The structure of the human brain is extremely complex. It is made up of billions of neurons that are linked together by trillions of connections. Each part of the brain performs a certain set of functions. Damage to a specific area of the brain causes distinct clinical symptoms. Knowledge of neuroanatomy, functioning of different sections of the brain, and clinical manifestations caused by injury to a part of the brain are critical in locating a neurological lesion. The complexity of this knowledge frequently presents a problem to health practitioners. This activity emphasizes the significance of the physical examination in the localization of a neurological lesion. It is intended to provide a concise and easy-to-review summary of the subject.

1. HOW TO LOCALIZE
NEUROLOGICAL LESION

2. 1. What is the pattern of motor deficit?

3. 4 basic
patterns of
features for
motor deficit:
Upper motor neuron lesion
features:
•Little muscle atrophy
•Spasticity
•Weakness or paralysis
•Increased reflexes, extensor plantar
response (Babinski positive), absent
superficial abdominal reflexes, with or
without clonus

4. Lower motor neuron lesion features:
•Muscle atrophy, fasciculations
•Flaccidity i.e. hypotonia
•Decreased or absent reflexes (more prominant with
demyelinating disease), flexor plantar response (Babinski
negative), normal or absent superficial abdominal reflexes

5. Neuromuscular junction features:
•No atrophy
•Normal or reduced tone
•Weakness: patchy i.e. doesn’t conform to an anatomic
structure, fluctuation with time & exercise i.e. fatigability
•Normal or depressed reflexes
•No sensory changes
•Fatigability of weakness or facilitation of power. Weakness that
gets worse or better with muscle exertion.

6. Myopathy features:
•Muscle may be normal, wasted or pseudo-hypertrophied, depending on the disease & time
of presentation
•Weakness, usually more proximal than distal
•Usually proximal rather than distal weakness, but there are distal myopathies. Also, some
myopathies are restricted to certain muscle groups e.g. ocular and pharygeal muscles
•Usually symmetric weakness
•Pure motor weakness without sensory signs
•Tendon reflexes are usually preseved until late in the disease. They may be depressed later
on in the disease. Normal abdominal & plantar reflexes
•Make an attempt to characterize which muscle groups are affected:
upper limb shoulders girdle (deltoids, rotator cuff), lower limb girdle (gluteal, quadreceps),
distal muscles (finger flexors, peroneal muscles), occular muscles, pharyngeal muscles,
diaphgram or heart.
Bowel and bladder sphincters are usually spared

7. 2. Pattern of weakness

9. 3. UMN lesion: Ipsilateral or contralateral?
ipsilateral
hemiplegia=same side of
face and body is involved
(hemispheric lesions)
Contralateral
hemiplegia=opposite side
of face and body is involved
(brainstem lesion)

10. upper motor neuron lesion with Ipsilateral hemiplegia
CEREBRAL
CORTEX:
 CORTICAL SENSORY LOSS(ASTEROGNOSIS)
 SEIZURES ARE COMMON.
 MAY BE ASSOCIATED WITH DYSFUNCTION OF HIGHER CENTERS E.G. BROCA’S
APHASIA ETC.
 MAY CONFORM TO THE TERRITORY SUPPLIED BY ONE OF THE CEREBRAL
ARTERIES:
 CONTRALATERAL LEGS: ANTERIOR CEREBRAL ARTERY
 CONTRALATERAL FACE & ARM: MIDDLE CEREBRAL ARTERY
 VISION: POSTERIOR CEREBRAL ARTERY
 HEMIPARESIS: MIDDLE CEREBRAL ARTERY
 IF PARASAGITTAL, IT AFFECTS BOTH LEGS & THEN MAYBE BOTH ARMS

11. Subcortical
lesions
Subcortical lesions can produce similar symptoms to
the cortical ones. without seizures and without
sensory loss
Internal
capsule:

Usually a severe “dense” hemiparesis with or
without sensory symptoms, because the fibres are
packed closed to one another.
Hemianesthesia
Homonymous hemianopia

12. Thalamus: •Sensory: Loss of sensation of one half of the body, pain in one half of
the body
•Thalamic pain a.k.a. thalamic syndrome: pain on touching the skin
•Motor: hemiparesis, less common than sensory dysfunction
•Cognitive dysfunction because of reciprocal connections with the
cortex:
•Frontal network syndrome may occur; i.e. symptoms/signs of frontal
lobe disease
•Aphasia may occur with left-sided lesions.
•Agnosia may occur with right-sided lesions.
•Decreased level of consciousness due to interruption of the reticular
activating system

13. upper motor neuron lesion with contralateral hemiplegia
Brainstem:
•Cranial nerve involvement
•The D’s of brainstem lesions:
•Diplopia ‘Double vision’, dysphagia, dysarthria, ‘dizziness’
Vertigo & ataxia
•Crossed deficits may occur: e.g. with a left-sided lesions: a
facial palsy on the left side & hemiparesis of the right side
•Bilateral signs may occur e.g. quatraparesis
•Later on or in larger lesions, respiratory function may be
impaired

14. A.MIDBRAIN
LESIONS
WEBER SYNDROME:3rd nerve palsy with crossed
hemiplegia
BENEDICTS SYNDROME: crossed hemiplegia with red
nucleus affection-tremors, ataxia, rigidity on opposite
side.
B.PONS LESION MILLARD-GUBLER SYNDROME: 7th nerve palsy+crossed
hemiplegia
FOVILLE SYNDROME: 6th+7th nerve palsy +crossed
hemiplegia
C.MEDULLA LESION 12th nerve palsy +crossed hemiplegia

15. lower motor neuron lesion: Is it with or without
sensory deficit?
What is the pattern of dysfunction? Does it
fit within the distribution of one nerve,
within the distribution (segment) of one
nerve root, within the distribution of many
nerves or glove and stocking.

16. LMN lesion without sensory involvement
Alpha motor neuron: •Fasciculations •Atrophy
•Usually develops
asymmetrically i.e. starts in
one limb & then other limbs
are affected, so at a late
stage it affects all the limbs
•May develop in the bulbar
muscles first; causing
dysphagia, dysarthria
•Progresses to involve the
phrenic nerve & nerves
supplying the accessory
muscles of respiration
•Very importantly, there is
no sensory deficit
•In ALS, the most common
motor neuron disease, the
UMN is involved as well

17. LMN lesion with sensory involvement
Myelopathy: (spinal cord lesion)
Myelopathy is an injury to the spinal cord due to severe compression that may result from
trauma, congenital stenosis, degenerative disease or disc herniation.

If above C5: quadriparesis more commonly than hemiparesis that spares the cranial
nerves

If below T1: the arm is completely spared but the legs are affected

A sensory level is very helpful finding

Lesions are usually bilateral:

Associated with bladder or sexual dysfunction

18. If unilateral:

Ipsilateral motor deficit, vibration & proprioception impairment
Contralateral loss of pain & temperature a.k.a. Brown-Sequard
syndrome

A focal lesion may cause an associated lower motor neuron (LMN)
lesion at the level, especially if the process also affects the nerve root,
we call this a myeloradiculopathy (this is rare though)

T1-T9 lesions interrupting the sympathetic outflow, Neurogenic shock
may occur: this is a form of distributive shock occurring with
bradycardia & loss of vascular tone ‘hypotension’. T1-T4 innervate the
heart,T5-T9 innervate the vessels

19. Peripheral nerves
1.Radiculopathy:
 LMNL due to nerve root disease
 In other words, the deficit conforms to the segmental innervation of the affected motor roots
 Sensory modalities e.g. Pain may be a feature, for example sciatica with weakness
2.Polyradiculopathy:
LMNL due to nerve root disease of multiple nerves, may also be sensory
3.Plexopathy (brachial or lumbosacral):
 LMN lesion due to damage of a plexus (brachial or lumbar)
 The deficit that does not conform to mononeuropathies or polyneuropathy
 upper arm & shoulder involvement in upper branchial plexus lesions, forearm & hand
involvement in lower brachial plexus lesions.

20. 4.Mononeuropathy:

LMN lesion due to single nerve disease

The deficit conforms to the distribution of a single nerve, e.g. ulnar nerve palsy or radial nerve
palsy, median nerve palsy

Sometimes the nerve is palpable

Tinel’s phenomenon may occur tapping the nerve causes a tingling sensation
5.Mononeuritis multiplex:

LMN lesions that begin like a mononeuropathy, but other nerves then become involved

Therefore, it starts asymmetrically i.e. in one arm then progresses to involve other nerves in other
limbs

If seen at the late stage, the disease is diffuse & symmetrical. Therefore, the history & progression is
important in this case

Sometimes the nerve is palpable

Tinel’s phenomenon may occur tapping the nerve causes a tingling sensation

21. 6.Polyneuropathy:

Develops symmetrically & distally leading to a glove & stocking distribution

It does not fit into a nerve root (segmental) or multiple peripheral nerve
distribution

Motor, sensory or both

If sensory: small fibres, large fibres or both

Small fibers: decreased pinprick & temperature sensation (painful & burning),
autonomic dysfunction, but relative sparring of power & reflexes

Large fibres: areflexia, sensory ataxia

22. SUMMURY

23. Patterns for localizing motor or sensory deficits:
Lateralized symptoms (e.g. hemiparesis):
 Hemispheric lesions
 Thalamus
 Brain stem
 Less commonly, spinal cord
Associated with cortical signs (aphasia, apraxia, visual field defect):
Think of hemispheric lesions
Associated cranial nerve dysfunction (vertigo, diplopia, dysarthria, ataxia):
Think of brainstem lesions

24. CRANIAL NERVE ABNORMALITIES:
 Ocular: cranial neuropathy III, IV, VI or midbrain or pons
 Facial: cranial neuropathy VII (motor), V (sensory), or pons
 Bulbar: cranial neuropathy IX, XII, or medulla
One limb or Part of a limb is affected:
 Cortical lesion
 Nerve root (Radiculopathy)
 Mononeuropathy
 Early mononeuritis multiplex

25. All limbs are affected:
 Cervical spinal cord lesions
 Brainstem lesions (accompanied by cranial nerve findings)
Peripheral neuropathy:
 Polyneuropathy
 Polyradiculopathy
 Mononeuroritis multiplex
Only lower limbs affected:
 Thoracic spinal cord lesions
 Lumbar spinal cord lesions
Peripheral neuropathy:
 Polyneuropathy
 Polyradiculopathy
 Mononeuroritis multiplex