Presentation on theme: "頭暈 新光醫院 神經科 許維志 醫師. Balance and Equilibrium Equilibrium The ability to maintain orientation of the body and its parts in relation to external space. Interaction."— Presentation transcript:
頭暈 新光醫院 神經科 許維志 醫師
Balance and Equilibrium Equilibrium The ability to maintain orientation of the body and its parts in relation to external space. Interaction between self and environment. Sensory input from visual, vestibular, and proprioceptive information. Integration in the brain stem and cerebellum.
Disorders of Equilibrium Diseases affect Central or peripheral vestibular pathways Cerebellum Proprioceptive sensation Mismatch of input signals and disintegration Symptoms Vertigo Ataxia
Vertigo and Dizziness Vertigo 眩暈 Illusion of movement of the body or the environment. Impulsion, oscillopsia, nausea, vomiting, cold sweating, or unsteadiness Dizziness 頭昏 No association of illusion of movement Light-headedness, faintness, giddiness, swimming
Vestibular System Semicircular canal Sense angular acceleration Head rotation Otolith organs Sense linear acceleration Head translation and uprightness
Functions of Semicircular Canals, Saccule and Utricle
Cerebellar System Archicerebellum Flocculonodular lobe vestibulocerebellum Paleocerebellum Anterior lobe Spinocerebellum Neocerebellum Posterior lobe Pontocerebellum The oldest cerebellum Caudal part Eye/head movement The next oldest Midline Neck/trunk movement The newest cerebellum Hemsiphere Limb movement
Origin and Classification of Vertigo
The Saccades, Pursuit, and Vestibular Control of Eye Movements
Dizziness History VertigoDisequilibrium without vertigo Near-faintPsychological dizziness Physiological dizziness Central originPeripheral origin
Distinguishing Vestibular From Nonvestibular Dizziness VestibularNonvestibular DescriptionSpinning, falling, drunkenness, motion sickness, tilting Floating, near-fainting, fatigue, head fullness, out-of body sensation Precipitating factorsHead movements, position changes Standing after sitting or lying, cardiac disease, agoraphobia Associated featuresNausea, vomiting, unilateral tinnitus or hearing loss, imbalance, oscillopsia Palpitation, diaphoresis, syncope, loss of concentration, dyspnea
Physiological Vertigo TypeProvocative stimulusMechanism Motion sicknessProlonged passive head movement or movement of the environment Vestibular-visual conflict Visual vertigoExcessive visual stimulation Vestibular-visual conflict Mal de debarquementLong voyage on ship or plane Maladaptation to chronic vestibular stimulation Height vertigoStanding in a high place looking out Lack of nearby stationary objects in peripheral vision Space sicknessZero gravityCanal-otolith conflict
Causes of Pathological Vertigo Peripheral vertigo Vestibular end organs: inner ear, labyrithine apparatus Vestibular nerve Central vertigo Brainstem: vestibular nucleus Archicerebellum (flocculonodular lobe)
Peripheral Causes of Vertigo Benign paroxysmal positional vertigo Meniere ’ s disease Acute peripheral vestibulopathy (vestibular neuritis) Head trauma Cerebellopontine angle tumor Toxic vestibulopathies
Disorders of the Semicircular Canal Vertigo (spinning of the environment or the self) Nystagmus Past-pointing of the limbs Ataxia Positive Romberg sign Turning during steppage test Tilt, a false sense of linear motion Vertical diplopia Skew deviation Ataxia Positive Romberg sign Translation on the steppage test Disorders of the Otolith Organs
Differentiating Peripheral From Central Vertigo PeripheralCentral Nausea/vomitingSevereVariable, mild ImbalanceMild-moderateSevere Hearing lossCommonRare Neurological symptoms RareCommon NystagmusUnidirectional in all gaze; inhibit with fixation Direction-changing in different gaze; not inhibited with fixation CompensationRapidSlow
Causes of Dysequilibrium without Vertigo Disorders of afferent senses Bilateral vestibular loss Sensory ataxia Multisensory disequilibrium Disorders of central processing and motor responses Cerebellar degeneration Frontal lobe syndrome Extrapyramidal syndrome
Approach to Vertigo and Dizziness General examination BP in the lying and standing Look for cardiac arrhythmia Examination of extracranial and peripheral vasculature
Approach to Vertigo and Dizziness Neurological examination (1) Consciousness and mental status Visual acuity and visual field Fundus Screening for hearing impairment Ocular motor examination Nystagmus Ocular motor palsy Slow or ataxic ocular movement
assessing current history Ask the patient to describe the symptoms without using the word dizzy. Have the patient differentiate vertigo from presyncope or near-syncope. Determine if the patient has a sense of being pushed down or pushed to one side (pulsion). A peculiar sense of movement of objects viewed when the patient moves is termed oscillopsia. Ascertain whether the symptoms are related to an anxiety attack; patients with agoraphobia may describe their symptoms as dizziness. Determine if the sensation is continuous or episodic (ie, attacks); if episodic, find out if the sensation is fleeting or prolonged. Ascertain whether the onset and progression of symptoms were slow and insidious or acute.
Ask the patient about head trauma and other illnesses to determine the setting of the initial symptoms. Trauma resulting in damage to an ear often manifests as unilateral hearing loss, which may be the cause of episodic vertigo even years later (posttraumatic hydrops). Determine if the attacks are associated with turning the head, lying supine, or sitting upright. Determine if symptoms of an upper respiratory infection or flu-like illness preceded the onset of vertigo. Inquire about associated symptoms such as hearing loss or tinnitus (ringing in the ears), aural fullness, diaphoresis, nausea, or emesis. Determine if the patient has an aura or warning before the symptoms start. If hearing loss is evident, find out if hearing fluctuates. Determine if the patient has a headache or visual symptoms such as scintillating scotoma. Ask the patient about brainstem symptoms such as diplopia, dysarthria, facial paresthesia, or extremity numbness or weakness. Ascertain the degree of impairment during an attack
Examination of Vestibulo-ocular Reflexes Spontaneous nystagmus Elicit slow phases with slow head rotation, in yaw (horizontal), pitch (vertical), and roll (torsion), and with high accelerations in yaw and pitch (head thrust) Caloric test Head-shaking nystagmus
Vestibulospinal Testing Past-pointing with arms, with eyes closed Romberg: feet apposed, in tandem, in tandem on toes, on one foot at a time, standing on compliant foam rubber Fukuda stepping test or walking around a circle Tandem gait, forward and backward
Approach to Vertigo and Dizziness Neurological examination (2) Motor system examination Focal or diffuse weakness Reflex changes Sensory examination Stock-and-gloving sensation loss: polyneuropathy Loss of vibratory and proprioceptive sensation: Vit B12 deficiency or tabes dorsalis Romberg ’ s sign
Approach to Vertigo and Dizziness Neurological examination (3) Cerebellar examination Observation of sitting and standing and walking Bending backward Tandem gait Walking around a chair Finger-nose-finger Heel-knee-shin
Approach to Vertigo and Dizziness Neurological examination (3) Cerebellar examination Pronation-supination Knee-patting Rapid touching of each finger to the thumb Arm deviation Arm tapping Rebound test
The Most Common Causes of Vertigo Syndromes Seen in a Neurological Clinic Benign paroxysmal positioning vertigo Phobic postural vertigo Basilar migraine Meninere ’ s disease Vestibular neuritis (T. Brandt, “ Vertigo, its multisensory syndrome ” )
Benign Paroxysmal Positioning Vertigo
The Vertical Vestibulo-ocular Projections Excitatory afferents Inhibitory afferents
Characteristic Nystagmus of BPPV
Benign Paroxysmal Positional Vertigo (BPPV) – Symptoms & Signs Brief attacks of rotational vertigo and concomitant rotatory nystagmus precipitated by rapid head tilt, turning or extension. The symptoms can be induced by Hallpike maneuver. Typical peripheral vestibular nystagmus, short latency, limited duration, reversal on returning to the upright position, and fatigability on repeated provocation.
Benign Paroxysmal Positional Vertigo (BPPV) – Pathogenesis & Treatment Otolith debris floats freely within the endolymph of the semicircular canal: canalolithiasis. Heavy debris settles on the cupula transforming it as a transducer of angular acceleration into a transducer of linear acceleration: cupulolithiasis. Treatment by canal repositioning or libratory maneuvers.
Brandt-Daroff vestibular exercise
Meriere ’ s Disease
Meniere ’ s Syndrome – Symptoms & Signs Fluctuating hearing loss, tinnitus, episodic vertigo and a sensation of fullness or pressure in the ear. Attacks lasted for hours but dizziness and unsteadiness remain for a few days. Repeated attacks lead to progressive tinnitus, hearing loss, and impaired vestibular function. Usual in the fourth to sixth decades.
Endolymphatic hydrops: increase of volume of endolymph associated with distension of entire endolymph system. The attacks are caused by rupture of membranous labyrinth leading to paralysis of the surrounding vestibular or cochlear hair cells and neural structures. Symptomatic treatment of acute spells. Salt restriction and diuretics. Intratympnic treatment with ototoxic antibiotics. Labyrinthectomy or vestibular neurectomy. Meniere ’ s Syndrome – Pathogenesis & Treatment
Basilar Migraine – Symptoms & Signs Vertigo may occur in about one-fourth of migraine patients, and can occur without headache. Other symptoms of basilar migraine include ataxia, dysarthria, diplopia, visual symptoms, tinnitus, decreased hearing, bilateral pareses or paresthesia and decreased level of consciousness. Benign paroxysmal vertigo of childhood. Benign recurrent vertigo of adulthood. Motion sensitivity with frequent bouts of motion sickness occurs in at least one-half of patients with migraine.
Basilar Migraine – Pathogenesis & Treatment Vasoconstriction (?). Neuronal depression (?). Genetic. Channelopathy. Symptomatic treatment of acute attack Antivertiginous medications. Antiemetics. Sumatriptans and ergotamines often are ineffective and even aggravate vertigo. Prophylactic treatment of attacks Beta-blockers. Calcium channel blockers. Valproic acid. Tricyclics.
Vestibular Neuritis – Symptoms & Signs Vertigo, nausea, and vomiting developed over several hours, reach a peak within 24 h, and resolve gradually over several weeks. Generally without hearing symptoms. Diagnosis is based on acute unilateral peripheral vestibular loss and exclusion of other inner ear diseases. Ramsay Hunt syndrome by varicella-zoster infection may causes facial paresis, tinnitus, hearing loss, and a vestibular defect.
Presumed of viral origin. Similar to Bell ’ s palsy caused by reactivation of dormant herpes infection in the Scarpa ’ s ganglion within the vestibular nerve. Treatment is symptomatic. Antivertiginous medication should not be given as long as nausea and vomiting subsides. These drugs suppress central compensation. Corticosteroid may shorten the clinical course. Vestibular rehabilitation exercise. Vestibular Neuritis – Pathogenesis & Treatment
Drugs That Can Cause Dizziness or Be Harmful to the Dizzy Patient DrugDrugs that causes dizziness Drug that interfere with vestibular compensation Ototoxic Anti-arrythmics amiodarone, quinine+ Anticonvulsants barbiturates, CBZ, PHT+ Antidpressant amitiptyline, imipramine+ Antihypertensives+ Diuretics hydrochlorothiazide, furosemid+ Antiinflammatory Drugs ibuprofen, indomethacin, ASA++ Antibiotics aminoglycosides+ Chemotherapeutics cisplatin+ Hypnotics+ Muscle relaxants+ Tranquilizers BZD++ Vestibular suppressants meclizine, scapolamine++