Brain Injury, May 2009; 23(5): 445–449

Post-traumatic mutism in children

XI JIAN, WANG JUNYU, & LIU JINFANG

Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, Hunan Province, PR China

(Received 7 May 2008; accepted 18 February 2009)

AbstractObjective: To explore the pathological mechanism of post-traumatic mutism (PTM) in children.Methods: A retrospective study of 16 children who suffered from severe head injury and developed PTM.Results: Post-traumatic coma lasted from 2–72 days, average 15.5 days; while post-traumatic mutism lasted from 2–56 days,average 11.94 days. The correlation between duration of coma and mutism was significant (p< 0.001). SPECT found thatmultiple persistent ischaemic brain regions occurred in all patients; the mean number of regions was 5.6. The patients weresub-divided into three groups based on the number of ischaemic regions: group 1, � 4; group 2, 5� 6; group 3, � 7. Theduration of mutism did not differ significantly between groups 1 and 2, but the difference between group 3 and the othertwo groups combined was significant (p< 0.05).Conclusion: Most PTM occurred in patients with diffuse brain injury. The duration of mutism was related to the number ofischaemic brain regions and the duration of post-traumatic coma.

Keywords: Children, brain injury, mutism, SPECT, brain region, ischaemia

Introduction

Post-traumatic mutism (PTM) occurs rarely and ischaracterized by the short-term dysfunction of verbalexpressing ability after trauma without a significantdecrease in comprehension. Levin et al. [1] reportedthat the incidence of PTM was 3% in patients withsevere brain trauma and was slightly higher inchildren than adults, which the incidence of PTMin children has no issued statistical results yet. Twoprevious publications also showed that PTM wasrare in adult patients with severe brain trauma [2, 3].

PTM is not caused by damage to Broca’s speechcentre. It can be differentiated from psychogenicmutism, akinetic mutism, post-traumatic aphasiaand cerebellar mutism by a period of total absence ofvocal emission associated with a gradual recovery ofverbal comprehension and communication skills,preserved oropraxies and vocalizations related topain and emotions [4]. However, there are still

considerable arguments about the mechanism ofonset of PTM. Dayer et al. [4] summarized theimaging information from six children who sufferedfrom PTM and suggested that none had an occupy-ing effect after intracranial injury. In contrast, someother case reports suggested that PTM resulted fromdiffuse cerebral trauma [5–8].

Such studies only involved in imaging data lackinginformation about focal cerebral metabolism orblood flow, which might underlie the discrepanciesbetween the studies. The imaging data alone, whichis restricted by resolution and other factors, isinsufficient to reflect the general post-trauma con-dition. SPECT can provide information about focalcerebral blood flow, which should help to completelyanalyse the functions of injured brain and explorethe mechanism of onset of PTM.

This study reports a retrospective study of 16children hospitalized with PTM (Table I) fromApril 1999 to October 2006. The clinical

Correspondence: Wang Junyu, Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha 410008, Hunan Province, PR China.E-mail: wjy5907@yahoo.com.cn

ISSN 0269–9052 print/ISSN 1362–301X online � 2009 Informa Healthcare Ltd.DOI: 10.1080/02699050902838157

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manifestation, Glasgow Coma score (GCS) atadmission, coma duration, the manifestation onCT, MRI and SPECT, the duration of PTM afterthe end of coma (spontaneous eye opening) and thedegree of recovery were analysed.

Patients and methods

General data

Sixteen patients (12 boys and four girls) with anaverage age of 7.34 years and a GCS of 7.37 atadmission were studied: two cases with acutesubdural haematoma combined with contusion andlaceration of the brain, two cases with intracerebralhaematoma, 12 cases with severe Diffuse AxonalInjury (DAI) and two cases with pre-operativeplatycoriasis.

Patient management

Two patients received craniotomy, one of which alsounderwent single decompressive craniectomy. Allpatients were treated in the ICU. Early tracheotomywas performed in patients with airway obstruction orSaO2 below 95%. All patients received multiplelumbar punctures until the CSF became clear. Allcases also received vasodilators and neurotrophicmedication as routine. Hyperbaric oxygenationwithout corticosteroids was given to patients in astable condition. Families tried to communicate withthe children in various ways, including speech andsign language, during PTM. The patients were askedto make finger movements. The older patients wereasked to read newspapers and books silently and tomake corresponding lip movements.

Mutism recovery

All patients recovered emotional expression andunderstood the power of language after the end ofcoma. The duration of mutism until oral expressionwas recorded. At first patients uttered incoherentmonotonic words such as mom, pain, urine and soon, followed by coherent sentences 2–3 days later,but most speech was still slow and in some patientswas accompanied with dysarthria. Two-to-threeweeks later, oral expression returned to normal inmost children.

CT, MRI and SPECT

CT and SPECT were performed on all cases. Theencephalic ischaemic regions detected by SPECTwere divided into two sides and 10 sites includingfrontal lobe, temporal lobe, parietal lobe, occipitallobe, thalamus and basal ganglia. MRI was per-formed on 12 cases.

Tab

leI.

Gen

eral

info

rmat

ion

and

SP

EC

Tre

sult

sof

pat

ien

ts.

Du

rati

on

(day

s)Is

chem

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dis

trib

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on

inS

PE

CT

Pat

ien

tn

o.

Age

(yea

rs)

Sex

Inju

rym

ech

anis

mC

om

aM

uti

smG

CS

on

adm

issi

on

fron

tal

tem

pora

lp

arie

tal

occ

ipit

alth

alam

us

Ou

tcom

e(G

OS

)

111

MF

allin

g3

28

Lef

tL

eft

Rig

ht

Good

reco

very

27

MT

raff

icac

cid

ent

22

8L

eft

Lef

tL

eft

Good

reco

very

313

MT

raff

icac

cid

ent

10

12

8R

igh

tR

igh

tB

ilat

eral

Lef

tB

ilat

eral

Good

reco

very

43.5

MT

raff

icac

cid

ent

24

13

5R

igh

tR

igh

tB

ilat

eral

Bilat

eral

Mod

erat

ed

isab

ilit

y5

13

FT

raff

icac

cid

ent

53

8B

ilat

eral

Rig

ht

Rig

ht

Rig

ht

Good

reco

very

62

MF

allin

g7

77

Lef

tL

eft

Lef

tL

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Lef

tG

ood

reco

very

77

MT

raff

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85

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tR

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tB

ilat

eral

Mod

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8M

Tra

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den

t9

88

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reco

very

94

FF

allin

g8

58

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8M

Tra

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acci

den

t26

18

6B

ilat

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Bilat

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Rig

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ht

Bilat

eral

Sev

ere

dis

abilit

y11

3M

Tra

ffic

acci

den

t72

56

4W

hole

bra

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ypop

erfu

sion

Sev

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dis

abilit

y12

5F

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t11

12

6L

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9M

Tra

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acci

den

t5

38

Rig

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Lef

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Lef

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very

14

14

MT

raff

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cid

ent

99

7B

ilat

eral

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ht

Lef

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15

4M

Tra

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acci

den

t32

24

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dis

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y16

6F

Tra

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acci

den

t17

12

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igh

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igh

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eral

Rig

ht

Bilat

eral

Mod

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ed

isab

ilit

y

446 X. Jian et al.

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Statistical analysis

The rank sum test and the correlative analysis wereprocessed by SPSS10.0 software.

Results

Mutism and coma

Coma lasted from 2–72 days (average 15.50 days)and PTM lasted from 2–56 days (average 11.94days) (Table I). The duration of mutism waspositively related to duration of coma (Figure 1).

Imaging data

A CT scan was performed on all patients 1–2 daysafter trauma and the main imaging changes were:subarachnoid haemorrhage in 12 cases, acute sub-dural haematoma combined with cerebral contusionin two cases, linear fracture in six cases, intracerebralhaematoma in two cases and DAI in 12 cases. MRIobtained at 7–30 days after trauma in 12 childrenshowed no significant cerebellar lesions, with a smallencephalomalacia in the body of the corpus callosumin one child at 30 days post-trauma (Figure 2).

SPECT

All patients received a SPECT scan, showing morethan one ischaemic brain region in each case. Asshown in Table I, the distribution of ischaemicregions can be summarized as follows: all cases hadischaemic changes in one or both sides of the frontallobe (left side, five cases; right side, seven cases; bothsides, four cases) and the temporal lobe (left side, sixcases; right side, seven cases; both sides, three cases).Fifteen of 16 cases had ischaemic regions in thethalamencephalon (left side, three cases; right side,four cases; both sides, eight cases). Two cases had noischaemic changes in the parietal lobe. The leastinvolved region was the occipital lobe.

The patients were classified into three groupsaccording to the number of ischaemic encephalicregions detected by SPECT: group 1,� 4; group 2,5� 6; group 3, � 7. The rank sum test was used tocompare the number of ischaemic regions andduration of mutism among the three groups. Therewas no significant difference between groups 1 and 2( p> 0.10); groups 1 and 2 combined were signifi-cantly different from group 3 ( p<0.05). Theseresults suggested that the duration of mutism wasprolonged when the number of ischaemic regionsexceeded seven. Statistical analysis failed to find asignificant correlation between the number ofischaemic regions either in the left or right hemi-sphere and the duration of PTM ( p¼ 0.265).

Discussion

In this study, 12 cases (75%) were due to DAI, whileanother four patients with intracranial haematoma,which had an occupying effect, also displayedsignificant multiple ischaemic brain regions afteroperation. It seems that PTM is more commonlyseen in patients with diffuse brain injury, especiallyin DAI, than in those with simple focal brain injury.

Comparing with the patients with psychogenicmutism, cerebellar mutism or akinetic mutism,almost all patients with PTM have experiencedcoma after trauma. After a coma lasting from 2–72days (average 15.5 days), the patients included inthis study suffered from PTM lasting for 2–56 days(average 11.94 days). The further statistical analysisshowed that the duration of PTM was positivelycorrelated with the duration of coma. The correla-tion of PTM with coma duration could predict afavourable, complete and rapid recovery of speecheven after many weeks of total mutism and, there-fore, support the child, his family and the nursingstaff during this distressful situation, even benefit forthe family and patient’s management.

Imaging data (CT and MRI) may give somesuggestions for the mechanism of PTM in children.However, there are still considerable argumentsabout the anatomical orientation of children withPTM and related brain regions containing cerebel-lum, callosum, thalamencephalon, diencephalons,brainstem and periaqueductal grey [4–9]. In thisstudy, CT and MRI showed diffuse brain injury in14 out of 16 patients. A punctated haemorrhagicfocus also appeared unexpectedly in early CTimaging. CT at 6 hours post-trauma in 14 childrenshowed a punctated haemorrhagic focus in the rightfrontal and temporal lobe. Encephalomalacia in thecallosum or cerebral atrophy were found by CT orMRI in some cases in the middle or late post-

Figure 1. Correlation of coma and mutism duration (days).

PTM in children 447

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traumatic period. Unfortunately, none of the aboveimaging changes were linked with the anatomicallocation of PTM. Moreover, the information derivedfrom CT or MRI images was not adequate for theunderstanding of the whole status of injured brain.Thus, this report processed SPECT for the patientsto learn the regional cerebral blood flow. SPECT ofthese patients at the same stage of disease showedmuch more severe changes than CT and MRI andeach patient had ischaemia in multiple brain regions,involving almost all the regions mentioned above.The further statistical analysis indicated that theduration of mutism was prolonged when the numberof ischaemic regions exceeded seven. The SPECTanalysis is a benefit for the prediction of PTMduration. Moreover, it was considered that theimprovement of ischaemic status of injury brainwould make better for PTM recovery, which isunder further investigation in the laboratory.

Human language function gradually develops inthe dominant hemisphere after birth. The languagecentre is less consummate in younger children. MRIand PET have shown that more than 10 brainregions are related to language function and that along time is required to build various languagenetworks, with numerous acquired language storesbeing located in the extensive brain region. Gaillaret al. [10] reported that children need to activatemore brain regions than adults to achieve the sameverbal fluency, which has the same condition in theright hemisphere in children, because of theirincomplete brain development. Thus, it is easy to

understand that in children more brain regions,including the right hemisphere, need to be involvedto complete a verbal fluency task. Three cases ofinjury mainly in the right hemisphere were observedin a sample of six children in imaging data collectedby Dayer et al. [4] Both the fMRI by Schlaggar et al.[11] and Wood et al. [12] and the cortex electricalstimulation during surgery by Stevenet et al. [13]revealed that maturation of the brain languageregion correlates significantly with age. The lefthemisphere damage was not as severe as the rightside in CT and MRI data shown in the results andthe correlation between the number of ischaemicregions in both hemispheres and the duration ofmutism was not significant ( p¼0.265). The dis-tribution of ischaemic brain regions in another studyon severe post-trauma coma adult patients revealedthat there was no significant PTM, which wasconsistent with this study [2]. The imaging data ofsix patients with PTM summarized by Dayer et al.[4] suggested that the involvement of mesencephalicstructures played a key role in the aetiology ofPTM. From these data, it is assumed that PTM inchildren may be related to their incomplete braindevelopment.

In summary, most PTM in children resulted fromdiffuse brain injury and ischaemic changes usuallyappeared in multiple brain regions. PTM durationwas correlated with coma duration. However, therelationship between PTM and damage to thelanguage centre in the dominant hemisphere wasnot significant. Although it appears that no lastingmemory or painful recollection of this situationoccurred in these patients, children with PTM mayexpress definite frustration at being unable to speak.One should be aware of this and look for alternativeways for the child to communicate in PTM duration,which will be of benefit for the future development ofthe child.

Declaration of interest: The authors report noconflicts of interest. The authors alone are respon-sible for the content and writing of the paper.

References

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2. Wang J, Xi J, Jiang B. The research of persistent coma aftersevere head injury and brain ischemia. Chinese Journal ofNeurosurgical Disease Research 2005;4:34–36.

3. Wang J, Jiang B, Zhang M. Clinical characteristics andprognosis of 34 patients with cerebral diffuse axonal injury.Chinese Journal of Traumatology 2001;17:26–28.

Figure 2. MRI at 28 days after trauma in a 3.5-year-old child:Encephalomalacia in callosum (white arrow).

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PTM in children 449

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