Vertigo

Vertigo refers to hallucination of movement. It is defined as an abnormal perception of movement of the environment or self, and occurs because of conflicting visual, proprioceptive and vestibular information about a person’s position in space. Vertigo commonly arises from imbalance of vestibular input and is within the experience of most people, since this is the ‘dizziness’ that occurs after someone has spun round vigorously and then stops.¹

Vertigo is a cardinal symptom of vestibular disease.

Most patients with vertigo have acute vestibular failure, benign paroxysmal positional vertigo or Ménière’s disease.¹

Frequently accompanied by nausea, postural unsteadiness, and gait ataxia; may be provoked or worsened by head movement.

CLINICAL MANIFESTATIONS

Depending on the frequency and duration of attacks, vertigo can be classified into 3 clinical types:

• Prolonged Spontaneous Attacks of Vertigo

This occurs when due to unilateral loss of vestibular function. The vertigo is acute in onset, may last for days and is aggravated by head movement. The patient prefers to sit upright with the head still or to lie with the intact side down. On movement the patient may fall towards the affected side. The vertigo is associated with nausea, vomiting and malaise. This type of vertigo may be peripheral or central. Common causes of this type of vertigo include acute labyrinthine/vestibular dysfunction due to infection, trauma or ischemia, brainstem or cerebellar infarction/hemorrhage, multiple sclerosis and brainstem tumors/vascular malformations.²

• Recurrent Spontaneous Attacks of Vertigo

The vertigo is sudden, temporary and reversible due to impairment of labyrinthine function. The vertigo of vascular origin like transient ischaemic attacks (TIA) lasts for minutes, whereas, that due to disease of the inner ear may last for hours. The common causes of recurrent spontaneous vertigo include Meniere’s disease, autoimmune inner ear disease, syphilitic labyrinthitis and vertebro-basilar TIA.²

• Recurrent Positional Vertigo

Positional vertigo is precipitated by the movement of the head either to the right or to the left from the recumbent position, triggering the vestibular pathway. The peripheral type of positional vertigo is more common than that of central origin.²

Benign Paroxysmal Positional Vertigo (BPPV)

BPPV is characterized by sudden onset of a peripheral vestibular syndrome with no auditory component. The vertigo occurs when the patient rolls to the side on lying down, or while gazing upwards, or bending forwards. The episode lasts for 10 to 20 seconds. BPPV occurs in bouts lasting for a few days or weeks and may recur after several weeks or months. BPPV can be caused by head injury, stapes surgery, otitis media, labyrinthine ischemia and viral infection of the ear. Occasionally, the cause is not obvious. The diagnosis is confirmed by standard positional testing test (Dix-Hallpike test).^{2 and 3}

TYPES OF VERTIGO

Peripheral Vertigo

Usually severe, accompanied by nausea and emesis. Tinnitus, a feeling of ear fullness, or hearing loss may occur. A characteristic jerk nystagmus is almost always present. The nystagmus does not change direction with a change in direction of gaze; it is usually horizontal with a torsional component and has its fast phase away from the side of the lesion. It is inhibited by visual fixation. The patient senses spinning motion away from the lesion and tends to have difficulty walking, with falls toward the side of the lesion, particularly in the darkness or with eyes closed. No other neurologic abnormalities are present.^{2and 3}

Central Vertigo

Identified by associated brainstem or cerebellar signs such as dysarthria, diplopia, dysphagia, hiccups, other cranial nerve abnormalities, weakness, or limb ataxia; depending on the cause, headache may be present. The nystagmus can take almost any form (i.e., vertical or multi directional) but is often purely horizontal without atorsional component and changes direction with different directions of gaze. Central nystagmus is not inhibited by fixation. Central vertigo may be chronic, mild, and is usually not accompanied by tinnitus or hearing loss. It may be due to vascular, demyelinating, neurodegenerative, or neoplastic disease. Vertigo may be a manifestation of migraine or, rarely, of temporal lobe epilepsy.^2and3

Psychogenic Vertigo

The vertigo develops gradually, increasing with associated anxiety and terminates abruptly. Organic vertigo occurs

Abruptly and disappears gradually. Psychogenic vertigo is sometimes called phobic postural vertigo, associated with panic attacks or agoraphobia (fear of large open spaces or crowds).The vertigo is not associated with nystagmus or vomiting. Most patients adapt to being ‘house-bound’, whereas inorganic vertigo patients attempt to function in spite of theincapacity.^2and3

VERTIGO MAY BE DUE TO PHYSIOLOGICAL OR PATHOLOGICAL CAUSES²

Physiological vertigo is seen in normal individuals with unfamiliar head movements, unusual head and neck position or following spinning.²

Pathological vertigo results from lesions of the visual, somatosensory or vestibular system. Visual vertigo is caused by incorrect eye-glasses, and extra-ocular muscle paresis. Somatosensory vertigo is due to myelopathy or peripheral neuropathy and is rarely seen in isolation.²

The most common cause of pathological vertigo is vestibular dysfunction. If may involve the end organ (labyrinth), the nerve or central connections. Vertigo is associated with jerk nystagmus frequently accompanied by nausea, postural unsteadiness and gait ataxia.²

APPROACH TO THE PATIENT

Vestibular dysfunction is demonstrated by a simple ‘headshaking nystagmus test’. The patient is asked to close his eyes and bend his head down 30°. The head is oscillated horizontally 20 times. Elicitation of nystagmus after the manoeuvre suggests vestibular imbalance. Further evaluation of vestibular dysfunction is essential to determine the side of the lesion, the type of lesion and to distinguish central from peripheral lesions. The standard tests include head thrust test, Dix-Hallpike test and electro-nystamography. If a central aetiology is suspected, MRT is mandatory.²

MANAGEMENT OF VERTIGO

Treatment of acute vertigo consists of bed rest for 1 to 2days and use of anti-vertiginous drugs. These drugs give

Symptomatic relief in acute vestibulopathy (Meniere’s syndrome, vestibular neuritis), acute brain-stem lesions near the vestibular nuclei and prevent motion sickness. These are also used in frequent attacks of vertigo, vomiting and severe BPPV. Surgical procedures like labyrinthectomy, and section of 8th nerve are used in selected patients. In chronic and recurrent vertigo, exercises which provoke vertigo may be tried in order to habituate the patient. Patients who are refractory to conventional therapy may benefit from a formal rehabilitation programme, habituation customized programme and use of instruments, like tilt tables.²

SCOPE OF HOMEOPATHY

Homeopathic literature has a great deal of data which covers symptoms of vertigo and can play an important role in management of vertigo. Oral Homeopathic medicines aid to resolve the symptoms of vertigo. There are medicines especially targeting the labyrinth inflammation. Finding the correct cause is an important aspect of vertigo management. Response to homeopathic medicines is usually very fast and relief is long lasting.

MEDICINES FOR VERTIGO⁴