This document provides an outline and overview of localisation in neurology. It discusses the history and examination in neurology, focusing on good listening skills and avoiding assumptions. It then covers the anatomy and blood supply of the brain and cerebral cortex. Specific sections discuss lesions of the frontal, parietal, temporal and occipital lobes and their associated signs and symptoms. Other topics include the internal capsule, aphasia syndromes, stroke syndromes involving different arteries, and involvement of various cranial nerves.

1. LOCALISATION IN NEUROLOGY
DR. TARUN BETHA
1

2. OUTLINE
History and examination
Blood supply of cerebral
hemisphere
Frontal lobe lesions
Parietal lobe lesions
Temporal lobe lesions
Occipital lobe lesions
Internal capsule
Aphasia
Stroke syndromes
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3. HISTORY AND EXAMINATION
• The secret of good history taking is to be good
listener.
• It is essential to avoid the presumption that
because the patient is in neurological clinic they
must have a disease and it must be neurological.
• Some identical phrases the patient may say that
point towards identical syndromes- déjà vú
(temporal lobe), ‘red hot needle’ (tic douloureux).
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4. • Neurological examination should be tailored to
the patients history to make quick neurological
examination.
• Assessment of the mental status of the patient is
important before proceeding with history.
• A useful rule in neurology is that a more bizarre
and unusual the symptom, the more likely it to be
organic.
• The family history, past history have to be asked
with further direct questioning.
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5. BLOOD SUPPLY OF BRAIN
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6. BLOOD SUPPLY OF BRAIN
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7. ANATOMY OF CEREBRAL
CORTEX
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10. FRONTAL LOBE LESIONS
Dorsolateral
planning, strategy formation, and executive
function.
Apathy, personality changes, abulia, lack of
ability to plan or sequence tasks.
Ventrolateral
Broca’s aphasia.
Defective verbal retrieval.
Orbitofrontal
dif
fi
culty with disinhibition, emotional lability,
and memory disorders.
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11. FRONTAL MOTOR AREAS
• Primary frontal cortex.
• Premotor and supplementary motor cortex.
• Betz cells- corticospinal and cortico bulbar tracts.
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12. Premotor area
Planning and execution of movements (sequences of
movements)
Receives afferents from sensory cortex and projects to
motor cortex and motor thalamus.
Supplementary
motor area
Present on the medial aspect of hemisphere just anterior to
primary motor cortex.
Planning of motor movements, temporal organisation of
movements.
Frontal eye
fi
eld
area
Middle frontal gyrus.
Control movement of eye to opposite side
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13. PARIETAL LOBE AREAS
• Primary sensory cortex (3,2 and 1)
• Secondary sensory cortex
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14. agnosia: abnormality of perception despite normal sensory
pathways
two point discrimination: ability to determine whether one or two
points are being applied at the same time (normal discrimination on
fi
nger tips: 2-3 mm)
astereognosis: inability to recognise familiar shapes and textures
when felt in either hand with both eyes shut
graphanaesthesia: inability to identify numbers drawn on the
palms with both eyes shut
sensory inattention: inability to correctly recognise and report a
stimulus (visual or tactile) coming from the side opposite the lesion
when the two stimuli are presented together to both sides at the
same time.
PARIETAL LOBE LESIONS
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15. • Apraxia- inability to perform learned purposeful
movements.
• Acalculia- inability to perform mental arithmetic
• Gerstmann syndrome- alexia (inability to read),
acalculia,
fi
nger agnosia, right-left disorientation.
• Gerstmann syndrome seen in dominant parietal
lobe lesion.
• Homonymous inferior quadrantanopia.
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16. TEMPORAL LOBE LESIONS
• Homonymous superior quandrantinopia
• Prosopagnosis (dif
fi
culty in recognising faces)
• Wernicke’s aphasia
• Memory impairment
• Auditory agnosia
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17. OCCIPITAL LOBE
• Primary visual cortex (17).- primary visual
impressions (colour, shape, form, motion,
illumination). - it causes visual hallucinations or
fl
ashes of light
• Congruous, contralateral, macular sparing
hemianopia.
• Parastriatal areas (18,19) useful in recognition
of objects.
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18. • Lesions of occipital lobes bilaterally causes cortical
blindness- or bilateral scotomas.
• Pupillary light re
fl
exes are preserved.
• Colour agnosia, prosopagnosia.
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19. CORONARADIATA
• Subcortical white matter.
• Continues as internal capsule.
• It carries axons from cerebral cortex.
• Associated tracts: corticopontine tract, corticobulbar,
corticospinal tract.
• Affected as part of lacunar syndromes.
• Diseases effecting: MS, NPH.
• Causes dense neurological de
fi
cit.
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20. INTERNAL CAPSULE
• Upper motor
neurons supplying
face, arms, trunk
and lower limb.
• Corticobulbar
tracts and
corticospinal tracts.
• Thalami radiation-
3rd order sensory
fi
bres.
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21. APHASIA SYNDROMES
Broca's area or Brodmann area 44 - posterior inferior
frontal gyrus, controls the output of spoken language.
Wernicke's area or Brodmann area 22 - posterior two-
thirds of the superior temporal gyrus, receives
information from the auditory cortex and accesses a
network of cortical associations to assign word
meanings.
Angular gyrus- inferior parietal lobule is adjacent to
visual receptive areas - perception of written language,
as well as other language-processing functions.
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22. Syndrome Flu Rep Comp Read Write Localization
Broca - - + + - Broca area: left inferior frontal, MCA branch occlusion
Wernicke + - - - -
Wernicke area: left superior temporal and inferior parietal
region. MCA branch
Anomic + + + +/- +/-
Temporal, parietal and occipital regions outside of classic
language areas
Conduction + - + + +/- Superior temporal gyrus, inferior parietal region.
Transcortical
motor
- + + + - Left mesial frontal, supplementary motor area, ACA
Transcortical
mixed
- + - - -
Anterior and posterior watershed zones, disconnecting
parasylvian cortex from other cortical regions
Global - - - - - Large MCA or left carotid occlusion.
Pure word
deafness
+ + - + + Left or bilateral superior temporal gyrus
Pure alexia + + + - + Left occipital lobe with involvement of corpus callosum
Aphemia - + + + + Motor cortex out
fl
ow to articulators
Pure agraphic + + + + - Left inferior frontal region
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23. STROKE SYNDROMES OF
CEREBRUM
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24. Anterior cerebral
artery
Areas involved
• Motor leg area
• Coronaradiata
• Sensory foot and leg
• Sensorimotor paracentral
lobule
• Medial surface of posterior
frontal lobe
• Corpus callosum
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25. Middle cerebral
artery
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26. Posterior cerebral artery
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27. Stroke type Clinical course Risk factors Other clues
Intracerebral
hemorrhagic
Gradual onset
Progression in minutes or hours.
May present abruptly with maximal
de
fi
cit at onset
Hypertension
Trauma
Bleeding diastheses
Vascular malformation
Illicit drugs (cocaine,
amphetamine)
May be precipitated with sex
or other physical activity.
Subarachnoid
haemorrhage
Abrupt onset of sudden, severe
headache. Focal brain dysfunction less
common
Smoking
Hypertension
Alcohol intake
PCKD
Drugs (cocaine)
May be precipitated with sex
or other physical activity.
Ischemic
(thromobotic)
Stuttering progression with periods of
improvement. May develop over hours
or to most a few days
Atherosclerotic risk factors
(diabetes, smoking, age).
Men > women
May have neck bruit
Ischemic (embolic)
Suddenly onset
De
fi
cit max at onset
Clinical
fi
ndings improve quickly
H/o heart disease (valvular,
AF, endocarditis),
Atherosclerotic risk factors
(diabetes, smoking, age).
Men > women
Can be precipitated by getting
up at night to urinate or
sudden coughing or sneezing.
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28. CRANIAL NERVES INVOLVED
IN CRANIAL FOSSA
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29. CRANIAL
NERVES- I
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CRANIAL
NERVES- II
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CRANIAL
NERVES- III
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36. • complete ptosis (partial ptosis may occur with an
incomplete lesion)
• divergent strabismus (eye ‘down and out’)
• dilated pupil
• unreactive to direct light (the consensual reaction
in the opposite normal eye is intact)
• unreactive to accommodation.
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37. CRANIAL
NERVE IV
• Failure to intort the eye
• The patient may walk around
with his or her head tilted away
from the lesion – that is, to the
opposite shoulder (this allows
the patient to maintain
binocular vision)
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39. CRANIAL
NERVE V
• Absent corneal re
fl
ex
• Absent sensation in the sensory
distribution
• Weakness/wasting of the
muscles of mastication (masseter
and temporalis)
◦ The motor supply is carried
by the mandibular branch.
◦ The mandible will deviate
towards the paralysed side
when the mouth opens.
◦ Chronic unilateral lesions will
present with unilateral
temporalis atrophy.
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40. Causes of a unilateral lesion of the trigeminal nerve
A higher central lesion (eg. cerebral or thalamic) will have to be contralateral to the clinical
fi
ndings.
• A hemispheric infarct of the MCA territory may produce sensory loss in the trigeminal
distribution on the same side as the hemiparesis.
• With hemispheric lesions, masseter strength is usually preserved. The supranuclear control
of trigeminal nerve motor functions is bilateral, so a hemispheric infarct is never going to
produce a unilateral lesion (although voluntary control of the masseter will be lost).
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A sensory lesion con
fi
ned to a branch distribution suggests the lesion cannot
be nuclear - i.e. it must be somewhere beyond the trigeminal ganglion:
◦ Craniofacial trauma
◦ Base of skull fracture
◦ Maxillary sinusitis
◦ Tumour
◦ Aneurysm of the internal carotid artery
◦ Cavernous sinus thrombosis
Bilateral lesions are rare in isolation
• Diabetic neuropathy
• Large pontine tumours
• Cavernous sinus thrombosis (extensive)
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42. 42
Brainstem lesions would be ipsilateral.
• Pontine stroke (lateral rostral pons or above) - with ipsilateral body
sensory loss
• Medullary stroke (lateral medulla) - with contralateral body sensory loss
• Mid-pontine stroke (ipsilateral pons) - if only the face is affected
◦ Isolated masticatory motor failure suggests that the lesion is actually
limited to a small area of the mid-pons.
• Raised intracranial pressure (a "false localising sign")
• Pontine tumours
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CRANIAL
NERVE VI

44. 44
Causes of a unilateral lesion:
• Head injury (most common) with BOSF
• Raised intracranial pressure
• Localising lesion.... at any number of levels:
◦ Damage to the frontal eye
fi
eld of the frontal lobe, which occupies some of the middle
frontal gyrus
◦ Damage to the posterior hemispheres, which would be accompanied by a hemianopia
◦ Brainstem (tumour, stroke) - the paramedian prepontine reticular formation mentioned in
this question, which receives information from higher cortical centres and transmits them
to the abducens nucleus.
◦ Petrous portion of temporal bone (otitis media-associated osteomyelitis, mastoiditis)
◦ Clivus (intraforaminal extension of nasopharyngeal carcinoma or similar)
◦ Cavernous sinus (thrombosis)
◦ Superior orbital
fi
ssue (base of skull fracture)
◦ basal forms of meningitis, eg sarcoidosis, tuberculosis,cryptococcosis.
Dr. Tarun betha

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CAVERNOUS SINUS
THROMBOSIS
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CRANIAL
NERVE VII

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Obvious features
• Facial paralysis:
◦ Supranuclear "central" lesions spare the
forehead and brow
◦ Peripheral lesions take out the whole hemiface
Subtle features
• Failure of lacrimation
• Failure of salivation
• Loss of taste in the anterior 2/3rds of the tongue
• Loss of sensation from tympanic membrane, part of
external auditory canal, lateral surface of ear, and
area behind the ear.
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Causes of a unilateral lesion of the facial nerve
Unilateral lesion:
• Peripheral (complete) lesions: ipsilateral paralysis
◦ Trauma
◦ Tumour (cerebellopontine angle)
◦ Otitis media
◦ Parotidectomy
◦ Meningitis
◦ Diabetic neuropathy
◦ Bell's Palsy
• Central (forehead-sparing) lesions:
◦ Traumatic brain injury
◦ Tumour
◦ Stroke
◦ Maxillary sinusitis
◦ Tumour
◦ Aneurysm of the internal carotid artery
◦ Cavernous sinus thrombosis

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51. THANK YOU
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Dr. Tarun betha