Vertigo Research Paper

Vertigo, in itself, does not refer to one disease, but is rather a symptom of many and varied disorders. It is one of the most common presented complaints, with an estimated 30% lifetime prevalence. A survey of over 30,000 persons showed that the frequency of vertigo as a function of age lies around 17% and rises up to 39% in those over 80 years of age (Neuhauser, 2007; Neuhauser et al, 2008). Vertigo is defined as the sensation of rotational motion in stationary individuals. In healthy individuals, motion is processed via three main sensory inputs: visual, vestibular (inner ear) and somatosensory. These collective signals are continuously processed in the brain to create an approximation of spatial orientation. The vestibular apparatus includes
Drugs that act on the vestibular apparatus have many cellular targets. These targets are involved in such processes as the homeostasis of liquids and electrolytes in the inner ear, and in the modification of sensory processes including mechanoelectrical transduction in hair cells and the postransductional processing of sensory information (Hain & Uddin, 2003). It is generally believed that vestibular suppressants act on the neurotransmitters responsible for carrying the vestibular signal from primary vestibular neurons. That is, these drugs seek to block the conduction of impulses from the semicircular canals and otolith organs, before these nerve impulses reach central vestibular structures (Smith & Darlington, 1996). The vestibulo-ocular reflex is a reflex eye movement, which is imperative in the control of balance. It functions to stabilize images on the retinas. Six primary neurotransmitters have been identified between the three-neuron arc that drives the vestibulo-ocular reflex (VOR) (Halmagyi, 2003; Itoh & Sakata, 1991) . These include: Glutamate, which maintains the resting discharge of the central vestibular neurons, and may control synaptic transmission in all three neurons of the VOR arc; acetylcholine, which appears to function as an excitatory neurotransmitter in both the peripheral and central synapses and gamma-Aminobutyric acid (GABA), which is believed to be inhibitory
The primary control of nausea and vomiting arises from the vomiting centre, located in the medulla. There are five primary pathways involved in stimulating the vomiting centre. These are: the chemoreceptor triggering zone, the vagal mucosal pathway in the gastrointestinal system, neuronal pathways from the vestibular system, reflex afferent pathways from the cerebral cortex and midbrain afferents (Miller, 1999). Stimulation of one of these afferent pathways can activate the vomiting centre through cholinergic, dopaminergic, histaminergic, or serotonergic receptors. Vomiting can also be induced by chemicals carried in the blood that are detected by the chemosensitive trigger zone (CTZ), an area of the medulla oblongata that receives inputs from hormones in the blood. This is potentially exploitable, as the CTZ is functionally outside the blood–brain barrier. Animal studies have shown that the area contains high concentrations of 5-HT3, and dopamine (D2). In humans, drugs acting as antagonists at these receptors help to ease nausea and vomiting. These are called antiemetic drugs (Aapro,et al,