Vertigo PDF

10-Nov-23 Vertigo Mahmoud Elsayed AbdEl-Kader Midan 1 VESTIBULAR SYSTEM OVERVIEW The primary function of the vestibular system is to inform the brain of head position and acceleration. The labyrinth performs this through two organe...

10-Nov-23 Vertigo Mahmoud Elsayed AbdEl-Kader Midan 1 VESTIBULAR SYSTEM OVERVIEW The primary function of the vestibular system is to inform the brain of head position and acceleration. The labyrinth performs this through two organelles: 1. The semi-circular canals responsible for angular head acceleration. inertia of the endolymph within the semicircular canals during angular acceleration displaces hair cells. 2. The otolith responds for linear acceleration (gravity) Linear acceleration results in displacement of the otoliths within the utricle or saccule. This distorts the hair cells. 2 1  10-Nov-23 Pathway of vestibular system The cochlear & vestibular divisions travel together to the internal auditory meatus and then to The brainstem, vestibular neurons synapse in the vestibular nuclei in the dorsolateral medulla. Vestibular nuclei project to: 1. Cerebellum. 2. ocular motor nuclei the ascending (MLF) to control VOR. 3. the spinal cord through the lateral vestibulospinal tracts to mediate postural reflexes. 4. the thalamus, which projects to the postcentral gyrus. 3 Vestibular ocular reflexes (VOR) mediated by: vestibular nuclei MLF ocular motor nuclei CN III, IV and VI. maintain steady gaze during head movement (read a street sign) This “visual gyroscope” moves the eyes an equal & opposite amount to compensate head movement (if the head moves 30 to the right, the eyes must move 30 to the left to maintain fixation) 4 2  10-Nov-23 Right head rotation A tonic level of activity is present within each vestibular nerve, the two vestibular organs act in a push-pull fashion with one side increasing activity and one side decreasing activity in response to head acceleration. 5 An imbalance of the vestibular inputs leads to asymmetric information transmitted to the brain, and vestibular nystagmus occurs. The brain is able to compensate for these asymmetries given time (probably involves cerebellum to a large degree) by tuning up or down the three static vestibular inputs. The VOR is the reflex arc assessed with doll’s head maneuver or caloric testing (for vertigo or in comatose patients). 6 3  10-Nov-23 Nystagmus: it is an involuntary rhythmic oscillation of eyes in horizontal, vertical, torsional or mixed direction. Usually, there is slow drift of the eyes in one direction followed by quick jerk in the opposite direction. Nystagmus is named for the direction of the fast component. The normal maintenance of ocular posture and alignment of the eyes with the environment depends on: retinal input. labyrinthine input. central connections including vestibular nuclei and cerebellum. Thus, nystagmus may result from visual disease, labyrinthine disease, or disorders affecting the cerebellum or brainstem. 7 VERTIGO Vertigo is defined as the sensation of movement of self or environment, often rotary. Vertigo is a subjective symptom defined as the illusion of movement accompanied by an objective sign (nystagmus) and neurovegetative signs (nausea and vomiting). Vertigo results from a mismatch of the brain’s three primary information systems: visual vestibular Sensory (proprioception). Vertigo is the historical hallmark of a vestibulopathy. 8 4  10-Nov-23 iiiii iiiii ii i 9 Classification Peripheral Vertigo Central Vertigo Benign paroxysmal VBI,TIA and brainstem positional vertigo infarction. (BPPV). Tumor or mass. Vestibular neuritis. Migraine. Ménière's disease. Multiple Sclerosis. Trauma. 10 5  10-Nov-23 Peripheral 1- BPPV: Short-lived episodes of vertigo (rotary) precipitated by head movements (especially with neck extension as during lying down or looking up - “top shelf” vertigo). Usually less than 45 seconds, although patients may report symptoms for minutes. It is the most common cause of vertigo. Correct diagnosis avoids costly and unnecessary testing. Trauma is a common antecedent event (50%), while other cases are idiopathic or occur following vestibular neuritis. The key physical exam finding is observed on Dix-Hallpike testing 11 Peripheral 2-Vestibular neuritis: Typically produces a monophasic episode of vertigo lasting from days to weeks. Often accompanied in the acute phase by severe nausea and vomiting. Peripheral 3- Ménière's disease: It appears to be caused by endolymphatic regulatory dysfunction. Spells of vertigo usually last hours. Classically preceded by ear pressure/fullness, tinnitus and change in hearing function Spells may be precipitated by high salt intake. 12 6  10-Nov-23 Peripheral 4- Vestibular/acoustic neuroma (nerve sheath tumors of CN 8) typically present with progressive unilateral hearing loss. the slow pace of vestibular loss allows central compensation until very late. Peripheral 5- Trauma: Produce several types of vertigo including BPPV Direct labyrinth trauma/contusion (persistent imbalance). Non-vertiginous, non-specific “dizziness” as part of the post concussive syndrome. The details of the history and physical exam will help define the specific diagnosis. 13 Central Vertigo 1- VBI, TIA and brainstem infarction: Spells characterized not only by vertigo but also (diplopia, dysarthria, dysphagia, drop attack, numbness, and incoordination) VBI may be cased by - Cervical degenerative changes. - Atherosclerosis - Embolism - Vertebral or basilar artery dissection. - subclavian steal: blood is diverted from the vertebrobasilar system due to a subclavian stenosis. Brainstem ischemia is an important cause of vertigo because further ischemia in this region may be acutely life threatening. These patients commonly have traditional risk factors (hypertension, diabetes, hyperlipidemia, tobacco use). 14 7  10-Nov-23 2- Tumor or mass: Brainstem tumors rarely present with isolated vertigo. 3- Migraine: Approximately 10-30% of patients with migraine cephalgia develop episodic vertigo lasting minutes to hours. Physical examination between episodes is normal. 4- Multiple Sclerosis: Demyelinating disease is an important cause of central vestibular lesions in young patients. Approximately 33% of MS patients present with visual symptoms, while an additional 7% present with vestibular symptoms. Examination may evidence central, peripheral or mixed patterns of nystagmus. 15 Cervical Vertigo described a syndrome of disequilibrium and disorientation in patients with many different diagnoses of neck pathology including cervical spondylosis, cervical trauma, and cervical arthritis. controversial diagnosis (no diagnostic tests to confirm that it is the cause of the dizziness). Diagnosis of exclusion diagnosis that is provided to people have neck injury or pain and dizziness, and other causes of dizziness ruled out. 16 8  10-Nov-23 Characterized by: usually last minutes to hours. worse in head movements or maintaining one head position occurs after the neck pain and may be accompanied by a headache often occurs as a result of whiplash or head injury Pathophysiology Abnormal sensory input from neck proprioceptors. 17 Abnormal sensory input from neck proprioceptors Sensory information from the neck is combined with vestibular and visual information to determine the position of the head on the neck, and space. (Brandt 1996) This mechanism was investigated by injecting local anesthetics into the necks. Such injections caused unsteadiness and minor amounts of dizziness Disturbances of gait have been noted in animals in whom the upper cervical sensory supply was disturbed in whom the neck. On the other hand, Loudon et al (1997) found that persons with whiplash injury had deficits in reproducing neck position after whiplash injury and inaccuracy in assessing neutral position. 18 9  10-Nov-23 Clinical Presentation of vertigo Relevant historical features of dizziness/vertigo include: Duration Character or description Frequency Precipitants Associated symptoms 19 Clinical Presentation According to temporal profile Vertigo Seconds BPPV,centeral episodic continous Minutes TIA,centeral Hearing + Meniere's labyrinthitis hours Meniere's loss - BPPV Vestibular days Labyrinthitis neuritis 20 10  10-Nov-23 ASSESSMENT 1. Electro/Video nystagmography 2. Positional nystagmus test 3. Dix-Hallpike test 4. Bithermal caloric test 21 1- Electro/Video nystagmography The standard ENG test battery is composed of: A) Saccadic test Evaluate voluntary fast-eye movements. B) Gaze test The gaze test is used to evaluate the ability to generate and hold a steady gaze without drift or gaze-evoked nystagmus. c) Pursuit eye-movement test Pursuit eye movements prevent slipping of an image on the retina while the patient is tracking moving objects. D) Head-shake nystagmus test (VOR) Head movements produce vestibular responses with an extremely short latency (< 15 msec). 22 11  10-Nov-23 1 23 A) Saccadic test Evaluate voluntary fast-eye movements. The neural substrate of the saccadic system includes: (the frontal eye fields, the brainstem reticular formation, the oculomotor nuclei, and the cerebellum). The test should be performed by recording each eye separately, especially if conjugate eye movement dysfunction is suspected. Common saccadic abnormalities include dysmetria, slow saccadic velocity, and dysconjugate saccades. 24 12  10-Nov-23 B) Gaze test The gaze test is used to evaluate the ability to generate and hold a steady gaze without drift or gaze-evoked nystagmus. The neural substrates of the gaze system are similar to those of the saccadic system. The most common abnormalities detected by the gaze test are gaze- evoked nystagmus. 25 c) Pursuit eye-movement test Pursuit eye movements prevent slipping of an image on the retina while the patient is tracking moving objects. The neural substrate of the pursuit system includes the occipital and parietal cortex, the brainstem reticular formation, the cerebellum, the vestibular nuclei, and the oculomotor nuclei. Pursuit abnormalities occur with brainstem and cerebellar lesions. 26 13  10-Nov-23 D) Head-shake nystagmus test (VOR) Head movements produce vestibular responses with an extremely short latency (< 15 msec). Oculomotor responses are slower than this, with latencies approaching 100-200 msec. The compensation for this temporal discrepancy is the ability of the central vestibular system to maintain a memory of head motion, so that eye movements can be accurately matched to head movement. usually impaired with unilateral vestibular deficit. In this test, 20 cycles of low-amplitude, high-velocity active or passive head movements are performed, followed by observation for nystagmus. 27 2- Positional nystagmus test recording eye movements without visual fixation in 3 cardinal positions: Supine head right head left. positional nystagmus is usually peripheral and an objective sign of vestibular asymmetry, even if it is present in only a single head position. 28 14  10-Nov-23 3- Dix-Hallpike test Positioning nystagmus is a classic finding in patients with benign paroxysmal positional vertigo (BPPV). It is elicited by moving the patient rapidly from the sitting position to the head-right- down and head-left-down positions while observing and recording resulting nystagmus and symptoms. 29 Torsional nys = posterior canal horizontal nys = lateral /horizontal canal vertical nys = anterior/superior canal 30 15  10-Nov-23 4- Bithermal caloric test Although it remains the standard for evaluating unilateral vestibular deficit, it is a nonphysiologic test of the vestibular system. Cold (30°C) and warm (44°C) water are used to irrigate one ear at a time. Cold irrigation is an inhibitory stimulus, and warm irrigation is excitatory. The direction of postcaloric nystagmus is determined by the quick-phase direction cold opposite, warm same. findings from the caloric test are: unilateral weakness bilateral weakness due to peripheral vestibular disease. 31 32 16  10-Nov-23 5- Rotating-Chair Test The rotating-chair test is used to evaluate the integrity of the vestibulo-ocular reflex (VOR). The measured parameters are VOR gain, phase (latency), and symmetry. The test is most useful in determining the degree of central vestibular compensation and the residual vestibular function in cases of bilateral vestibular loss. It is not advised on a routine basis for all patients who report dizziness. 33 2 34 17  10-Nov-23 Clinical testing Pursuit eye-movement test Saccadic test 35 Vertigo rating scales Vertigo is a subjective symptom defined as the illusion of movement accompanied by an objective sign (nystagmus) and neurovegetative signs (nausea and vomiting). For this reason, any evaluation of a dizzy patient must address all components of the vestibular syndrome : vertigo motion intolerance neurovegetative signs instability. 36 18  10-Nov-23 A) The Dizziness Handicap Inventory ( DHI ) It was proposed by Jacobson in 1990. Require answers for 25 questions Questions are designed to incorporate functional (F), physical (P), and emotional (E) impacts on disability. Keys: → No=0 Sometimes=2 Yes=4 Any Score greater than 10 points should be referred to balance specialists for further evaluation. 16-34 Points (mild handicap) 36-52 Points (moderate handicap) 54+ Points (severe handicap) 37 yo u a n k T h 38 19