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 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