LOCALISATION IN NEUROLOGY Localisation in neurology is not difficult, but the principal of "garbage ingarbage 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 nasolabial 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 its 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 (912) (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.

rologic Localization
Introduction
the goal is to try to explain neurological signs by a single lesion should be able to localize signs from the physical exam to cerebral, brainstem, spinal cord, nerve, or muscle Brodmans areas the basics o area 4: precentral gyrus primary motor cortex corticospinal tract: nerve fibers decussate at the pyramids and terminate at the ventral horn of the spinal cord corticobulbar tract: fibers dessucate immediately rostral to where they terminate at brain stem nucleii o areas 1,2,3: post central gyrus primary sensory regions o area 17: occipital pole primary visual cortex o areas 18, 19: rostral to the occipital pole visual association areas

Upper and Lower Motor Neurons

upper: begins in cortex and terminates on motor neuron either in brain stem or spinal cord o lesions: paralysis or paresis, tone, DTRs, cutaneous reflexes, pathological reflexes present (Babinski), minimal atrophy, normal EMG lower: begins at the nucleus in the brainstem or anterior horn of the spinal cord; proceeds peripherally as a nerve o lesions: paralysis/paresis, tone, all reflexes, no pathological reflexes present, marked atrophy, fasciculations and fibrillations present on EMG

Sensation all synapse in thalamus except for smell

pain and temperature: ascend in contralateral spinalthalamic tract after decussation several segments above where the root enters; synapse in VPL of thalamus; pass through posterior limb of internal capsule to sensory cortex touch: ascend in ipsilateral DCML, decussate in the medulla and continue to VPL of thalamus sensation of the face: all via CN V o touch: synapse in main sensory nucleus o pain/temperature: descend in trigeminal tract and terminate in trigeminal nucleus according to onion skin face model (peri-oral region highest, regions

near ears most caudal); after synapse, fibers decussate and ascend in contralateral trigeminal tract to VPM peripheral facial palsy: in CN VII or nucleus total facial paralysis central facial palsy: cerebral lesion upper face is spared because of bilateral innervation

Effects of Lesions
Visual Pathways o retina and optic nerve monocular visual defects; usually associated with decreased visual acuity o optic chiasm bitemporal hemianopsia o optic tract, lateral geniculate body, optic radiation, visual cortex contralateral homonymous hemianopsia o Meyers Loop (optic radiation within the temporal lobe) contralateral superior quadrantanopsia Hemispheric Lesions o right hemisphere: left hemiplegia or paresis with upper facial sparing; contralateral anesthesia; left homoynmous hemianopsia; speech is normal in right-handers, aphasia in 40% of left-handers; UMN lesion reflex manifestations; normal consciousness, fund of info and orientation, hearing, taste, smell o left hemisphere: same signs on contralateral side, but aphasia in all righthanders, and 60% of left-handers o capsular triad: a lesion in the posterior limb of the internal capsule can produce the same signs of hemiplegia, hemianopsia, and hemianesthesia (but not aphasia) Cortical Lesions o Focal: depends on location of lesion motor or sensory loss from contralateral motor or sensory cortex aphasia from peri-Sylvian lesions in the dominant hemisphere silent areas such as the anterior frontal lobes do not produce neurological signs lesions of the cortex can become epileptic foci o Generalized: decorticate state destruction of cortex or disconnection from rest of nerv. system (white matter disease) total bilateral destruction coma (although reticular formation destruction is a more common cause of coma) partial cortical destruction acute: delerium; chronic: dementia

Basal Ganglia Disease

sustantia nigra parkinsonism (resting tremor, rigidity, bradykinesia) subthalamic nucleus hemiballismus caudate, putamen, globus pallidus chorea and athetosis Brain Stem: disruption of motor or sensory tracts is the same in any area; cranial nerves make localization possible o general rules: first two nuclei are outside brainstem; next two are midbrain, next four are pons, last four are medulla lesions of nuclei cause ipsilateral signs except for CN IV (which crosses the midline) o Webers syndome: midbrain lesion that causes 3rd nerve palsy and contralateral hemiparesis o Wallenbergs syndrome: lesion of nucleus ambiguous and fascicle ipsilateral palatal and vocal cord weakness

other signs (variable depending on extent of lesion): sensory loss of ipsilateral face and contralateral body, ipsilateral Horners syndrome, ataxia, nystagmus; no extremity weakness if lesion is limited to lateral medulla Cerebellum: difficult to separate from brainstem lesions of cerebellar pathways o lateral syndrome (involves hemisphere): ipislateral ataxia and incoordination o midline syndrome (involves vermis): truncal unsteadiness and ataxia Spinal Cord: the important tracts spinothalamic, lateral corticospinal, posterior columns o transection: total paralysis and asesthesia below lesion; initial flaccid paralysis with spinal shock, later spastic paralysis o hemisection (Brown-Sequard syndrome): ipsilateral weakness and touch sense, contralateral pain and temp loss o ALS (amyotrophic lateral sclerosis): loss of anterior horn cells and demyelinization of corticospinal tracts o posterolateral sclerosis: involves posterior columns, corticospinal tracts, and dorsal roots o vascular disease: usually presents as anterior spinal artery syndrome involving the ventral 2/3 of the cord

Peripheral Nervous System

may be mononeuropathy, mononeuropathy multiplex (two or more nerves affected), polyneuropathy (all nerves) presents with distal weakness and sensory loss (glove-stocking sensory loss), hyporeflexia Myopathies: primary disease of muscle o presents with proximal weakness, but no sensory or reflex loss o muscular dystrophy: myopathy that is genetically determined Note: despite standard texts, position and vibration do not only travel in the posterior columns; ascending pathways seem to be located throughout the spinal cord, but we do not know exactly where