It occurs in 0.6% of the population yearly with 10% having an attack during their lifetime. It is believed to be due to a mechanical malfunction of the inner ear. BPPV may be diagnosed with the Dix-Hallpike test and can be effectively treated with repositioning movements such as the Epley maneuver. Ménières disease
Ménières disease is an inner ear disorder of unknown origin, but is thought to be caused by an increase in the amount of endolymphatic fluid present in the inner ear (endolymphatic hydrops). However, this idea has not been directly confirmed with histopathologic studies, but electrophysiologic studies have been suggestive of this mechanism. Ménières disease frequently presents with recurrent, spontaneous attacks of severe vertigo in combination with ringing in the ears (tinnitus), a feeling of pressure or fullness in the ear (aural fullness), severe nausea or vomiting, imbalance, and hearing loss. As the disease worsens, hearing loss will progress. Labyrinthitis
Labyrinthitis presents with severe vertigo with associated nausea, vomiting, and generalized imbalance and is believed to be caused by a viral infection of the inner ear, although several theories have been put forward and the cause remains uncertain. Individuals with vestibular neuritis do not typically have auditory symptoms, but may experience a sensation of aural fullness or tinnitus. Persisting balance problems may remain in 30% of people affected. Vestibular migraine
Vestibular migraine is the association of vertigo and migraines and is one of the most common causes of recurrent, spontaneous episodes of vertigo.
The high prevalence of diabetes mellitus type 2 and hypertension in Afro-Caribbeans in the West could be directly related to the incidence of G6PD deficiency in those populations.Although female carriers can have a mild form of G6PD deficiency (dependent on the degree of inactivation of the unaffected X chromosome – see lyonization), homozygous females have been described; in these females there is co-incidence of a rare immune disorder termed chronic granulomatous disease (CGD). Diagnosis
The diagnosis is generally suspected when patients from certain ethnic groups (see epidemiology) develop anemia, jaundice and symptoms of hemolysis after challenges from any of the above causes, especially when there is a positive family history.Generally, tests will include:
Complete blood count and reticulocyte count; in active G6PD deficiency, Heinz bodies can be seen in red blood cells on a blood film;
Liver enzymes (to exclude other causes of jaundice);
Lactate dehydrogenase (elevated in hemolysis and a marker of hemolytic severity)
Haptoglobin (decreased in hemolysis);
A "direct antiglobulin test" (Coombs test) – this should be negative, as hemolysis in G6PD is not immune-mediated;When there are sufficient grounds to suspect G6PD, a direct test for G6PD is the "Beutler fluorescent spot test", which has largely replaced an older test (the Motulsky dye-decolouration test). Other possibilities are direct DNA testing and/or sequencing of the G6PD gene.The Beutler fluorescent spot test is a rapid and inexpensive test that visually identifies NADPH produced by G6PD under ultraviolet light. When the blood spot does not fluoresce, the test is positive; it can be falsely negative in patients who are actively hemolysing.