CBL

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Localization

Objectives:
★ Master the ability of history-taking of neurological symptoms.
★ Importance of asking about functional limitations caused by the deficit.
★ Know the importance of detailed neurological examination to pinpoint
the deficit.
★ Understand the concept of upper and lower motor findings.
★ Know the difference between spasticity and rigidity.
★ Know the motor (corticospinal) pathways and the effect of their damage
★ Discuss the importance of a review of systems and systemic examination,
even in pure neurological presentations

Color index:
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Original text Females slides Males slides
Doctor’s notes Textbook Important Golden notes Extra
 Review of basics 2

Sources: Sensory tracts

- BnB
- Kaplan

2- Dorsal column
1- Spinothalamic tract
(Medial lemniscus)

Function: Vibration/proprioception/fine touch

Function: Pain/temperature/crude touch
Neurons:
Neurons:
1st: Spinal root up cord
1st: Spinal root to cord
2nd: Gracilis (LL) Cuneatus (UL)
2nd: Dorsal Horn to Thalamus
3rd: VPL Thalamus to Cortex
3rd: VPL Thalamus to Cortex
Crossing: in the spinal cord at the same level

Check the lesions box Check the lesions box

 Review of basics 3
Sources:
- BnB
- Kaplan Note: There are more tracts
other than the ones
mentioned here, but these 3
tracts (2 sensory, 1 motor) are
Motor tract what you should know.

3- Corticospinal tract

Function: Motor
Neurons:
1st (UMN): Cortex to Anterior Horn
2nd (LMN): Anterior Horn to muscle
Note: Decussation at Lower Medulla
A lesion in the spine will cause ipsilateral weakness (because the fibers
already crossed in the medulla) while a brain lesion will cause
contralateral weakness

Facial nerve

Lesion A: left lower

face weakness
Lesion B: complete
left face weakness

Summary
 CASE 4

◄ Case study
❖ Mr. Fahad is a 75-year-old man who complains of right-hand weakness and clumsiness.

What information do you need to know?

● HPI: he is right handed , weakness started gradual, 1 month ago, progressive, worsening over the last
2 weeks. He cannot write properly. He cannot hold objects and cannot open a jar. He is right-handed.
Also, numbness in his right hand and forearm. No leg weakness. No fluctuation of symptoms. No
pain. No headache. No vision changes. No speech changes. No seizures.
● Systemic review: positive for weight loss (7 kgs for the last month), poor appetite, chronic cough, and
shortness of breath on exertion. No fever.
● PMH: hypertension, dyslipidemia, and history of MI (stent).
● PSH: none.
● Medications: aspirin, atorvastatin, and candesartan.
● Social: married. Three kids. He retired math professor.
● Habits: ex-heavy smoker (1.5 p/d) for 25 years. Quit 5 years ago after MI. No alcohol. No drugs
● Family history: uncle died of colorectal cancer. Father had a stroke and hypertension. Mother is
healthy. Otherwise unremarkable.

Based on this history list all possible localizations for the lesion.
Work systematically, exclude one by one:
● Off the top, muscle and NMJ are excluded due to the sensory involvement
● Nerve and root are still possible
● Cord is unlikely (Because if it was transverse, it usually causes weakness in both lower limbs, and if it
affects upper spinal cord it usually causes weakness in all 4 limbs) but still on the list (if lesion is small
i.e. hemisection)
● Brain stem: excluded due to negative CN involvement in history (however, in the examination you
should perform CN exam to confirm that, in case the patient did have CN involvement but hasn’t noticed
it).
● Brain is in
● Thalamus: Excluded, because the pt has motor deficit. Recall that the corticospinal tract doesn’t
synapse nor pass through the thalamus (Only sensory pathways do)

What will you check on the examination?

❖ General: looks tired and thin. He was sitting on the bed. No use of accessory muscles. He is alert and
oriented to time, place, and person.
❖ V/S: BP: 142/70. HR : 80 regular, SpO2 96% on R/A. RR is 14 b/m. Temperature is 36.7 (temp is important
for any patient with significant weight loss, for TB or other infection)
❖ Neurological Examination:
➢ HMF: normal comprehension, expression, fluency, repetition, and naming. Normal 5-word
registration and recall after 5-minutes.
➢ Cranial nerve examination
■ Normal fundus, fields, and pupils.
■ Mild flattening of the nasolabial fold on the right side (UMN CN VII lesion)

Deltoid Biceps Triceps Wrist W. flexion Finger Finger

extension extension flexion

R 4+ 5 4+ 4 4 3 3

L 5 5 5 5 5 5 5
 CASE 5

◄ Case study (cont.)

Hip Hip Hip Hip Knee Knee ADF AFP
Flexion adduction abduction extension flexion extension

R 5 5 5 5 5 5 5 5

L 5 5 5 5 5 5 5 5

❖ Muscle tone: spastic in the right arm and leg.

❖ DTRs: +3 in the right biceps and right brachioradialis. +2 everywhere else.
❖ Babinski sign present in the right and absent on the left.
❖ Cerebellar: normal.
❖ Sensory examination: reduced pinprick, temperature, and vibration
perception over the right arm and hand. Otherwise, normal. Note the arm is adducted and
flexed, and the wrist is flexed (bc
❖ Gait examination: normal. extensors are weaker than
❖ Chest, heart, abdomen, and skin: within normal apart from stony flexors in UL in case of UMNL)
Note that his leg is extended (Bc
dullness and reduced air entry over the right lung base. No flexors are weaker than
lymphadenopathy extensors in LL in case of
UMNL)
➢ Why do it? Chest examination should be performed to examine
the lung for any masses (patient is an ex-heavy smoker, what he
has could be a metastatic brain lesion)

Based on the previous findings, where is the abnormality in the nervous system? Explain why?
● Patient has spasticity, positive babinski and hyperreflexia which indicates that there’s an UMN lesion.
So, with this info we can exclude any lesion at the level of the AHC and after. Now, is the lesion in the
spinal cord, brainstem or cerebral cortex? Given the signs of the UMNL of the corticospinal tract and
UMNL of the facial nerve, it has to be above the pons, bc the nucleus of the facial nerve is at the pons
(any lesion at the level of the nucleus and below is considered a LMNL). Furthermore, given the patient’s
sensory deficit (reduced pinprick, temperature and vibration perception), the sensory tracts must be
involved.
Note: babinski is much more important than hyperreflexia, because in cases where hyperreflexia is
bilateral, in could be normal. But babinski is 100% pathological (lesion in brain, brain stem or spinal
cord (A lesion in the spinal cord will cause loss of LMN at the level of the lesion and UMN loss below it))
What site would cause all these deficits?
● The only place that could cause this is the cerebral cortex (the motor and somatosensory cortices)
Could his weakness be caused by a spinal cord tumor?
● No, for 2 reasons:
○ UMN of facial nerve is involved (So, it has to be above the pons)
○ All the sensory and motor deficits are at the same side. If it was a spinal cord lesion then there
will be an ipsilateral motor loss (corticospinal tract), an ipsilateral loss of vibration and
proprioception (Dorsal column) and contralateral loss of pain and temperature (Spinothalamic
tract), there would also be an ipsilateral LMN involvement at the level of the lesion, which is not
the case here bc all deficits are at the same side.
Could his weakness be caused by a slipped cervical disc or a brachial plexus lesion?
● No, because these will cause LMN signs
 CASE 6

◄ Case study (cont.)

How will you investigate this patient?

● Imaging
○ See the CT pic, what are the possible causes of this lesion?
■ Metastasis, hemorrhage (amyloid),
■ This patient has likely had metastasis from a primary lung
tumor.

Would you change your investigations if his biceps and BR reflexes are
absent and muscle tone is low on the right?
● MRI cervical +/_ brachial plexus MRI
● NCS/EMG

How would you investigate if his symptoms and examination findings

occur in both hands and his facial nerve was normal?
● Cervical MRI
● NCS/EMG

Myopathy Neuropathy

Weakness Proximal Distal

Sensory Normal Impaired

Reflexes Normal Decreased

Fasciculations Absent May be present

Click here Brown-Séquard Syndrome

(Hemisection)

Transverse spinal cord lesion

Disrupt all motor and sensory pathways at
and below the level of the lesion. When a
patient comes with a bilateral progressive
weakness and loss of sensation in the lower
limb, it is important to think of transverse
spinal cord lesion and investigate urgently
& accordingly. Because any delay in the
diagnosis may lead to irreversible damage
that could make the patient
wheelchair-bound forever. Typically, a
patient might tell you that they feel as if a
“belt” is around a certain level in the trunk,
where they are normal above it and numb
and weak below it, or you could detect it
through examination.
 THANKS!!
This lecture was done by:
- Mashal AbaAlkhail
- Raghad AlKhashan

Females co-leaders: Males co-leaders:

Raghad AlKhashan Mashal AbaAlkhail
Amirah Aldakhilallah Nawaf Albhijan

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