Abu Zubair meriwayatkan dari Jabir bin Abdullah bahwa Nabi Muhammad SAW bersabda:
"Setiap penyakit ada obatnya. Jika obat yang tepat diberikan dengan izin Allah, penyakit itu akan sembuh".
(HR. Muslim, Ahmad dan Hakim).
Selasa, 01 Desember 2009
Reflex testing incorporates an assessment of the function and interplay of both sensory and motor pathways. It is simple yet informative and can give important insights into the integrity of the nervous system at many different levels.
Physiology of Reflexes
Assessment of reflexes is based on a clear understanding of the following principles and relationships:
Tendons connect muscles to bones, usually crossing a joint. When the muscle contracts, the tendon pulls on the bone, causing the attached structure to move.
When the tendon is struck by the reflex hammer, stretch receptors contained within it generate an impulse that is carried via sensory nerves to the spinal cord. At this juncture, the message is transmitted across a synapse to an appropriate lower motor neuron. An upper motor neuron, whose cell body resides in the brain, also provides input to this synapse.
The signal then travels down the lower motor neuron to the target muscle.
The sensory and motor signals that comprise a reflex arc travel over anatomically well characterized pathways. Pathologic processes affecting discrete roots or named peripheral nerves will cause the reflex to be diminished or absent. This can obviously be of great clinical significance. The Achilles Reflex (see below) is dependent on the S1 and S2 nerve roots. Herniated disc material (a relatively common process) can put pressure on the S1 nerve root, causing pain along its entire distribution (i.e. the lateral aspect of the lower leg). If enough pressure if placed on the nerve, it may no longer function, causing a loss of the Achilles reflex. In extreme cases, the patient may develop weakness or even complete loss of function of the muscles innervated by the nerve root, a medical emergency mandating surgical decompression. The specific nerve roots that comprise the arcs are listed for each of the major reflexes described below.
A normal response generates an easily observed shortening of the muscle. This, in turn, causes the attached structure to move.
The vigor of contraction is graded on the following scale:
0 No evidence of contraction
1+ Decreased, but still present (hypo-reflexic)
3+ Super-normal (hyper-reflexic)
4+ Clonus: Repetitive shortening of the muscle after a single stimulation
Deep Tendon Reflexes
Using a reflex hammer, deep tendon reflexes are elicited in all 4 extremities. Note the extent or power of the reflex, both visually and by palpation of the tendon or muscle in question.
The Reflex Hammer
You will need to use a reflex hammer when performing this aspect of the exam. A number of the most commonly used models are pictured below. Regardless of the hammer type, proper technique is critical. The larger hammers have weighted heads, such that if you raise them approximately 10 cm from the target and then release, they will swing into the tendon with adequate force. The smaller hammers should be swung loosely between thumb and forefinger.
The muscle group to be tested must be in a neutral position (i.e. neither stretched nor contracted).
The tendon attached to the muscle(s) which is/are to be tested must be clearly identified. The extremity should be positioned such that the tendon can be easily struck with the reflex hammer.
If you are having trouble locating the tendon, ask the patient to contract the muscle to which it is attached. When the muscle shortens, you should be able to both see and feel the cord like tendon, confirming its precise location. You may, for example, have some difficulty identifying the Biceps tendon within the Antecubital Fossa. Ask the patient to flex their forearm (i.e. contract their Biceps muscle) while you simultaneously palpate the fossa. The Biceps tendon should become taut and thus readily apparent.
Strike the tendon with a single, brisk, stroke. While this is done firmly, it should not elicit pain. Occasionally, due to other medical problems (e.g. severe arthritis), you will not be able to position the patient's arm in such a way that you are able to strike the tendon. If this occurs, do not cause the patient discomfort. Simply move on to another aspect of the exam.
This grading system is rather subjective. Additional levels of response can be included by omitting the '+' or adding a '-' to any of the numbers. As you gain more experience, you'll have a greater sense of how to arrange your own scale.
Specifics of Reflex Testing � The peripheral nerves and contributing spinal nerve roots that form each reflex arc are listed in parentheses:
Achilles (S1, S2 � Sciatic Nerve):
This is most easily done with the patient seated, feet dangling over the edge of the exam table. If they cannot maintain this position, have them lie supine, crossing one leg over the other in a figure 4. Or, failing that, arrange the legs in a frog-type position.
Identify the Achilles tendon, a taut, discrete, cord-like structure running from the heel to the muscles of the calf. If you are unsure, ask the patient to plantar flex (i.e. "step on the gas"), which will cause the calf to contract and the Achilles to become taut.
Achilles Tendon:Tendon is outlined in pen on left, grasped by forceps (gross dissection) on right.
Position the foot so that it forms a right angle with the rest of the lower leg. You will probably need to support the bottom of the foot with your hand.
Strike the tendon directly with your reflex hammer. Be sure that the calf if exposed so that you can see the muscle contract. A normal reflex will cause the foot to plantar flex (i.e. move into your supporting hand).
Positions for Checking Achilles Reflex
Patellar (L3, L4 � Femoral Nerve):
This is most easily done with the patient seated, feet dangling over the edge the exam table. If they cannot maintain this position, have them lie supine (i.e. on their backs).
Identify the patellar tendon, a thick, broad band of tissue extending down from the lower aspect of the patella (knee cap). If you are not certain where it's located, ask the patient to extend their knee. This causes the quadriceps (thigh muscles) to contract and makes the attached tendon more apparent.
Patellar Tendon: Outlined in pen on left, grasped by forceps (gross dissection)on right.
Strike the tendon directly with your reflex hammer. If you are having trouble identifying the exact location of the tendon (e.g. if there is a lot of subcutaneous fat), place your index finger firmly on top of it. Strike your finger, which should then transmit the impulse.
Patellar Reflex Testing, seated patient
For the supine patient, support the back of their thigh with your hands such that the knee is flexed and the quadriceps muscles relaxed. Then strike the tendon as described above.
Patellar Reflex, supine patient
Make sure that the quadriceps are exposed so that you can see muscle contraction. In the normal reflex, the lower leg will extend at the knee.
Biceps (C5, C6 � Musculocutaneous Nerve):
This is most easily done with the patient seated.
Identify the location of the biceps tendon. To do this, have the patient flex at the elbow while you observe and palpate the antecubital fossa. The tendon will look and feel like a thick cord.
Biceps Tendon:Tendon is outlined in pen on left, grasped by forceps (gross dissection) on right.
The patient's arm can be positioned in one of two ways:
Allow the arm to rest in the patient's lap, forming an angle of slightly more then 90 degrees at the elbow.
Biceps Reflex Testing
Support the arm in yours, such that your thumb is resting directly over the biceps tendon (hold their right arm with your right; and vice versa).
Biceps Reflex Testing,arm supported
Make sure that the biceps muscle is completely relaxed.
It may be difficult to direct your hammer strike such that the force is transmitted directly on to the biceps tendon, and not dissipated amongst the rest of the soft tissue in the area. If you are supporting the patient's arm, place your thumb on the tendon and strike this digit. If the arm is unsupported, place your index or middle fingers firmly against the tendon and strike them with the hammer.
Make sure that the patient's sleeve is rolled up so that you can directly observe the muscle as well as watch the lower arm for movement. A normal response will cause the biceps to contract, drawing the lower arm upwards.
Brachioradialis (C5, C6 � Radial Nerve):
This is most easily done with the patient seated. The lower arm should be resting loosely on the patient's lap.
The tendon of the Brachioradialis muscle cannot be seen or well palpated, which makes this reflex a bit tricky to elicit. The tendon crosses the radius (thumb side of the lower arm) approximately 10 cm proximal to the wrist.
Brachioradialis Tendon: Tendon is outlined in pen on left, grasped by forceps (gross dissection) on right.
Strike this area with your reflex hammer. Usually, hitting anywhere in the right vicinity will generate the reflex.
Observe the lower arm and body of the Brachioradialis for a response. A normal reflex will cause the lower arm to flex at the elbow and the hand to supinate (turn palm upward).
Triceps (C7, C8 � Radial Nerve):
This is most easily done with the patient seated.
Identify the triceps tendon, a discrete, broad structure that can be palpated (and often seen) as it extends across the elbow to the body of the muscle, located on the back of the upper arm. If you are having trouble clearly identifying the tendon, ask the patient to extend their lower arm at the elbow while you observe and palpate in the appropriate region.
Triceps Tendon:Tendon is outlined in pen on left, grasped by forceps (gross dissection) on right.
The arm can be placed in either of 2 positions:
Gently pull the arm out from the patient's body, such that it roughly forms a right angle at the shoulder. The lower arm should dangle directly downward at the elbow.
Triceps Reflex, arm supported
Have the patient place their hands on their hips.
Triceps Reflex, arm unsupported
Either of these techniques will allow the triceps to completely relax.
If you are certain as to the precise location of the tendon, strike this area directly with your hammer. If the target is not clearly apparent or the tendon is surrounded by an excessive amount of subcutaneous fat (which might dissipate the force of your strike), place your index or middle finger firmly against the structure. Then strike your finger.
Make sure that the triceps is uncovered, so that you can observe the response. The normal reflex will cause the lower arm to extend at the elbow and swing away from the body. If the patient's hands are on their hips, the arm will not move but the muscle should shorten vigorously .
Making Clinical Sense of Reflexes:
Normal reflexes require that every aspect of the system function normally. Breakdowns cause specific patterns of dysfunction. These are interpreted as follows:
Disorders in the sensory limb will prevent or delay the transmission of the impulse to the spinal cord. This causes the resulting reflex to be diminished or completely absent. Diabetes induced peripheral neuropathy (the most common sensory neuropathy seen in developed countries), for example, is a relatively common reason for loss of reflexes.
Abnormal lower motor neuron (LMN) function will result in decreased or absent reflexes. If, for example, a peripheral motor neuron is transected as a result of trauma, the reflex dependent on this nerve will be absent.
If the upper motor neuron (UMN)is completely transected, as might occur in traumatic spinal cord injury, the arc receiving input from this nerve becomes disinhibited, resulting in hyperactive reflexes. Of note, immediately following such an injury, the reflexes are actually diminished, with hyper-reflexia developing several weeks later. A similar pattern is seen with the death of the cell body of the UMN (located in the brain), as occurs with a stroke affecting the motor cortex of the brain.
Primary disease of the neuro-muscular junction or the muscle itself will result in a loss of reflexes, as disease at the target organ (i.e. the muscle) precludes movement.
A number of systemic disease states can affect reflexes. Some have their impact through direct toxicity to a specific limb of the system. Poorly controlled diabetes, as described above, can result in a peripheral sensory neuropathy. Extremes of thyroid disorder can also affect reflexes, though the precise mechanisms through which this occurs are not clear. Hyperthyroidisim is associated with hyperreflexia, and hypothyroidism with hyporeflexia.
Detection of abnormal reflexes (either increased or decreased) does not necessarily tell you which limb of the system is broken, nor what might be causing the dysfunction. Decreased reflexes could be due to impaired sensory input or abnormal motor nerve function. Only by considering all of the findings, together with their rate of progression, pattern of distribution (bilateral v unilateral, etc.) and other medical conditions can the clinician make educated diagnostic inferences about the results generated during reflex testing.
If you are unable to elicit a reflex, stop and consider the following:
Are you striking in the correct place? Confirm the location of the tendon by observing and palpating the appropriate region while asking the patient to perform an activity that causes the muscle to shorten, making the attached tendon more apparent.
Make sure that your hammer strike is falling directly on the appropriate tendon. If there is a lot of surrounding soft tissue that could dampen the force of the strike, place a finger firmly on the correct tendon and use that as your target.
Make sure that the muscle is uncovered so that you can see any contraction (occasionally the force of the reflex will not be sufficient to cause the limb to move).
Reinforcement is accomplished by asking the patient to clench their teeth, or if testing lower extremity reflexes, have the patient hook together their flexed fingers and pull apart. This is known as the Jendrassik maneuver.
Sometimes the patient is unable to relax, which can inhibit the reflex even when all is neurologically intact. If this occurs during your assessment of lower extremity reflexes, ask the patient to interlock their hands and direct them to pull, while you simultaneously strike the tendon. This sometimes provides enough distraction so that the reflex arc is no longer inhibited.
Occasionally, it will not be possible to elicit reflexes, even when no neurological disease exists. This is most commonly due to a patient's inability to relax. In these settings, the absence of reflexes are of no clinical consequence. This assumes that you were otherwise thorough in your history taking, used appropriate examination techniques, and otherwise identified no evidence of disease.
Pathological Reflexes :
The Hoffman response is elicited by holding the patient's middle finger between the examiner''s thumb and index finger. Ask the patient to relax their fingers completely. Once the patient is relaxed, using your thumbnail press down on the patient's fingernail and move downward until your nail "clicks" over the end of the patient's nail. Normally, nothing occurs.
A positive Hoffman's response is when the other fingers flex transiently after the "click". Repeat this manuever multiple times on both hands.
Abdominal reflexes = contractions of the abdominal muscles on stimulation of the abdominal skin.
Cremasteric reflex = stimulation of the skin on the front and inner thigh retracts the testis on the same side.
Anal reflex = contraction of the anal sphincter on irritation of the anal skin.
Oppenheim reflex = dorsiflexion of the big toe on stroking downward along the medial side of the tibia, seen in pyramidal tract disease.
The Babinski response is a test used to assess upper motor neuron dysfunction and is performed as follows:
Use the handle end of your reflex hammer, which is solid and comes to a point.
The patient may either sit or lie supine.
Start at the lateral aspect of the foot, near the heel. Apply steady pressure with the end of the hammer as you move up towards the ball (area of the metatarsal heads) of the foot.
When you reach the ball of the foot, move medially, stroking across this area.
Then test the other foot.
Some patients find this test to be particularly noxious/uncomfortable. Tell them what you are going to do and why. If it's unlikely to contribute important information (e.g. screening exam of the normal patient) and they are quite averse, simply skip it.
Interpretation: In the normal patient, the first movement of the great toe should be downwards (i.e. plantar flexion). If there is an upper motor neuron injury (e.g. spinal cord injury, stroke), then the great toe will dorsiflex and the remainder of the other toes will fan out. A few additional things to remember:
Babinski Response Present
Newborns normally have a positive Babinksi. It usually goes away after about 6 months.
Sometimes you will be unable to generate any response, even in the absence of disease. Responses must therefore be interpreted in the context of the rest of the exam.
If the great toe flexes and the other toes flair, the Babinski Response is said to be present. If not (i.e. normal), it is recorded as absent. For reasons of semantics, the Babinski is not recorded as '+' or '-'.
Withdrawal of the entire foot (due to unpleasant stimulation), is not interpreted as a positive response.
Chaddock's reflex in lesions of the pyramidal tract, stimulation below the external malleolus causes extension of the great toe.
Finally, test clonus if any of the reflexes appeared hyperactive. Hold the relaxed lower leg in your hand, and sharply dorsiflex the foot and hold it dorsiflexed. Feel for oscillations between flexion and extension of the foot indicating clonus. Normally nothing is felt.
Diposkan oleh FX di 18.05
Cranial Nerve 1 (Olfactory): Formal assessment of ability to smell is generally omitted, unless there is a specific complaint. If it is to be tested:
Each nostril should be checked separately. Push on the outside of the nares, occluding the side that is not to be tested.
Have the patient close their eyes. Make sure that the patient is able to inhale and exhale through the open nostril.
Present a small test tube filled with something that has a distinct, common odor (e.g. ground coffee) to the open nostril. The patient should be able to correctly identify the smell.
If you wish to test olfaction and don't have any "substance filled tubes" use an alcohol pad as a screening test. Patients should be able to identify its distinctive odor from approximately 10 cm .
Alcohol Pad Sniff Test
Cranial Nerve 2 (Optic): This nerve carries visual impulses from the eye to the optical cortex of the brain by means of the optic tracts. Testing involves 3 phases (also covered in the section of this site dedicated to the Eye Exam):
Each eye is tested separately. If the patient uses glasses to view distant objects, they should be permitted to wear them (referred to as best corrected vision).
A Snellen Chart is the standard, wall mounted device used for this assessment. Patients are asked to read the letters or numbers on successively lower lines (each with smaller images) until you identify the last line which can be read with 100% accuracy. Each line has a fraction written next to it. 20/20 indicates normal vision. 20/400 means that the patient's vision 20 feet from an object is equivalent to that of a normal person viewing the same object from 400 feet. In other words, the larger the denominator, the worse the vision.
Snellen chart for measuring visual acuity
There are hand held cards that look like Snellen Charts but are positioned 14 inches from the patient. These are used simply for convenience. Testing and interpretation are as described for the Snellen.
Hand held visual acuity card
If neither chart is available and the patient has visual complaints, some attempt should be made to objectively measure visual acuity. This is a critically important reference point, particularly when trying to communicate the magnitude of a visual disturbance to a consulting physician. Can the patient read news print? The headline of a newspaper? Distinguish fingers or hand movement in front of their face? Detect light?Failure at each level correlates with a more severe problem.
Visual Field Testing: Specific areas of the retina receive input from precise areas of the visual field. This information is carried to the brain along well defined anatomic pathways. Holes in vision (referred to as visual field cuts) are caused by a disruption along any point in the path from the eyeball to the visual cortex of the brain. Visual fields can be crudely assessed as follows:
The examiner should be nose to nose with the patient, separated by approximately 8 to 12 inches.
Each eye is checked separately. The examiner closes one eye and the patient closes the one opposite. The open eyes should then be staring directly at one another.
The examiner should move their hand out towards the periphery of his/her visual field on the side where the eyes are open. The finger should be equidistant from both persons.
The examiner should then move the wiggling finger in towards them, along an imaginary line drawn between the two persons.The patient and examiner should detect the finger at more or less the same time.
The finger is then moved out to the diagonal corners of the field and moved inwards from each of these directions. Testing is then done starting at a point in front of the closed eyes. The wiggling finger is moved towards the open eyes.
The other eye is then tested.
Meaningful interpretation is predicated upon the examiner having normal fields, as they are using themselves for comparison.
If the examiner cannot seem to move their finger to a point that is outside the patient's field don't worry, as it simply means that their fields are normal.
Interpretation: This test is rather crude, and it is quite possible to have small visual field defects that would not be apparent on this type of testing. Prior to interpreting abnormal findings, the examiner must understand the normal pathways by which visual impulses travel from the eye to the brain.
Pupils: The pupil has afferent (sensory) nerves that travel with CN2. These nerves carry the impulse generated by the light back towards the brain. They function in concert with efferent (motor) nerves that travel with CN 3 and cause pupillary constriction. Seen under CN 3 for specifics of testing.
CN 3 (Occulomotor): This nerve is responsible for most of the eyeball's mobility, referred to as extra-occular movement. CN 3 function is assessed in concert with CNs 4 and 6, the other nerves responsible for controlling eyeball movement. CN 4 controls the Superior Oblique muscle, which allows each eye to look down and medially. CN 6 controls the Lateral Rectus muscle, which allows each eye to move laterally. CN 3 controls the muscles which allow motion in all other directions. The pneumonic "S O 4 � L R 6 � All The Rest 3" may help remind you which CN does what (Superior Oblique CN 4 � LateralRectus CN 6 � All The Rest of the muscles innervated by CN 3). Testing is done as follows:
Ask the patient to keep their head in one place. Then direct them to follow your finger while moving only their eyes.
Move your finger out laterally, then up and down.
Then move your finger across the patient's face to the other side of their head. When it is out laterally, move it again up and down. You will roughly trace out the letter "H", which takes both eyeballs through the complete range of movements. At the end, bring your finger directly in towards the patient's nose. This will cause the patient to look cross-eyed and the pupils should constrict, a response referred to as accommodation.
CN 3 also innervates the muscle which raises the upper eye lid. This can first be assessed by simply looking at the patient. If there is CN 3 dysfuntion, the eyelid on that side will cover more of the iris and pupil compared with the other eye. This is referred to as ptosis.
Right CN3 Lesion: Note patient's right eye is deviated laterally and there is ptosis of the lid (picture on left),
and the right pupil (middle picture) is more dilated than the left pupil (picture on far right).
CN6 Palsy: This patient is unable to move left eye lateral of midline due to left CN6 lesion.
It's also worth noting that disorders of the extra ocular muscles themselves (and not the CN which innervate them) can also lead to impaired eye movement. For example, pictured below is a patient who has suffered a traumatic left orbital injury. The inferior rectus muscle has become entrapped within the resulting fracture, preventing the left eye from being able to look downward.
Entrapment of Left Inferior Rectus Muscle
The response of pupils to light is controlled by afferent (sensory) nerves that travel with CN 2 and efferent (motor) nerves that travel with CN 3. These innervate the ciliary muscle, which controls the size of the pupil. Testing is performed as follows:
It helps if the room is a bit dim, as this will cause the pupil to become more dilated.
Using any light source (flashlight, oto-ophtahlmoscope, etc), shine the light into one eye. This will cause that pupil to constrict, referred to as the direct response.
Remove the light and then re-expose it to the same eye, though this time observe the other pupil. It should also constrict, referred to as the consensual response. This occurs because afferent impulses from one eye generate an efferent response (i.e. signal to constrict) that is sent to both pupils.
If the patient's pupils are small at baseline or you are otherwise having difficulty seeing the changes, take your free hand and place it above the eyes so as to provide some shade. This should cause the pupils to dilate additionally, making the change when they are exposed to light more dramatic. If you are still unable to appreciate a response, ask the patient to close their eye, generating maximum darkness and thus dilatation. Then ask the patient to open the eye and immediately expose it to the light. This will (hopefully) make the change from dilated to constricted very apparent.
Under normal conditions, both pupils will appear symmetric. Direct and consensual response should be equal for both.
Asymmetry of the pupils is referred to as aniosocoria. Some people with anisocoria have no underlying neuropathology. In this setting, the asymmetry will have been present for a long time without change and the patient will have no other neurological signs or symptoms. The direct and consensual responses should be preserved.
A number of conditions can also affect the size of the pupils. Medications/intoxications which cause generalized sympathetic activation will result in dilatation of both pupils. Other drugs(e.g. narcotics) cause symmetric constrictionof the pupils. These findings can provide important clues when dealing with an agitated or comatose patient suffering from medication overdose. Eye drops known as mydriatic agents are used to paralyze the muscles, resulting marked dilatation of the pupils. They are used during a detailed eye examination, allowing a clear view of the retina. Addiitonally, any process which causes increased intracranial pressure can result in a dilated pupil that does not respond to light.
If the afferent nerve is not working, neither pupil will respond when light is shined in the affected eye. Light shined in the normal eye, however, will cause the affected pupil to constrict. That's because the efferent (signal to constrict) response in this case is generated by the afferent impulse received by the normally functioning eye. This is referred to as an afferent pupil defect.
If the efferent nerve is not working, the pupil will appear dilated at baseline and will have neither direct nor consensual pupillary responses.
CN 4 (Trochlear): Seen under CN 3.
CN 5 (Trigeminal): This nerve has both motor and sensory components.
Assessment of CN 5 Sensory Function: The sensory limb has 3 major branches, each covering roughly 1/3 of the face. They are: the Ophthlamic, Maxillary, and Mandibular. Assessment is performed as follows:
Use a sharp implement (e.g. broken wooden handle of a cotton tipped applicator).
Ask the patient to close their eyes so that they receive no visual cues.
Touch the sharp tip of the stick to the right and left side of the forehead, assessing the Ophthalmic branch.
Touch the tip to the right and left side of the cheek area, assessing the Maxillary branch.
Touch the tip to the right and left side of the jaw area, assessing the Mandibular branch.
The patient should be able to clearly identify when the sharp end touches their face. Of course, make sure that you do not push too hard as the face is normally quite sensitive. The Ophthalmic branch of CN 5 also receives sensory input from the surface of the eye. To assess this component:
Pull out a wisp of cotton.
While the patient is looking straight ahead, gently brush the wisp against the lateral aspect of the sclera (outer white area of the eye ball).
This should cause the patient to blink. Blinking also requires that CN 7 function normally, as it controls eye lid closure.
Assessment of CN 5 Motor Function: The motor limb of CN 5 innervates the Temporalis and Masseter muscles, both important for closing the jaw. Assessment is performed as follows:
Place your hand on both Temporalis muscles, located on the lateral aspects of the forehead.
Ask the patient to tightly close their jaw, causing the muscles beneath your fingers to become taught.
Then place your hands on both Masseter muscles, located just in from of the Tempero-Mandibular joints (point where lower jaw articulates with skull).
Ask the patient to tightly close their jaw, which should again cause the muscles beneath your fingers to become taught. Then ask them to move their jaw from side to side, another function of the Massester.
CN6 (Abducens): See under CN 3.
CN7 (Facial): This nerve innervates many of the muscles of facial expression. Assessment is performed as follows:
First look at the patient's face. It should appear symmetric. That is:
There should be the same amount of wrinkles apparent on either side of the forehead� barring asymmetric Bo-Tox injection!
The nasolabial folds (lines coming down from either side of the nose towards the corners of the mouth) should be equal
The corners of the mouth should be at the same height
If there is any question as to whether an apparent asymmetry if new or old, ask the patient for a picture (often found on a driver's license) for comparison.
Ask the patient to wrinkle their eyebrows and then close their eyes tightly. CN 7 controls the muscles that close the eye lids (as opposed to CN 3, which controls the muscles which open the lid). You should not be able to open the patient's eyelids with the application of gentle upwards pressure.
Ask the patient to smile. The corners of the mouth should rise to the same height and equal amounts of teeth should be visible on either side.
Ask the patient to puff out their cheeks. Both sides should puff equally and air should not leak from the mouth.
Interpretation: CN 7 has a precise pattern of inervation, which has important clinical implications. The right and left upper motor neurons (UMNs) each innervate both the right and left lower motor neurons (LMNs) that allow the forehead to move up and down. However, the LMNs that control the muscles of the lower face are only innervated by the UMN from the opposite side of the face.
CN7 - Facial Nerve
Precise Pattern of Innervation
Thus, in the setting of CN 7 dysfunction, the pattern of weakness or paralysis observed will differ depending on whether the UMN or LMN is affected. Specifically:
UMN dysfunction: This might occur with a central nervous system event, such as a stroke. In the setting of R UMN CN 7 dysfunction, the patient would be able to wrinkle their forehead on both sides of their face, as the left CN 7 UMN cross innervates the R CN 7 LMN that controls this movement. However, the patient would be unable to effectively close their left eye or raise the left corner of their mouth.
Right central CN7 dysfunction: Note preserved abiltiy to wrinkle forehead. Left corner of mouth, however, is slightly lower than right. Left naso-labial fold is slightly less pronounced compared with right.
LMN dysfunction: This occurs most commonly in the setting of Bell's Palsy, an idiopathic, acute CN 7 peripheral nerve palsy. In the setting of R CN 7 peripheral (i.e. LMN) dysfunction, the patient would not be able to wrinkle their forehead, close their eye or raise the corner of their mouth on the right side. Left sided function would be normal.
Left peripheral CN7 dysfunction: Note loss of forehead wrinkle, ability to close eye, ability to raise corner of mouth, and decreased naso-labial fold prominence on left.
This clinical distinction is very important, as central vs peripheral dysfunction carry different prognostic and treatment implications. Bell's Palsy (peripheral CN 7 dysfunction)tends to happen in patient's over 50 and often responds to treatment with Acyclovir (an anti-viral agent) and Prednisone (a corticosteroid). Over the course of weeks or months there is usually improvement and often complete resolution of symptoms. Assessment of acute central (UMN) CN 7 dysfunction would require quite a different approach (e.g. neuroimaging to determine etiology).
CN 7 is also responsible for carrying taste sensations from the anterior 2/3 of the tongue. However as this is rarely of clinical import, further discussion is not included.
CN8 (Acoustic): CN 8 carries sound impulses from the cochlea to the brain. Prior to reaching the cochlea, the sound must first traverse the external canal and middle ear. Auditory acuity can be assessed very crudely on physical exam as follows:
Stand behind the patient and ask them to close their eyes.
Whisper a few words from just behind one ear. The patient should be able to repeat these back accurately. Then perform the same test for the other ear.
Alternatively, place your fingers approximately 5 cm from one ear and rub them together. The patient should be able to hear the sound generated. Repeat for the other ear.
These tests are rather crude. Precise quantification, generally necessary whenever there is a subjective decline in acuity, requires special equipment and training.
The cause of subjective hearing loss can be assessed with bedside testing. Hearing is broken into 2 phases: conductive and sensorineural. The conductive phase refers to the passage of sound from the outside to the level of CN 8. This includes the transmission of sound through the external canal and middle ear. Sensorineural refers to the transmission of sound via CN 8 to the brain. Identification of conductive (a much more common problem in the general population) defects is determined as follows:
Grasp the 512 Hz tuning fork by the stem and strike it against the bony edge of your palm, generating a continuous tone.
Place the stem of the tuning fork on the mastoid bone, the bony prominence located immediately behind the lower part of the ear.
The vibrations travel via the bones of the skull to CN 8, allowing the patient to hear the sound.
Ask the patient to inform you when they can no longer appreciate the sound. When this occurs, move the tuning fork such that the tines are placed right next to (but not touching) the opening of the ear. At this point, the patient should be able to again hear the sound. This is because air is a better conducting medium then bone.
The above testing is reserved for those instances when a patient complains of a deficit in hearing. Thus, on the basis of history, there should be a complaint of hearing decline in one or both ears.
In the setting of a conductive hearing loss (e.g. wax in the external canal), the Webber test will lateralize (i.e. sound will be heard better)in the ear that has the subjective decline in hearing. This is because when there is a problem with conduction, competing sounds from the outside cannot reach CN 8 via the external canal. Thus, sound generated by the vibrating tuning fork and traveling to CN 8 by means of bony conduction is better heard as it has no outside "competition." You can transiently create a conductive hearing loss by putting the tip of your index finger in the external canal of one ear. If you do this while performing the Webber test, the sound will be heard on that side.
In the setting of a sensorineural hearing loss (e.g. a tumor of CN 8), the Webber test will lateralize to the ear which does not have the subjective decline in hearing. This is because CN 8 is the final pathway through which sound is carried to the brain. Thus, even though the bones of the skull will successfully transmit the sound to CN 8, it cannot then be carried to the brain due to the underlying nerve dysfunction.
In the setting of conductive hearing loss, bone conduction (BC) will be better then air conduction (AC) when assessed by the Rinne Test. If there is a blockage in the passageway (e.g. wax) that carries sound from the outside to CN 8, then sound will be better heard when it travels via the bones of the skull. Thus, the patient will note BC to be better then or equal to AC in the ear with the subjective decline in hearing.
In the setting of a sensorineural hearing loss, air conduction will still be better then bone conduction (i.e. the normal pattern will be retained). This is because the problem is at the level of CN 8. Thus, regardless of the means (bone or air) by which the impulse gets to CN 8, there will still be a marked hearing decrement in the affected ear. As AC is normally better then BC, this will still be the case.
Grasp the 512 Hz tuning fork by the stem and strike it against the bony edge of your palm, generating a continuous tone. Alternatively you can get the fork to vibrate by "snapping" the ends between your thumb and index finger.
512 Hz Tuning Fork
Hold the stem against the patient's skull, along an imaginary line that is equidistant from either ear.
The bones of the skull will carry the sound equally to both the right and left CN 8. Both CN 8s, in turn, will transmit the impulse to the brain.
The patient should report whether the sound was heard equally in both ears or better on one side then the other (referred to as lateralizing to a side).
Identifying conductive v sensorineural hearing deficits requires historical information as well as the results of Webber and Rinne testing. In summary, this data is interpreted as follows:
First determine by history and crude acuity testing which ear has the hearing problem.
Perform the Webber test. If there is a conductive hearing deficit, the Webber will lateralize to the affected ear. If there is a sensorineural deficit, the Webber will lateralize to the normal ear.
Perform the Rinne test. If there is a conductive hearing deficit, BC will be greater then or equal to AC in the affected ear. If there is a sensorineural hearing deficit, AC will be greater then BC in the affected ear.
CN9 (Glosopharyngeal) and CN 10 (Vagus): These nerves are responsible for raising the soft palate of the mouth and the gag reflex, a protective mechanism which prevents food or liquid from traveling into the lungs As both CNs contribute to these functions, they are tested together.
Testing Elevation of the soft palate:
Ask the patient to open their mouth and say, "ahhhh," causing the soft palate to rise upward.
Look at the uvula, a midline structure hanging down from the palate. If the tongue obscures your view, take a tongue depressor and gently push it down and out of the way.
The Uvula should rise up straight and in the midline.
If CN 9 on the right is not functioning (e.g. in the setting of a stroke), the uvula will be pulled to the left. The opposite occurs in the setting of left CN 9 dysfunction.
Left CN9 Dysfunction: Patient status post stroke affecting left CN9. Uvula therefore pulled over towards right.
Be aware that other processes can cause deviation of the uvula.A peritonsilar abscess, for example, will push the uvula towards the opposite (i.e. normal) tonsil.
Left peritonsillar abscess: infection within left tonsil has pushed uvula towards the right.
Testing the Gag Reflex:
Ask the patient to widely open their mouth. If you are unable to see the posterior pharynx (i.e. the back of their throat), gently push down with a tongue depressor.
In some patients, the tongue depressor alone will elicit a gag. In most others, additional stimulation is required. Take a cotton tipped applicator and gently brush it against the posterior pharynx or uvula. This should generate a gag in most patients.
A small but measurable percent of the normal population has either a minimal or non-existent gag reflex. Presumably, they make use of other mechanisms to prevent aspiration.
Gag testing is rather noxious. Some people are particularly sensitive to even minimal stimulation. As such, I would suggest that you only perform this test when there is reasonable suspicion that pathology exists. This would include two major clinical situations:
If you suspect that the patient has suffered acute dysfunction, most commonly in the setting of a stroke. These patients may complain of/be noted to cough when they swallow. Or, they may suffer from recurrent pneumonia. Both of these events are signs of aspiration of food contents into the passageways of the lungs. These patients may also have other cranial nerve abnormalities as lesions affecting CN 9 and 10 often affect CNs 11 and 12, which are anatomically nearby.
Patient's suffering from sudden decreased level of consciousness. In this setting, the absence of a gag might indicate that the patient is no longer able to reflexively protect their airway from aspiration. Strong consideration should be given to intubating the patient, providing them with a secure mechanical airway until their general condition improves.
CN 9 is also responsible for taste originating on the posterior 1/3 of the tongue. As this is rarely a clinically important problem, further discussion is not included.
CN 10 also provides parasympathetic innervation to the heart, though this cannot be easily tested on physical examination.
CN11 (Spinal Accessory): CN 11 innervates the muscles which permit shrugging of the shoulders (Trapezius) and turning the head laterally (Sternocleidomastoid).
Place your hands on top of either shoulder and ask the patient to shrug while you provide resistance. Dysfunction will cause weakness/absence of movement on the affected side.
Place your open left hand against the patient's right cheek and ask them to turn into your hand while you provide resistance. Then repeat on the other side. The right Sternocleidomasoid muscle (and thus right CN 11) causes the head to turn to the left, and vice versa.
CN12 (Hypoglossal): CN 12 is responsible for tongue movement. Each CN 12 innervates one-half of the tongue.
Ask the patient to stick their tongue straight out of their mouth.
If there is any suggestion of deviation to one side/weakness, direct them to push the tip of their tongue into either cheek while you provide counter pressure from the outside.
If the right CN 12 is dysfunctional, the tongue will deviate to the right. This is because the normally functioning left half will dominate as it no longer has opposition from the right. Similarly, the tongue would have limited or absent ability to resist against pressure applied from outside the left cheek.
Left CN 12 Dysfunction: Stroke has resulted in L CN 12 Palsy.
Tongue therefore deviates to the left.
Diposkan oleh FX di 17.39
The Holy Al-Qur'an (English version)
- Surah 1 - Al Fatiha THE OPENING
- Surah 2 - Al Baqarah THE HEIFER
- Surah 3 - Ali 'Imran - THE FAMILY OF 'IMRAN
- Surah 4 - Al-Nisa' THE WOMEN
- Surah 5 - Al Ma'idah THE REPAST
- Surah 6 - Al An'am THE CATTLE
- Surah 7 - Al A'raf THE HEIGHTS
- Surah 8 - Al Anfal THE SPOILS OF WAR
- Surah 9 - Al Tawbah THE REPENTANCE
- Surah 10 - Yunus JONAH
- Surah 11 - Hud THE PROPHET HUD
- Surah 12 - Yusuf JOSEPH
- Surah 13 - Al Ra'd THE THUNDER
- Surah 14 - Ibrahim ABRAHAM
- Surah 15 - Al Hijr THE ROCKY TRACT
- Surah 16 - Al Nahl BEES
- Surah 17 - Al Isra' THE NIGHT JOURNEY
- Surah 18 - Al Kahf THE CAVE
- Surah 19 - Maryam MARY
- Surah 20 - TA HA
- Surah 21 - Al Anbiya THE PROPHETS
- Surah 22 - Al Hajj THE PILGRIMAGE
- Surah 23 - Al Mu'minun THE BELIEVERS
- Surah 24 - Al Nur THE LIGHT
- Surah 25 - Al Furqan THE CRITERION
- Surah 26 - Al Shu'ara' THE POETS
- Surah 27 - Al Naml THE ANTS
- Surah 28 - Al Qasas THE NARRATIONS
- Surah 29 - Al 'Ankabut THE SPIDER
- Surah 30 - Al Rum THE ROMANS
- Surah 31 - Luqman LUQMAN
- Surah 32 - Al Sajdah THE PROSTRATION
- Surah 33 - Al Ahzab THE CONFEDERATES
- Surah 34 - Saba' SHEBA
- Surah 35 - Fatir THE ORIGINATOR OF CREATION
- Surah 36 - Ya Sin YA SIN
- Surah 37 - Al Saffat THOSE RANGED IN RANKS
- Surah 38 - Sad SAD
- Surah 39 - Al Zumar CROWDS
- Surah 40 - Ghafir FORGIVER
- Surah 41 - Fussilat EXPOUNDED
- Surah 42 - Al Shura CONSULTATION
- Surah 43 - Al Zukhruf THE GOLD ADORNMENTS
- Surah 44 - Al Dukhan THE SMOKE
- Surah 45 - Al Jathiyah THE KNEELING DOWN
- Surah 46 - Al Ahqaf WINDING SAND-TRACTS
- Surah 47 - Muhammad MUHAMMAD
- Surah 48 - Al Fath THE VICTORY
- Surah 49 - Al Hujurat THE CHAMBERS
- Surah 50 - Qaf QAF
- Surah 51 - Al Dhariyat THE WINDS THAT SCATTER
- Surah 52 - Al Tur THE MOUNT
- Surah 53 - Al Najm THE STAR
- Surah 54 - Al Qamar THE MOON
- Surah 55 - Al Rahman THE MOST GRACIOUS
- Surah 56 - Al Waq'iah THE INEVITABLE
- Surah 57 - Al Hadid IRON
- Surah 58 - Al Mujadilah THE WOMAN WHO PLEADS
- Surah 59 - Al Hashr THE MUSTERING
- Surah 60 - Al Mumtahinah THAT WHICH EXAMINES
- Surah 61 - Al Saff THE BATTLE ARRAY
- Surah 62 - Al Jumu'ah FRIDAY
- Surah 63 - Al Munafiqun THE HYPOCRITES
- Surah 64 - Al Taghabun THE MUTUAL LOSS AND GAIN
- Surah 65 - Al Talaq DIVORCE
- Surah 66 - Al Tahrim PROHIBITION
- Surah 67 - Al Mulk THE DOMINION
- Surah 68 - Al Qalam THE PEN
- Surah 69 - Al Haqqah THE SURE REALITY
- Surah 70 - Al Ma'arij THE WAYS OF ASCENT
- Surah 71 - Nuh NOAH
- Surah 72 - Al Jinn THE SPIRITS
- Surah 73 - Al Muzzammil THE ENFOLDED ONE
- Surah 74 - Al Muddaththir THE ONE WRAPPED UP
- Surah 75 - Al Qiyamah THE RESURRECTION
- Surah 76 - Al Insan MAN
- Surah 77 - Al Mursalat THOSE SENT FORTH
- Surah 78 - Al Naba' THE GREAT NEWS
- Surah 79 - Al Nazi'at THOSE WHO TEAR OUT
- Surah 80 - 'Abasa HE FROWNED
- Surah 81 - Al Takwir THE FOLDING UP
- Surah 82 - Al Infitar THE CLEAVING ASUNDER
- Surah 83 - Al Mutaffifin THE DEALERS IN FRAUD
- Surah 84 - Al Inshiqaq THE RENDING ASUNDER
- Surah 85 - Al Buruj THE CONSTELLATIONS
- Surah 86 - Al Tariq THE NIGHT STAR
- Surah 87 - Al A'la THE MOST HIGH
- Surah 88 - Al Ghashiyah THE OVERWHELMING EVENT
- Surah 89 - Al Fajr THE DAWN
- Surah 90 - Al Balad THE CITY
- Surah 91 - Al Shams THE SUN
- Surah 92 - Al Layl THE NIGHT
- Surah 93 - Al Duha THE GLORIOUS MORNING LIGHT
- Surah 94 - Al Sharh THE EXPANSION OF THE BREAST
- Surah 95 - Al Tin THE FIG
- Surah 96 - Al Alaq THE CLINGING CLOT
- Surah 97 - Al Qadr THE NIGHT OF POWER
- Surah 98 - Al Bayyinah THE CLEAR EVIDENCE
- Surah 99 - Al Zalzalah THE EARTHQUAKE
- Surah 100 - Al 'Adiyat THOSE THAT RUN
- Surah 101 - Al Qari'ah THE GREAT CALAMITY
- Surah 102 - Al Takathur THE PILING UP
- Surah 103 - Al 'Asr TIME THROUGH THE AGES
- Surah 104 - Al Humazah THE SCANDALMONGER
- Surah 105 - Al Fil THE ELEPHANT
- Surah 106 - Quraysh THE TRIBE OF QURAYSH
- Surah 107 - Al Ma'un THE NEIGHBOURLY ASSISTANCE
- Surah 108 - Al Kawthar THE ABUNDANCE
- Surah 109 - Al Kafirun THOSE WHO REJECT FAITH
- Surah 110 - Al Nasr THE HELP
- Surah 111 - Al Masad THE PLAITED ROPE
- Surah 112 - Al Ikhlas THE PURITY OF FAITH
- Surah 113 - Al Falaq THE DAYBREAK
- Surah 114 - Al Nas MANKIND
- Acute Coronary Syndromes
- Angina Pectoris
- Anomalous Left Coronary Artery From the Pulmonary Artery
- Aortic Coarctation
- Aortic Dissection
- Aortic Regurgitation
- Aortic Stenosis
- Aortic Stenosis, Subaortic
- Aortic Stenosis, Supravalvar
- Ashman Phenomenon
- Atrial Fibrillation
- Atrial Flutter
- Atrial Myxoma
- Atrial Septal Defect
- Atrial Tachycardia
- Atrioventricular Block
- Atrioventricular Dissociation
- Atrioventricular Nodal Reentry Tachycardia (AVNRT)
- Benign Cardiac Tumors
- Brugada Syndrome
- Complications of Myocardial Infarction
- Coronary Artery Atherosclerosis
- Coronary Artery Vasospasm
- Digitalis Toxicity
- Dissection, Aortic
- Ebstein Anomaly
- Eisenmenger Syndrome
- First-Degree Atrioventricular Block
- HACEK Group Infections (Infective Endocarditis)
- Heart Failure - Decompensatio Cordis
- Holiday Heart Syndrome
- Hypertensive Heart Disease
- Junctional Rhythm
- Loeffler Endocarditis
- Long QT Syndrome
- Lutembacher Syndrome
- Mitral Regurgitation
- Mitral Stenosis
- Mitral Valve Prolapse
- Myocardial Infarction
- Myocardial Rupture
- Paroxysmal Supraventricular Tachycardia
- Patent Ductus Arteriosus
- Patent Foramen Ovale
- Pericardial Effusion
- Pericarditis Acute
- Pericarditis, Constrictive
- Pericarditis, Constrictive-Effusive
- Pulmonic Regurgitation
- Pulmonic Stenosis
- Right Ventricular Infarction
- Saphenous Vein Graft Aneurysms
- Second-Degree Atrioventricular Block
- Sinus of Valsalva Aneurysm
- Sudden Cardiac Death
- Tetralogy of Fallot
- Third-Degree Atrioventricular Block
- Torsade de Pointes
- Tricuspid Regurgitation
- Tricuspid Stenosis
- Unstable Angina
- Ventricular Fibrillation
- Ventricular Septal Defect
- Ventricular Tachycardia
- Wolff-Parkinson-White Syndrome