subarachnoid haemorrhage and akinetic mutism

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SHORT REPORT Subarachnoid haemorrhage and akinetic mutism K. A. CHOUDHARI Department of Neurosurgery, Regional Neurosciences Unit, Royal Victoria Hospital, Belfast, UK Abstract Two rare cases of akinetic mutism induced by aneurysmal subarachnoid haemorrhage are reported. The literature is reviewed, the possible pathophysiological mechanism of akinetic mutism is considered and the association between these two conditions is explored with an attempt to address the roles of medical treatment and surgery and to discuss prognosis. Key words: Akinetic mutism, aneurysm, anterior cerebral artery, cingulate gyrus, subarachnoid haemorrhage. Introduction Cairns and coworkers 1 in 1941 introduced the term ‘akinetic mutism’ (AM) to denote a syndrome characterized by lack of responsiveness in the presence of apparently preserved vigilance. 2 It is a neurological state with total immobility (but not paralysis) except for eye movements and complete absence of all other types of communication. 3 A person with akinetic mutism has sleep-waking cycles. When apparently awake, he may be able to indicate alertness with eyes open, but lies mute, immobile and unresponsive. The condition is known to be associated with trauma, neoplasia and ischaemia of the brain. Two cases of AM associated with aneurysmal subarachnoid haemor- rhage (SAH) are reported—one as a presenting feature and the other as a delayed sequel of the SAH. Comprehensive MEDLINE search was carried out via the British Medical Association’s OVID Medline + system, as well as via National Library of Medicine’s PUBMED using ‘subarachnoid haemorrhage’ and ‘akinetic mutism’ as primary key words, initially focused and exploded on these key words, and later combined. Relevant literature is reviewed to explore the anatomical association between these two condi- tions, to discuss its pathophysiology and management. Illustrative cases Case 1 A 41-year-old woman presented with collapse at work and was thought to be unconscious at the scene. In the casualty department, she was noticed to be in a state of akinetic mutism. CT of the head showed an inter- hemispheric clot situated dorsal to the corpus callosum splaying the cingulate gyri (Fig. 1). There was associated diffuse subarachnoid haemorrhage. Angiography showed the presence of a saccular aneurysm arising at the junction of left pericallosal and calloso-marginal arteries (Fig. 2). This was treated with right frontal craniotomy, clipping of the aneurysm and complete evacuation of the clot via an interhemispheric approach (Fig. 3). Her postopera- tive course was complicated by chest infection and vasospasm leading to further neurological deteriora- tion. One month later she improved to the state of AM again. Very little improvement has been noticed after 3 months despite satisfactory radiological appearances. Case 2 A 40-year-old woman presented with devastating subarachnoid haemorrhage and remained comatose for several weeks. An anterior communicating artery (AComA) aneurysm was diagnosed, but was not treated owing to the patient’s poor grade. It was uneventfully coiled as an elective procedure after 6 months. Her condition at that stage was of akinetic mutism. CT revealed infarcts in the distribution of the distal anterior cerebral arteries (DACA). One year following treatment she has shown very little neurological improvement. Discussion Akinetic mutism (AM) describes a standard clinical state characterized by akinesia (inability to move) Received for publication 3 September 2003. Accepted 8 March 2004. Correspondence: Mr K. A. Choudhari, Department of Neurosurgery, Regional Neurosciences Unit, Royal Victoria Hospital, Belfast BT12 6BA, UK. Tel: + 44 (0)2890 635395. Fax: + 44 (0)2890 237733. E-mail: [email protected] British Journal of Neurosurgery, June 2004; 18(3): 253 – 258 ISSN 0268-8697 print/ISSN 1360-046X online/04/030253–06 # The Neurosurgical Foundation DOI: 10.1080/02688690410001732698 Br J Neurosurg Downloaded from informahealthcare.com by Universitaets- und Landesbibliothek Duesseldorf on 11/19/13 For personal use only.

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Page 1: Subarachnoid haemorrhage and akinetic mutism

SHORT REPORT

Subarachnoid haemorrhage and akinetic mutism

K. A. CHOUDHARI

Department of Neurosurgery, Regional Neurosciences Unit, Royal Victoria Hospital, Belfast, UK

AbstractTwo rare cases of akinetic mutism induced by aneurysmal subarachnoid haemorrhage are reported. The literature is reviewed,the possible pathophysiological mechanism of akinetic mutism is considered and the association between these two conditionsis explored with an attempt to address the roles of medical treatment and surgery and to discuss prognosis.

Key words: Akinetic mutism, aneurysm, anterior cerebral artery, cingulate gyrus, subarachnoid haemorrhage.

Introduction

Cairns and coworkers1 in 1941 introduced the term

‘akinetic mutism’ (AM) to denote a syndrome

characterized by lack of responsiveness in the presence

of apparently preserved vigilance.2 It is a neurological

state with total immobility (but not paralysis) except

for eye movements and complete absence of all other

types of communication.3 A person with akinetic

mutism has sleep-waking cycles. When apparently

awake, he may be able to indicate alertness with eyes

open, but lies mute, immobile and unresponsive. The

condition is known to be associated with trauma,

neoplasia and ischaemia of the brain.Two cases ofAM

associated with aneurysmal subarachnoid haemor-

rhage (SAH) are reported—one as a presenting feature

and the other as a delayed sequel of the SAH.

Comprehensive MEDLINE search was carried out

via theBritishMedicalAssociation’sOVIDMedline+

system, as well as via National Library of Medicine’s

PUBMED using ‘subarachnoid haemorrhage’ and

‘akinetic mutism’ as primary key words, initially

focused and exploded on these key words, and later

combined. Relevant literature is reviewed to explore

the anatomical association between these two condi-

tions, to discuss its pathophysiology andmanagement.

Illustrative cases

Case 1

A 41-year-old woman presented with collapse at work

and was thought to be unconscious at the scene. In the

casualty department, she was noticed to be in a state of

akinetic mutism. CT of the head showed an inter-

hemispheric clot situated dorsal to the corpus

callosum splaying the cingulate gyri (Fig. 1). There

was associated diffuse subarachnoid haemorrhage.

Angiography showed the presence of a saccular

aneurysm arising at the junction of left pericallosal

and calloso-marginal arteries (Fig. 2). This was

treated with right frontal craniotomy, clipping of the

aneurysm and complete evacuation of the clot via an

interhemispheric approach (Fig. 3). Her postopera-

tive course was complicated by chest infection and

vasospasm leading to further neurological deteriora-

tion. Onemonth later she improved to the state of AM

again. Very little improvement has been noticed after 3

months despite satisfactory radiological appearances.

Case 2

A 40-year-old woman presented with devastating

subarachnoid haemorrhage and remained comatose

for several weeks. An anterior communicating artery

(AComA) aneurysm was diagnosed, but was not

treated owing to the patient’s poor grade. It was

uneventfully coiled as an elective procedure after 6

months. Her condition at that stage was of akinetic

mutism. CT revealed infarcts in the distribution of

the distal anterior cerebral arteries (DACA). One

year following treatment she has shown very little

neurological improvement.

Discussion

Akinetic mutism (AM) describes a standard clinical

state characterized by akinesia (inability to move)

Received for publication 3 September 2003. Accepted 8 March 2004.

Correspondence: Mr K. A. Choudhari, Department of Neurosurgery, Regional Neurosciences Unit, Royal Victoria Hospital, Belfast BT12 6BA, UK.

Tel: + 44 (0)2890 635395. Fax: + 44 (0)2890 237733. E-mail: [email protected]

British Journal of Neurosurgery, June 2004; 18(3): 253 – 258

ISSN 0268-8697 print/ISSN 1360-046X online/04/030253–06 # The Neurosurgical Foundation

DOI: 10.1080/02688690410001732698

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Page 2: Subarachnoid haemorrhage and akinetic mutism

and mutism (inability to speak). Although, its

clinical expression is fairly typical irrespective of

the cause, aetiological factors are diverse and

various anatomical sites are known to be involved.

Common neurosurgical causes of AM are summar-

ized in Table I. Non-traumatic AM is most

commonly caused by tumours arising from dience-

phalic structures or those arising in the midline

from the skull base4 or in the region of the third

ventricle. Common vascular causes of AM include

ischaemia of the basilar artery (BA) or the ACA4,5

territories, bilateral thalamic infarction of athero-

sclerotic origin,6 ACA dissection7 or, in rare

circumstances, purely due to abnormal morphology

of the ACA.8

Review of the literature

AM has been rarely linked directly to aneurysms and

aneurysmal SAH (Table II). A literature review

suggests that the most common cause of AM in

patients with SAH is secondary infarction in the

DACA territory.4,9 Sometimes post-SAH hydroce-

phalus has also been implicated in a delayed form of

AM following SAH.10 Rarely, low intracranial

pressure caused by decompressive craniectomy and

FIG. 1. Preoperative plain CT axial scan images showing interhemispheric clot with SAH.

FIG. 2. Angiogram showing distal anterior cerebral artery aneurysm (white arrow).

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Page 3: Subarachnoid haemorrhage and akinetic mutism

theco-periotoneal shunt following SAH has been

reported to result in AM.11 AM has also been noted

during the natural course12 or recovery phase13 of

coma-producing SAH. Expanding or thrombosing

midline giant aneurysms are known to present with

AM without the SAH.14,15 AM as a presenting

feature of a poor-grade SAH as in our first case has

been sporadically reported,3,16 but is rare and usually

carries poor prognosis.

Pathophysiology of akinetic mutism

The syndrome of AM usually can be classified either

according to the anatomical site affected or depend-

FIG. 3. Postoperative CT scan showing satisfactory appearances, but residual hypodensities in the region of cingulate gyri.

TABLE I. Anatomical classification and neurosurgical causes of akinetic mutism

Anatomical level Structures affected Common pathologies

Telencephalic Cingulate gyri of the mesial frontal Lobes Vascular (ischaemic28, aneurysmal14,29), neoplastic

Diencephalic Thalamus (or thalamo-cortical tracts), caudate nucleus Neoplastic30, vascular (ischaemic)6, drugs31,32, hydrocephalus10

Mesenecephalic Upper brain-stem reticular activating system Traumatic 33

TABLE II. Akinetic mutism associated with Intracranial aneurysms and SAH

Author, year,

Reference

No of

cases

Cause of

AM

Site of the

aneurysm

Anatomical level

of the lesion

Patricolo, 197134 1 Postoperative complication AComA Hypothalamus

Buge,19754 1 Infarction of ACA region AComA Cingulate gyri

Koh, 197915 1 Mass effect caused by the aneurysm Basilar artery Mesencephalic compression

Von Cramon, 198035 1

Hydrocephalus and bilateral ACA

territory infarction AComA Cingulate gyri + diencephalons

Nemeth, 19883 1 Presenting feature of SAH

Left internal carotid

artery bifurcation Cingulate gyri

Nishigaya, 199036 1 Vasospasm in DACA territories DACA Cingulate gyri

Danilewicz, 199010 8 Secondary hydrocephalus – Diencephalic

Lechevalier, 199637 1 Infarction in the left ACA territory AComA Cingulate gyrus+dienecephalic ischaemia

Ushikoshi, 199927 1 Post- GDC coiling complication Superior cerebellar A Brain stem

Burruss, 19999 1 Unknown, intermittent – –

Hodozuka, 200011 1

Low pressure due to craniectomy

and T–P shunt AComA ?Diencephalic

Kanemoto, 200014 1 Mass effect caused by the aneurysm Azygous ACA Diencephalic compression

Present study 2

Intracerebral clot and DACA

territory infarction AComA and DACA Cingulate gyri

Subarachnoid haemorrhage and akinetic mutism 255

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Page 4: Subarachnoid haemorrhage and akinetic mutism

ing on the underlying pathological condition. The

author prefers to classify it anatomically as:

. telencephalic (mainly affecting medial frontal

lobes- cingulate gyri;

. diencephalic (thalamic/basal ganglia);

. mesencephalic (upper brain-stem reticular

activating system; Fig. 4).

Two pathological mechanisms of AM can be

described:

. reduced ‘arousal’ of cortical function due to

lesions at or rostral to the meso-diencephalic

junction;

. impaired activation of the motor system

following bilateral damage to the frontal lobes.

Neither of these mechanisms in isolation is likely to

be responsible in the causation of AM and it is

possible that both mechanisms may play some roles

in varying combination in an individual case. Some

authors such as Ackerman et al., however, group the

frontal AM (type i in the anatomically-based

classification) separately from the mesodiencephalic

AM (types ii and iii in the anatomically-based

classification). Since perceptual and cognitive func-

tions are also severely disturbed in the latter variety,

they have labelled it as the ‘apallic syndrome’ if it is

in a milder form or ‘vegetative state’ if it is in its

extreme form, thus restricting the term ‘akinetic

mutism’ to reduced motor activation following

bilateral medial frontal damage.2 Unless the anato-

mical localization in a given patient is discrete, there

may be some overlapping of clinical features. This

may lead to usages of different terms interchangeably

by different authors, mainly depending upon their

perception of the severity of akinesia and mutism.

Thus, it appears that the conditions akinetic mutism,

apallic syndrome and vegetative state are not

mutually exclusive. Rather there is an overlap

between them and patients may improve or deterio-

rate from one into another.

In its classic form, regardless of the cause, the

underlying biochemical mechanism of AM is postu-

lated to be selective disruption of mesocoeruleo,

diencephalospinal and/or mesocorticolimbic dopa-

minergic pathways.17 Nemeth and colleagues, in

their study of akinetic mutism and locked-in

syndrome (LiS) analysed morphological observa-

tions in relation to the neurochemical findings and

found a consistent correlation between pathways of

dopaminergic neurons and the lesions associated

with AM. They concluded that dopaminergic sys-

tems are selectively damaged in AM but spared in

LiS.17 Echiverri et al. described reversible akinetic

mutism induced by bromocriptine in four children.18

Apart from isolated case reports, this theory has not

gained wide support in the clinical field, nor does it

tie in convincingly with the anatomical subtypes

described above. In cases where routine imaging

(CT/MRI) is not able to pin-point the anatomical

site affected, Tc99m brain SPECT imaging is said to

be of localizing value.19

Role of cingulate gyri

Aneurysmal SAH classically results in the frontal or

telencephalic AMwith affection of cingulated gyri and

almost always from aneurysms in the region of

anterior cerebral arteries. Each cingulate gyrus has

complex reciprocal connections with other limbic

structures and frontal cortex, and appears to provide

an interface between the decision-making process of

the frontal lobe and the emotional world of the limbic

system. Stimulation of the cingulate gyrus in humans

often produces negative or positive feelings, and in

lower animals, stimulation causes erection of the penis

and grooming. Most cases of aneurysmal AM result

from destruction of both cingulate gyri manifested by

immobility and speechlessness. Conversely, increased

activity in this region may contribute to Tourette’s

syndrome, characterized by increased movement

such as muscular and vocal tics, facial grimacing,

pacing, twirling, coughing, sniffing and grunting.

Medical treatment

AM caused by primarily neuronal damage may have

slightly better prognosis than that caused by mainly

white matter disruption and may also show better

response to medical therapy than the latter. Several

workers have reported encouraging response of the

AM state to medical treatments with agents like

levodopa20,21 or bromocriptine18,22 – 26 However,

AM in all these cases has been meso-diencephalicFIG. 4. Schematic diagram depicting various anatomical regions

affected in akinetic mutism.

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Page 5: Subarachnoid haemorrhage and akinetic mutism

in contrast to the AM seen after SAH that is mostly

telencephalic (frontal). Although there is no strong

evidence to support routine administration of these

medications, a short therapeutic trial with dopamine

agonists may not be unjustified in cases of SAH-

induced AM if spontaneous improvement plateaus.

Role of surgery and prognosis

The author believes that SAH presenting with AM

carries similar prognosis to that of any poor-grade

SAH despite a preserved sensorium. In most

literature reviews, the presence of AM invariably

led to poor outcome irrespective of whether AM was

present before or after the treatment of the aneur-

ysm. The only exception seems to be that resulting

from secondary hydrocephalus, where promising

results have been reported.10 At our Institute, we

have achieved good results by radical evacuation of

intracranial clot together with clipping of the

ruptured aneurysm in poor-grade SAH patients

(unpublished). However, our efforts to radically

evacuate the clot and to treat the aneurysm urgently

in an attempt to reverse the AM (case 1) have yielded

slightly disappointing result. The author now be-

lieves that, in the absence of a localized haematoma,

acute surgical intervention may, in fact, worsen a

patient’s neurological condition if the patient already

has AM. Interventional workers have also reported

similar disappointing results with GDC coiling.27

Usually, we are firm advocates of early intervention

for aneurysmal SAH. However, in the presence of

AM, any intervention, whether surgical or endovas-

cular, may be deferred for weeks or months following

the onset of AM. Although the literature provides

scanty evidence to help in prognosticating in this

uncommon condition, the author believes that

delayed intervention may perhaps optimize the

chances of maximal spontaneous neurological im-

provement. Generally, the dismal prognosis carried

by the AM in presence of aneurysmal SAH makes

‘re-bleeding’ hardly a threatening consequence.

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