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IV. DIAGNOSIS
A.
Patients with memory complaints, whether self-reported or reported by an informant,
should have a thorough history and physical and laboratory and imaging studies to evaluate
for reversible or treatable causes. Equivocal evaluations can be further assessed with formal
neuropsychiatric testing. More profound memory loss indicative of dementia or delirium is
addressed elsewhere in this book.
B. Some mild memory loss associated with aging is considered normal. The phenomenon has
many names, including age-associated cognitive decline and age-associated memory impair-
ment. It also lacks definition, but can be characterized by isolated memory deficits without
impact on daily functioning (3).
C. MCI is a separate, if still poorly defined, clinical entity. It is characterized by cognitive and
memory decline that is more severe than seen with age-associated cognitive decline but less
severe than dementia, with overall preserved independent function. Patients with MCI are
at higher risk for progression to dementia, at a rate of approximately 10% per year (3).
For patients with MCI, the physician should establish a plan for periodic reevaluation and
discuss the risk for progression to dementia, the role of emerging testing, and potential
strategies to prevent further decline.
REFERENCES
1. Budson AE, Price BH. Memory dysfunction. N Engl J Med 2005;352:692–699.
2. Blazer DG, Hays JC, Fillenbaum GG, Gold DT. Memory complaint as a predictor of cognitive decline:
a comparison of African-American and white elders. J Aging Health 1997;9:171–184.
3. Peterson RC. Mild cognitive impairment. N Engl J Med 2011;364:2227–2234.
4. Nasreddine ZS, Phillips NA, Bédirian V, et al. The Montreal Cognitive Assessment, MoCA: a brief
screening tool for mild cognitive impairment. J Am Geriatr Soc 2005;53:695–699.
5. Saxton J, Morrow L, Eschman A, et al. Computer assessment of mild cognitive impairment. Postgrad
Med 2009;121(2):177–185.
6. American Geriatrics Society. A guide to dementia diagnosis and treatment. Accessed at American
Geriatrics Society (http://dementia.americangeriatrics.org/) on August 22, 2010.
I. BACKGROUND. Paresthesia is a skin sensation, such as burning, prickling, itching, or tingling,
with no apparent physical cause. Dysesthesia is defined as either the impairment of sensation,
especially that of touch, or a condition in which an unpleasant sensation is produced by ordi-
nary stimuli.
II. PATHOPHYSIOLOGY
A. Etiology.
Paresthesias and dysesthesias are due to dysfunction of the nervous system that
can occur anywhere along the pathway of sensation between the cortex and the sensory
receptor. Dysfunction can be related to either lack of function (e.g., numbness due to carpal
tunnel syndrome) or excess function (e.g., pain from postherpetic neuralgia) (1).
B. Epidemiology. The most common source of paresthesia is peripheral neuropathy. The
most common causes in the United States are diabetes and alcoholism. Other common
causes include hypothyroidism, vitamin B12 deficiency, postherpetic neuralgia, and nerve
entrapments such as carpal tunnel syndrome (2).
4.6
Paresthesia
andDysesthesia
Toby D. Free
58
III. EVALUATION
A. History.
The history should include time of onset, duration, and location. Past medi-
cal history should be obtained for illnesses that can cause paresthesias or dysesthesias
(e.g., diabetes, human immunodeficiency virus [HIV], hypothyroidism, and rheumatoid
arthritis). Social history may reveal substance abuse (e.g., alcoholism, or intravenous drug
use, which would raise the suspicion of HIV) or occupational exposures (e.g., exposure
to lead or mercury, or mechanical repetition). Family history may disclose a hereditary
neuropathy (2).
B. Physical Examination. The patient should have a general physical examination and
complete neurologic examination, paying particular attention to the sensory portion of the
examination. Complicating the physical examination is the fact that the examiner must rely
on the patient’s subjective response to the examination. The examination should test for
pain (using a pin or needle), light touch (using a cotton-tipped swab or wisp of cotton),
vibration (using a tuning fork), temperature, and position sense (performed with the eyes
closed). The examination should delineate the distribution of abnormal sensation as this
may be enough to establish a diagnosis. The patient may be asked to map the affected area.
Other aspects of the neurologic examination should include testing of muscle strength and
reflexes. Muscle wasting may be noted (1, 2). Flexion of the patient’s neck (Lhermitte’s sign)
causing electric shock-like pain in the back or extremities may be present in patients with
multiple sclerosis, cervical spinal cord disease, or vitamin B12 deficiency. Tinel sign, which
is a reproduction of the paresthesia with percussion on or just proximal to the carpal tunnel,
and Phalen’s maneuver, involving full flexion of the wrist for greater than 60 seconds, can
aid in the diagnosis of carpal tunnel syndrome.
C. Testing. If clinical examination does not reveal a cause for the patient’s symptoms, then
initial laboratory workup should include complete blood count, renal function, fasting
serum glucose, vitamin B12 level, urinalysis, thyroid-stimulating hormone, and erythrocyte
sedimentation rate. Further laboratory testing might include folate, the Venereal Disease
Research Laboratory or rapid plasma reagin test, antinuclear antibody, serum immunoelec-
trophoresis, purified protein derivative, and blood levels of heavy metals (e.g., lead) (2, 3).
Electromyography and nerve conduction testing are often helpful in delineating either the
anatomic source of the neuropathy (e.g., carpal tunnel syndrome) or the systemic cause
(e.g., paraneoplastic syndromes) (3). Radiologic studies such as computed tomography or
magnetic resonance imaging may be indicated for specific causes, such as a suspected lumbar
disc herniation.
D. Genetics. There are several hereditary causes of neuropathies. These include
Charcot-Marie-Tooth disease, Denny-Brown’s syndrome, and familial amyloidotic
polyneuropathy (2).
IV. DIAGNOSIS
A. Differential Diagnosis.
The differential diagnosis of paresthesias and dysesthesias is
broad (see Table 4.6.1).
B. Clinical Manifestations. The cause of paresthesias and dysesthesias can frequently be
determined clinically. Distal sensory loss is the most common and is frequently due to
metabolic or toxic causes such as diabetes, alcoholism, vitamin B12 deficiency, or heavy
metal exposure. Some causes, such as diabetes or alcoholism, can have various clinical pat-
terns. Diabetes most commonly causes a symmetric distal sensory loss, but can also cause
multifocal neuropathies, autonomic neuropathies, or even symmetrical proximal motor
neuropathies (3).
Most nerve entrapments are distinguished by an examination consistent with their
nerve distribution (e.g., loss of sensation of the fifth finger and adjacent half of the fourth
finger in ulnar neuropathies, which are usually caused by compression at the cubital tunnel
in the elbow).
Dermatomal distributions would point to either a radiculopathy or postherpetic neural-
gia. Neuropathies involving the cranial nerves are rare, but may be caused by Guillain-Barré
syndrome, diabetes, HIV, or Lyme disease (3).
59
REFERENCES
1. Asbury AK. Numbness, tingling, and sensory loss. In: Braunwald E, Hauser SL, et al. eds. Harrison’s
principles of internal medicine, 15th ed. New York, NY: McGraw Hill, 2001:128–132.
2. McKnight JT, Adcock BB. Paresthesias: a practical diagnostic approach. Am Fam Physician
1997;56(9):2253–2260.
3. Poncelet AN. An algorithm for the evaluation of peripheral neuropathy. Am Fam Physician
1998;57(4):755–760.
TABLE 4.6.1 Causes of Paresthesia and Dysesthesia
Endocrine Diabetes, hypothyroidism, acromegaly
Nutritional Vitamin B12/folate deficiencies
Toxic Chemotherapy, heavy metals, chronic overdose of pyridoxine,
alcohol, medications such as nitrofurantoin
Connective tissue disorders Polyarteritis nodosa, rheumatoid arthritis, lupus
Entrapment syndromes Carpal and cubital tunnel syndromes, thoracic outlet syndrome,
lateral femoral cutaneous syndrome, tarsal tunnel syndrome,
spinal disc herniations
Trauma
Central nervous system Cerebrovascular accident, tumors
Infectious Syphilis, Lyme disease, postherpetic neuralgia, human
immunodeficiency virus, leprosy
Malignancy Paraneoplastic syndromes from small cell carcinoma of the lung
and cancers of the breast, ovary, and stomach
Miscellaneous Guillain-Barré syndrome, multiple sclerosis, critical illness
polyneuropathy (2, 3)
4.7
I. BACKGROUND. A seizure is characterized as temporary neurologic signs or symptoms as a
result of abnormal, transient, synchronous neuronal activity in the cerebral cortex. Epilepsy is
a group of disorders characterized by recurrent seizures that are unprovoked and not caused by
an easily reversible condition.
II. PATHOPHYSIOLOGY
A. Etiology.
Causes of seizures include primary central nervous system (CNS) dysfunctions
as well as metabolic derangement or systemic disease. Distinguishing between the two is vital
since therapy must be directed at correcting the underlying condition as well as at seizure
control. However, over two-thirds of new onset seizures are idiopathic (1).
1. Primary CNS dysfunctions. Head trauma, stroke or vascular malformations, mass
lesions (tumors), intracranial hemorrhage, CNS infections, encephalitis, meningitis,
febrile seizures, primary epilepsy disorders, and dementia.
Seizures
Denae M. Torpey
60
2. Systemic disease or metabolic. Hypoglycemia, hyponatremia, hypocalcemia, hypo-
magnesemia, uremia, hepatic encephalopathy, eclampsia, drug toxicity or withdrawal,
porphyria, hyperthermia, and genetic disorders.
The age of the patient may help in establishing a cause of the seizure. In the
elderly, they are more likely to result from dementia, cerebrovascular disease, or tumors.
Children and infants are more likely to experience seizures caused by trauma and infec-
tion or idiopathic seizures.
B. Epidemiology. The incidence of epilepsy is bimodal with a peak high in childhood,
decreases in midlife, then peaks again in the elderly. The overall lifetime risk of having a
seizure is 10%; however, only 3% will go on to develop epilepsy (2). The annual incidence
of epilepsy is 50 per 100,000 population, with a prevalence of about 5–10 per 1,000 (2).
III. EVALUATION
A. History.
Care should be taken to elicit risk factors for seizures pertinent to the patient’s
age (including a family history of seizures and developmental history), possible seizure pre-
cipitants (medication, alcohol or drugs of abuse, sleep deprivation, intense exercise, flashing
lights, trauma, and fever), and the clinical features, setting, chronology, and duration of
the seizure. In many cases, information about the seizure must be obtained from a witness
because of the patient’s age or level of consciousness. Given that 20% of childhood seizures
occur only at night, it is important to inquire about early morning behavior in children,
including disorientation and transient neurologic dysfunction (1). The following questions
are especially important in determining the etiology of the seizure:
1. Was there an aura prior to the seizure?
2. Was there a fall or injury prior or during the seizure?
3. Was there a loss or impairment of consciousness?
4. Was there staring, eye blinking, vocalizations, or automatisms (repetitive purposeless
movements such as lip smacking, chewing, or facial grimacing)?
5. Was there a loss of bowel or bladder continence?
6. Was there rhythmic muscular jerking and/or rigidity?
7. Was there a postictal period?
The two features most indicative of a seizure include the presence of an aura associated with
seizures of focal onset and postictal confusional state following a generalized tonic–clonic
seizure. Having urinary incontinence or a few tonic or jerking movements is not sufficient
to discern seizures from other causes of transient loss of consciousness (1).
B. Physical Examination. The examination is usually normal in patients with epilepsy,
but occasionally some signs of trauma, an underlying systemic or neurologic disorder, or
stigmata of chronic alcoholism may be evident. Additionally, it is important to look for
cutaneous manifestations of some genetic disorders (facial nevus flammeus of Sturge-Weber
syndrome, adenoma sebaceum of tuberous sclerosis, or café au lait macules and cutaneous
neurofibromas of neurofibromatosis).
C. Testing. Laboratory studies in adults and children should be ordered on the basis of
suggestive historical or clinical findings. In children with a first simple febrile seizure
(<10 minutes, isolated, and generalized), laboratory testing should be directed toward iden-
tifying the cause of the fever. Studies that may be appropriate for evaluation of a first seizure
include a complete blood count, glucose, electrolytes, calcium, magnesium, renal, liver and
thyroid function tests, urinalysis, pregnancy screen, and drug and heavy metal toxicology
screening (if there is a question of substance abuse or possibility of exposure).
1. A lumbar puncture should be performed if there is a concern about meningitis or
encephalitis or if the patient is immunocompromised. The American Academy of
Pediatrics suggests that a lumbar puncture be “strongly considered” when a febrile sei-
zure occurs in an infant younger than 12 months of age or all children on prior antibiotic
treatment, “considered” in infants 12–18 months of age, and “recommended” if menin-
geal signs are present in infants older than 18 months of age (3). If increased intracranial
pressure is suspected, the lumbar puncture should be preceded by computed tomography
(CT) scan or magnetic resonance imaging (MRI) of the head.
61
2. An electroencephalogram (EEG) is essential in the evaluation of epileptic seizures. An
abnormal EEG may confirm the diagnosis, but a normal or nonspecifically abnormal
EEG does not exclude the diagnosis of a seizure. Sleep deprivation and provocative mea-
sures such as hyperventilation and photic stimulation may increase the yield of an EEG.
3. Neuroimaging is often necessary to rule out a structural lesion of the brain. Any patient
with neurologic findings on examination, with mental deficiency, or older than 25 years
of age when presenting with new-onset seizure warrants neuroimaging. A brain MRI is
more sensitive and is preferred over a CT scan. An EEG and neuroimaging need not be
performed in the evaluation of an otherwise neurologically healthy child with a simple
febrile seizure.
IV. DIAGNOSIS
A. Differential Diagnosis.
A variety of events, either physiologic or psychogenic, can often
be mistaken as seizures. These include syncope, complex migraines, breath-holding spells,
transient ischemic attacks, sleep disorders (parasomnias and narcolepsy), transient global
amnesia, movement disorders, and psychiatric disorders (panic attacks, anxiety with hyper-
ventilation, dissociative states, and psychogenic seizures).
B. Clinical Manifestations. The clinical expression of a seizure depends on the location and
extent of propagation of the discharging neurons.
1. Partial seizures. A partial (focal) seizure begins in a localized area of the cortex. The
signs and symptoms of a partial seizure depend on the cortical region involved and may
range from a subjective perception (aura) to motor, autonomic (flushing and hypersaliva-
tion), somatosensory, or psychic phenomena.
a. Simple partial seizures. Consciousness is preserved with simple partial seizures.
However, they may evolve into a complex partial seizure, and both may evolve into a
generalized seizure.
b. Complex partial seizures. A complex partial seizure implies spread of the seizure
discharge to allow impairment of consciousness. Usually, they arise in the temporal
lobe or medial frontal lobe. Patients with complex partial seizures usually exhibit
automatisms or some other complex coordinated motor activity that is not directed or
purposeful.
2. Generalized seizures. A generalized seizure involves both the cerebral hemispheres at the
onset. Generalized seizures begin with an abrupt loss of consciousness (except myoclonic
seizures). They are subdivided based on the presence or absence and character of ictal
motor manifestations.
a. Generalized tonic–clonic seizures (Grand mal). Consciousness is lost and usually
is not preceded by an aura. Tonic contractions of limb muscles occur first, producing
flexion and extension, followed by clonic phase characterized by rhythmic muscular
jerking.
b. Absence seizures (Petit mal). Absence seizures are characterized as brief (5–10 sec-
onds) loss of consciousness without loss of postural tone. These may be exhibited with
staring, blinking, or slight head turn and are usually inducible by hyperventilation.
c. Other. This includes tonic (not followed by clonic phase), clonic (not preceded by
tonic phase), atonic (sudden collapse due to loss of postural tone), and myoclonic
(sudden, brief muscular contractions affecting any group of muscles).
REFERENCES
1. Simon RP, Greenberg DA, Aminoff MJ, eds. Seizures & syncope. In: Clinical neurology, 7th ed. New
York, NY: McGraw-Hill, 2009:270–291.
2. Middleton DB. Seizures. In: South-Paul JE, Matheny SC, Lewis EL, eds. Current diagnosis & treatment:
family medicine, 2nd ed. New York, NY: McGraw-Hill, 2008:88–102.
3. American Academy of Pediatrics. Practice parameter: the neurodiagnostic evaluation of the child with
a first simple seizure. Pediatrics 1996;97(5):769–772; discussion 773–775.
62
4.8
I. BACKGROUND. Stroke is defined as an acute neurologic deficit that lasts more than 24 hours.
Events lasting <24 hours are referred to as transient ischemic attacks.
II. PATHOPHYSIOLOGY
A. Etiology.
Stroke is caused by occlusive vascular disease (thrombotic or embolic) leading to
ischemia 85% of the time and hemorrhagic vascular disease 15% of the time.
B. Epidemiology. Risk factors for stroke include uncontrolled hypertension, hyperlipidemia,
diabetes mellitus, tobacco smoking, cardiac disease, coagulopathies, obesity, and hormone
therapy. Stroke is the fourth most common cause of death (1) and the most common acute
neurologic event in the United States.
III. EVALUATION (2, 3)
A. History.
Historical factors of note include
1. Time of abrupt onset of symptoms, last time at previous baseline
2. Unilateral change in motor control, vision, gait, strength, or sensation
3. Other neurologic disorders such as migraine, systemic lupus, vasculitis, seizure disorder,
previous brain hemorrhage, or recent head trauma
4. Sudden onset of unusual headache
5. Presence of one or more risk factors
B. Physical Examination. Physical findings include
1. Alteration of mental status and/or consciousness
2. Slurred or inappropriate speech, aphasia
3. Hemiparalysis, hemiparesis
4. Altered sensation
5. Visual field defect, diplopia, nystagmus
6. Hypertension
7. Cardiac dysrhythmia
8. Ataxia and other gait abnormalities
9. Vascular tenderness to palpation or bruit, temporal and carotid arteries
10. Document findings in standard fashion with the National Institutes of Health (NIH)
Stroke Scale initially and serially during evolution of stroke
C. Testing. Studies and laboratory tests include
1. Computed tomography (CT) scan of the head to identify hemorrhage. CT perfusion
and angiography as well as magnetic resonance imaging diffusion weight images are
promising for the detection of smaller strokes earlier.
2. Complete blood count, with platelet count, basic metabolic panel, cardiac enzymes,
prothrombin time, international normalization ration (INR), and partial thromboplas-
tin time for underlying diseases and baseline if thrombolytic or anticoagulant therapy
is anticipated.
3. Special studies such as hepatic function panel, toxicology screen, blood alcohol level,
antiphospholipid antibodies, protein S and C, antithrombin III, and others if indicated
by history or physical examination.
4. Electrocardiogram to help diagnose dysrhythmias or preceding myocardial infarction.
5. Echocardiogram to visualize structural defects such as patent foramen ovale or mural
thrombi. Transesophageal echocardiography may possibly be appropriate if concern for
patent foramen ovale or valve vegetations.
6. Carotid/intracranial Doppler studies to find occlusive vascular disease or source of
artery to artery emboli.
Stroke
Kathryn K. Garner
63
IV. DIAGNOSIS
A. Differential Diagnosis.
The differential diagnosis of stroke includes aberrant migraine,
seizure disorder, metabolic disorders, psychogenic condition (hysterical conversion reaction
and hyperventilation), and tumor with hemorrhage.
B. Clinical Approach. With the availability of thrombolytic therapy, a rapid diagnosis upon
presentation has become critical. A history and physical examination should be completed
as quickly as is practical, with special attention to the neurologic examination. Quantitative
assessment of strength and function on the affected side should be documented for com-
parison with subsequent examinations (NIH Stroke Scale is preferred). Laboratory studies
are ordered to assess for stroke mimickers and a noncontrast head CT scan is obtained to
rule out hemorrhage, provided the patient is clinically stable. Appropriate interventions to
control blood pressure, seizures, hyperglycemia, and cardiac dysrhythmias should proceed
concomitantly with the evaluation. Acetyl salicylic acid (ASA) and dipyridamole therapy
are superior to ASA alone for secondary prevention but equivocal to clopidogrel alone. Full
anticoagulation is appropriate only for cardiac emboli causing a stroke. Statin administration
and lipid measurement should be considered for all stroke patients. Optimal LDL levels are
<100 mg/dl or <70 mg/dl if the patient has multiple stroke risk factors including diabetes
mellitus, history of previous stroke, hypertension, hypercoagulability, or tobacco smoking.
REFERENCES
1. CDC FASTATS: www.cdc.gov/nchs/fastats/stroke.htm, 2009.
2. American Heart Association Stroke Outcome Classification. Executive summary. Circulation
1998:97:2474–2478.
3. Harrison’s Online: Part 15. Neurological disorders. Section 2. Diseases of the Central Nervous system.
Chapter 349. Cerebrovascular diseases.
4. Update to the AHA/ASA recommendations for the prevention of stroke in patients with stroke and
transient ischemic attack. Stroke 2008;39:1647–1652.
4.9
I. BACKGROUND. Tremor is one of the most common movement disorders and is characterized
by an oscillatory and usually rhythmic movement. The first step in the evaluation of any move-
ment disorder is to recognize the movement phenomenology, to be able to generate a list of
different etiologies (1). Jumping straight to the differential leads to misdiagnoses. Thirty to fifty
percent of cases with action tremor are misdiagnosed and do not have essential tremor (2).
II. PATHOPHYSIOLOGY. Assessment of patients with tremor still depends upon the history and
physical examination. This chapter will review only a few of the many types of tremors.
A. Resting Tremor. Resting tremor is one in which the amplitude decreases or disappears
as soon as the muscles involved with the tremor get voluntarily contracted. Therefore, this
is predominantly present during rest. This tremor might also appear after the patient has
been holding arms up in front for a while (usually in the wrist or fingers), the so-called
re-emergent tremor. Re-emergent tremor will usually disappear by contracting the involved
muscles, helping differentiate this tremor from other postural tremors.
B. Action/Kinetic/Postural Tremors. These tremors are those that appear or in which
amplitude increases as soon as the muscles involved get voluntarily contracted.
C. Intention Tremor. Intention tremor is a posture-kinetic tremor in which amplitude
increases with target-directed movements (e.g., while comparing the tremor during finger-
to-nose-finger maneuver vs. just holding the arms straight). Intention tremor is regarded as
a sign of disturbed function of the cerebellum and its pathways.
Tremors
Diego R. Torres-Russotto
64
D. Posture-specific or task-specific tremor. This is commonly due to dystonia. Examples
include the tremor present during flexion of a limb but not during extension; or the inter-
mittent, jerky, irregular, arrhythmic head tremor of patients with cervical dystonia. Particular
features that differentiate dystonic tremor from other tremors include the presence of
abnormal posturing, muscle hypertrophy, null point (a place in the range of motion of the
joint involved where tremor amplitude significantly decreases), and sensory tricks (aka geste
antagoniste, a sensory stimulus like touching the area can improve the dystonic tremor).
This category includes the task-specific tremors (e.g., those present only during writing or
while playing an instrument) (2).
III. EVALUATION AND DIFFERENTIAL DIAGNOSIS
A. Initial Workup
1. Diagnoses not to miss: medication induced, pregnancy, Wilson disease, thyroid abnor-
malities, liver, kidney, or electrolyte/glucose abnormalities, vitamin B12, D, and E
deficiencies. Psychogenic tremors are rare and always a diagnosis of exclusion.
2. Basic initial workup to consider: pregnancy test, ceruloplasmin, thyroid function, CMP,
vitamin B12 level, MMA, homocysteine, folate, 25-OH vitamin D3, and vitamin E.
Environmental exposures and use of over-the-counter, herbal, or illegal drugs should be
ascertained. Consider heavy metals and urine drug screen testing.
3. Structural imaging (usually with magnetic resonance imaging of the brain) could be
considered in cases suspicious for multiple sclerosis (MS), strokes, ataxia, primary and
metastatic tumors; in those with rapid or unusual progression; or with associated abnor-
mal neurologic examination.
4. Functional imaging (like positron emission tomography (PET) or single photon emis-
sion computed tomography (SPECT)) can help differentiate between Parkinson disease
and essential tremor. Referral to a movement disorders center might be the most cost-
effective measure.
B. Resting Tremor. Differential includes parkinsonism of any cause (idiopathic, secondary
to dopamine blockers [anti-psychotics, anti-emetics], lithium, amiodarone, and strokes),
Wilson disease, dystonia, midbrain/Holmes tremor (trauma, strokes, and MS), etc.
Ascertainment of presence of rigidity and bradykinesia is very important as it would com-
plete the triad for parkinsonism.
C. Action/Kinetic/Postural Tremor. The two most common etiologies are medication
induced and essential tremor.
1. Medication-induced action/kinetic tremor: almost all drugs that affect the CNS have
the potential to cause or worsen tremors. Most common drugs include anti-depressants,
anti-epileptics, benzodiazepines, opioids, anesthetics, and dopamine blockers (both anti-
psychotics and anti-emetics).
2. Essential or primary tremor: tends to be a familial action tremor of hands (can also have
tremor in face, neck, voice, and lower limbs), slowly progressive and responsive to alco-
hol (in some). Currently, the definition of essential tremor is under debate, as it is felt to
encompass multiple diseases under the same umbrella term. The prevalence is about 2%
to 6%. Essential tremor is underdiagnosed, misdiagnosed, and undertreated, leading to
inadequate patient satisfaction. Treatment options include propranolol, primidone, and
topiramate. After treatment failure with two drugs, referral to a deep brain stimulation
surgery center should be offered to the patient.
D. Intention Tremor. Etiologies for ataxia should be entertained, although medications and
essential tremor remain important causes. Fragile X-associated tremor and ataxia syndrome
is a high-prevalence condition, a common cause for tremor and ataxia, and can also display
parkinsonism (please refer to Chapter 4.1, Ataxia).
REFERENCES
1. Fahn S. Involuntary movements. In: Lewis PR, Timothy AP. Merritt’s neurology, 12th ed. Philadelphia,
PA: Lippincott Williams & Wilkins, 2010:50–53.
2. Louis ED. Essential tremor. In: Lewis PR, Timothy AP. Merritt’s neurology, 12th ed. Philadelphia, PA:
Lippincott Williams & Wilkins, 2010:825–826.
3. Torres-Russotto D, Perlmutter J. Task-specific dystonias: a review. Ann N Y Acad Sci 2008;1142:179–199.
65
I. BACKGROUND. Blurred vision is the most common visual complaint (1). “Blurred vision is
the loss of sharpness of vision and the inability to see small details” (2).
II. PATHOPHYSIOLOGY
A. Etiology.
The causes of blurred vision range from mild to potentially catastrophic. Most
causes involve the orbit (anterior and posterior segments), although a number of extraocular
causes must be considered (medications, viral infections such as herpes simplex virus, sys-
temic causes such as sarcoidosis, and cerebrovascular events) (see Table 5.1.1).
B. Epidemiology. In younger patients, blurred vision is often acquired through trauma,
occupational exposures, and infections. Certain age-related eye disorders such as macular
degeneration, cataracts, and temporal arteritis may cause blurred vision, potentially contrib-
uting to the risk of falling (3).
III. EVALUATION
A. History.
Careful attention should be paid to the rapidity of the onset, associated eye pain,
and whether the blurring is unilateral or bilateral. Blurred vision that worsens at night
may indicate a cataract (4). Intermittently blurred vision may be caused by excess tearing,
allergies, uncontrolled diabetes, acute glaucoma, transient ischemic attacks, cerebrovascular
insufficiency, and multiple sclerosis (5). Other important factors include a family history
of eye disorders (macular degeneration and glaucoma), any work exposures (chemicals and
prolonged computer use), medications (such as corticosteroids and antibiotics), and past
medical history (diabetes and hypertension) (6).
B. Physical Examination. The physical examination should include the following elements:
1. Conjunctival erythema and discharge should be noted. The corneal light reflex should
be symmetric and sharp; fluorescein staining should be performed to evaluate for the
evidence of trauma, ulcers, or herpetic lesions. The anterior chamber (space between the
cornea and the iris) should be evaluated with a penlight for blood (hyphema) and pus
(hypopyon).
2. Careful documentation of visual acuity (corrected and uncorrected) is important to
monitor the progression of the disease. If the patient is unable to discern letters on the
Snellen eye chart, the examiner should determine the extent of acuity impairment by
testing the distance from the patient’s eyes at which the patient can first see the exam-
iner’s fingers.
3. Visual field testing may indicate an underlying stroke (homonymous field defect) or
retinal detachment (quadrant or hemispheric loss of vision).
4. Ocular muscle involvement may be detected by testing the cardinal positions of the orbit
through range of motion.
Blurred Vision
Norman Benjamin Fredrick
5.1
Eye Problems
Shou Ling Leong
CHAPTER 5
66
5. In up to 20% of the cases, pupillary examination may be the only clue to serious underly-
ing pathology. Using a penlight, the abnormalities of pupillary size or shape (the pupils
should be symmetric; a unilateral miotic pupil may indicate iritis) or color (black is
normal) may be detected. Other findings may include cataracts, ruptured globes (with
eccentric pupils), and optic nerve disease (afferent papillary defect—paradoxical papillary
dilatation in response to light).
6. Direct ophthalmoscopy may reveal an abnormal red reflex that suggests a hemorrhage,
cataract, or retinal detachment. Papilledema warrants further evaluation.
C. Testing. An elevated sedimentation rate may suggest a diagnosis of temporal arteritis.
Computed tomography is appropriate to evaluate blurred vision following trauma or when
there is concern for mass effect (1).
D. Genetics. Macular degeneration, glaucoma, collagen vascular diseases, diabetes, and mul-
tiple sclerosis (optic neuritis) are potentially heritable conditions.
IV. DIAGNOSIS
A. Differential Diagnosis.
See Table 5.1.1.
B. Clinical Manifestations. A careful history and physical examination often limit the dif-
ferential diagnosis. Conditions that require immediate ophthalmologic referral include acute
glaucoma, retinal detachment, vitreous hemorrhage, retinal-vein occlusion, herpes simplex
infection, and orbital cellulitis.
TABLE 5.1.1 Causes of Blurred Vision
Painless Painful
Sudden onset Gradual onset Sudden onset Gradual onset
Unilateral Vitreous
hemorrhage,
macular
degeneration,
retinal detachment,
retinal-vein
occlusion,
amaurosis fugax,
cataracts
Cataracts,
“dry” macular
degeneration,
tumor
Corneal abrasion,
infection or
edema, uveitis,
traumatic
hyphema, acute
glaucoma,
temporal arteritis,
optic neuritis,
orbital cellulitis
Rare
Bilateral Poorly controlled
diabetes,
medications
(anticholinergics,
cholinergics,
corticosteroids),
migraines,
psychological
trauma
Cataracts,
macular
degeneration,
medications
(hydrochloroquine,
ethambutol, digoxin
toxicity), optic
chiasm mass,
fatigue, computer
vision syndrome (7),
refractive errors
(myopia, hyperopia,
astigmatism,
presbyopia);
incorrect eyewear
Trauma,
chemical spill,
welder’s exposure
Rare (sarcoidosis,
collagen vascular
disease)
Compiled from Shingleton BJ, O’Donoghue MW. Primary care: blurred vision. N Engl J Med
2000;343(8):556–562.
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