LOCALISATION IN NEUROLOGY

Localisation in neurology is not difficult, but the principal of "garbage in-garbage out"
does apply: if you fail to identify the clinical signs correctly, then you will be unable
to identify where the problem is. Fortunately, clues frequently come from each of
the various systems such as cranial nerves, motor and sensory, so that the
localisation of the lesion may be confirmed by examining each system.

(1) The cardinal point is that the history is of the greatest importance and
must be used as a vehicle to assist you in localisation. If the patient was dizzy
and saw double, the lesion is in the brainstem, whereas, if their right hand had
became numb and they could not speak they in all likelihood had aphasia and a
left cortical lesion.

(2) Use basic clinical signs such as hemiparesis to decide on the possible side of
the lesion, and then use more advanced techniques to further localise and
confirm what you expect to find. This is the same principal as in aortic
incompetence, the pulse tells you what you expect to hear when you listen
specifically for a blowing diastolic murmur at the left sternal edge.

RULE NUMBER 1
Only one lesion. It is an error of the inexperienced to assume that there are multiple
lesions present. Obviously, bilateral lesions may occur, in which case there should be
bilateral signs: typically bilateral hemiparesis or bilateral increased tone.

RULE NUMBER 2
The lesion is on the opposite side of the hemiparesis.

If there is weakness, and the lesion is above the foramen magnum, the site of the
lesion causing the weakness is in the opposite brainstem or opposite hemisphere.
Thus, from a distance of a few metres you can say: "this patient's lesion is in the left
hemisphere or the left brainstem".

RULE NUMBER 3
There are 4 major sites causing hemiparesis:

In order of importance
(1) Cortex
(2) Internal Capsule
(3) Corona Radiata (between 1 and 2)
(4) Brainstem
RULE NUMBER 4
The face is always weak on the same side as the arm and leg if it is an upper motor
neurone facial weakness. This means that it is not really necessary to talk about "a
patient with a right hemiparesis and right facial upper motor neurone weakness"...
this is saying the same thing twice. The presence of hemiparesis means that there is
usually an obvious or subtle upper motor neurone weakness of the face on the same
side, providing that the lesion is not in the brainstem. Upper motor facial weakness
may be mild, with the only signs being flattening of the naso-labial fold and widening
of the palpebral fissure.

RULE NUMBER 5
AVOID talking about "upper motor lesion of cranial nerve VII": you will only confuse
yourselves, since as soon as many people use the phrase "cranial nerve", their next
statement is: therefore, the lesion is in the brainstem. It is better to talk about
upper motor neurone weakness of the face.

Can a brainstem lesion cause an upper motor neurone VII? Rarely, but this will occur
if there is a lesion of the cerebral peduncle in the midbrain. The nucleus of VII is in
the pons, so only a lesion above the pons may cause an upper motor neurone type of
weakness.

A lesion of the cerebral peduncle of the midbrain causes weakness of the opposite
side of the body and an upper motor neurone facial weakness of the opposite side of
the face.

RULE NUMBER 6: EVERYTHING CROSSES

THIS IS TRUE

EVERYTHING, absolutely everything crosses if it’s going to the hemispheres. Your

left brain receives sensation and visual input from the right side and sends out its
motor output to the right side.

RULE NUMBER 7: THE LAW OF EXPECTATIONS

If there is a left sided hemiparesis, which is an easy thing to observe: it follows that
you can expect to find: (if there is not a brainstem lesion):

there will be a left-sided upper motor neurone facial weakness.

there will be left sided sensory loss
there will be a left homonymous hemianopia
if the lesion is in the cortex you expect cortical signs
If presented with a hemiparesis, the problem is to decide where the lesion lies in the
opposite side of the brainstem or hemisphere.

CORTEX:
A lesion of the cortex is associated with cortical dysfunction: a right hemiparesis is
associated with aphasia and a left hemiparesis with neglect, dressing apraxia etc.

Cortical sensory loss: (2-point discrimination, graphasthesia, and stereognosis) :

there is no point in testing for cortical sensory loss if the patient cannot feel
touch or pain or the basic modalities of sensation. Usually, when one is able to
check for cortical sensory loss, basic modalities are mildly abnormal, but there
is at least sufficient touch and perception to distinguish between sharp or dull
for pin, or for light touch, to say "I feel it, but it is not like the other side". If
the patient says "Ek voel niks" you cannot test cortical sensation.

With most lesions giving rise to cortical sensory loss, there is loss of joint position
sense.

Vibration sense is poorly localising, and, in my opinion, there is little place for the
tuning fork in the examination of a patient with a possible brainstem or hemisphere
lesion.

To make another important point, joint position sense loss or loss of two point
discrimination does not mean the lesion must be in the hemispheres: peripheral
neuropathies can cause loss of all or any modalities, as can spinal cord lesions: it is
the dissociation between, on the one hand, the ability to feel primary modalities like
touch and pain, and on the other hand, the inability to synthesise this information to
decide if there are two pins or one, or a key in ones hand, that defines cortical
sensory loss.

Visual Fields:
The presence of a homonymous hemianopia implies a lesion of the optic radiation of
occipital cortex: if acute, this suggests a vascular lesion, typically an infarction of the
middle cerebral artery territory.

INTERNAL CAPSULE LESION:

The typical features of an internal capsule lesion are: arm and leg affected equally,
often quiet severely weak. There should be no cortical fall-out such as aphasia, and if
the patient has sufficient sensation to enable testing there should be no cortical
sensory loss present. Hemianopia may occur if the retrolentiform area is involved, but
this is rare.

BRAINSTEM:
Like the spinal cord, lesions of the brainstem cause lower motor neurone disturbance
on the level where the lesion is and long tract signs below the lesion. In the case of
the brainstem, naturally, the hemiparesis is on the opposite side to the lesion, as is
the sensory loss, just like a lesion of the cerebral hemisphere. (Remember a unilateral
lesion of the spinal cord produces a Brown-Sequard syndrome).

The brainstem has only 3 sections: midbrain, pons and medulla. The respective cranial
nerves are 3 & 4 (midbrain), 5-8 (pons) and the rest (9-12) (medulla).

A midbrain lesion: CN III : ptosis, dilated pupil, eye down and out
: vertical gaze palsy

A lesion of the pons: CN 6 or 7 (this is a LOWER motor neurone type 7)

: Horizontal gaze palsy or INO
: Unilateral facial numbness from CN 5
(results in CROSSED SENSORY LOSS)
: Unilateral deafness

A lesion of the medulla : bulbar palsy

: Unilateral facial numbness from CN V
(Descending spinal tract and nucleus)

Nystagmus is a clear indication of a brainstem problem most commonly of the

medullo-pontine junction.

Lesions of the cerebellum give rise to signs on the same side as the lesion. Brainstem
lesions often damage the cerebellar peduncles giving rise to cerebellar disturbance on
the side of the lesion.

Lesions of the sympathetic system:

Causes of ipsilateral Homer's syndrome

: thalamic lesion
: medullary lesion
: lesion of C8T1 roots or a lesion of sympathetic fibres as they climb up the carotid
and pass through the cavernous sinus on their way to the eye.

Causes of bilateral Homer's syndrome

: pontine bleed: pinpoint pupils
Remember: The sympathetic pathway starts in the area of the thalamus, descends
down through the brainstem and leaves the skull with the cord, and then exits with
the C8T1 roots. It then ascends with the carotid artery and goes back into the skull
and then to the eye. The most inefficient nerve in the body.

Supranuclear control of the cranial nerves:

Remember that a lesion of the nucleus or of the nerve leaving the nucleus causes
LOWER motor neurone signs.

The lower part of the face receives control only from the opposite hemisphere's
facial motor cortex. (This may be so that one has better control of ones expression.)

Both hemispheres (Try and lift one side of your forehead) control the forehead. The
facial nerve nucleus is divided into two parts: the upper part for the forehead is
bilaterally innervated, the lower part is supplied from the opposite hemisphere.

Cranial nerves 3 4 and 6 are controlled by the hemispheres via the horizontal and
vertical gaze centres in the brainstem. Lesions of the hemispheres produce gaze
palsies, as may lesions of the brainstem. Brainstem lesions also cause deficits of
individual cranial nerves.

Cranial nerves 5 and 9-12 are bilaterally innervated, like the forehead. Again, observe
the obvious fact that the tongue and palate and muscles of swallowing move as a
whole, both sides moving at the same time together.

Usually, the supply to those brainstem nuclei coming from the hemisphere of the
same side is not as good as that from the opposite side: therefore after a cerebral
lesion, there is often transient weakness which recovers in a few days. Thus, a left-
sided cortical/corona radiata/ internal capsule lesion cause upper motor neurone
weakness of the right face and transient weakness of the right palate and tongue and
some dysphagia, as well as a right hemiparesis. Sometimes, if the supply from the
hemisphere of the same side as the lesion is good, only facial weakness is seen and
the palate, tongue and swallowing muscles are normal, like the forehead.

In summary, the forehead is completely bilaterally innervated, the muscles of the

tongue and palate are mostly bilaterally innervated and the lower part of the face is
not bilaterally innervated at all.