Localization in Neurology

Alissa Willis, MD

Objectives
Understand the importance of localization in guiding the work-up and determining the correct diagnosis. Realize the importance of the history in localization. Be able to describe basic localization: brain, brain stem, spinal cord, motor neuron, peripheral nerve, neuromuscular junction, and muscle.

Go Where the Money Is

Localization helps you do this! Guides your work-up
Labs Imaging EEG EMG

Puts your differential in the right ballpark. Usually need a where before the what. Push and pull as hard as you please, but fit it all into one disease.

Where is the lesion?

CNS
Hemisphere Brainstem Cerebellum Spinal cord Motor neuron Plexus Root Peripheral nerve NMJ Muscle

PNS

Getting started
HISTORY, HISTORY, HISTORY In no other branch of medicine is it possible to build up a clinical picture so exact with reference to localization and pathologic anatomy as in clinical neurology. Dr. Armin Haerer

Mr. N
Came to the ED because he couldnt open his R eye. Thought it was exposure to concrete solvent at work. Says his lid is open when he wakes up in the AM but it slowly falls down during the day. Has also had double vision at the end of the day for the past 2 months. Where is the lesion and what is his problem?

Clue: Diplopia
Can only be brainstem, nerve (3/4/6), muscle, or NMJ Horizontal or vertical? Binocular or monocular? Intermittent or persistent? Intermittent, binocular diplopia worsening with fatigue can only be NMJ Dx: Myasthenia gravis No imaging needed. Only AchR Ab panel

The history will also help focus your physical exam:

Pain in 1 limbspend more time on sensory testing Off balancemore detailed cerebellar and sensory testing Visual complaintsfocus on fields, fundi, eye movements, pupils Memory troublemore time on mental status exam

When something is not normal, what do you call it?

It doesnt really matter. Just describe what you see. Interpret later. incomplete adduction of right eye and left nystagmus on look to the left or right INO Can follow commands but cant name or repeat or expressive aphasia

Use your neuroanatomy

Motor signs/symptoms
Testing UMN vs LMN Hemiparesis Paraparesis Quadraparesis Monoparesis

Medical Research Councils Scale for Assessment of Muscle Power

Scale 0 1 2 3 4 5 Description No muscle contraction visible Flicker or trace of contraction, but no movement Active joint movement when effect of gravity is eliminated Active movement against gravity Active movement against gravity and resistance, but weaker than normal Normal power

Describe pattern of weakness: Proximal vs. distal UE vs. LE +/- face

Reflexes
Reflex Jaw jerk Biceps Triceps Brachioradialis Knee jerk Ankle jerk Nerve CN V C5 C7 C6 L4 S1

Grading of Muscle Stretch Reflexes 0 Tr or 1 1+ to 3 3+ 4 Areflexia Hyporeflexia Normoreflexia Hyperreflexic Hyper- +clonus

UMN vs LMN
Upper Motor Neuron Weakness Spasticity Hyperreflexia Clonus Spasms (most often flexor) Lower Motor Neuron Weakness Flaccidity Hyporeflexia Fasiculations Atrophy

BUT..damage to UMN initially produces flaccid weakness.

Hemiparesissome basic rules

Usually cortex, subcortex (internal capsule and corona radiata), or brainstem Lesion is opposite weak side Facial weakness follows the hemiparesis
If above pons, expect sparing of upper face and weakness on same side as body weakness

Lesion is located where the pathways cross

Example: Mr. R
53 y/o WM smoker with DM2, HTN, CAD has acute onset slurred speech, L facial droop, and L sided weakness. On exam, no sensory deficits. L face and arm weaker than the leg.
Location: (1) Above cervical cord due to facial weakness (2) Pure motor thus unlikely to be stem R posterior limb of internal capsule Mechanism: Stroke

Paraparesis
Cerebrum
Parasagittal meningioma

Cervical or thoracic cord

Transverse myelitis Cord tumor Look for sensory level

Peripheral
Guillain-Barre syndrome Bilateral plexopathies (rare)

Example: Mrs. M
62 y/o WF has developed bilateral LE weakness with sensory loss as well as behavioral changes gradually over the past 18 months. Location:
(1) Behavior change puts it in brain (2) Bilat LE weakness makes it parasagittal

Mrs. M

Quadraparesis
Cervical spinal cord
Cervical stenosis Spinal trauma Neuromyelitis optica

Peripheral (rare)
Guillain-Barre

Brain stem
Central pontine myelinolysis Pontine stroke

Monoparesis
UMN vs LMN most helpful here Rely on other findings such as sensory involvement Hemisphere
ACA infarctionLE weakness

Spinal cord Root, plexus, or nerve

Should have sensory involvement and reflex

Sensory signs/symptoms
Test posterior column (vib/prop) and ALS modalities (pain/temp/LT)
Localization of sensory abnormalities Peripheral nerve Dorsal root Spinal cord Brainstem Thalamus Cerebrum All modalities affected in dermatome

Polyneuropathy Distal symm sensory loss Irritative symptoms Loss of vib/prop onlyposterior column Loss of pain/temp contralatALS Loss of sensation on side opposite weakness Loss of all sensory modalities on one side Weakness/sensory loss on same side

Cerebellar Generalizations
Cerebellar fibers cross 2x ipsilateral ataxia Midline cerebellar lesion truncal ataxia Cerebellar hemisphere lesion limb ataxia +/- Nystagmus +/- Dysarthria

Example: Mr. S
55 y/o RH BM smoker with HTN complained of sudden onset severe posterior headache and difficulty walking. Held onto walls to walk and saw images overlapping. +Nausea
Awake and alert. Slurred speech. Nystagmus Dysmetria on R fnf. Wide based gait with tendency to fall to R.

Mr. S: R cerebellar hemisphere

Walk this way.

Steppage gait
Usually severe neuropathy +/- bilat foot drop

Waddling gait
Severe proximal muscle weakness Common in myopathies

Spastic gait/scissor gait

Corticospinal tract lesions

Parkinsonian gait Magnetic gait/apractic gait

Frontal lobes

Cortical or subcortical?
Cortical signs Aphasia* (dominant) Apraxia* Agnosia Neglect (parietal) Weakness/sensory follow homunculi Subcortical signs Equal involvement of face/arm/leg Sensory abnormalities Visual field cuts Normal cerebellar and higher cortical functions

*Thalamic lesions can also cause aphasia and apraxia

Visual Disturbances
Ask About: Time course Binocular or monocular Does it go away if you close one eye? Positive phenoma Floaters? Sparkles? Pain Check For: Visual acuity in each eye Visual fields in each eye separately Pupils Fundus

A homonymous defect can only be brain!

Brainstem
Crossed findings = brainstem Cranial nerve deficit localizes lesion The lesion is where the 2 pathways cross. Example
L UE and LE weakness. Tongue deviates to the R. Location: Medulla

Spinal cord
Sensory level Hypertonia Weakness:
Extensors>flexors Distal>proximal

Bowel/bladder problems Normal CN

Example: Mrs. R
48 y/o WF with no sig PMHx c/o bilat LE weakness and numbness developing over the past 3 days. She cannot empty her bladder and feels like she has a belt cinched around her waist. Exam: Flaccid LEs. C7 sensory level to pinprick. post void residual. Poor rectal tone.

Mrs. R: Transverse myelitis

Peripheralroot
Asymmetric weakness, atrophy; often in a myotome Dysesthesias confined to a dermatome Hyporeflexia
Example: 56 y/o man c/o low back pain and numbness/tingling down his L leg into the sole and lateral side of his foot. L gastroc and hamstrings are weak. LT/PP on L lateral calf and foot. Absent L ankle jerk. Diagnosis: L S1 radiculopathy

PeripheralNerve
Distal predominant, asymmetric weakness Distal predominant dysesthesias Hyporeflexia May have autonomic involvement (skin changes, hair loss, nail changes)

Neuromuscular Junction
Fatiguability Weakness
Proximal and bilateral Normal bulk and tone May affect facial muscles

Sensation is preserved

Muscle
Sensory normal Reflexes normal Usually proximal more than distal weakness Face can be involved May complain of cramps, aches

Where does altered mental status come from?

Brainstem and RAS Both sides of diencephalon Both cerebral hemispheres
If there are no focal deficits, think toxic/ metabolic cause of diffuse cerebral dysfunction. Otherwise, use deficits to help you identify the structural lesion.