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 Table of Contents  
ORIGINAL ARTICLE
Year : 2020  |  Volume : 26  |  Issue : 1  |  Page : 27-31

An electronystagmographic study in post head injury vertigo patients


Department of ENT, DR. B.R.A.M.C.H, Bangalore, Karnataka, India

Date of Submission03-Feb-2019
Date of Acceptance26-Mar-2019
Date of Web Publication19-Feb-2020

Correspondence Address:
Dr. Shruthi Dechamma
#293, 4th Main, 4th Cross, Coffee Board Layout, Hebbal Kempapura, Bengaluru - 560 024, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/indianjotol.INDIANJOTOL_7_19

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  Abstract 


Vertigo is a well-known sequelae in post head injury patients. Etiopathology is multifactorial. Vertigo is recognized in all types of head injury-mild-to-severe and is a part of the post-concussion syndrome. However, it may also present later due to degenerative process involving the vestibular system. The observations made by the analysis of the tracings of electronystagmography and by noting the corresponding code we can identify the site and side of the vestibular lesion. The present study intends to understand post head injury vertigo using electronystagmography. Objectives of the Study: To evaluate post head injury vertigo using electronystagmography, to determine the side and site of origin of vertigo, and to localize the level of lesion – peripheral, central, or combined. Methodology: Fifty patients with post head injury vertigo presenting to ENT OPD of Dr. B. R. Ambedkar Medical College and Hospital were included in the study after taking their consent. Observations and Results: Fifty patients with post head injury vertigo were subjected to electronystagmography. Young adults between the age group of 20 and 30 years were found to be the most common group involved, constituted 34% of the patients. Equal gender predisposition was observed. 1111 ENG CODE was found to be the most common type seen in 18% of the cases, followed by 0000 in 16% of patients, and 0222 seen in 16% of the patients. Bilateral peripheral lesion was the most common type seen in 36% of patients followed by unilateral peripheral lesion in 20% of patients, central lesion in 22%, and normal in 20%. Conclusion: Electronystagmography is an effective tool in the assessment of post head injury vertigo. It is useful in identifying the cause of vertigo and to localize the lesion for timely management and early vestibular rehabilitation of the patient providing better clinical outcome.

Keywords: Central lesion, Claussen's butterfly chart, electronystagmography, ENG code, peripheral lesion, post head injury vertigo


How to cite this article:
John S, Dechamma S. An electronystagmographic study in post head injury vertigo patients. Indian J Otol 2020;26:27-31

How to cite this URL:
John S, Dechamma S. An electronystagmographic study in post head injury vertigo patients. Indian J Otol [serial online] 2020 [cited 2020 Jul 14];26:27-31. Available from: http://www.indianjotol.org/text.asp?2020/26/1/27/278739




  Introduction Top


Vertigo, dizziness, and imbalance are frequent symptoms of patients suffering from injury to head, neck, or craniovertebral junction which can result in vestibular dysfunction. Etiopathology of the vestibular dysfunction is multifactorial.[1]

Vertigo following head injury is reported in 25%–90% of cases.

Head injuries are sustained by 5% of the population annually.[2]

Trauma may be as a result of road traffic accidents, falls, assault, contact sports, and blast injuries. Patients following trauma to the cervical vertebral junction – whiplash injury also develop vertigo. Possible cause could be an imbalance in the afferent impulses from the mechanoceptors of the cervical vertebrae to the vestibular nuclei.

Nystagmus is an important sign of vestibular lesion. It is defined as the involuntary, rhythmic, and oscillatory movement of the eyes. Nystagmus may be horizontal, vertical, or rotatory. It has a slow component to one side followed by quick return to the opposite side. Direction of nystagmus is designated toward the quick phase.

Barany (1906) introduced nystagmus as a clinical test of vestibular function. The method of recording nystagmus by electronystagmography was developed by Jung and Mittermair in 1939 and Hallpike and Fitzgerald in 1942.[3]

In the central nervous system, electroencephalography (EEG) is used to record the activity of cerebral cortex but has a blind spot in the brainstem as it cannot satisfactorily record the activity there. ENG fulfils this blind spot and records the neurophysiological activities of the brainstem as the vestibular reflex has main connections in the brainstem.[4]

Most common clinically relevant forms of post head injury vertigo are as follows:

  1. Post traumatic otolithic vertigo/benign paroxysmal positional vertigo (BPPV)
  2. Labyrinthine concussion
  3. Rupture of round window/oval window
  4. Injury to vestibulocochlear nerve complex
  5. Post traumatic endolymphatic hydrops
  6. Late degeneration of labyrinthine hair cells
  7. Fracture temporal bone
  8. Central vertigo due to concussion of brainstem and cerebellum or secondary to dissection of vertebral artery
  9. Unilateral vestibular deficit due to concussion of temporal lobe.


Nature of trauma and force of injury determine multiple points of injury to the vestibular system.[5] Electronystagmography is an electrical test to evaluate patients with vertigo. It helps in the diagnosis of the cause of vertigo when combined with clinical and radiological investigations. Electronystagmography provides qualitative and quantitative assessment of vertigo.

Jonkees (1964) concluded that nystagmus can be observed four times more frequently with electronystagmography. The principle of electronystagmography is the electrical recording of the corneoretinal potential difference (Dubios, Reymond, 1849). Retina-like neural tissue bears a negative charge and cornea a positive charge. Electronystagmography records the potential difference between the cornea and retina during nystagmus.[3]

The objective record obtained by electronystagmography facilitates proper documentation, accurate record, evidence for medicolegal cases, teaching tool, and easier patient follow-up.

Disturbances of the vestibular system can be peripheral, central, and combined. Depending on the etiology of vertigo, management of the patients has to be tailor-made. The present study intends to understand and evaluate post head injury vertigo using electronystagmography by analyzing the vestibulograms of the patients presenting with vertigo post head injury.[4],[5]


  Methodology Top


This prospective study was conducted in the Department of Otorhinolaryngology and Head-and-Neck Surgery of Dr. B. R. Ambedkar Medical College and Hospital, Bengaluru, Karnataka, India.

Fifty patients clinically diagnosed with vertigo following head injury were included in the study.

Mean age of patients is 37.22 years, ranging from 20 to 60 years. The most common age group presenting with post head injury vertigo is between the age group of 20 and 30 years [Figure 1]. 50% of patients were male, 50% were female, equal predisposition was found in both the gender [Figure 2]. Patients were selected after a thorough history, detailed otoneurological assessment – balance tests – Romberg's test, Unterberger's test, straight line test, spontaneous nystagmus, positional tests, head shaking test, and head thrust test.
Figure 1: Age distribution

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Figure 2: Gender distribution

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Procedure of electronystagmography

(Nystagmorite mark II) RMS Digital Electronystagmography: Two channeled ENG Machine was used to carry out the electronystagmography procedure. The patient was instructed to avoid alcohol, sedatives and antivertiginous drugs for at least 24 h before the test. External ear is cleared of wax, infection if any is treated. Intactness of the tympanic membrane was confirmed. The wires are thin, flexible, and insulated and shielded. The cups of the leads are secured with adhesive tapes. The electrodes are secured lateral to the outer canthi, neutral electrode over the forehead. For a monochanneled record of conjugate horizontal eye movement, electrodes are applied to the side of the temple lateral to the outer canthi, and a neutral electrode is placed on the forehead.

Butterfly chart consists of four quadrants for four caloric responses, each with its corresponding normal range. For convenience the response is designated normal = 0, hypoactive + 1, hyperactive = 2.

Inclusion criteria

  1. Age >18 years
  2. History of vertigo after head injury (Immediate to 10 years following head injury).


Exclusion criteria

  1. Age <18 years
  2. History of vertigo (k/c/o BPPV, Meniere's disease, labyrinthitis, otosclerosis)
  3. Perforation of the tympanic membrane
  4. Patients under the influence of alcohol and sedative drugs
  5. Patients with other causes of vertigo
    1. Cardiogenic causes – cardiogenic syncope, vertebrobasilar insufficiency
    2. Epileptic vertigo
    3. Vertigo associated with migraine
    4. Neurological causes – cerebellar causes of imbalance, stroke, transient ischemic attack, multiple sclerosis
    5. Cervicogenic vertigo
    6. Psychogenic vertigo.
    7. Patient who does not give consent.


Objectives of the study

  1. To document the abnormalities of vestibular system post head injury using electronystagmography
  2. To determine the site of origin of the lesion – peripheral/central
  3. To determine the side of the lesion.



  Results Top


Fifty patients with post head injury vertigo were subjected to electronystagmography. Young adults between the age group of 20 and 30 years were found to be the most common group involved, constituted 34% of the patients. Equal gender predisposition was observed, as shown in [Table 1] [Table 2] [Table 3].
Table 1: Age distribution

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Table 2: Gender distribution

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Table 3: Type of lesion

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Results of butterfly code

1111 ENG code was found to be the most common type followed by 0222 and 0000 seen in 18%, 16%, 16%, respectively. Bilateral peripheral lesion was found to be the most common type followed by 0222 and 0000 seen in 18%, 16%, 16% respectively. Bilateral peripheral lesion was found to be the most common type [Table 4].
Table 4: ENG codes

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Bilateral peripheral lesion was found to be the most common type in 36% cases, followed by central lesion in 22% cases [Figure 3].
Figure 3: Sector plot - distribution of causes of vertigo

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  Discussion Top


Vertigo has been defined as the “sensation of motion when no motion is occurring relative to earth's gravity.”[6]

International classification of diseases define vertigo as a feeling of movement, a sensation as if the external world was revolving around the patient (objective vertigo), or as if he himself was revolving in space (subjective vertigo). Vertigo tends to be recurrent in 88% of cases. In over 80% of cases, it affects their daily lives and leads to sick leave or frequent medical consultations. It can lead to reduced quality of life, psychiatric problems, and occupational problems.[7]

Patients with dizziness often have vague symptoms, determining the cause can be challenging. Knowledge of history, physical examination and radiological findings were used to determine the cause of vertigo, to establish the diagnosis and provide appropriate treatment in most cases.[8],[9]

According to Kushner, the organically conditioned dizziness that occurs after head trauma is usually peripheral rather than central in origin. The late onset of the symptomatology can be explained by the slow degeneration that sets in after concussion. The most frequent peripheral form of vertigo after head trauma is BPPV thought to be due to dislodgment of otoliths from the macula of the utricle. Clinical experience and the most recent literature show that post traumatic paroxysmal positional vertigo (canalolithiasis) is usually unilateral and less frequently bilateral.

However, bilateral BPPV is recognized to have a post traumatic etiology. When canalolithiasis is bilateral, paroxysmal vertigo, and related nystagmus are more pronounced on one side. The symptoms may persist for between a day and up to more than a year. Vestibular dysfunction after labyrinthine concussion has often been ascribed to unilateral microscopic hemorrhages in the labyrinth. Labyrinthine concussion is often manifested by vertigo, nausea, and/or vomiting, but the vestibular examination focuses on pathological nystagmus that occurs spontaneously and is exacerbated during rapid head movements.

In general, labyrinthine concussion resolves through adaptation over a period of weeks or months, a process known as vestibular compensation. While vestibular suppressants dramatically improve the symptoms during the early period after trauma, they generally delay compensation and subsequently recovery.

Loss or reduction of function in a semicircular canal can also lead to peripheral vestibular symptoms. This may be the result of the injury or also occur as a side effect of medication prescribed after head trauma (e.g., ototoxic aminoglycoside antibiotics. Trauma can also cause vertigo by creating a perilymphatic fistula between the middle and inner ear. Rupture of the oval or round windows of the inner ear may lead to the development of a perilymphatic fistula and provoke inappropriate stimulation of labyrinthine receptors. Such fistulas may even occur following minor head trauma or barotraumas (high altitude or underwater), strenuous exercise, suppressed sneezing, or air travel. In general, the symptoms are dizziness, fluctuating hearing loss, ear pressure and tinnitus, chronic nausea and exertional headaches, and their expression depends on head position, movement, or air pressure. A perilymphatic fistula may, in rare instances, heal spontaneously, whereas a chronic perilymphatic fistula has to be corrected surgically.

Acute evolving vertigo may be associated with even mild traumatic brain injury. Frequently, such patients also complain of headache and have difficulty concentrating (post-concussion syndrome). Central vestibular syndromes are mostly due to concussion of vestibular nuclei or central vestibular pathways. Direct traumatic damage to the brainstem or cerebellum may be followed by the occurrence of imbalance and transitional vertigo. All the parts of the brainstem and the cerebellum can be affected, but the mesencephalon is affected more often.

Symptoms of a central origin may include nausea with nonpositional vertigo and imbalance. Up to 50% of patients with mild traumatic brain injury develop a post concussion syndrome) (dizziness, headache, tinnitus, hearing loss, blurred vision, diplopia, anxiety, irritability, depression, emotional lability, a decrease in intentional information processing, and fatigue). These symptoms are attributed to the diffuse microscopic changes that accompany mild concussion, the most common form of closed head injury. Even mild concussion can cause significant attentional and information processing impairments that last for months in the absence of any apparent neurological problem. Animal experiments have shown that minor head trauma can produce petechial cerebral hemorrhages due to distortion forces, especially in the brainstem and the vestibular nuclei.[10]


  Conclusion Top


Head injuries are sustained by 5% of population annually. Post traumatic vertigo refers to giddiness that follows the head or neck injury. In the central nervous system, EEG is used to record the activity of cerebral cortex but has a blind spot in the brainstem as it cannot satisfactorily record the activity there. ENG fulfills this blind spot and records the neurophysiological activities of the brainstem as the vestibular reflex has main connections in the brainstem. Head injury is an important etiological factor in vestibular disorders – peripheral lesions were found to be more common-BPPV, Meniere's were the most common types. Vestibular system is found to be more susceptible to the effects of trauma compared to the cochlea. Nature of vestibular dysfunction is not related to the type/severity of trauma. Patients with vertigo following head injury must be assessed using electronystagmography to identify the lesion for appropriate management.

Vestibular testing of patients with head trauma shows that head trauma may damage the peripheral and central vestibular structures, simultaneously or separately. Many authors support the hypothesis that traumatic brain injury with vestibular symptoms affects both the peripheral and central vestibular structures.

ENG provides an objective record for documentation, tool for teaching, publication, and better patient follow-up. ENG with a thorough history, examination, and radiological tests can aid in timely diagnosis and treatment of vestibular disorders.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Pathak A, Panda N, Mathuriya SN. Department of Neurosurgery, Otorhinolaryngology Postgraduate Institute of Medical Education and Research, Chandigarh: Post head injury vertigo. Indian J Neurotrauma 2007;4:31-3.  Back to cited text no. 1
    
2.
Jennet B. Epidemiology of head injury. J Neurol Neurosurg Psychiatry 1996;60:362-9.  Back to cited text no. 2
    
3.
Sarma AC. Electronystagmography in labyrinthine lesions. J NEBAO HNSI2014;8:19.  Back to cited text no. 3
    
4.
Kirtane MV. Electronystagmography – A systemic approach. In: Biswas A, editors. Clinical Audio Vestibulometry. 4th ed. Kolkata;1982. p. 180-2.  Back to cited text no. 4
    
5.
E Medicine. Available from: http://www. Medscape.com/article.overview/884361. [Last accessed on 2018 Nov 30].  Back to cited text no. 5
    
6.
Thomas S, Cherian A. Vertigo An Overview. IAN Guidelines on Vertigo. Guidelines on Vertigo. Indian Academy of Neurology; 2013. p. 1-6.  Back to cited text no. 6
    
7.
Available from: http://www.icd9.data.com/2012/volumeI/780–799/780–789. [Last accessed on 2018 Nov 30].  Back to cited text no. 7
    
8.
Moulin T, Sablot D, Vidry E, Belahsen F, Berger E, Lemounaud P, et al. Impact of emergency room neurologists on patient management and outcome. Eur Neurol 2003;50:207-14.  Back to cited text no. 8
    
9.
Schappert SM, Nelson C. National ambulatory medical care survey, 1995-96 summary. National centre for health statistics. Vital Health Stat 1999;142:1-122.  Back to cited text no. 9
    
10.
Benson BE, Meyers AD. Post traumatic vertigo : Background Pathophysiology, Epidemiology Available from:https:// e medicine.medscape.com [Last accessed on 2018 Nov 30].  Back to cited text no. 10
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4]



 

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