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LOCALIZATION
NEUROLOGY
EPISODE V
VISUAL LOSS AND WRIST DROP
EPISODE V 2012
VISUAL LOSS
LOCALIZATION NEUROLOGY
PAWUT MEKAWICHAI MD
DEPARTMENT of MEDICINE
MAHARAT NAKORNRAJSIMA HOSPITAL
CN II : OPTIC NERVE
VISUAL PATHWAY
Retina
Optic nerve
Lateral geniculate body
Optic radiation
Optic chiasma
Optic tract
Occipital lobe
CN II : OPTIC NERVE
VISUAL PATHWAY
Optic nerve
Optic chiasma
Optic tract
Lateral geniculate body
Optic radiation
Occipital lobe
VISUAL LOSS
PRECHIASMATIC LESION: pupil impair
POSTCHIASMATIC LESION: intact pupil
PRECHIASMATIC LESION
Monocular blindness
• Transient monocular blindness
• Optic neuritis
• Anterior ischemic optic neuropathy
• Giant cell (temporal) arteritis
Binocular blindness
• Papilledema
• Papillitis
TRANSIENT MONOCULAR
BLINDNESS
Amaurosis Fugax
Sudden onset of visual loss
Retinal TIA
Risk of infarction = 14 % in 7 yr.
Rx as TIA esp. carotid stenosis
OPTIC NEURITIS
Eye pain with visual loss in day
Demyelinating disease of optic nerve
Central scotoma (enlarge blind spot)
VA drop, fundi – pale disc (optic atrophy)
Pupil – RAPD (+)
OPTIC NEURITIS
Multiple sclerosis
Meningeal/ parameningeal/ ocular inflammation
Post viral infection
Autoimmune disease – SLE
Rx pulse Methylprednisolone 1g/d X 3 d
No oral steroid alone (high recurrence)
ANTERIOR ISCHEMIC
OPTIC NEUROPATHY
Infarction of optic nerve
Painless sudden onset of visual loss
CRAO, CRVO
Ipsilateral disc swelling with hemorrhage
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2
1. CRVO
2. OPTIC ATROPHY
3. CRAO
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GIANT CELL (TEMPORAL) ARTERITIS
Vasculitis at temporal artery
Involve retinal artery (blindness)
Age > 60 with unilateral headache
Abnormal temporal artery (decrease pulse, nodule,
abnormal biopsy)
increase ESR 90 % (> 50 mm/h) or increase CRP level
Rx prednisolone 1 MKD
Associated with Polymyalgia rheumatica
POLYMYALGIA RHEUMATICA
Healey criteria, 1984, 6/6
1. Persistent pain (> 1 month) involve two of :
neck, shoulder, pelvic
2. Morning stiffness > 1 hour
3. Rapid response to prednisolone (< 20 mg/d)
4. Age over 50
5. ESR > 40 mm/hr
6. No others disease (negative for ANA, RF)
Grade I papilledema is
characterized by a C-shaped
halo with a temporal gap
Grade II papilledema, the halo
becomes circumferential
Grade III papilledema is
characterized by loss of major
vessels AS THEY LEAVE the disc
(arrow)
Grade IV papilledema is
characterized by loss of
major vessels ON THE DISC.
Grade V papilledema has the
criteria of grade IV plus partial
or total obscuration of all
vessels of the disc.
BINOCULAR BLINDNESS
Papilledema
• Increase ICP, headache with VA drop
• Increase CSF protein spinal cord tumor, GBS
• Idiopatic (Drusen)
• Happen in hour or day but resolve in 2-3 mo.
Papillitis/Uveitis
• Eye pain with severe VA drop
• Fundi – optic disc swelling
• Infiltrative or inflammatory
• Leukemia, SY, CA, Sarcoidosis, uveominigitis syndrome
UVEITIS
Anterior (involving the iris)
Intermediate (involving the ciliary body),
Posterior (involving the choroid)
Panuveitis (involving all the parts).
involves the middle layers eye, also called the uveal tract or uvea
many veins and arteries transport blood to the eye
Iritis: most common form of uveitis
affects the iris
often associated with autoimmune disease: RA or sarcoidosis.
Cyclitis: inflammation of the middle portion of the eye
may affect the muscle that focuses the lens.
Retinitis: affects the back of the eye
may be rapidly progressive
may be caused by infectious agent
Choroiditis : an inflammation of the layer beneath the retina
may caused by an infection such as tuberculosis.
MENINGO-UVEITIS SYNDROME
Cause
infection: CMV, TB, SY, toxoplasmosis
immune: Bechet, VKH, sarcoid, lymphoma
SLE, AS, JRA, MS, Sjorgen
MENINGO-UVEITIS SYNDROME
VKH = Vogt-Konayaki-Harada
Uveitis with meningitis,
Strand depigmentation of hair
and skin around eye
(poliosis circumscripta)
Loss of eyelashes
Deafness
POST CHIASMATICS LESION
Spare pupil
VF defect follow lesion
Bilateral occipital lobe infarction
• Tip of basilar lesion
• Posterior leukoencephalopathy
• Cortical blindness/Anton’s syndrome
• Macular sparing
• DDx with psychologic blindness
VISUAL FIELD DEFECT
CORTICAL BLINDNESS
bilateral loss of vision with normal pupillary
responses and no other ocular abnormalities
bilateral retrogeniculate lesions
some patients deny their blindness (Anton syndrome)
sometimes perceive moving targets (Riddoch phenomenon)
unformed visual hallucination
causes
cardiopulmonary arrest, cardiac surgery, CVA, head trauma,
central nervous system infection, epilepsy, cerebral or
vertebral angiography, uremia, hypoglycemia, carbon
monoxide poisoning and irradiation
Visual loss
Pupil
Poor
Good
Prechiasmatic
Postchiasmatic
Monocular blindness
Amaurosis fugax
ON
AION
Temporal arteritis
Binocular blindness
Papilledma
Papillitis
VF
Visual pathway
Cortical blindness
EPISODE V 2012
WRIST DROP
LOCALIZATION NEUROLOGY
PAWUT MEKAWICHAI MD
DEPARTMENT of MEDICINE
MAHARAT NAKORNRAJSIMA HOSPITAL
Wrist Drop
Increased reflexes
Pyramidal pattern of weakness
UMN lesion
eg. Lesion at motor cortex
(hand area), ALS
Decreased reflexes
Unilateral
Bilateral
Polyneuropathy
- lead
LEAD NEUROPATHY
C7 lesion
Post. cord
Radial Nerve
axilla lesion
spiral groove lesion
Post. interosseous Nerve
WRIST DROP with DECREASE REFLEX
C7 lesion (atypical)
Posterior cord of brachial plexus
weakness: radial N.+ axillary N. (deltoid)
Radial N. at axilla eg. from crutches
weakness: all radial m.
Radial N. at spiral groove
weakness: radial m. except triceps
Posterior interosseous n.
spare brachioradialis, supinator,ext. carpi radialis
finger drop without wrist drop
radial deviation of wrist, no sensory loss
POSTERIOR INTEROSSEOUS NERVE
finger drop without wrist drop
radial deviation of wrist, no sensory loss
POSTERIOR CORD
Action
Muscle
Root
Nerve
Extend wrist
Ext. carpies
C 7,8
Radial
Extend fingers
Ext. digitorum
C 7,8
Radial
Abduct thumb
Abd. pollicis brevis
C8,T1
Median
Flex 2,3 fingers
Flex. digit. Profundus
II, III
Opp. Pollicis
C8, T1
Median
C8, T1
Median
Flex 4,5 fingers
Flex. digit. Profundus
IV, V
C8, T1
Ulnar
Abduct fingers
Dorsal interossei
C8,T1
Ulnar
Adduct fingers
Palmar interossei
C8 , T1
Ulnar
Opponens
LOCALIZATION
NEUROLOGY
EPISODE VI
HEARING LOSS AND GAIT ATAXIA
EPISODE VI
HEARING LOSS
APPROACH and DIAGNOSIS
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Cochlea and Auditory nerve
Pons (superior olive)
lateral lemniscus
Inferior colliculus
Thalamus (median geniculate body)
Auditory cortex
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TUNNING FORK TEST
RINNE’S Test and WEBBER’S Test
Rinne’s test:
Air Conduction > Bone Conduction = normal or SNHL
Bone Conduction > Air Conduction = CHL or dead ear
Webber’s test:
in CHL heard loudest in the affected ear
In SNHL heard louder in the unaffected ear
CAUSE of HEARING LOSS
Acoustic Trauma (Noise)
Age related
Genetic
Ototoxic Drugs: aminoglycoside, furosemide
Infection: VDRL
Illness (examples)
– Autoimmune Disease
– Meniere’s Syndrome
– Acoustic Neuromas
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DIPOLPIA
Infranuclear
Supranuclear
Long tract sign
Extraaxial
INO
1 1/2
Intraaxial
Exclude NMJ, muscle
group
Foramen syndrome
Ungroup
Subarachnoidal space
SNHL
Unilateral
Bilateral
bilateral lesion
IMPOSSIBLE
long tract signs
Bilateral CN8
Intrinsic
Extrinsic
Exclude NMJ, muscle
Ungroup
EXACTLY
Subarachnoid space
Pontine lesion
CN8 lesion
Group: foramen syndrome
Ungroup: subarchnoid space or base of skull
Isolated CN8 : vestibular neuritis, Meniere’s disease
EPISODE VI
ATAXIAS
APPROACH and DIAGNOSIS
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Ataxia Approach
1. Weakness ?
2. Sensory ataxia:
failure of proprioceptive information to the CNS
disorders of spinal cord or peripheral nerves
can be compensated for by visual inputs
3. Vestibular: vestibular organ, brain stem lesion
4. Cerebellar: cerebella signs/acute or chronic
Midline Cerebellar Lesion
anterior and posterior parts of the vermis
concerned with posture, locomotion, position of head
relative to trunk, control of EOM’s
cerebellar signs resulting from midline cerebellar disease
disorders of stance/gait
truncal ataxia
postural disturbances
rotated postures of the head (titubation)
disturbances of eye movements
Hemispheric Cerebellar Lesion
cerebellar hemisphere and dentate nucleus on each side
concerned with the planning of movement in connection
with neurons in the Rolandic region of the cerebral cortex
(fine skilled)
lesions result in
abnormalities of skilled voluntary movements
hypotonia, dysarthria, dysmetria, dysdiadochokinesia,
excessive rebound (over shoot) and pendulum reflexes
impaired check, kinetic and static tremors, past-pointing
(dysmetria)
Cerebellar Signs
“Over shoot”
Cerebellar Ataxia
acute
Stroke or Transient ischemic attack (TIA)
brain stem syndromes, cerebellar
Multiple sclerosis (MS)
Postviral infection (cerebellitis) eg. Chickenpox
uncommon complication, appear in healing stages of the infection
and last for days or weeks, resolves completely
Toxic reaction
phenobarbital, benzodiazepines, alcohol, heavy metal (lead or
mercury), solvent poisoning (paint thinner)
Cerebellar Ataxia
chronic
Cerebral palsy
Arnild Chiari malformations: type I, II, III
Paraneoplastic syndromes: Anti Yo
rare, degenerative disorders triggered
by immune response to tumor
most commonly from lung, ovarian, breast or lymphatic
Tumor: metastasis, hemangioma
Degeneration: alcohol, phenytoin
Genetic disease: SCA, EA
Autosomal Dominant Ataxias
Spinocerebellar ataxias
labeled 28 autosomal dominant ataxia genes (SCA1-SCA28) according to
their order of discovery
cerebellar ataxia and cerebellar degeneration are common to all types, but
other signs and symptoms- age of onset are differ depending on the
specific gene mutation
Episodic ataxia
six types of ataxia that are episodic rather than progressive (EA1-EA6)
all but the first two are rare.
EA1 : brief ataxic episodes last seconds or minutes, triggered by stress,
being startled or sudden movement, associated with muscle twitching
EA2: longer episodes from 30 minutes to six hours, triggered by stress
some cases symptoms resolve in later life, not shorten life span
symptoms may respond to medication, such as acetazolamide (Diamox) or
phenytoin
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Repeats and autosomal dominant ataxias
Anticipation – repeat size expands during transmission, the larger the repeat size the
earlier the age of onset and more severe symptoms
Spino-Cerebellar Ataxia Type 3 (SCA 3)
MJD
Clinical features: Adult (after 40) onset gait ataxia, Parkinsonian
signs, ophthalmoparesis or nystagmus, leg areflexia, Babinski
signs, nystagmus, mild cerebellar tremors, diabetes
Inheritance: Autosomal dominant
About 40 % of dominant ataxias in one study
Chromosome: 14q24.3-q32
Mutation: CAG repeat expansion in ATXN3 gene
Testing: Gene testing available
Autosomal Recessive Ataxias
Friedreich's ataxia:
involves damage to cerebellum, spinal cord and peripheral nerves
Progressive limb and gait ataxia usually beginning before 25
rate of disease progression varies (wheelchair within 15 years)
axonal polyneropathy: absent DTR but BBK (+)
muscles weaken , waste and deformities (pes clavus)
slow-slurred speech fatigue
death from cardiomyopathy and heart failure
GAA trinucleotide repeat expansions in frataxin gene (9q13)
Ataxia-telangiectasia
Congenital cerebellar ataxia:
type refers to ataxia that results from damage to the cerebellum
that's present at birth
Wilson's disease
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