Dizziness

Dizziness
David Newman-Toker, neuro-otology
Senior author of "HINTS to diagnose stroke"

What is dizziness?
-Dizziness→ impaired perception of spatial orientation without vertigo
-Vertigo→ illusion of motion (spinning/non-spinning)
>Subjective (person)→ MC peripheral
>Objective (environment)→ MC central
-Oscillopsia 'world bounces'
>can’t read signs while walking
>B/L vestibular hypofunction
-Lightheadness, syncope→ LOC
-Imbalance→ severe truncal ataxia

Red flags associated sx
-Headache→ new
-Neck pain→ dissection
-AMS→ toxic
-CP→ PE & MI

Dizziness Ddx
“If you are sitting still with your eyes closed, are you still dizzy?”
Y→ Acute (Continuous) Vestibular Syndrome
N→ Episodic Vestibular Syndrome
Triggers
Positional, orthostatic, motion, auditory, visual, dietary
VPPB
-Position‑change + Short + Intense + Torsional
-Hx of TBI
-3-types
>Posterior→ vertical + MC BPPV + typical torsional nystagmus
>Horizontal→ lateral + turning + geotropic/apogeotropic nystagmus
>Superior→ vertical + rare + downbeat torsional pattern

Middle ear disease (otitis/effusion)
-Otalgia
-Does not produce vertigo, but sense of imbalance
-Rare syphilis

Vestibular neuritis ≠ labyrinthitis
-Neuritis→ No hearing loss; labyrinthitis→ Y
-DDx: Neuritis→ PICA; Labyrinthitis→ AICA
-Post-viral, self-resolution wks-mo

Meniere disease
-VERT→ Vertigo (recurrent); Ear fullness (pressure); Ringing (tinnitus); Thump/low-tone hearing loss
-2015 Barany criteria→ ≥2 spontaneous vertigo episodes 20 min–12 hr

Vestibular migraine
-Episodic dizziness + migraine features + motion sensitivity + no hearing loss
-NOT req headache, and headache may come before, during, or after the vertigo

Persistent Postural‑Perceptual Dizziness (PPPD)
-Chronic + worse with motion/visual stimuli + triggered by a past event + normal exam
-Grows out when another problem ends (PMH of VN, BPPV, VM, TBI, psych)

Medications
-CALM EAR→ Cisplatin, Aminoglicoside, Loop diuretics, Malaria; Erythromycin, Asa, Redman (vancomycin)
-Others: taxane, bevacizumab

Perilymphatic Fistula (PLF) and Superior Canal Dehiscence (SCD)
-PLF→ sudden hearing loss + pressure-triggered vertigo after trauma
-SCD→ conductive hearing loss + sound-triggered vertigo + autophony

Carotid‑Cavernous Fistula (CCF)
-Pulsatile tinnitus + red eye + diplopia
-DSA

Acoustic neuroma
-U/L hearing loss + U/L tinnitus + chronic imbalance (not vertigo)
>CPA→ facial numbness
-NF2

VBI
-Vertigo + brainstem signs (diplopia/dysarthria/ataxia) + no hearing loss
-Sx occur at rest, NOT positional
≠Bow Hunter→ triggered ONLY by head rotation
>Dynamic imaging showing mechanical compression
-CTA w/ post circ stenosis

Stroke syndromes assoc w/ dizziness
-Hearing loss→ AICA
-Sensory→ Thalamus
-Vision→ PCA
-Quadriplegia→ Basilar
Physical exam
-POC & T° & BP
-Otoscopy→ cerumen, infection
-OH BP + telemetry→ cardiac source
-HINTS→ only w/ dizzy or nystagmus
>HINTS (SN100) vs MRI[<48h](SN88)→ to dx post circ stroke
>HINTS-plus→ add hearing test eval
-Cerebellar signs
-Gait
-Dix-Hillpike→ episodic and triggered by head movement
>Roll test→ positional, but Dix-Hillpike
-Romberg Test
-Fukuda test

HI-N-TS & IN-FA-RCT
Impulse Normal
Fast-phase Alternating
Refix on Cover Test
Head-Impulse
-Abnormal→ peripheral; Abnormal→ good
-Normal is absence of saccades
Nystagmus
-Horizontal-Torsional and unidirectional
-Look at other side decrease (Alexander's law)
Test of Skew
-No vertical skew
≠CN IV
Dix–Hallpike
Maneuver
Positive Dix Hallpike
Roll test
-Vertigo is positional, BUT ⊖Dix‑Hallpike
-Nystagmus looks horizontal
-Sx triggered by rolling in bed
-Suspect horizontal canal BPPV (geo = affected; apo = unaffected)
Romberg test
→ verstibular dysf or sensory (peripheral neuropathy, post column disease)
*Sharpened (Tandem) Romberg test→ feet in tandem + arms crossed
Fukuda (Unterberger) test
-Marches in place, 50 steps
-Do: chronic imbalance; suspected unilateral vestibular loss
-Positive: ≥30° rotation→ peripheral vestibular weakness
Investigation
Labs
CBC→ sev anemia, infection
CMP→ all associated w/ dizziness/imbalance
POC→ hypo/hperG

Others: 
A1c, OGTT, lipid profile (triglycerides), TSH, vit (B12 & D)
Lyme titers→ if vertigo + cranial neuropathies
HIV/RPR→ if encephalopathy, neuropathy, or atypical findings
Cardiac markers→ troponin, BNP
UDS + alcohol level

ILR/MCOT→ recurrent events
+/-routine-EEG

Neuroimaging
If classic BPPV→ no need; otherwise→ do it

Acute→ CTH & CTA H&N→ post circ infarcts & stenosis
bMRI D/H→ c/f central etiology
IAC-MRI→ U/L SNHL, U/L tinnitus
CT Temporal bone→ PLF, SCD, temporal bone trauma

Audiometry→ hearing loss, tinnitus, aural fullness, unexplained vertigo

Treatment
-NO long-term vestibular sedation→ blocks recovery
-General (vestibular sedatives)
>Meclizine PO 25q8
>Diphenhydramine PO/IV 25q8;
>Scopolamine TD 1.5q3d behind ear
>Diazepam 2q8 or lorazepam 0.5q8
-Medrol dose pack
-Vestibular rehabilitation therapy

VNeuritis/Labyrinthitis
<72h→ pred 60q24 for 5d
-Vestibular sedative→ meclizine

Meniere disease
-Low‑salt diet
-Limit caffeine/alcohol
-Thiazide‑type diuretics→ HCTZ 25q24
-Betahistine (no USA 2/2 lack efficacy)
-Steroids (intratympanic or PO) for flare‑ups
-ENT referral for refractory cases:
>Intratympanic gentamicin (caution: hearing risk)
>Endolymphatic sac decompression

Vestibular migraine
-Treat migraine

PPPD, Anxiety‑Related Dizziness
-SSRIs/SNRIs (sertraline/venlafaxine)
-CBT
>If anxiety, breathing techniques
-Treat underlying vestibular event that triggered PPPD

BPPV
-Reposition→ Epley, Semont, Gufoni
-Teach home Epley if recurrence

Epley maneuver
-Worse sx→ consider, sedative
-Rotate 1st to affected side
-Steps: 1) Turn head 45° toward affected ear. 2) Lie back into Dix Hallpike position. 3) Wait for symptoms to stop. 4) Turn head 90° to the opposite side. 5) Roll onto side (nose toward floor). 6) Sit up slowly
Home Epley
Semont maneuver
-Rotate 1st to non-affected side
-Steps: 1) Turn head 45° away from affected ear. 2) Drop rapidly to affected ear down side. 3) Hold 1 minute. 4) In one motion, swing to opposite side. 5) Hold 1 minute. 6) Sit up
Foster (Half‑Somersault)
-Steps: 1) Kneel and place head on floor. 2) Turn head 45° toward affected ear. 3) Lift head halfway (back straight). 4) Sit up
BBQ Roll (Lempert)
-Rotate 1st to affected side
-Steps: 1) Lie on back with head flexed 30°. 2) Turn head 90° toward affected side. 3) Turn head to midline. 4) Turn head 90° to opposite side. 5) Roll body onto stomach (face down). 6) Roll onto side and sit up
Gufoni
-Steps: 1) Sit upright. 2) Fall quickly to unaffected side. 3) After 1 min, turn head 45° downward. 4) Hold 2 min. 5) Sit up
-Appiani is when fall to affected side
Casani
Zuma‑e‑Maia
Yacovino
-Steps: 1) Sit upright. 2) Move quickly to head hanging supine position. 3) Hold 30 seconds. 4) Bring head up to chin to chest. 5) Sit up

227. Accepted

Mirror Movements

Mirror Movements (Spiegelschrift)
1st described by Dr. Friedrich Albrecht Erlenmeyer (1849–1926)
Grundzüge ihrer Physiologie und Pathologie, 1879

Definition
"Involuntary movements on one side that mirror voluntary actions on the other"
-Normal in <7–10yo (CC myelination), 70% healthy children (on speed-based task)

Pathophysiology
Three teories
-Overflow
> signal 'overflows' to the other hand 
-Weak interhemispheric inhibition
> both hemispheres fire together
-Abnormal crossing motor pathways
>same commands go to both hands
Key quests
-Development & family history
-Cognitive & neuropsych

Exam
-Rapidly finger‑tap, open/close the fist, or perform pronation-supination
>MC in UEs
>Watch the “quiet” hand

-Woods & Teuber scale
0→ none
1→ barely
2→ clear, mod amplitude (<50%); 2a (slight) & 2b (strong)
3→ clear, large amplitude (>50%)
4→ complete, unable to supress
W&T=0
No clear imitative movements. Right hand is active and left hand is scored
W&T=1
Barely discernible repetitive movements. Right hand is active and left hand is scored
W&T=2a
Slight mirror movements. Right hand is active and left hand is scored
W&T=2b
Stronger, but briefer, repetitive movements. Right hand is active and left hand is scored
W&T=3
Strong and sustained repetitive movements. Left hand is active and right hand is scored
W&T=4
Movements equal to those observed in the active hand. Left hand is active and right hand is scored
Diagnostic work-up
-Affect QoL, otherwise no need
>Children unable to climb a ladder because releasing one hand makes the other involuntarily release too
>Painful compensatory shoulder contractions while writing
-Adults→ secondary (affecting CST)
>normal: fatigue, stress, high cognitive load, and aging
>investigate, if new in adulthood

Electrophysiology
-TMS
>Patho: simultaneous response & normal latency
>Physio: delayed responses & longer latency
-EMG: synchronous recruitment of homologous muscle groups, often with near‑identical timing to the voluntary contraction
-CMM demonstrates coactivation without delay

Neuroimaging
-bMRI to evalaute CC
>DTI→ ↓FA CC
>Asymmetric sigmoid bundle
-fMRI→ resting‑state   
-c-spine MRI
>spine abnormality
>vertebral fusion→ KFS

Genetic
-DCC (>80% of cases), followed by RAD51, NTN1, and ARHGEF7

Clinical Pearls
MM vs synkinesias
-Synkinesia→ no mirror

MM vs Imitation
-Imitation→ frontal lobe disinhibition (≠ behavior)

MM vs affected hand
-PD→ less affected hand
-CBS/CJD→ more affected hand
*MM co-exist w/ alien hand phenomenon: early (CJD) vs late (CBS)
-ET→ either
-HD→ UHDRS TMS correlated w/ MM

Treatment
-PT/OT→ bimanual independence, adpt at school/work
>HABIT-ILE→ CP-related MM
-Botox→ contralateral dystonia
-PD→ dopamine therapy adjustment
-Surgical→ no effect
-TMS→ research

Etiology
CMM
Mutations affecting CST
-DCC: req for CST axon guidance
-NTN1: chemoattractant for decussating CST axons
-RAD51: axonal migration & midline crossing indirectly
-ARHGEF7: cytoskeletal remodeling for CST

DCC
DCC
RAD51
PD
May precede motor asymmetry
-Asymmetric DA degeneration
-Loss of striato‑thalamo‑cortical regulation of motor suppression
-Inc motor overflow 2/2 impair inhibition

PD
PD
PD
-not really MM, but overflow
-RSM w/ mouth moves
LID


Others
-Focal hand dystonia
>if contralateral use, MM-dystonia 
>Botox contralateral
>Rare sensory coupling
-Klippel-Feil syndrome
#FND→ TMS
-Other craniovertebral anomalies
#KFS
-Kallmann syndrome
-Joubert syndrome
-Stroke
>R MCA territory infarct
>Limitation QoL
-CJD
-Tumor
>M1 resection
-KMT2B
Others
-ALS
-HD

Syncope vs Seizure

Syncope vs Seizure
Fainting by love in Philadelphia Museum of Art
The Doctor's Visit by Jan Steen

Syncope spectrum
-Normal
-Prodrome→ early autonomic sx
-Presyncope→ near-syncope
-Intermediary→ gray-out/ syncope threshold
-Syncope
-Recovery
 
Clinical history

What EXACTLY happened before, during, and after the event?
-open-ended quest at begining, than close
-LOC, incotinence
-Witness and recurrence
*avoid term fainting
-Triggers (sleep dep, drugs, stand) vs premonitory symptoms
-Eyes (open & position & pupil)
-Tunnel vision/ Black curtain
-Chest palpitations before fall
-BP & POC at arrival of EMS
Ask szs risk factors
-FH and personal PMH
-Developmental delay
-TBI/ consussion
-Febrile seizure

Fall pattern & awareness
-Velocity, stiffness, injury pattern, movement, color, sound, timing, and recovery
-Time to return to baseline, not for to be awake!
Convlusive syncope (aka syncopizing szs)
-Szs provoked by syncope (hypoperfusion)
-Myoclonic > tonic moves
≠Recovery-time, color, and trigger
≠Myoclonus <10 movs, irreg amplitude, asynchronous
≠Abnormal move start after LOC (Szs start at same time)

Etiology
Szs 2/2 electrical discharge and syncope 2/2 hypoperfusion
-Syncope etiology-based classification→ ROCks!
Differentials of LOC
-Syncope vs szs
-FNDs (syncope and szs)
-TIA (posterior circ)
-Metabolic (HypoGlycemia, drugs)
-Concussion
-Sleep disorders (cataplexy)
-Drop attacks
-Panic attacks
-Migraines

Physical exam
-Look at skin and tongue/mouth s/f bruises & sweat
>Lat lac→ szs (SN 33%, SP 96%)
-Pupils→ autonomic fx
>szs→ midriasis, rare hippus; syncope→ no chage (usual) 
-Orthostatic BP measurement
>OH vs nOH→ HR response
±Ewing battery s/f dysautonomia

Investigation
Inhospital
-EKG+Telemetry
-TTE
-rEEG±cEEG
±Neck vessel imaging→ s/f stenosis
±Lactate + CPK + Bicarb
±HypoP (SN20, SP93) + prolactin

Outpatient
±Ambulatory EEG
±MCOT/ILR

Indications for Tilt Table Test study
Cases non-diagnostic by H&P, ECG
-Vasovagal syncope vs POTS vs functional
-Syncope from szs
-Dx of delayed orthostatic ⬇️BP
-To recognize prodromes and perform countermeasures

Seizure likelihood
-Sheldon score
>"Have you ever woken up somewhere unusual with no memory of how you got there—blood in your mouth or strange, hard‑to‑explain sensations?"
Follow-up
≥ 2 episodes of LOC→ DMV (state-dependent)

Video
Seizure
Syncope
-Reflex orthostatic posture
Syncope
-Reflex orthostatic posture
Seizure
Syncope in heavy weight lifters
-Heavy lift + breath holding
Syncope (MSs)
-Induction of syncope
-Falls
-Akinetic syncope
-Myoclonus
-Other Movements
-Eye Movements

Cognitive changes

Cognitive Changes
Alois Alzheimer (1864 – 1915), German psychiatrist and neuropathologist

Referral
-word-finding difficulty (tip-of-the-tongue phenomenon)
-memory complaints (often vague, sometimes language-related)
-dissect complaints into domains

Cognitive Domains
Use SAMPLE
-Social→ behavior
-Attention→ focus
-Memory→ retention
-Perceptual/ visuospatial→ navigation
-Language→ only language
-Executive function→ multisteps

Information gather
-pt & collateral equally
>Anosognosia vs high self-aware
   high-performer→ subtle changes
   low-performer→ under-recognize
-Normalize aging
"Have you noticed anything like that for yourself compared to your friends?"
-Comparative qs (now vs 1y ago)
>ADLs after baseline

ADLs
-Basic
>Eat, bath, dress, toilet, transfer, grooming
-Instrumental
>Managing meds, finances, cook, shop, housekeep, transportation

Multifactorial nature
-Avoid attributing changes solely to lab abnormalities
-Acute events (UTI) may unmask underlying impairment
-NDG vs non-NDG

Considerations
- LATE is an histopath dx
- PPA is divided into FTD (svPPA & nfvPPA) and AD (lvPPA) like

Physical exam
-Focal deficits→ sugg vasc
-EOM abnormality
-PD sx
-Gait
-Palmomental rfx & Myerson

Diagnostic tools
-MoCA (preferred)
> assess sAMPLE, 's' is talking w/ pt
If unclear pattern, do
>Trail A&B→ processing & executive
>BNT→ language
>Dig span→ attention + work memory
-MMSE
> if severe dementia (higher ceiling effect)
> assess mainly sa'M'p'L'e
> convert MoCA to MMSE

-Others
>ACE→ specialist
>Minicog→ PCP screening
>Fluency→ phonemic (AD) vs category 

-NeuroPsych test→ domain-level profile
>High-performers for subtle complaints
>Discrepancy btw pt & family
>Legal quests
>Suspected FTD, PPA, atypical AD
>Mood vs cognitive

Investigation
-Reversible causes of dementia
>CBC, BMP (Ca), vitamins (B12 & MMA & HMC, folate, D, thiamine/ETKA), TSH, HIV, RPR
±ATN profile ±pTau217 (outpatient)
±APOE genotyping
±CSF amyloid

-if rapidly progressive→ LP
> CJD→ RT-QuIC, 14-3-3, t-tau
> AIE→ serum&CSF AIE panel
>SREAT→ anti-TPO, anti-TG, TSH cascade

-Neuroimaging s/f WMC, infarcts, atrophies
>bMRI ± NeuroQuant
±Amyloid PET (outpatient)

AD Treatment
*divided by severity 2/2 insurance

Traditional meds
-AChEi (donepezil, rivastigmine, galantamine)
> N/V & diarrhea; check EKG 2/2 QT
*PDD RVS Patch
-Memantine
> early confusion & dizziness; CI szs

Anti-amyloid therapy
-Lecanemab & donanemab
-Specialist

Lifestyle
-Sensory optimization: hearing and vision tests
-Exercise
-Healthy diet
-Cognitive & social engagement
-Always assess caregiver burden

Headache - basics

Headache
Basics
Figure from Codex Vindobonensis 93 (12th century)

Primary or Secondary?

1st question - onset

Hyperacute→ think vascular
Acute/subacute→ broader ddx
Chronic→ reassure if unchanged

Use SNOOP4 for screen secondary causes
Characterize

-Pain features - "SOCRATES"
> quality (throbbing, pressure, stabbing)
> duration & frequency
> associated sx (photo/phonophobia, N/V, auto sx)
*open-ended, avoid anchoring
*migraine term is freq 'mis'used
*reverse-HA hx, ask
"How many days per month do you NOT have HA?"
≠ bad vs mild HAs
>medication use freq

What NOT to miss

-GCA ESR/CRP, visual changes, chew
-IIH worse laying, pulsatile tinnitus, visual obscuration, VI palsy
-CVST focal neurological sx, pointing sign
-IHypo worse standing, post-LP
-RCVS recur thunderclap; stimulant, marijuana
-MOH Vit A (seal liver), decongestant

Primary etiologies

-Migraine→ U/L, pulsatile, photo/phonophobia, aura, nausea
-TTH→ B/L, pressure-like
-TACs→ tear, rhinorrhea, ptosis
> cluster, PH, SUNCT/ SUNA, HC
-Others (Ten list)
> cough, exercise, sexual, thunderclap, cold, external-pressure, stabbing, nummular, hypnic, NDPH

Non-HA mimics

-Sinusitis
-TMJ dysfunction
-Cervicogenic pain
-Refractive errors
-Neuralgias
Physical exam

-Fundoscopy - papilledema
-CN - vision, facial pain, diplopia
-Weakness or sensory loss
-Meningeal signs
-Touch head, s/f tender & triggers
>TMJ, OCN, cervical, MSK (traps)

Work-up

NO imaging, if all
-HA is clearly migraine or TTH
-Normal NE
-Long-stand stable pattern
-No red flags

Order imaging, if
- ⊕SNOOP4 screen

Do LP, if
-C/f IIH; check OP
-High c/f SAH w/ ⊖ CTH; check RBC
-C/f infection, inflammatory, neoplastic

Management

-Aim near-full improvement (last guideline 2025), before 50%
*Caution: improvement w/ meds do NOT  define if HA is 1st or 2nd

Inpatient
HA cocktail
-Hydration + sleep (benadryl & compazine) + antiemetics (metoclopramide) + IV Mg +/- NSAIDs (ketorolac 30q8, max 5d)
*order standing
- if refractory:
> MTP 125 mcg 1x/d for 5 d
> VPA 500q8h for 5d

-DHE
> 1mg IV, max 3 mg/d
> need telemetry; check EKG, avoid if CAD or aura

Outpatient
Acute/ abortive
- OTC (ibuprofen, acetaminophen)
* adv freq and MOH

-Triptans
> sumatriptan 50q2hr; max 200 mg/d
> if PO fails→ nasal/ SC
> adv max dose and avoid CAD

-Gepants (nurtec, qulipta, ubrelvy)
> Nurtec & qulipta can acute&prev
> Ubrelvy 50-100 q2h, max 200

-Fioricet (butalbital–acetaminophen–caffeine)
> avoid, high-risk MOH, HA ≤2 d/mo

Preventive
Consider when > 2 HAs/wk

-Supplements
-TCA
-BB/ CCB
-ASMs
-CGRPs
-Botox
Lifestyle
-Avoid triggers (advised the pt to observe)
-Healthy diet
-Sleep, hydration, exercise, and avoid stress
-Moderate caffeine

Pt education
-Set expectations: trial-and-error is normal
-Emphasize early use of abortive meds
-Avoid medication overuse
-Encourage HA diary
>day, features, medication

Diagnosing neuropathy

Diagnosing Neuropathy
Clinical Pearls
"There are numbness, tingling, and burning pains in the feet, with weakness of the legs, so that the patient walks with difficulty and unsteadiness"
Sir William Osler (1849 – 1919), Canadian physician

Presentation
Referral "neuropathy," self-dx googling numbness/tingling
-hard numbness≠tingling≠weakness

-true negative sx (loss) are more specific
>unable to feel floor T°
>unable to sense sand/cold surfaces

-positive sx (gain) are nonspecific
>dd: CVI, MSK, compression, positional

Localizing

P.neuropathy patterns
-stocking-glove distribution
>1st stocking knee level → 2nd hands: likely DM
-dist → prox progression in limbs
-symmetric sensory loss

Ddx patterns
-only the legs, not feet → unlikely neuropathy
-nocturnal hand numbness relieved by shaking → CTS
-lat thigh numbness in obese/tight clothing → meralgia paresthetica
-shooting pain into arm → cervical radiculopathy

Constant vs Intermittent

Constant → more likely neuropathy
Intermittent → more likely non-neuropathic

Clinical pearl:
Ask patients to close their eyes, focus internally, and report any abnormal sensation in their feet
>If they report nothing, neuropathy becomes less likely

Pain

Neuropathy pain: burn, electric/shock, stab

Less likely neuropathy
-isolated focal spot pain
-predominantly aching pain (usually MSK)
> foot palpation/press (plantar fasciitis)
> flat-foot (arthritis)

Neuropathic pain typically
-worsens at night
-worsens with walking/standing

If pain improves by walking at night → consider RLS

Review of systems
-always ask autonomic, bulbar, fever, weight, and skin changes

-autonomix sx
Orthostatic lightheadedness/syncope
Gastroparesis (early satiety, bloating, vomiting)
Abnormal sweating
Urinary retention
Bowel dysfunction

Autonomic sx

Auto sx are SN but not SP of true auto dysfx (AD)
Ex dry mouth/eyes (medications, Sjögren’s, etc.)
-complain w/o ask → ⬆️ SP

High SP clues:
True OH symptoms require stabilization
Severe early satiety with minimal intake

PE

Gait
Walk normal, heels (dorsiflex), toes (plantarflex), tandem, Romberg
*Normal gait & toe/heel walk usually no severe neuropathy

Motor ex
Focus on strong msc
-tibialis ant (dorsiflex)
-gastrocnemius (plantarflex)
Not able to break in a nml pt
-toe strength is too easy to overpower

Sensory ex
If no TF
-cotton/kleenex for light touch
*cotton → finger → press
*monofilament more SN for % of ulcer

-pin/ pinprick
*compare toe → ankle → knee for gradient
Ask: “do these feel the same?” (not “is this normal?”)
*if toe is 100%, how much is knee? >80% → normal
*if ask to repeat → normal
*if not feel pin, do dull part; if not feeling both → absent pinprick

Temperature
-ice pack/ metal can is more objective

Proprioception & vibration
Subjective
Vibration is more objective
test toe → ankle → knee

Reflexes
Absent ankle reflex support neuropathy
If ankle reflex are present, neuropathy is usually not severe

Other PE clues
Foot ulcers → severe neuropathy; often DM or hereditary
-ulcer is sensory & autonomic (heal impair)
-avoid nerve bx → wound not heal
High arches + hammertoes → possible CMT
Marked leg atrophy → chronic neuropathy

Initial lab workup
CBC, BMP, LFTs, A1C, lipid panel, Vit B12, folate, B1, Cu & Zn, B6
Avoid ordering initially unless referring
SPEP/ UPEP

When EMG
Do NOT order EMG/NCS
-obvious cause (malnutrition, uncontrolled DM)
-check baseline

Order EMG/NCS
-motor weakness
-gait impair
-rapid progression
-phenotype is unclear
-refer to neuro

U&L limb testing prevents mislabeling severity
*if upper nml → no severe

Small fiber neuropathy
True isolated SFN is rare

Criteria:
-normal EMG
-abnormal exam (temp/pinprick)
-abnormal confirmatory test (QST, skin biopsy)
*biopsy abnormal in high% of population

SFN vs fibromyalgia; exam findings are key

Time as a diagnostic tool
Following the patient over 2–3 months helps differentiate
-static sx → less likely serious
-progressive sx → refer & evaluate urgently
Patients often misjudge onset; serial exams are invaluable