Head & Neck ModuleSmall Group Discussion for the Ear and Temporal Bone

Student Guide The temporal bone is an extremely important part of the body, not only because it contains vital sensory organs and helps protect the brain, but also because it is traversed by vascular structures that supply key areas of the central nervous system and by neural structures that provide important cranial nerve functions. This session will illustrate the myriad problems that may occur when the temporal bone is affected by pathology.

Learning Objectives: At the end of this session, the learner must be able to:1) Describe the signs and symptoms of a temporal bone fracture2) Explain the anatomical basis for injuries that may occur in a temporal bone fracture3) Explain the physiological basis for the hearing loss and the findings on clinical testing of hearing4) Explain the physiological basis for the vertigo and the findings on clinical testing of the vestibular balance system5) Discuss the treatment options for the different injuries that may occur in a temporal bone fracture6) Discuss the societal issues (general safety, economic, etc.) that may be involved in the proliferation of motorcycles as a form of transportation in Metro Manila Case History: A 35-year old male motorcyclist suffered a left-sided temporal bone fracture when he was thrown from his motorcycle after it collided with a taxicab. He was immediately transported to the emergency room of The Medical City, where he was examined by the ER physicians and the otolaryngology resident-on-call. Although the man was conscious and communicable, he complained of severe dizziness described as a whirling sensation, and preferred to lie still with his eyes closed. Clinical examination revealed the following findings:1) Bilaterally intact tympanic membranes with evidence of slightly reddish middle ear fluid in the left ear2) Dripping of clear fluid from the left nostril when the patient leans forward3) Weber test : lateralizes to the right ear4) Rinne test : AC>BC in right ear, AC<BC in the left ear5) A hematoma in the left post-auricular and mastoid area6) Spontaneous right-beating nystagmus (fast component to the right)7) A total loss of voluntary movement of the muscles of facial expression on the left Guide Questions: 1) What are the signs and symptoms of a temporal bone fracture? (Balazo Bugayong) Symptoms of a skull fracture may include:● Headache

● Scalp swelling● Scalp tenderness

○ Bone tenderness● Scalp contusion● Skin wound to the scalp:

○ Scalp abrasion○ Scalp laceration○ Scalp puncture wound

● Deformed skull:○ A depressed area, or indentation, in the skull

A fracture to the base of the brain, called a basilar skull fracture, may cause additional symptoms. Additional symptoms of a basilar skull fracture include:● Loss of hearing● Tinnitus:

○ Ringing in the ears● Blood behind the eardrum● Bruising behind the ear (Battle sign) ● Ear discharge:

○ Clear or bloody fluid leaking from the ear● Bruising around both eyes ● Runny nose:

○ Clear fluid leaking from the nose A skull fracture may occur with an injury to the brain. Symptoms of a minor brain injury include:● Dizziness● Poor balance● Headache● Nausea● Excessive sleepiness● Fatigue Symptoms of a serious brain injury include:● Severe headache● Repeated vomiting● Amnesia:

○ An inability to remember events prior to or just after the injury● Bruising around the eyes:

○ Black eyes on both sides ● Confusion● Lethargy:

○ Excessive sleepiness or drowsiness● Loss of consciousness● Numbness in one arm or leg:

○ Arm numbness (unilateral)○ Hand numbness (unilateral)

○ Leg numbness (unilateral)○ Arm and leg numbness (unilateral)

● Weakness in one arm or leg:○ Arm weakness (unilateral)○ Hand weakness (unilateral)○ Leg weakness (unilateral)○ Arm and leg weakness (unilateral)

● Vision impairment:○ Double vision

● Neck pain● Difficulty walking● Difficulty speaking● Seizures● Coma Nice to Know : (eto nalang add ko. -Raine)The head is the most frequently injured part of the body. Head injuries occur in approximately 75% of all motor vehicle accidents. Approximately 30% of head trauma cases result in skull fracture. The ear is the most frequently damaged sense organ. Temporal bone injuries reportedly occur in 14-22% of all skull fractures. Motor vehicle accidents are the cause of 31% of temporal bone fractures. Other causes, in descending order of frequency, are physical assaults, falls, motorcycle accidents, pedestrian injuries, bicycle accidents, and gunshot wounds. Men aged 21-30 years comprise the most commonly involved group. The predisposition in males is based on an increased number of males involved in high-risk activities compared with females, Types of Temporal bone fractureA. LongitudinalThe fracture line parallels the long axis of the petrous pyramid. It starts in the pars squamosa (mastoid or external auditory canal; as seen in the image below), extends through the posterosuperior bony external canal, continues across the roof of the middle ear space anterior to the labyrinth, and ends anteromedially in the middle cranial fossa in close proximity to the foramen lacerum and ovale. Signs and symptoms include bleeding into the ear canal from skin and tympanic membrane laceration, hemotympanum, external auditory canal fractures, ossicular chain disruption that produces conductive hearing loss, and facial nerve paralysis. Twenty percent of longitudinal fractures injure the facial nerve and cause paralysis. The injury site is usually the horizontal segment of the nerve distal to the geniculate ganglion. CSF otorhinorrhea is common but usually temporary. Sensorineural hearing loss may occur as a result of concussive damage. Vertigo occurs but is not related to the severity of the fracture. B. Transverse FractureThey are usually caused by a frontal or parietal blow but may result from an occipital blow. The fracture line runs at a right angle to the long axis of the petrous pyramid and starts in the middle cranial fossa (close to the foramen lacerum and spinosum). It then crosses the petrous pyramid

transversely and ends at the foramen magnum. It may also extend through the internal auditory canal and injure the nerves directly. Cochlear and vestibular structures are usually destroyed, producing a profound sensorineural hearing loss and severe ablative vertigo. The intensity of the vertigo will decrease after 7-10 days and then continues to decrease steadily over the following 1-2 months, leaving only an unsteady feeling that lasts approximately 3-6 months, until compensation finally occurs. Intense nystagmus (third degree) is present since the initial fracture, with the fast component beating away from the fracture site. The nystagmus is easily seen by the naked eye. Nystagmus also decreases progressively in intensity (third degree, second degree, first degree) and then finally disappears. Rarely, a mixed hearing loss may occur. Facial nerve injury occurs in 50% of transverse fractures. The injury site is anywhere from the internal auditory canal to the horizontal segment distal to the geniculate ganglion. I guess ours is a transverse fracture. Kasi first, hindi perforated ang tympanic membrane. Second, severe ung vertigo and ung hemotympanum not associated with otorrhagia. Refer to the table below. Feature Longitudinal Fractures Transverse Fractures

Incidence Approximately 80% Approximately 20%

Mechanism Temporal or parietal trauma Frontal or occipital trauma

CSF otorrhea Common Occasional

Tympanic membrane perforation

Common Rare

Facial nerve damage

20% (most often temporary and frequently delayed in onset)

50% (severe, usually permanent, and immediate in onset)

Hearing loss Common (conductive type and possibly high tone neurosensorial secondary to concomitant inner ear concussion)

Common (severe sensorineural or mixed)

Hemotympanum

Common (associated with otorrhagia)

Possible (not associated with otorrhagia)

Nystagmus Common (usually spontaneous, usually less intense [first or second degree] or positional; nystagmus absence also possible)

Common (intense [third degree], spontaneous, fast component beating to the opposite ear, long lasting; positional nystagmus also possible before and after compensation period)

Otorrhagia Common Rare

Vertigo Common (less intense, and/or positional; absence is also possible)

Common (intense, usually associated in the acute phase with nausea and possibly vomiting)

2) Explain the pathophysiology of the clear fluid from the nose when the patient leans forward. How is the type of fluid determined clinically? (Haw Liechtenstein) Pathophysiology Cerebrospinal fluid (CSF) Leaks

● 2 kinds: rhinorrhea (nose) or otorrhea (ears)● seen as middle ear effusion, hearing loss, or unilateral rhinorrhea secondary to

Eustachian tube drainage. ● The diagnosis must be either confirmed or excluded as the risk of meningitis is high, with

reported rates varying between 2-88%. The clinician must be aware of the diagnostic and treatment options available in order to best manage such patients.

● most common cause: blunt trauma● implies an abnormal communication between the subarachnoid space and the nasal

cavity or tympanomastoid space. ● immediate leak: a dural tear and a bony defect or fracture has occurred.● delayed traumatic leak:

○ a previously intact dural layer that has slowly become herniated through a bony defect, finally tearing the dura and causing the leak.

○ the tear and bony defect are present from the time of the original injury, but the leak occurs only after the masking hematoma dissolves.

Temporal bone CSF leak

● indication of an abnormal communication or series of communications between the subarachnoid space and the temporal bone

● may be either acquired or congenital○ Acquired - most common: trauma (temporal bone fractures), postoperative

(delayed or immediate), temporal bone infections, and benign or malignant neoplasms (abnormal mass of tissues).

● most common cause of CSF otorrhea: fractures of the temporal bone. ○ Blunt trauma produce fractures in the temporal bone with tearing of dura and

foramina causing acute leakage. ● Fractures may also produce defects in the bony tegmen plate, predisposing one to

encephaloceles or meningoceles with resultant delayed CSF leakage. Temporal bone fractures have been traditionally divided into transverse or longitudinal, based on the relationship of the fracture line to the otic capsule and axis of the petrous ridge. In reality, however, most fractures are actually oblique in nature. An important factor in temporal bone fracture classification is whether the fracture passes through the otic capsule. Tympanic membrane or EAC lacerations are frequently seen in longitudinal

fractures which allows for the egress of CSF from the ear. However, with transverse fractures, the tympanic membrane is typically intact and the fluid may build within the middle ear and mastoid and eventually drain though the eustachian tube producing CSF rhinorrhea. CSF otorrhea in temporal bone fractures usually occurs within minutes of the accident but may be delayed in its presentation if it is draining through the nasopharynx. After trauma, CSF otorrhea is typically serosanginous and can be mistaken for blood byproducts.

Determining type of fluid Confirm or exclude the presence of CSF in leaking fluid by means of an immunoelectrophoretic study of the fluid for beta-2 transferrin (B2Tr) or, where available, beta-trace protein. For this specialized laboratory study, 0.5-1.0 mL of the fluid may be required. An absorptive sponge pad placed at or near the presumed site of fluid leak can facilitate the collection of the fluid. Perform high-resolution, thin-section axial and coronal cranial and facial computed tomography (CT) scanning. Include all of the paranasal sinuses and petrous temporal bones in the scans.Perform magnetic resonance (MR) cisternography. This study may also be useful for detecting inactive fistulas. CT cisternography or radionuclide cisternography may be useful if CT and MR cisternography do not show the CSF fistula. Radionuclide cisternography may be useful to detect an intermittently active CSF fistula. Cisternography with an intrathecal injection of radioisotope or nonionic iodinated myelographic contrast medium or noninvasive magnetic resonance imaging (MRI) cisternography usually localizes the CSF leak. Brain and spinal MRI is useful in demonstrating meningocele and meningoencephalocele when associated with CSF leak, as well as for examining patients with spontaneous intracranial hypotension syndrome. On occasion, the methods listed above do not help in localizing the CSF fistula, and surgical exploration is necessary. Fluid leaking from the nose or external auditory canal must first be positively identified as CSF. Drops of fluid from a CSF leak placed on absorbent filter paper may result in the double-ring sign, which is a central circle of blood and an outer clear ring of CSF. Results of glucose, chloride, and total protein tests of the fluid are not specific or conclusive for CSF. All methods of cisternography—radionuclide, CT, and MR—provide improved or optimal CSF fistula detection when the fistula is active and when a Valsalva maneuver or jugular venous compression is added to the imaging protocol. CSF fistula can usually be demonstrated by using some method of cisternography, but localization of the leak to the right or left nasal cavity may be difficult because of the tendency of the fluid to cross sides and flow from both nostrils. In a study of 4 patients who underwent radionuclide cisternography (RNC), as well as MRI and/or CT, for suspected CSF leaks, Thomas et al found that RNC accurately detected and localized the leaks in all patients. Each patient subsequently underwent a procedure for an epidural blood patch, and all patients experienced symptomatic relief.

Methods for detecting CSF fistulas with intrathecal injections of dye pose a risk of chemical meningitis. Methylene blue, indigo carmine, and phenolsulfonphthalein (PSP) dyes are no longer in use. Some otolaryngologists use a dilute solution of fluorescein to localize CSF fistulas both preoperatively and during surgery. Typically, 0.5 mL of a 10% fluorescein solution is injected into the lumbar subarachnoid space over more than 1 minute. Cotton pledgets are placed in the nose, as for radionuclide cisternography. The dye reaches the skull base in 6 hours and is present over the cerebral convexities in 24 hours. The pledgets are examined for green fluorescence in a dark room with ultraviolet light 6 hours after the intrathecal PSP injection.

Limitation of techniquesSkull radiographs are of limited diagnostic use in cerebrospinal fluid (CSF) leaks, but they may show a skull fracture or suggest the presence of empty sella.Computer-reconstructed coronal images are less accurate and are acceptable only until direct coronal images can be obtained. ---- ● Glucose determination

○ A rapid but highly unreliable test is glucose-content determination with the use of glucose oxidase paper. This method of detecting CSF rhinorrhea is not recommended as a screening or confirming lab test to detect the presence of CSF in the nasal cavity for the following reasons:

■ Reducing substances present in the lacrimal-gland secretions and nasal mucus may cause false-positive results.

■ Glucose, at a concentration of 5 mg/dL, can lead to a positive result with this test.○ Active meningitis can lower the glucose level in the CSF and may lead to false-negative

readings.○ This test is not specific for the side or site of leak.

● Beta-trace protein○ Also known as prostaglandin D synthase, this protein is synthesized primarily in

arachnoid cells, oligodendrocytes, and the choroids plexus within the CNS.○ Beta-trace protein is also present in the human testes, heart, and serum, making it not

specific for CSF.○ It is altered by the presence of renal failure, multiple sclerosis, cerebral infarction, and

certain CNS tumors.○ This test has been used to diagnose CSF rhinorrhea in multiple studies, with a sensitivity

of 92% and specificity of 100%.○ This test is not specific for side or site of leak and can be difficult to collect if the leak is

intermittent.● Beta-2 transferrin

○ Beta2-transferrin is produced by neuraminidase activity within the central nervous system; therefore, B-2 transferrin is located only within the CSF, perilymph, and aqueous humor.

○ The assay has a high sensitivity and specificity, it is performed rapidly, and it is noninvasive.

○ A minimum of 0.5 mL of fluid is necessary for electrophoresis, but difficulties in collection of this fluid have been noted, especially in intermittent, low-volume leaks.

○ Beta-2 transferrin is stable at room temperature for approximately 4 hours; therefore, immediate refrigeration following collection is recommended as the protein will remain stable for up to 3 days. Specimens should not be frozen.

○ Not specific for side or site of leak; can be difficult to collect if leak is intermittent in nature.

○ This is currently the recommended single lab test for identifying the presence of CSF in sinonasal fluid.

Sources:http://emedicine.medscape.com/article/338989-overviewhttp://www.utmb.edu/otoref/grnds/CSF-leaks-050112/CSF-leaks-050112.htmhttp://emedicine.medscape.com/article/857365-workup 3) Why does hearing loss occur? What explains the findings on tuning fork testing? (Manalastas Palmares) REASONS WHY HEARING LOSS OCCUR:I. Problems in the External Ear:1. Blockage in the external canal - usually earwax or cerumen2. Infections with swelling that may shut the ear canal3. Foreign body4. Birth defects5. Growth in the ear canalII. Problems in the Middle Ear:1. Middle ear infections causing swelling in the lining of the middle ear and accumulation of pus. Fluid accumulates behind the ear drum and the ossicles - improper functioning of the structures = hearing loss2. Chronis otits media with effusion or Glue ear - fluid not caused by infection accumulates commonly in children, and sometimes in adults. The condition is known as glue ear, or chronic otitis media with effusion (OME). It sometimes requires drainage through a myringotomy or with the placement of ear tubes. This ordinarily eliminates the hearing loss almost instantly.Fluid in the ear usually is due to malfunction of the eustachian tube, which connects the ear with the back of the throat. The job of the eustachian tube is to keep the pressure in the middle ear approximately the same as that in the ear canal and outside world.

● The eustachian tube does this by opening momentarily when we swallow or yawn.● If it fails to open because of swelling, allergy, or other reasons, the air already in the

middle ear becomes trapped.● Gradually, this air is absorbed into the bloodstream. The middle ear space is bony

except for the eardrum. As absorption occurs and less and less air is present, its disappearance creates a vacuum (negative pressure), which sucks the eardrum toward the middle ear (retracted ear drum).

● When the negative pressure is great enough, it causes fluid to seep out of the blood vessels that line the middle ear. This is the fluid that constitutes glue ear.

The presence of fluid causes hearing loss, and sometimes frequently recurring ear infections. In some cases, the eustachian tube starts to work again spontaneously and the condition resolves. In others, decongestants may be helpful. When allergy is the cause, allergy treatments may improve the problem.

When the condition causes frequent middle ear infections (acute otitis media) some physicians recommend the long-term use of antibiotics, although this treatment is currently controversial. 3. Otosclerosis - hereditary disease in which new bone is deposited around one of the tiny bones in the middle ear, specifically around the footplate of the stapes (or 'stirrup') bone. This prevents normal bone transmission of sound from the eardrum to the inner ear, and consequently, conductive hearing loss results.This type of hearing loss can be cured by a surgical procedure called stapedectomy, in which the stapes bone is replaced by an artificial bone. This procedure usually only takes 30 or 40 minutes, and it is performed under local anesthesia (in which the person is awake). In many cases, hearing can return to normal after surgery.4. Birth defectsVarious birth defects may also involve the middle ear and cause hearing loss. Some are major and cause obvious external defects. Many involve only the inner ear structures. In any case, most conductive hearing loss, in which sound waves are not transmitted effectively to the inner ear, is surgically treatable. 5. Tumors of the middle ear may be responsible for hearing loss. They may be cancerous (malignant) or noncancerous (benign).

● Examples of cancerous tumors are rhabdomyosarcoma, a very rare muscle tumor, in children or squamous cell carcinoma in adults.

● Examples of noncancerous tumors are glomus tumors (which also cause pulsating ear noises) or neuromas of the facial nerve.Cholesteatoma is a common noncancerous skin cyst that grows slowly and dissolves adjacent bone as it grows. It is a fairly common problem, especially in people who have had repeated ear infections; but it may also occur from birth. It generally requires surgery to remove the cyst.

Problems in the Inner Ear1. Otosclerosis (the hereditary disease in which bone deposits collect around the small bone in the middle ear known as the stirrup) can also affect the cochlea (the coiled tube in the inner ear), and cause hearing loss in some people.2. Presbycusis - natural aging process also causes sensorineural hearing loss, in which the damage lies in the inner ear, the hearing nerve, or both. Beginning shortly after birth, we begin to lose hair cells and nerve endings within the cochlea (the region that hears very high frequencies). As this loss pattern progresses over a lifetime, sensorineural hearing loss develops.There also are other age-related causes of hearing loss, including stiffening of portions of the cochlea and loss of nerve endings in the acoustic nerve.3. Fistula - (opening) is an abnormal connection between the inner ear and middle ear. The inner ear is filled with fluid, and the middle ear is filled with air. If a fluid leak occurs from the inner ear, hearing loss and dizziness commonly result. This kind of hearing loss often is cured by surgically repairing the fistula. Such leaks are usually caused by trauma. The trauma may be direct, such as a blow to the ear or a head injury in a car accident. However, it may also be the

result of air pressure changes in an airplane trip, a forceful sneeze, or lifting a heavy object.4. Head injury - Direct head trauma, particularly trauma severe enough to cause unconsciousness, can cause inner ear concussions and hearing loss.5. Meniere's syndrome - a condition characterized by fluctuating hearing loss (usually more prominent in the lower frequencies where we hear speech), dizziness, fluctuating ear pressure, and tinnitus (a noise sensation heard in one or both ears). It is due to a swelling and fluid overload of the middle compartment of the inner ear (a condition known as endolymphatic hydrops).There are many treatable causes of Meniere's syndrome. When all tests have revealed none of the known causes, the condition is classified as Meniere's disease.6. Noise - important cause of hearing loss. An estimated 7 to 10 million people in American industry have noise-induced hearing loss, virtually all of which was preventable. In addition to industrial noise, recreational noise can damage hearing. Such noise is encountered commonly from gunfire, power tools, snow blowers, motorcycles, loud music (especially with earphones) and other causes.In some cases, the playing of musical instruments can damage hearing. This has been reported not only with loud, electrical rock and roll instruments, but also with classical music performance such as violin playing and flute playing. One can minimize such problems by using ear protection whenever practical, such as during selected practice sessions. 7..Infections involving the inner ear and hearing nerve can also produce deafness. Middle ear infections can spread to the inner ear, causing loss of hearing and, usually, dizziness. Infections may also involve the hair cells or acoustic nerve, causing hearing loss and even sudden total deafness. 8. Sudden deafness may be caused by a variety of problems. Treatment is controversial, but there is some evidence to suggest that aggressive treatment may improve the chances for hearing recovery even after a sudden profound loss. Once the condition has been present for more than two or three weeks, even the most aggressive treatments generally do not work. 10. Neural (nerve-related) problems may also produce hearing loss. Among the more common are:

● Acoustic neuroma, a common tumor of the acoustic nerve● Multiple sclerosis● Autoimmune sensorineural hearing loss, in which the body attacks its own ear● Ototoxicity, which is hearing loss caused by a substance that gets into the body; most

often the substance is a medication, particularly certain antibiotics, but other toxins (such as lead) may also cause hearing loss

Tuning Fork

1. Indication: Differentiate Hearing Loss causea. Sensorineural Hearing Lossb. Conductive Hearing Loss

2. Preparationa. Tuning fork should be 512 Hz (preferred) to 1024 Hz

3. Test: Webera. Technique: Tuning Fork placed at midline foreheadb. Normal: Sound radiates to both ears equallyc. Abnormal: Sound lateralizes to one ear

i. Ipsilateral Conductive Hearing Loss ORii. Contralateral Sensorineural Hearing Loss

PerformanceIn the Weber test a vibrating tuning fork (either 256 or 512 Hz) is placed in the middle of

the forehead, chin, or head equidistant from the patient's ears. The patient is asked to report in which ear the sound is heard louder.

In a normal patient, the sound is heard equally loud in both ears (no lateralization). However, a patient with symmetrical hearing loss will hear the sound equally as well. Thus, there is diagnostic utility only in asymmetric hearing losses.

In an abnormal patient, the sound is heard louder in one ear (lateralization). This should be confirmed by repeating the procedure and having the patient occlude one ear with a finger; the sound should be heard best in the occluded ear.Detection of conductive hearing loss

A patient with a unilateral conductive hearing loss would hear the tuning fork loudest in the affected ear. This is because the conduction problem masks the ambient noise of the room, whilst the well-functioning inner ear picks the sound up via the bones of the skull causing it to be perceived as a louder sound than in the unaffected ear. Another theory, however, is based on the occlusion effect described by Tonndorf et al. in 1966. Lower frequency sounds (as made by the 512Hz fork) that are transferred through the bone to the ear canal escapes from the canal. If an occlusion is present, the sound cannot escape and appears louder on the ear with the conductive hearing loss

Conductive hearing loss can be mimicked by plugging one ear with a finger and performing the Rinne and Weber tests, which will help clarify the above. The simulation of the Weber test is the basis for the Bing test.Detection of sensorineural hearing loss

A patient with a unilateral sensorineural hearing loss would hear the sound louder in the unaffected ear, because the affected ear is less effective at picking up sound even if it is transmitted directly by conduction into the inner ear.Incompleteness

This test is most useful in individuals with hearing that is different between the two ears. It cannot confirm normal hearing because it does not measure sound sensitivity in a quantitative manner. Hearing defects affecting both ears equally, as in Presbycusis will produce an apparently normal test result.1. Test: Rinne

a. Techniquei. First: Bone Conduction

1. Vibrating Tuning Fork held on Mastoid2. Patient covers opposite ear with hand3. Patient signals when sound ceases4. Move the vibrating tuning fork over the ear canal

a. Near, but not touching the earii. Next: Air Conduction

1. Patient indicates when the sound ceasesb. Normal: Air Conduction is better than Bone Conduction

i. Air conduction usually persists twice as long as boneii. Referred to as "positive test"

c. Abnormal: Bone conduction better than air conduction

i. Suggests Conductive Hearing Lossii. Referred to as "negative test"

ProcedureThe Rinne test is performed by placing a vibrating tuning fork (512 or 256 Hz) against

the patient's mastoid bone and ask the patient to tell you when the sound is no longer heard. Time this interval of bone conduction with a watch, noting the number of seconds. Quickly position the still vibrating tines 1-2 cm from the auditory canal, and again ask the patient to tell you when the sound is no longer heard. Continue timing the interval of sound due to air conduction heard by the patient. Compare the number of seconds sound is heard by bone conduction versus air conduction; air conducted sound should be heard twice as long as bone conducted sound (e.g., if bone-conducted sound is heard for 15 seconds, air-conducted sound should be heard for 30 seconds).Air VS Bone conduction hearing loss

Air conduction uses the apparatus of the ear (pinna, eardrum and ossicles) to amplify and direct the sound whereas bone conduction bypasses some or all of these and allows the sound to be transmitted directly to the inner ear albeit at a reduced volume, or via the bones of the skull to the opposite ear.

Description Relative Positive/Negative

In a normal ear, air conduction (AC) is better than bone conduction (BC)

AC > BC this is called a positive Rinne

In conductive hearing loss, bone conduction is better than air

AC < BC negative Rinne

In sensorineural hearing loss, bone conduction and air conduction are both equally depreciated, maintaining the relative difference of bone and air conductions

AC > BC positive Rinne

In sensorineural hearing loss patients there may be a false negative Rinne

AC < BC negative Rinne

Note that the words positive and negative are used in a somewhat confusing fashion

here, other than their normal use in medical tests. Positive or negative means that a certain parameter that was evaluated was present or not. In this case, that parameter is if air conduction (AC) is better than bone conduction (BC). Thus, a "positive" result indicates the healthy state, in contrast to many other medical tests. Therefore, if presenting your findings to a physician, to avoid confusing yourself, it may be wise to avoid using the term 'positive' or 'negative', and simply state if the test was normal or abnormal e.g. 'Rinnes test was abnormal in the right ear, with bone conduction greater than air conduction'.Hazards

This test and its complement, the Weber test, are quick screening tests and are no replacement for formal audiometry. Recently, its value as a screening test has been questionedIn relation to Weber’s test

The Rinne test is used in cases of unilateral hearing loss and establishes which ear has the greater bone conduction. Combined with the patient's perceived hearing loss, it can be determined if the cause is sensorineural or conductive.

For example, if the Rinne test shows that air conduction (AC) is greater than bone conduction (BC) in both ears and the Weber test lateralizes to a particular ear, then there is sensorineural hearing loss in the opposite (weaker) ear. Conductive hearing loss is confirmed in the weaker ear if bone conduction is greater than air conduction and the Weber test lateralizes to that side. Combined hearing loss is likely if the Weber test lateralizes to the stronger ear and bone conduction is greater than air conduction in the weaker ear.

Weber w/o lateralization

Weber lateralizes to the left

Weber lateralizes to the right

Rinne both ears AC>BC

Normal Sensorineural loss in right

Sensorineural loss in left

Rinne left BC>AC Conductive loss in left Combined loss : conductive and sensorineural loss in left

Rinne right BC>AC Combined loss : conductive and sensorineural loss in right

Conductive loss in right

Rinne both ears BC>AC

Combined loss in right and conductive loss on left

Combined loss in left and conductive loss on right

In relation to the patient

1) Weber test : lateralizes to the right ear2) Rinne test : AC>BC in right ear, AC<BC in the left ear

Conclusion: Sound is perceived louder in the right ear suggesting that there could be something wrong in left ear. The right ear is also positive for Rinne’s test, meaning it is “normal” (air conduction is better than bone conduction). The left ear has a combined loss of conductive and sensorineural. 4) Why does the patient present with nystagmus? Why does it beat to the right? (Roldan Sabili)

Nystagmus may be defined as a periodic rhythmic ocular oscillation of the eyes. The oscillations may be sinusoidal and of approximately equal amplitude and velocity (pendular nystagmus) or, more commonly, with a slow initiating phase and a fast corrective phase (jerk nystagmus).[1]

Nystagmus may be unilateral or bilateral, but, when the nystagmus appears unilateral, it is more often asymmetric rather than truly unilateral. Nystagmus may be conjugate or disconjugate (dissociated). It may be horizontal, vertical, torsional (rotary), or any combination of these movements superimposed upon each other.

Nystagmus may be congenital or acquired. When acquired, it most often is caused by abnormalities of vestibular input. Congenital forms may be associated with afferent visual pathway abnormalities (sensory nystagmus).[2]

To understand the mechanisms by which nystagmus may occur, it is important to discuss the means by which the nervous system maintains position of the eyes. Foveal centration of an object of regard is necessary to obtain the highest level of visual acuity. Three mechanisms are involved in maintaining foveal centration of an object of interest: fixation, the vestibulo-ocular reflex, and the neural integrator.

Fixation in the primary position involves the visual system's ability to detect drift of a foveating image and signal an appropriate corrective eye movement to refoveate the image of regard. The vestibular system is intimately and complexly involved with the oculomotor system.

The vestibulo-ocular reflex is a complex system of neural interconnections that maintains foveation of an object during changes in head position. The proprioceptors of the vestibular system are the semicircular canals of the inner ear. Three semicircular canals are present on each side, anterior, posterior, and horizontal. The semicircular canals respond to changes in angular acceleration due to head rotation.

The third mechanism is the neural integrator. When the eye is turned in an extreme position in the orbit, the fascia and ligaments that suspend the eye exert an elastic force to return toward the primary position. To overcome this force, a tonic contraction of the extraocular muscles is required. A gaze-holding network called the neural integrator generates the signal. The cerebellum, ascending vestibular pathways, and oculomotor nuclei are important components of the neural integrator.

http://emedicine.medscape.com/article/1199177-overview#a0104 Acquired nystagmus may be caused by the following

● Brain tumor● Drug overdose or toxicity● Head trauma● Stroke

Horizontal nystagmusHorizontal nystagmus is a well-recognized finding in patients with a unilateral disease of the cerebral hemispheres, especially with large, posterior lesions. It often is of low amplitude. Such patients show a constant velocity drift of the eyes toward the intact hemisphere with fast saccade directed toward the side of the lesion.-- If the patient’s nystagmus beats to the right(right-beating nystagmus), then it is characterized by a rightward-moving quick phase. According to medscape, the quick movement is directed towards the side of the lesion so this indicates that the lesion is found on the right hemisphere. However this is a bit odd because according to the case, the injury was on the left side of the skull.-- Another type of Nystagmus that is possibly presented in the case if Vestibular Nystagmus

Vestibular nystagmusVestibular nystagmus may be central or peripheral. Important differentiating features between central and peripheral nystagmus include the following: peripheral nystagmus is unidirectional with the fast phase opposite the lesion; central nystagmus may be unidirectional or bidirectional; purely vertical or torsional nystagmus suggests a central location; central vestibular nystagmus is not dampened or inhibited by visual fixation; tinnitus or deafness often is present in peripheral vestibular nystagmus, but it usually is absent in central vestibular

nystagmus. According to Alexander's law, the nystagmus associated with peripheral lesions becomes more pronounced with gaze toward the side of the fast-beating component; with central nystagmus, the direction of the fast component is directed toward the side of gaze (eg, left-beating in left gaze, right-beating in right gaze, up-beating in upgaze).--In this type of nystagmus, the fast phase is directed opposite the lesion, this means that if the nystagmus is right-beating, the lesion is found on the left. Since the case presents trauma on the left side of the patient’s head, this type of nystagmus is a better match than horizontal nystagmus.

5) Why does the patient have weakness of the left facial musculature? (Sandoval)FACIAL NERVE INJURY

● Facial nerve injuries are more common after transverse fractures of the temporal bone. ○ About 50% of patients with transverse fractures have associated facial nerve paralysis,

whereas 20% of patients with longitudinal fractures have associated facial nerve paralysis.

○ The higher incidence of longitudinal (80%) versus transverse fractures (20%) makes facial nerve injuries after longitudinal fractures a more common occurrence.

○ The site of injury of the facial nerve in temporal bone fractures is in the perigeniculate region 82-93% of the time.

● In longitudinal fractures, the middle ear is almost always involved, although the otic capsule is

spared. ○ The most common site of facial nerve involvement is the horizontal segment of the

intratympanic portion. ○ The injury is usually caused by compression and ischemia, rather than disruption. ○ Multiple sites are involved in 20% of cases, usually in the mastoid portion. ○ Onset may be immediate or delayed and partial or complete.

● In transverse fractures, otic capsule injury is present.○ Facial nerve paralysis is usually immediate in onset and complete. ○ Frequently, the nerve is avulsed or severed by the comminuted bone fragments. ○ The usual location of injury is anywhere from the internal auditory meatus to the

horizontal segment distal to the geniculate ganglion. FACIAL NERVE PARALYSIS

● The eye cannot close and constantly weeps. ● The mouth dribbles, the speech is interfered with and mastication impaired. ● The delicate shades of continence are lost. ● Joy, happiness, sorrow, shock, surprise, all the emotions have for their common expression the

same blank stare. ● Speech, mastication, and expression of moods and emotions are based on the ability to move

facial musculature—be it voluntary or involuntary. Facial nerve injury can be complete or partial

● Generally, partial disruption of axonoplasmal flow reveals a greater chance of complete functional recovery.

● Loss of motor function can be observed immediately after facial nerve injury. ● Depending on the affected trunk and localization (proximal or distal), various patterns of motor

function loss can be seen and used for primary diagnosis of the lesion site. ● Significant muscle fiber decay has been demonstrated when denervation has been present for

more than 3 years.● Early changes at cellular level (approximately 1 wk after denervation) include chromatin changes

and increased mitochondria number, DNA, and satellite cells, thus reflecting the plastic state of denervated muscle.

● In addition to clinical and Histopathologic Findings, parasympathetic functions such as salivation, lacrimation, and taste sensation also may be impaired.

Reference: Kim, J. (2010). Facial Nerve Paralysis. Retrieved September 25, 2011 from http://emedicine.medscape.com/article/1290547-overview#a0104March, A. (2010). Temporal Bone Fractures: Treatment and Management. Retrieved September 26, 2011 from http://emedicine.medscape.com/article/857365-treatment#showallCONCLUSION

● Facial nerve supplies all the muscles of facial expression ○ Orbicularis occuli both the palpebral and orbital part○ Corrugator supercilii○ Compressor nasi○ Dilator naris○ Procerus○ Orbicularis oris

● Facial nerve also supplies the dilator muscles of the lips○ Levator labii superioris alaeque nasi○ Levator labii superioris○ Zygomaticus major○ Zygomaticus minor○ Levator anguli oris○ Risorius○ Depressor anguli oris○ Depressor labii inferioris○ Mentalis○ Buccinator○ Platysma

● DAMAGE TO THE LEFT FACIAL NERVE Reference: Snell, R. (2008). Clinical Anatomy By Regions. 8th ed. Lippincott Williams & Wilkins. 6) What are the general management options for the injuries suffered by the patient? (Sandoval)Common complications of temporal bone fractures include hearing loss, CSF fistula, facial nerve paralysis, external auditory canal stenosis, cholesteatoma formation, and vascular injuries.

Conductive hearing loss● Conductive hearing loss is frequently observed with longitudinal fractures and is caused

by hemotympanum, tympanic membrane perforation, or partial or complete ossicular chain disruption.

○ Ossicular chain dislocation is more common than ossicular chain fracture.○ Tympanic membrane perforations and hemotympanum usually resolve in 3-4 weeks.○ Axial and coronal HRCT scans are helpful for diagnosing ossicular chain dislocation.

● The most common ossicle involved in temporal bone trauma is the incus because it is less stable, having weak attachments to the malleus and stapes.

○ Furthermore, the malleus is anchored by the tensor tympani muscle and its tendon, and the stapes is anchored by the stapedius muscle and its tendon.

○ They contract during trauma and pull the incus medially. ○ This movement is accentuated by the trauma, causing medial dislocation of the incus.

The following chain abnormalities have been identified with temporal bone fractures:

● Incudostapedial joint separation: The incudostapedial joint is the most common site of traumatic separation. (82%)

● Incus dislocation (57%)● Fracture of the stapes crura (30%)● Fixation of the ossicles in the attic (25%)● Incudomalleolar joint separation

● Other lesions, such as delayed necrosis of the long process of the incus, dislocation of the stapes

footplate, and dislocation of the malleus are possible but are not commonly seen.○ Most nondisruptive conductive hearing losses resolve spontaneously. ○ If conductive hearing loss is present at greater than 30 dB after 2 months, consider

surgical exploration unless the conductive hearing loss is in the only hearing ear.

Sensorineural hearing loss● Severe-to-profound sensorineural hearing loss most commonly occurs in patients who have ● transverse fractures with otic capsule involvement.

○ Partial sensorineural loss is also possible. ○ Mild high-frequency loss (5-kHz notch) may occur in longitudinal fractures from cochlear

concussion. ○ Blood products and cellular disruption are present on histopathology.

● Before considering cochlear implant, labyrinthitis ossificans must be considered when bilateral severe sensorineural hearing loss is present.

● Progressive sensorineural hearing loss has also been reported with and without vertigo. ● When vertigo is present with fluctuating or progressive loss, traumatic endolymphatic hydrops or

perilymphatic fistula is the diagnosis.● Autoimmune hearing loss may account for some cases of progressive hearing loss.

Mixed hearing loss● Mixed conductive and sensorineural hearing loss may be difficult to detect in the presence of

severe sensorineural hearing loss. ● Surgical correction is considered when gain from correction of the conductive component is

desired.

Vertigo/nystagmus● These conditions are difficult to assess during the acute injury phase because of associated

neurologic trauma and/or life threatening injuries. ○ Therefore, the incidence of vertigo has been estimated on a wide spectrum to comprise

24-78% of cases. ● Spontaneous nystagmus observed by the naked eye is an important clinical sign in the acute

phase of temporal bone trauma. ○ It is usually related to a transverse temporal bone fracture with damage to the cochlea

and semicircular canals. ○ The spontaneous nystagmus in this instance is a severe one, horizontal or horizonto-

rotatory, third degree, and beating to the opposite ear. ○ It represents a peripheral vertigo and it is suppressed or diminished by fixation

(nystagmus in central vertigo can have a vertical direction, horizontal, horizonto-rotatory, or a changing direction, and its intensity can be enhanced by fixation).

● The accompanying vertigo is also severe, with a spinning sensation, and can be associated with nausea and vomiting.

○ Once the acute phase has passed, the spontaneous nystagmus and vertigo resolve within 3-6 months.

○ At this time, the ENG reveals absent vestibular responses in the affected labyrinth.

○ Spontaneous nystagmus, horizontal or horizonto-rotatory, of lesser degree, not easily seen by the naked eye, can also occur in longitudinal fractures and in general is less severe and intense than that seen in transverse fractures.

○ Also, posttraumatic vertigo is usually found in concussive injuries to the labyrinth associated with temporal bone trauma that does not involve the otic capsule or vestibular apparatus.

○ Note that these injuries may not be observed radiographically, nor does the incidence of vertigo or its intensity and duration correlate well with the severity of the temporal bone injury.

Posttraumatic benign paroxysmal positional vertigo● Posttraumatic benign paroxysmal positional vertigo (BPPV) is common.

○ BPPV is defined by a latent onset of postural related nystagmus and fatiguing which is nonreproducible.

○ In BPPV, a geotropic rotatory nystagmus is elicited with the Dix-Hallpike maneuver.○ After positioning the injured ear down, a latency period of 10 seconds occurs before the

nystagmus is seen. ○ The elicited nystagmus is fixed, horizontal, or horizonto-rotatory and, after a few seconds,

fatigues. ○ With repetition, the nystagmus is not reproducible at a point; contrarily, central positional

vertigo is a changing-direction nystagmus that has no latency period, is nonfatiguing, and is easily reproducible.

○ Postural vertigo of central etiology could be related to injury or hemorrhage in the brainstem, resulting in dysfunction of the vestibular nuclei.

● In both benign paroxysmal positional vertigo and central postural vertigo, the spontaneous nystagmus and vertigo usually resolve over 3-6 months and the remaining symptoms by 10-12 months; however, these symptoms may persist in elderly patients.

○ A combination of both central and peripheral causes are highly possible in the pathophysiology of vertigo after head and temporal bone trauma.

○ Vestibular rehabilitation or canal repositioning may be of value, in particular in BPPV.

Perilymphatic fistula● Perilymphatic fistula may also cause paroxysmal vertigo.

○ The onset of fistula and its symptoms may be delayed. ○ This diagnosis is considered when fluctuating hearing loss and vertigo are present in the

near posttraumatic period. ○ A fistula test in the ear canal should not be performed in the acute setting to avoid further

trauma or complications.○ Medical treatment initially consists of bed rest, head elevation, and stool softeners.○ Surgical exploration may be indicated in persistent perilymphatic fistulas.

Traumatic endolymphatic hydrops● Traumatic endolymphatic hydrops as a cause of posttraumatic vertigo has the following

etiologies: bony labyrinthine fistula, direct membranous labyrinth injury, injury to the endolymphatic drainage system, or surgical trauma.

● The onset of traumatic hydrops may be delayed for months or years.

Cerebrospinal fluid fistula● CSF fistula may occur as a result of a dural tear after any type of temporal bone fracture (17%).

○ The leak almost always closes within 4 weeks. ○ The average duration of the leak is approximately 4 days. ○ Longitudinal fractures tend to leak more severely, and this occurs through the middle

cranial fossa.

○ Transverse fractures cause leaks through the posterior cranial fossa. ○ The most common sites of fistula are the tegmen tympani and tegmen mastoideum when

the leak originates in the middle cranial fossa. ○ Most CSF leaks are obvious by their clear watery appearance in the immediate

posttrauma period. ○ CSF leak may be delayed after the initial trauma in approximately 28% of the cases. ○ Pneumatoceles and brain herniations are rare. ○ Pneumatoceles may resolve but occasionally expand.

● CSF contains decreased potassium and protein and elevated glucose concentration levels. Qualitative testing of the fluid for glucose is helpful but lacks specificity.

○ Quantitative testing for potassium, protein, and glucose is more precise. ○ The halo test performed by using a filter paper may be helpful (as the paper separates

CSF from blood). ○ Nevertheless, if available, beta2- transferrin assay is the most accurate diagnostic test for

CSF.● Otorrhea through a canal laceration or tympanic membrane laceration is usually the presenting

symptom, or rhinorrhea may be the only symptom. ○ The rate of flow is increased with exertion or learning forward. ○ CSF can also be observed in the middle ear behind an intact tympanic membrane after

the blood is resorbed.● The use of antibiotics in the presence of CSF fistula is controversial.

○ In studies before 1970, MacGee and colleagues reported that 16% of patients who receive prophylactic antibiotics developed meningitis.

○ Rathmore found no difference in the rate of meningitis with or without prophylactic antibiotics.

○ Demetriades and colleagues found that the incidence of meningitis and other co-infections was higher in the group that did not receive prophylaxis.

○ Villalobos et al combined 12 studies (1970-1996) of 1241 subjects and concluded that antibiotic prophylaxis does not appear to decrease the risk of meningitis.

○ To date, no clear answers exist, although the literature generally seems to support prophylactic use of antibiotics in patients with CSF fistulas, particularly in the presence of open laceration or co-infection.

● CSF leaks tend to close spontaneously with elevation of the head, bed rest, stool softeners, and cessation of sneezing, straining, and nose blowing.

○ Intermittent lumbar punctures or indwelling lumbar drains may help if the leak persists. ○ However, surgical exploration may be indicated for CSF fistulas that last longer than 14

days.● Radiography is necessary before surgical repair is considered.

○ The usefulness of HRCT and CT cisternography in localizing the site of CSF leaks is debatable.

○ HRCT alone shows bony defects in 70% of patients with fistulas and is the most specific test.

○ MRI may be the next step. ○ If the fracture is seen but the site of the fistula is not identified, CT cisternography with

intrathecal contrast agent (Omnipaque) is the next diagnostic procedure of choice. ○ However, if the bony defect cannot be demonstrated with HRCT, CT cisternography

rarely depicts the site of leakage. ○ The method of surgical closure of CSF fistulas after temporal bone fractures depends

on the location of the fistula, hearing status of both ears, presence of brain herniation through the tegmen, and patency of the external canal.

Facial nerve paralysis● The controversies regarding facial nerve paralysis involve the decision to operate, the timing of

the operation, and the preferred surgical approach to the injured segment.

○ Initial evaluation in the emergency department is extremely important because patients with delayed-onset paralysis almost always recover.

○ Therefore, delay in onset is the most important predictive factor for nerve recovery. ○ Those patients with immediate paralysis of an incomplete nature also almost always

recover. ○ Incomplete paralysis implies a functional nonsevered facial nerve with good prognosis. ○ Electrodiagnostic testing is usually unnecessary, and these patients should be treated

conservatively. ○ Determining whether immediate paralysis is partial may be difficult in the emergency

department or ICU. ○ Middle ear and mastoid infection can cause a partially denervated nerve to become

totally denervated.● Immediate complete paralysis is usually the result of a severed nerve.

○ Recovery rates are lower for immediate-onset paralysis, a fact that generates the main controversy.

○ Turner treated 30 patients with complete paralysis conservatively and reported good recovery in 63%.

○ Maiman and associates treated 21 patients with complete traumatic facial paralysis and reported full recovery in 52% and partial recovery in 43%.

○ When these recovery rates are compared with the expected recovery rate of 55% with facial nerve decompression, decompression surgery does not appear to be indicated.

○ Determining if the facial nerve is severed is difficult and sometimes impossible without surgical exploration.

● The decision to operate is made with the assistance of the electrodiagnostic studies. ○ Generally, surgery should be performed in the case of "nerve degeneration," whether the

paralysis is immediate or delayed. ○ The electrodiagnostic studies help the clinician to differentiate degeneration and

percentage of degeneration on the traumatized side as compared with the normal side.● The most common electrical tests are the maximum stimulation test (MST), the nerve excitability

test (NET), electroneuronography (ENOG), and electromyography (EMG).

Unusual complications of temporal bone fractures● Paralysis of cranial nerves IX (glossopharyngeal), X (vagus) and XI (spinal accessory): These

cranial nerves can be affected at the jugular foramen in petrous apex fractures. The treatment is conservative

● Paralysis of cranial nerve VI (abducens): This condition usually occurs in the area of the Meckel cave and the Dorello canal. Recovery within 6 months is usual. Alternate eye patching may be the only treatment necessary.

● Paralysis of cranial nerve V (trigeminal): This condition usually occurs in the area of Meckel cave. Treatment is conservative. Mastication muscles may be involved.

● Sigmoid sinus thrombosis: This condition occurs but is rare. Sigmoid sinus thrombosis is usually aseptic and nonsymptomatic. It may cause elevated CSF pressure and septicemia if infection is present. Diagnosis is made by means of MRI, magnetic resonance angiography, magnetic resonance venography, or angiography. The Griesinger sign (mastoid emissary vein thrombosis due to thrombus extension) may be noted. Treatment may require exploration of the sinus and ligation of the jugular veins in the neck.

● Posttraumatic cholesteatoma: This is a late complication of temporal bone fracture and is caused by skin entrapment in the cranial vault or temporal bone. It can grow undetected for years and become extremely invasive, owing to its size. Treatment is surgical.

● Classic Eagle syndrome: This condition may follow tonsillectomy. It consists of pain in the throat with foreign body sensation associated with difficult and painful swallowing. Referred otalgia is common. Traumatic fracture of an ossified styloid and stylohyoid ligament can cause pressure on the external or internal carotid artery and pain may be referred to the cheek or eye, producing atypical pain. Diagnosis is somewhat difficult after trauma and is made by means of palpation and CT scanning. Relief of symptoms by intraoral anesthetic injection may help the diagnosis. Treatment is surgical.

● Sympathetic cochleolabyrinthitis: This is a rare complication of temporal bone fracture. The condition is clinically significant because of the potential for hearing loss in the sole ear with hearing. Etiology may be related to the initiation of autoimmune inner ear damage with development of autoantibodies directed against inner ear proteins, as seen in polyarteritis nodosa. Cochlear fracture may release inner ear antibodies and cause host sensitization. Diagnosis is difficult and requires a high index of clinical suspicion. Results of Western blot assays for anticochlear antibodies may or may not be positive. Treatment includes immunosuppression.

Reference: March, A. (2010). Temporal Bone Fractures: Treatment and Management. Retrieved September 26, 2011 from http://emedicine.medscape.com/article/857365-treatment#showall 7) Why are more people using motorcycles as a form of transport? How can this form of transport be made safer for the passenger as well as the walking public to whom they are exposed? (Tamon) Situationer: FACT: Road accidents are one of the leading causes of death in the Philippines (5th!! next only to heart disease, pulmonary diseases, cancer and stroke)DOH: motorcycle accidents have the highest fatality rate at 23% out of 122 accidents in 2006! Number of road accidents [Jan-Oct 2010]: 18,391Motor vehicles involved: 14,847Motorcycles: 2,829 [Far second! but still!!] Total number of registration [Automobiles vs Motorcycles] 2002Type Number % Automobiles 749,553 (18.00%)Utility Vehicles 1,554,619 37.34Sport Utility Vehicles 97,6952.35Trucks 257,774 6.19Buses 33,915 0.81Motorcycles and Tricycles 1,470,383 (35.31%)Total 4,163,939 100.00Source: Land Transportation Office. Rapid Increase in the number of motorcycles: 2008: 762,000 automobiles vs 2.9 million motorcycles registered for the year!! Motorcycles in the Philippines have outnumbered all vehicle types! These statistics and the lack of available bicycle lanes for two-wheeled modes of transports streets, become recipe for accidents. Motorcycles as preferred form of transportationSales of motorcycles in the Philippines: 7000 motorcycles per week! (PNP via ABS CBN)

WHY MOTORCYCLES?: 1. Inefficiency of public transportation2. Cheaper gasoline consumption and travel costs 3. Reduce road congestion and pollution4. Free up parking spaces5. Easier to maintain6. Faster in traffic7. Sense of “ownership” for the common man Recommendations:

The Problem with Lack of RegulationAs convenient as the informal carriers may be the fact remains, these forms of transportation are dangerous. The lack of regulation means that vehicles that are not roadworthy are on the road. Moreover, unskilled and/or reckless drivers are transporting members of the public. Part of the responsibility of the state is to look after its citizens. Many developing nations do not have the resources to provide public transport but, they should be able to regulate it. Ways to regulate:Intellectual Property Office of the Philippines (Quality control) “. . .A fake medicine, equipment, or motorcycle parts, can instantly cause the death not only the buyer but that of innocent bystanders as well. It is in this light that IPOPHL partnered with MDPPA to help protect the public from the proliferation of fake motorcycle parts. MDPPA President Raul M. Gener responded by saying that their concern is first and foremost the safety of the public and consumers. . . This agreement will not only protect and enforce IPR but will also ensure road safety which may save our lives and our love ones.” Strict enforcement of laws:RA 10054“wearing helmets mandatory among motorbike owners. . . wearing a helmet reduces injuries from motorbike accidents by as much as 70%, deaths by as much as 20%.” Counter MeasuresOne counter measure is to actually implement the road safety exams. No exam no license.

> But LTO is inefficient and problem of red tape/corruption In line with this, stricter drivers' education should be implemented.

> Driver’s education as a priority. Go beyond the 2-3 hours classroom lesson; ask the help of NGO to augment LTO

Punish the traffic enforcers who violate the very traffic rules that they are supposed to enforce

> Very people who enforce the traffic rules often have a limited knowledge and understanding of what they are supposed to enforce. Change in infrastructure

> Accommodate for growing number of motorcyclists by creating motorcycle lanes

Establish specific set of rules for motorcyclists Mandatory motorcycle insurance Some practical guidelines for riders:

● Ride assuming that you and your motorcycle are totally invisible to motorists.● Leave plenty of space in front and back and to the sides from all other vehicles.● Anticipate trouble situations and know what to do when you see them.● Beware of motorists turning left in front of you at intersections. This is a leading cause of injuries

to motorcycle riders.● Slow down as your motorcycle enters an intersection and be prepared to make an evasive

maneuver if necessary.● Never drink or take drugs and try to ride a motorcycle.● Don’t ride if you are on medication that makes you sleepy.● Avoid riding at night.● Beware of riding your motorcycle into sun glare.● Do not give in to road rage and try to “get even” with another rider or motorist.● If someone is tailgating you, either speed up to open more space or pull over and let them pass.

references:http://www.iieom.org/ieom2011/pdfs/IEOM126.pdfhttp://ezinearticles.com/?Motorcycles-As-an-Alternative-Mode-of-Transport&id=1850778http://loqal.ph/nation-and-world/2010/04/16/a-considerable-problem-of-motorcycle-safety/http://www.motorcyclephilippines.com/news/more-anti-motorcycle-laws-proposed/http://odilile-ayodele.suite101.com/addressing-the-challenge-of-the-3rd-world-a80516http://www.adb.org/documents/reports/arrive-alive/country-reports/ctry-rep-07-phi.pdfhttp://ipophil.gov.ph/viewwhatsnew.php?id=204