Examination of the Cranial Nerves

Post your experience There are 12 pairs of cranial nerves although the ophthalmic nerve is really an extension of the brain rather than a peripheral nerve. The ability to test them swiftly, efficiently and to interpret the findings should be a core competency for general practice. The article on Neurological History and Examination includes a description of a brief examination of the cranial nerves. Here the aim is to give a slightly fuller account of examination whilst interpretation of the findings is discussed elsewhere under cranial nerve lesions. There are also more specific articles on diplopia and cranial nerves and visual field defects. Principles of Examination There is no single way to perform a clinical examination but the following is offered as one effective way. Everyone should develop his own protocol. Protocols are easy to use, efficient in use of time and reduce the chance of missing something significant. With most examinations, the clinician will detect and interpret the signs. With neurological examination, especially of the sensory system, the doctor relies on the patient to interpret what he feels. He must be encouraged to report when there is a change in sensation or if anything feels different from normal. Very often there will not be an absence of sensation but a dulling or diminution and this is just as important. Comments such as, "I can feel it but it's not so sharp over there," are very useful. By and large, the muscles supplied by the cranial nerves are not as large and powerful as those supplied by spinal nerves, with the exception of those supplied by XI. The following table lists the grading of power for muscles of the limbs and it can be modified accordingly to give a meaningful scale. 0 1 2 3 4 5 Grading Muscle Power There is no muscle contraction Contraction may be felt by palpation but it is ineffective Active movement is possible with gravity eliminated. The muscle can overcome gravity but not resistance from the examiner The muscle group can move against some resistance from the examiner Full and normal power against resistance

It makes sense to examine the nerves in roughly numerical order but there are exceptions where nerves are best grouped together and their numbers may not be sequential. Olfactory Nerve Most of what we call taste is really smell. Testing the olfactory nerve is often omitted. Before starting, check that there is free flow of air by occluding each nostril in turn and asking the patient to sniff in. The nerves are tested by having bottles containing characteristic substances such as peppermint, coffee or heather and asking the patient to identify each in turn. If you do not have such tools available, ask the patient to close his eyes and then hold a bar of soap under

his nose for him to smell. It is possible to occlude one nostril and then the other to assess each side in turn. If there is doubt about the claim of anosmia, try testing with ammonia solution. Ammonia causes a physical irritation and so will cause an abreaction even in the presence of anosmia. Denying a response to ammonia suggests malingering. Ophthalmic Nerve Two important aspects of the optic nerve are visual acuity and visual field.

Visual Acuity
Visual acuity can easily be tested with Snellen type. Charts are also available to test ability to read small print. If the patient normally wears spectacles both tests may be done with them on as it may be assumed that they give good correction and that what is important is any rapid deterioration in visual acuity. Deterioration of at least 2 lines of the Snellen chart is significant. Colour vision can be tested with Ishihara plates. Deterioration may be significant but remember that 8% of men and 0.5% of women have congenital X-linked colour blindness.

Visual Fields
A small item, such as the top of a pen, may be used to test visual fields by confrontation. Sit about 50cm away from the patient and ask him to keep his eyes fixed on your nose. Hold the point half way between you and move it around, asking him to say when it disappears from view. If you also fix on his nose, you can compare his response with yours, taking your own as normal. Plotting visual field defects by confrontation is very crude and if an accurate picture is required, it is necessary to ask an optometrist to plot visual fields by perimetry.

Use of the Ophthalmoscope
Many people find use of the ophthalmoscope daunting. It can only be mastered with practice and this means using it over the course of years. Do not bother clicking through the lenses until you are adept in its use but use the 0 dioptre lens to view the retina. It is very difficult to see much through a small pupil in a bright room. It should be possible to take the patient to a darker room or to dim the light with curtains or a blind. Better still, a mydriatic agent such as 1% homatropine eyedrops can be used, provided that the patient does not have to drive for the rest of the day. The effect can last up to 24 hours. Take the ophthalmoscope and ask the patient to fix his gaze on something in the distance such as a picture on the wall and to ignore you. Do the pupils look equal? First shine the light on the eye and then remove it. The pupil should be brisk in its response of both constriction and dilatation. This is testing both the ophthalmic and oculomotor nerves as the response is dependent upon appreciation of light and the motor response of the muscles of the iris. There is also a consensual response in that the contralateral pupil will also respond but less markedly. Then use the ophthalmoscope to examine the eye. First hold it away from the patient and look through it at the eye. There should be an orange reflex from light reflected from the retina. This means that the lens is clear and there is no significant cataract. Check that the optic disc is clear.

Note the vessels of the retina and try to see the periphery. Repeat on the other side. It is not reasonable to assume that because one side is normal that the other side will be too. Only by seeing many normal discs is it possible to be confident about abnormality. Try to learn:

The normal colour of a disc. It is usually pink but in people with dark skin it appears grey. People with blond hair tend to have paler retinae than those with darker hair. Hair may go grey with the passage of time or blond or coloured with the contents of a bottle but the retina is constant. A clear and distinct optic disc. Only by be being familiar with a normal disc is it possible to recognise papilloedema when it occurs. Cupping of the disc, as with glaucoma, brings the vessels up over the disc. Learn to follow the 4 arteries and veins. Follow then to the periphery. Note tortuosity. Note any silver wiring or A-V nipping. The appearance of central retinal artery thrombosis and retinal vein thrombosis is described in the respective articles. A detached retina is avascular and may appear as a crescent or a grey cloud. Only by learning the normal appearance of a retina will such abnormalities as neovascularization, cotton wool spots and haemorrhages be recognised.

Oculomotor, Abducent and Trochlear Nerves These 3 nerves are examined together as they control the external ocular muscles. The oculomotor nerve supplies the internal muscles of the eye including sympthetic fibres to dilate the pupil and parasympathetic fibres to constrict it and to reduce the focal length of the lens for accommodation.

Internal Ocular Muscles
The pupillary response to light has already been tested. It is possible to complement this test by moving a finger from about 40cms to about 10cm from the patient's nose, asking him to follow it, and note if the pupil constricts in response to accommodation. This is not normally very marked. If the pupils are unequal, which eye is the abnormal one? • • • Darken the room and note if the difference increases. If it does the problem is due to failure of sympathetic tone to the smaller pupil. Brighten the room and if the difference increases, the problem is due to failure of parasympathetic tone to the larger pupil. If the difference remains constant in dim or bright light, the difference may be physiological.

Failure of sympathetic tone is a feature of Horner's syndrome that is discussed elsewhere. There is lack of sweating on that side of the forehead and possibly a ptosis too. Horner's syndrome is a very good lateralising sign but a poor localising sign. The Argyll-Robertson pupil is small, does not react to light, but constricts on accommodation. If it is bilateral, the pupils are frequently unequal in size (anisocoria). Argyll-Robertson pupils are almost always related to neurosyphilis but similar pupils are occasionally found in diabetic

neuropathy and in some hereditary neuropathies. The myotonic pupil (Holmes-Adie syndrome) reacts very slowly both to light and accommodation, but especially to light. It may be unilateral or bilateral and is commoner in women than men. Myotonic pupils may be associated with absence or depression of the tendon reflexes and occasionally with anhidrosis in the limbs.

External Ocular Muscles
Hold the patient's head still with the left hand and hold out the extended right index finger about 40cm in front of the patient. Ask him to follow your finger with his eyes. Move the finger up and down and left and right. There should be a full range of movements of both eyes. Note any ptosis or lid lag. Then move the finger to the left and hold it there for several seconds whilst the eyes are observed for nystagmus. Repeat to the right. False positive tests for nystagmus can result from holding the finger too close and by moving it too far to the extreme of vision. It may be apparent that some of the movements are incomplete in one eye. There may also have been a complaint of diplopia. A more sensitive way to test ocular movements is with a small torch. This test is also very useful when assessing children for strabismus and tends to be easier than the "cover test". • • • • Hold the torch about 40cms away and shine it in the patient's eyes. Note the reflection of the light in the centre of the pupil. Holding the patient's head still, move the torch up, down, left and right, asking him to follow the light with his eyes. Note if the reflection of the light becomes eccentric from any direction. If so, note in which pupil it was eccentric and the direction of stare. The lesion is in the muscle that moves that eye in that direction.

External Ocular Paralysis Muscle Direction of pull Result of paralysis Cranial nerve Medial rectus Medial Lateral III Superior rectus Upwards Downwards III Lateral rectus Laterally Medial VI Inferior rectus Downwards Upwards III Superior oblique Down and out Up and in IV Inferior oblique Up and out Down and in III The superior and inferior recti are set slightly medial to the midline. Hence they tend to move the eye slightly medially as well as up or down. This movement is offset by coordination with the lateral rectus and obliques.

Ignore the reflection in the pupils as the patient is not looking at the light. There is complete failure of the left eye to move laterally due to paralysis of the lateral rectus supplied by VI. Trigeminal Nerve The trigeminal nerve is largely a sensory nerve but it does have a motor component in the mandibular division. Lightly touch each side of the face with a piece of cotton wool and ask if it feels normal and symmetrical. Alternatively, a light touch with a finger will suffice. Test the areas supplied by the ophthalmic, maxillary and mandibular branches. The spinal nerves from segments C2,3 supply the face for about 3 fingers breadth in front of the ear. Ask the patient to clench his teeth. Both masseters should feel firm and strong. The contracting temporalis may also be felt. The pterygoids may jut the jaw forwards. Many neurologists omit the corneal reflex unless a sensory deficit is found, especially in the ophthalmic division, or if there is a lesion of another cranial nerve. Take a clean piece of cotton wool and ask the patient to look away from the side being tested. Gently touch the cornea with the cotton wool and the patient will blink. This requires the sensation of V but also the motor of VII. There may be a positive jaw jerk reflex in spasticity. This is difficult to elicit and is not described here. Facial Nerve • Ask the patient to give a broad toothy grin, demonstrating what you want. Do not say, "Show me your teeth," or he may remove his dentures and hand them to you. Is the grin full and symmetrical? Ask him to screw up his eyes. Gently try to prise them open. You should fail.

Ask him to raise his eyebrows. Are the furrows of the forehead symmetrical?

Paralysis of the facial nerve causes face drop. This is more marked with a lower motor neurone (LMN) lesion than an upper motor neurone (UMN) lesion. The best way to differentiate the two is to test the muscles of the forehead. They have bilateral innervation at the upper motor neurone level and so in a UMN lesion such as a pseudobulbar palsy, they are spared. A LMN lesion such as Bell's palsy will involve the forehead. Vestibulo-cochlear Nerve Testing of the vestibular component is described with such tests as Hallpike's manoeuvre in the article on vertigo. Formal testing of the cochlear component requires audiometry. Hearing tests are discussed elsewhere. Either whispering or use of a high frequency tuning fork can give a very crude assessment of hearing. A 516Hz (upper C) tuning fork is usually employed. • Strike the tuning fork and hold it about 2cm from the ear, asking the patient to tell you when it stops. Then listen to it yourself and the intensity of the sound indicates the degree of loss in that ear. If it is marked, place the still vibrating fork on the mastoid process and ask if it is heard. If it is heard by bone but not air conduction, there is a marked conductive loss. With profound nerve deafness, the patient may be hearing it by bone conduction in the other ear. If there is significant loss in one ear the Weber test can be employed. Strike the tuning fork and place it on the centre of the forehead. Ask the patient in which ear it seems louder. The vibration is conducted through bone and it will be quieter in the bad ear with nerve deafness but louder with conductive deafness as the affected ear becomes more sensitive.

Glossopharyngeal and Vagus Nerves Assessment of the glossopharyngeal and vagus nerves is difficult. Ask the patient to swallow. Is there any difficulty? Ask the patient to open his mouth wide and to say, "Arhh". Phonation should be clear and the uvula should not move to one side. The quality of the dysarthria differs for central and peripheral lesions. Central lesions produce a strained, strangled voice quality, while peripheral lesions produce a hoarse, breathy and nasal voice. It is also possible to test the gag reflex by touching the pharynx with a tongue depressor. Most people omit this unless there is evidence of a local lesion. It is unpleasant and around 20% of normal people have a minimal or absent response. Isolated lesions of the IX nerve are very rare. Taste to the anterior two thirds of the tongue travels with the VII nerve until it leaves in the chorda tympani to join the V nerve. The posterior third of the tongue is supplied from the IX nerve that also provides parasympathetic fibres to the salivary glands. It is possible to test taste with small bottles and a dropper. The bottles usually contain sugar or sale solution. Most generalists do not perform this test. Hypoglossal Nerve

It is often more convenient to assess the XII cranial nerve before the XI as the mouth is examined for IX and X. Ask the patient to protrude his tongue and note any deviation. A fluttering motion called fibrillation rather than fasiculation may be seen with a lower motor neurone lesion. If the tongue deviates to one side when protruded, this suggested a hypoglossal nerve lesion. If it is a lower motor neurone lesion, the protruded tongue will deviate towards the side of the lesion.With an upper motor neurone lesion, the tongue will deviate away from the side of the lesion.

Note the wasted left side of the tongue and deviation to the left suggesting a left lower motor neurone lesion. Accessory Nerve The accessory nerve supplies the trapezius and sternomastoid muscles. Is there any wasting? Ask the patient to shrug his shoulder up and try to push them down. Ask him to push his head forwards against your hand. Both these movements should be very difficult to resist. LMN lesions produce weakness of both muscles on the same side. UMN lesions produce ipsilateral sternomastoid weakness and contralateral trapezius weakness, because of differing sources of cerebral innervation. This article is far from exhaustive and the 2 Internet sites below give further detail. The second site also offers video if sound and Realplayer are available. Internet and further reading

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Russell F, Triola R;; The Precise Neurological Examination.; From New York University School of Medicine.; Cranial Nerves Blumfield H; Neuroanatomy through Clinical Cases; Cranial Nerves

This is a PatientPlus article. PatientPlus articles are written for doctors and so the language can be technical. However, some people find that they add depth to the articles found in the other sections of this website which are written for non-medical people.

Neurological History and Examination
Post your experience • Taking a detailed history and performing a careful examination can help the doctor to determine the site of a specific neurological lesion and reach a diagnosis, or at least differential diagnoses.1 A systematic approach is required. This is a general article, attempting to cover all aspects of neurological history and examination. You are referred to other related articles where relevant for more detail. Mental state examination may also be an important consideration and this is covered in the separate article Mini Mental State Examination (MMSE). Gait: ○ ○ ○ • Look at the patient's gait as they walk in to the room. Is there evidence of e.g. hemiparesis, footdrop, ataxic gait, a typical Parkinsonian gait. Separate articles discuss Abnormal Gait and Gait Disturbance in Children in more detail. Is there a problem with articulation (dysarthria)? Here comprehension is retained and speech construction is normal. There is usually weakness or incoordination of the orolingual muscles. Ask the patient to say 'West Register Street' if you are uncertain.1 Is there a problem with phonation (dysphonia)? This is usually due to laryngeal problems which can cause voice hoarseness. There may be reduced speech volume.1 Is there a problem with language function (dysphasia)? This is due to a lesion in the language areas of the dominant hemisphere. A separate article discusses Dysarthria and Dysphasia in more detail.

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Observation of the patient •

Speech: ○

○ ○ •

Involuntary movements:

○ History

Is there evidence of, e.g. tremor, tics, chorea, hemiballismus, orofacial dyskinesias?

Specific emphasis should be placed on the following:

Presenting complaint
• Ask about the symptoms: ○ ○ ○ ○ ○ ○ ○ • What are they? Which part of the body do they affect? Are they localised or more widespread? When did they start? How long do they last for? Were they sudden, rapid or gradual in onset? Is there a history of trauma? Are the symptoms static or deteriorating, or are there exacerbations and remissions? Does anything trigger the symptoms, e.g. exercise, sleep, posture or external stimuli such as light or smell? Headache Numbness, pins and needles, cold or warmth Weakness, unsteadiness, stiffness or clumsiness Nausea or vomiting Visual disturbance Altered consciousness Psychological changes, e.g. agitation, tearfulness, depression or elation, sleep disturbance For children ask about performance at school

Ask about any associated symptoms (other features of neurological disease):1 ○ ○ ○ ○ ○ ○ ○ ○

Try to understand how the symptoms may affect the patient's life, ask about activities of daily living.

Past medical history
Some neurological problems can present years after a causative event.1
• Enquire about other medical problems, past and present. These may give clues to the diagnosis. For example: ○ ○ ○ A person in atrial fibrillation may be producing multiple tiny emboli. There may be vascular problems or recurrent miscarriage to suggest antiphospholipid syndrome. There may be diabetes.

• •

Ask about pregnancy, delivery and neonatal health. Ask about any infections, convulsions or injuries in infancy, childhood or adult life. Particularly ask about head or spinal injury, meningitis or encephalitis.

Systematic enquiry
The systematic enquiry is very important here. For example:
• • • Loss of weight and appetite may suggest malignancy and this may be a paraneoplastic syndrome. Gain in weight may have precipitated diabetes. Polyuria may suggest diabetes. Difficulty with micturition or constipation may be part of the neurological problem but was not volunteered in the general history. In men, enquire about erectile dysfunction. Note smoking and drinking habits. Alcohol is a significant neurotoxin, both centrally and peripherally. Ask about drugs including prescribed, over-the-counter and illicit. This includes complementary and alternative medicines. Ask about occupation and what it involves. There may be exposure to toxins. Is repetitive strain injury likely? Is there prolonged visual work which may predispose to tension headache or migraine?1 The job may involve driving but the patient has admitted to convulsions. He may work at heights or in a dangerous environment. Ask about marital status. Has there been recent bereavement or divorce which may have affected symptoms? Ask about sexual orientation and consider likelihood of sexually transmitted infection, e.g. syphilis, HIV

Social history
• • •

• •

Family history
Consider if there may be a genetic basis or predisposition.1 For example:
• • • A cousin with Duchenne muscular dystrophy or Becker muscular dystrophy would be very important for a boy who cannot run like his peers. Huntingdon's chorea is unusual in that it is a familial disease that does not present until well into adult life. A family history of, e.g. type 2 diabetes, cerebral aneurysm, neuropathies, epilepsy, migraine or vascular disease may be important.1

Examination

Examination of speech1
• • Look for spontaneous speech, fluency and use of appropriate words during conversation. Ask the patient to name objects.

• • • •

Ask the patient to carry out some commands to assess their comprehension. Ask the patient to read aloud. This can show evidence of any dyslexia. Ask the patient to repeat a simple sentence. Inability to do this suggests a conduction dysphasia. Look at the patient's handwriting. There may be problems with form, grammar or syntax which may suggest a more global language problem and not just a speech disorder. Examine the neck movements: ○ Is there evidence of degenerative disease which may be producing radicular symptoms in the upper limbs? Examine flexion, extension and rotation. Look for Lhermitte's sign. This is when neck flexion causes an electric shock-like feeling on the limbs. It is due to disease in cervical spinal cord sensory tracts (seen in, e.g. multiple sclerosis, syringomyelia, tumours).1 Is there any neck stiffness (can be a sign of meningeal irritation)? The chin can normally touch the chest when the neck is flexed but this is not possible if neck stiffness is present. This may be a sign of meningitis or subarachnoid haemorrhage. Look for enlarged lymph nodes or cervical ribs. Listen at the carotid bifurcation at the angle of the jaw for carotid bruits. Listen over the supraclavicular fossa for vertebral or subclavian bruits. A common carotid bruit may be heard by listening between these two sites. Listen with the bell of the stethoscope over a closed eyelid for bruits due to cerebral arteriovenous malformations. Listen for cardiac murmurs to ensure that any bruit heard is not just due to transmission of these. Note that just because a bruit is not heard, it does not mean that there is no significant stenosis present.

Examination of the neck

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Palpate the supraclavicular fossae: ○ ○ ○ ○ ○ ○ ○ Listen for any bruits:1

Cranial nerves
• Examination of the cranial nerves takes practice. The cranial nerves and their function is summarised below.2 ○ ○ ○ I (olfactory nerve): smell II (optic nerve): visual acuity, visual fields and ocular fundi II, III (optic nerve and oculomotor nerve): pupillary reactions

○ ○ ○ ○ ○ ○ ○ ○ •

III, IV, VI (oculomotor, trochlear and abducent nerves): extra-ocular movements, including opening of the eyes V (trigeminal nerve): facial sensation, movements of the jaw, and corneal reflexes VII (facial nerve): facial movements and gustation VIII (vestibulocochlear nerve): hearing and balance IX, X (glossopharyngeal and vagus nerves): swallowing, elevation of the palate, gag reflex and gustation V, VII, X, XII (trigeminal, facial, vagus and hypoglossal nerves): voice and speech XI (accessory nerve): shrugging the shoulders and turning the head XII (hypoglossal nerve): movement and protrusion of tongue

A separate article describes Examination of the Cranial Nerves in detail.

Brief cranial nerve examination
• Olfactory nerve: ○ Tested using bottles containing characteristic substances such as peppermint, coffee or vanilla and ask the patient to identify each in turn. Test each nostril separately and occlude the other. Patient's eyes should be closed. If such bottles are not available, simply ask the patient if he has any problems with smell or taste. Remember that most of what we call taste is really smell. Visual acuity can easily be tested with a Snellen chart. If the patient normally wears spectacles, they should wear these. Test the visual fields by confrontation. Sit about 40cm away from the patient and ask them to keep their eyes fixed on your nose. Ask them to cover one eye. Hold your finger half way between you and the patient with your arm extended. Test each quadrant of their visual field in that eye by moving your finger laterally to medially along the diagonal. Move inwards from the periphery at a number of points in the upper and lower, nasal and temporal quadrants. Ask the patient when your finger appears into view. If you also fix on their nose, you can compare their response with yours, taking your own as normal. Repeat for the other eye. Take the ophthalmoscope and ask the patient to fix their gaze on something in the distance. First shine the light on each eye and then remove it. The pupil should be brisk in its response. Check direct and consensual reflexes (the reaction of the pupil on the side that you shine the light in is called the direct light reflex; the constriction of the other

○ ○ ○ ○ • ○ ○

Optic nerve:

pupil is the consensual light reflex). ○ ○ Test accommodation by asking the patient to look in the distance and then at an object close up. Look for any change in pupil size. Then use the ophthalmoscope to examine the back of each eye. Check that the optic disc is clear and that there is no papilloedema. Note the vessels of the retina and try to see the periphery. Hold the patient's head still with your left hand on their forehead. With your arm extended, hold out your right index finger about 40cm in front of the patient. Ask them to follow your finger with their eyes. Move your finger up and down and left and right. There should be a full range of movements of both eyes. Then move the finger to the left and hold it there for several seconds whilst the eyes are observed for nystagmus. Repeat to the right and up and down. False positive tests for nystagmus can result from holding the finger too close and by moving it too far to the extreme of vision. Test convergence by bringing in your finger from a distance towards the tip of the patient's nose and asking them to focus on it. Lightly touch each side of the face in the three sensory regions (forehead, cheek/side of nose and chin) and ask if it feels normal and symmetrical. Ask the patient to clench their teeth. Both masseters should feel firm and strong. Ask the patient to open their jaw against resistance.1 In this brief assessment it is fair to omit the corneal reflex. Ask the patient to give a smile, demonstrating what you want. Is it full and symmetrical? Ask them to screw up their eyes. Gently try to prise them open. You should fail. If there is any facial weakness, ask them to raise their eyebrows. The upper motor neurone innervation of the muscles of the forehead is bilateral. Hence a lower motor neurone lesion will cause asymmetry but an upper motor neurone lesion will not. Either whispering into each ear or using a high frequency tuning fork can give a very crude assessment of hearing. The separate article entitled Hearing Tests gives more details. Ask the patient to open their mouth wide and to say, "Arhh". Phonation should be clear and the uvula should not move to one side. Elicit the gag reflex by touching the tonsil or the pharynx. There should be elevation of the pharynx and the palate. Test each side.1 Ask the patient to puff out the cheeks.

Oculomotor, trochlear and abducent nerves: ○ ○ ○ ○ ○

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Trigeminal and facial nerves: ○

Vestibulocochlear nerve: ○

Glossopharyngeal, vagus nerves: ○ ○ ○

Accessory nerve: ○ ○ This nerve supplies the trapezius and sternomastoid muscles. Ask the patient to shrug their shoulders up and try to push them down. Then ask them to rotate their head to the right against resistance on the right side of the chin from your hand. Repeat for the left side. Both these movements should be very difficult to resist. Ask the patient to protrude their tongue and note any deviation or wasting. Assess tongue movement from side to side.1

Hypoglossal nerve: ○

Examination of the sensory system
There are separate articles that describe sensory examination in detail:
• • Neurological Examination of the Upper Limb Neurological Examination of the Lower Limb

Both the upper and lower limbs should be examined. Work in a methodical way. A logical progression is required when examining each sensory modality.
• With the lower limbs, you may want to start testing over the groin and to move down the front of the leg and up the posterior side as this moves progressively from L1 to S3 dermatomes. With the upper limbs, you may want to start testing over the shoulder and to move along the lateral aspect of the arm and up the medial side as this moves progressively from C4 to T3 dermatomes. The dermatomal (segmental) and peripheral nerve innervation is labelled in the diagrams below.

The following sensory modalities should be tested: • Light touch and pin prick (sharp touch) ○ ○ Both light touch and pin prick are conducted along the same pathways. Light touch can be tested by using a light touch of the finger, a piece of cotton wool or a small brush. It is important to touch and not to stroke as moving sensations, such as rubbing and scratching are conducted along pain pathways. Test sharp touch using a dedicated disposable pin. Test light touch using the light touch of a finger, a piece of cotton wool or a piece of tissue paper. One approach is to touch the patient with a tuning fork as the metal feels cold. Containers of warm and cool water may be used for more accurate assessment. Ask the patient to distinguish between warm and cool on different areas of the skin with their eyes closed.1 This can be tested at the distal interphalangeal joint of the index finger and at the interphalangeal joint of the big toe. The examination technique is described in the articles on neurological examination of the upper and lower limbs. This can be examined using vibrating 128 Hz tuning fork. Please refer to the above mentioned articles for examination technique. This is usually just performed on the pulp of the fingers using a twopoint discriminator. The technique is described in the article neurological examination of the upper limbs (link below).

Temperature ○ ○

Proprioception (joint position sense) ○ ○

Vibration sense ○ ○

Two-point discrimination ○ ○

Examination of the motor system
There are separate articles that describe motor examination in detail:
• • Neurological Examination of the Upper Limb (click here) Neurological Examination of the Lower Limb (click here)

Both upper and lower limbs should be examined. The following gives a brief outline of the examination.
• Inspection ○ Start by looking at the patient.

○ ○

Note the resting posture. Is there unusual rotation or posture of a joint? Is the patient symmetrical? Look for muscle wasting or hypertrophy. Is it focal or diffuse? An upper motor neurone (UMN) lesion will produce disuse atrophy but a lower motor neurone (LMN) lesion or myopathy will produce much more marked wasting. Look for muscle fasciculation (sign of lower motor neurone disease process). These are subcutaneous twitches over a muscle belly at rest. Tapping the belly may stimulate fasciculation.1 Hypertonia is found in upper motor neurone lesions; hypotonia is found in lower motor neurone lesions and cerebellar disorders.1 In the upper limbs:    Ask the patient to let their shoulders and arms 'go floppy'. Flex and extend their shoulder passively and feel for abnormality of tone. Repeat for the elbow and wrist. Ask the patient to let their legs 'go floppy'. Internally and externally rotate the 'floppy' leg. Assess for any increased or reduced tone. Then lift the knee off the bed with one of your hands. Does the ankle raise off the bed as well signifying increased tone? Ankle clonus can also be tested and is discussed in the article on Neurological Examination in the Lower Limbs.

Tone ○ ○

In the lower limbs:    

Power ○ ○ ○ As with sensation, test each group of muscles in a systematic order. The Medical Research Council (MRC) has a recommended grading system for power (see table). Examination of power in both the upper and lower lower limbs is described in the articles on neurological examination of the upper and lower limbs and so will not be repeated here.

MRC scale for muscle power 0 No muscle contraction is visible 1 Muscle contraction is visible but there is no movement of the joint 2 Active joint movement is possible with gravity eliminated 3 Movement can overcome gravity but not resistance from the examiner The muscle group can overcome gravity and move against some resistance 4 from the examiner 5 Full and normal power against resistance

Deep tendon reflexes ○ ○ ○ Eliciting deep tendon reflexes requires good technique and an appropriate tendon hammer is required. How to elicit the various tendon reflexes is described in the articles on neurological examination of the upper and lower limbs. Tendon reflexes tend to be brisk when there is an UMN lesion and depressed in a LMN lesion. Isolated loss of a reflex can point to a radiculopathy affecting that segment. Reflexes can either hyperactive (+++), normal (++), sluggish (+) or absent (-). ± is used when the reflex is only present on reinforcement.1 In the lower limbs, this is the plantar response. To elicit this, the patient should be lying down with their legs extended. Use a blunted point and run this along the lateral border of the foot, starting at the heel and moving towards the big toe. Stop on the first movement of the big toe. An extensor plantar response (upgoing big toe) is pathological and signifies an upper motor neurone lesion. The cerebellum helps in the coordination of voluntary, automatic and reflex movement.1 Tests of cerebellar function in the upper limbs are described in the article neurological examination of the upper limbs (link above) and include:   ○ The finger-nose test Rapid alternating movement

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Superficial tendon reflexes ○ ○ ○ ○ ○

Coordination ○ ○

Tests of cerebellar function in the lower limbs are described in the article neurological examination of the lower limbs and include:   The heel-shin test The heel-toe test

Romberg's test examines lower limb cerebellar function but also tests balance mechanisms that rely on the cerebellar, vestibular and proprioceptive systems.    Ask the patient to keep their eyes open and stand with their feet together, arms by their sides. Then ask them to maintain this position when they close their eyes. Patients who have cerebellar lesions often cannot stand in this position even with their eyes open. If balance is only lost when

the eyes are closed, this signifies a proprioceptive or vestibular lesion.1  Be ready to catch the patient by standing behind.

Document references 1. Macleod's Clinical Examination. Churchill Livingstone. 2000. 2. Russell F, Triola R;; The Precise Neurological Examination.; From New York University School of Medicine.; Cranial Nerves 3. Russell F, Triola R;; The Precise Neurological Examination.; From New York University School of Medicine.; Cranial Nerves Internet and further reading • • Russel S, Triola M; The Precise Neurological Exam. From New York University School of Medicine. Blumenfeld H; Neuroexam.com. Neurological examination including short realtime demonstrations.; requires Realplayer and sound turned on.

Acknowledgements EMIS is grateful to Dr M Preston for writing this article. The final copy has passed scrutiny by the independent Mentor GP reviewing team. ©EMIS 2009. Document ID: 2509 Document Version: 22 Document Reference: bgp59 Last Updated: 19 Feb 2009 Planned Review: 19 Feb 2011

The authors and editors of this article are employed to create accurate and up to date content reflecting reliable research evidence, guidance and best clinical practice. They are free from any commercial conflicts of interest. Find out more about updating.

PATIENT UK Hearing Impairment Survey
We are investigating the sorts of problems people with any form of deafness have when attending surgery. If you have hearing problems we would be grateful if you could complete our (anonymous and non-commercial) survey. We will publish the results on Patient UK once we have gathered sufficient numbers (eg 250).

Facial Pain

Post your experience See others (3 there) Facial pain has a long list of possible causes but the diagnosis can often be made by a good history and examination. The common causes are often benign and self-limiting but it is essential not to miss those conditions that require urgent treatment, e.g. temporal arteritis, or early diagnosis, e.g. malignancy. There is a tendency to overdiagnose bacterial sinusitis when the real cause may be a viral upper respiratory tract infection or, much less frequently, a more serious cause of facial pain. Causes •
• • • • • • • • • • • • • •

Sinus: sinusitis, trauma, carcinoma Nose: upper respiratory tract infection, nasal injury and foreign bodies Ear: otitis media, otitis externa Mastoid: mastoiditis Teeth: dental abscess Neurological: trigeminal neuralgia, herpes zoster Parotid gland: mumps, other causes of parotitis, abscess, duct obstruction, calculi, tumour Eye: orbital cellulitis, glaucoma Temporomandibular joint dysfunction and pain Cluster headaches, migraine Temporal arteritis Tumours: nasopharyngeal, oral, posterior fossa Bone: maxillary or mandibular osteitis, cyst Atypical facial pain: more common in the elderly and in women; often linked with depression Lung cancer (upper lobe)1

Presentation

Symptoms
• Site: ○ Pain in the region of the ear may be referred from the skin, teeth, tonsils, pharynx, larynx or neck. ○ Tenderness over the maxilla may be due to sinusitis, dental abscess or carcinoma. • Character: ○ Trigeminal neuralgia: intermittent sharp, severe pain in the distribution of the divisions of the trigeminal nerve. ○ Infections of teeth, mastoid and ear: often dull, aching quality.

Precipitating factors:

Precipitated by food or chewing: dental abscess, salivary gland disorder, temporomandibular joint disorder or jaw claudication due to temporal arteritis.

○ Trigeminal neuralgia: even slightest touch of the skin causes intense pain. • Associated symptoms:
○ ○ ○

Obstruction of the lacrimal duct by nasopharyngeal carcinoma may cause watering of the eyes. Otorrhoea and/or hearing loss suggest an ear or mastoid cause. Nasal obstruction and rhinorrhoea may be due to maxillary sinusitis or carcinoma of the maxillary antrum. Carcinoma of the maxillary antrum may also present with unilateral epistaxis. Proximal muscle weakness and pain may be due to polymyalgia rheumatica, associated with temporal arteritis.

Signs
• • • • • •

Unilateral erythema and vesicles in the distribution of the trigeminal nerve: herpes zoster infection (may not be present in the early stages of the disease). Localised erythema or swelling: localised infection or carcinoma. Inspection of nose and throat may demonstrate a nasopharyngeal tumour. Facial palsy: may be due to a tumour of the parotid gland. Tenderness of the superficial temporal artery associated with temporal arteritis. Cervical lymphadenopathy: infection or carcinoma. Full blood count: raised white cell count in infection or malignancy. ESR, CRP: increase in infection, malignancy, temporal arteritis. X-rays:
○ ○ ○

Investigations •

Opacification of the sinus and destruction of bone with carcinoma of sinuses. Opacification may also occur in sinusitis. Mastoid films may show opacification in cases of mastoiditis.

• • •

CT or MRI scan: carcinoma sinuses, nasopharyngeal carcinoma, parotid conditions. Extent of tumours and invasion. Sialography: parotid conditions, e.g. duct stones, sialectasis. Fine needle aspiration: parotid tumours. The essential aspect of management in primary care is to make an accurate diagnosis. The management will then depend on the identified cause of facial pain. Tricyclic antidepressants may be useful for persistent pain.

Management •