Blurred Vision

Blurred vision is the most common visual complaint vision is the loss of sharpness of vision and the inability to see small details

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 (medication, cerebrovascular event, sarcoidosis, herpes simplex).

Epidemiology
Certain age-related eye disorders such as macular degeneration, cataracts, and temporal arteritis may cause blurred vision. In younger patients, blurred vision is often acquired through trauma, occupational exposures, and infections.

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 (2). Intermittently blurred vision may be caused by excess tearing, allergies, uncontrolled diabetes, acute glaucoma, transient ischemic attacks, cerebrovascular insufficiency, and multiple sclerosis (3). Other important factors include a family history of eye disorders (macular degeneration, glaucoma), any work exposures (chemicals), medications (such as corticosteroids, antibiotics), and past medical history (diabetes, hypertension).

Physical examination
The physical examination should include the following elements:
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 examiner's fingers.
Visual field testing may indicate an underlying stroke (homonymous field defect) or retinal detachment (quadrant or hemispheric loss of vision).
Ocular muscle involvement may be detected by testing the cardinal positions of the orbit through range of motion.
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).
In up to 20% of the cases, pupillary examination may be the only clue to serious underlying 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).
Direct ophthalmoscopy may reveal an abnormal red reflex that suggests a hemorrhage, cataract, or retinal detachment. Papilledema warrants further evaluation.

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

Causes of Blurred Vision

Painless conditins

Sudden onset Unilateral- Vitreous hemorrhage, macular degeneration, retinal detachment, retinal-vein occlusion, amaurosis fugax, cataracts

Sudden onset Bilateral- Poorly controlled diabetes, medications (anticholinergics, cholinergics, corticosteroids), migraines, psychological trauma.

Gradual onset Unilateral -Cataracts,macular degeneration, tumor

Gradual onset Bilateral - Cataracts, macular degeneration, medications (hydrochloroquine, ethambutol, digoxin toxicity), optic chiasm mass, fatigue, refractive errors (myopia, hyperopia, astigmatism, presbyopia); incorrect eyewear

Painful conditions

Sudden onset Unilateral - Corneal abrasion, infection or edema, uveitis, traumatic hyphema, acute glaucoma, temporal arteritis, optic neuritis, orbital cellulitis

Sudden onset Bilateral- Trauma, chemical spill, welder's exposure

Gradual onset Unilateral- Rare

Gradual onset Bilateral - Rare (sarcoidosis, collagen vascular disease)

Genetics
Macular degeneration, glaucoma, collagen vascular diseases, diabetes, and multiple sclerosis (optic neuritis) are potentially heritable conditions.

Clinical manifestations
A careful history and physical examination often limit the differential diagnosis. Conditions that require immediate ophthalmologic referral include acute glaucoma, retinal detachment, vitreous hemorrhage, retinal-vein occlusion, herpes simplex infection, and orbital cellulitis.

Ataxia

Ataxia is the loss of the ability to coordinate muscular movement.

Etiology
Ataxia is caused by the dysfunction of the cerebellum and its afferent and efferent pathways. Ataxia has a broad list of causes, including:

Drugs, such as alcohol, barbiturates, lithium, or chemotherapeutic drugs
Toxins, such as mercury, solvents, lead, gasoline, or glue
Infections, such as coxsackievirus, human immunodeficiency virus (HIV), Legionella, Lyme disease, or varicella
Nutritional conditions, such as vitamin B1, B12, or E deficiency
Endocrine conditions, such as hypothyroidism
Vascular conditions, such as cerebellar infarction or hemorrhage
Hereditary conditions, such as Friedreich's ataxia, ataxia telangiectasia, or Machado-Joseph (SCA-3)
Neoplastic conditions, such as cerebellar glioma, metastatic tumors, or paraneoplastic syndromes
Congenital conditions, such as Chiari or Dandy-Walker malformations .

Epidemiology
Friedreich's ataxia is the most common cause of hereditary ataxia, constituting about half of hereditary ataxias. The incidence of Friedreich's ataxia is approximately 1 to 2 per 50,000 in the United States .

History
The history should include time of onset of the development of ataxia, whether it is symmetric or asymmetric, and whether it is focal or diffuse. A gradual onset with symmetric and bilateral symptoms suggests a biochemical, immune, metabolic, or toxic cause. Focal and asymmetric ataxias with other symptoms such as headaches and cranial nerve palsies suggest a cerebellar mass. The history should also include questioning regarding medications that can cause ataxia (e.g., lithium), exposure to toxins (e.g., mercury), and history of ethanol intake. The age of onset can be helpful in differentiating some of the hereditary ataxias. The patient should be questioned about recent or chronic infections because there are several that can cause ataxia (e.g., varicella, Lyme disease, or HIV).

Physical examination
The examination should include an evaluation of the type of ataxia. The patient's speech should be observed for difficulties such as dysarthria or scanning speech. The patient's gait should be observed. Eye movements should be examined for nystagmus or cranial nerve palsies. The patient's movements should be evaluated for tremor, loss of proprioception, weakness, loss of fine motor control, spasticity, rigidity, bradykinesia, and dystonia. In addition, the history and physical examination should search for other problems that can mimic ataxia from cerebellar causes, such as vertigo from vestibular disease, or difficulties in gait that are actually due to leg weakness .

Testing
Computed tomography or magnetic resonance imaging (MRI) of the brain (preferably MRI) to evaluate for causes such as a neoplasm, hemorrhage, or infarction. This should be done as soon as possible, because some causes may be surgical emergencies (e.g., mass effect leading to brain stem herniation).
Many other causes may be discovered by laboratory testing. Possible tests include thyroid-stimulating hormone, vitamin B1 and vitamin B12 levels, HIV,
P.54rapid plasma reagin, Lyme, and toxicology. Antibodies to Yo, Ri, and PCD may be present in paraneoplastic syndromes. In children, screening for inherited metabolic disorders may be warranted.
Lumbar puncture may be helpful for diagnosing causes such as multiple sclerosis, viral cerebellitis, and other infections. An electroencephalogram may reveal seizure-related ataxia .

Genetics
There is a long list of hereditary ataxias. The most common of these is Friedreich's ataxia. The hereditary ataxias are subdivided by the mode of inheritance. The most common are autosomal recessive (e.g., Friedreich's ataxia). Autosomal dominant ataxias are classified by a sequential numbering system (e.g., SCA-3 which is most common in the United States). There are also X-linked and mitochondrial forms of hereditary ataxias .

Differential diagnosis
Ataxia has diverse causes, ranging from toxins (e.g., mercury), infections (e.g., Lyme disease), and neoplasms to hereditary degenerative causes (e.g., Friedreich's ataxia)(1). Friedreich's ataxia usually starts before 25 years of age. It most commonly presents with lower extremity symptoms including gait disturbances, diminishing reflexes, and loss of proprioception. Other symptoms (which can occasionally be presenting symptoms) include dysarthria, scoliosis, nystagmus, and foot deformities. Approximately 25% of patients have hypertrophic cardiomyopathy and 10% have diabetes mellitus .

Clinical manifestations
The speed of the onset and the type of symptoms (symmetric vs. focal) can be very helpful in diagnosing the cause of ataxia.
A common example of acute symmetric ataxia is alcohol intoxication with its clumsiness, slurred speech, unbalanced gait, nystagmus, and inaccurate finger-to-nose testing. An acute and symmetrical onset would lead a clinician to suspect drugs, toxins, or infection. Examples of more chronic symmetrical ataxias include hypothyroidism, paraneoplastic disorders, inherited disorders, or vitamin B12 deficiency.
A rapid but focal onset would lead a clinician to suspect vascular or infectious causes. For example, the sudden onset of right-sided clumsy movements, the inward gaze of the right eye, and a headache would lead one to suspect a right-sided (cerebellar symptoms are ipsilateral) mass in the posterior fossa such as a hemorrhage or abscess.
A slower onset of focal or asymmetric findings would lead one to suspect neoplasms, multiple sclerosis, vascular lesions, or congenital malformations .

Anxiety Diagnosis

The experience of anxiety is ubiquitous in society. Anxiety can be part of an adaptive or protective response to threat (e.g., the fight-freeze-flight response) or a natural reaction to physical and emotional stress, but it can also be debilitating and a serious health concern. At its core, anxiety is a complex bio-psychosocial-spiritual experience that requires comprehensive assessment and treatment. Undiagnosed anxiety disorders contribute to inappropriate or overutilization of healthcare resources, but as many as 80% of the individuals with anxiety disorders can be significantly helped through appropriate treatment.
Etiology
Many factors contribute to both the development and experience of anxiety. These include genetic/neurologic predisposition, family history, acute and chronic stressors, resources for coping, comorbid conditions, and overall physical health. Extreme anxiety responses, known as anxiety disorders, are often comorbid with mood disorders or other chronic health conditions (e.g., coronary artery disease, cancer). These disorders usually include debilitating physical and emotional symptoms and may be due, at least in part, to primary medical problems such as hyperthyroidism or hypoxia. Consequently, anxious patients present to the emergency room or primary care setting with complaints that can be difficult to assess and diagnose.
Epidemiology
According to the National Institute of Mental Health (NIMH), 19 million Americans experience an anxiety disorder at any one time. Estimates of the prevalence of the various anxiety disorders vary from study to study but generally are as follows: generalized anxiety disorder (GAD)—4 million, 2.8% (women twice as likely as men); obsessive compulsive disorder—3.3 million, 2.3% (equally common among men and women); panic disorder—2.4 million, 1.7% (women twice as likely); posttraumatic stress disorder—5.2 million, 3.6% (women more likely than men); social anxiety disorder—5.3 million, 3.7% (equally common among men and women); and specific phobia—6.3 million, 4.4% (women twice as likely as men). The various anxiety disorders affect approximately 10% of primary care patients .
History
Patients with anxiety disorders frequently describe experiencing physical symptoms such as chest pain, dizziness, palpitations, fatigue, shortness of breath, sweating, muscle aches or tension, or a variety of gastrointestinal complaints. Common psychologic symptoms can include shakiness, nervousness, fear of dying or going crazy, or a sense of unreality or detachment from oneself.
Some patients attribute their anxiety to their physical symptoms (“Of course, I was anxious. I thought I was having a heart attack”). Consequently, the assessment of anxiety disorders should include the nature, frequency, and duration of the preceding symptoms and the extent to which the symptoms have impacted the individual's life and activity.
The patient should also be asked about precipitants of the symptoms, including stressors, medications (e.g., stimulants), and other drug use (e.g., caffeine, cocaine).
Questions about the patient's general medical condition are also appropriate.
Physical examination
As with all patients, those whose clinical picture is suspected of including a significant component of anxiety should be examined carefully.
P.44The extent of the physical examination should be dictated by the patient's personal health and medical history.
The examination may include the following: blood pressure (hypertension, hypovolemia), cardiovascular (angina, arrhythmia, congestive heart failure, valvular heart disease), respiratory (chronic obstructive lung disease, pulmonary embolism, pneumonia), and neurologic (tumor, encephalopathy, vertigo).
Patients frequently present with nervous agitation, intermittent eye contact, somewhat pressured speech, and, in the primary care context, a worried focus on the somatic concerns described in the preceding text.
Testing
Useful laboratory tests include serum calcium (hypocalcemia), hematocrit (anemia), and thyroid-stimulating hormone (hyperthyroidism/hypothyroidism). Depending on the clinical scenario, an exercise stress test to evaluate chest pain or other tests to rule out organic causes (such as drug screen, oximetry (hypoxia), glucose (hypoglycemia), and electrolytes) may be useful as well.
Differential diagnosis
GAD is characterized by persistent and excessive worry about a number of issues on most days for a period of at least six months. GAD usually begins by early adulthood, is exacerbated by situational stressors, and usually involves a combination of psychologic and physical symptoms.
Panic disorder, with or without agoraphobia, presents with recurrent panic attacks—discrete episodes of anxiety involving shortness of breath, fear of dying, impending doom or losing control, pounding heart, sweating, chest pain, paresthesias, trembling, and nausea. The panic attacks may be provoked by identifiable stressors or situations but often seem to “come out of the blue.” Individuals with panic disorder may be so fearful of being in a situation in which they have another panic attack and are unable to escape that they develop agoraphobia (an intense fear of being in open or crowded places, which often contributes to the individuals being reluctant to leave the perceived safety of their home).
Acute stress disorder (ASD) and Posttraumatic stress disorder (PTSD) are characterized by reexperiencing (through recollections, flashbacks, nightmares) an extremely traumatic and possibly life-threatening experience (e.g., rape, murder, motor-vehicle accident, war), followed by hyper-arousal, panic, depressed mood, sleep disturbance, and hyper-vigilance. The individual usually attempts to avoid these memories or the chance of being in danger again through numbing, dissociation, repression, and behavioral changes. The main distinction between ASD and PTSD is the duration of symptoms (i.e., in PTSD symptoms last longer than one month).
Specific phobia is excessive anxiety provoked by exposure to a specific feared object or situation. Common phobias include fear of animals or insects, natural environment (e.g., heights, storms, water), blood-injection-injury, or situations (e.g., tunnels, bridges, elevators, flying, driving).
Social phobia is an excessive anxiety provoked by exposure to social or performance situations and unfamiliar individuals or surroundings. As a result, individuals with social phobia avoid these types of situations.
Obsessive-compulsive disorder is characterized by obsessions that cause anxiety (e.g., germs on hands) and compulsions (behaviors aimed at reducing the anxiety such as hand-washing). The obsessions usually fall into one or more of the following categories: infection/contagion, safety, religiosity, sexuality, death/dying, orderliness.
Adjustment reaction with anxious features is a condition in which a patient experiences significant anxiety in reaction to a specific stressor such as a major life event or interpersonal conflict. To qualify for this diagnosis, the level of anxiety should be assessed as being more than expected under the circumstances. In addition to these conditions, the clinician should investigate the possibility of mood, substance abuse, and other psychiatric disorders .
Clinical manifestations
Most anxious patients present in the primary care setting with a primary focus on their bodies and somatic symptoms rather than “their
P.45minds.” But inevitably there is a significant component of worry, fear, apprehension, and so on in the background. Because an exclusive focus on physical complaints (e.g., chest pain, dizziness) can obscure the diagnosis, it is important to ask patients about their psychologic state, living situation, and current stressors, as well as evaluate them for underlying medical issues.