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Dizziness And Vertigo PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "Dizziness and Vertigo” by V. Abbasi, MD.

This medical PowerPoint presentation is about dizziness and vertigo, two terms that are often used interchangeably, but they actually refer to different sensations.

Dizziness is a feeling of lightheadedness or unsteadiness that can be accompanied by a range of symptoms, such as nausea, headache, or difficulty concentrating. It can be caused by a variety of factors, including low blood pressure, dehydration, medication side effects, or underlying health conditions like anemia or heart disease.

Vertigo, on the other hand, is a specific type of dizziness that is characterized by a sensation of spinning or motion even when you are still. It is often associated with a feeling of nausea or vomiting and can be triggered by changes in position, such as standing up quickly. Vertigo can be caused by a problem in the inner ear, such as an infection or inflammation, or by a neurological condition like migraines or multiple sclerosis.

If you are experiencing dizziness or vertigo, it is important to see a healthcare provider to determine the underlying cause and receive appropriate treatment. Depending on the cause, treatment may involve medication, changes in diet or lifestyle, or physical therapy. In some cases, more advanced interventions like surgery or other medical procedures may be necessary.

Tags : Dizziness, Vertigo, neurological condition, migraines, multiple sclerosis, Neurology, Neurology PowerPoint presentation

Published on : Jun 07, 2023 | Views : 1390 | Downloads : 4

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Slide 1-

Dizziness and Vertigo V. Abbasi, M.D.
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Dizziness Vertigo: illusion of movement Ataxia: inability to co-ordinate movements (walking or of extremities), “feel as if drunk” Dizziness Non-specific term (lightheadedness, swimming sensation inside of head) Different meanings to different people Could mean Vertigo - Syncope - Presyncope Weak - Giddiness - Anxiety Anemia - Depression - Unsteady
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Syncope Transient loss of consciousness with loss of postural tone Presyncope Lightheadedness-an impending loss of consciousness Psychiatric dizziness Dizziness not related to vestibular dysfunction Disequilibrium Feeling of unsteadiness, imbalance or sensation of “floating” while walking
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Prevalence 1 in 5 adults report dizziness in last month Increases in elderly Worsened by decreased visual acuity, proprioception and vestibular input Vertigo and Dizziness
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Evaluation of the Dizzy Patient What type of dizziness is it? How long does it last? Continuous or episodic Spontaneous or positional Duration of vertigo if episodic Are there otologic symptoms? Are there focal neurological symptoms?
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Vestibular Labyrinth Pathophysiology Complex interaction of visual, vestibular and proprioceptive inputs that the CNS integrates as motion and spatial orientation 3 semicircular canals rotational movement cupula 2 otolithic organs utricle & saccule linear acceleration Macula
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Normally there is balanced input from both vestibular systems Vertigo develops from asymmetrical vestibular activity Abnormal bilateral vestibular activation results in truncal ataxia Vertigo and Dizziness
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Nystagmus Rhythmic slow and fast eye movement Direction named by fast component Slow component due to vestibular or brainstem activity Slow component usually ipsilateral to diseased structure Fast component due to cortical correction Physiologic Vertigo “motion sickness” A mismatch between visual, proprioceptive and vestibular inputs Not a diseased cochleovestibular system or CNS Vertigo and Dizziness
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Otologic Symptoms in theDizzy Patient Hearing Loss: progressive, sudden SNHL,congenital, fluctuating Tinnitus: continuous or episodic Aural fullness Ear pain, or chronic drainage History of ear surgeries/infection
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Focal Neurological Symptoms Vertigo if secondary to cerebrovascular insufficiency is indicative of posterior circulatory problems Visual loss Loss of consciousness Numbness especially if on one side Weakness especially if on one side Incoordination as if drunk Difficulty swallowing Slurring of the speech
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Evaluation of the Dizzy Patient Family History: Hearing Loss Vertigo Spells Headaches or visual auras Gait ataxia or imbalance
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Is it true vertigo? Autonomic symptoms? Pattern of onset and duration Auditory disturbances? Neurologic disturbances? Was there syncope? Unusual eye movements? Any past head or neck trauma? Past medical history? Previous symptoms? Prescribed and OTC medications? Drug and alcohol intake? Vertigo-History
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Cerumen/FB in EAC Otitis media Pneumatic otoscopy Tympanosclerosis or TM perforation Nystagmus Fundoscopic exam Pupillary abnormalities Extraocular muscles Cranial nerves Internuclear ophthalmoplegia Auscultate for carotid bruits Orthostatic vital signs BP and pulse in both arms Dix-Hallpike maneuver Gross hearing Weber-Rinne test External auditory canal vesicles Muscle strength Gait and Cerebellar function Vertigo-Physical Exam
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Nystagmus: Features of Peripheral Spontaneous nystagmus from imbalance of signals from the right and left vestibular periphery The resulting nystagmus is a combined torsional, horizontal. Alexander’s law: Increased frequency and amplitude of nystagmus with gaze in direction of fast component, reverse effect with gaze opposite to the fast component. Inhibited by fixation
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Features of Central Nystagmus Prominent with and without fixation Can be purely vertical (always central), horizontal, or torsional, of have some combination The rule is if the nystagmus is vertical (upbeat or downbeat), it is central i.e. not coming from the inner ear Cerebellar: spontaneous downbeat with vertical amplitude increasing with horizontal gaze deviation or brought out when placed in supine position
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Bedside Tests of Vestibular Function:Dynamic Visual Acuity Oscillopsia : perception of environment jumping up and down when walking. Ask the patient: “Can you read the print on the cans while walking down the grocery store aisle?” May be a sign of bilateral loss of VOR function Horizontal passive rotation at 2 Hz. Normal is loss of 1 line of Snellen acuity card, bilateral vestibular loss will lose 5 lines.
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Bedside Tests of Horizontal VOR: Head Thrust Test Rapid, high-acceleration head thrust with patient fixating on examiner’s nose Corrective saccade (catch-up saccade) when head is rotated toward the affected vestibular periphery is positive Positive in vestibular neuritis, gentamicin ototoxicity (bilateral), idiopathic and autoimmune vestibulopathy May be normal to have slight VOR hypometria bilaterally in older patients
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Vertigo-Characteristics
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Etiologies of Vertigo BPPV Labyrintitis Acute suppurative Serous Toxic Chronic Vestibular neuronitis Vestibular ganglionitis Ménière’s Acoustic neuroma Perilymphatic fistula Cerumen impaction CNS infection (TB, Syphillis) Tumor (Benign or Neoplastic) Cerebellar infarct Cerebellar hemorrhage Vertebrobasilar insufficiency AICA syndrome PICA syndrome Multiple Sclerosis Basilar artery migraine Hypothyroidism Hypoglycemia Traumatic Hematologic (Waldenstroms) Vertigo-Differential Diagnoses
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Labyrinthine Disorders Most common cause of true vertigo Five entities Benign paroxysmal positional vertigo (BPPV) Labyrinthitis Ménière disease Vestibular neuronitis Acoustic Neuroma Peripheral Vertigo-Differential
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Benign Paroxysmal Positional Vertigo Otolithic calcium carbonate crystals become loose, and fall into the posterior semicircular canal Common with head trauma, older age, inner ear disease One of the most common cause of vertigo seen in neurotology clinics, estimated at 20-30% of patients
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Benign Paroxysmal Positional Vertigo Typical complaint: spells of vertigo when turning over in bed No hearing loss or tinnitus Usually a single position that elicits vertigo Horizontorotary nystagmus with crescendo-decrescendo pattern after slight latency period Examine the patient for nystagmus and vertigo in the Dix-Hallpike position : head-hanging R and L Vertigo lasts shorter than 1 minute torsional nystagmus with upbeat component Brought on only by positional changes Latency of few seconds up to 45 sec Fatigues with repeated testing
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Modified Epley Maneuver
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Epidemiology of BPPV Lifetime prevalence of 3.2% in females and 1.6% in males Of 100 unselected elderly patients, a prevalence of 9% was reported Median duration of two weeks Female preponderance likely reflects the association of migraine with BPPV Association of BPPV with hypertension and hyperlipidemia Vascular damage to the inner ear facilitates detachment of the otoconia
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Otoconia in BPPV
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Labyrinthitis Associated hearing loss and tinnitus Involves the cochlear and vestibular systems Abrupt onset Usually continuous Four types of Labyrinthitis Serous Acute suppurative Toxic Chronic
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Labyrinthitis Serous Adjacent inflammation due to ENT or meningeal infection Mild to severe vertigo with nausea and vomiting May have some degree of permanent impairment Acute suppurative labyrinthitis Acute bacterial exudative infection in middle ear Secondary to otitis media or meningitis Severe hearing loss and vertigo Treated with admission and IV antibiotics
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Labyrinthitis Toxic Due to toxic effects of medications Still relatively common Mild tinnitus and high frequency hearing loss Vertigo in acute phase Ataxia in the chronic phase Common etiologies -Aminoglycosides -Vancomycin -Erythromycin -Barbiturates -Phenytoin -Furosemide -Quinidine -Salicylates -Alcohol
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Labyrinthitis Chronic Localized inflammatory process of the inner ear due to fistula formation from middle to inner ear Most occur in horizontal semicircular canal Etiology is due to destruction by a cholesteatoma
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Meniere’s Disease Symptoms: Fluctuating hearing loss, tinnitus, ear fullness, and vertigo. May have initially only hearing loss or only vertigo spells. Possibly sudden falls (Tumarkin crisis) Hearing loss, tinnitus, and aural fullness increase during the vertigo attack Typically lasts 20 minutes or more in duration
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Meniere’s Disease On temporal bone histopathology, there is a distension of the entire endolymphatic system Audiogram: often low-frequency sensorineural hearing loss that increases during attacks.
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Meniere’s Disease: Tumarkin falls In about 7-10% of Meniere’s disease, there are associated sudden falls “drop attacks” No warning, sudden, violent fall without loss of consciousness Subjective sensation of being pushed by an external force Surgical ablation is curative of these dangerous and frightening drop attacks
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Meniere’s Disease Variant:Delayed Endolymphatic Hydrops Delayed hydrops develops in an ear that has h/o profound SNHL years before (up to 70 years before) Many years later: recurrent spells of vertigo of 20 minutes duration or longer Often without accompanying otologic symptoms of aural fullness, increased tinnitus and hearing fluctuation Can also have Tumarkin falls
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Ménière Disease First described in 1861 Triad of vertigo, tinnitus and hearing loss Due to cochlea-hydrops Unknown etiology Possibly autoimmune
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Ménière Disease Often patients have eaten a salty meal prior to attacks May occur in clusters and have long episode-free remissions Usually low pitched tinnitus Symptoms subside quickly after attack No CNS symptoms or positional vertigo are present
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Positional and Spontaneous Vertigo:Multiple Sclerosis Vertigo is the initial symptom of MS in 5%, and presents in 50% of MS patients at some time in the course. 25% of patients with MS have caloric paresis 80% have eye movement abnormalities Oftentimes abnormalities on ABR and occasionally retrocochlear hearing loss from involvement at the root entry zone near pons May have any type of nystagmus
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Brainstem aud itory evo ked potentials (BAEPs)
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Positional and Spontaneous Vertigo:Multiple Sclerosis Demyelinating disease of unknown etiology Onset usually in 3rd and 4th decade of life Common associated signs and symptoms: INO (internuclear ophthalmoplegia), optic neuritis, Llermitte’s sign, vibratory loss, spasticity, sensitivity to temperature MRI with FLAIR: plaques
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Migraine-associated Vertigo Vestibular Meniere’s, migraine-associated vestibulopathy, benign paroxysmal vertigo 25% of patients with migraine have vertigo spells Duration of the vertigo varies: 31% few min-2 hr 49% > 24 hrs 7% seconds 25% of patients with migraine have caloric paresis Isolated vertigo without headache are termed migraine equivalent
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Migraine-associated Vertigo Migraine is an inherited, likely metabolic syndrome with multiple causes, likely autosomal dominant with variable penetrance Always ask about the family history Ask about h/o motion sickness (50%) Ask about h/o altitude sickness Ask about sensitivity to visual stimuli (bright lights/ patterns, computer work)
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Migraine-associated Vertigo Ask about h/o recurrent abdominal pains or cyclical vomiting as child, which is usually migraine equivalent Ask women specifically regarding menses: some will call migraine headaches “PMS” Migraine-associated vertigo often has a catamenial component, or worsened by OCP in women
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International Headache SocietyCriteria for Migraine Headaches At least 5 attacks fulfilling B-D B. Headache lasting 4-72 hrs C. At least 2 of: unilateral, pulsating, moderate or severe, aggravation by physical activity D. At least one of N/V, photophobia and phonophobia Other causes ruled out
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Variants of Migraine Migraine visual aura: Visual aura may occur isolated without headache: fortification spectra, scotoma, stars, patterns of colored lights lasting usually 15-20 minutes Retinal migraine: retinal artery vasospasm which can cause monocular blindness: prophylaxis with verapamil Benign paroxysmal vertigo of childhood: recurrent spells of vertigo in child is usually migraine, may or may not have H/A
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Association between Migraineand Vestibulopathy Tumarkin falls may be associated with migraine Out of 55 patients with Tumarkin falls, 6 had >1yr h/o normal hearing 5 out of 6 had h/o migraine Tumarkin falls are known to localize to the vestibular periphery since surgery is curative
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Vestibular Neuritis Subacute onset of vertigo, often with nausea and vomiting Vertigo lasts a few days, and crescendos in few hours, and decreases in severity with time Suspicion for viral cause but evidence for ischemic causes Mild vertigo may last for several weeks May have auditory symptoms Highest incidence in 3rd and 5th decades Temporal bone histopathology: Scarpa’s ganglion neuronal loss
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Vestibular Ganglionitis Usually virally mediated-most often VZV Affects vestibular ganglion, but also may affect multiple ganglions May be mistaken as BPPV or Ménière disease Ramsay Hunt Syndrome -Deafness -Vertigo -Facial Nerve Palsy -EAC Vesicles
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Peripheral vertigo that ultimately develops central manifestations Tumor of the Schwann cells around the 8th CN Vertigo with hearing loss and tinnitus With tumor enlargement, it encroaches on the cerebellopontine angle causing neurologic signs Earliest sign is decreased corneal reflex Later truncal ataxia Most occur in women during 3rd and 6th decades Acoustic Neuroma
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Central Vertigo Vertebrobasilar Insufficiency Atheromatous plaque Subclavian Steal Syndrome Wallenberg Syndrome Cerebellar Hemorrhage Multiple Sclerosis Head Trauma Neck Injury Temporal lobe seizure Vertebral basilar migraine Metabolic abnormalities Hypoglycemia Hypothyroidism Central Vertigo-Differential
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Vertebrobasilar Insufficiency Important causes of central vertigo Related to decreased perfusion of vestibular nuclei in brain stem Vertigo may be a prominent symptom with ischemia in basilar artery territories Unusual for vertigo to be only symptom of ischemia
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Vertebrobasilar Insufficiency Most commonly will also have: -Dysarthria -Ataxia -Facial numbness -Hemiparesis -Diplopia -Headache Tinnitus and hearing loss unlikely Vertical nystagmus is characteristic of a (superior colliculus) brain stem lesion
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Vertebrobasilar insufficiency 20% of all strokes are in the vertebrobasilar distribution Usually from atherosclerotic disease, but 1/5 of infarcts may be cardioembolic Common cause of episodic, spontaneus vertigo of abrupt onset in older patients Several minutes (3-4 min) duration is always suspicious for TIA
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Vertebrobasilar insufficiency Visual (diplopia/ illusions, field defects in 69% Drop attacks in 33% Imbalance/ incoordination in 21% Extremity weakness in 21% Confusion in 17% Headache in 14% Hearing loss in 14% Loss of consciousness in 9.5% Extremity numbness in 9.5% Dysarthira in 9.5% Tinnitus in 9.5% Perioral numbness in 5%
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Abruptly falls without warning, but does not loose consciousness Believed to be caused by transient quadraparesis due to ischemia at the pyramidal decussation Drop attack
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Subclavian Steal Syndrome Rare, but treatable Arm exercise on side of stenotic subclavian artery usually causes symptoms of intermittent claudication Blood is shunted away from brainstem into ipsilateral vertebral artery Classic history occurs only rarely
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Stroke syndrome with vertigo:Wallenberg syndrome Dorsolateral medullary syndrome PICA (posterior inferior cerebellar artery) Vertebral atherosclerotic disease (artery to artery emboli) prior to takeoff Consider vertebral dissection Look for h/o neck trauma or manipulation
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Wallenberg symptoms Right Dorsolateral medullary stroke Nystagmus and vertigo (vestibular nuclei) Difficulty swallowing, hoarse voice, absent gag on R (nucleus ambiguus) Difficulty limb coordination on the right FTN, HTS (right cerebellum) On walking, veers and falls to the right Pain and temperature loss on right face and left leg, trunk, arm (spinothalamic) Right Horner’s: ptosis, miosis, anhydrosis (reticulospinal fibers in lateral medulla)
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Wallenberg Syndrome Occlusion of PICA Relatively common cause of central vertigo Associated Symptoms: -nausea -vomiting -nystagmus -ataxia -Horner syndrome -palate, pharynx and laryngeal paresis -loss of pain and temperature on ipsilateral face and contralateral body
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Stroke syndrome with vertigo: Anterior inferior cerebellar artery Vertigo Tinnitus, hearing loss secondary to infarct of cochlea/nerve or cochlear nucleus Ataxia Facial paralysis and numbness Ispilateral Horner’s
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Stroke syndrome with vertigo: Labyrinthine infarction Occlusion of the internal auditory artery Sudden, profound hearing loss Acute onset of spontaneous vertigo lasting days Consider the diagnosis in older patients with h/o TIA, stroke, or atherosclerotic vascular disease
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Cerebellar Hemorrhage Etiology is hypertensive vascular disease in 2/3 of patients Acute onset of vertigo, nausea, and vomiting and severe headache, inability to stand Spontaneous or gaze evoked nystagmus, dysmetria, truncal ataxia Often requires prompt evaluation and surgical decompression to prevent progression to coma or even death from herniation Motor-sensory exam usually normal Gait disturbance often not recognized because patient appears too ill to move
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Head and Neck Trauma Due to damage to the inner ear and central vestibular nuclei, most often labyrinthine concussion Temporal skull fracture may damage the labyrinth or eighth cranial nerve Vertigo may occur 7-10 days after whiplash Fistula may provide direct route to CNS infection
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Syndrome of vertigo, dysarthria, ataxia, visual changes, paresthesias followed by headache Distinguishing features of basilar artery migraine -Symptoms precede headache -History of previous attacks -Family history of migraine -No residual neurologic signs Symptoms coincide with angiographic evidence of intracranial vasoconstriction Vertebral Basilar Migraine
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Duration of vertigo Duration BPPV Seconds, always < 1 min VBI Few minutes,  focal neurological signs Migraine Varies sec, minutes, hours or days Meniere’s 20 minutes to hours Vest.neuritis Days Stroke Days
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Hypoglycemia Suspected in any patient with diabetes with associated headache, tachycardia or anxiety Hypothyroidism Clinical picture of vertigo, unsteadiness, falling, truncal ataxia and generalized clumsiness Metabolic Abnormalities
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Severe Ménière disease may require chemical ablation with gentamicin Attempt Epley maneuver for BPPV Mainstay of peripheral vertigo management are antihistamines that possess anticholinergic properties -Meclizine -Diphenhydramine -Promethazine -Scopolamine Management
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Epley Maneuver
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University of Baltimore 107 patients Diagnosed with BPPV Right ear affected 54% Posterior semicircular canal in 105 patients Treated with 1.23 treatments Successful in 93.4% Laryngoscope. 1999 Jun;109(6):900-3 Epley Maneuver
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Ensure you understand what the patient means by “dizzy” Try to differentiate central from peripheral Often there is significant overlap Not every patient needs a head CT Central causes are usually insidious and more severe while peripheral causes are mostly abrupt and benign Most can be discharged with antihistamines Summary
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