Epilepsy and driving
General considerations
Correct diagnosis of your seizure type is
extremely important. It means appropriate management is commenced, and
assessment for driving safely can be considered.
Any person experiencing a seizure or
recurrent seizures should see an appropriate consultant for evaluation, so the
risk of further seizures and the need for treatment can be determined.
Individual responsibility means personal
accountability for management of your condition in conjunction with the support
of a medical practitioner.
Where non-compliance with medication is suspected
your doctor may notify the Driver Licensing Authority who may then choose to
issue a driver licence conditional upon periodic drug level monitoring.
It is a legal requirement for the person
with epilepsy to notify the Driver Licensing Authority in their state or
territory.
The following aspects of epilepsy
management should be taken into account in the assessment of driver fitness:
You must have been free of seizures for the
specified period (see Medical Standards below)
You must continue to take anti-epileptic
medication regularly when prescribed
You should ensure adequate sleep and not
drive if sleep-deprived
You may need to abstain from alcohol and
other drugs (it has been found that a repeated episode of seizure may be
precipitated by consumption of alcohol or drugs not under prescription for
epilepsy).
Your
responsibilities It is
a legal requirement
for the person
with epilepsy to
notify the DLA
in their state
or territory that
they have epilepsy. The
driver is responsible
for making sure
that they are
well enough to
drive safely -
by managing good seizure
control and complying
with medical treatment.
If issued with
a conditional licence
the person with epilepsy
is expected to
comply with any
enforced driving restrictions. The Australian
guidelines concerning seizures
and driving may
seem severe but
these laws were
created to protect public
safety. You must be seizure
free for a
specified period (see www.austroads.com.au ) You must continue to
take anti-epileptic medication
regularly as prescribed
unless your specialist recommends changes
You should ensure that
you have adequate
sleep and not
drive if sleep-deprived You may need to abstain
from alcohol and
other drugs (it
has been found
that a repeated
episodes of seizures may be
precipitated by consumption of alcohol or drugs not prescribed for epilepsy) Who tells
the authorities? The
laws requires you
to report to
your DLA, any
permanent or long-term
illness that is
likely to affect
your ability to drive
safely. In some
cases, the DLA
may issue you
a conditional licence.
This means that
you may continue
to drive as
long as certain conditions
or restrictions are
met. The DLA
always makes the
final decision about
your licence status.
They will consider
the advice of
your doctor and other
factors such as
your accident history
and the type
of vehicle you
drive (for example
a truck, car
or a public passenger
vehicle). What if I don’t
tell the authorities?
Driving against medical
advice is illegal
and dangerous to
you, your passengers
and the general
public. There are many
safety factors to
consider as seizures
often occur without
warning. If you
continue to drive
despite your doctor’s
advice and you
do not report
your condition to
the DLA, you
are not fulfilling your
legal responsibility. If
you are involved
in a crash
during the recommended
non-driving period and
it is found
that your epilepsy
was a contributing factor,
you may be
prosecuted, charged and/or
jailed and your
insurance may not
be valid. You may
also have difficulty
obtaining insurance in the future.
Conditional
Licences Treatment advances in
recent years mean
that many medical
conditions can be
well managed and
drivers can remain on
the road, sometimes
on a conditional
licence. Conditional licences
are not a
new feature of the
licensing system, however
revised standards place
greater emphasis on the use
of conditional licences
as a means of
balancing safety requirements
with the needs
of drivers. A conditional
licence means that
the person may
continue to drive
as long as
certain conditions or
restrictions are met. Your responsibilities It
is a legal
requirement for the
person with epilepsy
to notify the
DLA in their
state or territory
that they have epilepsy. The
driver is responsible
for making sure
that they are
well enough to drive safely
- by managing
good seizure control and
complying with medical
treatment. If issued
with a conditional
licence the person
with epilepsy is expected
to comply with
any enforced driving
restrictions. The Australian guidelines
concerning seizures and
driving may seem
severe but these
laws were created
to protect public safety.
You must be seizure free
for a specified
period (see www.austroads.com.au ) You must continue to
take anti-epileptic medication
regularly as prescribed
unless your specialist recommends changes
You should ensure that
you have adequate
sleep and not
drive if sleep-deprived You may need to abstain from
alcohol and other
drugs (it has
been found that
a repeated episodes
of seizures may be precipitated by consumption of alcohol or drugs
not prescribed for epilepsy)
Newly Diagnosed Epilepsy
Once treatment is started nearly three out of
four patients achieve long term control? Epilepsy from this perspective has a
good prognosis and driving need be curtailed for no more than 3-6 months if the
patient is seizure-free from the start of treatment.
Lipomas are the most common soft-tissue tumor.
These slow-growing, benign fatty tumors form soft, lobulated masses enclosed by
a thin, fibrous capsule
In the GI tract, lipomas present as
submucosal fatty tumors. The most common locations include the esophagus,
stomach, and small intestine
The outcome and prognosis are excellent for
benign lipomas. Recurrence is uncommon but may develop if the excision was
incomplete.
Atypical lipomatous tumors are considered
to be well-differentiated liposarcomas. They have a predilection for local
recurrence but do not generally metastasize. This diagnosis should be suspected
when a fatty tumor is encountered in an intramuscular or retroperitoneal
location.
Liposarcomas are malignant tumors that
arise from adipocytes. They may recur locally and may metastasize. Fatty tumors
of the retroperitoneum or in intramuscular locations should be considered to be
potential liposarcomas until proven otherwise.
In the breast, a lipoma will be
mammographically radiolucent. It must be differentiated from a similar benign
tumor, a mammary hamartoma, and a pseudolipoma (
lipoma
Biopsies are normally not indicated for
small subcutaneous lesions, because the entire tumor is usually removed
benign melanocytic nevus refers to a
heterogeneous group of nonmalignant melanocytic nevi manifesting either as
pigmented or nonpigmented cutaneous lesions.
prototypical benign melanocytic nevus is
the common acquired nevus, which typically appears within the first 6 months of
life, reaches maximal size and number in young adulthood, then disappears with
advancing age.
bening melanotic naevi
3 major types are classified acording to
possition of melanocyte
1.intradefmal(majority of benign hairy
congenital mole)
2.junctional naevi(neavhs cells at the
junction)
3.compound naevi(neavus cells completely in
the dermis)
Malignant melanoma is believedcto occur the
juctional component
leucolakia are whitish leasikn in the oral
cabity
Bowen's disease is a very early form of
skin cancer, which is easily curable. The main sign is a red, scaly patch on
the skin. The abnormal growth takes place in the squamous cells – the outermost
layer of skin – and Bowen's disease is sometimes referred to as "squamous
cell carcinoma in situ".
Bowen disease is a squamous cell carcinoma
(SCC) in situ with the potential for significant lateral spread.
Bowen disease is a form of intraepidermal
carcinoma, a malignant tumor of keratinocytes.
A solar keratosis is the most common skin
condition resulting from skin damaged by the sun over many years. Solar
keratoses (also known as actinic keratoses) are usually rough, scaly patches on
sun-exposed areas such as the head and face. They are common, especially in
older people, many of whom have more than one.
its premalignent condition
soler kerstodis
Monday, January 4, 2016
7:00 PM
seborrhoaeic keratoses(seborrhoeic
warts)
Seborrheic keratoses are the most common
benign tumor in older individuals
specially trunc and face
brown to black pigmentation
sebboriec keratisis
Monday, January 4, 2016
7:08 PM
seboratic dermatitis is benign condision
Lentigo Maligna Melanoma/ Hutchinson melanotic freckle
superficial spredibg melsnoma/melanoma
insitu
usually face of elderly female
Lentigo maligna (LM) is a subtype of
melanoma in situ, and it has a slight female preponderance.
the disease continues to be called
Hutchinson melanotic freckle on occasion
Lentigo maligna melanoma is a melanoma that
has evolved from a lentigo maligna. :695. They are usually found on chronically
sun damaged skin such as the face and the forearms of the elderly. The
nomenclature is very confusing to both patients and physicians alike.
lentigo malignant melanoma
Mycosis fungoides, also known as
Alibert-Bazin syndrome or granuloma fungoides, is the most common form of
cutaneous T-cell lymphoma. It generally affects the skin, but may progress internally
over time. Symptoms include rash, tumors, skin lesions, and itchy skin.
mixed parotid Tumour (pleomopic adenoma )
are the most common parotid tumour.
It DOES NOT CAUSE facial NERVE PARALISIs even its very karge
he most common intraparotid mass is the
benign lymph node, as a significant number of lymph nodes are present in the
parotid. The most common benign tumor in children is the hemangioma. Of the
benign epithelial tumors, the mixed tumor (pleomorphic adenoma) is the most
common.
second most common benignntumour is
Adenolymphoma(WARTHIN Tumour)
Warthin tumor (papillary cystadenoma
lymphomatosum or adenolymphoma)
See the list below:
Second most common benign parotid tumor
(5%)
Most common bilateral benign neoplasm of
the parotid
uperficial parotidectomy is the treatment
of choice for most benign tumors in the superficial lobe.
Avoid enucleation (except for Warthin
tumors and lymph nodes), since it greatly increases the likelihood of
recurrence (up to 80%) and nerve damage. Deep lobe tumors demand total
parotidectomy with preservation of the facial nerve.
Approximately 25% of parotid masses are
nonneoplastic; the remaining 75% are neoplastic.
Signs of trismus. The most obvious effect
of trismus is difficulty in opening the mouth.
Trismus often indicates advanced disease
with extension into the masticatory muscles or, less commonly, invasion of the
temporomandibular joint.
Mucoepidermoid carcinoma is the most common
malignant tumor of the parotid gland, accounting for 30% of parotid
malignancies.
other types
Adenoid cystic carcinoma
Malignant mixed tumors
Adenocarcinoma
Mucoepidermoid carcinoma is the most common
malignant tumor of the parotid gland, accounting for 30% of parotid malignancies
pleomophic adenoma=mixed parotid
tumours
anterior hone of hyoid bone some time mimic
malignet lymp node of anterior trangle
Branchial cleft cysts are congenital
epithelial cysts, which arise on the lateral part of the neck from a failure of
obliteration of the second branchial cleft in embryonic development
Surgical excision is definitive treatment
for branchial cleft cysts.
branchial cyst first appernace in 2nd and
3rd decade
situated upper 1/3 of anterior trangle
usually line by squarmous epithilium
often cotain lymp tissue
Cystic hygroma (meaning "moist
tumor") belongs to a group of diseases now recognized as lymphatic
malformations.
A cystic hygroma, also known as cystic
lymphangioma and macrocystic lymphatic malformation, is an often congenital
multiloculated lymphatic lesion that can arise anywhere, but is classically
found in the left posterior triangle of the neck and armpits.
Cystic hygromas are benign, but can be
disfiguring. It is a condition which usually affects children; very rarely it
can present in adulthood.
Cystic hygromas are increasingly diagnosed
by prenatal ultrasonography. 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
Cystic hygromas are also often seen in
Turner's syndrome, although a patient who does not have Turner's syndrome can
present with this condition.
Treatments for removal of cystic hygroma
are surgery or sclerosing agents which include:
Bleomycin
Doxycycline
Ethanol (pure)
Picibanil (OK-432)
Sodium tetradecyl sulfate
branchial cyst
branchial cyst - Google Search
cystic hygroma
cystic hygroma - Google Search
medullary ca of thyroid
Rare form of thyroid CA
produce calcitonine and presented with
hypocalceamia rather than swelling in the neck
cause MEN(multiple endocrine neoplacia
) type 2A abd 2B
Medullary carcinoma of the thyroid (MTC) is
a distinct thyroid carcinoma that originates in the parafollicular C cells of
the thyroid gland. These C cells produce calcitonin.
MEN syndrome
Medullary thyroid cancer (MTC) is usually
diagnosed on physical examination as a solitary neck nodule, and early spread
to regional lymph nodes is common. Distant metastases occur in the liver, lung,
bone, and brain.
medullary Ca
In addition to producing calcitonin, MTC
cells can produce several other hormones, including corticotropin, serotonin,
melanin, and prostaglandins; moreover, paraneoplastic syndromes (eg, carcinoid
syndrome, Cushing syndrome) can occur in these patients.
Medullary carcinoma of the thyroid (MTC)
has a genetic association with multiple endocrine neoplasia (MEN) 2A and 2B; h
atients may present with various
paraneoplastic syndromes, including Cushing or carcinoid syndrome
Papillary carcinoma (PTC) is the most
common form of well-differentiated thyroid cancer, and the most common form of
thyroid cancer to result from exposure to radiation.
Papillary tumors have a propensity to
invade lymphatics but are less likely to invade blood vessels.
At the time of diagnosis, 10-15% of
patients with papillary thyroid carcinoma have distant metastases to the bones
and lungs.
lymphatic infiltration is common
Capture Dec 30, 2015
Wednesday, December 30, 2015
4:25 PM
sebaceous cyst attsched go the skin and
move with skin
lipoma nit attachnto the skin and freely
moving
secacious cyst smoogh serface.but lipoma
lobulated .
follicuer CA
FTC originates in follicular cells and is
the second most common cancer of the thyroid, after papillary carcinoma.
The most common thyroid tumor to develop
after exposure to radiation is papillary thyroid cancer
thyroid ca
prognosis is better for younger patients
than for patients who are older than 45 years.
follicuer thyroid ca
The bone metastases in FTC are osteolytic.
Older patients have an increased risk of developing bone and lung metastases.
papillary ca of thyroid atimulated by TSH
submandibuler duct stone clinically diagnose by bimanual
palpation.
confirm by Intra Oral Xray
commonly tonsiller LN(jugulo digastric)
enlarge due to paryngeal and tonciller pathalogy
A ranula is a type of mucocele found on the
floor of the mouth. Ranulas present as a swelling of connective tissue
consisting of collected mucin from a ruptured salivary gland caused by local
trauma.
ranula
Tuesday, January 5, 2016
9:58 AM
mucocele or ranula
Collectively, the mucocele, the oral
ranula, and the cervical, or plunging, ranula are clinical terms for a
pseudocyst that is associated with mucus extravasation into the surrounding
soft tissues. These lesions occur as the result of trauma or obstruction to the
salivary gland excretory duct and spillage of
ranula resulting from obstructed miner
salivery gland
pemberton sign ususally due to
obstruction of venus flow due to retrosternal extention ...patien may hv
disinusand singcope due to venus obstruction
pemberton sign - Google Search
sub clavian steal syndrom
Watch "Subclavian Steal Syndrome"
on YouTube
In medicine, subclavian steal syndrome
(SSS), also called subclavian steal phenomenon or subclavian steal
steno-occlusive disease, is a constellation of signs and symptoms that arise
from retrograde (reversed) flow of blood in the vertebral artery or the
internal thoracic artery, due to a proximal stenosis (narrowing) ...
papillary TCA well differentiated
medallaray ca is leaset differentiated
foliculer CA is in between
medullaray CA of thyrodid secread
calcitonian and serotonin ect and cause CARCINOID SYNDROM
Horner syndrom
ptosis
meosis
anhydrosis
enopthalmus
stuffy nostril
most important sign of prognosis of
headninjury patient is level of conciousness
subdural haematoma
chronic subdural haematoma
Often, the torn blood vessel is a vein that
connects the cortical surface of the brain to a dural sinus (termed a bridging
vein). In elderly persons, the bridging veins may already be stretched because
of brain atrophy (shrinkage that occurs with age).
chronic SDH
presented with Nohx of headtroma or mild
head injura 2 to 4 weeks back
alcoholic
elderly
complain of headacheh and demntia some time gait abnormalities
on anticoagulant
treat with burr hole
Watch "The Ulnar Nerve Review - Everything You Need To Know - Dr.
Nabil Ebraheim" on YouTube
brachial plexus
Watch "Funky Anatomy EXAM ANSWERS
Brachial Plexus Made Easy AMENDED" on YouTube
ulnar nerve
Watch "Anatomy Of The Ulnar
Nerve" on YouTube
ulnervnerve
ulnar nerve supply - Google Search
ulnar nerve palsy - Google Search
ulnar nerve
Background
The ulnar nerve is an extension of the
medial cord of the brachial plexus. It is a mixed nerve that supplies
innervation to muscles in the forearm and hand and provides sensation over the
medial half of the fourth digit and the entire fifth digit (the ulnar aspect of
the palm) and the ulnar portion of the posterior aspect of the hand (dorsal
ulnar cutaneous distribution). Entrapment of the ulnar nerve is the second most
common entrapment neuropathy in the upper extremity (after entrapment of the
median nerve).[1, 2, 3]
The most common site of ulnar nerve
entrapment is at or near the elbow region, especially in the region of the
cubital tunnel[4] or in the epicondylar (ulnar) groove; the second most likely
site is at or near the wrist, especially in the area of the anatomic structure
called the canal of Guyon
When the ulnar nerve is divided at the
wrist, only the opponens pollicis, superficial head of the flexor pollicis
brevis, and lateral 2 lumbricals are functioning.
The ulnar nerve is the terminal branch of
the medial cord of the brachial plexus and contains fibers from C8, T1,
ulnar never pass through the cubital tunnel
n the forearm, the ulnar nerve extends
motor branches to the flexor carpi ulnaris and the flexor digitorum profundus
of the ring and small fingers.
Anatomy
Course of ulnar nerve
The ulnar nerve is the terminal branch of
the medial cord of the brachial plexus and contains fibers from C8, T1, and,
occasionally, C7.[8, 9] It enters the arm with the axillary artery and passes
posterior and medial to the brachial artery, traveling between the brachial
artery and the brachial vein.
At the level of the insertion of the
coracobrachialis in the middle third of the arm, the ulnar nerve pierces the
medial intermuscular septum to enter the posterior compartment of the arm.[10,
11] Here, the nerve lies on the anterior aspect of the medial head of the
triceps, where it is joined by the superior ulnar collateral artery. The medial
intermuscular septum extends from the coracobrachialis proximally, where it is
a thin and weak structure, to the medial humeral epicondyle, where it is a
thick, distinct structure.
The next important site along the course of
the ulnar nerve is the arcade of Struthers. This structure is found in 70% of
patients, 8 cm proximal to the medial epicondyle, and extends from the medial
intermuscular septum to the medial head of the triceps. The arcade of Struthers
is formed by the attachments of the internal brachial ligament (a fascial
extension of the coracobrachialis tendon), the fascia and superficial muscular
fibers of the medial head of the triceps, and the medial intermuscular septum.
It is important to distinguish the arcade
of Struthers from the ligament of Struthers, which is found in 1% of the
population and extends from a supracondylar bony or cartilaginous spur to the
medial epicondyle. This supracondylar spur can be found on the anteromedial
aspect of the humerus, 5 cm proximal to the medial epicondyle, and it can often
be seen on radiographs. The ligament of Struthers may occasionally cause
neurovascular compression, usually involving the median nerve or the brachial
artery but sometimes affecting the ulnar nerve.
Next, the ulnar nerve passes through the
cubital tunnel, which is the space bounded by the following:
The medial epicondyle (medial border)
The olecranon (lateral border)
The elbow capsule at the posterior aspect
of the ulnar collateral ligament (floor)
The humeroulnar arcade (HUA), or Osborne
fascia or ligament (roof)
The deep forearm investing fascia of the
flexor carpi ulnaris and the arcuate ligament of Osborne, also known as the
cubital tunnel retinaculum, form the roof of the cubital tunnel. The cubital
tunnel retinaculum is a 4-mm-wide fibrous band that passes from the medial
epicondyle to the tip of the olecranon. Its fibers are oriented perpendicularly
to the fibers of the flexor carpi ulnaris aponeurosis, which blends with its
distal margin.
The elbow capsule and the posterior and
transverse portions of the medial collateral ligament form the floor of the
cubital tunnel. The medial epicondyle and olecranon form the walls.
O’Driscoll suggested that the roof of the
cubital tunnel (ie, the Osborne ligament or fascia), is a remnant of the
anconeus epitrochlearis,[12] an aberrant muscle that has been found in 3-28% of
cadaver elbows and in as many as 9% of patients undergoing surgery for cubital
tunnel syndrome. This muscle arises from the medial humeral condyle and inserts
on the olecranon, crossing superficially to the ulnar nerve, where it may cause
compression.[13]
O’Driscoll also identified a retinaculum at
the proximal edge of the arcuate ligament in all but 4 of 25 cadaveric
specimens.[12] He classified this retinaculum into the following four types:
Absent retinaculum
Thin retinaculum that becomes tight with full
flexion without compressing the nerve
Thick retinaculum that compresses the nerve
between 90° and full flexion
Accessory anconeus epitrochlearis
Upon entering the cubital tunnel, the ulnar
nerve gives off an articular branch to the elbow. It then passes between the
humeral and ulnar heads of the flexor carpi ulnaris and descends into the
forearm between the flexor carpi ulnaris and the flexor digitorum profundus.
About 5 cm distal to the medial epicondyle, the ulnar nerve pierces the
flexor-pronator aponeurosis, the fibrous common origin of the flexor and
pronator muscles.
The ligament of Spinner is an additional
aponeurosis between the flexor digitorum superficialis of the ring finger and
the humeral head of the flexor carpi ulnaris. This septum is independent of the
other aponeuroses and attaches directly to the medial epicondyle and the medial
surface of the coronoid process of the ulna. With anterior transposition of the
ulnar nerve, it is important to recognize and to release this structure to prevent
kinking.
In the forearm, the ulnar nerve extends
motor branches to the flexor carpi ulnaris and the flexor digitorum profundus
of the ring and small fingers. The ulnar nerve may extend as many as 4 branches
to the flexor carpi ulnaris, ranging from 4 cm above to 10 cm below the medial
epicondyle. Proximal dissection of the first motor branch to the flexor carpi
ulnaris from the ulnar nerve may be performed up to 6.7 cm proximal to the
medial epicondyle, facilitating anterior transposition of the nerve.
Posterior branches of the medial
antebrachial cutaneous nerves cross the ulnar nerve anywhere from 6 cm proximal
to 4 cm distal to the medial epicondyle. These branches are often cut in the
course of making the skin incision for a cubital tunnel release, creating an
area of dysesthesia or resulting in potential neuroma formation.
As the ulnar nerve courses down the forearm
toward the wrist, the dorsal ulnar cutaneous nerve leaves the main branch. A
little further down, the palmar cutaneous branch takes off. Thus, neither of
these two branches goes through the canal of Guyon.[1] The remainder of the
ulnar nerve enters the canal at the proximal portion of the wrist. This is
bounded proximally and distally by the pisiform bone and the hook of the hamate
bone.
Ulnar compression[36] in the medial
epicondylar region is generally from a valgus deformity of the bone.
After the ulnar nerve passes distal to the
elbow,[41, 42, 19] it makes several important divisions. The first branches to
come off are those that go to the flexor carpi ulnaris. Further distally, the
branches to the flexor digitorum profundus muscles of digits 4 and 5 arise
ulnar nervr
Overview
Background
The ulnar nerve is an extension of the
medial cord of the brachial plexus. It is a mixed nerve that supplies
innervation to muscles in the forearm and hand and provides sensation over the
medial half of the fourth digit and the entire fifth digit (the ulnar aspect of
the palm) and the ulnar portion of the posterior aspect of the hand (dorsal
ulnar cutaneous distribution). Entrapment of the ulnar nerve is the second most
common entrapment neuropathy in the upper extremity (after entrapment of the
median nerve).[1, 2, 3]
The most common site of ulnar nerve
entrapment is at or near the elbow region, especially in the region of the
cubital tunnel[4] or in the epicondylar (ulnar) groove; the second most likely
site is at or near the wrist, especially in the area of the anatomic structure
called the canal of Guyon.[1, 5, 6, 7] However, entrapment can also occur in
the forearm between these two regions, below the wrist within the hand, or
above the elbow.
Pressure on or injury to the ulnar nerve
may cause denervation and paralysis of the muscles supplied by the nerve.
Affected patients often experience numbness and tingling along the little
finger and the ulnar half of the ring finger. This discomfort is often
accompanied by weakness of grip and, rarely, intrinsic wasting. One of the most
severe consequences is loss of intrinsic muscle function in the hand. When the
ulnar nerve is divided at the wrist, only the opponens pollicis, superficial
head of the flexor pollicis brevis, and lateral 2 lumbricals are functioning.
Conservative nonsurgical treatment may play
a useful role in management. If such treatment fails or the patient has severe
or progressive weakness or loss of function, surgical treatment is warranted.
Several surgical approaches have been employed, each of which has its
advocates; results for all of them appear to be satisfactory.
Anatomy
Course of ulnar nerve
The ulnar nerve is the terminal branch of
the medial cord of the brachial plexus and contains fibers from C8, T1, and,
occasionally, C7.[8, 9] It enters the arm with the axillary artery and passes
posterior and medial to the brachial artery, traveling between the brachial
artery and the brachial vein.
At the level of the insertion of the
coracobrachialis in the middle third of the arm, the ulnar nerve pierces the
medial intermuscular septum to enter the posterior compartment of the arm.[10,
11] Here, the nerve lies on the anterior aspect of the medial head of the
triceps, where it is joined by the superior ulnar collateral artery. The medial
intermuscular septum extends from the coracobrachialis proximally, where it is
a thin and weak structure, to the medial humeral epicondyle, where it is a
thick, distinct structure.
The next important site along the course of
the ulnar nerve is the arcade of Struthers. This structure is found in 70% of
patients, 8 cm proximal to the medial epicondyle, and extends from the medial
intermuscular septum to the medial head of the triceps. The arcade of Struthers
is formed by the attachments of the internal brachial ligament (a fascial
extension of the coracobrachialis tendon), the fascia and superficial muscular
fibers of the medial head of the triceps, and the medial intermuscular septum.
It is important to distinguish the arcade
of Struthers from the ligament of Struthers, which is found in 1% of the
population and extends from a supracondylar bony or cartilaginous spur to the
medial epicondyle. This supracondylar spur can be found on the anteromedial
aspect of the humerus, 5 cm proximal to the medial epicondyle, and it can often
be seen on radiographs. The ligament of Struthers may occasionally cause
neurovascular compression, usually involving the median nerve or the brachial
artery but sometimes affecting the ulnar nerve.
Next, the ulnar nerve passes through the
cubital tunnel, which is the space bounded by the following:
The medial epicondyle (medial border)
The olecranon (lateral border)
The elbow capsule at the posterior aspect
of the ulnar collateral ligament (floor)
The humeroulnar arcade (HUA), or Osborne
fascia or ligament (roof)
The deep forearm investing fascia of the
flexor carpi ulnaris and the arcuate ligament of Osborne, also known as the
cubital tunnel retinaculum, form the roof of the cubital tunnel. The cubital
tunnel retinaculum is a 4-mm-wide fibrous band that passes from the medial
epicondyle to the tip of the olecranon. Its fibers are oriented perpendicularly
to the fibers of the flexor carpi ulnaris aponeurosis, which blends with its
distal margin.
The elbow capsule and the posterior and
transverse portions of the medial collateral ligament form the floor of the
cubital tunnel. The medial epicondyle and olecranon form the walls.
O’Driscoll suggested that the roof of the
cubital tunnel (ie, the Osborne ligament or fascia), is a remnant of the
anconeus epitrochlearis,[12] an aberrant muscle that has been found in 3-28% of
cadaver elbows and in as many as 9% of patients undergoing surgery for cubital
tunnel syndrome. This muscle arises from the medial humeral condyle and inserts
on the olecranon, crossing superficially to the ulnar nerve, where it may cause
compression.[13]
O’Driscoll also identified a retinaculum at
the proximal edge of the arcuate ligament in all but 4 of 25 cadaveric
specimens.[12] He classified this retinaculum into the following four types:
Absent retinaculum
Thin retinaculum that becomes tight with
full flexion without compressing the nerve
Thick retinaculum that compresses the nerve
between 90° and full flexion
Accessory anconeus epitrochlearis
Upon entering the cubital tunnel, the ulnar
nerve gives off an articular branch to the elbow. It then passes between the
humeral and ulnar heads of the flexor carpi ulnaris and descends into the
forearm between the flexor carpi ulnaris and the flexor digitorum profundus.
About 5 cm distal to the medial epicondyle, the ulnar nerve pierces the
flexor-pronator aponeurosis, the fibrous common origin of the flexor and
pronator muscles.
The ligament of Spinner is an additional
aponeurosis between the flexor digitorum superficialis of the ring finger and
the humeral head of the flexor carpi ulnaris. This septum is independent of the
other aponeuroses and attaches directly to the medial epicondyle and the medial
surface of the coronoid process of the ulna. With anterior transposition of the
ulnar nerve, it is important to recognize and to release this structure to
prevent kinking.
In the forearm, the ulnar nerve extends
motor branches to the flexor carpi ulnaris and the flexor digitorum profundus
of the ring and small fingers. The ulnar nerve may extend as many as 4 branches
to the flexor carpi ulnaris, ranging from 4 cm above to 10 cm below the medial
epicondyle. Proximal dissection of the first motor branch to the flexor carpi
ulnaris from the ulnar nerve may be performed up to 6.7 cm proximal to the
medial epicondyle, facilitating anterior transposition of the nerve.
Posterior branches of the medial
antebrachial cutaneous nerves cross the ulnar nerve anywhere from 6 cm proximal
to 4 cm distal to the medial epicondyle. These branches are often cut in the
course of making the skin incision for a cubital tunnel release, creating an
area of dysesthesia or resulting in potential neuroma formation.
As the ulnar nerve courses down the forearm
toward the wrist, the dorsal ulnar cutaneous nerve leaves the main branch. A
little further down, the palmar cutaneous branch takes off. Thus, neither of
these two branches goes through the canal of Guyon.[1] The remainder of the
ulnar nerve enters the canal at the proximal portion of the wrist. This is
bounded proximally and distally by the pisiform bone and the hook of the hamate
bone. It is covered by the volar carpal ligament and the palmaris brevis.
The following two nerve anomalies should be
mentioned because they may confuse the diagnosis in the setting of ulnar
neuropathy:
Martin-Gruber anastomosis in the forearm -
In this anomaly, fibers that supply the intrinsic muscles are carried in the
median nerve to the middle of the forearm where they leave the median nerve to
join the ulnar nerve; functioning intrinsic muscles could be observed with
injury above this anastomosis, though the ulnar nerve dysfunction is proximal
Riche-Cannieu anastomosis - In this
anomaly, the median and ulnar nerves are connected in the palm; even with an
injury at the wrist, there is some intrinsic function
Blood supply
The extrinsic blood supply to the ulnar
nerve is segmental and involves the following three vessels:
Superior ulnar collateral artery
Inferior ulnar collateral artery
Posterior ulnar recurrent artery
Typically, the inferior ulnar collateral
artery (and often the posterior ulnar recurrent artery) is sacrificed with
anterior transposition. At the level of the medial epicondyle, the inferior
ulnar collateral artery is the sole blood supply to the ulnar nerve. In an
anatomic study, no identifiable anastomosis was found between the superior
ulnar collateral artery and the posterior ulnar recurrent arteries in 20 of 22
arms; instead, communication between the two arteries occurred through proximal
and distal extensions of the inferior ulnar collateral artery.
The intrinsic blood supply is composed of
an interconnecting network of vessels that run along the fascicular branches
and along each fascicle of the ulnar nerve itself. The surface microcirculation
of the ulnar nerve follows an anastomotic stepladder arrangement. The inferior
ulnar collateral artery is consistently found 5 mm deep to the leading edge of
the medial intermuscular septum on the surface of the triceps.[14]
Sites of nerve entrapment
As diagnostic and surgical methodologies
have evolved over the past century, physicians’ ability to recognize and
describe sites of entrapment has improved. However, the terminology used to
describe ulnar nerve entrapment has become confusing, in that not all
clinicians use the same words for the same things. This confusion can be
illustrated by examining the terms applied to ulnar nerve entrapment in the
elbow region,[15] of which the two most commonly used (and misused) are tardy
ulnar palsy[16] and cubital tunnel syndrome.[17]
In 1878, Panas first described what is now
often called tardy ulnar palsy, in which either prior trauma or osteoarthritis
gradually caused damage to the ulnar nerve.[18] Additional cases were reported
over the ensuing decades,[19, 20] usually associated with trauma (eg, fractures
in the elbow region) and typically occurring in the epicondylar groove.[21, 22]
Initially denoting time (ie, appearing years after trauma), the term came to
have an anatomic connotation (ie, usually seen in or very near the epicondylar
groove).[23]
From 1922 on, physicians began to recognize
ulnar entrapments in the HUA.[24, 25] In 1958, the term cubital tunnel syndrome
was coined to describe the effects of the ulnar nerve entrapment[26] at the
HUA. Numerous other reports ensued.
Although the current state of knowledge is
still incomplete, it is possible to identify approximately five sites in the
elbow region at which the ulnar nerve is most likely to be compressed. (Five is
not a firm figure; some of the sites are so close together that certain
authorities categorize them differently to get a different number.) This
article principally follows Posner’s classification,[27] which lists the
following sites (see the image below):
Above the elbow in the region of the
intermuscular septum
The medial epicondylar region
The epicondylar (ie, ulnar) groove
The region of the cubital tunnel
The region where the ulnar nerve exits from
the flexor carpi ulnaris, at which the usual cause of compression is the deep
flexor-pronator aponeurosis
Schematic diagram of elbow region, with 5
main sites (as given by Posner) labeled 1-5; other sites and structures are
also named. Main regions of interest are circled with pastel-colored arrows.
Sites 2 and 3 are close together and cannot be distinguished by means of
electromyography and nerve conduction studies. This location is referred to as
ulnar (or epicondylar) groove.
View Media Gallery
Region of intermuscular septum
Halikis et al[28] divided this region into
2 areas, the arcade of Struthers[29, 30] and the medial intermuscular septum.
According to the standard anatomic definition, the arcade of Struthers is a
thin fibrous band that usually extends from the medial head of the triceps to
the medial intermuscular septum. It is often said to be about 6-10 cm proximal
to the medial epicondyle.
Considerable anatomic variation exists, and
in fact, there is outright controversy about the arcade of Struthers.[31] One
component of the controversy is quite trivial: There is no evidence that
Struthers discovered this structure or was even aware of it; his name was
attached to it by Kane et al in a 1973 paper.[32]
Siqueira, in an autopsy study of 60 upper
limbs, found a structure reasonably approximating the definition given above in
8 limbs (13.5%).[31] Ulnar nerve entrapment occurred in none of them (but there
was no clinical reason to expect that it might have).
Bartels et al could not find the arcade of
Struthers in their dissections, and they expressed doubts about its
existence.[33]
Wehrli and Oberlin described a different
structure in the same region that might be involved in ulnar entrapment in some
cases—the internal brachial ligament.[34] This structure was in fact described
by Struthers, but not in relation to ulnar nerve entrapment. Wehrli and Oberlin
advocated abolishing the concept of the arcade of Struthers.
Von Schroeder and Scheker described yet
another structure, a fibrous tunnel in roughly the same region.[35] They
maintained that the ulnar nerve goes through this tunnel and could be trapped
therein and suggested naming this structure the arcade of Struthers.
Settling this anatomic controversy is
beyond the scope of this article. It is sufficient to note that in rare cases,
the ulnar nerve may be compressed considerably above the ulnar groove and that
surgeons may find it entrapped in a fibrous or ligamentous structure that may
correspond to one of the aforementioned anatomic descriptions.
Medial epicondylar region
Ulnar compression[36] in the medial
epicondylar region is generally from a valgus deformity of the bone. If a
patient is placed in standard anatomic position with the palms rotated toward
the front and the thumb away from the midline, a valgus deformity means that
the elbow would be deformed away from midline of the body.
Epicondylar groove
The epicondylar (ulnar) groove is a
fibro-osseous tunnel holding the ulnar nerve and its vascular accompaniment. It
is slightly distal to the medial epicondyle, or at least to the beginning of
it.
Campbell used slightly different
terminology, lumping the epicondylar groove together with the medial
epicondylar region and labeling the entire region the area of the retrocondylar
groove. Halikis et al considered the medial epicondylar region and the
epicondylar groove to be the area of the medial epicondyle.[28]
The medial epicondylar region and the
epicondylar groove are generally considered to be the classic locations (or
location, if considered as a single area) for tardy ulnar palsy. In the
author’s personal experience, electromyographers and orthopedic surgeons more
commonly refer to a tardy ulnar palsy at the retrocondylar groove, thus using
the Campbell terminology.
Region of cubital tunnel
The cubital tunnel is the passage between
the two heads of the flexor carpi ulnaris, which are connected by a
continuation of the fibroaponeurotic covering of the epicondylar groove
(Osborne ligament). During elbow flexion, the tunnel flattens as the ligament
stretches, causing pressure on the ulnar nerve.[37, 38, 39]
Campbell’s classification was basically the
same for this region, except that he preferred to call it the region of the
HUA, apparently because he believed that too many clinicians loosely used the
term cubital tunnel to refer to a place anywhere in the elbow.
Halikis et al divided this region into two
parts, the cubital tunnel and the Osborne fascia.[28] This is a good example of
the problems with the terminology: Different terms are used for locations that
are virtually the same. For all practical purposes—certainly with regard to
anything that can be distinguished on electromyography (EMG)—the Osborne
ligament is equivalent to the Osborne fascia, and both are equivalent to the HUA.
Region where ulnar nerve exits from flexor
carpi ulnaris
Campbell[40] and Halikis et al[28] agreed
with Posner in listing this region as the final entrapment site in the elbow
area. As the nerve exits the flexor carpi ulnaris, it perforates a fascial layer
between the flexor digitorum superficialis and the flexor digitorum profundus.
Entrapment can occur here also.
More distal entrapment sites
After the ulnar nerve passes distal to the
elbow,[41, 42, 19] it makes several important divisions. The first branches to
come off are those that go to the flexor carpi ulnaris. Further distally, the
branches to the flexor digitorum profundus muscles of digits 4 and 5 arise.
Although the nerve could be injured or
entrapped at any point along its course, four sites have been identified as the
most common locations of entrapment in relation to the canal of Guyon (see the
image below).
Diagram shows ulnar nerve distal to elbow
region. Dorsal ulnar cutaneous nerve (lavender) branches off main trunk (blue).
Although course is not followed in detail after that, lavender region on
sensory dermatome diagram shows where this sensory nerve innervates skin.
Similarly, palmar cutaneous sensory nerve (yellow) branches off to innervate
skin area depicted in yellow. Superficial terminal branch is mostly sensory
(see green-colored skin on palmar surface), though it also gives off branch to
palmaris brevis. Deep terminal branch has no corresponding skin area, because
it is solely motor-innervating muscles shown, as well as others not explicitly
depicted. Nerve could be pinched or injured anywhere, but sites labeled I-IV
are more commonly involved.
View Media Gallery
The canal of Guyon may be conveniently
divided into 3 zones as follows:
Zone 1 (encompassing the area proximal to
the bifurcation of the ulnar nerve) - Compression in zone 1 causes combined
motor and sensory loss; it is most commonly caused by a fracture of the hook of
the hamate or a ganglion
Zone 2 (encompassing the motor branch of
the nerve after it has bifurcated) - Compression in zone 2 causes pure loss of
motor function to all of the ulnar-innervated muscles in the hand; ganglion and
fracture of the hook of the hamate are the most common causes
Zone 3 (encompassing the superficial or
sensory branch of the bifurcated nerve) - Compression in zone 3 causes sensory
loss to the hypothenar eminence, the small finger, and part of the ring finger,
but it does not cause motor deficits; common causes are an aneurysm of the
ulnar artery, thrombosis, and synovial inflammation
Pathophysiology
As the elbow moves from extension to
flexion, the distance between the medial epicondyle and the olecranon increases
by 5 mm for every 45° of elbow flexion. Elbow flexion places stress on the
medial collateral ligament and the overlying retinaculum. The shape of the
cubital tunnel in cross-section changes from round to oval, with a 2.5-mm loss
of height, because the cubital tunnel rises during elbow flexion and the
epicondylar groove is not as deep on the inferior aspect of the medial
epicondyle as it is posteriorly.
The cubital tunnel’s loss in height with
flexion leads to a 55% volume decrease in the canal, which causes the mean
ulnar intraneural pressure to increase from 7 mm Hg to 14 mm Hg.[43, 44] A
combination of shoulder abduction, elbow flexion, and wrist extension results
in the greatest increase in cubital tunnel pressure, with ulnar intraneural
pressure increasing to about 6 times normal.[45, 46, 47, 48, 36]
Traction and excursion of the ulnar nerve
also occur during elbow flexion, as the ulnar nerve passes behind the axis of
rotation of the elbow. With full range of motion of the elbow, the ulnar nerve
undergoes 9-10 mm of longitudinal excursion proximal to the medial epicondyle
and 3-6 mm of excursion distal to the epicondyle.[49] In addition, the ulnar
nerve elongates by 5-8 mm with elbow flexion.
In addition to prior cadaver and surgical
studies of ulnar nerve motion, recently developed sonographic methods
facilitate monitoring the motion in the intact arm.[50] Interestingly, in
patients with ulnar neuropathies, the nerve is somewhat more motile than in
individuals with normal ulnar nerves.
Within the cubital tunnel, the measured
mean intraneural pressure is significantly greater than the mean extraneural
pressure at elbow flexion of 90° or more.[51] With the elbow flexed 130°, the
mean intraneural pressure is 45% higher than the mean extraneural pressure.
With this degree of flexion, significant flattening of the ulnar nerve occurs;
however, with full elbow flexion, there is no evidence for direct focal
compression, which suggests that traction on the nerve in association with
elbow flexion is responsible for the increased intraneural pressure.
In addition, studies have shown that the
intraneural and extraneural pressures within the cubital tunnel are lowest at
45° of flexion. As a result of these studies, 45° of flexion is considered to
be the optimum position for immobilization of the elbow to decrease pressure on
the ulnar nerve.
Subluxation of the ulnar nerve is common.
Childress, in a study of 2000 asymptomatic elbows, found that although none of
the patients were aware of ulnar nerve subluxation, 16.2% had this condition
after flexion past 90°.[52] Of the 325 patients with ulnar nerve subluxation,
only 14 had unilateral subluxation. Subluxation does not appear to cause
cubital tunnel syndrome, but the friction generated with repeated subluxation
may cause intraneural inflammation, and the subluxed position may render the
nerve more susceptible to inadvertent trauma.
Sunderland described the internal
topography of the ulnar nerve at the medial epicondyle.[53] The sensory fibers
and intrinsic muscle nerve fibers are located superficially. In contrast, the
motor fibers to the flexor carpi ulnaris and the flexor digitorum profundus are
located deep within the nerve.[54, 55, 56] The central location protects the
motor fibers and explains why weakness of these two muscles is not typically
seen in ulnar neuropathy.[57, 58, 27, 59]
Proximal compression of a nerve trunk, such
as occurs with cervical radiculopathy, may lead to increased vulnerability to
nerve compression in a distal segment. This "double crush" condition
can affect the ulnar nerve and results from disruption of normal axonal
transport.[60]
The nerve, axon, and myelin can be
affected. Within the axon, fascicles to individual muscles may be involved
selectively. Axonal involvement leads to motor unit loss and amplitude/area
reduction. Conduction block implies impaired transmission through a segment of
nerve. In the absence of changes indicating axonal damage, conduction block
implies myelin damage to the involved segment. Significant slowing of
conduction or significant spreading out of the temporal profile of the recorded
response with preserved axonal integrity suggests demyelination.
Various systems have been proposed for
classifying nerve injuries. Seddon in 1972 and Sunderland in 1978 took similar
approaches to this classification. Seddon stratified nerve injuries into the
following three levels[61] :
Neurapraxia - This is a transient episode
of complete motor paralysis with little sensory or autonomic involvement,
usually occurring secondary to transitory mechanical pressure; once the
pressure is relieved, complete return of function follows
Axonotmesis - This is a more severe injury
involving loss of continuity of the axon with maintenance of continuity of the
Schwann sheath; motor, sensory, and autonomic paralysis is complete, and
denervated muscle atrophy can be progressive; recovery can be complete but
depends on a number of factors, including timely removal of the compression and
axon regeneration; the time necessary to recover function depends on the
distance between the denervated muscle and the proximal regenerating axon
Neurotmesis - This is the most serious
level of injury, entailing complete loss of continuity both of the axon and of
the Schwann sheath; recovery rarely is complete, and the amount of loss can
only be determined over time; regenerating axons without intact neural tubes
reinnervate muscle fibers that were not part of their original network
Sunderland’s classification specifies five
degrees of nerve damage.[62] The first degree corresponds to neurapraxia in
Seddon’s schema; the second corresponds to axonotmesis; and the third, fourth,
and fifth correspond to increasingly severe levels of neurotmesis. In a
Sunderland third-degree injury, axons and Schwann sheaths are disrupted within
intact nerve fascicles. In a fourth-degree injury, the perineurium surrounding
the fascicles is damaged, as is the endoneurium. In a fifth-degree injury, the
nerve trunk is severed.
McGowan established the following
classification system for ulnar nerve injuries[63] :
Grade I - Mild lesions with paresthesias in
the ulnar nerve distribution and a feeling of clumsiness in the affected hand;
no wasting or weakness of the intrinsic muscles
Grade II - Intermediate lesions with weak
interosseous muscles and muscle wasting
Grade III - Severe lesions with paralysis
of the interosseous muscles and a marked weakness of the hand
In a study of the validity of the
Disabilities of Arm, Shoulder and Hand (DASH) questionnaire for elbow ulnar
neuropathy, Zimmerman et al found that the DASH questionnaire accurately
reflected the clinical staging of ulnar neuropathy.[64] There was a high
correlation between DASH scores, severity of symptoms, and functional status.
Correlations were identified as significant between DASH and biomechanical
measures, but correlation coefficients were lower. All measures showed significant
improvement postoperatively.
Etiology
Cubital tunnel syndrome may be caused by
constricting fascial bands, subluxation of the ulnar nerve over the medial
epicondyle, cubitus valgus, bony spurs, hypertrophied synovium, tumors,
ganglia, or direct compression. Occupational activities may aggravate cubital
tunnel syndrome secondary to repetitive elbow flexion and extension. Certain
occupations are associated with the development of cubital tunnel syndrome;
however, a definite relation to occupational activities is not well
defined.[65, 66, 67]
Factors that may cause ulnar neuropathy at
or near the elbow include the following:
Compression during general anesthesia
Blunt trauma
Deformities (eg, rheumatoid arthritis)
Metabolic derangements (eg, diabetes)
Transient occlusion of the brachial artery
during surgery [68]
Subdermal contraceptive implant [69]
Venipuncture [70]
Hemophilia [71] leading to hematomas
Malnutrition leading to muscle atrophy and
loss of fatty protection across the elbow and other joints
Cigarette smoking [72]
Factors that may cause ulnar neuropathy at
or distal to the wrist (ie, at the canal of Guyon) include the following:
Ganglionic cysts
Tumors
Blunt injuries, with or without fracture
Aberrant artery
Idiopathic
Ulnar neuropathy at or distal to wrist
The following physical findings are
significant with respect to ulnar neuropathy at or distal to the wrist:
Weakness of the interosseous and hypothenar
muscles only, with no sensory loss - This would most likely be due to
compression of the deep motor branch in the hand after it had separated from
the superficial terminal sensory branch but before the branch to the hypothenar
muscles had taken off
muscle of hand - Google Search
The interosseous muscles of the hand are
muscles found near the metacarpal bones that help to control the fingers. They
are considered voluntary muscles.
They are generally divided into two sets:
4 Dorsal interossei - Abduct the muscles
away from the 3rd digit (away from axial line) and are bipennate.
3 Palmar interossei - Adduct the muscles
towards the 3rd digit (towards the axial line) and are unipennate.
This is often remembered by the mnemonic
PAD-DAB, as the Palmar interosseous muscles ADduct, and the Dorsal interosseous
muscles ABduct. The axial line goes down the middle of the 3rd digit, towards
the palm of the hand (it's an imaginary line).
The lumbricals are intrinsic muscles of the
hand that flex the metacarpophalangeal joints and extend the interphalangeal
joints
ulnar nerve palsy cause ,inability to
abduct /spread fingers of hand
opposition of thumb
opposition of thumb to index finger week due to median nerve palsy which inervate
theana muscle
opposition of thumb to little finger weeken
due to ulnar palsy ( coz ulnar nerve support little finger movemrnt)
flexion of distal interphalangial joints of
the 4th and 5th fingers is funtion of
flexure digitirum profundus which inervated by ulner nerve where highr in
forearm.
lesion to ulnar nerve where at wrist is not
cause to affect funtion of flexure digitorum profundus
flexure carpi radialis is flesure of the wrist and inervated by median
nerve
extenser carpi radialis is the main wrist
extenser inervated by radial nerve
rheumatoid hand - Google Search
volkmann ischeamic contracture of
hand cause claw hand
volkmann contracture - Google Search
The Achilles reflex checks if the S1 and
S2[3] nerve roots are intact and could be indicative of sciatic nerve
pathology. It is classically delayed in hypothyroidism. This reflex is usually
absent in disk herniations at the L5—S1 level. A reduction in the ankle jerk
reflex may also be indicative of peripheral neuropathy.
Common causes
sensory innervation of leg - Google Search
ankle jerk reflex arc - Google Search
ankle jerk reflex arc - Google Search
qcute sever trauma cause fat emolism
syndrome and ARDS. ventilatory failure
is the most common cause of death after masive tissue injury.(folloving
sucsesful resacitaion)
shoulder
abduction
first
30 degree(may be 90) definitly by supra spinater muscle
then
mainly by deltoids muscle
some
ither muscle contribute too
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