19. reported similar results: of 29 patients with vertebrobasilar peduncle, and anterior inferior cerebellum including the floc-
insufficiency, 21% had episodic vertigo for at least 4 weeks culus.9 Since AICA always supplies the lateral pontine teg-
as the only presenting symptom.5 I recently reported three pa- mentum and middle cerebellar peduncle, AICA territory in-
tients with anterior inferior cerebellar artery (AICA) infarction farcts usually involve the brainstem and are virtually never
who experienced isolated episode of recurrent vertigo, fluctu- limited to the cerebellum itself whereas infarcts in the territory
AICA 塞による急性前庭神経障害
ating hearing loss, and/or tinnitus (similar to MeniereMs dis- of the PICA or SCA usually involve only the cerebellum.
ease) as initial symptoms 1-10 days prior to the infarction. 6 There are common anatomic variants, in which AICA domi-
All of these data suggested that isolated episodic vertigo with nance on one side and PICA dominance on the opposite side
or without auditory symptom can be the only manifestation are commonly seen in normal person. At times either the AI-
of transient ischemia within the vertebrobasilar circulation. CA or PICA is absent or hypoplastic, in which case one AI-
Isolated vertigo especially can occur when there is a stenosis CA-PICA supplies the usual territory of both arteries. The in-
AICAは前庭神経 末梢, 中枢双方へ栄養している血管. of the caudal or middle portion of the basilar artery (presuma-
bly close to the AICA origin) or widespread slow vertebroba-
ternal auditory artery (IAA) is a usual branch of AICA and
supplies the eight cranial nerve, the cochlea and vestibular
silar flow on MRA.4,6 However, it is still unclear whether iso- labyrinth. In terms of collateral circulation, in addition to the
脳底動脈下半分より起始し, 内耳, 橋側面, 中脳脚, 小脳の前下部を栄養.
lated episodic vertigo originate from the brain or the inner ear.
When isolated vertigo occurs in transient ischemia of the pe-
dorsolateral pons and middle cerebellar peduncle, which are
known to be sensitive to ischemia, inner ear is also particular-
ripheral vestibular labyrinth,1 the superior part of the vestib- ly vulnerable to ischemia since it is supplied entirely by the
AICA 塞は殆どが脳幹を含み, 小脳に限局することは先ず無い.
ular labyrinth may selectively be vulnerable to ischemia, pos- IAA that is an end artery with minimal collaterals from the
sibly due to the small caliber of the anterior vestibular artery otic capsule and has complete absence of collateral circula-
PICA, SCA領域の 塞では小脳に限局することがある.
(AVA) and little collateralization.7 Patients with AVA infarc- tion.1,10,11 By contrast, the retrocochlear eight nerve has an
tion may subsequently develop typical episodes of benign par- abundant collateral blood supply arising from the lateral med-
oxysmal positional vertigo; these have been ascribed to is- ullary artery, the arteries supplying the adjacent dura matter
内耳動脈はAICAから分岐する動脈であり, chemic necrosis of the utricular macule and release of otoco- and the petrous bone, and the inferior lateral pontine artery.12-14
nia into the posterior canal. Since the posterior canal is suppli- A typical pattern of AICA territory infarction on brain MRI
前庭神経, 核, 内耳への血流支配はAICAが強く関連.ed by the posterior vestibular artery, a branch of the common is shown in Fig. 1.
cochlear artery, it may be spared in AVA infarction.7,8 Although
迷路 塞はAICA 塞の重要な所見の1つ. isolated episodic vertigo can occur as a manifestation of ver-
tebrobasilar insufficiency, long-lasting (>6 months) recurrent
episodes of vertigo without other symptoms are almost never
AICA 塞11/12(92%)で迷路 塞を合併.
caused by vertebrobasilar disease.
Three Cerebellar Ischemic
内耳動脈 塞は殆どがAICA, 脳底動脈の
Stroke Syndromes
動脈硬化による生じる.are three major cerebellar arteries: the posterior inferior
There
cerebellar artery (PICA), the AICA, and the superior cerebel-
lar artery (SCA). After supplying branches to the brainstem,
each of these arteries supplies the part of the cerebellum in-
dicated by its name.
Acute vestibular Clin Neurol 2009;5:65-73
J syndrome due to anterior inferi-
or cerebellar artery territory cerebellar infarction
24. bone-conducted signals in an acoustic booth. The pure-tone average latencies and interpeak latencies. middle cerebellar peduncle
also showed that the
was obtained by averaging hearing thresholds at 500, 1000, and 2000 We defined hearing loss of cochlear origin as Six days later,
and dorsolateral pons were spared. follows13–17: (1)
Hz. A pure-tone average Ͼ25 dB was regarded as indicative of axial T2-weighted (C) and diffusion-weighted (D)
speech recognition scores corresponded well with the increasing
hearing loss. Mild, moderate, severe, and profound hearing loss was MRI of the brain demonstrated hyperintense foci
hearing thresholds on PTA; (2) despite the hearing loss on PTA, the
defined as 26 to 40, 41 to 70, 71 to 90, and Ͼ90 dB, respectively. We in the left middle cerebellar peduncle, left dorso-
ABR showed no abnormalities or delay in absolute latencies of all
performed additional tests to discriminate between neural and lateral pons, and ventral pons.
waves, but interpeak latencies of wave I-III-V were within normal
AICA 塞と難聴
cochlear causes of hearing loss. Speech discrimination testing was limits; and (3) stapedial reflex testing showed normal reflex thresh-
done with AB Wordlists according to the Korean Hearing Services olds. Vestibular function tests were performed by a computer-based
standard protocol. The stapedial reflex thresholds of each ear at electronystagmography (ENG) system (Nicolet ENG system) and
frequencies of 500, 1000, 2000, and 4000 Hz were measured. included examination of oculomotor movements (saccade, smooth
Measurements of stapedial reflex were performed with a GSI 33 Stroke. 2002;33:2807-2812
pursuit, and optokinetic nystagmus), spontaneous and gaze-evoked
Middle Ear Analyzer, which allows determination of stapedial reflex nystagmus, and caloric responses. All neurotologic evaluations were
12例のAICA 塞 + 突然発症の難聴症例のReview
thresholds up to the 110-dB hearing level. The activating stimuli
Illustrative Cases steps ipsilateral to the examined ear. Reflex
were presented in 5-dB
ness. Ten days before, she had 3 episodes of transient
performed during the acute period.
Case 1: Patient 10 Withthe lowest activatorUnilateral
threshold was defined as Cochlear-Type level that resulted in an left-sided tinnitus and hearing loss lasting a few minutes. One
observable meter deflection.
Hearing Loss
Results
day before, she had 2 episodes of transient isolated vertigo
最も多い責任病変は中小脳脚(11/12). lasted no more than several minutes. On neurologic
A 60-year-old woman with type 2was performed on 12 patients
Auditory brainstem response (ABR) diabetes mellitus and all that
Clinical Features
(Medelec ER94a) with previously described techniques. Rarefac-
回転性めまい, 眼振は全例で合併. examination, she wereafemale; 5 patients were male. Clinical
hypertension developed the sudden onset of vertigo, nausea,
tion click stimuli were used. For ABR, the auditory stimulation was
Seven patients had spontaneous right-beating horizontal
vomiting,ofand hearing loss insoundleft side. presented monaurally
a click 0.1-ms-long, 90-dB the that was On examination, nystagmus with aof admission are summarized component and
data at the time counterclockwise torsional in Tables 1 in
she had aof 10 Hz,4/12で2d-2moの間に前駆症状としてのめまい, 難聴の報告あり.
at a rate spontaneous right-beating horizontal nystagmus
and broadband masking (40 dB less intense than primary and rightward gaze, which changed to a left-beating
2. All patients were alert and orientated on admission.
with a counterclockwise torsional component in primary horizontal nystagmus with a clockwise torsional component
position and Classic featuresthe AICA Infarction* and showed a 12
TABLE 2. with gaze to of right or left. PTA Findings in Patients
on leftward gaze. There were diminished left facial sensation,
moderate sensorineural hearing loss of 50 dB on the left side. left limb dysmetria, and gait ataxia. MRI of the brain
Patient
Stapedial reflexes were recorded at normal levels from both demonstrated hyperintense lesions on axial T2-weighted im-
sides. Speech discrimination scores were 85%Involved left side. 1
Signs and Symptoms Structures Possibly on the 2 3 4 5 6 7 8 9 10 11
ages situated in the left middle cerebellar peduncle and left 12
Normal waveform responses were vestibular bilaterally on ABRϩ
Vertigo, nystagmus Labyrinth,
evoked nerve, vestibular ϩlateral pons (Figure 2). PTA showed a ϩ
ϩ ϩ ϩ ϩ ϩ ϩ mild (40 dB)ϩ
ϩ senso-
ϩ
testing. ENG showed no response to caloric stimulation of the
nuclei, flocculus rineural hearing loss on the left side even though she did not
left side. Axial T2- and diffusion-weighted MRI of nucleibrainϩ
Tinnitus, hearing loss Cochlea, auditory nerve, cochlear
the ϩcomplain of decreased hearing in the ϩ side during the
ϩ ϩ ϩ ϩ ϩ ϩ left ϩ Ϫ ϩ
showed a small infarct in the left ventrolateral pons, but the attack of vertigo.ϩSpeech discrimination ϩ scoresϩwere 30% on
Gait and limb ataxia MCP, anterior inferior cerebellum ϩ ϩ ϩ ϩ ϩ ϩ ϩ ϩ ϩ
middle cerebellar peduncle and dorsolateral pons were appar- the left side and ϩ on the Ϫ
90% Ϫ right ϩ
side. No stapedial reflexes
ently spared. Brain MRA Spinal trigeminal tract, nucleus
Facial hemianesthesia showed moderate stenosis ofϩ ϩ Ϫ Ϫ ϩ ϩ Ϫ
were elicited from the left side. On ABR testing, no responses
Ϫ
the middle third of the basilar artery. fascicle
Facial paralysis Facial nerve Low-dose aspirinϩ Ϫ Ϫ Ϫ ϩ Ϫ Ϫ Ϫ ϩ Ϫ
were evoked by stimulation on the left side, whereas there
Ϫ Ϫ
(100 mg)sensory signs started. The hearing loss persisted, butϪ
Crossed therapy was Spinothalamic tract Ϫ
were Ϫnormal waveforms on Ϫ right side (Figure 3). ENG
Ϫ ϩ Ϫ
the Ϫ ϩ Ϫ Ϫ Ϫ
the vertigo improved steadily over a few days. Six days afterϪ
Horner’s syndrome Sympathetic fibers Ϫshowed noϪresponse to caloric stimulation ofϪ left side.
Ϫ ϩ Ϫ Ϫ Ϫ ϩ the Ϫ Ϫ
the initial onset of hearing losspeduncle. side and vertigo, the
MCP indicates middle cerebellar in the left
patient complained1 of an exacerbation of AICA infarction. com-
*Based on Adam’s clinicopathological study of the vertigo,
25. disappearance. All patients with acute auditory syndrome
also had transient vertigo lasting a few minutes, consistent inferior pontine infarction who presented w
with a transient ischaemic attack in the vertebrobasilar deafness, facial palsy, Horner’s syndrome, and
circulation.9 Furthermore, the tinnitus preceding the infarc- 2002, Toyoda et al reported two patients with
tion was identical to that experienced at the time of occlusion who had bilateral hearing loss as a wa
infarction, and isolated vertigo preceding the infarction was an impending stroke.19 No large consecutive clin
identical in quality to the vertigo experienced at the time of AICA infarction has focused on an acute audito
AICA 塞の前駆症状, 前兆として, infarction. as a warning sign of impending infarction.
Most previous reports of an isolated neuro-otological It is well recognised that the tinnitus is a v
symptom as a manifestation of vertebrobasilar insufficiency complaint, not only in association with deafnes
have focused on the acute vestibular symptom of vertigo.10–17 individuals with normal hearing, and it is not u
一過性の耳鳴, 難聴を認める例も報告されている. There have been few reports of an acute auditory syndrome
as an initial manifestation of vertebrobasilar insufficiency. In
as a warning sign of an impending stroke. How
the episodes of tinnitus, the patient No 2 also c
1981, Stephan et al described a patient with sudden bilateral episodic vertigo lasting a few minutes, which
hearing loss caused by basilar artery occlusion who later duration of ischaemia within the posterior
中小脳脚の 塞で多い. developed multiple brain stem dysfunctions with quadriple-
gia and mental change.6 In 1993, Huang et al described seven
Furthermore, the quality of tinnitus was ide
tinnitus experienced at the time of infarction.
patients with sudden bilateral hearing loss caused by It was surprising that all the patients had
同部位では前庭神経症状が主に生じる vertebrobasilar occlusive disease.7 Six had an acute auditory paresis to caloric stimulation yet an incomplete
1646
Figure 3 Magnetic resonance imaging findings in patient 5 with episodic prodromal unilateral hearing loss and tinnitus. (A) T2 weigh
of the brain shows a hyperintense lesion situated in the right middle cerebellar peduncle and right dorsolateral pons. (B) Magnetic r
angiography shows proximal basilar artery stenosis close to the origin of the anterior inferior cerebellar artery.
J Neurol Neurosurg Psychiatry 2003;74:1644–1648
25
![DIZZINESSの原因
South Med J. 2000 Feb;93(2):160-7
• 12 trialのMeta-analysis (primary care 2, ER 4, Referral center 6)
• 12 trials, N=4536での解析. 原因 頻度
Peripheral vestibular BPPV 16%[4-44]
• 末梢性前庭神経症状 44%, 迷路炎 9%[3-23]
メニエール病 5%[0-10]
中枢性前庭神経症状 11%,
その他(薬剤など) 14%[0-30]
精神疾患 16%,
Central vestibular 脳血管疾患 6%[0-20]
その他 39% 脳腫瘍 <1%[0-6]
その他(MS, 片頭痛) 3%[0-12]
Psychiatric 精神疾患 11%[2-26]
過換気症候群 5%[0-24]
非前庭N, 非精神 Presyncope 6%[0-16]
平衡障害 5%[0-15]
その他 13%[0-53]
不明 不明 13%[0-37]](data:image/gif;base64,R0lGODlhAQABAIAAAAAAAP///yH5BAEAAAAALAAAAAABAAEAAAIBRAA7)