NEUROLOGICAL SIGN

Auditory hallucination in basilar
occlusion: I heard it was the basilar
Siew Mei Yap,1 Gerald Wyse,2 J Nicholas P Higgins,3 Eoin O’Brien,4
Simon Cronin1,5

1

Department of Neurology, Cork
University Hospital, Cork, Ireland
2
Department of Radiology, Cork
University Hospital, Cork, Ireland
3
Department of Radiology,
Addenbrooke’s Cambridge NHS
University Hospital, Cambridge,
UK
4
Department of Stroke Medicine,
Addenbrooke’s Cambridge NHS
University Hospital, Cambridge,
UK
5
Department of Clinical
Neuroscience, College of
Medicine and Health, University
College Cork, Cork, Ireland
Correspondence to
Dr Simon Cronin, Department of
Neurology, Cork University
Hospital, Cork, Ireland; simon.
cronin@hse.ie
Accepted 4 November 2015

To cite: Yap SM, Wyse G,
Higgins JNP, et al. Pract
Neurol Published Online First:
[ please include Day Month
Year] doi:10.1136/
practneurol-2015-001189

ABSTRACT
Acute basilar artery occlusion is a neurological
emergency. Unlike anterior circulation stroke
presenting with hemiparesis, the symptoms of
basilar artery occlusion are challenging to
recognise in the emergency setting. Basilar artery
occlusion can rarely lead to ischaemia of the
auditory pathways, resulting in bizarre, positive
auditory hallucinations. Here, we report two
cases of basilar artery occlusion presenting with
positive auditory phenomena; in both cases the
auditory phenomenon resolved upon arterial
recanalisation. We discuss the phenomenology of
this unusual and distinctive neurological
symptom. Acute auditory hallucinosis in the
setting of sudden vomiting, dizziness, visual
disturbance or other posterior circulation
symptoms should prompt emergency imaging of
the basilar artery, to avoid a potentially
devastating posterior circulation stroke.

CASE 1
A woman in her 30s, partially awake, was
startled by ‘the sudden sound of war’—her
description of a dramatic and persisting
auditory hallucination. In addition, she
had severe ataxia, diplopia and right face
and limb weakness. A family member
found her 2 h later and a thrombolysis call
was made to the stroke team 40 min after
that. On examination, she was anxious,
nauseated, kept her eyes shut and complained persistently of the ‘deafening
noise’; there was a right homonymous
hemianopia, impaired upgaze of the right
globe, nystagmus of the left globe on
attempted upgaze, left hypertropia, leftsided ataxia and right spinothalamic
sensory loss. Non-contrast CT scan of the
head was normal but CT angiogram of the
intracranial and extracranial vessels
showed occlusion of the upper third of the
basilar artery (figure 1A, B). There was no
evidence of vertebral dissection. We proceeded to emergency intra-arterial intervention with thrombectomy. Subsequently,

we retrieved a thrombus ‘cast’ of the
basilar and bilateral posterior cerebral
arteries (figure 1C, D); the ‘sound of war’
immediately stopped.
Pathological examination of the cast
confirmed ‘red thrombus’. Twenty-four
hour Holter monitor showed no arrhythmia. Thrombophilic and vasculitic screens
were negative. A transoesophageal echocardiogram showed a large patent foramen
ovale with associated atrial septal aneurysm. We prescribed warfarin and had an
implantable loop recorder placed. She
spent several weeks in the rehabilitation
unit and her vision, strength and sensation
improved tremendously. Her diplopia corrected with prism glasses. She returned to
work within 3 months and the ‘sound of
war’ did not return.
CASE 2
A 64-year-old woman with type 2 diabetes mellitus presented to the emergency
department having awoken with a ‘loud,
devastating noise’ in her left ear. She
noted dimming of vision bilaterally, dysarthria and left-sided paraesthesia. The
loud auditory phenomenon remained
continuous and severe for 2 h, then spontaneously resolved. The other neurological signs disappeared over the next
hour and she recovered completely.
Although her symptoms had resolved, we
requested
urgent
CT angiography,
prompted by the striking similarity of the
described auditory phenomenon to that in
case 1. This showed non-occlusive thrombus causing a 60% stenosis of the mid
section of the basilar artery (figure 2A,B).
In addition, there was atherosclerotic
occlusion of the left vertebral artery from
its origin to the V3 segment. Presumably,
the basilar itself had been occluded when
symptomatic, but had now partially recanalised. We monitored her in the intensive
care unit, and treated her with fluids,

Yap SM, et al. Pract Neurol 2015;0:1–4. doi:10.1136/practneurol-2015-001189

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Figure 1 Basilar artery occlusion. (A) CT angiogram reconstruction of the intracranial circulation, showing occlusion at the top of
the basilar (black arrow). (B) Angiogram showing tapering and occlusion of the basilar artery with absence of blush from the superior
cerebellar artery and posterior cerebral artery territories. (C) Injection post-thrombectomy confirms recanalisation with normal arterial
blush. (D) The removed ‘thrombus cast’ of the basilar artery and bilateral posterior cerebral arteries.

therapeutic dose low molecular weight heparin and
dual antiplatelet therapy (aspirin and clopidogrel)
aiming to avert re-occlusion of the basilar. She had no
further neurological events. After 72 h, a repeat CT
angiogram showed complete resolution of the thrombus within the basilar artery (figure 2C, D), although
the left vertebral artery remained occluded.
MR scan of the brain showed a small area of subacute infarction in the right cerebellar hemisphere
(figure 2E). A transoesophageal echocardiogram
showed a patent foramen ovale with an atrial septal
aneurysm. Her thrombophilia screen was normal.
During 4 days of cardiac monitoring there was no
atrial fibrillation. She was discharged well and the
‘loud devastating noise’ did not return.
DISCUSSION
Basilar artery occlusion is a neurological emergency
which, untreated, may lead to particularly devastating
stroke syndromes including the ‘locked in’ state.
Unfortunately, the clinical signs in basilar artery occlusion (hemianopia, ataxia, sensory loss, vomiting) are
not as intuitively recognisable as stroke symptoms
when compared with the FAST (Face Arm Speech
Test) positive picture of an acute middle cerebral
artery syndrome. Rapid recognition of basilar artery
occlusion is key to emergency recanalisation. Here,
we add to reports of an important but

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underappreciated clinical symptom in basilar artery
occlusion—acute onset auditory hallucinations.
The auditory phenomena described in the above
case histories, that is, ‘the sound of war’, ‘loud devastating noise’ may be labelled as auditory hallucinations.1 A hallucination is defined as ‘a perception in
the absence of external stimulus that has qualities of
real perception’. Cogan (1973) categorised neurogenic hallucinations into irritative and release
forms.2
▸ Irritative forms are caused by abnormal electrical discharges in the brain secondary to an insult such as
migraine, epilepsy and tumour formation.
▸ Release forms are associated with spontaneous activity of
the cells of the particular sensory pathway involved that
may occur secondary to peripheral sensory deprivation,
or a central negative event such as cerebral ischaemia.

There are two main hypotheses to explain the generation of auditory release hallucinations.3 They may
result from interruption of signals passing along
central auditory pathways, depriving higher auditory
areas of their normal input and resulting in compensatory overactivity in these areas. Alternatively, they may
result from interruption of descending inhibitory
feedback pathways within the auditory system. The
more familiar visual analogues are peduncular hallucinosis, described in 1922 by Lhermitte as visual hallucinations secondary to an infarct in the midbrain and
pons; and the Charles Bonnet syndrome, which is the
Yap SM, et al. Pract Neurol 2015;0:1–4. doi:10.1136/practneurol-2015-001189

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Figure 2 Basilar artery thrombus. CT angiogram of the head, imaged hours following spontaneous resolution of auditory
hallucinations. (A and B) There is non-occlusive thrombosis of the basilar artery seen in sagittal (A, white arrow) and axial (B, black
arrow) cuts. (C and D) CT angiogram after 72 h of medical management shows resolution of the thrombus and restoration of the
normal calibre of the basilar artery lumen. (E) MRI fluid-attenuated inversion recovery sequence at 1 week showing established right
cerebellar infarct.

experience of complex visual hallucinations in person
with significant visual loss due to bilateral ocular or
anterior visual pathway lesions.
A handful of case reports in the literature have
described auditory hallucinations as a result of ischaemic lesions of brain tissue confirmed radiologically or
pathologically.3–5 Like our cases, many of the descriptions involve elementary, unstructured auditory phenomena such as ringing, buzzing, roaring, etc. For
example, Galtrey et al4 described a 60-year-old man
with fluctuating midbrain ischaemia from basilar
artery thrombosis who reported hearing ‘white noise’.
Fischer and Tapia described a 71-year-old woman
reporting intermittent ‘roaring’ in the left ear at the
onset of a pontomedullary stroke.5 However, occasional stroke patients have reported complex structured auditory hallucinations, such as elaborate music
or people’s voices.3 6
Yap SM, et al. Pract Neurol 2015;0:1–4. doi:10.1136/practneurol-2015-001189

Auditory hallucinations occur very rarely in stroke,
presumably owing to decussation of the auditory pathways at multiple levels and to the rich collateral blood
supply they receive. In the emergency department,
most patients reporting acute onset auditory hallucinations will be found to have a psychiatric cause. It
seems unlikely that this symptom would occur as an
isolated manifestation of basilar occlusion, but when
occurring together with other symptoms of brainstem
ischaemia it warrants careful consideration.
In summary, we report two patients who experienced prominent auditory hallucinations at the onset
of basilar artery occlusion, with resolution upon arterial recanalisation. Clinicians involved in the evaluation
of patients with stroke for thrombectomy and/or
thrombolysis should be aware of the implications of
this distinctive, and perhaps under-appreciated,
symptom.
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Competing interests None declared.

Key points
▸ Acute basilar artery occlusion in a neurological
emergency.
▸ Acute basilar artery occlusion has protean and sometimes non-specific clinical features including dizziness, hemianopia and hemisensory loss, making
syndrome recognition a challenge.
▸ Acute basilar artery occlusion can occasionally cause
additional ischaemia of brain stem auditory pathways
resulting in the patient describing a unique auditory
hallucination, often a ‘loud, devastating noise’.
▸ Detection of this symptom in the acute setting
should prompt emergency imaging of the basilar
artery.

Contributors SMY: literature search, preparation of manuscript
and revision of manuscript. GW, JNPH: neuroimaging,
interventions and revision of manuscript. SC, EO’B: revision of
manuscript, overall responsibility for care of patients

4

Patient consent Obtained.
Provenance and peer review Not commissioned; externally
peer reviewed. This paper was reviewed by Richard Perry,
London, UK.

REFERENCES
1 Hausler R, Levine RA. Auditory dysfunction in stroke. Acta
Otolaryngol 2000:120:689–703.
2 Cogan DG. Visual hallucinations as release phenomena.
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3 Braun CMJ, Dumont M, Duval J, et al. Brain modules of
hallucination: an analysis of multiple patients with brain
lesions. J Psychiatry Neurosci 2003;28:432.
4 Galtrey CM, MacKinnon AD, Pereira AC. Localization of
bilateral auditory hallucinations and correlation to imaging in
posterior circulation stroke. Neurologist 2012;18:4 18–22.
5 Fischer CM, Tapia J. Lateral medullary infarction extending to
the lower pons. J Neurol Neurosurg Psychiatry 1987;50:620–4.
6 Celesia G, Hickok G. The human auditory system:
fundamental organization and clinical disorders. Elsevier
2015:509–36.

Yap SM, et al. Pract Neurol 2015;0:1–4. doi:10.1136/practneurol-2015-001189