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by available data and is unlikely, considering the 48-h delay after the bite to a tran-
sient episodic vertigo, followed thereafter in approximately 4 more days by vertigo
and other related vestibular symptoms. The symptoms resulted in an emergency-room
review. These symptoms constitute some of the most common presenting complaints
in general medicine. A well-grounded interpretation of this case requires a carefully
and accurately considered differential diagnosis. The duration of discrete vertiginous
events comprises the foundation for a likely diagnosis.
Vertiginous symptoms and signs are categorized as peripheral or central. These
have been reviewed in detail elsewhere (Fauci et al., 2007), but an important distin-
guishing feature is the paroxysmal onset of vertigo of peripheral etiologies [vestibular
neuronitis, benign paroxysmal positional vertigo (BPPV), cervical vertigo, Ménière's
syndrome, etc.] versus the gradual onset of vertigo from central causes (vertebrobasi-
lar insufficiency, cerebellar, pons or medullary lesions, multiple sclerosis, migraines,
etc.; Chan, 2009; Karatas, 2008; McPhee and Papadakis, 2009). Peripheral vertigo
often includes horizontal nystagmus and may also feature tinnitus and/or some abnor-
mal auditory testing. Central vertigo usually does not cause abnormal auditory testing.
Recommended investigations include MRI of the brain with gadolinium, electronystag-
mography, and videonystagmography.
The authors reported a negative CT of the head (MRI was unavailable in their facil-
ity), an absence of nystagmus, and unremarkable neurological exam, as well as audi-
tory testing (Peichoto et al., 2007a). Although, as the imaging study was not optimal,
there is a chance of an undetected central lesion, the published medical history and
symptoms/signs of the patient suggest that the described course is most likely related
to a vestibular neuronitis. This form of labyrinthitis is often of unknown etiology
and results from a disruption of afferent neuronal input from one of the two vestib-
ular apparatuses. In some cases, a viral etiology has been demonstrated (unspecified
enterovirus; Ergul et al., 2006), while in others it is strongly suspected (adenovirus;
Zannolli et al., 2006). Reactivation of latent herpes simplex-1 in vestibular ganglia may
account for some cases of this syndrome (Gacek, 2008). Paroxysmal vestibular neu-
ronitis (PVN) frequently occurs over several days to a week or two with gradual clear-
ing. In some patients, a brief prodrome occurs days or hours prior to sustained episodes
(Lee et al., 2009). Nystagmus may be present (often it is not) and an absent response
to caloric stimulation is noted. It is not clear if such testing was performed in this case,
although many features of this syndrome are compatible with the history as reported.
Another differential that must be considered is BPPV, which may present simi-
larly to PVN except that it tends to occur in cluster episodes lasting several minutes
or longer, following specifically provoking head movements/position. The etiology
probably is related either to canalithiasis or cupulolithiasis that results in abnormal
stimulation of the crista ampullaris (for details of the proposed pathophysiological
models; see Schuknecht, 1969 and Epley, 1992). Some surgical data lend support to
the canalithiasis theory (Parnes and McClure, 1991). The presentation of BPPV may
be variable and its onset described quite differently by various patients (SAW, per-
sonal observations). Diagnosis may be assisted by response to and/or reproduction of
the transient vertigo by Hallpike, Epley, or Semont canalith repositioning maneuvers.
The transient episode of vertigo experienced by the patient several days prior to the
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