(WCS 19 & 20) Where and what is the lesion

JC WCS 19&20: WHERE IS THE LESION
Dr SL Ho

Medicine

Thu/Fri 14/15-11-02
WHERE IS THE LESION?

Cerebral cortex

Subcortex

Brainstem: midbrain, pons, medulla

Spinal cord, root, plexus

Peripheral nerves

NMJ

Muscle

GOOD HX

The principle of taking a good history is the same whatever the system

History will provide clues to the location and the nature of the lesion

Taking a history in NOT THE SAME as a dictation

Avoid irrelevant or too much details in your history and examination

Make use of important "negatives" (eg. m weakness but no numbness - unlikely to be peripheral n (contain S + M) b/c peripheral neuropathies affecting only S or M rare ® could be NMJ? Fatigability ® M? Prox m weakness

Experience and knowledge are essential in deciding what is important in the history and examination

Don't present irrelevant and tedious details

Extent of investigations can never replace the history and physical examination, especially for neurological problems

COMPETENT EXAM

No ideal neurological technique (be systematic)
Practice makes perfect
General observation, state of consciousness (eg. depressed, drowsy, comatose), gait (eg. broad-based, unsteady)
Hx: focus on relevant parts
Signs manifest as abn in

Body contour + posture (eg. m wasting - UL: 1^st dorsal interossei, (hypo)thenar m's)
High mental function
Motor - eg. gait, tone, m power, reflexes, incoord'n
Sensory

Correlation of clinical signs to anat
Making up signs is as misleading as missing signs (if signs do not fit with your Dx, you must have DDx)

UMN LESION VS LMN LESION

UMN Lesion	LMN Lesion
No early wasting	Wasting ± fasciculation
Tone, weak, reflexes	¯ Tone, weak, ¯ reflexes
Babinski sign	No Babinski sign

NEUROLOGICAL LOCALISATION (many o'lap but not full picture alone)

Practice makes perfect
Focus on examining what is relevant (a good history is crucial)

Cerebral cortex

Higher mental functions

¯ memory/ orientation/ consciousness/ understanding/ expression of speech (receptive vs. expressive dysphagia)

Apraxia: difficulty with familiar and purposeful task despite normal strength (eg. tie, buttons, make-up)

Hallucinations, seizures

Test the sensorium (consciousness, orientation, attention span, memory, insight, judgement, calculation)

Lobes

Frontal: disinhibition, emotional lability, ¯ planning ability, expressive dysphagia (Broca's - inferior frontal gyrus)

Temporal: amnesia, aggression, TLE (temporal lobe epilepsy), receptive dysphagia (Wernicke's - superior temporal gyrus), upper quadratic VF defect

Parietal: agnosia (tactile, visual), apraxia (draw clockface), acalculia, hemineglect (esp. if non-dominant lobe), lower quadratic VF defect

Occipital: contralat hemianopia with macula sparing, visual hallucination

Consider

Lesion of dominant or non-dominant hemisphere? (Dominant - apraxia, agnosia, dysphagia most easily observed)
Diffuse cortical lesion (eg. encephalopathy)?

Higher mental function

Take into acc state of consciousness

Orientation: t, place, person

Conc'n: no ifs ands or buts

Memory: immediate recall, ST, LT (general knowledge relevant to era eg. last HK governor = Chris Patten)

Calculation: serial 7's

Language: u'standing, expression (3-step instruction, do not demonstrate to Pt)

Visual-spatial orientation (apraxia): intersecting pentagons

Knowledge: dep on educ'n level

Mood

Judgement (concrete): man #'ed both legs and ran to AED - what is wrong with this? (Similarity bet apple and banana ® fruits: abstract, have skin: concrete)

Content of thought: paranoia, schizophrenia, delusion (psychiatrists)

Eg. MMSE

Total score = 30 (>24 normal)
< 24 abn but total score not as important as specific domain affected (eg. AD - OK LT memory but deficient other domains like insight - realisation that something is wrong)
Brief screening measure of cognitive impairment
Tests various domains of cognition

Pyramidal (somatic motor) system

Corticospinal and corticobulbar tracts
Differentiate: ask if facial/ H&N symptoms (speech, numbness, etc.)
Motor functions: weakness, dysphagia, abn gait

Corticospinal - PMC to SC

H&N spared

(numbers refer to SC not vertebrae - SC ends at L1-2, then corda equina)

Above C5: UMN signs below level of lesion (eg. quadriplegia) if affecting both sides
C5-T1: LMN signs UL, UMN LL
T2-12: sensory level trunk, UL spared, UMN signs LL
L1-S5: UL spared, LMN signs LL, sphincter disturbance

Corticobulbar - PMC to BS

Vertical nystagmus (cf. cerebellar = horiz), prob with conjugate gaze

Specific CN deficit (ie. H&N) - diplopia, dysphagia, facial numbness, deafness, difficulty talking/ chewing

UMN signs below level of lesion (eg. spastic quadriplegia) - b/c CB + CS tracts meet in midbrain at cerebellar peduncles \ lesion in midbrain downwards usu affects both sides

Other signs - dep on intrinsic struc in BS

Perform tests for tone, power, limb reflexes, reinforcement, Babinski’s response
Recognise wasting, fasciculation, spasticity, hyper/hyporeflexia,
Differentiate between an upper and lower neurone lesion
Correlate the signs to the level of the lesion

Thalamus

Input for sensory afferents, cerebellar + BG output to cerebral cortex
Contralat sensory loss/ impairment

Extrapyramidal system

Basal ganglia

Caudate nucleus, putamen, globus pallidum, substantia nigra
Parkinsonian features, dystonia
Various movement disorders

Co-ordination of movement (unsteadiness, stiffness, tremor, dysphagia)

Abnormal gait and movements, rigidity, bradykinesia, gait disturbance
Abnormal speech

Brain Stem

Specific syndrome: lateral/ medial medullary syndrome
May develop

UMN signs in limbs (esp. contralat aspect b/c pyramidal tract crosses in pyramid - hemiparesis)

Specific CN deficit (at level of lesion) (pons: CN VII nucleus \ LMN lesion)

Internuclear ophthalmoplegia (medial longitudinal bundle)

Vertical nystagmus

Coma (RAF)

Pin-point pupils

Dysarthria, dysphagia (esp. if medulla affected)

DIAG: midbrain from dorsal aspect: mesencephalic nucleus of V very long (sensory) from midbrain to upper cervical cord \ lesion at C1-2 may inv this tract (innervates nose)

Cerebellar system

Vermis: truncal ataxia (eg. difficulty sitting up), dysarthria
Cerebellar hemispheres

Dysmetria (past-pointing, intention tremor, finger-nose + heel-shin test)
Dysdiodochokinesis (abn rapid repetitive movt)
Dysarthria, "rebound phenomenon", broad-based gait, nystagmus (lateral)

Spinal Cord

Cervical C1-8
Thoracic T1-12
Sacral S1-5
Brachial plexus C5-T1
Lumbosacral plexus L4-S5
Ventral root motor
Dorsal root sensory (cell body outside SC)

These form one spinal root \ if only one spinal root affected, must be close to SC

Cauda equina: n root of lower SC
Glove and stocking sensory loss: all nerves (rather than specific nerve or n roots)
Spinal cord level

LMN at level of lesion
UMN signs below lesion
Unaffected above level of lesion
Dermatomal sensory level
May get different specific deficits dep on area of SC affected

Spinal root

Eg. radiculopathy affecting only T1 ® supplies intrinsic m of hand

Pancoast tumour at apex, lower trunk brachial plexus
False cervical rib: prominent transverse process in C8, lig presses on T1
Thoracic outlet syndrome

LMN signs
Dematomal sensory level
Cauda equina (multiple n roots, sphincter affected)

Plexus (plexopathy)

a) Multiple n's affected

NMJ

Power (weakness in eyelid, external ocular m's, resp m's, pharyngeal m's, neck, jaw, limbs ® \ diurnal variation in muscle strength, double vision, drooping of eyelids, dysphagia)

No sensory deficit

Learn the anatomy of NMJ and correlate anatomy with fatigability (worse twd end of day)

Muscle

Eg. Polymyositis

Power (proximal weakness especially with climbing stairs, standing from sitting, or combing hair)

± M tenderness/ pain

± Wasting

No sensory disturbance

Recognise and distinguish between (EMG) weakness induced by a myopathy and a disorder of the pyramidal system

Sensory system

Numbness, pin/needles
Different sensory modalities (posterior column/spinothalamic)
Distribution of the dermatomes
Dermatomal sensory versus "glove and stocking" distribution
Significance of the distribution and modalities of sensory deficit
Correlate the deficit with the location of the lesion

Peripheral nerves

Both motor and sensory functions - usu all sensory modalities (some > others)
Weakness, numbness, pin/needles, LMN signs
General neuropathy

LMN signs in UL + LL
Distal > proximal weakness
Glove and stocking sensory loss
Resp m's may be affected

Isolated compressive neuropathy

LMN sign of n affected

Dermatomal deficit of n affected

Eg. Ulnar: C8-T1 ® intrinsic hand m's (hypothenar, dorsal interossei) + sensory loss in C8-T1)

WHAT IS THE LESION

Common causes are more common

Congenital/ Developmental: ¯ age, +ve fam Hx, consanguineous birth (eg. Pakistani/ Wilson's disease, Jews)

Vascular: sudden onset (infarct or haemorrhage), transient nature, risk factors of vasc dis

Degenerative: age, gradual onset, progressive course

(Para)neoplastic: insidious onset, progressive, other gen features (eg. ¯ wt/ app)

Demyelinating: exacerbating/ remitting course (episodic)

Inflammatory: infective/ autoimmune, fever (acute/ chronic), general malaise, signs of infection/ inflammation - eg. LN, skin rash, jt pain

Metabolic/ Toxic: precipitating cause (eg. drugs), exacerbation of previous system disorder (eg. encephalopathy)

Trauma/ Physical: cause and effect usu seen/ from Hx

Clues to the nature of the lesion: location of lesion, spectrum and pattern of clinical features

Demyelinating lesions: usu at paraventricular region
Haemangioblastoma: usu in posterior fossa
Commonest cause of CN VII palsy = Bells palsy (do not say surgeon cut it!)

Note: lymphadenopathy

Infection
Neoplasm (eg. lymphoma)
Autoimmune (eg. vasculitis)

SYRINGOMYELIA

Expansion in central canal (eg. cyst) at foramen magnum \ presses on central canal

If lesion central in cord ® spinothalamic affected ® loss of temp and pain in (eg.) C5-T1

If horizontal, elongated lesion ® dermatomes (pin-prick, temp), corticospinal (UMN lesion in LL), anterior horn cells (LMN lesion of C8 + T1)

BROWN-SEQUARD SYNDROME

Eg. T7-8 left side

Ipsilateral loss of sensation at level affected
Below level of lesion

Contralat loss pain and temp
Ipsilateral loss proprioception, 2-pt discrimination, jt + pos'n sensation

LATERAL MEDULLARY SYNDROME (WALLENBERG'S SYNDROME)

Eg. From stroke (most common syndrome in BS)

Spinal nucleus and desc tract: ipsilateral loss trigeminal (pin-prick, cannot do proprioception + vib's in face!) + temp at level
Descending sympathetic pathway: ipsilat Horner's syndrome (partial ptosis, sm pupils, anhydrosis, enophthalmos)
Spinothalamic tract: contralat loss of pain and temp sensation in trunk and limb, occasionally face
Inv some/ all struc in open-medulla on dorsolat side

Inf cerebellar peduncle: ipsilat cerebellar ataxia

Vestibular nuclei: nystagmus, vertigo, nausea + vomiting

Fibres or nuclei of IX + X: palatal paralysis + ¯ gag reflex, vocal cord paralysis ® hoarseness

Normal and abnormal physical signs

In general, do not rely entirely on just one isolated symptom or physical sign, especially if it goes against the rest of the history or other examination findings

Examples of "hard" physical signs:

Wasting

Fasciculations: regen'n of MU \ not always present

Limb reflexes

Babinski’s sign

Nystagmus

Dysconjugate gaze

Gag reflex

Corneal and pupillary reflexes

Cog-wheel rigidity

Examples of "soft" physical signs

(especially if they are isolated and do not correlate with the other findings):

Power
Sensory deficits
Unsteadiness

Important messages

Core lecture notes or core lectures can never replace recommended textbooks
These core lectures provide only a guide
You should read your textbooks

Davison’s Principles and Practice of Medicine. Edited by C Haslett, ER Chilvers, JAA Hunter, NA Boon. Eighteenth Edition, Churchill Livingstone
Neurology in Practice. Edited by YL Yu, JKY Fong, SL Ho. Second Edition, Hong Kong University Press

Long case: check

Fundi
BP
Bedside urine
Reflexes - may not c/o probs (eg. M) but has absent ankle reflexes