When & How To Do a Basic Neurologic Evaluation of Your Patient

Transcription

When & How To Do a Basic Neurologic Evaluation of Your Patient
When & How To Do a Basic
Neurologic Evaluation of
Your Patient
David Sendrowski, O.D.
Professor / SCCO
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Disclosure
Information
Lecture Bureau
for:
’ Alcon Pharm.
’ Allergan Pharm.
’ VSP
’ Ista Pharm.
’ Inspire Pharm.
’ Pfizer Pharm.
Nor do I or any immediate family member have any
personal business interests, affiliation or activity
with any entity in the Optometric health care field
that would give rise to a Conflict of Interest in this
lecture.
No animals were harmed during the development of
this lecture!!
Afferent vs Efferent Problems
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Afferent—
‰ Visual Acuity
‰ Color perception
‰ Contrast
Sensitivity
‰ Visual Fields
‰ Higher cortical
visual function
(obj. recognition)
‰ TIA’s
N
Efferent--‰ Pupils
‰ Eyelids
‰ Facial nerve
‰ Ocular Alignment
and Motility
(EOMs)
‰ Orbital disease
CASE HISTORY
#1 source of information
Patient Profile
’ Age/ Race/ Sex (kids: congenital
neuro disorder and neoplasm,
adults: vascular or degen. or
neoplasm)
’ Height / Weight
’ Right-handed or Left-handed
Chief Complaint:
’ When was the problem first
noticed?
’ How was the problem first
noticed? – Very important!
’ Frequency: How often? Last
episode?
’ Duration: How long does it last?
How long have you had this?
– Prog: compressive mass /
episodic: migraine, carotid.
Chief Complaint:
’
’
’
’
’
When or where is it worse?
Location (flashes central –ONH)
Aggravating Factors
Relieving Factors
Severity
Ocular History
’ Injuries – Important to consider
old contusion injuries.
’ Surgeries
’ Eye diseases
Medical History:
’ Last physical exam
’ Systemic Diseases: current
medical ailments and duration
’ Past illnesses – Strokes, MI,
Cancer, etc.
’ Past surgeries/ Hospitalizations/
Blood Loss
’ Past injuries: Head, neck, back
’ Current medications / Allergies
– Isoniazid--TB
– Lithium – bipolar/ depression
– Cogentin—Parkinson Dz
Family History
’ Similar condition
’ Eye diseases
’ Medical problems
Ex: Leber’s, migraines, MS, have
genetic predispositions and
should be considered.
Lifestyle
’ Occupation
’ Alcohol consumption / Smoking /
Recreational Drug use
’ Diet – Well-balanced?
Children’s History:
’ Birth weight (6 to 9lbs) / APGAR score
(7/10)
’ Full term?
’ Complications with pregnancy?
– Consider maternal drug / alcohol
abuse in some cases
’ Development: Age of walking
and
talking
– Loss – degenerative / delayed with
slow achievement static disease
(encephalopathy from hypoxia)
Neuro-developmental Milestones
Behavioral Event ---------------Age
Lifts head in sitting position
Rolls over
Sits up
Crawls
Walks unassisted
Walks up / down stairs holding
Can stand on one foot
‰
Associated
Neurological
Symptoms
’ Paralysis
’ Paresthesia
’ Weakness
(Asthenia)
’ Seizures
’ Dizziness and
vertigo
’ Gait Disturbances
’ Pain
’ Hearing Loss and
tinnitus
’ Disordered
mentation,
memory or
behavior
’ Endocrine
Irregularities
’ Chewing or
swallowing
difficulties
’ Uhthoff’s symptom
4 mo
6 mo
9–10 mo
10–11 mo
12–15 mo
18 mo
3 yr
EXTERNAL EXAMINATION
N
N
Gross
‰ Physical Disability: Paralysis, etc.
‰ Difficulty with mobility
’ Observe while patient walks to
the examination room
Head Position
‰ Head turn, depression or elevation,
tilt, bobbing
Watch for Neuro Dysfunction ??
Observation is priceless!!
N
Facial Appearance
‰ Symmetry
‰ Forehead: Brow, skin texture,
prominent vessels
‰ Eyelids: Ptosis, retraction
‰ Eyes: Proptosis, enophthalmos,
deviation
‰ Mouth: Droop on one side
OCULAR EXAMINATION
Afferent System Evaluation
‰
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Visual acuity
’ Best Corrected with refraction
’ Pinhole
’ Neutral density filter test – 2 log
– Amblyopia – Less impact on
VA in amblyopic eye
– Optic Nerve disease – worsens
Pupils
‰ Pupil size
‰ Direct response
‰ Look for APD on SFLT !
‰ Subjective Marcus Gunn / APD
‰ Dilation Lag – Horner’s syndrome
‰
Accommodation
’ Will be decreased in cases of
cycloplegia and Adie’s pupil
Evaluation of Horner’s Syndrome
1.
2.
Step one: Confirm that there is a
Horner Syndrome (HS)
N Cocaine supplanted with 0.5%
apraclonidine
Step two: Previous accidental or
surgical trauma to the neck, upper
spine or chest that will explain the HS
N If so, no further work up is
necessary
Evaluation of HS
3.
Step three: Determine is there are
localizing clinical features for the HS
N Ataxia and nystagmus–--medullary
lesion
N Arm pain/weakness/numbness –-lung apex, brachial plexus, and
cervical spine
N Acute neck pain---cervical carotid
artery
Evaluation of HS
4. Step Four: Perform non-targeted
(nonselective) imaging of the upper
chest and neck as far up as the base of
the skull
Anticipate the yield of the
causative lesion will be low
(unknown)
But!! Even if one tumor is found–
gesture may be “life-saving”
Pharmacologic Testing : Pupils
N
N
N
N
N
N
Cocaine (4 or 10%)
Apraclonidine (0.5%) alpha 2 agonist (D/H)
Paredrine (1% Hydroxyamphetamine) or
Pholedrine 5% (derivative)
Phenylepherine (1%) (H>>N)
Pilocarpine (0.1% --- 1.0%)
‰ Objective test to define anterior visual
pathway disorders
New Test (2007- eyelid ptosis from partial
Horner’s – Naphazoline nitrate: Privina)
Anisocoria
Pathway
Involved area
Other signs
Phys Aniso
Dark=Light
Normal
None
None
Pharm Test
None
Horner’s
Dark>Light
Sympathetic
Sympathetic
Ptosis
Anhydrosis
Cocaine (+)
Paredrine (-)
third order /
(+) second
order
Adie’s
Light>Dark
Parasympath
Ciliary Gang
↓Accomm
↓Reflexes
Pilocarpine
0.125% (+) or
0.5% (+)
IIIrd nerve
Light>Dark
Parasympath
Pupil fibers
Ptosis
Diplopia
Pilocarpine
0.12% (+)
&1% (+)
Pharmacol
Light>Dark
Parasympath
Iris Sphincter
↓Accomm
Pilocarpine
0.12% (-)
&1% (-)
Third Nerve Paralysis / Paresis
Adults:
Diabetes
Hypertension
Atherosclerotic
Children:
Trauma
PCA -- most feared
and deadly
Fourth Nerve intact
--- you see incyclorotation
Sixth nerve intact
--- you see abduction
N
Visual Fields
‰ Confrontations
’ Look for the extinction
phenomenon
‰ Red cap test
’ Comparison between two eyes
’ Comparison in each quadrant
‰ Tangent Screen
’ Good for determining functional
vision loss
Amsler Grid
Great for central 10 degrees of field
Red Amsler Grid – Toxic Maculopathies
N
N
Photostress Test
’ Aids in the diagnosis of “wet”
versus “dry” macular disease
’ Prolonged photostress time in
cases of fluid in the macula
(CSC)
Contrast Sensitivity
1. Threshold perimetry:
Goldmann – Kinetic
Automated – Static
N
Where does the VF go to??
N
Color vision
’ Color saturation comparison
’ Kollner’s rule:
– Optic Nerve: Red-Green
– Inner Retina
– Ex: Optic Neuritis, Toxic
neuropathy
– Macula-Retina: Blue-Yellow
– Outer retina
– ARMD, Diabetic Retinopathy
’ Color Plates
’ D-15
’ Munsell 100 hue test
’ Remember:
–
–
–
–
–
–
‰
NS Cataracts affect Blue-Yellow
Monocular!-- Always
Test the more severe eye first!
Good VA with CV loss – think ONH
Poor VA with CV loss – think Macula
Occipital Lobe
Stereoacuity
’ Will be reduced in patients with
chiasmal disease, parietal lobe
lesions and small angle strabismus
Macular vs. ONH Disease
Visual Symptoms
Onset
Visual Acuity
Afferent Pupil Defect
Color Vision
Refractive Error
Photostress Test
Visual Fields
Pain
Macular Disease
Distortion
Gradual
Impaired
Absent or small
B-Y
Hyperopic Shift
Yes, if “wet”
Central scotoma
Never
Optic Nerve Disease
Dimming
Acute or progr essive
Variable
Yes
R-G
None
No
Variable
Sometimes
Efferent System Evaluation – hey doc
check this out??
N
N
Eyelids – MRD 1 and MRD 2
‰ Exophthalmometry
’ Evaluation of enophthalmos or
proptosis – young females
‰ Retropulsion
’ Aids in r/o of retrobulbar mass
‰ Comparison of old photos
’ Determination of duration of
ptosis
Ocular Motility evaluation
‰ Position Maintenance – Primary gaze
‰ Vergences / Ductions
‰ Saccades
‰ Vergence – NPC
’ May indicate midbrain lesion, MS,
encephalitis, if impaired
‰ Oculocephalic – Doll’s head
’ Abnormal eye mvts overcome by OC
stimulation are usually supranuclear.
’ Comatose patients – if OK, nuclear and
intranuclear connections are intact.
Causes Of Slow Saccades
N
Olivopontocerebellar atrophy and spinocerebellar degenerations
Huntington's disease
Progressive supranuclear palsy
Parkinson's disease (advanced cases) and diffuse Lewy body
disease
Whipple's disease
Lipid storage diseases
Wilson's disease
Drug intoxications: anticonvulsants, benzodiazepines
Tetanus
In dementia: Alzheimer's disease (stimulus-dependent) and in
association with AIDS
Lesions of the paramedian pontine reticular formation
Internuclear ophthalmoplegia
N
Cover Test
N
Maddox Rod / Red lens
N
N
N
N
N
N
N
N
N
N
N
‰
Neutralize in 9 fields of gaze Vert and
Horiz
’ Must determine comitancy of the
deviation
Park’s Bielschowski Three Step
Step 1: Determine which eye is hypertropic.
Paralysis of the superior oblique is one cause
of hypertropia.
Step 2: Determine whether the hypertropia is
greater in left or right gaze. Hypertropia due
to superior oblique paralysis is greater on gaze
to the contralateral side.
Step 3: Determine whether the hypertropia is
greater in left or right head tilt. Hypertropia
due to superior oblique paralysis is greater in
a head tilt to the ipsilateral side
N
Forced Duction Testing
‰ Utilization of cotton-tipped
applicator or forceps on an
anesthetized eye
‰ Differentiate restrictive vs.
neuropathic myopathy
N
Bell’s phenomenon
‰ May indicate supranuclear disorders
‰ Pt. can’t look up but Bell’s intact:
brain stem pathway, EOMs, nuclear
cell complex, and motor neurons -OK
N
Optokinetic Nystagmus
‰
Useful for “blind” patients or malingerers
‰
Parietal lobe lesions and midbrain
disorders
Etiology of Fourth N. Problems
Adult: Trauma, congenital, other
Children: Congenital, Trauma
Elderly: Vascular, idiopathic, other
‰
Double Maddox rod test
’ when you suspect bilateral SO palsies
’ Greater than 10 degrees of torsion is
suggestive of bilateral SO
Sixth Nerve Etiologies:
Adult: Idiopathic, other, neoplasm
Children: Neoplasm, trauma, inflamm.
Ocular Motor Combinations.
3rd and 4th N– think aneurysm or neoplasm
3rd and 6th N. – think neoplasm or idiopathic
All three – think neoplasm.
N
Ocular Health Evaluation
‰ Biomicroscopy
‰ Tonometry
‰ Gonioscopy – if indicated
‰ Fundus Evaluation
N
Systemic Evaluation
‰ Blood Pressure / Pulse
‰ Carotid Auscultation
‰ Cranial Nerve Testing
’ Indications: Orbital Fracture,
neuropathy, Pulsating red eye
’ Olfactory: Detection and
Identification
’ Corneal Sensitivity – Trigeminal
’ Superficial Stimulation (V)
’ Facial Smile (VII)
’ Hearing/ Webers (VIII)
’ Vowel Pronunciation (IX, X)
’ Shoulder Shrug (XI)
’ Tongue Twister (XII)
‰
Neurologic Screening
’ Mental Status
’ Sensory System – Spinothalamic Tract
’ Motor System – Corticospinal Tract
’ Coordination – Cerebellum
’ Spinal Reflexes
ADDITIONAL TESTS
N
Neuroimaging
‰
Computed Tomography (CT):
’ Collimated X-rays are sent
through a structure
’ Density of the tissue determines
the amount of X-ray
attenuation
CT Scans: Orbit, solid tumors, great
anatomical evaluation of the head and
neck.
’ Computer reconstructs an image based
on amount the attenuation in a grayscale
format
’ The denser the media, the lighter
the structure appears
’ Sometimes vascular lesions are
enhanced with an iodine based
contrast substance
’ Best for calcified lesions and
fresh hemorrhages
– ORBITAL DISEASE
CT Scan
of Cerebral
Hemorrhage
‰
N
T1
‰
‰
‰
N
Magnetic Resonance Imaging (MRI)
’ Strong magnetic field is applied
to the tissue which cause the
hydrogen protons to resonate
and emit radiowaves
’ Preferred for analysis of
infarctions, demyelinating
plaques, and soft tissue
involvement
’ Gadolinium is used as a contrast
agent with MRI
N
Brain tissue
- Light
CSF, H20, Fat
- Dark
Anatomical Detail
T2
‰
‰
‰
Brain Tissue
- Dark
CSF, H20, Fat
- Light
Pathological Detail
Laboratory Tests – Most Common
‰ Utilized to rule out systemic causes
of neuro-ophthalmic dz
’ Complete Blood Count (CBC)
with Differential
’ Westergren Erythrocyte
Sedimentation Rate (ESR)
’ Fasting Blood Sugar
’
’
’
’
’
Lipid Profile
VDRL and FTA-ABS
AntiNuclear Antibody (ANA)
Thyroid Function Tests
PPD