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.
