TIA with cranial nerve examination

New Station on 7th August 2018

50 years old male presented with the history of TIA symptoms yesterday.
Take history do the cranial nerve examination and discuss the further management with the
patient.
[ Do not do fundoscopic examination]

History

How can I help you ?

I had facial weakness, weakness of arms and legs yesterday which lasted for few hours.
Do you have those symptoms now ? No

Did you see any doctor for this yesterday ? No

Did you have such problems before ? No

Do you have high blood pressure, diabetes, high cholesterol, heart problems ( abnormal heart
rhythms), stroke or mini stroke before ? No
Any medications ?

Ask about life style ( smoking, alcohol, exercise, diet)

Family history of stroke or mini strokes or heart problems ?

Examination

[ watch the video in you tube - www.youtube.com/watch?v=sJBpai74tlU]

Olfactory nerve

Did you notice any change in the smell at all ? No

Optic 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. If the patient normally wears spectacles
both tests may be done with them on.

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
Ophthalmoscopic examination ( do not do it in the exam)

3rd Oculomotor, 4th Abducent ( SO4) and 6th Trochlear nerves ( LR 6)

These three nerves are examined together, as they control the external ocular muscles.

The oculomotor nerve is the third cranial nerve (CN III). It innervates extrinsic eye muscles
that enable most movements of the eye and that raise the eyelid. The nerve also contains
fibers that innervate the intrinsic eye muscles that enable pupillary constriction and
accommodation (ability to focus on near objects as in reading). 

Internal ocular muscles : Direct and consensual light reflex and accommodation reflex

External ocular muscles: H test

5th 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. Test the areas supplied by the ophthalmic, maxillary and mandibular branches.

Ask the patient to clench his/her teeth. Both masseters should feel firm and strong. The
contracting temporalis may also be felt.

Corneal reflex ( do not do in the exam)

7th Facial nerve

Ask the patient to raise his/her eyebrows. Are the furrows of the forehead symmetrical?

Ask the patient to screw up his/her eyes. Gently try to prise them open. You should fail.

Ask the patient to give a broad toothy grin, demonstrating what you want. Do not say, 'Show
me your teeth', or he/she may remove any dentures and hand them to you. Is the grin full and
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 between 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. An LMN lesion such as Bell's palsy will involve the forehead.

8th Vestibulocochlear nerve

Testing of the vestibular component is - Hallpike's manoeuvre ( do not do).
Formal testing of the cochlear component requires audiometry. Hearing tests – Rinnes and
Webers tests ( examiner may say no need to do).
Either whispering or use of a high-frequency tuning fork can give a very crude assessment of
hearing. A 516 Hz (upper C) tuning fork is usually employed:

Strike the tuning fork and hold it about 2 cm 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, Weber's 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.

9th Glossopharyngeal and 10th 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/her mouth
wide and to say 'Ahh'. 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 salt solution. Most generalists do not perform this test.

Accessory nerve
The accessory nerve supplies the trapezius and sternomastoid muscles. Is there any wasting?
Ask the patient to shrug his/her shoulders up and try to push them down.

Ask the patient to push his/her 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.

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/her tongue and note any deviation. A fluttering motion called
fibrillation rather than fasciculation may be seen with an LMN lesion.

If the tongue deviates to one side when protruded, this suggests a hypoglossal nerve lesion. If
it is an LMN lesion, the protruded tongue will deviate towards the side of the lesion. With a
UMN 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 LMN lesion.

Tell the examiner that you would like to do neurological examination of the upper and lower
limbs – examiner may they are normal
 
Diagnosis investigations and management

Mr... on examination everything looks normal at the moment.

With what you have told me and after examination I think you had a condition what we call
Transient ischemic attack.

Dr: A TIA is a medical condition where there is a momentary decrease or loss in blood supply to the
brain. This could either be because of some narrowing of the blood vessels in the neck that supply
blood to the brain... or because of some rhythm problems in the heart. Are you following me Mr...?

P: Yes doctor.. Is it serious?

Dr: Mr... A TIA as such is not serious as it usually resolves by itself within 24 hours. But there is a risk
of having stroke next time which is a very serious condition.

We need to do investigations to find what exactly caused this problem and treat that condition so as
to reduce the chances of you getting a stroke. Is that Okay ? Yes

P: What kind of tests doctor?

Dr: First we will have to do a CT scan of head... to make sure that there is no evidence of a stroke.
We will then do an ECG or a heart tracing to look for any rhythm problems. We will also do some
blood tests to check her sugar and cholesterol levels ( high cholesterol is a risk factor for stroke).

Additionally, we will have to do a scan called a Doppler... of the blood vessels of your neck to see if
they are narrowed. Are you with me Mr...? P: Yes

Treatment:

Dr: Mr... There is no need to egt admitted to the hospital at the moment. We will also start you on
Aspirin, which can help prevent such attacks in the future. We will refer you to the Neurologist
urgently. Do you have any questions for me Mr...?

Treat other conditions if the patient has like HTN or Diabetes.

Advise life style. ( diet, exercise, smoking, alcohol).

Warning signs :

I would like to inform you about the warning signs of a stroke [FAST – Facial weakness, Arm
weakness, Speech problem – Time to call the ambulance]. If you ever notice any weakness in face
or limbs... or any slurring of her speech, please call an ambulance and come to the hospital
immediately as the next time, it can be even stroke. Do you have any questions for me ?

H: No doctor.. Thank you.

Tiredness – COPD patient on inhalers

Old lady presents with tiredness for 2 months. Known COPD patient. GP did blood
investigations and referred to the hospital. History and management.
Pt has COPD for 20 years. Taking Blue and brown inhalers.

Blood test shows low sodium ( 129 mmols).

Cause of tiredness ? due to hyponatremia ? due to Corticosteriod inhalers.

Ask about diarrheoa, vomit ( can cause hypovolumic hyponatremia).

Admit for investigations to rule out and serious causes.

Check morning cortisol, Urine sodium, TFT ( hypothyroidism can cause hyponatremia),
If no other cause - stop steroid inhalers and give alternative medicines talk to seniors and
discharge.
(Sodium is not very low to correct by treatment. It is chronic condition – so need to admit and
treat for hyponatremia).

Causes of hyponatremia
Hypovolemic hyponatremia Euvolemic hyponatremia Hypervolemic hyponatremia

Renal loss SIADH Congestive Cardiac failure

Diuretic therapy Cerebral salt
wasting Adrenocortical
insufficiency Salt wasting
nephropathy
Extra renal loss
Diarrhoea Vomiting Excessive
sweating
Drugs: (not complete list) Liver cirrhosis
SSRI, Carbamazepine Nephrotic syndrome
Desmopressin, Phenothiazines
Tricyclic antidepressants,
Cyclophosphamide, Opioids
Vincristine, NSAIDS,
Clofibrate, Proton pump
inhibitor

Third space loss: Pulmonary causes:

Small bowel obstruction Pneumonia,
Pancreatitis Pulmonary abscess
Burns Tuberculosis
 Neoplastic: Small cell lung
cancer Lymphoma
CNS: Meningitis Stroke
Tumours
Post operative pain

Adrenocortical insufficiency

Hypothyroidism

Primary polydipsia

When to admit and treat

If serum sodium between