Neuro

Case Based Learning:
Topic 1
Dr Hassan Bhatti
Clinical Tutor in Neurology
Hassan.bhatti@nuigalway.ie

Learning Outcomes
• How to approach history and examination in neurology (why, what,
where)
• Recognise patterns of motor and sensory loss
• Anatomy of the spinal tracts: Corticospinal tract, Dorsal Columns,
Spinothalamic tract
• Spinal cord syndromes

The Case
You are the neurology SHO and you are helping with consults. You have
been asked by the consultant to see Jacky Walsh who is a 27-year-old
right-handed accountant referred by her GP to the Acute Medical Unit.
She has been complaining of heaviness and numbness in her arms and
legs.
 What further information do you want to obtain when taking Jacky’s
history?

What further information do you want to
obtain when taking Jacky’s history?

Approach to the neurology patient

Approach to the neurology patient
Why? What?
Where?

History taking in neurology
Why is the patient really here?
• Clarify what symptoms the patient is complaining of
What is the lesion?
• Timing of symptoms
• Patient characteristics
Where is the lesion?
• Pattern recognition of signs and symptoms

First: Why is the patient really here?
• What exactly is the patient describing?
 Heaviness – is this a change in sensation or does she find it difficult to move
her arm (weakness)?
 Numbness – numbness (lack of sensation) vs pins and needles/tingling
• What parts of her body are affected?
• Both arms and legs or one side?
• Does numbness and heaviness affect the same sides?

Next: What is the lesion? = Timing
• Onset: Sudden, seconds, minutes, hours, days, weeks, months
• Progression:
• Continuous or Intermittent
• Static, improved or progressed (gradually vs stepwise)
• Pattern: if intermittent – duration and frequency

Timing is everything
• Sudden onset/acute – Vascular
• Subacute – inflammation, infection, neoplasia
• Progressive – neoplasia or degenerative
• Stepwise – vascular or inflammation
• Relapsing-Remitting - Inflammation

Other questions to ask
• Precipitating/Relieving Factors
• Examples of how function is impacted
• Associated symptoms
• Including systemic symptoms like weight loss, fever, infective symptoms

Associated Symptoms - Neurology Sieve
• Fits/Faints/Blackouts
• Headaches
• Visual Disturbance
• Hearing Disturbance
• Numbness/Tingling/Weakness
• Bowel/Bladder Symptoms

Past medical history and Family history
• Smoking, Hypertension, Diabetes – Vascular
• History of seizures, migraine etc
• History of malignancy – metastases, paraneoplastic
• Any neurological disorders in the family? - genetic

The Case
Jacky tells you she has had her symptoms for around 10 days. It started with pins and needles in her
left arm, then began to involve her left leg. It has gradually progressed over the past week now she
describes numbness “like getting an injection at the dentist”. She has a heavy sensation in her right
arm and leg and on clarification she feels this is weakness. She has noticed she has started to drag
her right leg and has had difficulty opening jars with her right hand.
She has no other medical problems and no significant family history. She lives with her partner and
two young children, does not smoke and drinks alcohol occasionally.
 Summarise her complaints (i.e. why is she really here?)
 What do you think the lesion is?

Summarise her complaints (Why is she here?)

Summarise her complaints (Why is she here?)
1. Weakness in right upper and lower limb
2. Loss of sensation in left upper and lower limb

What do you think the lesion is?

What do you think the lesion is?
Onset over days to weeks (gradual) = subacute
 think inflammation, infection, neoplasia
1. Inflammation: demyelination (multiple sclerosis)
2. Infection: cerebral or spinal abscess
3. Neoplasia: primary CNS tumour, metastases, spinal cord
compression, paraneoplastic (tumour makes antibodies that attack
nervous system)

The Case
Next you proceed to examination. You begin by assessing her motor
function. You believe the patient will have weakness on her right side
based on your history. You test tone, power and reflexes.
• How do you grade power?
• Explain the mechanism behind tendon reflexes
• Describe the pathway that carries impulses from the primary motor
cortex to the muscles
• What is meant by an upper motor neuron and a lower motor neuron?
• How would you distinguish between damage to an upper motor
neuron and a lower motor neuron on examination?

Examination in neurology
Where is the lesion?
•Pattern recognition of signs and symptoms
What is the lesion?
•Timing of symptoms
•Patient characteristics

How do you grade power?
Grade Meaning
5 Normal power
4 Active movement against gravity and resistance
3 Moves against gravity but not resistance
2 Moves with gravity eliminated
1 Flicker
0 No movement

Explain the mechanism behind tendon
reflexes

reflexes
• If a muscle is stretched it responds
by contracting = maintain a
constant length
1. Sensory fibres respond to stretch
2. Monosynaptic reflex arc with
quadriceps muscle (contraction)
3. Motor neurons of antagonistic
muscles (hamstrings) are
inhibited by interneurons
(relaxation)

Ankle Jerk
• One-two, buckle my shoe (S1,2)
Knee Jerk
• Three-four, kick the door (L3,4)
Biceps and Brachioradialis
• Five-six, pick up sticks (C5,6)
Triceps
• Seven-eight, lay them straight (C7,8)
reflexes

Describe the pathway that carries impulses
from the primary motor cortex to the muscles

Upper Motor Neuron
1. Motor cortex
2. Internal capsule
3. Brainstem
4. Spinal Cord
Lower Motor Neuron
1. Anterior Horn or Brainstem Nucleus
2. Peripheral Nerves
3. Neuromuscular Junction
4. Muscles

NB. The corticospinal tracts
decussate in the medulla just
before reaching spinal cord

What is meant by upper motor neurons and
lower motor neurons?

What is meant by upper motor neurons and
lower motor neurons?
• Relay race
• The first runner (upper motor neuron) starts
at the motor cortex and travels to brainstem
(for cranial nerves) or continues in spine (for
peripheral nerves)
• The upper motor neuron hands over the
baton (electrical impulse) to the second
runner (lower motor neuron)
• The lower motor neuron starts in the cranial
nerve nucleus in the brainstem (if it is a
cranial nerve) or the anterior horn of the
spinal cord (if it is a peripheral nerve)

How would you distinguish between damage to an
upper motor neuron and a lower motor neuron?

How would you distinguish between damage to an
upper motor neuron and a lower motor neuron?
UMN Signs (“Up”) LMN Signs (“Down”)
 Tone  Tone
 Reflexes  Reflexes
Plantars (Babinski reflex) Fasciculations
Clonus (Sometimes) Wasting

Upper Motor Neuron Signs
1. Hypertonia
• Descending motor pathways modulate nerve
circuits within the spinal cord
• Modulation can be inhibitory or excitatory
• The loss of descending inhibitory inputs tends
to result in an increased firing rate of lower
motor neurons
• The higher firing rate causes an increase in
the resting level of muscle activity, resulting in
hypertonia
2. Hyperreflexia
• Because of the loss of inhibitory modulation
from descending motor pathways, the stretch
reflex is exaggerated in upper motor neuron
disorders
3. Clonus
• Sometimes the stretch reflex is so strong that
the muscle contracts a number of times in a
rhythmic oscillation when the muscle is
rapidly stretched and then held at a constant
length

Upper Motor Neuron Signs
4. Babinski’s Sign
• Test = scratch lateral aspect of foot
• Normal response = all toes flex (curl downwards)
• Babinski Sign = dorsiflexion (upward movement) of
the big toe and fanning of the other toes
• Normally positive in babies
• As the descending motor pathways mature the
response is inhibited
• If there is damage to the descending motor tracts
there is loss of inhibition and become Babinski sign
positive

Lower Motor Neuron Signs
1. Muscle atrophy
When lower motor neurons die, the muscle
fibres that they innervate become deprived
of necessary growth factors and eventually
the muscle itself atrophies
2. Fasciculation
Damaged lower motor neurons can
produce spontaneous action potentials.
These spikes cause the muscle fibres that
are part of that neuron’s motor unit to fire,
resulting in visible twitching

The Case
As you examine the patient you are hypothesis testing.
• What findings might you expect if the lesion was at the different
levels of the motor pathway described previously?

Cerebral Cortex
• Pattern:
• UMN
• Contralateral weakness of face
and upper/lower limb
• Expressive or receptive aphasia
• Visual Field Deficits
• Visual or spatial neglect
• Sensory symptoms (all modalities)
X
X

Internal Capsule
• Contralateral weakness of the
face and arm and leg
• “Pure motor stroke”
• Pure motor stroke caused by an
infarct in the internal capsule is
the most common lacunar
syndrome
• UMN Signs
• No cortical signs

Internal Capsule
Lacunar Syndrome = small subcortical
stroke caused by occlusion of a
penetrating artery

Brainstem
• Pattern:
1. UMN
2. Often crossed signs
• Nearly all cranial nerves control
ipsilateral functions in the head
• The corticospinal tracts cross at the
end of the brainstem and control
contralateral functions in the body
3. Cranial nerve signs

Spinal cord
• Spinal cord is relatively small
• Common for disease processes affecting it to cause
bilateral symptoms and signs
• Small lesions within the spinal cord or unilateral
external compression of the spinal cord can lead to
unilateral symptoms
• No cranial nerve or cortical signs
• Bowel and urinary symptoms
• Sensory level
• Cervical spine: arms + legs + bowels/bladder
• Thoracic spine: legs + bowels/bladder

Spinal cord
• Spinal cord ends between L1 and L2 vertebral bodies (conus
medullaris)
• Injuries below L2 usually involve the cauda equina and represent
injuries to spinal roots rather than to the spinal cord (lower motor
neuron)

Peripheral nerve
• LMN
1. Mononeuropathy
• Single nerve distribution (e.g. median nerve)
2. Polyneuropathy
• Glove and stocking distribution = distal weakness
• Chronic = diabetes, alcohol
• Acute = Guillain-Barré syndrome
3. Mononeuropathy multiplex
• More than one single nerve
• Systemic disease
• e.g. right radial and left peroneal nerve

Peripheral nerve
1. Abductor Policis Brevis
(“bring your thumb up
to the ceiling”)
2. Opponens Pollicis
(“bring your thumb
over to baby finger”).

Peripheral nerve
1. Palmar interossei (hold a
apiece of paper between two
fingers as you attempt to pull
away)
2. Dorsal Interossei (spread the
fingers and don’t let me push
them together)

Peripheral nerve
1. Wrist drop (wrist extensors)
2. Weakness straightening fingers
at the knuckles (finger
extensors)
3. Weak elbow extension (Triceps)

Muscles and neuromuscular junction

Muscles and neuromuscular junction
• Lower motor neuron
• Sensation intact
• Myopathy
• Endocrine (hypothyroidism, Cushing’s
Disease)
• Inflammatory (polymyositis, inclusion
body myositis)
• Steroids
• NMJ – Myasthenia gravis
(autoimmune)
• Fatigability!!
• Ocular, respiratory and bulbar
involvement too

The Case
The patient also complains of sensory symptoms
• What are the different modalities of sensation you test for on
neurological exam? How do you test for each?
• Describe the pathway that carries impulses from the sensory nerve
endings to the primary somatosensory cortex for:
1. Sharp touch and temperature
2. Vibration and proprioception

What are the different modalities of sensation
on examination?

on examination?
Sharp Touch Fine Touch Temperature
Proprioception Vibration

on examination?
Sharp Touch Fine Touch Temperature
Proprioception Vibration
Small Fibres

Spinothalamic Tract
Large Fibres

Dorsal Columns

Pathway from nerve endings to the cortex

The Case
As you examine you are hypothesis testing.
• What findings would you expect at the level of each sensory pathway
described in the section above?

Peripheral nerves
• Pattern recognition of each
individual nerve
• Also pattern of dermatomes
(nerve root impingement)

Spinal cord
• Sensory level
• e.g. cord compression at T10 = no
sensation bellow belly button
• Know key landmarks
• Associated UMN motor, urinary
and bowel symptoms with no
cortical or cranial nerve signs
• If the lesion is unilateral:
1. Absent proprioception and
vibration on the same side as the
lesion
2. Absent pinprick on the opposite
side of the lesion (early decussation
of spinothalamic tract)

Brainstem
1. Crossed signs
2. Cranial nerve signs

Thalamus
• Unilateral complete sensory loss
on contralateral side
• No motor signs
• No cortical signs

Cerebral Cortex
• Contralateral sensory loss
• Expressive or receptive aphasia
• Visual Field Deficits
• Visual or spatial neglect
• Motor deficits
X
X

Summarise
3 main tracts
1. Spinothalamic
2. Corticospinal
3. Dorsal Columns

Back to the case …
• Lorna 27 yo female
• Gradual onset of:
1. Weakness in right upper and lower limb
2. Sensory changes in left upper and lower limb

The Case
Examination revealed:
• Increased tone on the right
• Grade 3/5 power on the right upper and
lower limb with normal power on the left side
• Deep tendon reflexes were brisk on the right
side of body and were normal on the left side
• Right side plantar reflex showed extensor
response and left side was flexor
• Sensory system examination revealed loss of
pin-prick and thermal sensations on the left
from the neck down and was normal on the
right side
• Proprioception was impaired on the right side
of body
• Cranial nerve examination is normal
Right Side
• Increased tone
• Power 3/5
• Brisk Reflexes
• Babinski +ve
• Impaired
proprioception
and vibration
Left Side
• Loss of
pinprick
• Loss of
thermal
Cranial Nerves = Normal
Cortical Function = Normal
• Speech
• Vision
• Cognition

Where would you localize the lesion in the
nervous system?
A. Brain
B. Brainstem
C. Spinal Cord
D. Nerves
E. NMJ/Muscles

What part of the spine is responsible for the
lesion?
A. Cervical
B. Thoracic
C. Lumbar
D. Sacral

What area of the spine is affect?
A. Anterior Spinal Cord
B. Posterior Spinal Cord
C. Right Half of Spinal Cord
D. Left Half of Spinal Cord

Cross sectional anatomy of the spine

(1) Segmental Syndrome
• Total cord transection =
loss/impairment of all types of
sensation and loss of movement
below the level of the lesion
Acute Subacute
Trauma Abscess
Infarct Tumours
Haemorrhage “Transverse Myelitis” (MS)

(2) Anterior Cord Syndrome
• Affects:
• Corticospinal Tracts (weakness and reflex
changes)
• Spinothalamic tracts (bilateral loss of
pain and temperature sensation)
• Spares:
• Dorsal Columns: joint position and
proprioception
• Commonly caused by anterior spinal artery
syndrome (e.g. thrombosis, surgeries, aortic
aneurysm/dissection)

(3) Dorsal (Posterior) Cord Syndrome
• Affects:
• Dorsal columns: gait ataxia and
paraesthesia
• Corticospinal tract: weakness and
reflex changes
• Causes:
• Multiple sclerosis
• Syphilis
• Friedreich’s ataxia
• Vitamin B12 deficiency

(4) Brown-Sequard (Hemicord) syndrome
• Lateral hemi-section syndrome
• Involves the dorsal column,
corticospinal tract and
spinothalamic tract unilaterally
• This produces weakness, loss of
vibration, and proprioception
ipsilateral to the lesion and loss of
pain and temperature on the
opposite side
• Trauma (knife or bullet injuries)
and demyelination

Summary
• 27 year old lady
• Weakness on her right side and numbness on her left side
• Subacute onset over 10 days think inflammation, infection, tumour
• Examination consistent with right cervical spine lesion
• Brown-Sequard Syndrome

How would you confirm your localization?

• Imaging – MRI

• Imaging – MRI
White matter lesion at C2 level in
cervical spine

What is the most likely diagnosis?

What is the most likely diagnosis?
• Multiple sclerosis
• Immune mediated disease that
affects the central nervous
system only
• More common in young women
• Relapsing remitting course
• Relapse treatment = steroids
• Prevent relapse = disease
modifying therapy

Take home points
• History and examination = why, what, where?
1. Figure out why the patient is really there
2. Timing is everything when determining the aetiology
3. Hypothesis testing using the examination
• Recognise patterns of motor and sensory loss
• Anatomy of the spinal tracts: Corticospinal tract, Dorsal Columns,
Spinothalamic tract
• Spinal cord syndromes: transverse, anterior, posterior, Brown-Sequard
• Basic knowledge of diagnosis and treatment of multiple sclerosis

Questions?
hassan.bhatti@nuigalway.ie

Neuro

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