The Nervous System Flashcards
Neurological history: An approach to neurological symptoms
Symptoms can vary wildly in neurology. The exact nature of the symptom. The onset (sudden? slow- hours? days? weeks? months?). Change over time (progressive, intermittent, episodes of recovery). Precipitating factors. Exacerbating and relieving factors. Previous episodes of the same symptom. Previous investigations and treatment. Associated symptoms. Any other neurological symptoms.
Neurological history: Dizziness
Narrow the exact meaning down without appearing aggressive or disbelieving.
A sense of rotation = vertigo.
Swimminess or lightheadedness- a non-specific symptoms which can be related to pathology in many different systems.
Pre-syncope- the unique feeling prior to fainting.
Incoordination- many will say they are dizzy when they can’t walk straight due to either ataxia or weakness.
Neurological history: Headache
This should be treated as any other type of pain.
Establish character, severity, site, duration, time course, frequency, radiation, aggravating and relieving factors, and associated symptoms.
Ask about facial and visual symptoms.
Neurological history: Numbness and weakness
These 2 words are often confused by patients- describing a leg as ‘numb’ when it is weak with normal sensation.
May report numbness when they are experiencing pins and needles or pain.
Neurological history: Tremor
Does the tremor occur only at rest, only when attempting an action, or both?
Is it worse at any particular time of day?
Severity can be established in terms of its functional consequence (can’t hold a cup/ put food to mouth?).
Establish what is being described- a tremor is a shaking, regular, or jerky involuntary movement.
Neurological history: Common symptoms
Dizziness Headache Numbness and weakness Tremor Syncope Seizures Visual symptoms Falls and loss of consciousness
Neurological history: Falls and loss of consciousness
An eyewitness account is vital.
Establish also whether the patient actually lost consciousness or not.
People often describe ‘blacking out’ when in fact they simply fell to the ground (drop attacks have no LOC).
‘Can you remember hitting the ground?’
Ask about preceding symptoms and warning signs- may point towards a different organ system (sweating or weakness could be a marker of hypoglycaemia, palpitations may indicate a cardiac dysrhythmia).
Neurological history: Seizures
Establish early on if there was any impairment of consciousness and seek collateral histories.
Syncopal attacks can often cause a few tonic-clonic kegs which may be mistaken for epilepsy.
True tonic-clonic seizures may cause tongue-biting, urinary and faecal incontinence, or both.
People presenting with pseudoseizure can have true epilepsy, as well as vice versa.
Neurological history: Visual symptoms
Commonly visual loss, double vision, or photophobia (pain when looking at bright lights).
Establish what is being experienced- ‘double vision’ (diplopia) is often complained of when the visit is blurred or sight is generally poor (amblyopia) or clouded.
Neurological history: Direct questioning for specific symptoms
Headaches.
Faints, fits and ‘funny turns’, and ‘blackouts’.
Visual symptoms.
Pins and needles, tingling.
Numbness.
Weakness.
Incontinence, constipation, or urinary retention.
Neurological history: Past medical history
A birth history is important here, particularly in patients with epilepsy- brain injury at birth has neurological consequences. Hypertension- if so, what treatment? Diabetes mellitus- what type? what treatment? Thyroid disease. Mental illness (e.g. depression). Meningitis or encephalitis. Head or spinal injuries. Epilepsy, convulsions, or seizures. Cancers. HIV/AIDs.
Neurological history: Drug history
Anticonvulsant therapy (current or previous)? Oral contraceptive pill? Steroids? Anticoagulants? Anti-platelet agents? Tobacco, alcohol?
Neurological history: Family history
Ask about neurological diagnoses and evidence of missed diagnoses (seizures, blackouts, etc.).
Neurological history: Social history
Occupation: neurological disease can impact significantly on occupation so ask about this at an early stage- some suggest right at the beginning of the history; also ask about exposure to heavy metals or other neurotoxins.
Driving?- many neurological conditions have implications here.
Ask about the home environment thoroughly (will be very useful when considering handicaps and consequences of the diagnosis).
Ask about support systems- family, friends, home-helps, day centre visits, etc.
Neurological history: Characteristic headaches
Tension Subarachnoid haemorrhage Sinusitis Temporal (giant cell) arteritis Meningitis Cluster Raised intracranial pressure Migraine
Neurological history: Characteristic headaches, tension
Bilateral- frontal, temporal.
Sensation of tightness radiating to neck and shoulders.
Can last for days.
No associated symptoms.
Neurological history: Characteristic headaches, subarachnoid haemorrhage
Sudden, dramatic onset ‘like being hit with a brick’.
Occipital initially, may become generalised.
Associated with neck stiffness and sometimes photophobia.
Neurological history: Characteristic headaches, sinusitis
Frontal, felt behind the eyes or over the cheeks.
Ethmoid sinusitis is felt deep behind the nose.
Overlying skin may be tender.
Worse on bending forwards.
Lasts 1-2 weeks, associated with coryza.
Neurological history: Characteristic headaches, temporal (giant cell) arteritis
Diffuse, spreading from the temple- unilateral.
Tender overlying temporal artery (painful brushing hair).
?jaw claudication whilst eating.
?blurred vision- can lead to loss of vision if severe and untreated.
Neurological history: Characteristic headaches, meningitis
Generalised.
Associated with neck stiffness and signs of meningism.
Nausea, vomiting, photophobia.
Purpuric rash is caused by septicaemia, not meningitis per se.
Neurological history: Characteristic headaches, cluster
Rapid onset, usually felt over one eye.
Associated with a blood-shot, watering eye, and facial flushing.
May also have rhinorrhoea.
Last for a few weeks at a time.
Neurological history: Characteristic headaches, raised intracranial pressure
Generalised headache, worse when lying down, straining, coughing, on exertion, or in the morning.
Headache may also wake the patient in the early hours.
May be associated with drowsiness, vomiting, and focal neurology.
Neurological history: Characteristic headaches, migraine
Unilateral- rarely crosses the midline.
Throbbing/pounding headache.
Associated with photophobia, nausea, vomiting, and neck stiffness.
May have preceding aura.
Neurological examination: Framework
Inspection, mood, conscious level. Speech and higher mental functions. Cranial nerves II-XII. Motor system. Sensation. Coordination. Gait. Any extra tests. Other relevant examinations, e.g. skull, spine, neck stiffness, ear drums, blood pressure, anterior chest, carotid arteries, breasts, abdomen, lymph nodes.
Neurological examination: General inspection and mental state
Are they accompanied by carers- and how do they interact with those people?
Do they use any walking aids or other forms of support?
Any abnormal movements?
Observe the gait as they approach the clinic room, if able.
Any speech disturbance?
What is their mood like?- ask the patient how they feel. what is the state of their clothing, hair, skin and nails? restlessness, inappropriately high spirits, pressure of speech? obviously depressed with disinterest? denying disability?
Neurological examination: Cognitive function, The Abbreviated Mental Test Score
AMTS (10 points) is a brief screening tool.
Neurological diseases may affect function such that patients’ appearance or communication skills are at odds with their educational level- formal assessment allows for any future change to be noted and monitored.
Explain the purpose of the questions and ask their permission to proceed.
1) Date of birth: ‘What is your date of birth?’
2) Age: ‘How old are you?’
3) Time: ‘What time is it?’
4) Year: ‘What year is it now?’
5) Place: ‘Where are we?’ or ‘What is this place?’
6) Head of state: ‘Who’s the Prime Minister at the moment?’ or ‘Who is the current monarch?’
7) War II: ‘What year did the second world war start?
8) 5-minute recall: Tell the patient an address (e.g. 42 West Street) and ask them to repeat it back to you to ensure they’ve heard it correctly. Ask them to remember it. 5 minutes later, ask them to recall the address- must remember in full to score the point.
9) 20-1: ‘Count backwards from 20 to 1. Patients sometimes need a prompt, ‘follow on from me: 23, 22, 21…’
10) Recognition: ‘What job do I do?’ and ‘What job does this person do?’ - both must be correct to score the point.
Neurological examination: Speech and language
Speech and language problems may be evident from the start of the history and require no formal testing.
You should briefly test language function by asking the patient to read or obey a simple written command (e.g. close your eyes) and write a short sentence.
If apparently problematic, speech can be tested formally by asking the patient to respond to progressively harder questions: yes/no questions, simple statements or instructions, more complicated sentences, and finally by asking them to repeat complex phrases or tongue-twisters.
Before jumping to conclusions, ensure that the patient is not deaf (or that their hearing aid is working) and that they can usually understand the language you are speaking.
Neurological examination: Speech and language, dysarthria
A defect of articulation with language function intact (writing will be unaffected).
There may be a cerebellar lesion, an LMN lesion of the cranial nerves, an extrapyramidal lesion, or a problem with muscles in the mouth and jaws or their nerve supply.
Listen for slurring and the rhythm of speech.
Test function of different structures by asking the patient to repeat: ‘yellow lorry’ or words with ‘d’, ‘l’ and ‘t’ (tongue function); ‘peter piper picked a pickle’ or words with ‘p’ and ‘b’ (lip function).
Cerebellar lesions: slow, slurred, low volume with equal emphasis on all syllables (‘scanning’).
Facial weakness: speech is slurred.
Extrapyramidal lesions: monotonous, low volume and lacking in normal rhythm.
Neurological examination: Speech and language, dysphonia
Defective volume- huskiness.
Usually from laryngeal disease, laryngeal nerve palsy or, rarely, muscular disease such as myasthenia graves.
May also be ‘functional’ (psychological).
Neurological examination: Speech and language, dysphasia
This is a defect of language, not just speech, so reading and writing may also be affected (some patients attempt to overcome speaking difficulties with a notepad and pen only to be bitterly disappointed).
Types: expressive, receptive, conductive, nominal, and global.
Neurological examination: Speech and language, expressive dysphasia
‘Anterior’, ‘motor’, ‘Broca’s’ dysphasia.
Lesion in Broca’s area (frontal lobe), involved in language production.
Understanding remains intact.
Unable to answer questions appropriately.
Speech is non-fluent, broken with abnormal word ordering.
Unable to repeat sentences.
Neurological examination: Speech and language, receptive dysphasia
‘Posterior’, ‘sensory’, ‘Wernicke’s’ dysphasia.
Lesion in Wernicke’s area creates problems understanding spoken or written language (dyslexia) and problems with word-finding.
Unable to understand commands or questions.
Speech is fluent with lots of meaningless grammatical elements.
May contain meaningless words.
Unable to repeat sentences.
Patients are often unaware of their speech difficulty and will talk nonsense continually- although may become frustrated with other people’s lack of understanding.
Neurological examination: Speech and language, conductive dysphasia
Lesion in the arcuate fascicles and/or other connections between the 2 primary language areas.
Patient can comprehend and respond appropriately.
Unable to repeat a sentence.
Neurological examination: Speech and language, nominal dysphasia
All language function is intact except for naming of objects.
Caused by lesion at the angular gyrus.
Patient may function with ‘circumlocution’, e.g. says ‘that thing I write with’ instead of ‘pen’.
Neurological examination: Speech and language, global dysphasia
Both Broca’s and Wernicke’s areas affected.
The patient is unable to speak or understand speech at all.
Neurological examination: Cranial nerve I, olfactory, applied anatomy
Sensory: smell.
Motor: none.
Fibres arise in the mucous membrane of the nose.
Axons pass across the cribriform plate to the olfactory bulb.
The olfactory tract runs backwards below the frontal lobe and projects, mainly, in the uncut of the ipsilateral temporal lobe.
Neurological examination: Cranial nerve I, olfactory, examination
Not routinely tested unless the patient complains of a loss of sense of smell (anosmia) and exhibits other signs suggestive of a frontal or temporal lobe cause (e.g. tumour).
‘Have you noticed any change in your sense of smell or taste recently?’
Casual: take a nearby odorous object, e.g. coffee or chocolate, and ask the patient if it smells normal.
Formal: a series of identical bottles containing recognisable smells are used, the patient is asked to identify them, e.g. coffee, vanilla, camphor, vinegar.
Test each nostril separately and determine if any loss of smell is uni- or bilateral.
Neurological examination: Cranial nerve I, olfactory, findings
Bilateral anosmia: usually nasal, not neurological; causes include upper respiratory tract infection, trauma, smoking, old age, Parkinson’s disease, tumours of the ethmoid bone or congenital ciliary dysmotility syndromes.
Unilateral anosmia: mucus-blocked nostril, head trauma, subfrontal meningioma.
Neurological examination: Cranial nerve V, trigeminal, applied anatomy
Sensory: face sensation in 3 branches: ophthalmic (V1), maxillary (V2), mandibular (V3).
Motor: muscles of mastication.
Nerve originates in the pons, travels to trigeminal ganglion at the petrous temporal bone and splits.
V1 passes through the cavernous sinus with III and exits via the superior orbital fissure.
V2 leaves via the infraorbital foramen (also supplies the palate and nasopharynx).
V3 exits via the foramen oval with the motor portion.
Neurological examination: Cranial nerve V, trigeminal, inspection
Inspect the patient’s face- wasting of the temporalis will show as hollowing above the zygomatic arch.
Neurological examination: Cranial nerve V, trigeminal, testing motor function
Ask the patient to clench their teeth and feel both sides for the bulge of the masseter and temporalis.
Ask the patient to open their mouth wide- the jaw will deviate towards the side of a V lesion.
Again ask them to open their mouth but provide resistance by holding their jaw closed with one of your hands.
Neurological examination: Cranial nerve V, trigeminal, testing sensory function
Assess light touch for each branch and ask the patient to say ‘yes’ if they can feel it. Forehead, cheek, and midway along the jaw, like-for-like.
For each branch, compare left to right: ‘does it feel the same on both sides?’
Test pin-prick sensation at the same spots using a sterile pin.
Neurological examination: Cranial nerve V, trigeminal, findings
Wasting of muscles: long term V palsy, MND, myotonic dystrophy.
Loss of all sensory modalities: V ganglion lesion (?herpes zoster).
Loss of light touch only, with loss of sensation on ipsilateral side of the body: contralateral parietal lobe (sensory cortex) lesion.
Loss of light touch in V only: lesion at the sensory root pons.
Loss of pin-prick only, along with contralateral side of body: ipsilateral brainstem lesion.
Loss of sensation in a ‘muzzle’ distribution (nose, lips, anterior cheeks): damage to the lower part of the spinal sensory nucleus (syringomyelia, demyelination).
Neurological examination: Cranial nerve V, trigeminal, reflexes
Jaw jerk.
Corneal reflex.
Neurological examination: Cranial nerve V, trigeminal, reflexes, jaw jerk
Explain to the patient what is about to happen as this could appear rather threatening.
Ask the patient to let their mouth hang loosely open.
Place your finger horizontally across their chin and tap your finger with a patella hammer.
Feel and watch jaw movement- there should be a slight closure of the jaw but this varies widely in normal people; a brisk and definite closure may indicate an UMN lesion above the level of the pons (e.g. pseudobulbar palsy).
Neurological examination: Cranial nerve V, trigeminal, reflexes, corneal reflex
Afferent = V1. Efferent = VII.
Ask the patient to look up and away from you.
Gently touch the cornea (overlies the iris) with a wisp of cotton wool.
Bring this in from the side so it cannot be seen approaching.
Watch both eyes. A blink is a normal response.
No response = ipsilateral V1 palsy.
Lack of blink on 1 side only = VII palsy.
Neurological examination: Cranial nerve VII, facial, applied anatomy
Sensory: external auditory meatus, tympanic membrane, small portion of skin behind ear, taste anterior 2/3 of tongue.
Motor: muscles of facial expression, stapedius.
Autonomic: parasympathetic supply to lacrimal glands.
The nucleus lies in the pons, the nerve leaves at the cerebellopontine angle with VIII.
The nerve gives off a branch to the stapedius at the geniculate ganglion whilst the majority of the nerve leaves the skull via the stylomastoid foramen and travels through the parotid gland.
Neurological examination: Cranial nerve VII, facial, muscles of facial expression
Test both left and right at the same time.
Some patients have difficulty understanding the instructions- quickly demonstrate to allow the patient to mirror you.
Look at the patient’s face at rest. Look for asymmetry in the nasolabial folds, angles of the mouth, and forehead wrinkles.
Ask the patient to raise their eyebrows (‘look up’) and watch the forehead wrinkle. Attempt to press their eyebrows down and note any weakness.
Ask the patient to ‘close your eyes tightly’. Watch, then test against resistance with your finger and thumb. ‘Don’t let me open them’.
Ask the patient to puff out their cheeks. Watch for air escaping on one side.
Ask the patient to bare their teeth, ‘show me your teeth’. Look for asymmetry.
Ask the patient to purse their lips, ‘whistle for me’. Look for asymmetry. The patient will always smile after whistling.
Neurological examination: Cranial nerve VII, facial, the ‘whistle-smile’ sign
A failure to smile when asked to whistle (whistle-smile negative) is usually due to ‘emotional paresis’ of the facial muscles, synonymous with Parkinsonism.
Neurological examination: Cranial nerve VII, facial, external auditory meatus
This should be examined briefly if only VII is examined- can be done as part of VIII if examining all the cranial nerves.
Neurological examination: Cranial nerve VII, facial, taste
Rarely tested outside specialist clinics.
Each side is tested separately using cotton buds dipped in solutions applied to each side of the tongue in turn.
Swill the mouth with distilled water between each taste sensation.
Test: sweet, salty, bitter (quinine), and sour (vinegar).
Neurological examination: Cranial nerve VII, facial, findings
Upper motor nerve lesion: will cause loss of facial movement on the contralateral side but with preservation of forehead wrinkling- both sides of the forehead receive bilateral nervous supply. Unilateral = CVA, etc. Bilateral = pseudobulbar palsy, motor neurone disease.
Lower motor neuron lesion: will cause loss of all movement on the ipsilateral side of the face. Unilateral = demyelination, tumours, Bell’s palsy, pontine lesions, cerebellopontine angle lesions. Bilateral = sarcoid, GBS, myasthenia gravis.
Bell’s palsy: idiopathic unilateral LMN VII paresis.
Ramsay-Hunt syndrome: unilateral paresis caused by herpes at the geniculate ganglion (look for herpes rash on the external ear).
Neurological examination: Cranial nerve VIII, vestibulocochlear, applied anatomy
Sensory: hearing (cochlear), balance/equilibrium (vestibular).
Motor: none.
The 8th nerve comprises 2 parts: the cochlear branch originates in the organ of Corti in the ear, passes through the internal auditory meatus to its nucleus in the pons.
Fibres pass to the superior gyrus of the temporal lobes.
The vestibular branch arises in the utricle and semicircular canals, joins the auditory fibres in the facial canal, enters the brainstem at the cerebellopontine angle, and ends in the pons and cerebellum.
Neurological examination: Cranial nerve VIII, vestibulocochlear, examination
Enquire first about symptoms- hearing loss/changes or balance problems.
Peripheral vestibular lesions cause ataxia during paroxysms of vertigo but not at other times.
Begin by inspecting each ear.
Test hearing.
Test vestibular function.
Neurological examination: Cranial nerve VIII, vestibulocochlear, hearing
Test each ear separately. Cover one by pressing on the tragus. Simple test of hearing: rub your fingers together at the external auditory meatus with patient's eyes closed, ask which side the sound is on and if it's the same on both sides. Rinne's test. Weber's test.
Neurological examination: Cranial nerve VIII, vestibulocochlear, hearing, Rinne’s test
Tap a 512Hz tuning fork and hold adjacent to the ear (air conduction).
Then apply the base of the tuning fork to the mastoid process (bone conduction).
Ask the patient which position sounds louder.
Normal = air conduction > bone conduction = ‘Rinne’s positive’.
In neural (or perceptive) deafness, Rinne’s test will remain positive.
In conductive deafness, the findings are reversed (bone >air).
Neurological examination: Cranial nerve VIII, vestibulocochlear, vestibular function, turning test
Ask the patient to stand facing you, arms outstretched.
Ask them to march on the spot, then close their eyes (continue marching).
Watch.
The patient will gradually turn towards the side of the lesion, sometimes 180 degrees.
Neurological examination: Cranial nerve VIII, vestibulocochlear, vestibular function, Hallpike’s manoeuvre
A test for benign positional vertigo (BPV).
Do not test those with known neck problems or possible posterior circulation impairment.
Warn the patient what is about to happen.
Sit the patient facing away from the edge of the bed such that when they lie back their head will not be supported (over the edge).
Turn their head to one side and ask them to look in that direction.
Lie them back quickly- supporting their head so that it lies about 30 degrees below the horizontal.
Watch for nystagmus (affected ear will be lowermost).
Repeat with the head turned in the other direction.
No nystagmus = normal.
Nystagmus, with a slight delay (~10secs) and fatiguable (can’t be repeated successfully for 10-15mins) = BPV.
Nystagmus, no delay, and no fatiguing = central vestibular syndrome.
Neurological examination: Cranial nerves IX and X, glossopharyngeal and vagus, applied anatomy
The 9th and 10th nerves are considered together as they have similar functions and work together to control pharynx, larynx, and swallow.
IX, sensory: pharynx, middle ear, taste on posterior 1/3 of tongue.
IX, motor: stylopharyngeus.
IX, autonomic: parotid gland.
IX originates in the medulla, passes through the jugular foramen.
X, sensory: tympanic membrane, external auditory canal, and external ear, proprioception from thorax and abdomen.
X, motor: palate, pharynx, and larynx.
X, autonomic: carotid baroreceptors.
X originates in medulla and pons, leaves the skull via jugular foramen.
Neurological examination: Cranial nerves IX and X, glossopharyngeal and vagus, applied anatomy
The 9th and 10th nerves are considered together as they have similar functions and work together to control pharynx, larynx, and swallow.
IX, sensory: pharynx, middle ear, taste on posterior 1/3 of tongue.
IX, motor: stylopharyngeus.
IX, autonomic: parotid gland.
IX originates in the medulla, passes through the jugular foramen.
X, sensory: tympanic membrane, external auditory canal, and external ear, proprioception from thorax and abdomen.
X, motor: palate, pharynx, and larynx.
X, autonomic: carotid baroreceptors.
X originates in medulla and pons, leaves the skull via jugular foramen.
Neurological examination: Cranial nerves IX and X, glossopharyngeal and vagus, examination, pharynx
Ask the patient to open their mouth and inspect the uvula (use a tongue depressor if necessary).
Is it central or deviated to one side? which side?
Ask the patient to say ‘ahh’. Watch the uvula. It should move upwards centrally. Does it deviate to one side?
Neurological examination: Cranial nerves IX and X, glossopharyngeal and vagus, examination, gag reflex
This is unpleasant for the patient and should only be tested if a IX or X nerve lesion is suspected (afferent signal = IX, efferent = X).
With the patient’s mouth open wide, gently touch the posterior pharyngeal wall on one side with a tongue depressor or other sterile stick.
Watch the uvula (it should lift up).
Repeat on the opposite side.
Ask the patient if they felt 2 touches- and was there any difference in sensation?
Neurological examination: Cranial nerves IX and X, glossopharyngeal and vagus, examination, larynx
Ask the patient to cough- normal character? gradual onset/ sudden?
Listen to the patient’s speech- note volume, quality, and whether it appears to fatigue (quieter as time goes on).
Test swallow.
At each stage, watch the swallow action- 2 phases or 1 smooth movement? delay between fluid leaving mouth (oral phase) and pharynx/larynx reacting (pharyngeal phase)? any coughing/choking? any ‘wet’ voice?
Terminate the test at the first sign of the patient aspirating.
Offer the patient a teaspoon of water to swallow, repeat x3.
Offer the patient a sup of water, repeat x3.
Offer the patient the glass for a mouthful of water, repeat x3.
Neurological examination: Cranial nerves IX and X, glossopharyngeal and vagus, findings, uvula
Moves to one side = X lesion on the opposite side.
No movement = muscle paresis.
Moves with ‘aah’ but not gag and decreased pharyngeal sensation = IX palsy.
Neurological examination: Cranial nerves IX and X, glossopharyngeal and vagus, findings, cough
Gradual onset of a deliberate cough = vocal cord palsy.
‘Wet’, bubbly voice and cough (before the swallow test) = pharyngeal and vocal cord palsy (X palsy).
Poor swallow and aspiration = combined IX and X or lone X lesion.
Neurological examination: Cranial nerve XI, accessory, applied anatomy
Sensory: none.
Motor: sternocleidomastoids and upper part of trapezii.
The accessory nerve is composed of ‘cranial’ and ‘spinal’ parts.
The cranial accessory nerve arises from the nucleus ambiguus in the medulla.
The spinal accessory nerve arises from the lateral part of the spinal cord down to C5 as a series of rootlets.
These join together and ascend adjacent to the spinal cord, passing through the foramen magnum to join with the cranial option of the accessory nerve.
It leaves the skull via the jugular foramen.
The cranial portion joins with the vagus nerve (X).
The spinal portion innervates the sternocleidomastoids and the upper fibres of the trapezii.
Each cerebral hemisphere controls the ipsilateral sternocleidomastoid and the contralateral trapezius.
Neurological examination: Cranial nerve XI, accessory, examination
The cranial portion of the accessory nerve cannot be tested separately.
Inspect the sternocleidomastoids- look for wasting, fasciculation, hypertrophy, and any abnormal head position.
Ask the patient to shrug their shoulders and observe.
Ask the patient to shrug again, using your hands on their shoulders to provide resistance.
Ask the patient to turn their head to each side, first without then with resistance (use your hand on their cheek).
Neurological examination: Cranial nerve XI, accessory, findings
Isolated accessory nerve lesions are very rare.
XI lesions usually present as part of a wider weakness or neurological syndrome.
Bilateral weakness: with wasting caused by muscular problems or motor neuron disease.
Unilateral weakness (trapezius and sternomastoid same side): suggests a peripheral neurological lesion.
Unilateral weakness (trapezius and sternomastoid of opposite sides): usually with hemiplegia suggests an UMN lesion ipsilateral to the weak sternomastoid.
The action of the sternocleidomastoid is to turn the head to the opposite side, so poor head turning to the left indicates a weak right sternocleidomastoid.
Neurological examination: Cranial nerve XII, hypoglossal, applied anatomy
Sensory: none.
Motor: muscles of the tongue.
Nucleus lies on the floor of IV ventricle.
Fibres pass ventrally, leaving the brainstem lateral to the pyramidal tracts.
Leaves the skull via the hypoglossal foramen.
