Diagnosis of Nystagmus
Nystagmus Diagnosis: Book Excerpts
Diagnostic Tests for Nystagmus: Online Medical Books
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EYE PAIN:
Ask the following questions:
(Algorithmic Diagnosis of Symptoms and Signs)
- 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.
- If there is redness, is there periorbital edema as well? Periorbital edema should suggest a cavernous sinus thrombosis or herpes zoster.
- If there is periorbital edema, is there a rash? A rash, particularly vesicular rash, would suggest herpes zoster.
- 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.
- 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.
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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003
NYSTAGMUS:
Ask the Following Questions:
(Algorithmic Diagnosis of Symptoms and Signs)
- Is the nystagmus pendular? Pendular nystagmus without a fast or slow component suggests ocular nystagmus due to albinism, partial blindness, or other ocular disorders.
- Is it intermittent or fatigable? Intermittent or fatigable nystagmus suggests otologic disorders such as acoustic neuroma, Ménière's disease, vestibular neuronitis, and acute labyrinthitis.
- Is there associated tinnitus or deafness? The presence of nystagmus with tinnitus or deafness also suggests otologic disorders such as acoustic neuroma, Ménière's disease, or cholesteatoma. If there are long tract signs, multiple sclerosis and brain stem tumors must be considered.
- Is the nystagmus brought on by change of position? Nystagmus brought on by certain changes of position suggests benign positional vertigo. However, this also may be found in post-traumatic labyrinthitis and postconcussion syndrome.
- Are there associated long tract signs? The presence of long tract signs suggests multiple sclerosis, basilar artery insufficiency, syringomyelia, and Friedreich's ataxia. Certain brain stem tumors may also be associated with long tract signs.
DIAGNOSTIC WORKUP
The basic diagnostic workup includes visual acuity, visual fields, audiogram, caloric testing, and x-rays of the skull, mastoids, and petrous bones. If these are negative or indefinite, a CT scan or MRI of the brain will be necessary. A spinal fluid analysis will help diagnose central nervous system lues and multiple sclerosis. A BSEP or VEP study may be needed to diagnose multiple sclerosis. The help of a neurologic specialist should be sought before ordering expensive diagnostic tests. Cisternography, tomography, and vertebral basilar angiography are occasionally necessary to establish the diagnosis. Magnetic resonance angiography is an excellent noninvasive means of visualizing the vertebral-basilar circulation.
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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003
Nystagmus:
Differential Diagnosis
(In a Page: Signs and Symptoms)
- Vestibular
–Peripheral (horizontal rotary nystagmus, slow phase toward hypoactive side, latency, fatigability, and accompanied by vertigo, tinnitus, or deafness): Etiologies include labyrinthitis, vestibular neuronitis, Ménie're's disease, migraine, BPV
–Central (asymmetric, rotary nystagmus that changes direction in different gazes, no latency, not fatigable): Etiologies include lesions of cerebellum, pons, or cerebellopontine angle
–Horizontal
-
Gaze-evoked
–Physiologic: Fixing on objects with eyes when head is turned (e.g., ballerinas)
–Pathologic (asymmetric): Etiologies include toxic-metabolic lesions, cerebellar or pontine lesions
-
Dissociated (different nystagmus between eyes): Etiologies include internuclear ophthalmoplegia of multiple sclerosis or cerebral disease
-
Periodic alternating nystagmus (cervicomedullary junction)
-
Downbeat (cervicomedullary junction, characteristic of syringobulbia)
-
Upbeat (brainstem or cerebellum when present in primary gaze; drug effect if only present in upgaze)
-
Drug-induced (e.g., anticonvulsants, sedatives, alcohol)
-
Monocular visual loss (ipsilateral slow vertical oscillation)
- Head nodding, head turn (due to motor or sensory deficits)
–Latent nystagmus (occurs only when one eye is viewing, and is always associated with strabismus)
–Nystagmus blockage syndrome (convergence, esotropia, and head turn)
–Spasmus nutans: Onset 4–14 months, resolves by age 5; head nodding, torticollis, see-saw
Workup and Diagnosis
- History and physical examination
–Note age of onset, associated symptoms (e.g., oscillopsia, decreased vision, nausea/vomiting, vertigo, hearing loss, tinnitus, diplopia, dysarthria, facial numbness, dysphagia), medications, and drug use
–Complete ocular exam: Eye movements in primary gaze and all positions of gaze; iris transillumination (albinism), dilated fundus exam, careful refraction, vestibulo-ocular reflex
–Dix-Hallpike maneuver (for positional vertigo, peripheral
versus central)
–Caloric stimulation
–Complete neurologic examination
–Nystagmus is asymptomatic, unless acquired after age 8,
at which time the patient may have oscillopsia (a sense that the surroundings are oscillating)
-
Consider drug, toxin, and dietary screen of urine/serum
-
Consider MRI of brain
-
Consider visual field exam
-
Consider neurology and/or ophthalmology consultation
–Eye movement recording
–Electronystagmogram
–Visual evoked response
–Electroretinography
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Source: In a Page: Signs and Symptoms, 2004
Nystagmus:
Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)
-
Nystagmus occurs at the extreme lateral gaze in many normal individuals
–May also occur when tracking an object or row of objects horizontally
–Can be induced by rotatory visual stimuli or otic irrigation (vestibular stimuli) in normal individuals
-
Hereditary nystagmus
–Benign condition of horizontal nystagmus
–May not be accompanied by other neurologic
findings, but involuntary head-bobbing may be a feature
–May be XL or AD
-
Visual impairment
–Poor vision, ocular blindness, and cortical blindness can result in nystagmus
–May also have “searching” eye movements that are not true nystagmus
–Both are more likely to occur in patients born blind or blind from an early age
-
Spasmus mutans
–May be isolated or associated with intracranial mass
–Characterized by nystagmus, involuntary head-bobbing, and torticollis
-
Congenital jerking nystagmus
–Idiopathic; horizontal nystagmus with lateral gaze on one direction
-
Intracranial neoplasms
-
Arnold-Chiari malformation
-
Cerebellar etiologies
–Acute cerebellar ataxia
–Encephalitis or abscess involving the
cerebellum
-
Septo-optic dysplasia
–Optic nerve hypoplasia, associated with other midline brain defects
–Endocrine abnormalities are common
(diabetes insipidus, hypoglycemia,
hypopituitarism, failure to thrive)
-
Toxicity
–Medications include barbiturates, hydantoin,
antihistamines, and salicylates
–Lead toxicity
–Alcohol intoxication may involve vestibular
disturbances including vertigo, nystagmus
- Opsoclonus
–Not true nystagmus
–Eye movements that may be mistaken for
nystagmus (e.g., opsoclonus-myoclonus disorder)
Workup and Diagnosis
- History
–Onset, duration, progression
–Accompanying signs and symptoms, including
symptoms of intracranial space-occupying lesion such
as headache and vomiting
–Family history
–Birth and past medical history
- Physical exam
–Characterization of the eye movements that elicit nystagmus, the severity, and the type of eye movements
–Visual acuity in each eye
–Funduscopic examination for papilledema
–Extraocular muscle evaluation
–Pupillary red light reflex: White in retinoblastoma
–Preferred head position: Patients with congenital
jerking nystagmus frequently turn their faces in such a
way as to minimize nystagmus
–Positional test for benign paroxysmal vertigo
–Head circumference (hydrocephalus)
–Neurologic examination including cranial nerves and
cerebellar signs
-
Labs
–Toxicology screen and medication levels as applicable
-
Studies
–Imaging of the brain may be required to rule out malignancy, mass, midline defects
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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.
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Source: Differential Diagnosis in Primary Care, 2007
NYSTAGMUS:
Approach to the Diagnosis
(Differential Diagnosis in Primary Care)
The workup here is similar to the workup of vertigo. Nystagmus without other signs of CNS disease is usually ocular or peripheral in the middle or inner ear. Vertigo is almost invariably present in nystagmus of aural origin. Nystagmus with long tract signs such as hemiplegia or hemianesthesia is invariably brainstem in origin. Purely cerebellar nystagmus is not easily fatigued and is associated with dyskinesia and dyssynergia of the extremities as well as ataxia. There are no long tract or cranial nerve signs. Nystagmus with vertigo, nausea, vomiting, tinnitus, and deafness suggests Ménière disease.
Confirmation of the diagnosis is made by audiograms, caloric tests, skull x-rays (with special views of the mastoids and petrous bones), angiography, CT scans, and myelography. MRI scans are useful, especially in diagnosing brainstem lesions and multiple sclerosis. They also provide a better view of the internal auditory canal. A spinal tap will help in the diagnosis of multiple sclerosis and neurolues as well as acoustic neuromas.
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Source: Differential Diagnosis in Primary Care, 2007
TREMOR AND OTHER INVOLUNTARY MOVEMENTS:
Approach to the Diagnosis
(Differential Diagnosis in Primary Care)
The workup of tremor and other involuntary movements involves most of all a good history. The neurologic exam is important as it will determine the type of tremor. Rapid fine tremors (8–20/s) are suggestive of hyperthyroidism and emotional disorders. Coarser tremors at rest suggest parkinsonism, whereas a flapping tremor of 4 to 8 per second suggests Wilson disease. The association of other neurologic signs helps pin down the diagnosis. Spasms of pain suggest a thalamic syndrome, whereas ataxia suggests Friedreich ataxia and loss of memory suggests manganese toxicity. Laboratory tests will be useful in selected cases. Blood lead, manganese, copper, and ceruloplasmin levels may be necessary. A T3, T4, and FT4 index will confirm the diagnosis of Graves disease. Other tests that may be helpful may be found in the Appendix or listed below.
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Source: Differential Diagnosis in Primary Care, 2007
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
Ocular deviation:
History and physical examination
(Handbook of Signs & Symptoms (Third Edition))
If the patient isn’t in distress, find out how long he has had the ocular deviation. Is it accompanied by double vision, eye pain, or a headache? Also, ask if he’s noticed associated motor or sensory changes or a fever.
Check for a history of hypertension, diabetes, allergies, and thyroid, neurologic, or muscular disorders. Then obtain a thorough ocular history. Has the patient ever had extraocular muscle imbalance, eye or head trauma, or eye surgery?
During the physical examination, observe the patient for partial or complete ptosis. Does he spontaneously tilt his head or turn his face to compensate for ocular deviation? Check for eye redness or periorbital edema. Assess the patient’s visual acuity, and then evaluate extraocular muscle function by testing the six cardinal fields of gaze.
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Source: Handbook of Signs & Symptoms (Third Edition), 2006
Nystagmus:
History and physical examination
(Handbook of Signs & Symptoms (Third Edition))
Begin by asking the patient how long he’s had nystagmus. Does it occur intermittently? Does it affect his vision? Ask about recent infection, especially of the ear or respiratory tract, and about head trauma and cancer. Does the patient or anyone in his family have a history of stroke? Then explore associated signs and symptoms. Ask about vertigo, dizziness, tinnitus, nausea or vomiting, numbness, weakness, bladder dysfunction, and fever.
Begin the physical examination by assessing the patient’s level of consciousness (LOC) and vital signs. Be alert for signs of increased intracranial pressure (ICP), such as pupillary changes, drowsiness, elevated systolic pressure, and an altered respiratory pattern. Next, assess nystagmus fully by testing extraocular muscle function: Ask the patient to focus straight ahead and then to follow your finger up, down, and in an “X” across his face. Note when nystagmus occurs as well as its velocity and direction. Finally, test reflexes, motor and sensory function, and the cranial nerves.
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Source: Handbook of Signs & Symptoms (Third Edition), 2006
Ocular deviation:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
If the patient isn’t in distress, find out how long he has had the ocular deviation. Is it accompanied by double vision, eye pain, or headache? Also, ask if he has noticed any associated motor or sensory changes, or fever.
Check for a history of hypertension, diabetes, allergies, and thyroid, neurologic, or muscular disorders. Then obtain a thorough ocular history. Has the patient ever had extraocular muscle imbalance, eye or head trauma, or eye surgery?
During the physical examination, observe the patient for partial or complete ptosis. Does he spontaneously tilt his head or turn his face to compensate for ocular deviation? Check for eye redness or periorbital edema. Assess visual acuity, then evaluate extraocular muscle function by testing the six cardinal fields of gaze.
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Nystagmus:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
Begin by asking the patient how long he has had nystagmus. Does it occur intermittently? Does it affect his vision? Ask about recent infection, especially of the ear or respiratory tract, and about head trauma and cancer. Does the patient or anyone in his family have a history of stroke? Then explore associated signs and symptoms. Ask about vertigo, dizziness, tinnitus, nausea or vomiting, numbness, weakness, bladder dysfunction, and fever.
Begin the physical examination by assessing the patient’s level of consciousness (LOC) and vital signs. Be alert for signs of increased intracranial pressure (ICP), such as pupillary changes, drowsiness, elevated systolic pressure, and altered respiratory pattern. Next, assess nystagmus fully by testing extraocular muscle function: Ask the patient to focus straight ahead and then to follow your finger up, down, and in an “X” across his face. Note when nystagmus occurs, as well as its velocity and direction. Finally, test reflexes, motor and sensory function, and the cranial nerves.
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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
Nystagmus:
History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
A. Age of onset. Congenital nystagmus is either caused by poor vision (sensory) or motor nystagmus. Both develop early in life but sensory nystagmus does not present until 2 to 3 months of age. Nystagmus developing later in life (acquired nystagmus) is neuropathologic.
B. Family history. Is there a history of nystagmus, strabismus, or visual problem present at an early age in other family members? Hereditary motor nystagmus is not too uncommon.
C. Associated symptoms. Is oscillopsia (the sensation of environment “jiggling”) present? If present, then the nystagmus is likely acquired. Vertigo implies vestibular disease. Previous episodes of weakness, numbness, or loss of vision implicate multiple sclerosis. Associated ptosis suggests myasthenia.
D. Medications. Medications that can induce nystagmus include lithium, barbiturates, phenytoin, salicylates, benzodiazepines, phencyclidine, and other anticonvulsants or sedatives.
E. Social history. Alcohol intoxication produces a gaze-evoked nystagmus as well as alcohol-induced thiamin deficiency in Wernicke’s encephalopathy.
Physical examination
A. Visual acuity. Visual acuity is more depressed in acquired sensory nystagmus than in congenital nystagmus.
B. Ocular motility. The direction, plane, and amplitude of the eye movement are described. Nystagmus is conjugate if both eyes demonstrate the same movement and dissociated if they have different movements. Look for a null zone (field of gaze in which the nystagmus is minimal) or a neutral zone (field of gaze where nystagmus reverses direction).
C. Eye examination. Evaluate for any cause of poor vision that will help confirm sensory nystagmus. Look for aniridia (absence of iris) or iris transillumination as seen in albinism; both are associated with poor vision and nystagmus at an early age. Congenital cataracts or corneal opacities will have poor red reflexes. Analyze the optic nerve to assess for hypoplasia or atrophy. Latent nystagmus (seen only when one eye is covered) is present in congenital esotropia.
D. Other examinations. Head bobbing is usually present with congenital motor nystagmus and spasmus nutans (see below). A complete neurologic assessment should be done to screen for associated signs seen in cerebellar disease, multiple sclerosis, and so on.
Diagnostic assessment
(3,4). An accurate description of the nystagmus will help to categorize the type of eye movement disorder and to determine if any further diagnostic testing is needed.
A. Congenital nystagmus. The nystagmus develops at birth or in the perinatal period with small binocular and conjugate pendular eye movements. Over the first year of life, a jerk nystagmus develops with a null point. The nystagmus decreases with convergence and is abolished during sleep. Head nodding develops at any point up to age 20 years. Any cause of poor vision can cause sensory nystagmus. Two forms of acquired nystagmus when seen in the young merit concern.
1. Opsoclonus. Repetitive, irregular, and multidirectional (“dancing eyes” or saccadomania), opsoclonus is associated with cerebellar or brainstem disease, postviral meningitis, or neuroblastoma.
2. Spasmus nutans. Triad of head turn, nystagmus, and head bobbing that begins between 6 months to 3 years is seen in spasmus nutans. The nystagmus can be monocular or binocular and dissociated; of low amplitude and high frequency; and with horizontal or vertical pendular movements. This usually resolves between age 2 and 8 years. An identical clinical picture can be produced by a glioma of the optic chiasm.
B. Acquired nystagmus. The following are acquired forms of nystagmus with localized pathology.
1. See-saw. One eye rises and rotates in whereas the other descends and rotates out. Movements are pendular. This is frequently seen with lesions of the chiasm or third ventricle.
2. Downbeating. The fast phase of the nystagmus beats down and localizes the lesion at the cervicomedullary junction at the level of the foramen magnum. Arnold-Chiari malformation is the most common cause but spinocerebellar degeneration, brainstem stroke, multiple sclerosis, and platybasia will induce this type of nystagmus.
3. Upbeat. The fast phase beats up and can be of large or small amplitude. The lesion commonly involves the brainstem or vermis of the cerebellum.
4. Convergence-retraction. Here, is seen convergence of the eyes with jerk nystagmus and retraction of the globe on upgaze. Eyelid retraction, limitation in upgaze, and large unreactive pupils are associated with the nystagmus. Papilledema may be present. This is caused by midbrain abnormalities loosely correlated with age 10 years, pinealoma; 20 years, head trauma; 30 years, brainstem vascular malformation; 40 years, multiple sclerosis; 50 years, basilar artery stroke.
5. Periodic alternating. Jerk nystagmus has the fast phase in one direction with a head turn for 60 to 90 seconds, then reverses direction (neutral zone). The cycles repeat continuously with the nystagmus being horizontal throughout. This can be seen with vestibulocerebellar disease (stroke, multiple sclerosis, spinocerebellar degeneration), severe bilateral visual loss (optic atrophy, dense vitreous hemorrhage), or it can be congenital.
6. Gaze-evoked. Jerk nystagmus is present only when eyes look to the side. This is most commonly seen with alcohol or other central nervous system depressants. Cerebellar disease and brainstem disease can be associated with this nystagmus.
7. Vestibular. Nystagmus is caused by dysfunction of inner ear, nerve, or central nuclear complex. Peripheral vestibular disease produces unidirectional jerk nystagmus with fast phase opposite the lesion and usually horizontal. This is commonly associated with vertigo, tinnitus, and deafness (Chapters 6.8 and 6.9). It is caused by labyrinthitis, Ménière’s disease, neuronitis, vascular ischemia, trauma, or toxicity. Central (nuclear) disease is characterized by uni- or bidirectional nystagmus that may be purely horizontal jerk, vertical, or rotatory. Vertigo, tinnitus, and deafness are mild, if present, and symptoms are not relieved with eye fixation as in peripheral disease. This implies bilateral brainstem disease including demyelinating tumor, trauma, or stroke.
8. Latent nystagmus. As discussed, latent nystagmus is found in congenital esotropia.
9. Dissociated. The nystagmus in one eye is different than the other. This is seen in posterior fossa lesions; if an abduction nystagmus is present with an internuclear ophthalmoplegia, multiple sclerosis is likely.
C. Other ocular oscillations
1. Ocular bobbing is characterized by fast, conjugate, downward movement of the eye followed by a slow drift to primary position of gaze. This is seen in comatose patients with large pontine lesions (hemorrhage, stroke, or tumor). Obstructive hydrocephalus or metabolic encephalopathy can cause this type of eye movement.
2. Superior oblique myokymia is present with small unilateral, vertical, and rotatory movements of one eye. Symptoms of oscillopsia worsen when looking down and in. This is usually benign and self-limited, but has been noted with multiple sclerosis.
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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
Involuntary Weight Loss:
Differential Overview
(Field Guide to Bedside Diagnosis)
❑ Diabetes
❑ Depression
❑ Inadequate intake
❑ Drugs
❑ Hyperthyroidism
❑ Occult cancer
❑ Low cardiac output
❑ Anorexia nervosa
❑ Malabsorption
❑ Chronic infection
❑ Adrenal insufficiency
❑ Emphysema
Diagnostic Approach
Cachexia is accelerated loss of lean body mass in the context of a chronic inflammatory response, caused by a combination of decreased intake (with decreased appetite) and increased metabolic rate. The cause of the weight loss will usually be evident, based on concurrent symptoms. If not, first document that weight loss has occurred by using prior records of measured weights or the discovery of loose-fitting clothes (tightening belt notches) or dentures. If the cause is not found on the first pass, document the weight and re-examine several weeks later.
Weight loss in patients with congestive heart failure, cirrhosis, and
uremia may be masked by fluid retention, but temporalis and limb wasting will be prominent. Weight loss in malignancy of more than 5% of body mass prior to treatment portends a poor prognosis.
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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
Ocular deviation:
History
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)
If the patient isn’t in distress, ask how long he has had the ocular deviation. Is it accompanied by double vision, eye pain, or headache? Also, ask if he’s noticed associated motor or sensory changes or fever.
Determine whether the patient’shistory includes hypertension, diabetes, allergies, and thyroid, neurologic, or muscular disorders. Then obtain a thorough ocular history. Has the patient ever had extraocular muscle imbalance, eye or head trauma, or eye surgery?
Physical examination
During the physical examination, observe the patient for partial or complete ptosis. Does he spontaneously tilt his head or turn his face to compensate for ocular deviation? Check for eye redness or periorbital edema. Assess visual acuity, and then evaluate extraocular muscle function by testing the six cardinal fields of gaze. Test for near vision with a handheld eye chart held approximately 14"(35.5 cm) in front of the patient’s face.
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Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 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.
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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Ocular deviation:
History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
If the patient isn’t in distress, find out how long he has had the ocular deviation. Is it accompanied by double vision, eye pain, or headache? Also, ask if he has noticed any associated motor or sensory changes, or fever.
Check for a history of hypertension, diabetes, allergies, and thyroid, neurologic, or muscular disorders. Then obtain a thorough ocular history. Has the patient ever had extraocular muscle imbalance, eye or head trauma, or eye surgery?
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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Nystagmus:
History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Begin by asking the patient how long he’s had nystagmus. Does it occur intermittently? Does it affect his vision? Ask about recent infection, especially of the ear or respiratory tract, and about head trauma and cancer. Does the patient or anyone in his family have a history of stroke? Then explore associated signs and symptoms. Ask about vertigo, dizziness, tinnitus, nausea or vomiting, numbness, weakness, bladder dysfunction, and fever.
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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Nystagmus:
Clinical Features and Diagnosis
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)
Physiologic Nystagmus
Voluntary Nystagmus
Some individuals can voluntarily producebrief pendular nystagmus, which is usually rapid and horizontal.
End-Point Nystagmus
Is a jerk nystagmus of fine amplitude thatoccurs on extreme lateral gaze. It is brief and usually occurs innormal individuals who are anxious or tired. Fast phase is towardfield of gaze.
Opticokinetic Nystagmus
Is a jerknystagmus produced by watching repetitive visual stimuli movingacross field of vision.Can be produced by watching movinglights or sequence of vertical stripes on rotating drum or cloth.Following the moving object produces slow phase. Fast phase occurswhen eyes return to see next moving object.Nystagmus is horizontal or verticaldepending on direction of moving objects.Can be elicited to determine if inattentiveinfant sees or in cases of functional visual loss. Evoked Vestibular Nystagmus
Is a jerk nystagmus that can be producedin normal individuals by caloric (irrigation of ear canal with warmor cold water) or rotatory testing to determine integrity of labyrinthand its central connections. Direction of nystagmus (fast component)can be remembered by mnemonic COWS (cold, opposite; warm, same).
Pathologic Nystagmus
Idiopathic Congenital Nystagmus
Onset ofidiopathic congenital nystagmus is typically at 6–8 wksof age. It is frequently jerk nystagmus, but occasionally pendular.Different waveforms may be seen atvarious times in same individual. Almost always conjugate and mostoften horizontal.Often dampened by convergence, it isfrequently associated with a "null" point in whichintensity of oscillations decreases and visual acuity improves.Although amplitude and frequency ofnystagmus usually increase during first few months after presentation,they decrease later on. Many children have significant refractiveerrors, strabismus, or amblyopia, but there is no association withrecognizable structural lesions of the eye or anterior visual pathways.Eye muscle surgery is performed forany associated strabismus and sometimes to compensate for markedhead turns associated with nystagmus.Amplitude of nystagmus is not relatedto visual acuity, and many individuals have acuity sufficient toobtain driver's license. Latent Nystagmus
Is a congenitalnystagmus that is seen under conditions of monocular fixation. Etiologyis unknown but is most often seen in individuals with infantileesotropia. Generally not recognized until early childhood, whencover testing is done.It is a conjugate jerk nystagmus thathas its fast phase directed toward uncovered eye. Direction reverseswhen opposite eye is covered.Latent nystagmus may be superimposedon idiopathic congenital nystagmus. Nystagmus Associated with Visual Loss
Many eyedisorders can cause nystagmus, especially those that cause significantbilateral visual loss. These disorders include aniridia, congenitalcataract, retinopathy of prematurity, retinal dysplasia, macularcoloboma, glaucoma, optic nerve hypoplasia or atrophy, albinism,retinoblastoma, and strabismus. Because many of these causes ofimpaired vision are congenital, nystagmus may be the finding thatleads to their diagnosis.Before 2 yrs of age, lack of developmentof normal vision or visual loss is usually associated with nystagmus,which is usually horizontal and conjugate.From 2 to 6 yrs of age, nystagmus mayoccur after onset of visual loss.Acquired visual loss does not usuallycause nystagmus after 6 yrs of age.Severity of ocular oscillations doesnot predict visual acuity; rather, severity of visual pathway diseasedetermines severity of visual loss. Neurologic Disorders Associated with Nystagmus
Acquired Fixation Nystagmus
Posterior fossa lesion (e.g., tumor) mayproduce pendular or jerk, horizontal or vertical nystagmus withattempted fixation.
Periodic Alternating Nystagmus
Is a horizontal jerk nystagmus in which directionof fast phase changes in cyclic fashion every few minutes and isoften accompanied by alternating face turn. Can be seen with Chiarimalformations, demyelinating diseases, and cerebellar disorders.
Gaze-Evoked Nystagmus
Common causes are drugs (e.g., barbiturates,phenothiazines, tranquilizers, and anticonvulsants). If the drughistory is negative, other causes are brainstem or cerebellar dysfunction.
Seesaw Nystagmus
Unusual type of nystagmus in which 1 eyeelevates and intorts while other eye depresses and extorts. Maybe associated with parasellar tumors that compress optic chiasm(craniopharyngioma) or lesions of rostral midbrain.
Vestibular Nystagmus
Caused by disturbances in peripheral or centralportion of vestibular system.
Peripheral Lesions
With peripheralvestibular nystagmus (lesions of the labyrinth or eighth nerve),the jerk nystagmus is usually horizontal, with fast phase oppositethe side of the lesion.Common associated findings are vertigo,tinnitus, and hearing loss. Visual fixation inhibits nystagmus.Trauma and labyrinthitis are most commoncauses. Central Lesions
Lesionsinvolving vestibular nuclei, cerebellum, or their connections withcerebral cortex usually produce jerk nystagmus, which may be horizontal,vertical, or torsional.Hearing loss, tinnitus, and vertigodo not usually occur, and visual fixation does not inhibit nystagmus.Common causes include viral encephalitis,cerebellar or brainstem lesions, and multiple sclerosis. Spasmus Nutans
This disorderof unknown cause is characterized by the triad of nystagmus, headnodding, and torticollis.Usually begins after 4 mos of age andresolves by 5 yrs of age. Appears to only involve 1 eye, but finemovements also occur in other eye (dysconjugate nystagmus).Acquired mononuclear nystagmus maybe seen with chiasmal glioma, so that MRI may need to be performedif this tumor cannot be excluded on clinical exam by experiencedophthalmologist. Diagnostic Approach
Nystagmuscan usually be detected by simple observation, and type, direction,amplitude, frequency, and gaze should be determined.Whether nystagmus is physiologic orpathologic can usually be determined by history and physical exam.Careful eye exam can diagnose eye disordersassociated with nystagmus. If results of eye exam are normal, aneurologic disorder including a vestibular disturbance should beinvestigated.Association of nystagmus with hearingloss and vertigo suggests disturbance of peripheral vestibular system.Nystagmus associated with ataxia withouttinnitus and hearing loss suggests disturbance in brainstem or cerebellarfunction.CT and MRI are useful in diagnosisof neurologic disorders that may be associated with nystagmus.When considering causes of gaze-evokednystagmus, positive drug history may be diagnostic.Idiopathic congenital nystagmus isdiagnosis of exclusion.
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Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006
Involuntary Movements:
Clinical Features and Diagnosis
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)
Tics
Brief, sudden,repetitive movements that may be motor, vocal, or both.Motor tics usually involve face, neck,or shoulder and last 1–2 secs. Consist of eye blinking, grimacing,head jerking, and shoulder shrugging.Vocal tics include throat clearing,sniffing, coughing, grunting, and humming.Social impairing tics [e.g.,coprolalia (foul language) and copropraxia (foul gestures)] are lesscommon. Transient Tic Disorder
Usuallycharacterized by ≥1 simple tics, typically involving head orupper body.Duration of symptoms is <12mos.No markers identify which childrenwill progress to have Tourette syndrome. Tourette Syndrome
Autosomal-dominantdisorder characterized by motor and/or vocal tics of ≥1 yr'sduration.Gene locus has been mapped to chromosome11q23.Attention deficit hyperactivity disorder,obsessive compulsive behaviors, and other psychiatric disordersare commonly associated with Tourette syndrome. Drugs
Onset and severity of tics may be associatedwith stimulant use, although recent epidemiologic evidence appearsto make this association less clear. Other implicated drugs includeanticonvulsants, neuroleptics, and levodopa.
Chorea
Consists of repetitive, aimless, irregular,jerky movements of face, trunk, and extremities. Can be more apparentduring sustained muscle contraction or action movements.
Sydenham Chorea
Manifestationof acute rheumatic fever that can occur alone or with other manifestationsof rheumatic fever.May occur months after primary infectionwith group A Streptococcus.Besides chorea, characteristic featuresinclude emotional lability, slurred speech, difficulty in holdingobjects, and worsening handwriting. Anxiety, inattentiveness, anddeterioration in learning may occur before chorea becomes apparent.Antineuronal antibodies as well asantibodies to streptolysin O and DNAse B may be found in many childrenwith Sydenham chorea. Benign Familial Chorea
Onset isin infancy or early childhood.Both autosomal-dominant and -recessiveforms occur.Age of onset, family history, and lackof neurologic deterioration are diagnostic.Less pronounced in adolescence. Huntington Disease
Autosomal-dominantdisease that can appear as early as 5 yrs of age, but usual onset isin middle of adult life.Gene locus has been mapped to chromosome4p16.3.Characteristic features include chorea,rigidity, and dementia. Speech and behavioral changes may precedeintellectual deterioration.CT or MRI often shows atrophy of caudatenucleus and putamen.Clinical and radiologic findings alongwith family history are diagnostic. Molecular genetic analysis isconfirmatory. Drugs
Phenytoin, methylphenidate, dextroamphetamine,ethosuximide, and oral contraceptives can cause chorea-like movements.
Athetosis
Consistsof slow, writhing, purposeless, often continuous movements of head,neck, and extremities. Excitement or agitation increases their amplitude.Hypoxic-ischemic encephalopathy andcerebral palsy are common causes of these movements, which may mergewith chorea-like movements to produce choreoathetosis.Familial paroxysmal choreoathetosisis autosomal-dominant disorder that may occur in children who areotherwise normal. Dystonia
Slow, writhing,irregular, twisting movements of limbs, trunk, or face that produce abnormalpostures. Movements may begin with initiation of reaching or walking.Increases with anxiety and stress andtend to disappear during sleep. Dopa-Responsive Dystonia
May be transmittedas autosomal-dominant or -recessive trait. Dominant form is causedby mutations in GTP cyclohydrolase 1 gene on chromosome 14q22.1-q22.2,while recessive form is caused by mutations in tyrosine hydroxylasegene on chromosome 11p15.5.Onset is usually in childhood withgait disturbance produced by dystonic leg movements, which may worsenas day progresses. Posturing movements of arms also may occur. Eventually,parkinsonian features (e.g., rigidity and bradykinesia) develop.Diagnosis generally confirmed by clinicalresponse to small doses of levodopa. Molecular genetic analysisis definitive. Idiopathic Torsion Dystonia (Dystonia Musculorum Deformans)
There isevidence that mutations in DYP 1 gene on chromosome 9q34 can causethis autosomal-dominant disorder.Onset of this slowly progressive diseaseis usually 5–15 yrs of age.Posturing of trunk and neck interfereswith sitting, standing, and walking. Involvement of face and tonguemay impair speech and swallowing. Intellect is preserved and seizuresdo not occur.Molecular genetic analysis is confirmatory. Hypoxic-Ischemic Encephalopathy
1 of theprincipal causes of chronic dystonia in pediatric population.Some common causes of hypoxic-ischemicencephalopathy are perinatal asphyxia, head trauma, near drowning,and carbon monoxide poisoning. Wilson Disease
Autosomal-recessivedisorder of copper transport that is characterized by liver involvementand degenerative changes in brain, primarily basal ganglia.Neurologic findings (e.g., dystoniaand speech disturbance) usually occur after 10 yrs of age, whereashepatic disease usually occurs before this age.See Chap.36, Jaundice. Hallervorden-Spatz Disease
Mutationsin pantothenate kinase gene located on chromosome 20p12.3-p13 have beenfound to cause this autosomal-recessive disorder.Onset is usually 2–10 yrsof age with generalized dystonia followed by spasticity, speech difficulty,retinal degeneration, and intellectual deterioration.MRI shows lesions involving the globuspallidus. Molecular genetic analysis is confirmatory. Drugs
Acute dystonia may be due to phenothiazines,haloperidol, and metoclopramide.
Myoclonus
Fast, repetitivecontractions of muscle or muscle group in any part of body.Muscular jerks may be epileptic ornonepileptic. Epileptic form is discussed in Chap. 59, Seizures.Occurrence of myoclonus in restrictedgroup of muscles (arm or leg) is called myoclonus simplex, whereasgeneralized contraction of muscle groups is termed polymyoclonus. Benign Neonatal Sleep Myoclonus
Consistsof rhythmic jerks of extremities, which may last a few seconds orcontinue for a few hours, and cease on awakening. They usually disappearin a few months.Child's development and electroencephalogramare normal. Essential Myoclonus
Autosomal-dominantdisorder of unknown cause that consists of brief, shocklike musclecontractions with onset usually after several years of age.Proximal limb muscles are primarilyaffected.Course is benign, with no seizuresor other neurologic impairment. Myoclonic Encephalopathy
Myoclonic jerks of head and trunk; bizarre,chaotic, conjugate eye movements; and truncal ataxia characterizethis disorder, which can be associated with neuroblastoma or postviralencephalitis (see Chap. 4, Ataxia).
Other
Polymyoclonus may be associated with severaldisorders, including phenylketonuria, maple syrup urine disease,Tay-Sachs disease, Hallervorden-Spatz disease, tuberous sclerosis,hypoxic-ischemic encephalopathy, lead intoxication, and encephalitis.
Tremor
Regular, rhythmic, alternating contractionsof muscle group and its antagonists that may occur at rest or withmovement. Hands and fingers are usually affected.
Physiologic Tremor
All humanshave tremor of hands that may be detected by special electrophysiologic techniques.Enhanced physiologic tremor is actionthat is visible to naked eye. May be caused by fear, anxiety, fatigue,hyperthyroidism, caffeine, cigarette smoking, and drugs (beta adrenergicbronchodilators, lithium, valproate, selective serotonin reuptakeinhibitors). Pathologic Tremor
Includesresting, action, and intention tremors.Resting tremor occurs when extremityis relaxed, while action tremor is seen with sustained extensionof the arm, or while performing motor tasks (e.g., writing). Bothforms of tremor may occur with Wilson disease and Parkinson disease,though the latter is rare in pediatric population.Most common form of action tremor isessential tremor, which involves hands but can also affect head,trunk, and legs. This autosomal-dominant disorder may begin in childhoodand slowly progress.Intention tremor occurs when exactor precise movement is attempted (e.g., finger-to-nose maneuver).Often accompanied by other signs of cerebellar disease (e.g., ataxia,nystagmus, and slurred speech). Spasmus Nutans
Disorderof unknown cause that usually occurs after 6 mos of age and resolvesby 3–4 yrs of age.Consists of triad of nystagmus, headnodding, and torticollis, but all do not have to occur together.Usually disappears within a few monthsor 1 or 2 yrs. Ballismus
Flailingmovements of arms and legs.No meaningful distinction between choreaand ballismus exists except one of degree.In childhood, ballismus is most commonlyseen as extreme manifestation of chorea, usually Sydenham chorea. Habit Spasms
Occur mostoften in older children and adolescents and consist of sniffing,throat clearing, grimacing, head jerking, and eye blinking.Tension or stress may precipitate theiroccurrence.With passage of time, individual becomesunaware of them and cannot control them. Diagnostic Approach
Movementdisorders generally must be identified by clinical features, incontext of history, family history, and careful physical exam. Oncespecific type of movement is recognized, specific cause should beinvestigated.In absence of any associated neurologicdeficits, neuroimaging and electroencephalography are not routinelyuseful for childhood-onset movement disorders. >
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Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006
Ocular deviation:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
If the patient isn't in distress, find out how long he has had the ocular deviation. Is it accompanied by double vision, eye pain, or headache? Also, ask if he has noticed associated motor or sensory changes or fever.
Check for a history of hypertension, diabetes, allergies, and thyroid, neurologic, or muscular disorders. Then obtain a thorough ocular history. Has the patient ever had extraocular muscle imbalance, eye or head trauma, or eye surgery?
During the physical examination, observe the patient for partial or complete ptosis. Does he spontaneously tilt his head or turn his face to compensate for ocular deviation? Check for eye redness or periorbital edema. Assess the patient's visual acuity, and then evaluate extraocular muscle function by testing the six cardinal fields of gaze.
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Source: Nursing: Interpreting Signs and Symptoms, 2007
Nystagmus:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
Begin by asking the patient how long he has had nystagmus. Does it occur intermittently? Does it affect his vision? Ask about recent infection, especially of the ear or respiratory tract, and about head trauma and cancer. Does the patient or anyone in his family have a history of stroke? Then explore associated signs and symptoms. Ask about vertigo, dizziness, tinnitus, nausea or vomiting, numbness, weakness, bladder dysfunction, and fever.
Begin the physical examination by assessing the patient's level of consciousness (LOC) and vital signs. Be alert for signs of increased intracranial pressure (ICP), such as pupillary changes, drowsiness, elevated systolic pressure, and an altered respiratory pattern. Next, assess nystagmus fully by testing extraocular muscle function: Ask the patient to focus straight ahead and then to follow your finger up, down, and in an “X” across his face. Note when nystagmus occurs as well as its velocity and direction. Finally, test reflexes, motor and sensory function, and the cranial nerves.
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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.)
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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.
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Source: Differential Diagnosis in Primary Care, 2007
NYSTAGMUS:
Approach to the Diagnosis
(Differential Diagnosis in Primary Care)
The workup here is similar to that of vertigo. Nystagmus without other
signs of central nervous system (CNS) disease is usually ocular or
peripheral in the middle or inner ear. Vertigo is almost invariably present
in nystagmus of aural origin. Nystagmus with long tract signs such as
hemiplegia or hemianesthesia is invariably brainstem in origin. Purely
cerebellar nystagmus is not easily fatigued and is associated with
dyskinesia and dyssynergia of the extremities as well as ataxia. There are
no long tract or cranial nerve signs. Nystagmus with vertigo, nausea,
vomiting, tinnitus, and deafness suggests Ménière disease.
Confirmation of the diagnosis is made by audiograms, caloric tests, skull
x-rays (with special views of the mastoids and petrous bones), angiography,
CT scans, and myelography. MRI scans are useful, especially in diagnosing
brainstem lesions and multiple sclerosis. They also provide a better view of
the internal auditory canal. A spinal tap will help in the diagnosis of
multiple sclerosis and neurolues as well as acoustic neuromas.
