The Northern Neuroscience Centre

Chiang Mai University

NNC CMU

Symptomatologic
Approach in Neurology
Chayasak Wantaneeyawong MD
The Northern Neuroscience Center
Faculty of Medicine, Chiang Mai University
The Northern Neuroscience Centre
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Outline
• Concepts Vertigo

• Motor weakness Multiple CN palsy

• Sensory disturbance
Abnormal movement
• Speech problems
Parkinsonism
• Headache
Tremor
• Visual loss
Gait disorders
Ptosis
Ataxia
• Diplopia
Seizure
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Concepts
• 1. Identify symptoms

• 2. Clarify symptoms

• 3. Syndromic approach

• - Where is the lesion?

• - What is the lesion?

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What is the lesion
• VINDICATES HIM • Aging (Degenerative)

• Vascular • Trauma - Toxin - Transient

disorder (Seizure, Migraine,
• Infection TIA)

• Neoplasm • Endocrine - Metabolic -

Nutrition
• Demyelination
• Hematologic - HT
• Inflammation/Immune
• Iatrogenic (include RT)
• Congenital - Hereditary
• Mitochondrial
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Motor weakness
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Localisation in
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neuromuscular system
Signs UMNL LMNL

Tone Spastic Flaccid

Hypoactive/
Tendon reflex Hyperactive
Absent
Babinski’s sign
Present Absent
Clonus
Atrophy None Present

Fasciculation None Present

Proximal
Pyramidal
Distribution of weakness Distal
Regional
Segmental
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UMN
• Cortex

• Subcortex

• Brainstem

• Spinal cord
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Cortex
• Motor+Sensory: Contralateral

• Higher cortical function

• Broadmann area

• Corticobulbar dysfunction:
Contralateral

• Consciousness

• Seizure
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Higher cortical function

• Language: dominant hemisphere

• Agnosia

• Apraxia

• Non-dominant hemisphere

• Frontal lobe sign

• Parietal lobe sign

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Non-dominant hemisphere
• Drawing

• Topographic ability

• Constructional

• Dressing

• Facial recognition

• Awareness of body and space

• Prosody
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Frontal releasing signs Parietal lobe signs
• Snout reflex • Sensation

• Palmomental reflex • Two points discrimination

• Sucking reflex • Astereognosia

• Palmar grasp reflex • Agraphesthesia

• Glabellar tap sign • Sensory inattention

• Homonysmous inferior
quadrantanopia
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Subcortex
• Motor + Sensory: Contralateral

• Disproportional weakness

• No cortical signs

• Corticobulbar dysfunction: Contralateral

• BG: Abnormal movement

• Consciousness
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Internal capsule

http://www.prepare2pg.in/wp-content
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Thalamus

Powell R, et al. Pract Neurol 2014;14:440–445

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Brainstem
• Motor+Sensory: Contralateral

• Cranial nerve dysfuction: Ipsilateral

• Alternating hemiplegia/hemianesthesia

• Consciousness

• Autonomic dysfunction
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Brainstem stroke syndrome

Weber’s Millard- Dejerine • Wallenberg’s

syndrome: Gubler syndrome: syndrome:
Ipsilateral syndrome: Ipsilateral Alternating
CN 3 palsy + Ipsilateral CN CN 12 palsy hemianesthesia +
contralateral 6,7 palsy + + Ipsilateral
weakness contralateral contralateral Horner’s, Vertigo,
weakness weakness Dysarthia,
Dysphagia
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Stroke in the young
• ASCOD phenotype Prothrombosis: APS, PC/PS/ATIII def.,
MPN, Leukemia, TTP, PNH, NS, IVL, CA
• Atherosclerosis
Vasculopathy: RCVS, PRES, moyamoya
• Small vessel Infection: HIV, VZV, SY, TB, BM
disease
Inflammation: Vasculitis - SLE, Takayasu,
• Cardioembolism: NBD
structural, rhythm
Genetic: CADASIL, Fabry’s disease
• Other
Drug: cocaine, amphetamine
• Dissection Migraine

PRES
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Stroke in young adults

Hemorrhage Ischemic

Arterial stroke Venous stroke

Cardioembolic Vascular Prothrombotic state

Rhythm Structural Atherosclerosis Non-atherosclerosis

Courtesy of Dr.Jiraporn
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Cardioembolic

Rhythm Structural
- AF
- SSS

• VHD
- Mitral stenosis (NSR 8-14%; AF 30%; • PFO with ASA
• Atrial myxoma
prior embolism 30-65%) • Recent MI
- Endocarditis (infective, NBTE) • Aortic arch atherosclerosis

- Mechanical valves (mitral 3%/year;

aortic 1.5%/year)

Courtesy of Dr.Jiraporn
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Non-atherosclerosis Drug
• Cocaine
Genetic • Amphetamine
• CADASIL

Vascular:
Infection • Dissection
• TB • Reversible cerebral
• SY vasoconstriction
• VZV syndromes
• HIV • Moyamoya disease
• Vasculopathy: VZV
Inflammatory:
Vasculitis
• SLE
• SS Female hormone-related
• Takayasu’s • OCP – 4 times
syndrome • Pregnancy
• Puerperium
• eclampsia

Courtesy of Dr.Jiraporn
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Spinal cord
• Motor: Ipsilateral

• Sensory: Pain/Temp. - Contralateral

Propioception/Vibration - Ipsilateral

• Sensory level

• Bowel+Bladder+Sexual function involvement

• Neck or back pain

• LMN signs at level of involvement

• UMN signs below level of involvement

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Approach to spinal cord disorders
• 1. Longtitudinal plane

• 2. Horizontal plane

• 3. Causes
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Intra-axial VS Extra-axial lesion
Features Intra-axial Extra-axial

Progression of
Descending Ascending
weakness
Cape-liked
Sensation Sensory level
Hanging sensation
Bowel-Bladder
Early Late
involvement
Radicular,
Pain Funicular
Back tenderness
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Spinal cord syndrome

• Central cord syndrome

• Anterior cord syndrome

• Posterior cord syndrome

• Brown – Sequard
syndrome

• Complete cord
syndrome
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Central cord syndrome Brown – Sequard Syndrome
Flaccid weakness of arms > legs
• Cape-like sensory disturbance
• Perianal sensation & some lower
extremity movement and sensation
may be preserved
• Causes: Trauma, Syringomyelia,
NMOSD, Sjogren, Intracord tumor
NNC CMU
• Hemi-section of the cord
• Paralysis on affected side
(corticospinal)
• Loss of proprioception and fine
discrimination (dorsal columns)
• Pain and temperature loss on the
opposite side below the lesion
(spinothalamic)
• Causes: Trauma, MS
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Anterior cord syndrome Posterior cord syndrome
• Corticospinal and • Proprioception affected – ataxia
spinothalamic tracts are
damaged (anterior spinal • Usually good power and
arteries) sensation

• Causes: Trauma, B12 or

• Causes: Trauma, ASA
Copper def.(+corticospinal),
infarction, MS HIV, NeuroSY, MS
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Features Conus medullaris syndrome Cauda equina syndrome

Vertebral level L1-2 L2-Sacrum

Presentation Spinal cord & nerve root Nerve root

Onset Sudden, bilateral Gradual, unilateral

Low back pain More Less

Radicular pain Less severe More severe

Motor Symmetrical paraparesis Asymmetric paraparesis

Sensory Perianal area, symmetrical Saddle anesthesia, asymmetrical

Reflexes Hyperreflexia Hyporeflexia

Sphincter Early incontinence Late retention

Impotence Frequent Less frequent

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Causes of myelopathy
• 1. Extra-axial: Tumor (primary, secondary), Trauma,
Orthopedic condition, Hematoma

• 2. Intra-axial:

• 1) Myelitis: Idiopathic, Infectious(VZV)/parainfectious,

Post-vaccination, Demyelination, Autoimmune(SLE,
Sjogren), Paraneoplastic

• 2) Non-myelitis: Vascular(AVM, Dural AVF),

Infection(HIV, SY), Neoplasm, Hereditary(MND, LD),
Toxin(NO), RT, Nutrition(B12 def., Cu def.)
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CNS Demyelinating Diseases
Features MS NMOSD
85% RRMS 80-90% Relapse
Clinical course
15% PPMS 10-20% Monophonic
Median age at onset 29 39
Sex(F:M) 2:1 9:1
2ry progressive Common Rare
Dawson finger, U Fiber Periependymal, Area postrema,
Temporal, Cortical lesion Cervicomedullary junction,
MRI brain
Perivenous lesion Hemispheric tumefactive
“Ovoid or ring” EL “Cloud-like” EL
Short segment Long segment(>=3)
MRI spinal cord
Peripheral Central
Uni > Bilateral, less severe More bilateral, more severe
Optic neuritis
Short segment Long segment
Mild pleocytosis, Lym Occasional marked pleocytosis,
CSF WBC
predominate, OCB 85% PMN & Lym, OCB 15-30%
Maintenance Rx IFN-B, Fingolimod, GA AZA, Rituximab, MMF, IVCY
Adapted from Lancet Neurol 2007; 6: 805–15
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http://www.radiologyassistant.nl
Neurology® 2015;84:1165–1173
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• Core clinical characteristics

• 1.Optic neuritis

• 2. Acute myelitis

• 3. Area postrema syndrome

• 4.Acute brainstem syndrome

• 5.Symptomatic narcolepsy or acute

diencephalic clinical syndrome

• 6.Symptomatic cerebral syndrome

Neurology® 2015;84:1165–1173
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LMN
LMN/ Auto
Motor Sensory Reflex Pain Atrophy
Character nomic

Yes/ Yes/ Less

Nerve Abnormal Abnormal Reduced
No No prominent

NMJ Abnormal Normal Normal No No No

Yes/
Muscle Abnormal Normal Normal No Prominent
No
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Proximal muscle weakness Distal muscle weakness

• Anterior horn cell • Peripheral nerve

• Neuromuscular Junction • Muscle (Distal

myopathy, IBM,
• Muscle muscular dystrophy)

• Peripheral nerve (GBS)

• (Beware Cervical
myelopathy)
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Anterior horn cell / Lower motor neuron
• Motor: Predominant limb m.

• Sensory: Normal

• Reflex: Reduced

• Autonomic: No involvement

• Pain: None

• Other: Muscle atrophy with fasciculation, frequent

bulbar symptoms, usually asymmetric at onset
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Motor neuron diseases

• 1. LMN only

• Poliomyelitis, Kennedy, PMA: LMN signs begin in 1

limb

• 2. UMN only

• HSP, PLS

• 3. UMN + LMN

• ALS: UMN + LMN signs >= 3 regions (Possible = 2

regions)
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Kennedy disease
• X-linked bulbospinal neuronopathy (XBSN)

• SBMA: Spinobulbar muscular atrophy

• XR; Mutated androgen receptor gene

• Onset: adulthood(usually > 30 yo)

• Proximal muscle weakness +- bulbar symptoms

• Muscle & perioral fasciculation, muscle atrophy(tongue, limb

girdle), cramp

• Endocrine: Gynecomastia, Infertility, Testicular atrophy

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Nerve root & Plexus
• Motor: Myotomal weakness

• Sensory: Dermatomal sensory loss

• Reflex: Reduced

• Pain: Radicular pain

• Other: Bowel, Bladder, Sexual involvement

• E.g.: Spondylosis, HNP, trauma

• (Polyradiculopathy VS Multiple plexopathy: long thoracic n.)

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Peripheral nerve
• Motor: Distal weakness predominate, bulbar in some
disease

• Sensory: Glove-stocking pattern

• Reflex: Reduced

• Autonomic: +-

• Pain: Hyperesthesia/Allodynia

• Other: If prolonged ! muscle atrophy

• E.g.: Entrapment, GBS, Toxic, Hereditary

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Neuropathy
• 1. Mononeuropathy

• 2. Multiple mononeuropathy

• 3. Polyneuropathy

• Axonal pattern

• Demyelinating pattern
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Multiple
Polyneuropathy Axonal Demyelinating
Mononeuropathy

Length Non-Length
Clinical Asymmetric
dependent dependent

Asymmetric,
Weakness Distal weakness Distal +- proximal
nerve distribution
Glove and Asymmetric,
Numbness Varies
stocking nerve distribution

Depressed DTR Distal All DTRs Asymmetric

Present(if Less muscle Present(if

Muscle atrophy chronic)
chronic) atrophy
Common DM, Drug Vasculitis,
CIDP
etiologies deficiency Leprosy
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Causes of neuropathy
• Acquired causes - MINI

• Metabolic(Nutrition) & toxin: DM, Arsenic, CMT, CKD, B1, B6, B12

• Infection: HIV

• Neoplastic/paraneoplastic: Lymphoma, Anti-Hu

• Inflammation/Immune: amyloidosis, GBS, vasculitis

• Hereditary: HMSN, HSAN

• Hereditary neuropathy characters: Very slowly progressive, Family

history +ve, Foot deformity, No paresthesia
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Mononeuropathy
• Trauma

• Inflammation

• Pressure/compression

• Chemical induced
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Multiple mononeuropathy
• SLe DVT HAMC Tangier disease

• SLE HNPP

• Leprosy Amyloidosis

• DM MMN
• Vasculitis Monoclonal gammopathy

CIDP
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Axonal neuropathy
Sensorimotor Small fiber/ Sensory Pure
/Pure sensory autonomic neuronopathy motor

6 Pack So HIT 12 Im
DM B6 toxicity
Endocrine Amyloidosis Cisplatin
Dapsone
DM HIV Paraneoplastic
Lead
Drug Drug Sjogren synd.
poisoning
Toxin CMT(vincristine) HIV
Nutritional def. B12 def.
Immune mediated
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Demyelinating neuropathies
• Motor predominate: Por Lead Gil<GBS> Char Diph
Hom Mun

• CIDP

• Charcot Marie Tooth disease

• POEMS, monoclonal gammopathies

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CIDP
Chronic Inflammatory Demyelinating Polyradiculoneuropathy
• Heterogeneous, grossly symmetric, sensory and motor neuropathy

• Course: monophasic, relapsing, or progressive

• Develop over > 8 weeks

• Hallmark = inflammatory-mediated demyelination

• Associating conditions: DM, CNTD, Hep C, HIV, Lymphoma,

Monoclonal gammopathy, Organ transplantation, IBD

• Ix: EDx, MRI nerve root, CSF exam, pathology

• Rx: IVIg, Steroid > PLEX

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Neuromuscular Junction
• Motor: Proximal weakness predominate, oculobulbar in
some disease

• Sensory: No involvement

• Reflex: Normal (reduced in LEMS)

• Autonomic: normal in MG but abnormal LEMS, Botulism

• Other: Fluctuation, fatigability, Worsened(MG)/ Improved

after activity(LEMS)

• E.g.: MG, LEMS, Botulism

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http://image.slidesharecdn.com/
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MG VS LEMS VS Botulism
Features MG LEMS Botulism

Post-synaptic Pre-synaptic Pre-synaptic

Mechanism
(AchR Ab) (VGCC) (SNARE protein)

Chronic, marked Chronic Acute

Present illness oculobulbar weakness, Ascending weakness, Descending weakness,
Fatiguability, Fluctuation mild oculobulbar weakness prominent oculobulbar

Smoking (SCLC), Foodborne, wound,

Past history Autoimmune diseases
constitutional symptoms outbreak

Normal DTR, Slightly reduced or

Physical exam Reduced DTR with PEP
Fatiguability test normal DTR

NCS: small CMAPs

NCS: normal CMAP NCS: small CMAPs, PEF
RNS: decremental &
Electrodiagnosis RNS: decremental RNS: decremental &
incremental response(not
response incremental response
prominent as in LEMS)
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Muscle
• Motor: Proximal weakness predominate, bulbar in some
disease

• Sensory: No involvement

• Reflex: Normal (+-reduced in severe myopathy)

• Pain: Muscle pain

• Other: Muscle atrophy, elevated CPK level

• E.g.: Myositis, Rhabdomyolysis, Dyskalemic periodic

paralysis, Muscular dystrophy
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Myopathy types
• Hereditary: 2C4M Acquired: DIIETS

• Congenital Drug
• Channelopathy Infection
• Muscular dystrophy
Inflammation
• Metabolic
Endocrine
• Mitochondrial
Trauma/Toxin
• Myotonia
Systemic
• Characters: Very slowly progressive,
Family history +ve, Myotonia Rhabdomyolysis
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6 main questions in history taking
• DOSFAT

• Distribution of weakness: proximal, distal, neck, trunk, ocular, bulbar,

respiratory

• Onset & Progression

• Symptoms: positive & negative symptoms

• Family history of myopathy

• Associated S&S: rash, myoglobinuria, eye, cardiac symptoms,

dysmorphic features

• Trigger: illegal drug, exercise, exercise & high carbohydrate meal

then rest, fever or heat exposure
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Idiopathic inflammatory myopathy
• DM, PM IBM

• 1. Typical skin rash of DM 1. Proximal muscle

weakness(insidious onset)
• 2. Symmetrical proximal muscle weakness
(thigh)
• 3. Muscle enzyme
2. Distal muscle
• 4. EMG weakness(hands)
• 5. Muscle biopsy
3. Muscle enzyme
• Autoantibody:
4. EMG
• Myositis specific antibody: anti-Jo1, anti SRP,
antiMi-2, anti-HMGCR, anti p55/140, anti MDA-5, anti 5. Failure of muscle
SUMO-1
weakness to improve on
• Nonspecific autoantibody: ANA, RF, anti-PM-Scl, a high dose steroid
anti-Ro/SS-A, anti-La/SS-B, anti-U1RNP, anti-non-U1 (≥40-60 mg/day for 3-6
snRNP mo.)
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http://patient.info/health/muscular-dystrophies
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Myotonic dystrophy
• Trinucleotide repeat expansion disorders CTG

• Progressive muscular weakness: hand + thigh

• Ptosis c/o ophthalmoplegia

• Myotonia: Percussion, Hand grip, Tongue

• Appearance: Ptosis, Temporalis wasting, Sagging of jaw,

Sunken cheek, Swan neck

• Other: Gonadal atrophy*, Cataract, Cardiac arrhythmia, CNS

(apathy, inertia, hypersomnolence), Endocrine (hyperinsulinism,
elevated FSH & LH)
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Sensory disturbances
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Sensory disturbances
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http://fracp.bigpondhosting.com/
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Speech disturbances
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Speech disturbances
• 1. Motor speech disorder —> Dysarthria

• 2. Linguistic/Language disorders —> Aphasia

• 3 .Mutism
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Dysarthria
• 1. Spastic dysarthria

• 2. Flaccid dysarthria

• 3. Hyperkinetic dysarthria

• 4. Hypokinetic dysarthria

• 5. Ataxic dysarthria/slur speech

• 6. Mixed dysarthria
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Aphasia
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Mutism
• 1. Functional: depression, catatonia, conversion
disorder

• 2. Organic:

• 1) Diffuse lesion: Delirium, Dementia, Drug-

induced, Metabolic encephalopathy

• 2) Focal lesion: Aphasia, Severe dysarthria/

Anarthria, Akinetic mutism
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Headache
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Pain sensitive structures of head
• Intracranial structures • Extracranial structures

• 1. Meningeal arteries • 1. Subcutaneous tissue

• 2. Proximal portions of the • 2. Eyes

cerebral arteries
• 3. Ears
• 3. Dura at the base of the brain
• 4. Sinuses
• 4. Venous sinuses
• 5. Mucous membrane
• 5. Cranial nerves 5, 7, 9, and 10,
and cervical nerves 1, 2, and 3 • 6. TMJ

• 7. Blood vessel
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History taking
• LODCRAFST: Location & sides, Onset, Duration(with
and without medications), Characteristic, Radiation,
Associating symptom, Aura, Aggravating/alleviating
factor, Frequency, Severity, Temporal pattern

• Red flag signs

• Previous headache, past medication and

comorbidity

• Why today?
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Red flag signs - SNOOP4

• Systemic diseases

• Neurological deficit

• Onset: sudden-acute

• Onset: in age > 50 years old

• Papilledema

• Pattern change

• Precipitated by Valsava manoeuvre

• Postural related
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Primary headache Secondary headache
• Abnormal neuronal Secondary causes
network
Structural, Metabolic, Systemic abnormality
• Recurrence
-Extracranial: Sinusitis, Otitis media,
• Same characteristics Glaucoma, Dental problems, Temporal
arteritis, TMJ disorders, Cardiac
• Specific features cephalalgia

• -TTH: 10 atk. -Intracranial: SAH, ICH, RCVS, Dissection,

PRES, CVST, CNS infection(abscess,
• -Migraine: 2 or 5atk. meningitis), Tumour, Pachymeningitis,,
IICP, IIH, Low pressure
• -TACs
-Metabolic/systemic disorders: CO2
• -Other retention, CO poisoning, Drug, Systemic
infection
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Diffuse secondary headache
• Acute

• SAH, IICP(ICH, CVST, Abscess, SDH,

Hydrocephalus), Acute meningitis, Severe HT/
PRES, Systemic infection, Metabolic(CO2, CO)

• Chronic

• IICP(Tumor, SDH, CVST, Hydrocephalus), Chronic

meningitis, IIH, Low CSF pressure (SIH), Drug
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Thunderclap headache

Lancet Neurology
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Cerebral venous thrombosis
• Clinical AOC 40%

• Headache 95% FND 40%

• Seizure 50% Papilledema 40%

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Causes of CVT
• Prothrombosis: Pregnancy
Inherited, Acquired
Dehydration
• Infection:
Parameningeal
infection Trauma

• Inflammation: SLE, Cancer-related:

Behcet’s lung, breast

OCP, HRT
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Visual loss
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Visual pathway
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Visual loss
• Anterior visual Posterior visual pathway lesion
pathway lesion (Bilateral eye involvement)
(Unilateral > Bilateral
eye involvement) Optic chiasm (Bitemporal
hemianopia): Pituitary tumor,
• Refractive error Craniopharyngioma, Aneurysm

• Ocular media: Optic tract (Homonysmous

Cornea, AC, Lens, hemianopia or quadrantanopia):
Vitreous CVD, Tumor

• Sensory system: Occipital lobe (Homonysmous

Retina, Optic nerve hemianopia c macular sparing):
CVD, Tumor, Trauma
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Ocular media Retina Optic nerve
Neuritis
• Cornea: Abrasion, CRAO
Ulcer, Scar, Edema Ischemia
CRVO
• Anterior chamber: Compression
Hyphema, DR
Hypopian Granulomatous

Retinal Glaucoma
• Lens: Cataract
detachment
Hereditary
• Vitreous: Vitreous
hemorrhage, Trauma
Endophthalmitis
Toxin, Tobacco, Drug

Irradiation
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Ptosis
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Ptosis
• Look for: Eyelid, Pupil, EOM, Other CN, Neighbourhood
sign, Fatiguability test, Motor & sensory & reflex exam

• Nucleus & Fascicles: Neighborhood sign

• Nerve: Other CN, peripheral neuropathy(sensation, DTR)

• NMJ: Fatiguability, Fluctuation, Bulbar involvement, proximal

muscle weakness

• Muscle: Bilateral, Slowly progressive, Family history, proximal

muscle weakness

• +Horner’s
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rd
Ptosis with pupil dilatation - 3 nerve palsy
• Nuclear lesion: bilateral ptosis

• Fascicle lesion: Third nerve fascicle syndrome

• Subarachnoid space lesion: meninges

• Posterior communicating artery aneurysm

• Cavernous sinus/superior orbital fissure lesion

• Nerve lesion: ischemia(pupil spared), inflammation,

infiltrative, compressive lesion
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Ptosis with miosis - Horner’s
• FON pathology • SON pathology

• Hypothalamic • Pancoast tumors

lesions
• Sympathetic schwannoma
• Lateral medullary
plate syndrome • Neuroblastic tumors
(Wallenberg
syndrome) • Goiter
• Syringohydromyelia • Other: Surgery or trauma to
upper thorax or neck,
• Multiple sclerosis -
lesions destroy or compress
MS
nerve roots, neck mass,
• Spinal cord subclavian artery
neoplasms aneurysm
• TON pathology

• Lesion dilates or compresses the carotid artery

• Fibromuscular dysplasia (FMD)

• Carotid dissection

• Skull base, parasellar, and orbital lesions

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Ptosis c/o pupillary involvement in
Neuromuscular diseases
• Ptosis without Ptosis with
ophthalmoplegia ophthalmoplegia

• Myotonic dystrophy OPMD

• Congenital myopathy: OPDM

Centronuclear,
Nemaline, central core CPEO

• Myofibrillar myopathy NMJ disorders

GBS variants
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Diplopia
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Diplopia
• Monocular VS Binocular diplopia

• Causes of monocular diplopia

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 General approach to diplopia
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Binocular Diplopia
• Look for: EOM, Ptosis, Pupil, Other CN, Neighbourhood
sign, Fatiguability test, Motor & sensory & reflex exam

• Nucleus & Fascicles: Neighbourhood sign

• Nerve: Other CN, peripheral neuropathy(sensation, DTR)

• NMJ: Fatiguability, Fluctuation, Bulbar involvement, proximal

muscle weakness

• Muscle: Bilateral, Slowly progressive, Family history, proximal

muscle weakness

• +INO (CVD, MS)

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CN VI lesions
• VI1: Brainstem syndrome(Millard-Gubler)

• VI2: IICP and subarachnoid lesion(pachymeningitis/

leptomeningitis, leptomeningeal metastasis)

• VI3: Petrous apex syndrome(Gradenigo’s syndrome)

• VI4: Cavernous sinus syndrome(CA NP, Metastases,

Meningioma, Tolosa-Hunt, Thrombosis, ICA aneurysm, CCF)

• VI5: Orbital syndrome

• Isolated CN VI palsy: Ischemia, Neuritis, Trauma

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Multiple cranial neuropathies

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Intra-axial lesion Extra-axial lesion
• Presence of neighbourhood
• Subarachnoid space:
sign meningitis, metastasis
• 4-4-4: cranial nucleus —>
• CP angle<SAME>:
above pons, pons, below pons
Schwannoma,
Ependymoma,
• Medial 4M: motor pathway,
Aneurysm, Meningioma,
medial lemniscus, MLF
Metastasis & Lymphoma,
• Lateral 4S: spinothalamic
• Foramen, sinus, fissure
tract, spinocerebellar tract,
syndrome
sympathetic tract, spinal
trigeminal nucleus of CN V
• Nerve itself: GBS
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Foramen, sinus, fissure syndrome
• Cavernous sinus syndrome: CN 3, 4, 6,
V1, V2

• Causes: thrombosis, aneurysm, fistula,

inflammation, tumor(Pituitary, CA NP,
metastasis)

• Superior orbital fissure syndrome: CN

3, 4, 6, V1

• Orbital apex syndrome: CN 2, 3, 4, 6, V1

Gradenigo syndrome: CN 5, 6 , otitis media

Jugular foramen syndrome: CN 9, 10, 11

Causes: glomus jugulare, metastasis, meningioma, bone infection

www.skullanatomy.info
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Dizziness & Vertigo

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Dizziness
• 1. Vertigo

• 2. Presyncope

• 3. Dysequilibrium

• 4. Systemic diseases

• 5. Multisensory dizziness

• 6. Giddiness or functional
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Tips in vertigo: HINTS

• HINTS

• Head impulse test

• Nystagmus: Spontaneous

• Gaze evoked

• Test of skew (Vertical skew deviation)

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Central VS peripheral vertigo
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Peripheral vertigo
• True vertigo Vertigo, tinnitus & hearing
alone loss
• 1) Episodic: 1) Episodic: Meniere’s
BPPV, Vestibular disease, Perilymphatic fistula
paroxysmia
2) Persistent: Labyrinthitis,
• 2) Persistent:
Sudden SNHL, Ototoxicity,
Vestibular
Acoustic Neuroma,
neuronitis
Temporal bone fracture
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Central vertigo
1) Episodic: Migraine, VBI/TIA, MS

2) Persistent:

Acute: Posterior circulation stroke, TBI, CNS

infection

Chronic: Posterior fossa tumor, Chronic

cerebellar disorders
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Abnormal movement
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Key for assessment abnormal movement
• 1. True or Mimic

• 2. Hypo or Hyper kinetic

• 3. Voluntary or Involuntary

• 4. Nature

• 5. Associated features
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Hyperkinetic movement disorders
• 1. Sustained (Dystonia) VS Non-sustained

• 2. Rhythmic (Tremor) VS Non-rhythmic

• 3. Suppressed (Tics) VS Non-suppressed

• 4. Proximal (Myoclonus, Ballism) VS Distal (Chorea >

myoclonus)

• Flow, unpredictable = chorea

Jerk = myoclonus

Twist = dystonia
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Hypokinesia
• 1. Non-neurological hypokinesia

• Metabolic disease(Hypothyroidism), Depression, Pain

• 2. Neurological hypokinesia

• 1) Non-MMD: weakness(CNS, PNS), apraxia, cataplexy

• 2) MMD: (1) Parkinsonism

• (2) Non-parkinsonism —> Blocking tics,

Catatonia, Rigidity, Hesitant gait, Freezing phenomenon
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Parkinsonism
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Parkinsonism
TRAP 2F

Tremor

Rigidity

Akinesia/Bradykinesia

Postural instability

Freezing gait

Flexed posture
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Parkinsonism
1. Primary: Idiopathic PD 80%

2. Secondary parkinsonism: Drug, Structural,

Toxin, Vascular, Metabolic, CJD, Psychogenic

3. Parkinson-plus syndrome: MSA, PSP, DLB,

CBS

4. Heredodegenerative: AD, HD, SCA,

Neuroacanthocytosis, WD, X-linked dystonia-
parkinsonism, Fahr disease, NBIA
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Parkinson-plus syndrome
MSA: autonomic, cerebellar, anterocollis

PSP: vertical gaze palsy, early fall, retrocollis,

procerus sign, applause sign

DLB: dementia, visual hallucination, RBD,

fluctuating confusion

CBS: apraxia, alien limb, cortical sensory loss,

dystonia, myoclonus
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Tremor
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Tremor
• Rhythmic oscillation of body parts produced by
alternating or synchronous contraction of Agonist-
Antagonist muscle

• Step to approach

• 1. Inspection of tremor

• 2. Specific exam for assessment of signs related to

tremor (Neighbourhood sign)

• 3. Syndromic classification of tremor

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Signs related to tremor Inspection of tremor
• Bradykinesia Type

• Muscle tone: coactivation Distribution

• Postural abormalities
Frequency
• Dystonia
Direction
• Cerebellar signs
(Amplitude)
• Neuropathic signs
(Constancy: Persistent,
• Systemic signs Intermittent)
• Gait and stance
(Regularity)
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Tremor type
• 1. Resting : support against gravity —> Parkinsonism, Severe ET, Holmes’ T.

• 2. Action:

• 1) Postural tremor: Outstretched, wing-beating, leg stretching, standing —

> Physiologic T., ET, Neuropathic T.

• 2) Kinetic: flexion-extension, pronation-supination, FTNTF

• -Simple kinetic: Midbrain T., Palatal T., ET

• -Intention tremor: Cerebellar T.

• -Task-specific: writing, standing —> Primary writing T., Occupational T.

• -Isometric: against rapid object —> Sustained extension, dystonic T.

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Specific distribution of tremor
Dystonic
Site ET PD EPT Drug Cerebellar
tremor

Head 1+ - - - - 2+

Vocal 1+ 1+ 1+ - 1+ 2+

Jaw - 2+ - 1+ - 1+

Tongue - 2+ - 1+ - -

Lower limb 1+ 2+ - - - -

Trunk - - - - +2 -
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MDS Tremor consensus

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Gait disorders
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Gait exam Gait cycle anatomy
• Arising from chair Golgi tendon organs &
muscle spindle receptors
• Stance

• Walking base
Spinocerebellar tract

• Step height Anterior lobe cerebellum

• Stride length Dentatorubrothalamic

pathway
• Turning
Medial frontal lobe & SMA
• Stopping

• Arm swing Paracentral lobule

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Gait disorders
Lowest level Middle level Highest level

Bone and joint

Vestibular Pyramidal
Cerebrum
Visual Cerebellum
Cognition
PNS(proprio- Basal Ganglia
ception, LMN)
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Lowest level
• 1. Bone and joint: pain, deformity

• 2. Vestibular system: vertigo + unsteadiness + N/V +- tinnitus, HL

• 3. Visual system: visual impairment

• 4. Proprioception: sensory ataxia, pseudoathetosis, Romberg test

• 5. Nerve, NMJ, Muscle

• 1) Steppage gait: foot drop, compensate with elevate foot, flex hip
and knee, heel strike with loud noise

• 2) Waddling gait(duck): proximal muscle weakness esp. gluteal m.

• Hip extended with seperated feet, more circumduct of pelvic bone

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Middle level
• 1. Spastic gait: pyramidal lesion ! hypereflexia, clonus ! circumduction

• 1) Hemiplegic: CVA, tumor

• 2) Paraplegic: Cord injury, myelitis ! Scissoring gait; adductors

hyperfunction , narrow base ! imbalance, easily fall

• 2. Ataxic gait: cerebellum

• 3. Parkinsonian gait: Shuffling, short step, low height, slow move,

decreased arm swing, slow response to external force, en bloc turn, normal
base in PD

• 4. Dystonic gait: Bizarre, non-stereotyped, normal walking backward

• 5. Choreic gait: non-stereotyped, unpredictable, short continuous movement

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Highest level
• Cerebrum, Cognition

• 1. Cautious gait: slow movement, wide base, short step, small

movement of body while as flex elbow and knee

• 2. Gait apraxia/Magnetic gait:

• Walking disturbances: Ignition failure with feet glued to the floor,

Stiff walk, Difficulty in stopping and turning

• Disequilibrium

• Loss of postural reflexes

• Counterproductive parasitic movements

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Ataxia
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Features Vestibular Sensory Cerebellar
Vertigo + (acute) - +/-
Hearing loss/tinnitus +/- - -
Nausea/Vomiting + (acute) - +/-

+
Limb dysesthesia - +
(brainstem)

Impaired
- + -
proprioception

Coordination - - +
Nystagmus Peripheral - Central

Worsened ataxia +
without visual sense (bilateral + -
(Romberg’s test) vestibulopathy)
Courtesy of Dr.Thararak
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Cerebellar syndrome
• 1. Rostral vermis syndrome (anterior lobe)

• Gait ataxia > Speech

• 2. Caudal vermis syndrome (flocculonodular & posterior lobe)

• Truncal ataxia, Nystagmus

• 3. Hemispheric syndrome (posterior lobe)

• Limb ataxia/dysmetria, Speech, Finger movement

• 4. Pancerebellar syndrome (all lobes)

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Cerebellar function exam

• FTNTF: intention Tandem
tremor, dysmetria
Romberg
• Rapid alternating
movement
Nystagmus
• HTKTS
Saccadic, pursuit
• Tone eye movement

• DTR Speech
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Causes of Cerebellar Ataxia
Onset Acquired Genetic
Inborn errors of metabolism
Episodic -
Episodic Ataxia
Strokes (ischemic/hemorrhagic)
Multiple Sclerosis
Acute Infections (acute cerebellitis, EBV) -
Parainfectious syndromes
Toxic disorders (AED, Lithium, alcohol)
Neoplasm (metastasis)
Paraneoplastic
Infections (HIV, CJD)
Subacute -
Immune (SREAT)
Deficiency syndromes (Vit B1, B12)
Toxic disorder (Alcohol)
Neoplasm (primary, metastasis) Most genetic disorders
Deficiency syndromes (Vit E) -Spinocerebellar ataxia
Chronic Toxic disorder (AED, Alcohol) (SCA)
Idiopathic/sporadic cerebellar ataxia (Multiple -Progressive myoclonic
system atrophy) ataxia(PMA)
Courtesy of Dr.Thararak
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Seizure
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First seizure
• Is this a seizure?

• Is this the first seizure?

• What is the cause: provoked or unprovoked?

• What are the investigations needed?

• Is this epilepsy—what is the epilepsy syndrome?

• What is the risk of seizure recurrence?

• What are the risks and benefits of antiepileptic drug (AED) treatment

• Should this patient be treated with AEDs?

• What are the instructions on safety and lifestyle?

• If AED treatment is initiated, how long should it be continued?

Postgrad Med J 2009;85:667–673
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Seizure history
• Preictal period: aura, prodrome

• Ictal period: clinical seizure(including automatism), consciousness, eye deviation,

tongue biting, bowel & bladder(not confirm dx. of seizure) involvement

• Postictal period: drowsy, headache, todd’s paralysis

• Precipitating factor: physical stress, mental stress, sleep deprivation

• Frequency

• Age of onset

• Progression of symptom

• AED history

• Other medication or herb use

• Other subtle seizure in the past: myoclonic, absent, simple partial, aura
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Differential diagnosis of seizure
• (Faint - Fit - Fake)

• Convulsive syncope

• PNES

• Posterior circulation TIA

• Movement disorders

• TGA

• Migraine
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AAN 2007 recommendation for
investigation in first seizure
• In apparent unprovoked seizure and pt. return to baseline
function

• 1. EEG: should be considered (Lv.B); (high yield, risk of

recurrence) if possible within 24-48 hr.

• 2. CT/MRI should be considered (Lv. B): significant

abnormality 10%, some value in determining risk of recurrence

• 3. Lab studies (Level U): Blood sugar, Electrolyte, CBC,

Lumbar puncture (fever), Toxicology screening

• +-4. EKG: VT, WPW, Brigade, Long QT

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Common causes of seizure
Idiopathic
Trauma
Adolescent Drug or alcohol withdrawal
AVM

Trauma
Young adult Alcoholism
Brain tumor

Brain tumor
CVD
Elderly Metabolic disorder (Uremia, Liver
failure, Dysglycemia)
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Proposed cutoff values for acute symptomatic
seizure in common metabolic disorders

Biochemical parameters Value

Serum glucose < 36 or > 450 mg/dl

Serum sodium < 115 mg/dl

Serum calcium < 5.0 mg/dl

Serum magnesium < 0.8 mg/dl

BUN > 100 mg/dl

Creatinine > 10 mg/dl

ILAE
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When to start AED in first seizure
• Abnormal neuro exam

• High risk for injury

• Focal seizure

• Abnormal brain imaging

• Epileptiform discharge found on EEG

Thai epilepsy guideline 2015

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AED and seizure type

Thai epilepsy guideline 2015

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