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When & How To Do a Basic Neurologic Evaluation of Your Patient David Sendrowski, O.D. Professor / SCCO N N N 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 N 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  N 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