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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.
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.
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".
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
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.
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.
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.
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.
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
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
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.
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.
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
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
: 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
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.