6-thioguanine nucleotide analogues, which can lead to bone marrow toxicity and myelosuppression
  Alleles associated with decreased TPMT enzymatic activity are TPMT*2, TPMT*3A, and TPMT*3C
  
  
  

  IV & IM Information

  IV Incompatibilities

  Stable in neutral or acid solutions, but in alkaline solns is hydrolyzed to mercaptopurine
  

  IV Administration

  Can be administered IVP over 5 min at a concentration not exceeding 10 mg/mL
  Can be further diluted with NS or D5W & administered by intermittent infusion over 30-60 min (usual) but infusions ranging from 5 min to 8 hr have been done
  

  Storage

  Store powder at room temp protected from light
  Reconstituted soln is stable for 2 wk at room temp (25°C); may be less stable under refrigeration
  Use within 24 hr since no preservatives
  

  
  
  
  
  
  

   

Sarcoidosis

Sarcoidosis is a disease in which inflammation occurs in the lymph nodes, lungs, liver, eyes, skin, or other tissues.


Causes, incidence, and risk factors



The cause of the disease is unknown. In sarcoidosis, tiny clumps of abnormal tissue (granulomas) form in certain organs of the body. Granulomas are clusters of immune cells.



The disease can affect almost any organ of the body, but it most commonly affects the lungs.



Possible causes of sarcoidosis include:



*



Extreme immune response to infection

*



High sensitivity to environmental factors

*



Genetic factors



The condition is more common in African Americans than Caucasians, especially in Caucasians of Scandinavian heritage. Females are usually affected more often than males.



The disease typically begins between ages 20 and 40. Sarcoidosis is very rare in young children.



A person with a close blood relative who has sarcoidosis is nearly five times as likely to develop the condition.

Symptoms



There may be no symptoms. When symptoms occur, they can involve almost any body part or organ system in your body.



Almost all patients have lung or chest symptoms:



*



Chest pain (most often behind your breast bone)

*



Dry cough

*



Shortness of breath



Symptoms of general discomfort or uneasiness often occur:



*



Fatigue (one of the most common symptoms in children)

*



Fever

*



Joint achiness or pain (arthralgia)

*



Overall feeling of discomfort, illness, or lack of well-being

*



Weight loss (one of the most common symptoms in children)



Skin symptoms:



*



Hair loss

*



Raised, red, firm skin sores (erythema nodosum), almost always on the front part of the lower legs

*



Rash

*



Scars that become raised or inflamed



Nervous system symptoms may include:



*



Headache

*



Seizures

*



Weakness on one side of the face



Eye symptoms include:



*



Burning

*



Discharge from the eye

*



Dry eyes

*



Itching

*



Pain

*



Vision loss



Other symptoms of this disease:



*



Dry mouth

*



Fainting spells if the heart is involved

*



Nosebleed

*



Swelling in the upper part of the abdomen



Signs and tests



A physical exam may show the following:



*



Abnormal breath sounds (such as rales)

*



Enlarged liver

*



Enlarged lymph glands

*



Enlarged spleen

*



Rash



Often the disease is found in patients with visible physical signs who have an abnormal chest x-ray.



Different imaging tests may help diagnose sarcoidosis:



*



Chest x-ray to see if the lungs are involved or lymph nodes are enlarged

*



CT scan of the chest

*



Lung gallium scan



To diagnose this condition, a biopsy is needed. Biopsy of the lung using bronchoscopy is usually done. Biopsies of other body tissues may also be done.



This disease may affect the results of the following lab tests:



*



Calcium levels (urine, ionized, serum)

*



CBC

*



Immunoelectrophoresis - serum

*



Liver function tests

*



Quantitative immunoglobulins (nephelometry)

*



Serum phosphorus



Treatment



Sarcoidosis symptoms will often get better on their own slowly without treatment.



Patients whose eyes, heart, nervous system, or lungs are involved may need to be treated with corticosteroids (prednisone or methylprednisolone). Therapy may continue for 1 or 2 years. The most severely affected patients may need lifelong therapy.



Drugs that suppress the immune system (immunosuppressive medicines) are sometimes also needed:



*



The drug used most often is methotrexate, but azathioprine and cyclophosphamide are also sometimes recommended.

*



Hydroxychloroquine is useful for skin sarcoidosis.



Rarely, some people with end-stage heart or lung damage may need an organ transplant.

Expectations (prognosis)



Many people with sarcoidosis are not seriously ill, and the disease may get better without treatment. About 30 - 50% of cases get better without treatment in 3 years. About 20% of people whose lungs are involved will develop lung damage.



The overall death rate from sarcoidosis is less than 5%. Causes of death include:



*



Bleeding from the lung tissue

*



Heart damage, leading to heart failure and abnormal heart rhythms

*



Lung scarring (pulmonary fibrosis)



Complications



*



Fungal lung infections (aspergilloma)

*



Glaucoma and blindness from uveitis (rare)

*



Kidney stones from high calcium levels in blood or urine

*



Osteoporosis and other complications of taking corticosteroids for long periods of time.

*



Pulmonary hypertension
 

Narcolepsy

Narcolepsy is a sleep disorder that causes excessive sleepiness and frequent daytime sleep attacks.
Causes, incidence, and risk factors

Narcolepsy is a nervous system disorder. The exact cause is known.

In some patients, narcolepsy is linked to reduced amounts of a protein called hypocretin, which is made in the brain. What causes the brain to produce less of this protein is unclear.

There is a possibility that narcolepsy is an autoimmune disorder. An autoimmune disorder is when the body's immune system mistakenly attacks healthy tissue.

Narcolepsy tends to run in families. Certain genes are linked to narcolepsy.
Symptoms

Narcolepsy systems usually first occur during ages 15 to 30.

The most common symptoms are:

Periods of extreme drowsiness during the day. You may feel a strong urge to sleep, often followed by a short nap (sleep attack).

These periods last for about 15 minutes each, although they can be longer.

They may happen after eating, while driving, talking to someone, or during other situations.

Most often, you wake up feeling refreshed.

Dream-like hallucinations between sleep and wakefulness. They involve seeing or hearing, and possibly other senses.

Sleep paralysis. This is when you cannot move as you start falling asleep or when you first wake up. It may last up to 15 minutes.

Cataplexy. This is a sudden loss of muscle tone while awake that makes you unable to move. Strong emotions, such as laughter or anger, can trigger this.

Most attacks last for less than 30 seconds and can be missed.

Your head will suddenly fall forward, your jaw will become slack, and your knees will buckle.

In severe cases, a person may fall and stay paralyzed for as long as several minutes.

Signs and tests

The doctor will perform a physical exam and order blood work to rule out conditions that can cause similar symptoms. Conditions that can cause excessive sleepiness include:

Insomnia and other sleep disorders

Restless leg syndrome

Seizures

Sleep apnea

Other medical, psychiatric, or nervous system diseases

Other tests may include:

ECG (measures the heart's electrical activity)

EEG (measures the brain's electrical activity)

Genetic testing to look for narcolepsy gene

Sleep study (polysomnogram)

Multiple Sleep Latency Test (MSLT) to see how long it takes you to fall asleep during a daytime nap. Patients with narcolepsy fall asleep much faster than people without the condition.

Treatment

There is no known cure for narcolepsy. The goal of treatment is to control symptoms.

Lifestyle changes and emotional counseling may help you do better in work and social activities. This involves:

Eating light or vegetarian meals during the day and avoiding heavy meals before important activities

Planning naps to control daytime sleep and reduce the number of unplanned, sudden sleep attacks

Scheduling a brief nap (10 to 15 minutes) after meals, if possible

Telling teachers and supervisors about the condition so you are not punished for being "lazy" at school or work

You may need to take prescription medications to help you stay awake. The stimulant drug armodafinil is usually tried first. It is much less likely to be abused than other stimulants. Other stimulants include dextroamphetamine (Dexedrine, DextroStat) and methylphenidate (Ritalin).

Antidepressant medications can help reduce episodes of cataplexy, sleep paralysis, and hallucinations. Antidepressants include:

Selective norepinephrine reuptake inhibitors (SNRIs) such as venlafaxine

Selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine, paroxetine, or citalopram

Tricyclic antidepressants such as protriptyline or imipramine

Sodium oxybate (Xyrem) is prescribed to some patients for use at night.

If you have narcolepsy, you may have driving restrictions. Restrictions vary from state to state.
Expectations (prognosis)

Narcolepsy is lifelong (chronic) condition.

It is not deadly, but it may be dangerous if episodes occur during driving, operating machinery, or similar activities.

Narcolepsy can usually be controlled with treatment. Treating other underlying sleep disorders can improve symptoms of narcolepsy.
Complications

Difficulty functioning at work

Difficulty with social activities

Injuries and accidents, if attacks occur during activities

Side effects of medications used to treat the disorder

Calling your health care provider

Call your health care provider if:

You have symptoms of narcolepsy

Narcolepsy does not respond to treatment, or you develop other symptoms

Prevention

There is no known way to prevent narcolepsy. Treatment may reduce the number of attacks. Avoid situations that aggravate the condition if you are prone to attacks of narcolepsy.

Mnemonics for EYE

I.                   Bones of the Orbit

Roof: “Front-less”

            à frontal, lesser wing of sphenoid bone

Lateral Wall: “Great-Z”

                        à greater wing of sphenoid, zygomatic bone

            Medial Wall: “Smel(l)”

                        à sphenoid, maxillary, ethmoid, lacrimal bones

            Floor: “Zip My Pants”

                        à zygomatic, maxillary, palatine bones

II.                Eye Innervation

CN III - superior division = LPS, SR; inferior division = MR, IR, IO

CN IV – SO

CN VI – LR     

III.             Nerves in Relation to CTR (common tendinous ring)

• Nerves outside CTR: “Little Fairy Tots”

L = lacrimal    (V1)

F = frontal       (V1)

T = trochlear   (CN VI)

• Nerves within CTR: “Sits Naked In Anticipation”

S = sup. division of CN III

N = nasociliary    (V1)

I = inf. division of CN III

A = abducent     (CN VI)

[NOTE: optic nerve (CN II) runs with ophthalmic artery thru optic canal]

Head & Neck Mnemonics

Head Mnemonics

NERVES

¨ Cranial Nerves

I-optic, II-olfactory, III-oculomotor, IV-trochlear, V-trigeminal, VI-abducens, VII-facial, VIII-acoustic (vestibulocochlear), IX-glossophrayngeal, X-vagus, XI-spinal accessory, XII-hypoglossal

On Old Olympus Towering Tops, A Finn And German Viewed Some Hops

 You have I nose. You have II eyes. (I – Olfactory; II – Optic)

Motor and Sensory nerves

Some Say Marry Money, But My Brother Says Big Bras Matter More

¨ Innervation of Extraocularmotor Muscles

LR6 (SO4) 3

LR6--Lateral rectus--> VI abductens

SO4--Superior Oblique--> IV Trochlear

3--The remaining 4 eyeball movers = III

¨ Branches of Facial Nerve after Stylomastoid foramen

From superior to inferior:
Ten Zebras Bought My Car

To Zanzibar By Motor Car

Temporal, Zygomatic, Buccal, Masseteric, Cervical

PAssing Through Zanzibar By Motor Car (PA for Posterior Auricular).
Ten Zulus Buggered My Cat (PAinfully)
Temporal branch
Zygomatic branch
Buccal branch
Mandibular branch
Cervical branch
(Posterior auricular nerve)

¨ Cervical Spinal Nerves

C3-4-5 keeps the phrenic alive (innervation of phrenic nerve)

C3-4-5 keep the diaphragm alive (innervation of diaphragm)

C5-6-7 raise your arms to heaven (nerve roots of long thoracic nerve innervate serratus anterior)

¨ V3 innervated muscles

My A$$ Meets The Toilet

Mylohyoid                 Anterior digastric       Muscles of Mastication
Tensor veli palatini     Tensor tympani

¨V3: sensory branches

"Buccaneers Are Inferior Linguists"
Buccal                        Auriculotemporal      
Inferior alveolar                     Lingual

¨ Lacrimal nerve course

Lacrimal's story of 8 L's
Lacrimal nerve runs on Lateral wall of orbit above Lateral rectus, then Lets communicating branch join in, then supplies Lacrimal gland, then Leaves it and supplies Lateral upper eye Lid!

¨ CN VII innervated muscles (branchial arch 2 derivatives)

"Imagine someone making the facial expression to say 'PSS...'
Facial expression muscles:
Posterior belly of digastric
Stapedius
Stylohyoid

¨ Scalp: nerve supply

GLASS
Greater occipital/ Greater auricular
Lesser occipital
Auriculotemporal
Supratrochlear
Supraorbital

Bones/Spaces

¨ Cranial bones PEST OF 6 Parietal            Ethmoid          Sphenoid        Temporal         Occipital         Frontal The 6 just reminds that there's 6 of them to remember. Old Pygmies From Thailand Eat Skulls Old People From Texas Eat Spiders Occipital         Parietal            Frontal                        Temporal         Ethmoid          Sphenoid Prostitutes Offer Free Sex To Everyone Parietal            Occipital         Frontal                        Sphenoid        Temporal         Ethmoid          ¨ Orbit: bones of medial wall My Little Eye Sits in the orbit Maxilla (frontal process) Lacrimal Ethmoid Sphenoid (body) ¨ Foramen spinosum  location on base of skull Foramen spinosum is adjacent to the spine of sphenoid. ¨ Cavernous sinus contents O TOM CAT O TOM are lateral wall components, in order from superior to inferior. CA are the components within the sinus, from medial to lateral. CA ends at the level of T from O TOM. · See diagram.  Occulomotor nerve (III) Trochlear nerve (IV) Ophthalmic nerve (V1) Maxillary nerve (V2) Carotid artery Abducent nerve (VI) T: When written, connects to the T of OTOM. ¨ Cartilage derivatives of 1st pharyngeal arch (mandibular) I'M A Super Sexy Guy       (or Girl) Incus Malleus Anterior ligament of malleus Spine of sphenoid Sphenomandibular ligament Genial tubercle of mandible Muscles ¨ Face muscles groups cranial innervation Mandibular nerve: Mastication. Facial nerve: Facial expression. ¨ Pterygoid muscles Function of lateral vs. medial "Look at how your jaw ends up when saying first syllable of 'Lateral' or 'Medial' ": "La": your jaw is now open, so Lateral pterygoid opens mouth. "Me": your jaw is still closed, so Medial pterygoid closes the mandible. ¨ Eye rotation by oblique muscles I Love S&M Inferior oblique: Lateral eye rotation Superior oblique: Medial eye rotation Extrinsic muscles of tongue [for pro soccer fans] "Paris St. Germain's Hour": Palatoglossus Styloglossus Genioglossus Hyoglossus · PSG is a French soccer team (foreign), hence extrinsic comes to mind. Vessels Maxillary artery branches "DAM I AM Piss Drunk But Stupid Drunk I Prefer, Must Phone Alcoholics Anonymous": Deep auricular Anterior tympanic Middle meningeal Inferior alveolar Accessory meningeal Masseteric Pterygoid Deep temporal Buccal Sphenopalatine Descending palatine Infraorbital Posterior superior alveolar Middle superior alveolar Pharyngeal Anterior superior alveolar Artery of the pterygoid canal Neck Mnemonics Vessels ¨ Subclavian artery branches Very Tired Individuals Sip Strong Coffee Served Daily Vertebral artery Thyrocervical trunk ---Inferior thyroid ---Superficial cervical ---Suprascapular Costocervical ---Superior intercostal ---Deep cervical ¨ External carotid artery branches Some Aggressive Lovers Find Odd Positions More Stimulating Superior thyroid Ascending pharyngeal Lingual Facial Occiptal Posterior auricular Maxillary Superficial temporal Sister Lucy's Powdered Face Often Attracts Silly Medicos So Long For Acting Old Parenting Means Stability Sally Ate Lots Of Fresh Produce March Through September   Nerves ¨ Cervical plexus arrangement of the important nerves "GLAST" 4 compass points: clockwise from north on the right side of neck: Great auricular (North)  à  Lesser occipital  (East) à Accessory nerve (pops out between L and S) à Supraclavicular (South) à Transverse cervical (West) Other ¨ Thoracic Duct Location The duck is between two gooses (duck = thoracic duct) 2 gooses = azyGOUS and esophaGOUS ¨ Carotid sheath contents               "I See 10 CC's in the IV": I See (I.C.) = Internal Carotid artery 10 = CN 10 (Vagus nerve) CC = Common Carotid artery IV = Internal Jugular Vein Muscles Hyoid bone: muscle attachments Christ, He Didn't Screw Girls Much. That's Obvious, Stupid The first sentence is for 6 muscles attaching superiorly, the second sentence is for 3 muscles attaching inferiorly.   Both sentences are in order from lateral to medial: Constricter (middle) Hyoglossus Digastric Stylohyoid Geniohyoid Myloyoid Thyrohyoid Omohyoid Sternohyoid