Management of Central DizzinessMigraineMigraineis a common disorder, affecting 10% of men and 30% of women. About 25% of migraineurs have motion intolerance or sickness rather than true vertigo. The pathophysiology of migraine-associated vestibulopathy is not completely understood.[12]Vestibular symptoms usually are dissociated from headaches but sometimes can occur as an aura or as part of a headache. Patients can also have mild form of hearing loss mimicking Mnire disease.Symptoms that qualify for a diagnosis of vestibular migraine include various types of vertigo and head motioninduced dizziness with nausea. Symptoms must be of moderate or severe intensity. Duration of acute episodes is limited to a window of between 5 minutes and 72 hours.[13]Electro/videonystagmography is typically not helpful in differentiating migraine-associated vertigo from other vestibular pathologies. However, for patients with a longstanding history of dizziness, normal findings on electro/videonystagmography are suggestive of migraine-associated dizziness.For vestibular migraine, the theory of an ion-channel disorder is particularly interesting because different mutations of theCACNA1Agene coding for a transmembrane component of a neuronal calcium channel can provoke familial hemiplegic migraine or episodic ataxia type.[14]However, several candidate genes coding for ion-channel proteins have not been found in a population with vestibular migraine.[15]Treatment of migraine-associated vestibulopathy is the same as that of migraine, focusing on adequate control of the frequency and intensity of symptoms using both abortive and prophylactic medications. Triggers should be minimized/eliminated, including disturbed sleep pattern, diet, and lifestyle.[12]Prophylactic and abortive medications commonly used in treating migraine should be individually tailored. In the authors experience, topiramate and rizatriptan benzoate are associated with long-term control of vestibular migraine.Transient ischemic attacksTransient ischemic attacks (TIAs) are episodes of focal neurologic symptoms involving isolated or combined brainstem symptoms such as dizziness, diplopia, or weakness. These attacks are of sudden onset and resolve within 24 hours without residual subjective symptoms or objective signs on examination. TIAs are usually due either to reduced blood flow (the hemodynamic theory; eg, cardiac dysrhythmia) or to obstructed blood flow (the embolic theory; eg, plaques from the heart).TIAs are commonly (75% of cases) due to posterior circulation (vertebrobasilar territory). The differential diagnosis of TIAs includes migraine, partial seizures, hypoglycemia, syncope, and hyperventilation.Cerebrovascular diseaseStrokeis the third most common cause of death or disability in adults. The vertebrobasilar circulation supplies the brainstem, the cerebellum, and the inner-ear auditory and vestibular structures. Infarction of the cerebellar midline can cause acute vertigo without auditory or other neurologic features (eg, isolated vertigo).This potentially life-threatening event must be differentiated from vestibular neuronitis. A key difference between these 2 entities is that patients experiencing cerebellar strokes are unable to ambulate without support during the acute vertigo phase. About one half of patients have other features of bulbar or long tract involvement, which make the diagnosis of stroke clear.Evaluation of the patient with stroke is directed at identifying correctable vascular risk factors (eg, hypertension, diabetes, hyperlipidemia, and smoking) and at determining the mechanism of stroke (eg, small-vessel disease, large-vessel disease, cardioembolism, dissection, hypercoagulability, or vacuities). Secondary prophylactic therapy and rehabilitation are individualized. Both hearing loss and vertigo can occur in the setting of stroke due to central injury, peripheral injury, or both.Multiple sclerosisMultiple sclerosisis a disorder of recurrent, inflammatory CNS demyelination that is due to underlying autoimmune disease. The onset is usually at age 20-40 years. Episodes begin over hours to a few days and last weeks to months. Typical symptoms include the following: Optic neuritis Ocular motor dysfunction Trigeminal neuralgia Sensorimotor deficits Myelopathy Ataxia Bladder dysfunctionVertigo, at times mimicking vestibular neuronitis, is a presenting symptom in fewer than 10% of patients. Dizziness or vertigo occurs at some point in the course in one third of patients. Few patients present with hearing loss due to brainstem involvement.The diagnosis of multiple sclerosis requires the presence of dissemination in time and space (ie, different neurologic symptoms at different times). A careful history, a thorough examination, and serial follow-up combined with magnetic resonance imaging (MRI) and cerebrospinal fluid (CSF) analysis help establish the diagnosis; the diagnosis should not be based on MRI abnormalities alone. Disease-modifying therapy is available, but it is only modestly effective. The search for improved treatment is ongoing.Tumors and malformations of posterior fossaVestibular schwannoma (acoustic neuroma) is an uncommon lesion (incidence, 1.1 per 100,000) that typically manifests with slowly progressive unilateral hearing loss and tinnitus. Dizziness is not common, because the vestibular system can usually compensate for such gradual unilateral hypofunction. Dizziness can occur as the tumor expands in the cerebellopontine angle and effaces the brainstem and cerebellum. Arachnoid cysts can also occur in the posterior fossa and result in subtle and nonspecific dizziness and auditory symptoms.In a cross-sectional observational study in patients with small to medium-sized vestibular schwannomas, over 50% of patients reported ongoing dizziness at a mean of 8 years after treatment. All 538 patients had sporadic vestibular schwannomas of less than 3 cm and underwent primary microsurgery, stereotactic radiosurgery, or observation. The treatment modality was not found to influence long-term dizziness handicap.[16]Chiari malformation occurs in a few adults. It is congenital but often does not become symptomatic until age 20-40 years. Occipital headache precipitated by Valsalva maneuvers, coughing, exertion, or changing position is common. Dizziness may occur with the same precipitants.Once suspected, the diagnosis can be confirmed by means of MRI. Surgical treatment should be considered for patients whose symptoms are more than mild.FallsUpright balance and posture control are not a single physiologic function; they include visual, vestibular, and proprioceptive sensory inputs. During ambulation, the CNS must instantly integrate these inputs and execute appropriate motor plans and purposeful output via an adequate musculoskeletal system. This intricate system changes with age and disease-related decline in any of these systems. For example, bilateral vestibular failure is a contributor in one fourth of elderly patients with disequilibrium. Untreated BPPV can be a risk factor for falls.The most common fall is a simple event in which the patient has tripped but has no ominous underlying peripheral or central disorder. Hazards in the environment (eg, rugs, electrical wires, poor lighting), polypharmacy, and orthopedic factors often contribute to falls. Because of the substantial risk of injury and the resultant decline in independence or quality of life after a fall, a well-directed evaluation is indicated. Orthostatic hypotension due to aging or medications is also a common contributor. Normal pressure hydrocephalus is also a contributing factor to gait abnormalities and falling.