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Diseases » Vision Impairment » Diagnosis
 

Diagnosis of Vision Impairment

Vision Impairment Diagnosis: Book Excerpts

Diagnosis of Vision Impairment: medical news summaries:

The following medical news items are relevant to diagnosis and misdiagnosis issues for Vision Impairment:

Diagnostic Tests for Vision Impairment: Online Medical Books

16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about diagnostis of Vision Impairment.


DIPLOPIA: Ask the following questions:
(Algorithmic Diagnosis of Symptoms and Signs)

  1. Is it unilateral? Diplopia that is unilateral is rare, but it can be encountered in ectopia lentis as associated with Marfan's disease, as well as in congenital double pupil, cataracts, and corneal opacities.
  2. Is it intermittent? Intermittent diplopia would make one think of myasthenia gravis, but remember, Eaton-Lambert syndrome can do the same thing.
  3. Is there associated proptosis? If there is associated proptosis, one should consider hyperthyroidism or pituitary exophthalmos, especially if it is bilateral. However, when it is associated with chemosis and ecchymosis, one should consider an infectious process.
  4. Is there chemosis, ecchymosis, or periorbital edema? These findings should make one think immediately of cavernous sinus thrombosis, but an arteriovenous aneurysm can produce unilateral chemosis, ecchymosis, and exophthalmos.
  5. Are there associated long tract neurologic signs? The findings of associated pyramidal tract or other long tract signs would make one think of a brain stem infarct or a brain stem tumor. Advanced intercranial pressure will put pressure on the sixth nerve and cause diplopia. Multiple sclerosis may cause long tract signs along with extraocular muscle palsies.
  6. Is there fever or chills? Findings of fever and chills and diplopia should make one think of an orbital abscess, a brain abscess, or a cavernous sinus thrombosis. There is also the possibility of diphtheria.

DIAGNOSTIC WORKUP

An expensive diagnostic workup may be avoided by referring the patient to an ophthalmologist or a neurologist at the outset. If the diplopia is intermittent, a Tensilon test would be indicated. If there are fever and chills, one should do a CBC, sedimentation rate, possibly blood cultures, skull x-ray, and x-rays of the sinuses. However, under these circumstances, it will usually be necessary to perform a CT scan of the brain, sinuses, and orbits. If there is chemosis or ecchymosis, a cavernous sinus thrombosis is likely, and immediate admission to the hospital and administration of antibiotics after blood culture has been drawn are indicated. MRI of the brain may be necessary to diagnose multiple sclerosis and some of the brain stem infarcts.

 

» READ BOOK EXCERPT ONLINE »

Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

EYE PAIN: Ask the following questions:
(Algorithmic Diagnosis of Symptoms and Signs)

  1. Is there redness of the eye? Redness of the eye suggests definite eye pathology. Without redness, one should suspect disease in the adjacent structures or retrobulbar neuritis.
  2. If there is redness, is there periorbital edema as well? Periorbital edema should suggest a cavernous sinus thrombosis or herpes zoster.
  3. If there is periorbital edema, is there a rash? A rash, particularly vesicular rash, would suggest herpes zoster.
  4. In cases without redness of the eye, is there any abnormality on examination both with the naked eye and with the ophthalmoscope? A dilated pupil would certainly suggest glaucoma; ophthalmoscopic examination may show optic neuritis or retinal detachment. A visual field examination may detect optic neuritis, retrobulbar neuritis, and retinal artery occlusion. A visual acuity check may pick up a refractive error.
  5. Finally, is there headache associated with the eye pain? This would be suggestive of migraine or cluster headache.

DIAGNOSTIC WORKUP

The primary care specialist may want to treat cases of obvious conjunctivitis without a culture and sensitivity. However, a smear and culture is useful especially if Neisseria is suspected. A smear may also reveal eosinophils suggesting allergic conjunctivitis. The primary care specialist may also use fluorescein dye to diagnose a foreign body. Most primary care physicians feel competent to use tonometry to diagnose glaucoma and may feel competent to use a slit lamp. However, when there is any doubt about the diagnosis, the most cost-effective approach is to refer the patient to an ophthalmologist.

 

» READ BOOK EXCERPT ONLINE »

Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

HEMIANOPSIA: Ask the Following Questions:
(Algorithmic Diagnosis of Symptoms and Signs)

  1. Is it intermittent? Intermittent hemianopsia, whether it is bitemporal or homonymous in type, would suggest migraine, carotid artery insufficiency, or vertebral basilar artery insufficiency.
  2. Is the hemianopsia of sudden or gradual onset? Sudden onset of hemianopsia would suggest a vascular disorder such as cerebral thrombosis, embolism, or hemorrhage, but it may also suggest multiple sclerosis or a ruptured aneurysm. Gradual onset of hemianopsia would suggest a space-occupying lesion.
  3. What type of hemianopsia is it? A bitemporal hemianopsia often suggests a pituitary tumor, especially if there are endocrine changes, but it may also be due to an aneurysm compressing the optic chiasm. Homonymous hemianopsia suggests involvement of the optic tract or occipital cortex. This may be by a space-occupying lesion, an aneurysm, arterial thrombosis, an embolism, or a hemorrhage.
  4. Are there long tract signs? Neurologic signs of pyramidal tract involvement or posterior column involvement would suggest anterior or middle cerebral artery occlusion, epidural hematoma, or multiple sclerosis if it is acute and compression of the cortex by a subdural hematoma or brain tumor if it is chronic.
  5. Are there endocrine changes? The presence of weight loss, hair loss, or diabetes insipidus would suggest a chromophobe adenoma of the pituitary. On the other hand, a protruding jaw, enlargement of the hands and fingers, and hypertrophy of the other tissues suggest acromegaly.
  6. Is there macular sparing? The presence of macular sparing suggests that the lesion is in the optic cortex. This is most often a space-occupying lesion.

DIAGNOSTIC WORKUP

Referral to an ophthalmologist for a thorough visual field examination is suggested at the outset. A neurology consultation also needs to be obtained. The neurologist will probably order a CT scan of the brain to rule out a space-occupying lesion unless multiple sclerosis is suspected.

If multiple sclerosis is suspected, MRI would be the study of choice, even though it is more expensive. In addition, VEP studies and spinal fluid analysis may be ordered to rule out multiple sclerosis.

A carotid duplex scan will help diagnose carotid vascular insufficiency, but four-vessel cerebral angiography will most likely be done so that both carotid and vertebral basilar artery disease can be evaluated. If there are endocrine changes, an endocrinologist should be consulted.

If a cerebral embolism is suspected, a source for the embolism should be sought. A cardiologist can best determine what tests to order to search for an embolic source.

 

» READ BOOK EXCERPT ONLINE »

Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

PAPILLEDEMA: Ask the Following Questions:
(Algorithmic Diagnosis of Symptoms and Signs)

  1. Is the onset acute or gradual? An acute onset would suggest optic neuritis, hypertensive encephalopathy, cerebral hemorrhage, extradural hematoma, brain abscess, dural sinus thrombosis, meningitis, and subarachnoid hemorrhage. On the other hand, a gradual onset would suggest a space-occupying lesion such as brain tumor, abscess, or subdural hematoma.
  2. If the onset is acute, is there coma or focal neurologic signs? Findings of coma or focal neurologic signs should suggest cerebral hemorrhage, extradural hematoma, brain abscess, dural sinus thrombosis, meningitis, and subarachnoid hemorrhage. An acute onset without focal neurologic signs or coma would suggest hypertensive encephalopathy and optic neuritis.
  3. If onset is gradual, are there focal neurologic signs? Gradual onset of papilledema with focal neurologic signs suggests a brain tumor, abscess, or subdural hematoma.
  4. Is there hypertension? The presence of hypertension and papilledema suggests hypertensive encephalopathy, acute glomerulonephritis, and certain collagen diseases. If there is no hypertension and no focal neurologic signs, then a diagnosis of pseudotumor cerebri or pseudopapilledema should be suspected.

DIAGNOSTIC WORKUP

Regardless of whether there are focal neurologic signs or hypertension, a CT scan or MRI should be done, and a consultation with a neurologist should be made when papilledema is suspected.

If there is significant hypertension and the CT scan or MRI are negative, a hypertensive workup should be done .

With a normal CT scan or MRI and no focal neurologic signs or hypertension, a spinal tap and visual field examination will assist in the diagnosis of pseudotumor cerebri. However, a blood lead level should be done to rule out lead poisoning. Also, the visual field exam may show optic neuritis when the clinical examination was inconclusive.

An ophthalmologist will help diagnose optic neuritis and pseudopapilledema.

 

» READ BOOK EXCERPT ONLINE »

Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

SCOTOMA: Ask the Following Questions:
(Algorithmic Diagnosis of Symptoms and Signs)

  1. Is it transient? If the scotomas are transient, then migraine, transient ischemic attacks, and retrobulbar neuritis should be suspected.
  2. Are there abnormalities on the eye examination other than the optic nerve? On a careful eye examination, the clinician may find corneal opacities, muscae volitantes, cataracts, choroiditis, glaucoma, retinitis, retinal hemorrhage, and detached retina.
  3. Are there other neurologic signs? The presence of other neurologic signs may suggest multiple sclerosis, carotid artery thrombosis or insufficiency, basilar artery thrombosis or insufficiency, and pseudotumor cerebri, among other disorders.

DIAGNOSTIC WORKUP

This should include a careful eye examination with slit lamp, tonometry, and visual field examinations. If the initial findings suggest an ocular disorder, referral to an ophthalmologist should be made. If the neurologic examination is abnormal, the patient should be referred to a neurologist, rather than ordering expensive tests such as a CT scan, MRI scan, VEP studies, angiography, and spinal fluid examinations.

 

» READ BOOK EXCERPT ONLINE »

Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

Diplopia: Differential Diagnosis
(In a Page: Signs and Symptoms)

Binocular diplopia

  • Decompensated phoria (ocular deviation)
    • Third nerve palsy (vertical and horizontal diplopia)
      –Compressive lesions (especially if pupil is involved), including aneurysm, cavernous sinus or orbit tumor, pituitary apoplexy, and uncal herniation
      –Ischemic microvascular disease (e.g., diabetes mellitus, hypertension)
      –Midbrain infarct
      –Giant cell arteritis
      –Herpes zoster
      –Leukemia
      –Meningitis
      –Subarachnoid hemorrhage
      –Ophthalmoplegic migraine
      –Trauma
    • Fourth nerve palsy (vertical diplopia): Etiologies include trauma, ischemic microvascular disease, congenital, multiple sclerosis, and other causes as above
    • Sixth nerve palsy (horizontal diplopia): Etiologies include ischemic microvascular disease, trauma, increased ICP (bilateral palsy), tumor, multiple sclerosis, post-LP, sarcoidosis/vasculitis, pontine infarct, and other causes as above
    • Myasthenia gravis
    • Orbital disease (e.g., Graves’ orbitopathy, orbital inflammation, tumor)
    • Cavernous sinus or superior orbital fissure syndrome (multiple CN involvement)
    • Postocular surgery
    • Trauma
    • Brown's syndrome (restriction of superior oblique tendon)
    • Internuclear ophthalmoplegia (MS, CVA)
    • Vertebrobasilar insufficiency (vertigo)
    • Botulism
      Monocular diplopia
    • Refractive error (high astigmatism)
    • Corneal opacity or irregularity
    • Cataract
    • Dislocated lens or lens implant
    • Extrapupillary openings
    • Macular disease
    • Retinal detachment
    • Nonphysiologic

    Workup and Diagnosis

    • History, neurologic, and ocular examinations
      –Note onset, duration, associated symptoms (e.g., eye or orbit pain, headache, erythema), trauma, and past history (e.g., diabetes, HTN, CVA, infection, thyroid disease)
      –Complete neurological exam: Note focal neurological deficits, cranial nerve involvement, cerebellar signs, and symptoms of demyelination (e.g., abnormal Romberg)
      –Ocular exam: Vision, pupil size and reaction, eye motility ductions and versions, ptosis, fundus exam (optic nerve edema or pallor), visual field defect, proptosis, and ice test (myasthenia gravis)
    • Consider ophthalmology consultation
    • If suspect CNS lesion, MRI is usually the test of choice
    • If suspect orbital etiology (e.g., trauma, thyroid), CT is usually superior
    • MRI/MRA (and/or angiography) is indicated immediately in cases of pupil-involving third nerve palsy, if age <50 (to rule out demyelinating disease), if no improvement over 3 months, aberrant regeneration, multiple cranial nerve or systemic neurologic involvement exists
    • Further testing may include Tensilon test and acetylcholinesterase receptor antibodies to rule out myasthenia gravis, fasting blood glucose and HgbA1C to rule out diabetes, ESR or CRP to rule out giant cell arteritis (urgent temporal artery biopsy is indicated if arteritis is strongly suspected), thyroid function tests and orbital ultrasound or CT for Graves’ orbitopathy
    • Lumbar puncture may be necessary (after head CT is done, to rule out increased intracranial pressure)
    >

    » READ BOOK EXCERPT ONLINE »

    Source: In a Page: Signs and Symptoms, 2004

    Papilledema: Differential Diagnosis
    (In a Page: Signs and Symptoms)

    Optic disc swelling due to increased ICP

    • Pseudotumor cerebri (idiopathic intracranial hypertension)
      –Most common cause of papilledema
      –Young, obese, or pregnant females
      –Associated with vitamin A overdose, OCPs, tetracycline, steroid withdrawal
    • Cerebral tumor (primary or metastatic)
    • Hydrocephalus (e.g., tumor, Arnold-Chiari malformation, aqueductal stenosis, postinfectious)
    • Intracranial hemorrhage (papilledema may not be seen acutely because it takes about 24 hours to develop after the ICP increases)
      –Subdural hematoma
      –Subarachnoid hemorrhage
      –Hemorrhagic stroke
      –Epidural hematoma
    • Intracranial infection
      –Brain abscess
      –Encephalitis (e.g., herpes)
      –Neurosyphilis
      –Toxoplasmosis
    • Meningitis (e.g., bacterial, viral, TB)
    • Malignant hypertension
    • Pre-eclampsia
      Optic disc swelling not due to increased ICP
    • Pseudopapilledema (the vessels traversing the disk margins are obscured, as in true papilledema): Optic disc drusen or congenitally anomalous disc
    • Papillitis: Unilateral, painful, vitreous cells
    • Papillophlebitis: Mild visual loss and disk swelling in young, healthy patient
    • Central retinal vein occlusion: Unilateral, associated with an acute loss of vision
    • Diabetic papillopathy: Disk edema with minimal visual loss, resolves spontaneously
    • Optic-disc vasculitis/ischemic optic neuropathy (giant cell/temporal arteritis)
    • Orbital optic-nerve tumors
    • Graves’ ophthalmopathy: History of thyroid dysfunction; may be associated with lid lag, proptosis, increased intraocular pressure
    • Uveitis: Associated with pain, photophobia, and scleral injection
    • Atypical optic neuritis

    Workup and Diagnosis

    • Papilledema is considered a medical emergency caused by increased intracranial pressure until proven otherwise
    • Complete neurologic and ocular exam, including a color vision assessment, slit lamp exam, posterior vitreous evaluation for WBCs, and a dilated fundus exam
      –True papilledema presents as bilaterally swollen, hyperemic discs with blurring of the disc margin that often obscures the blood vessels
      –True papilledema is due to increased ICP; if spontaneous venous pulsations are present, then ICP is normal
    • Noncontrast CT and/or MRI of the head/orbit will identify cerebral tumors, hydrocephalus, and intracranial hemorrhage
      –Pseudotumor cerebri have normal CT/MRI
      –Cerebral tumors appear as space-occupying lesions
      –Hydrocephalus appears as enlarged ventricles
    • Lumbar puncture (if CT/MRI negative)
      –Opening pressure for pseudotumor cerebri
      –Definitive diagnosis of meningitis and encephalitis
      –CSF CBC, Gram stain, cultures (bacterial, viral, VDRL if neurosyphilis is suspected, and fungal), cryptococcal antigen, protein, glucose,
      –Bloody tap in subarachnoid hemorrhage
    • Further laboratory studies may include CBC, thyroid tests (e.g., TSH, T3, T4), and blood glucose

    » READ BOOK EXCERPT ONLINE »

    Source: In a Page: Signs and Symptoms, 2004

    Vision Loss: Differential Diagnosis
    (In a Page: Signs and Symptoms)

    Transient vision loss (<24 hours)

    • Papilledema: Lasts seconds, bilateral
    • Amaurosis fugax: Lasts minutes, unilateral
    • Vertebrobasilar artery insufficiency: Lasts minutes, bilateral
    • Migraine: Lasts 10–60 minutes
    • Impending central retinal vein occlusion
    • Ocular ischemic syndrome (carotid occlusive disease)
    • Sudden change in blood pressure; orthostatic hypotension
      • Transient acute increase in intraocular pressure (e.g., acute angle closure glaucoma, retro- or peribulbar hemorrhage)

      Vision loss >24 hours: Sudden, painless
    • Retinal artery or vein occlusion
    • Ischemic optic neuropathy (must rule out giant cell/temporal arteritis to prevent permanent bilateral vision loss)
    • Vitreous or aqueous hemorrhage (hyphema)
    • Retinal detachment
    • Other retinal or CNS disease (e.g., cortical blindness due to occipital lobe CVA)
    • Exposure (“Welder's flash”) or prolonged exposure to intense sunlight

    Vision loss >24 hours: Gradual, painless
  • Cataract
  • Refractive error
  • Open angle glaucoma
  • Chronic retinopathy (e.g., age-related macular degeneration, diabetic retinopathy)
  • Chronic corneal disease (e.g., corneal dystrophy)
  • Optic neuropathy/atrophy (e.g., compressive lesion, toxic-metabolic cause, dominant optic neuropathy, radiation)
  • Retinitis pigmentosa
  • Pseudotumor cerebri

    • Vision loss >24 hours: Painful
  • Acute angle closure glaucoma
  • Optic neuritis (pain with extraocular motion)
  • Orbital apex/superior orbital fissure/ cavernous sinus syndrome
  • Uveitis
  • Corneal hydrops (keratoconus)
    • Ocular onchocerciasis (“river blindness”)
      –Common cause of blindness in developing nations due to Onchocerca volvulus worm
    • Corneal abrasion or ulcer
    • Herpes simplex or zoster infection

    Workup and Diagnosis

    • History should include age, onset, tempo of vision loss, history of trauma, associated headache, medications, past history (e.g., carotid or cardiac disease, HTN, diabetes, vertigo, migraine, syphilis, ocular, orbital, cranial radiation, keratoconus), family history of vision loss, alcohol and tobacco use
    • Physical exam should include a thorough eye examination, vision acuity, refractive error, color vision, blood pressure, refractive error, cranial examination, cranial nerve innervation, intraocular pressure, ocular media opacity (corneal edema, dystrophy, anterior chamber or vitreous cells, cataracts), and fundus and optic disc exam
    • Consider a visual field exam and fluorescein angiogram
    • Initial laboratory evaluation may include ESR, CRP, fasting blood glucose, HgbA1C, PPD, RPR, FTA-ABS, ACE level, vitamin B12, and folate
    • Consider CT/MRI of orbits and head with contrast, carotid Doppler, echocardiogram, electroretinography, and VEP (retinal dystrophies, optic neuropathies, nonphysiologic)
    • Consider ophthalmologic consultation
    '>

    » READ BOOK EXCERPT ONLINE »

    Source: In a Page: Signs and Symptoms, 2004

    Diplopia: Differential Diagnosis
    (In A Page: Pediatric Signs and Symptoms)

    • Monocular diplopia
      –Rare, usually associated with the cornea, lens, vitreous, or refractive anomalies such as high uncorrected astigmatism
      –May occur in lens implant dislocation
      –Neurologic disorders may present as monocular diplopia with repetitive images
      • Binocular, decompensated phoria with
      • concomitant strabismus, nonpathologic
        –Recent ocular surgery
        –Ocular myasthenia (may be transient)
      • Binocular with proptosis, gaze restriction
        –Thyroid disease, orbital pseudotumor, cavernous sinus thrombosis or fistula
      • Binocular with isolated third nerve
        –Atherosclerosis, hypertension, diabetes, tumor, aneurysm
      • Binocular with isolated sixth nerve
        –Trauma, atherosclerosis, hypertension, diabetes, tumor, increased intracranial pressure, sinus disease
      • Binocular with isolated fourth nerve
        –Trauma, stroke, thyroid eye disease, atherosclerosis, hypertension, diabetes
      • Binocular with multiple muscle weakness in one eye
        –Cavernous sinus lesion
      • Binocular with multiple muscle weakness in both eyes
        –Progressive supranuclear palsy, CPEO, acute postinfectious disorders
      • Adduction weakness or abducting nystagmus
        –Inner nuclear ophthalmolplegia (INO), brainstem disease, stroke, MS, posterior fossa mass
    • Vertical diplopia with no fourth or third palsy
      –Stroke, multiple sclerosis, posterior fossa mass

    Workup and Diagnosis

    • History
      –Temporal history of the symptoms, including past incidences and transience of defect
      –Establish whether monocular (one eye covered) or binocular (both eyes open)
      –History of recent trauma or ocular surgery
      –Status of known systemic diseases, e.g., hypertension, diabetes, thyroid disease
    • Physical exam
      –Obtain visual acuity and confrontation visual fields
      –Pupillary evaluation
      –Observe for head tilt or torsion
      –Observe for proptosis
      –Extraocular muscle evaluation to isolate affected muscle
      –Observe for other neurologic signs or symptoms
      –Perform a dilated fundus evaluation to rule out associated retinal and/or optic nerve disorders
      –Perform Tensilon test for myasthenia
    • Workup for medical issues such as diabetes, hypertension, atherosclerosis, stroke, thyroid disease
    • Workup with imaging for MS, orbital and intracranial tumor, aneurysm, orbital pseudotumor, cavernous sinus lesions
    • Neurologic or neuro-ophthalmological consultation is in order

    » READ BOOK EXCERPT ONLINE »

    Source: In A Page: Pediatric Signs and Symptoms, 2007

    Vision Loss: Differential Diagnosis
    (In A Page: Pediatric Signs and Symptoms)

    • Vascular causes
      –Amaurosis fugax: TIA of the retina lasting 5–60 minutes
      –Stroke causes loss of side vision usually to the left or right, may be interpreted as loss of vision in the right or left eye
      –Retinal vascular occlusion: Venous shows gradual decline with retinal hemorrhaging; arterial has sudden onset with minimal to no retinal hemorrhaging
      • Transient monocular blindness (TMB)
        –Lasts seconds
        –Due to positional changes in optic disc edema with increased intracranial hypertension, orthostatic hypotension, thyroid eye disease, and space-occupying lesions
    • Migraine variants are transient and may be associated with headache after presentation
    • Optic nerve edema or swelling from demyelinating disease, nonarteritic and arteritic optic neuropathy, toxicity (e.g., lead, chloramphenicol)
    • Optic atrophy
      • Retinal etiologies
        –Retinal surface wrinkling disorders
        –Idiopathic central serous retinopathy often associated with stress
        –Retinal detachment with probable history of floaters before loss of vision
    • Angle closure glaucoma
      • Postsurgical
        –Endophthalmitis: Often associated with ocular surgery and red eye
        –Cystoid macular edema may occur after ocular surgery
    • Vitreous hemorrhage
      –You will not be able to see into the eye
      • Infectious causes
        –Retinitis and/or uveitis due to toxoplasmosis, cytomegalovirus, Lyme, histoplasmosis
    • Trauma
    • Hysterical blindness
    • Cataracts
    • Hypoglycemia
    • Retinitis pigmentosa

    Workup and Diagnosis

  • History
    –Be aware that patients often have vision reduction over time (e.g., from cataracts) and only perceive the loss as sudden
    –Onset, duration, trauma; transience vs permanence of visual loss or change
    –Associated signs and symptoms of demyelinizing disease, toxoplasmosis, bartonellosis, Lyme disease
    –PMH including migraines, hypertension, diabetes, thyroid disease, rheumatic disease, vascular disease, atrial fibrillation, lipid status
    • Physical exam
      –Obtain visual acuity and confrontation visual fields in both eyes
      –Redness, pain, photophobia
      –Pupillary evaluation: look for Marcus Gunn pupil, which usually differentiates optic nerve from other causes
      –Extraocular muscle evaluation
      –Perform a dilated fundus evaluation
      –Evaluate for proptosis
      • Radiology
        –CT or MRI of orbits and brain is indicated for associated neurologic signs, history of trauma
    • Evaluation for stroke if right- or left-sided
    • Ophthalmology consultation for dilated retinal exam, evaluation, and management

    » READ BOOK EXCERPT ONLINE »

    Source: In A Page: Pediatric Signs and Symptoms, 2007

    Papilledema (Optic Disc Swelling): Differential Diagnosis
    (In A Page: Pediatric Signs and Symptoms)

    • Pseudotumor cerebri
      –Other symptoms: Headache, nausea, and vomiting all worse in morning, transient visual obscurations, diplopia
      –Diagnosis includes increased ICP, normal imaging, normal CSF
      –More common in obese females
    • Optic neuritis
      –May be associated with postviral syndromes or meningoencephalitis
      –Loss of vision, pain on eye movement
      –Vision usually improves within a few weeks, but not full recovery
    • Optic neuropathy
      –Compressive: Associated with NF1 and optic nerve glioma, presents with progressive visual loss, strabismus, nystagmus, proptosis
      –Infiltrative: From cancers (leukemias, lymphomas), infection, or inflammation (sarcoidosis, TB, toxocariasis, toxoplasmosis, CMV); optic disc swelling, vision loss, and hemorrhages
      –Toxic/nutritional optic neuropathy: Symmetric neuropathy from nutritional deficiency (thiamine, B12), drugs (tobacco/alcohol, chloramphenicol, rifampin), toxins (lead, methanol); visual field and vision loss; may recover with treatment
      –Leber optic neuropathy: Mitochondrial DNA transmission, presents late teens to middle 20s; visual field and vision loss, may spontaneously improve
    • Increased ICP: Idiopathic intracranial hypertension, intracranial hemorrhage, space-occupying lesion
    • Growth hormone supplementation
    • Retinal hemorrhage and loss of vision
    • Retinal vein occlusion
    • Malignant hypertension: Associated with retinal hemorrhage, exudates, and cotton wool spots
    • Optic neuropathy, nonarteritic or arteritic
    • Demyelinating disease
    • Infectious conditions: Toxoplasmosis, Lyme disease, Bartonella; hard exudates may be visible funduscopically

    Workup and Diagnosis

    • History
      –History of HA, nausea or vomiting, recent viral illness
      –Family history of visual loss, neurologic disorder
      –PMH or signs and symptoms consistent with known systemic diseases; e.g., hypertension, diabetes, thyroid disease, growth hormone therapy
      –Nutritional deficiencies; exposure to toxins such as tobacco or alcohol; recent drug use; exposure to ticks and animals
    • Physical exam
      –Visual acuity, confrontational visual fields, pupillary response, extraocular muscle movements, proptosis
      –Dilated fundus evaluation
      –Neurologic exam for signs and symptoms of demyelinating disease, localizing deficit
    • Labs
      –Titers for CMV, Lyme, toxocariasis, toxoplasmosis
      • Radiology
        –CT or MRI of the brain and orbits for suspicion of intracranial mass, mass effect or hemorrhage
      • Studies
        –Lumbar puncture may be indicated to establish presence or absence of, or to relieve, increased intracranial pressure
    • Ophthalmologic consultation to rule out congenital variation to avoid unnecessary and expensive differential testing

    » READ BOOK EXCERPT ONLINE »

    Source: In A Page: Pediatric Signs and Symptoms, 2007

    EYE PAIN: Approach to the Diagnosis
    (Differential Diagnosis in Primary Care)

    The approach to the diagnosis of eye pain involves a careful search for inflammation of the various anatomic structures; then a drop or two of fluorescent dye is inserted and the cornea inspected for lacerations, herpes ulcers, and foreign bodies. Finally, tenometry may be done. Referral to an ophthalmologist is often necessary, but the astute clinician will want to x-ray the sinuses, ask about a history of migraine, do a visual field, and rule out systemic diseases beforehand.

    » READ BOOK EXCERPT ONLINE »

    Source: Differential Diagnosis in Primary Care, 2007

    PAPILLEDEMA: Approach to the Diagnosis
    (Differential Diagnosis in Primary Care)

    The approach to the diagnosis of papilledema in someone without hypertension or hypertensive retinopathy must include a thorough neurologic examination and a CT scan. If focal signs are present or the CT scan shows positive findings, referral to a neurosurgeon is indicated. He or she can decide if an MRI is indicated. A spinal tap is contraindicated. If there are no focal signs, it may be worthwhile to differentiate papilledema from optic neuritis by having an ophthalmologist perform a visual field examination. This may also be helpful in differentiating pseudotumor cerebri because there may be bilateral visual defects in the inferior nasal quadrants. Papilledema from increased intracranial pressure will show only an enlarged blind spot (unless there is a tumor of the optic tracts, radiations, or occipital cortex), whereas optic neuritis will show scotomata peripheral to the blind spot (disc). The Appendix will be useful for confirming the diagnosis of a specific disease.

    » READ BOOK EXCERPT ONLINE »

    Source: Differential Diagnosis in Primary Care, 2007

    Diplopia: History and physical examination
    (Handbook of Signs & Symptoms (Third Edition))

    If the patient complains of double vision, first check his neurologic status. Evaluate his level of consciousness (LOC); pupil size, equality, and response to light; and motor and sensory function. Then take his vital signs. Briefly ask about associated symptoms, especially a severe headache. Find out about associated neurologic symptoms first because diplopia can accompany serious disorders.

    Next, continue with a more detailed examination. Find out when the patient first noticed diplopia. Are the images side-by-side (horizontal), one above the other (vertical), or a combination? Does diplopia affect near or far vision? Does it affect certain directions of gaze? Ask if diplopia has worsened, remained the same, or subsided. Does its severity change throughout the day? Diplopia that worsens or appears in the evening may indicate myasthenia gravis. Find out if the patient can correct diplopia by tilting his head. If so, ask him to show you. (If the patient has a fourth nerve lesion, tilting of the head toward the opposite shoulder causes compensatory tilting of the unaffected eye. If he has incomplete sixth nerve palsy, tilting of the head toward the side of the paralyzed muscle may relax the affected lateral rectus muscle.)

    Explore associated symptoms such as eye pain. Ask about hypertension, diabetes mellitus, allergies, and thyroid, neurologic, or muscular disorders. Also, note a history of extraocular muscle disorders, trauma, or eye surgery.

    Observe the patient for ocular deviation, ptosis, proptosis, lid edema, and conjunctival injection. Distinguish monocular from binocular diplopia by asking the patient to occlude one eye at a time. If he still sees double out of one eye, he has monocular diplopia. Test his visual acuity and extraocular muscles. Check his vital signs.

    » READ BOOK EXCERPT ONLINE »

    Source: Handbook of Signs & Symptoms (Third Edition), 2006

    Eye pain: History and physical examination
    (Handbook of Signs & Symptoms (Third Edition))

    If the patient's eye pain doesn't result from a chemical burn, take a complete history. Have the patient describe the pain fully. Is it an ache or a sharp pain? How long does it last? Is it accompanied by burning, itching, or discharge? Find out when it began. Is it worse in the morning or late in the evening? Ask about recent trauma or surgery, especially if the patient complains of sudden, severe pain. Does he have headaches? If so, find out how often and at what time of day they occur.

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    Source: Handbook of Signs & Symptoms (Third Edition), 2006

    Hemianopsia: History and physical examination
    (Handbook of Signs & Symptoms (Third Edition))

    Suspect a visual field defect if the patient seems startled when you approach him from one side or if he fails to see objects placed directly in front of him. To help determine the type of defect, compare the patient’s visual fields with your own — assuming that yours are normal. First, ask the patient to cover his right eye while you cover your left eye. Then move a pen or similarly shaped object from the periphery of his (and your) uncovered eye into his field of vision. Ask the patient to indicate when he first sees the object. Does he see it at the same time you do? After you do? Repeat this test in each quadrant of both eyes. Then, for each eye, plot the defect by shading the area of a circle that corresponds to the area of vision loss.

    Next, evaluate the patient’s level of consciousness (LOC), take his vital signs, and check his pupillary reaction and motor response. Ask if he has recently experienced a headache, dysarthria, or seizures. Does he have ptosis or facial or extremity weakness? Hallucinations or loss of color vision? When did neurologic symptoms start? Obtain a medical history, noting especially eye disorders, hypertension, diabetes mellitus, and recent head trauma.

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    Source: Handbook of Signs & Symptoms (Third Edition), 2006

    Scotoma: History and physical examination
    (Handbook of Signs & Symptoms (Third Edition))

    First, identify and characterize the scotoma, using such visual field tests as the tangent screen examination, the Goldmann perimeter test, and the automated perimetry test. Two other visual field tests  —  confrontation testing and the Amsler grid   —  may also help in identifying a scotoma.

    Next, test the patient’s visual acuity and inspect his pupils for size, equality, and reaction to light. An ophthalmoscopic examination and measurement of intraocular pressure are necessary.

    Explore the patient’s medical history, noting especially eye disorders, vision problems, or chronic systemic disorders. Find out if he takes medications or uses eyedrops.

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    Source: Handbook of Signs & Symptoms (Third Edition), 2006

    Vision loss: History and physical examination
    (Handbook of Signs & Symptoms (Third Edition))

    Sudden vision loss can signal an ocular emergency. (See Managing sudden vision loss.) Don’t touch the eye if the patient has perforating or penetrating ocular trauma.

    If the patient’s vision loss occurred gradually, ask him if the vision loss affects one eye or both and all or only part of the visual field. Is the visual loss transient or persistent? Did the visual loss occur abruptly, or did it develop over hours, days, or weeks? What is the patient’s age? Ask the patient if he has experienced photosensitivity, and ask him about the location, intensity, and duration of any eye pain. You should also obtain an ocular history and a family history of eye problems or systemic diseases that may lead to eye problems, such as hypertension; diabetes mellitus; thyroid, rheumatic, or vascular disease; infections; and cancer.

    The first step in performing the eye examination is to assess visual acuity, with best available correction in each eye. (See Testing visual acuity, page 630.)

    Carefully inspect both eyes, noting edema, foreign bodies, drainage, or conjunctival or scleral redness. Observe whether lid closure is complete or incomplete, and check for ptosis. Using a flashlight, examine the cornea and iris for scars, irregularities, and foreign bodies. Observe the size, shape, and color of the pupils, and test the direct and consensual light reflex (See “Pupils, nonreactive,” page 521.) and the effect of accommodation. Evaluate extraocular muscle function by testing the six cardinal fields of gaze. (See Testing extraocular muscles, page 206.)

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    Source: Handbook of Signs & Symptoms (Third Edition), 2006

    Diplopia: History and physical examination
    (Professional Guide to Signs & Symptoms (Fifth Edition))

    If the patient complains of double vision, first check his neurologic status. Evaluate his level of consciousness (LOC); pupil size, equality, and response to light; and motor and sensory function. Then take his vital signs. Briefly ask about associated symptoms. First find out about associated neurologic symptoms, especially a severe headache, because diplopia can accompany serious disorders.

    Next, continue with a more detailed examination. Find out when the patient first noticed diplopia. Are the images side by side (horizontal), one above the other (vertical), or a combination? Does diplopia affect near or far vision? Does it affect certain directions of gaze? Ask if diplopia has worsened, remained the same, or subsided. Does its severity change throughout the day? Diplopia that worsens or appears in the evening may indicate myasthenia gravis. Find out if the patient can correct diplopia by tilting his head. If so, ask him to show you. (If the patient has a fourth cranial nerve lesion, tilting the head toward the opposite shoulder causes compensatory tilting of the unaffected eye. If he has incomplete sixth cranial nerve palsy, tilting the head toward the side of the paralyzed muscle may relax the affected lateral rectus muscle.)

    Explore associated symptoms such as eye pain. Ask about hypertension, diabetes mellitus, allergies, and thyroid, neurologic, or muscular disorders. Also, note a history of extraocular muscle disorders, trauma, or eye surgery.

    Observe the patient for ocular deviation, ptosis, exophthalmos, eyelid edema, and conjunctival injection. Distinguish monocular from binocular diplopia by asking the patient to occlude one eye at a time. If he still sees double out of one eye, he has monocular diplopia. Test visual acuity and extraocular muscles. Also, check vital signs.

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    Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

    Hemianopsia: History and physical examination
    (Professional Guide to Signs & Symptoms (Fifth Edition))

    Suspect a visual field defect if the patient seems startled when you approach him from one side or if he fails to see objects placed directly in front of him. To help determine the type of defect, compare the patient’s visual fields with your own—assuming that yours are normal. First, ask the patient to cover his right eye while you cover your left eye. Then move a pen or similarly shaped object from the periphery of his (and your) uncovered eye into his field of vision. Ask the patient to indicate when he first sees the object. Does he see it at the same time you do? After you do? Repeat this test in each quadrant of both eyes. Then, for each eye, plot the defect by shading the area of a circle that corresponds to the area of vision loss.

    Next, evaluate the patient’s level of consciousness (LOC), take his vital signs, and check his pupillary reaction and motor response. Ask if he has recently experienced headache, dysarthria, or seizures. Does he have ptosis or facial or extremity weakness? Hallucinations or loss of color vision? When did his neurologic symptoms start? Obtain a medical history, noting especially eye disorders, hypertension, diabetes mellitus, and recent head trauma.

    » READ BOOK EXCERPT ONLINE »

    Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

    Scotoma: History and physical examination
    (Professional Guide to Signs & Symptoms (Fifth Edition))

    First, identify and characterize the scotoma, using such visual field tests as the tangent screen examination, the Goldmann perimeter test, and the automated perimetry test. Two other visual field tests—confrontation testing and the Amsler grid—may also help in identifying a scotoma.

    Next, test the patient’s visual acuity and inspect his pupils for size, equality, and reaction to light. An ophthalmoscopic examination and measurement of intraocular pressure (IOP) are necessary.

    Explore the patient’s medical history, noting especially any eye disorders, vision problems, or chronic systemic disorders. Find out if he takes medications or uses eyedrops.

    » READ BOOK EXCERPT ONLINE »

    Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

    Vision loss: History and physical examination
    (Professional Guide to Signs & Symptoms (Fifth Edition))

    Sudden vision loss can signal an ocular emergency. Don’t touch the eye if the patient has a perforating or penetrating ocular trauma. (See Managing sudden vision loss, page 802.)

    If the patient’s vision loss occurred gradually, ask him if it affects one eye or both and all or only part of the visual field. Is the vision loss transient or persistent? Did it occur abruptly or develop over hours, days, or weeks? What is the patient’s age? Ask the patient if he has experienced photosensitivity, and ask about the location, intensity, and duration of any eye pain. Also, obtain an ocular history and a family history of eye problems or systemic diseases that may lead to eye problems, such as hypertension; diabetes mellitus; thyroid, rheumatic, or vascular disease; infections; and cancer.

    The first step in performing the eye examination is to assess visual acuity with the best available correction in each eye. (See Testing visual acuity, page 803.)

    Carefully inspect both eyes, noting edema, foreign bodies, drainage, or conjunctival or scleral redness. Observe whether lid closure is complete or incomplete, and check for ptosis. Using a flashlight, examine the cornea and iris for scars, irregularities, and foreign bodies. Observe the size, shape, and color of the pupils, and test the direct and consensual light reflex (see “Pupils, nonreactive,” page 654) and the effect of accommodation. Evaluate extraocular muscle function by testing the six cardinal fields of gaze. (See Testing extraocular muscles, page 246.)

    » READ BOOK EXCERPT ONLINE »

    Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

    Eye pain [Ophthalmalgia]: History and physical examination
    (Professional Guide to Signs & Symptoms (Fifth Edition))

    If the patient’s eye pain doesn’t result from a chemical burn or from acute angle-closure glaucoma, take a complete history. Have the patient describe the pain fully. Is it an ache or a sharp pain? How long does it last? Is it accompanied by burning, itching, or a discharge? Find out when it began. Is it worse in the morning or late in the evening? Ask about recent trauma or surgery, especially if the patient complains of severe pain that developed suddenly. Does he have headaches? If so, find out how often and at what time of day they occur.

    During the physical examination, don’t manipulate the eye if you suspect trauma. Carefully assess the eyelids and conjunctivae for redness, inflammation, and swelling. Then examine the eyes for ptosis or exophthalmos. Finally, test visual acuity with and without correction, and assess extraocular movements. Characterize any discharge. (See Examining the external eye, page 322.)

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    Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

    Diplopia: History
    (The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

     A. Characteristics of the diplopia. Is it true double vision or simply just blurred or hazy vision? Patients often confuse double vision with blurry vision. Close one eye or the other to test the double vision. If, in the process of covering one or the other eye, double vision is still noted, under the occluded condition, this defines monocular diplopia, a non–life-threatening cause. If double vision goes away when covering the left eye, and again when covering the right eye separately, this is binocular diplopia and the index of severity increases substantially for the underlying cause. Does diplopia get worse looking at a distance and improve when looking up close (i.e., probably a sixth nerve palsy)? Are there any recent headaches associated with this? Is there a problem with balance, coordination, nausea or vomiting, or drooping of the eyes? Is double vision separated horizontally or vertically? A vertical separation suggests either a third or fourth nerve palsy. If there is ptosis with the diplopia, it suggests a third nerve palsy. Is the diplopia sudden in onset? This suggests a vascular event if the headache is binocular.

     B. Concurrent conditions. Microvascular ischemia is often secondary to diabetes, hypertension, or peripheral vascular disease, which can often cause a third, fourth, or an acute sixth cranial nerve palsy (Chapters 7.8 and 14.1). Thyroid disease can cause a gradually worsening binocular diplopia with a waxing and waning symptom (Chapter 14.8). This is usually associated with obvious proptosis in one or both eyes.

    C. Duration of diplopia. A chronic subacute intermittent diplopia, with some blurred vision or floaters with decreased vision, usually suggests an eye-related problem such as cataracts, corneal opacity, irregular astigmatism, or vitreous opacity. An acute intermittent diplopia usually represents a cranial nerve palsy and often represents an intracranial condition.

    Physical examination. Focused physical examination (PE)

    This should include a visual acuity test for each eye. Ask the patient about diplopia being present when covering each eye. If double vision is still present while having one or the other eye covered, by definition, this is monocular diplopia. A rare patient will complain of triplopia, or triple vision. This usually is malingering, but occasionally can be caused by corneal surface irregularity. Other parts of the examination are important: check the ocular rotations; lack of abduction or external rotation of the eye would suggest a sixth nerve palsy. Check for monocular ptosis; if it is present, then a third nerve palsy is suggested. Pupillary responses, if fixed and dilated, suggest an acute pupillary-involving third nerve palsy. An optic nerve where papilledema is present suggests an intracranial-involving process. A red fundus reflex test showing an opacity in the red reflex suggests an ocular cause, such as cataracts or corneal opacity.

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    Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000

    Papilledema: History
    (The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

     Headache, nausea, vomiting, diplopia, and transient loss of vision lasting seconds, especially with the head in dependent positions, raise the index of suspicion for increased cranial pressure. Mood swings can be present in cases with prolonged increased intracranial pressure. Rarely is a decrease in visual acuity seen in increased intracranial pressure; if truly present, then it would suggest other causes (e.g., vein occlusion, anterior ischemic optic neuropathy, and optic neuritis). The red flags in the history include true binocular diplopia with increasing headache, disorientation, and nausea and vomiting.

    Physical examination

    A focused physical examination should include vital signs, such as blood pressure. Examine the head: check for neck stiffness, temporal artery tenderness, pain in and around the eyes, and pain on ocular rotations, such as occurs in optic neuritis. Afferent pupillary defect is another red flag that almost always signifies an ocular cause of disc edema, retinal vein occlusion, anterior ischemic optic neuropathy, or optic neuritis. Always examine both eyes. Normally papilledema is bilateral, but can be present asymmetrically. In true disc edema, nerve fiber layer swelling is seen, which obscures the margins of the blood vessels. Tiny splinter hemorrhages will be seen in and around the optic nerve. If the other eye has no disc swelling, look for spontaneous venous pulsations (SVP). If these SVPs are present, there is normal intracranial pressure, therefore, no true papilledema. Very prominent retinal hemorrhages suggest malignant hypertension or central retinal vein occlusion, rather than papilledema. Disc elevation can be measured using the diopteric overcorrection in the direct ophthalmoscope. Basically, focus on the retina and add in plus (red) power until the optic nerve blurs. Three diopters equals 1 mm of elevation. Ocular rotations are limited in both third and sixth nerve palsy. Sixth nerve palsies show limited lateral gaze and third nerve palsies have limitation in medial gaze, elevation, and depression. When ptosis and a dilated pupil are seen, suspect an aneurysm at the posterior communicating artery in the circle of Willis as the underlying cause. Decreased visual acuity is another red flag and normally is only mildly depressed in true papilledema. If the vision is decreased severely, look for other causes that are not related to increased intracranial pressure.

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    Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000

    Scotoma: History
    (The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

     A. Nature of the scotoma. Try to establish whether the field loss is monocular or binocular. Binocular scotomas, which imply chiasmal or posterior chiasmal lesions, are vascular (stroke, transient ischemic attack, migraine, ruptured arteriovenous malformation) or compressive in nature (pituitary mass, meningioma, glioma). Establish with the patient the location of the defect. Scotomas that migrate through the visual field include vitreous floaters, vitreous hemorrhage, scintillating scotoma of migraine, and so forth. An altitudinal field loss is likely a prechiasmal lesion [i.e., optic nerve disease (e.g., ischemic optic neuropathy, glaucoma) or retina disease (e.g., detached retina, retina vascular occlusion)]. Central scotomas are commonly seen in optic nerve and macular lesions with macular degeneration by far the most common in the elderly. Macular holes, optic neuritis, toxic or metabolic optic neuropathy, central serous choroidopathy, maculopathy secondary to medications (hydroxychloroquine, thioridazine, chlorpromazine, quinine, tamoxifen), and others are examples of macular-induced central scotomas. Peripheral vision loss, if bilateral and homonymous, indicates a stroke opposite the side of field loss. Tumors, arteriovenous malformations, and migraines can cause hemianopias. Glaucoma, detached retina, retinitis pigmentosa, chronic papilledema, and previous laser treatment for diabetes are also common entities affecting peripheral vision.

     B. Onset and timing of scotoma. A scotoma of sudden onset will be secondary to some kind of vascular event: embolic, hypoperfusion, inflammatory, or hemorrhagic. Transient vision loss lasting seconds can occur with temporal arteritis, papilledema, or vertebrobasilar insufficiency. Visual loss lasting minutes to hours occurs in temporal arteritis or amaurosis fugax. Visual changes lasting weeks to months represent retinal vein occlusion, expanding compressive lesion, papilledema, and if associated with pain on eye movement, optic neuritis. Gradual progressive visual field loss occurs with compressive masses; however, acute expanding lesions from infectious, inflammatory (e.g., sarcoid, Tolosa-Hunt), aneurysmal, or apoplexy of a pituitary mass can cause rapid vision loss. Monocular vision loss after head trauma suggests injury to the intracanalicular portion of the optic nerve, compressive fracture of the sphenoid bone, or edema to the optic nerve. Emergent computed tomography (CT) scan with neurosurgical or ophthalmic consultation and high-dose intravenous steroids are needed.

     C. Associated symptoms. The presence of neurologic signs or symptoms can localize the area of the pathology. Amaurosis fugax implies ipsilateral internal carotid disease or cardiac disease. History of vertigo, diplopia, and urinary incontinence in a young patient with a monocular central scotoma implies multiple sclerosis. Older patients with acute monocular vision loss associated with periorbital pain and headaches, fatigue, jaw claudication, or muscle aches strongly suggests temporal arteritis. Transient dimming or loss of vision in one or both eyes with orthostatic changes can be seen with papilledema of intracranial hypertension. Progressive monocular visual loss with proptosis obviously implies an orbital mass (optic nerve glioma, meningioma, cavernous hemangioma), but asymmetric thyroid-related orbitopathy can present a similar picture. Monocular loss progressing over time without orbital signs can be seen with an intracanalicular or intracranial optic nerve mass.

     D. Past medical and social history. Diabetes and hypertension are the two most common causes of ischemic optic neuropathy (ION). ION presents as a sudden painless monocular vision loss, altitudinal in nature, with an APD. The risk of retinal vascular occlusions is much greater in patients with diabetes mellitus or hypertension. The risk is greater with tobacco use. A history of rheumatic fever, heart murmur, or cardiomyopathy is significant for an embolic source. Sudden vision loss without an APD in a diabetic patient is most likely a vitreous hemorrhage. An acquired immunodeficiency syndrome patient with a CD4 count less than 50 × 103 with visual scotomas needs to be evaluated for cytomegalovirus retinitis. A history of alcohol abuse or a psychiatric patient with bilateral vision loss and change in mental status needs urgent chemistries for anion gap acidosis with hemodialysis if methanol ingestion is suspected. An intravenous drug user can suffer a vascular occlusion from talc.

    Physical examination

    A. Visual acuity. The vision of each eye should be assessed with spectacles or contact lenses in each eye independently. Central scotomas are seen with optic nerve, macular disease, or (rarely) an occipital tip lesion; and Snellen visual acuity will be decreased.

    B. Visual fields. Confrontation field test is performed with each eye independently. Briefly flash several fingers in each of the four quadrants. Bilateral field loss in the same field of vision in each eye indicates injury posterior to the chiasm. Bitemporal field defects are seen with chiasmal lesions (pituitary masses, craniopharyngiomas, and others). Monocular field defects are seen in retina and optic nerve disease.

     C. Pupil examination. The presence of a prominent APD, which implies optic nerve injury, will help to differentiate central scotomas caused by macular disease. An APD is commonly seen with optic neuritis, optic neuropathy (ischemic and traumatic), asymmetric glaucomatous damage, optic nerve tumors, and central retinal artery or vein occlusion. An APD is not seen in early papilledema and minimally with macular degeneration, macular holes, or choroidopathy.

    D. Fundus examination. Direct ophthalmoscopy can give a quick assessment of the red reflex (i.e., a dim red reflex in a diabetic with vitreous hemorrhage). Vitreous floaters can occasionally be seen as shadows in the red reflex. Examine the nerve for edema, pallor, or glaucomatous cupping. Macular scarring or pigmentary change is most commonly seen with macular degeneration.

     E. Other examinations. A neurologic assessment is needed for a patient with bilateral field loss, screening for contralateral paresis and other focal deficits, palpation of the temporal artery for tenderness or diminished pulse if the history suggests giant cell arteritis, as is auscultation of the carotids for bruits and the heart for a murmur in a patient with amaurosis fugax or stroke. Glaucoma can be screened with tonometry. Check arms and legs for signs of intravenous drug abuse.

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    Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000

    Memory Impairment: History
    (The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

    A. Presentation. Dementia patients are brought in by relatives about memory problems; whereas, depressed and age-associated memory impairment (AAMI) patients come in on their own to complain (3).

    B. Chronology. Determine if the onset is gradual as in Alzheimer’s disease (AD) or abrupt as in multi-infarct dementia (MID), subdural hematoma (SH), Creutzfeld–Jakob disease (CJD); and steady (AD) or stepwise (MID) deterioration. Check for history of past strokes (MID); head trauma (AD, SH); medication; sexually transmitted diseases; human immunodeficiency virus (HIV) risk; alcohol use; heavy metal exposure; past depression; and many “I don’t know” answers (depression).

    C. Family reports of change in the patient’s judgment and executive functioning indicate other nonmemory cognitive problems (dementia) or visual hallucinations, as in Lewy body dementia (LBD).

    D. Family history. Inquire about a possible familial tendency for Huntington’s disease (HD), AD, Parkinson’s disease with dementia (PDWD), Pick’s disease (PD), or alcoholism.

    Physical examination (PE)

    A. Normal physical findings are reported in most patients with AD, AAMI, and depression.

     B. Specific abnormalities that help classify dementias include resting tremor (LBD, PDWD), myoclonus (CJD, LBD), glabellar reflex (AD), palmomental reflex (AD, PD), cogwheel rigidity (LBD, PDWD), stooped shuffling gait (LBD, PDWD), asterixis (alcoholism), chorea (HD), focal motor or sensory deficits (MID), asymmetric reflexes (MID, CJD), apraxic gait-wide based, feet stuck to floor or magnetic (normal pressure hydrocephalus, NPH), diffuse muscle wasting early in clinical course (CJD, HIV, dementia), and gaze paresis especially downward (progressive supranuclear palsy, PSNP).

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    Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000

    Eye Pain: Differential Overview
    (Field Guide to Bedside Diagnosis)

    ❑ Conjunctivitis

    ❑ Corneal abrasion

    ❑ Foreign body

    ❑ Sinusitis

    ❑ Migraine

    ❑ Acute glaucoma

    ❑ Orbital cellulitis

    ❑ Zoster prodrome

    ❑ Orbital fracture

    ❑ Keratitis

    ❑ Scleritis

    ❑ Iritis

    ❑ Optic neuritis

    ❑ Temporal arteritis

    Diagnostic Approach

    A foreign body sensation occurs with a foreign body, corneal abrasion, or keratoconjunctivitis sicca. Itching is associated with allergic and vernal conjunctivitis. Photophobia occurs with iritis and herpes simplex keratitis. Deep pain suggests acute glaucoma or posterior scleritis. Pain on eye movement is found with optic neuritis, sinusitis, and influenza.

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    Source: Field Guide to Bedside Diagnosis, 2007

    Diplopia/Nystagmus: Differential Overview
    (Field Guide to Bedside Diagnosis)

    Diplopia

    ❑ Alcohol

    ❑ Diabetes

    ❑ Brainstem ischemia/lesion

    ❑ Grave disease

    ❑ Multiple sclerosis

    ❑ Ophthalmoplegic migraine

    ❑ Myasthenia gravis

    ❑ Wernicke encephalopathy

    ❑ Zygoma fracture

    ❑ Basilar meningitis

    ❑ Posterior communicating artery aneurysm

    ❑ Cavernous sinus thrombosis

    ❑ Syphilis

    ❑ Guillain-Barré variant

    ❑ Botulism

    Nystagmus

    ❑ Labyrinthitis

    ❑ Multiple sclerosis

    ❑ Oculogyric crisis

    ❑ Cerebellar lesion

    ❑ Brainstem lesion

    ❑ Frontal lesion

    ❑ Occipital lesion

    ❑ Dorsal midbrain lesion

    ❑ Heavy metal intoxication

    ❑ Congenital

    Diagnostic Approach

    The direction of gaze with the most prominent diplopia reflects the action of the paretic muscle. Binocular diplopia is due to ocular misalignment, and the patient will usually close one eye to compensate. Acute monocular diplopia can occur with corneal aberrations, cataract, or foveal traction.

    CN III paresis: The lateral rectus and superior oblique are unopposed, turning the eye outward and downward. An acute lesion may be peripheral (diabetic or ischemic) or central (posterior communicating artery aneurysm or
    cavernous sinus lesion). Both have ptosis, absent eye elevation, and adduction, but a peripheral lesion has normal pupil size and movement (“pupillary sparing”). A central lesion produces a pupil that is dilated and unresponsive to light or accomodation. Causes include tumor, aneurysm, or severe trauma. Unilateral third nerve palsy with contralateral superior rectus palsy and bilateral partial ptosis, and bilateral third nerve palsy always represents a central lesion. Unilateral external ophthalmoplegia with normal contralateral superior rectus function, unilateral internal ophthalmoplegia, and unilateral ptosis represents a peripheral lesion.

    CN IV paresis: Superior oblique weakness produces vertical diplopia. The patient tilts his or her head to the opposite side to lessen the displacement. Typical causes are a relatively minor head blow, and idiopathic.

    CN VI paresis: Lateral rectus palsy produces weakness in abduction and horizontal diplopia that is better in near than in distant vision. When CN V is also affected (reduced facial sensation around the upper face and cornea), a cavernous sinus lesion should be suspected. Papilledema should also be looked for, as it indicates a mass lesion displacing the brainstem.

    If the patient has an isolated lesion of one of the cranial nerves, pain will be localized to just above the eyebrow on the weak side. Intraorbital pathology is indicated by pain in the eye itself or on eye movement. The worst headache of the patient’s life raises concern for intracranial aneurysm.

    True nystagmus is characterized by rapid regular oscillations around a fixed point not just with lateral gaze but also when the eyes are looking forward. A few beats of nystagmus at extremes of gaze are not pathologic. Nystagmus of ocular causes has a pendular motion whereas disease in the central nervous system produces fast and slow components. Irregular bursts of rapid eye movements (saccadic intrusions) almost always indicate a cerebellar lesion.

    Internuclear ophthalmoplegia occurs when the oculomotor and abducens nerves (CN III and VI) are disconnected at the medial longitudinal fasciculus. When conjugate gaze is attempted, one eye will not adduct medially and the abducting eye (lateral gaze) will show nystagmus. This finding is seen in persons with multiple sclerosis and pontine vascular lesions.

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    Source: Field Guide to Bedside Diagnosis, 2007

    Eye pain: History
    (Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

    If the patient’s eye pain doesn’t result from a chemical burn, take a complete history. Have the patient describe the pain fully. Is it an ache or a sharp pain? How long does it last? Is it accompanied by burning, itching, or discharge? Find out when it began. Is it worse in the morning or late in the evening? Ask about recent trauma or surgery, especially if the patient complains of sudden, severe pain. Does he have headaches? If so, find out how often and at what time of day they occur.

    Physical examination

    During the physical examination, don’t manipulate the eye if you suspect trauma. Carefully assess the lids and conjunctiva for redness, inflammation, and swelling. Then examine the eyes for ptosis or exophthalmos. Finally, test visual acuity with and without correction, and assess extraocular movements. Characterize any discharge. (See Examining the external eye.)

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    Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007

    Vision loss: History
    (Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

    Sudden vision loss can signal an ocular emergency. Don’t touch the eye if the patient has perforating or penetrating ocular trauma.

    If the patient’s vision loss occurred gradually, ask him if it developed over hours, days, or weeks. Does it affect one eye or both? Does it affect all or part of the visual field? Is the vision loss transient or persistent? What’s the patient’s age? Ask whether he has experienced photosensitivity, and ask him about the location, intensity, and duration of eye pain. Obtain an ocular history, including history of eye problems or systemic diseases that may lead to eye problems, such as infections, cancer, hypertension, diabetes mellitus, and thyroid, rheumatic, or vascular disease.

    Physical examination

    Assess visual acuity and determine the best available vision correction in each eye. (See Testing visual acuity.)

    Carefully inspect both eyes, noting edema, foreign bodies, drainage, or conjunctival or scleral redness. Observe whether lid closure is complete or incomplete, and check for ptosis. Using a flashlight, examine the cornea and iris for scars, irregularities, and foreign bodies. Evaluate extraocular muscle function by testing the six cardinal fields of gaze. (See Testing extraocular muscles, page 306.) Observe the size, shape, and color of the pupils, and test the direct and consensual light reflex and the effect of accommodation. (See Vision loss: Causes and associated findings, pages 308 and 309.)

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    Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007

    Diplopia: History
    (Signs & Symptoms: A 2-in-1 Reference for Nurses)

    Briefly ask about associated symptoms, especially a severe headache. Find out about associated neurologic symptoms first because diplopia can accompany serious disorders. Find out when the patient first noticed diplopia. Are the images side-by-side (horizontal), one above the other (vertical), or a combination? Does diplopia affect near or far vision? Does it affect certain directions of gaze? Ask if diplopia has worsened, remained the same, or subsided. Does its severity change throughout the day? Diplopia that worsens or appears in the evening may indicate myasthenia gravis. Find out if the patient can correct diplopia by tilting his head. If so, ask him to show you. (If the patient has a fourth nerve lesion, tilting of the head toward the opposite shoulder causes compensatory tilting of the unaffected eye. If he has incomplete sixth nerve palsy, tilting of the head toward the side of the paralyzed muscle may relax the affected lateral rectus muscle.)

    Explore associated symptoms such as eye pain. Ask about hypertension, diabetes mellitus, allergies, and thyroid, neurologic, or muscular disorders. Also, note a history of extraocular muscle disorders, trauma, or eye surgery.

    » READ BOOK EXCERPT ONLINE »

    Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

    Eye pain: History
    (Signs & Symptoms: A 2-in-1 Reference for Nurses)

    If the patient’s eye pain doesn’t result from a chemical burn, take a complete history. Have the patient describe the pain fully. Is it an ache or a sharp pain? How long does it last? Is it accompanied by burning, itching, or discharge? Find out when it began. Is it worse in the morning or late in the evening? Ask about recent trauma or surgery, especially if the patient complains of sudden, severe pain. Does he have headaches? If so, find out how often and at what time of day they occur.

    » READ BOOK EXCERPT ONLINE »

    Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

    Hemianopsia: History
    (Signs & Symptoms: A 2-in-1 Reference for Nurses)

    Ask the patient if he has recently experienced headache, dysarthria, or seizures. When did neurologic symptoms start? Obtain a medical history, noting especially eye disorders, hypertension, diabetes mellitus, and recent head trauma. Suspect a visual field defect if the patient seems startled when you approach him from one side or if he fails to see objects placed directly in front of him. To help determine the type of defect, compare the patient’s visual fields with your own — assuming that yours are normal. First, ask the patient to cover his right eye while you cover your left eye. Then move a pen or similarly shaped object from the periphery of his (and your) uncovered eye into his field of vision. Ask the patient to indicate when he first sees the object. Does he see it at the same time you do? After you do? Repeat this test in each quadrant of both eyes. Then, for each eye, plot the defect by shading the area of a circle that corresponds to the area of vision loss.

    » READ BOOK EXCERPT ONLINE »

    Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

    Scotoma: History
    (Signs & Symptoms: A 2-in-1 Reference for Nurses)

    Explore the patient’s medical history, noting especially any eye disorders, vision problems, or chronic systemic disorders. Find out if he takes medications or uses eyedrops.

    » READ BOOK EXCERPT ONLINE »

    Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

    Vision loss: History
    (Signs & Symptoms: A 2-in-1 Reference for Nurses)

    Sudden vision loss can signal an ocular emergency. (See Managing sudden vision loss, page 690.)

    If the patient’s vision loss occurred gradually, ask him if the vision loss affects one eye or both and all or only part of the visual field. Is the visual loss transient or persistent? Did the visual loss occur abruptly, or did it develop over hours, days, or weeks? What is the patient’s age? Ask the patient if he has experienced photosensitivity, and ask him about the location, intensity, and duration of any eye pain. You should also obtain an ocular history and a family history of eye problems or systemic diseases that may lead to eye problems, such as hypertension; diabetes mellitus; thyroid, rheumatic, or vascular disease; infections; and cancer.

    » READ BOOK EXCERPT ONLINE »

    Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

    Diplopia: History and physical examination
    (Nursing: Interpreting Signs and Symptoms)

    If the patient complains of double vision, first check his neurologic status. Evaluate his level of consciousness (LOC); pupil size, equality, and response to light; and motor and sensory function. Then take his vital signs. Briefly ask about associated symptoms, especially a severe headache. Find out about associated neurologic symptoms first because diplopia can accompany serious disorders.

    Next, continue with a more detailed examination. Find out when the patient first noticed diplopia. Are the images side-by-side (horizontal), one above the other (vertical), or a combination? Does diplopia affect near or far vision? Does it affect certain directions of gaze? Ask if diplopia has worsened, remained the same, or subsided. Does its severity change throughout the day? Diplopia that worsens or appears in the evening may indicate myasthenia gravis. Find out if the patient can correct diplopia by tilting his head. If so, ask him to show you. (If the patient has a fourth nerve lesion, tilting of the head toward the opposite shoulder causes compensatory tilting of the unaffected eye. If he has incomplete sixth nerve palsy, tilting of the head toward the side of the paralyzed muscle may relax the affected lateral rectus muscle.)

    Explore associated symptoms such as eye pain or limited eye movement. Ask about hypertension, diabetes mellitus, allergies, and thyroid, neurologic, or muscular disorders. Also, note a history of extraocular muscle disorders, trauma, or eye surgery.

    Observe the patient for ocular deviation, ptosis, proptosis, lid edema, and conjunctival injection. Distinguish monocular from binocular diplopia by asking the patient to occlude one eye at a time. If he still sees double out of one eye, he has monocular diplopia. Test his visual acuity and extraocular muscles. Check his vital signs.

    » READ BOOK EXCERPT ONLINE »

    Source: Nursing: Interpreting Signs and Symptoms, 2007

    Hemianopsia: History and physical examination
    (Nursing: Interpreting Signs and Symptoms)

    Suspect a visual field defect if the patient seems startled when you approach him from one side or if he fails to see objects placed directly in front of him. To help determine the type of defect, compare the patient's visual fields with your own—assuming that yours are normal. First, ask the patient to cover his right eye while you cover your left eye. Then move a pen or similarly shaped object from the periphery of his (and your) uncovered eye into his field of vision. Ask the patient to indicate when he first sees the object. Does he see it at the same time you do? After you do? Repeat this test in each quadrant of both eyes. Then, for each eye, plot the defect by shading the area of a circle that corresponds to the area of vision loss.

    Next, evaluate the patient's level of consciousness (LOC), take his vital signs, and check his pupillary reaction and motor response. Ask if he has recently experienced a headache, dysarthria, or seizures. Does he have ptosis or facial or extremity weakness? Hallucinations or loss of color vision? When did neurologic symptoms start? Obtain a medical history, noting especially eye disorders, hypertension, diabetes mellitus, and recent head trauma.

    » READ BOOK EXCERPT ONLINE »

    Source: Nursing: Interpreting Signs and Symptoms, 2007

    Scotoma: History and physical examination
    (Nursing: Interpreting Signs and Symptoms)

    Explore the patient's medical history, noting especially eye disorders, vision problems, or chronic systemic disorders. Find out if he takes medications or uses eyedrops.

    Identify and characterize the scotoma, using such visual field tests as the tangent screen examination, the Goldmann perimeter test, and the automated perimetry test. Two other visual field tests—confrontation testing and the Amsler grid—may also help in identifying a scotoma.

    Next, test the patient's visual acuity and inspect his pupils for size, equality, and reaction to light. An ophthalmoscopic examination and measurement of intraocular pressure are necessary.

    » READ BOOK EXCERPT ONLINE »

    Source: Nursing: Interpreting Signs and Symptoms, 2007

    Vision loss: History and physical examination
    (Nursing: Interpreting Signs and Symptoms)

    Sudden vision loss can signal an ocular emergency. (See Managing sudden vision loss, page 628.) Don't touch the eye if the patient has perforating or penetrating ocular trauma.

    If the patient's vision loss occurred gradually, ask him if the vision loss affects one eye or both and all or only part of the visual field. Is the visual loss transient or persistent? Did the vision loss occur abruptly or did it develop over hours, days, or weeks? What's the patient's age? Ask the patient if he has experienced photosensitivity and ask him about the location, intensity, and duration of eye pain. You should also obtain an ocular history and a family history of eye problems or systemic diseases that may lead to eye problems, such as hypertension; diabetes mellitus; thyroid, rheumatic, or vascular disease; infections; and cancer.

    The first step in performing an eye examination is to assess visual acuity, with best available correction in each eye. (See Testing visual acuity, page 629.)

    Carefully inspect both eyes, noting edema, foreign bodies, drainage, or conjunctival or scleral redness. Observe whether lid closure is complete or incomplete and check for ptosis. Using a flashlight, examine the cornea and iris for scars, irregularities, and foreign bodies. Observe the size, shape, and color of the pupils, and test the direct and consensual light reflex (See “Pupils, nonreactive,” page 515.) and the effect of accommodation. Evaluate extraocular muscle function by testing the six cardinal fields of gaze. (See Testing extraocular muscles, page 197.)

    » READ BOOK EXCERPT ONLINE »

    Source: Nursing: Interpreting Signs and Symptoms, 2007

    Eye pain [Ophthalmalgia]: History and physical examination
    (Nursing: Interpreting Signs and Symptoms)

    If the patient's eye pain doesn't result from a chemical burn, take a complete history. Have the patient describe the pain fully. Is it an ache or a sharp pain? How long does it last? Is it accompanied by burning, itching, or discharge? Find out when it began. Is it worse in the morning or late in the evening? Ask about recent trauma or surgery, especially if the patient complains of sudden, severe pain. Does the patient wear contact lenses? How often are they removed or replaced if they're disposable? Does he have headaches? If so, find out how often and at what time of day they occur.

    During the physical examination, don'tmanipulate the eye if you suspect trauma. Carefully assess the lids and conjunctiva for redness, inflammation, and swelling. Then examine the eyes for ptosis or exophthalmos. Finally, test visual acuity with and without correction, and assess extraocular movements. Characterize any discharge. (See Examining the external eye.)

    » READ BOOK EXCERPT ONLINE »

    Source: Nursing: Interpreting Signs and Symptoms, 2007

    EYE PAIN: Approach to the Diagnosis
    (Differential Diagnosis in Primary Care)

    The approach to the diagnosis of eye pain involves a careful search for inflammation of the various anatomic structures; then a drop or two of fluorescent dye is inserted and the cornea inspected for lacerations, herpes ulcers, and foreign bodies. Finally, tonometry may be done. Referral to an ophthalmologist is often necessary, but the astute clinician will want to x-ray the sinuses, ask about a history of migraine, do a visual field, and rule out systemic diseases beforehand.

    » READ BOOK EXCERPT ONLINE »

    Source: Differential Diagnosis in Primary Care, 2007

    PAPILLEDEMA: Approach to the Diagnosis
    (Differential Diagnosis in Primary Care)

    The approach to the diagnosis of papilledema in someone without hypertension or hypertensive retinopathy must include a thorough neurologic examination and a computed tomography (CT) scan. If focal signs are present or the CT scan shows positive findings, referral to a neurosurgeon is indicated. He or she can decide if a magnetic resonance imaging (MRI) is indicated. A spinal tap is contraindicated. If there are no focal signs, it may be worthwhile to differentiate papilledema from optic neuritis by having an ophthalmologist perform a visual field examination. This may also be helpful in differentiating pseudotumor cerebri because there may be bilateral visual defects in the inferior nasal quadrants. Papilledema from increased intracranial pressure will show only an enlarged blind spot (unless there is a tumor of the optic tracts, radiations, or occipital cortex), whereas optic neuritis will show scotomata peripheral to the blind spot (disc). Appendix A will be useful for confirming the diagnosis of a specific disease.

    PARESTHESIAS, DYSESTHESIAS, AND NUMBNESS
    VIND
    VascularInflammatoryNeoplasmDegenerative
        
    Peripheral Nerve
    Causalgia Raynaud disease Buerger disease Arteriosclerosis Ischemic neuritis
    Pellagra Beriberi Nutritional neuropathy
    Nerve Plexus
    Leriche syndrome
    		 Pancoast tumor
     
     
    Nerve Root
    Tabes dorsalis Tuberculosis
    Metastatic and primary tumors of the cord and spine (multiple myeloma)
    Herniated disc Cervical and lumbar spondylosis
    Spinal Cord
    Anterior spinal artery occlusion Aortic aneurysm
    Poliomyelitis Epidural abscess Tuberculosis Syphilis
    Metastatic and primary tumors of the cord and spine
    Spondylosis Disc disease Pernicious anemia
    Brain
    Cerebral embolus, thrombus, hemorrhage Carotid or basilar artery insufficiency Migraine
    Neurosyphilis Encephalitis Brain abscess
    		 Brain tumorSenile dementia Presenile dementia

    PARESTHESIAS, DYSESTHESIAS, AND NUMBNESS
    ICATE
    IntoxicationCongenital AutoimmuneTraumaEndocrine
     Allergic  
    Alcoholic neuropathy Isoniazid toxicity Lead and arsenic neuropathy
    		 Porphyria
    Infectious neuronitis Periarteritis nodosa
    Trauma Hematoma Laceration Neuroma Frostbite
    Tetany of hypoparathyroidism Aldosteronism
     
    Scalenus anticus Cervical rib
    Infectious neuronitis
    Contusion Laceration Fracture
    Diabetic neuropathy
    Spondylolisthesis
    Fracture Herniated disc
     
    Transverse myelitis from radiation
    Spina bifida Myelocele Syringomyelia
    Guillain–Barré syndrome Multiple sclerosis
    Fracture Herniated disc Hematoma
     
    Alcoholism Bromism Encephalopathy Opiates, barbiturates, etc.
    Atrioventricular anomalies Aneurysm Epilepsy Cerebral palsy
    Lupus cerebritis Multiple sclerosis
    Depressed fracture Subdural hematoma
    		 Pituitary tumor Acromegaly

    » READ BOOK EXCERPT ONLINE »

    Source: Differential Diagnosis in Primary Care, 2007


     » Next page: Signs of Vision Impairment

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