Dizziness



Dizziness


Robert W. Baloh



DIZZINESS


Background


Description



  • 1. Dizziness is a sensation of altered orientation in space.


  • 2. Dizziness can be caused by many different pathophysiologic mechanisms.


History



  • 1. Describe the sensation.


  • 2. How it began.


  • 3. How long it lasts.


  • 4. How frequently it occurs.


  • 5. Circumstances that induce it.


  • 6. Associated symptoms.


  • 7. Medications.


Classification (Common Subtypes)



  • 1. Presyncope (near-faint dizziness): A light-headed sensation, the sensation one experiences before losing consciousness or fainting.


  • 2. Psychophysiologic dizziness: Feeling of dissociation, as though one has left one’s own body. Patients use terms such as “floating” or “swimming.”



  • 3. Disequilibrium: Patients may use the term “dizzy” to describe a sensation of imbalance that occurs only when they are standing or walking and is unrelated to an abnormal head sensation.


  • 4. Vertigo: An illusion of movement, usually that of rotation although patients occasionally describe a sensation of linear displacement or tilt.


Epidemiology



  • 1. Dizziness is common in all settings and patient groups.


  • 2. Dizziness tends to be more common in women than in men.


  • 3. The prevalence of dizziness increases with age.


  • 4. Presyncope and vertigo represent the most common dizziness subtypes, each occurring in about one-third of patients with dizziness.


Pathophysiology



  • 1. Presyncope (near-faint dizziness): The mechanism of presyncope is reduced blood flow to the entire brain. When the cerebral blood flow is partially reduced, patients experience light-headedness; when there is a greater reduction, syncope occurs.



    • a. Cardiac arrhythmias produce spontaneous episodes of presyncope that can occur in any position and can be associated with other cardiac symptoms including chest pain and palpitations.


    • b. Orthostatic hypotension is usually due to acute blood loss, volume depletion, and diuretics or antihypertensive medications. When the patient stands, gravitational pooling of blood occurs in the limbs and splanchnic vasculature.


    • c. Vasovagal, or neurally mediated presyncope, typically occurs when the patient is standing but, unlike orthostatic hypotension, the blood pressure is not necessarily reduced immediately upon standing. The mechanism is not fully understood but begins with an afferent signal from the arterial visceral mechanoreceptors.


    • d. Hyperventilation causes presyncope by lowering the carbon dioxide content of the blood, thus producing constriction of the cerebral vasculature.


  • 2. Psychophysiologic dizziness: The mechanism of psychophysiologic dizziness is poorly understood, but it is believed to result from impaired central integration of sensory signals. Associated symptoms of acute and chronic anxiety are common.


  • 3. Disequilibrium: This can result from loss of peripheral sensory input (most often vestibular, proprioceptive, or visual) or from central lesions involving the motor centers of the basal ganglia, cerebellum, and cortex.


  • 4. Vertigo: It indicates an imbalance in vestibular tone. It can result from loss of peripheral input caused by damage to the labyrinth or vestibular nerve, or it can be caused by a unilateral impairment of vestibular nuclear or vestibulocerebellar activity.



    • a. Benign positional vertigo (BPV) (also called “benign paroxysmal positional vertigo”) is by far the most common cause of vertigo. It results from free-floating calcium carbonate crystals (normally attached to the utricular macule) most commonly in the posterior semicircular canal. With positional change, the crystals move within the endolymph and displace the cupula.


    • b. Acute peripheral vestibulopathy (vestibular neuritis) often occurs after a viral illness, and pathologic studies show atrophy of one or more of the vestibular nerve trunks, most consistent with an infectious or postinfectious process.


    • c. Ménière syndrome: The principle pathologic finding is an increase in the volume of the endolymph associated with distention of the entire endolymphatic system (endolymphatic hydrops). Ruptures of the membranous labyrinth might explain the sudden episodes that are characteristic of the syndrome.


    • d. Migraine: Vasospasm or an inherited metabolic defect could explain the commonly associated episodic vertigo.



    • e. Vertebrobasilar insufficiency (VBI) is usually caused by atherosclerosis of the subclavian, vertebral, and basilar arteries. Vertigo is also common with infarction of the lateral brainstem or cerebellum.


    • f. Cerebellar pontine angle tumors grow slowly, allowing the vestibular system to accommodate, so that they usually produce a vague sensation of disequilibrium rather than acute vertigo.


Prognosis



  • 1. Presyncope



    • a. Usually benign.


    • b. Some cardiac causes may be life threatening.


    • c. Orthostatic hypotension associated with degenerative neurologic diseases, such as Shy-Drager and Parkinson disease, can be severely disabling.


  • 2. Psychophysiologic dizziness



    • a. Often persists for many years.


    • b. Can recur after long periods of remission.


    • c. Typically present throughout the day.


    • d. Intensity varies with stress level.


    • e. Associated panic and phobic symptoms can lead to agoraphobia.


  • 3. Disequilibrium



    • a. Peripheral sensory loss (vestibular, proprioceptive, or visual) tends to be mild, leading to a cautious gait, but patients remain mobile.


    • b. Central causes, such as cerebellar infarction or degeneration, lead to a more profound gait disorder that is only minimally compensated over time.


  • 4. Vertigo



    • a. BPV will typically have spontaneous remissions after weeks to months, but most patients will have recurrences. The incidence of BPV increases with age.


    • b. Acute peripheral vestibulopathy (vestibular neuritis) is usually a monophasic illness with onset over a few hours, gradually clearing over several days, and returning to baseline after a few weeks. Recurrences are rare.


    • c. Ménière syndrome is characterized by recurrent episodes of fluctuating hearing loss, tinnitus, and vertigo, typically lasting for several hours. The natural course is for a progressive unilateral loss of hearing over several years to reach a “burnt-out” stage where the episodes of vertigo subside.


    • d. Migraine: Episodic vertigo occurs in about a quarter of patients. The vertigo attacks can occur during the headache, before the headache, or more often, completely independent of headache. The typical duration is from minutes to hours and the attacks will occur at irregular intervals over many years.


    • e. VBI is typically abrupt in onset, usually lasting for several minutes and is usually associated with other neurologic symptoms. It can be the prodrome of infarction in the brainstem or cerebellum.


    • f. Tumors in the cerebellar pontine angle are usually associated with mild dizziness and disequilibrium and are not progressive unless the tumor becomes large enough to compress the brainstem or cerebellum.


Diagnosis



  • 1. Presyncope



    • a. Orthostatic hypotension: A documented drop in mean blood pressure of more than 10 to 15 mm Hg when the patient moves from a lying to standing position.


    • b. Cardiac arrhythmias: Any patient with episodic presyncope of unknown cause should undergo electrocardiogram (ECG) monitoring to search for sinus pauses, sinus bradycardia, atrial fibrillation, and sustained supraventricular tachycardia.



    • c. Vasodepressor presyncope: Characteristic history in a patient without neurologic or cardiovascular disease.


    • d. Hyperventilation: Characteristic-associated symptoms in the setting of anxiety dyspnea.


  • 2. Psychophysiologic dizziness



    • a. Associated symptoms of acute and chronic anxiety.


    • b. Patients may focus on the somatic symptoms, especially the dizziness and autonomic symptoms, rather than the intense anxiety associated with the attacks.


  • 3. Disequilibrium



    • a. The broad-based ataxic gait of cerebellar disorders is readily distinguished from the milder gait disorder seen with vestibular or sensory loss.


    • b. Bilateral vestibular loss may or may not be associated with hearing loss. The diagnosis rests on finding decreased or absent response to caloric and rotational stimulation.


  • 4. Vertigo



    • a. BPV: A burst of torsional vertical nystagmus is induced by rapidly moving the patient from the sitting to head-hanging position (the Dix-Hallpike test). There are typically a few seconds of latency, and fatigue with repeated positioning.


    • b. Vestibular neuritis: Characteristic clinical profile (spontaneous prolonged vertigo that gradually resolves over days), examination findings consistent with a unilateral peripheral vestibular loss (spontaneous nystagmus and positive head thrust test), and absence of associated neurologic symptoms and signs.


    • c. Ménière syndrome: Fluctuating hearing levels occur (particularly in the low frequencies) in a patient with the characteristic episodes of vertigo.


    • d. Migraine: Diagnosis of exclusion in the patient with long-standing recurrent attacks of vertigo, normal hearing, and headaches that meet the International Headache Society (IHS) criteria.


    • e. VBI: Comes on abruptly without any apparent precipitating factor, lasts for a few minutes, and then ends abruptly. There are nearly always associated symptoms such as visual loss, diplopia, dysarthria, weakness, or numbness.


    • f. Brainstem infarction: Stroke syndromes involving the posterior circulation are usually easily identified on the basis of their characteristic combination of neurologic symptoms and signs.


    • g. Cerebellar infarction: Can masquerade as a more benign inner ear disorder. However, profound truncal ataxia and a direction-changing, gaze-evoked nystagmus indicate a central lesion. Magnetic resonance imaging (MRI) is the procedure of choice for viewing brain structures supplied by the vertebrobasilar system.


    • h. C-P angle tumors: Detailed audiometric testing followed by neuroimaging with MRI will usually lead to a definitive diagnosis. MRI with contrast is the procedure of choice because it can identify small acoustic neuromas confined to the internal auditory canal, tumors that are missed with computed tomography (CT) scanning. CT scanning may be helpful for identifying bony erosion or calcification within tumors.


Treatment

May 28, 2016 | Posted by in NEUROLOGY | Comments Off on Dizziness
Premium Wordpress Themes by UFO Themes