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 pt 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.

Acute prolonged vertigo may be caused by infection, trauma, or ischemia. Often no specific etiology is found, and the term acute labyrinthitis (or vestibular neuritis) is used to describe the event. Acute bilateral labyrinthine dysfunction is usually due to drugs (aminoglycoside antibiotics), alcohol, or a neurodegenerative disorder. Recurrent labyrinthine dysfunction with signs and symptoms of cochlear disease is usually due to Ménière's disease (recurrent vertigo accompanied by tinnitus and deafness). Positional vertigo is usually precipitated by a recumbent head position; benign paroxysmal positional vertigo (BPPV) of the posterior semicircular canal is particularly common; the pattern of nystagmus is distinctive. BPPV may follow trauma but is usually idiopathic; it generally abates spontaneously after weeks or months. Vestibular schwannomas of the eighth cranial nerve (acoustic neuroma) usually present with hearing loss and tinnitus, sometimes accompanied by facial weakness and sensory loss due to involvement of cranial nerves VII and V. Psychogenic vertigo should be suspected in pts with chronic incapacitating vertigo who also have agoraphobia, panic attacks, a normal neurologic examination, and no nystagmus.