Dizziness and Vertigo _________________________________________________________________________
5% to 10% of cases [7]. The central task for providers is to distinguish benign from serious or life-threatening causes of dizziness and vertigo, such as posterior circulation stroke. Misdiagnoses are common and diagnostic testing can be costly, especially if too much reliance is placed on this outdated diag- nostic paradigm [8]. These factors can make the medical care of patients with dizziness/vertigo seem daunting. However, a new diagnostic paradigm has replaced the standard symptom-based approach with an algorithm that streamlines the differential diagnosis, increases diagnostic accuracy for benign and dangerous causes alike, and reduces the use of expensive and unhelpful brain imaging [3; 9]. A “timing and triggers” approach to patient history guides the diagnostic workup. The onset (timing), precipitating factors/ events (triggers), evolution, associated symptoms and signs, and the context of dizziness episodes can be used to classify cases as triggered or spontaneous forms of episodic, acute, or chronic vestibular syndromes. Placement within one of six vestibular syndromes informs the differential diagnosis, targeted physical exams, and testing. Targeted exams are a range of procedures that assess for peripheral or central causes of dizziness/vertigo without using less accurate, expensive brain imaging [8]. ANATOMY AND PHYSIOLOGY The labyrinth in each inner ear houses the systems that serve the functions of hearing (auditory) and balance (vestibular). The auditory system involves the cochlea, which transmits sound signals to the brainstem via the cochlear branch of the 8th cranial nerve. The vestibular system is comprised of the vestibular end-organs in the labyrinth, the vestibular nuclei in the brainstem and cerebellum, and the vestibular branch of the 8th nerve, which relays labyrinthine input to the vestibular nuclei. The 8th cranial nerve is also called the vestibulo-cochlear nerve [10; 11; 12]. Within each labyrinth are five vestibular end-organs (three semicircular canals and two otolith organs) that help maintain spatial orientation, postural control, and egocentric percep- tion. Changes in angular and linear head acceleration, move- ment, and orientation to gravity are detected and signaled via the 8th nerve to brainstem and cerebellar circuits, through thalamic and spinal vestibular projections, and finally to the cerebral cortex [13; 14; 15]. This vestibular input, along with visual input from the eyes and proprioceptive input from peripheral sensory nerves (via the spinal cord), is relayed to the cerebral cortex, which integrates the sensory inputs and adjusts outgoing motor responses to maintain balance, posture, and gaze stabilization of retinal images (via the vestibulo-ocular reflex) [11; 14; 16].
INTRODUCTION Mdvances in knowledge of pathophysiology and newer imag- ing techniques have led to a paradigm shift in the classifica- tion system and diagnostic algorithm for managing dizziness and vertigo. With this newly identified connectivity between vestibular, balance, and anxiety disorders comes an enhanced ability to identify the stroke mimics of benign dizziness or vertigo. These and other breakthroughs are transforming the clinical care of patients with dizziness and vertigo complaints, connecting clinical syndromes previously considered unrelated, and expanding the range of effective treatment options for patients. The modern paradigm for the clinical management of dizzi- ness and vertigo was introduced by Drachman and Hart in a seminal 1972 publication [1]. Based on patient response to the question “What do you mean by ‘dizzy?’,” dizziness was clas- sified into one of four types that best reflected the subjective descriptions of the symptoms [2; 3]: • Vertigo: Dizziness experienced as a definite sensation of movement or rotation in space • Presyncope: A sensation of impending faint or loss of consciousness • Disequilibrium: A sense of unsteadiness or loss of balance without head sensations • Lightheadedness: Cannot be classed as vertigo, syncope, or disequilibrium The Drachman-Hart model also suggested that vertigo had a vestibular cause, presyncope a cardiovascular cause, disequilib- rium a neurologic cause, and nonspecific dizziness (lighthead- edness) a psychiatric or metabolic cause [4]. In accordance with this framework, the character of symptoms reported by the patient determined the type (pathophysiology) of disorder and guided subsequent clinical evaluation, differential diagnosis, testing, and treatment [3]. By current standards, the Drachman-Hart model was based on weak evidence and developed in the absence of modern diagnostic imaging. In reality, patients often have difficulty describing their symptoms and may give conflicting accounts at different times. In one study, an estimated 62% of patients presenting to the emergency department (ED) with past-week dizziness selected more than one type of dizziness on a multi- response questionnaire, and 52% chose a different type when retested six minutes later [5; 6]. As such, the character and quality of symptoms alone does not reliably predict the cause of dizziness or serve as a dependable guide to management. Primary care providers see at least 50% of patients who seek medical attention for dizziness or vertigo. The differential diagnosis is large, and each common etiology accounts for
42
EliteLearning.com/Nursing
Book Code: ANCCTX2027
Powered by FlippingBook