my passion - SCI REHAB

http://www.apparelyzed.com/spinal-cord-injury/definitions.html

http://www.christopherreeve.org/site/c.ddJFKRNoFiG/b.4343879/k.D323/Research.htm

http://www.sci-info-pages.com/stem_cells.html

http://www.ninds.nih.gov/disorders/sci/detail_sci.htm

ACL REHAB PROTOCOL

http://www.palomarortho.com/protocols/antcruciateligament.pdf

Capsular pattern

The different capsular patterns The various capsular patterns Capsular pattern Jaw Increasing limitation of mouth opening. Capsular pattern Cervical spine Equal limitation of extension, both side flexions and both rotations. Flexion is the best movement. Capsular pattern Shoulder Limitation of abduction, more limitation of lateral rotation, less limitation of medial rotation. Capsular pattern Elbow Limitation of extension, more limitation of flexion. Capsular pattern Lower radio-ulnar joint Pain on passive pro- and supination, no limitation. Capsular pattern Wrist Equal limitation of flexion and extension. Capsular pattern Trapezio-first metacarpal joint Limitation of abduction and extension, no limitation of flexion. Capsular pattern Thumb and finger joints Flexion more limited than extension. Capsular pattern Thoracic spine Equal limitation of both rotations. Capsular pattern Lumbar spine Equal limitation of extension and both side flexions. Capsular pattern Hip Gross limitation of medial rotation and abduction ; flexion more limited than extension. Capsular pattern Knee Limitation of extension, more limitation of flexion. Capsular pattern Ankle joint Limitation of dorsiflexion, more limitation of plantiflexion. Capsular pattern Talocalcanean joint Increasing limitation of varus, in the end fixation in full valgus. Capsular pattern Midtarsal joints  Limitation of dorsiflexion, plantiflexion, adduction and medial rotation ; no limitation of abduction and lateral rotation. Capsular pattern First metatarsophalangeal joint Limitation of plantiflexion with more limitation of dorsiflexion. Capsular pattern II-V metatarsophalangeal joints Variable. Fixation in extension with flexed IP-joints.

MYOSITIS OSSIFICANS....

 In 1918, Dejerine and Ceillier first described heterotopic ossification (HO) in paraplegic patients injured in World War I, referring to the process as paraosteoarthropathy. HO has been defined as the formation of mature lamellar bone in soft tissues. The process involves true osteoblastic activity and bone formation. HO has been reported in cases of brain injury, spinal cord injury, stroke, poliomyelitis, myelodysplasia, tabes dorsalis, carbon monoxide poisoning, spinal cord tumors, syringomyelia, tetanus, and multiple sclerosis. This condition also has been reported after burns and total hip replacement.

Several terms have been used to describe the condition, including heterotopic ossification, ectopic ossification, and myositis ossificans. HO usually involves the large joints of the body (eg, hips, elbows, shoulders, knees). Excessive bone formation may result in significant disability by severely limiting the range of motion (ROM) of these joints (see Image 1).

The following 3 categories of HO have been described:

* Myositis ossificans progressiva is a rare metabolic bone disease in children with progressive metamorphosis of skeletal muscle to bone and is characterized by an autosomal dominant pattern of genetic transmission.

* Myositis ossificans circumscripta without trauma is a localized soft tissue ossification after neurologic injury or burns. This process also is referred to as neurogenic HO.

In relation to your original question some USA stastics showed:

An association has been cited between spasticity and HO. The incidence is higher in a spastic extremity; 84% of patients with HO had spasticity, and 54% of patients with HO had no spasticity. HO is seen in the elbow in 4% of patients with traumatic brain injury (TBI); however, if fracture or dislocation is associated with brain injury, the incidence of HO rises to 89%.Patients with brain injuries are at greater risk for developing HO if they have significant spasticity or increased muscle tone in the involved extremity, duration of unconsciousness longer than 2 weeks, long-bone or associated fractures, and decreased ROM. Therefore, the risk of development of HO in a patient with brain injury increases as the severity of injury, length of immobilization, and duration of coma increase.

* Traumatic myositis ossificans occurs from direct injury to the muscles. Fibrous, cartilaginous, and osseous tissues near bone are affected. The muscle may not be involved.

Pathophysiology: The specific cause and pathophysiology of HO remain unclear. HO may be due to an interaction between local factors (eg, the pool of available calcium in adjacent skeleton, soft tissue edema, vascular stasis tissue hypoxia, mesenchymal cells with osteoblastic activity) and an unknown systemic factor or factors. The basic defect in HO is the inappropriate differentiation of fibroblasts to bone-forming cells. Early edema of connective tissue proceeds to tissue with foci of calcification and then to maturation of calcification and ossification.


The typical Sport (post trauma) myositis ossificans is summarised below

Definition: Myositis ossificans is an unusual condition that often occurs in athletes who sustain a blunt injury that causes deep tissue bleeding. A typical story is a soccer player who is kicked forcefully in the mid-thigh, and develops pain and significant bruising.

The soft-tissues that were injured in the traumatic event initially develops a hematoma, and subsequently develop the myositis ossificans. The word myositis ossificans means that bone forms within the muscle, and this occurs at the site of the hematoma. No one knows exactly why this occurs in some people.

The common concern when abnormal bone is seen on a x-ray is that there is a tumor within the soft-tissues. Fortunately, myositis ossificans has some typical clues that usually make it easily differentiated from a tumor. If there is any question about the diagnosis, repeat x-rays will be obtained several weeks later to ensure the bone mass is a typical myositis ossificans.

Treatment of myositis ossificans consists of:

* Rest

* Immobilization

* Anti-Inflammatory Medication 

Rarely is surgical excision of the myositis ossificans warranted. If the myositis ossificans is removed before it is "mature," it will likely return. Therefore, most surgeons wait between 6 and 12 months before even considering removal. Furthermore, there is a chance of return even when removed very late. Generally, myositis ossificans is only removed surgically if it interferes with joint motion or if it is irritating a nerve

FACIAL NERVE PALSY

COMPONENTS OF FACIAL NERVE

Brancial motor (special visceral efferent)	Supplies the muscles of facial expression; posterior belly of digastric muscle; stylohyoid, and stapedius
Visceral motor (general visceral efferent)	Parasympathetic innervation of the lcrimal, submandibular, and sublingual glands, as well as mucous membranes of nasopharynx, hard and soft palate.
Special sensory (special afferent)	Taste sensation from the anterior 2/3 of tongue; hard and soft palates.
General sensory (general somatic afferent)	General sensation from the skin of the concha of the auricle and from a small area behind the ear.

 Functional Component Overview of Facial Nerve

Pathway of Cranial Nerve VII (Facial Nerve)

Origin and Central Course of Brachial Component of Facial Nerve

The branchial motor component originates from the motor nucleus of CN VII in the caudal pons. Fibers leaving the motor nucleus of CN VII initially travel medially and dorsally to loop around the ipsilateral abducens nucleus (CN VI) producing a slight bulge in the floor of the fourth ventricle - the facial colliculus.

Fibers then course so as to exit the ventrolateral aspect of the brainstem at the caudal border of the pons in conjunction with the nervus intermedius components of CN VII.

Intracranial course

Upon emerging from the ventrolateral aspect of the caudal border of the pons, all of the components of CN VII enter the internal auditory meatus along with the fibers of CN VIII (vestibulocochlear nerve). The fibers of CN VII pass through the facial canal in the petrous portion of the temporal bone. The course of the fibers is along the roof of the vestibule of the inner ear, just posterior to the cochlea.

At the geniculate ganglion the various components of the facial nerve take different.

Figure: Showing branches of facial nerve proximal to geniculate ganglion

Fibers of the branchial motor component pass through the geniculate ganglion without synapsing, turn 90 degrees posteriorly and laterally before curving inferiorly just medial to the middle ear to exit the skull through the stylomastoid foramen. The nerve to the stapedius muscle is given off from the facial nerve in its course through the petrous portion of the temporal bone.

Extracranial Course and Final Innervation

The posterior auricular nerve, nerve to the posterior belly of the digastric and the nerve to the stylohyoid muscle are given off upon the facial nerve's exit from the stylomastoid foramen. The remaining fibers enter the substance of the parotid gland and divide to form the temporal, zygomatic, buccal, mandibular, and cervical branches to innervate the muscles of facial expression.

Voluntary Control of the Muscles of Facial Expression

Signals for voluntary movement of the facial muscles originate in the motor cortex (in association with other cortical areas) and pass via the corticobulbar tract in the posterior limb of the internal capsule to the motor nuclei of CN VII.

Fibers pass to both the ipsilateral and contralateral motor nuclei of CN VII in the caudal pons .The portion of the nucleus that innervates the muscles of the forehead receives corticobulbar fibers from both the contralateral and ipsilateral motor cortex. The portion of the nucleus that innervates the lower muscles of facial expression receives corticobulbar fibers from only the contralateral motor cortex. This is very important clinically as central (upper motor neuron) and peripheral (lower motor neuron) lesions will present differently.

Facial Nerve Palsy

Etiology and Diagnosis

v     Many conditions can produce isolated facial nerve palsy identical to Bell's palsy

v     Patients with Bell's palsy usually progress from onset of symptoms to maximal weakness within three days and almost always within one week

v     Classically, Bell's palsy has been defined as idiopathic

v      infection with herpes simplex virus type 1 (HSV-1) is a possible cause because research has found elevated HSV-1 titers in affected patients

Differential Diagnosis for Facial Nerve Palsy

DISEASE	CAUSE	DISTINGUISHING FACTOR
NUCLEAR(PERIPHERAL)
LYME DISEASE	Spirochete Borrelia burgdorferi	History of tick exposure, rash, or arthralgias; exposure to areas where Lyme disease is endemic
OTITIS MEDIA	Bacterial pathogens	Gradual onset; ear pain, fever, and conductive hearing loss
RAMSY HUNT SDYNDROME	Herpes zoster virus	Pronounced prodrome of pain; vesicular eruption in ear canal or pharynx
SARCOIDOSIS OR GUILLAIN-BARRÉ SYNDROME	Autoimmune response	More often bilateral
TUMOR	Cholesteatoma, parotid gland	Gradual onset
SUPRANUCLEAR(CENTRAL)
MULTIPLE SCLEROSIS	Demyelination	Additional neurologic symptoms
STROKE	Ischemia,hemorrhage	Extremities on unaffected side often involve
TUMOR	Metastases, primary brain	Gradual onset; mental status Changes; history of cancer

Evaluation

Ø      A patient with an acute onset of unilateral facial weakness most likely has Bell's palsy

Ø       gradual onset of more than two weeks' duration is strongly suggestive of a mass lesion

Ø      Medical history should include recent rashes, arthralgias, or fevers; history of peripheral nerve palsy; exposure to influenza vaccine or new medications; and exposure to ticks or areas where Lyme disease is endemic

Ø       physical examination should include careful inspection of the ear canal, tympanic membrane, and oropharynx, evaluation of peripheral nerve function in the extremities and palpation of the parotid gland.

Two types of Lesion and their Differnces

Upper Motor Neuron Lesion (UMN)

Results from damage to neuronal cell bodies in the cortex or their axons that project via the corticobulbar tract through the posterior limb of the internal capsule to the motor nucleus of CN VII. With an UMN lesion, voluntary control of only the lower muscles of facial expression on the side contralateral to the lesion will be lost. Voluntary control of muscles of the forehead will be spared due to the bilateral innervation of the portion of the motor nucleus of CN VII that innervates the upper muscles of facial expression. UMN lesions are usually the result of a stroke.

Lower Motor Neuron (LMN) Lesion

Results from damage to the motor nucleus of CN VII or its axons. A LMN lesion results in the paralysis of all muscles of facial expression (including those of the forehead) ipsilateral to the lesion.

Clinical Correlation - Bell's Palsy

A Lower Motor Neuron lesion of CN VII which occurs at or beyond the stylomastoid foramen is commonly referred to as a Bell's Palsy. Characteristic indications of a LMN lesion or Bell's Palsy include the following, on the affected side:

· Marked facial asymmetry

· Atrophy of facial muscles

· Eyebrow droop

· Smoothing out of forehead and nasolabial folds

· Drooping of the mouth corner

· Uncontrolled tearing

· Loss of efferent limb of conjunctival reflex (cannot close eye)

· Lips cannot be held tightly together or pursed

· Diificulty keeping food in mouth while chewing on the affected side

Ø      A Lower Motor Neuron lesion of CN VII in conjunction with deficits associated with CN VI (abducens nerve) indicates a lesion in the brainstem which affects both the motor nucleus of CN VII and the abducens nucleus.

Ø       A Lower Motor Neuron lesion of CN VII in conjunction with deficits associated with CN VIII (vestibulocochlear nerve) are characteristic of a lesion in the region of the internal acoustic meatus. An example of this type of lesion is an acoustic neuroma.

Figure: Diagram showing Differences in Innervation and Lesions in Upper motor

Neuron and Lower Motor Neuron Lesion

Peripheral Lesions of Facial Nerve

Ø       Paralysis of all the muscles of facial expression ipsilateral to the lesion (LMN lesion of the branchial motor component of CN VII).

Ø      Loss of secretion from lacrimal gland and mucous membranes of nasal and oral pharynx ipsilateral to the lesion (lesion of the greater petrosal nerve, visceral motor component of CN VII).

Ø       Loss of secretion from submandibular and sublingual glands ipsilateral to the lesion (lesion of the chorda tympani, visceral motor component of CN VII).

Ø       Loss of taste from anterior 2/3 of tongue ipsilateral to the lesion (lesion of the chorda tympani, special sensory component of CN VII).

Ø       Loss of general sensation from concha of external ear and small area of skin behind the ear (general sensory component of CN VII).

Ø       Deficits in hearing and/or vestibular functions ipsilateral to the lesion  (associated with CN VIII).

Ø       Intact general sensation to the tongue (supplied by CN V3).

Examination

Ø      Upon noticing facial asymmetry, proceed to tests VII nerve functions

·         Look up (frontalis) and attempt to push the folds down, close your eyes (orbicularis oculi) and attempt to force them open, and frown (corrugator superficialis)

·         Look for exposure keratitis, tarsorraphy

·         Nasolabial fold, show your teeth and and blow against closed lips

·         Look for drooling of saliva

Ø      Determine UMN or LMN, unilateral or bilateral

Ø      UMN unilateral

·         Examine UL and look for hemiparesis on the same side of the facial weakness

·         Check for xanthelesma, DM signs and BP

Ø      LMN unilateral

·         Examine other CN

·         VI nerve and contralateral weakness in brainstem lesions

·         CPA lesion (V, VI, VII and VIII with cerebellar)

·         Other CN nerves involvement non-conforming type

·         Basal meningitis lesions

·         Mononeuritis multiplex, MG

·         Therefore proceed to examine the neck

Ø      Look at the Palate for vesicles

Ø      Examine the parotids and for surgical scars

Ø      Mastoid tenderness

Ø      Examine the neck for cervical LNs

Ø      Upper limbs

·         Contralateral hemiparesis

·         Ipsilateral cerebellar

Ø      Ask to examine

·         Otoscopy for vesicles in EC and otitis media

·         For hyperacusis (sensitive to high-pitched or loud sounds)

·         For loss of taste in the anterior two-thirds of the tongue

·         Urine dipstick for glucose and BP

Ø      Upon noticing facial diplegia, proceed with

Ø      Rule out MG (Bilateral ptosis)

Ø      Rule out Dystrophia myotonica or fascio-scapular-humeral dystrophy

Ø      Bilateral LMN VII

·         Test for frontalis, corrugator and orbicularis oculi

·         Ask patient to show teeth and blow against closed lips

·         Look for V, VI, VIII

·         Examine parotids (Sarcoidosis, amyloidosis)

·         Examine tongue (scrotal tongue for MR syndrome)

·         Examine the upper limbs for GBS, MND, leprosy, Lyme’s (radiculopathy) and bilateral cerebellar signs if suggestive of bilateral CPA tumors

·         Think of rare: Melkersson-Rosenthal syndrome, Mobius syndrome

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TIN KOSONG ....

recently i was posted to a well established hospital ....other college students n the ''so called'' clever studnts frm well established institutions was also posted there....they look down on my college...n of course on us n our lecturers...put that apart...even when a pt  came v r not given a chance to treat....priority is only given to the so called ''CLEVER'' students even when they no ''nothing'' .... they cant even assess a patient completely...dont know even the basic things...parasthesia??? dermatomes?? myotomes?? ask them anything...they will b blinking their eyes n scratching they heads while looking at us for answers....when asked whats the difference between SWD & HOT PACK?? they can say ''one uses electric n the other doesnt''....such a lame answer which a primary school children can answer....dont need to spend 4 years studying bachelors to know this....''gait analysis''....when asked to analyse gait....the girl just look at the patients hip and say ''his hip flexion is limited'' ...thats all.... but the very basic things...'' the stance and swing phase'' is altered....but they never bother it at all....then range of motion assessment......as far as i studied v use goniometer to assess the range of motion of a particular movement...but here they will ask the patient
therapist : ''mmm sir how much u think ur knee flexion??''
 patient answers..'' fexion?? whats that??
therapist ans: flexion means how much u can bend ur knee....
 patient : o i think around 80 to 90 degrees...hmmmm....
next muscle power : as far as i studied v assess muscle power for each n every muscle...but there they will write ''knee= 4'' but no one knows whether it for hams o quads....hmmmmm....v found ourselves much more better....but still they will say 'm' college student is weak...n bad!!!!