Depression or anxiety that the condition will worsen or progress to Menieres disease.As with Menieres disease, atypical, early, or mild cases may only present some symptoms. Diagnosis
Diagnosis is based on symptoms and a hearing test that documents a loss in the low and mid frequencies, usually only in one ear. For patients with mild or atypical hydrops, the hearing thresholds may be normal, but they may experience a subjective, unilateral distortion of sounds in lower frequencies, such as diplacusis or that voices are sounding "robotic". Patients may also mention a feeling of pressure or fullness in the ear.To objectively test for the presence of hydrops, an electrocochleography (or ECOG) procedure can be done to detect elevated inner ear pressure. It is also possible to reveal the presence of hydrops with an MRI.If vertigo is experienced, the diagnosis progresses to Menieres disease. This occurs if the fluid increase leads to a leak or rupture of the membranes in the inner ear, causing a mixture of perilymph and endolymph. Treatment
Treatment for cochlear hydrops is the same as for Menieres disease. Currently, no cure exists for either.If a patient has undergone sudden sensorineural hearing loss, a course of steroids is often prescribed in an attempt to recover the hearing. Steroids may be injected directly through the eardrum.Like Menieres Disease, a low salt diet is recommended as a preventative measure. A diuretic may be prescribed to help lower salt content.Betahistine is the most widely prescribed medication for the treatment of Menieres disease.
Pharmacology
The activity profile of pramipexole at various sites has been characterized as follows:

While pramipexole is used clinically (see below), its D3-preferring receptor binding profile has made it a popular tool compound for preclinical research. For example, pramipexole has been used (in combination with D2- and or D3-preferring antagonists) to discover the role of D3 receptor function in rodent models and tasks for neuropsychiatric disorders. Of note, it appears that pramipexole, in addition to having effects on dopamine D3 receptors, may also affect mitochondrial function via a mechanism that remains less understood. A pharmacological approach to separate dopaminergic from non-dopaminergic (e.g. mitochondrial) effects of pramipexole has been to study the effects of the R-stereoisomer of pramipexole (which has much lower affinity to the dopamine receptors when compared to the S-isomer) side by side with the effects of the S-isomer.Parkinsons disease is a neurodegenerative disease affecting the substantia nigra, a component of the basal ganglia. The substantia nigra has a high quantity of dopaminergic neurons, which are nerve cells that release the neurotransmitter known as dopamine. When dopamine is released, it may activate dopamine receptors in the striatum, which is another component of the basal ganglia. When neurons of the substantia nigra deteriorate in Parkinsons disease, the striatum no longer properly receives dopamine signals. As a result, the basal ganglia can no longer regulate body movement effectively and motor function becomes impaired.