DTIC ADP010465: Usefulness of Sleep Records After Mild Head Trauma to Predict Shift Work Effectiveness

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ADPO 10465

TITLE: Usefulness of Sleep Records After Mild
Head Trauma to Predict Shift Work Effectiveness

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TITLE: Individual Differences in the Adaptability
to Irregular Rest- Work Rhythms/Status of the Use
of Drugs in Sleep- Wakefulness Management [les
Differences entre individus concemant les
facultes d’ adaptation aux rythmes irreguliers
activite-repos/Le point sur V utilisation des
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veille-sommeil]

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ADPO 1045 3 thru ADP010473

USEFULNESS OF SLEEP RECORDS AFTER MILD HEAD TRAUMA
TO PREDICT SHIFT WORK EFFECTIVENESS

12-1

Grzegorz MAKSYMIUK, Wojciech JERNAJCZYJ
Polish Air Force Institute of Medicine
Institute of Psychiatry and Neurology
Krasinskiego Str. 54
01755 Warsaw
Poland

Summary

Validity of polysomnography for determining the post-traumatic sequelae was evaluated in 33 male patients
after a mild head trauma. The results indicate that shortly after the trauma accompanied by the brain
commotion disturbances in sleep architecture can be detected by means of polysomnography. We also
demonstrate that polysomnography is a sensitive method of evaluation of early post-traumatic alterations within
the CNS. Based on the results of the present study we conclude that the described diagnostic procedure should
become a steady element of the clinical evaluation and qualification of patients presenting with subjective
symptoms as the sequalae of a mild head trauma.

Introduction

Minor head trauma (MHT) accompanied by
brain concussions constitutes, as a clinical
syndrome, about 2/3 of all the scull and brain
injuries [8]. Most of the patients with the past
history of the MHT recover within a few weeks
without a need for a specific intervention. A third
of the patients, however, develop the subjective,
post-traumatic syndrome, and half of them never
return to work. One year after the injuiy, 15% of
the patients still complain of symptoms affecting
their lifestyle [1]. Probably the pathological process
developing after trauma could be considered the
reason of complaints of sleep disturbances too.
Therefore authors suspect that in early period after
MHT patient can develop disturbances in sleep.
We did not find any research work analizing a
sleep pattern in a group of patients in early period
after MHT.

The present paper is a part of the research
project carried out at the Polish Air Force Institute
of Medicine (PAFIM), the Central Clinical
Hospital of the Military Medical University School
(CCH) and the Institute of Psychiatry and
Neurology (IPN) in Warsaw. The project was
devoted to evaluation of the state of the central
nervous system in patients who had suffered from
MHT. Here, we evaluated the sleep pattern of
patients in early period after MHT.

Material

The study was conducted in a group of 40
males aged 19-29 years (mean age 22.5 y) who
were admitted to the Dept, of Neurology, PAFIM

for the MHT accompanied by the consecutive brain
concussion. The diagnosis was based on history,
physical examination, and the computerized
tomography (CT) results. The protocol of the study
was approved by the Ethical Committees of both
the PAFIM and the CCH and a written consent was
obtained from all the subjects allotted to the study.

Selection of the patients for the study was based
on the following criteria: skull and brain injuries
with brain commotion experienced for the first
time shortly before the study (i.e., 24 - 96 hours
before hospitalisation), 19-41 years of age, male
sex, and no detectable mental disorders, somatic
diseases or other physical abnormalities. In
addition, no past history of abnormal EEC
recordings and no family history of epilepsy were
required.

Seven patients should take medication and were
excluded from the survey (two of them because of
excessive emotional irritability, one because of
serious dizziness and three because of persisted
moderate and heavy headache).

Control group consisted of 30 healthy paid
male volunteers aged 19-29 years (mean age 22. 4y)
with normal EEG in wakefulness. All examined
persons described their sleep as good. None of
them abused alcohol, took daytime naps, or
underwent pharmacological treatment for at least
four weeks before the sleep examination.

Method.

After admission to the Clinic patients were
assessed from the point of view of cause of trauma,

Paper presented at the RTO HFM Workshop on “Individual Differences in the Adaptability to Irregular
Rest-Work Rhythms/Status of the Use of Drugs in Sleep -Wakefulness Management”,
held in Venice, Italy, 3-4 June 1999, and published in RTO MP-31.

12-2

duration of unconsciousness, appearance and
duration of posttraumatic amnesia (PTA).

The injuries were evaluated using the Glasgow
Coma Scale (GCS). Accordingly, the total score
(ranging from 3 points for the most serious
condition to 15 points for the least serious one)
obtained after the assessment of the eye-opening
capacity and the verbal and motor responses was
used to divide the patients into the following 3
groups: a) mild (scaled 13-15), b) moderate (scaled
8-12), and c) heavy head trauma (scaled 3- 7).

During the first 24 hours after the admission, the
brain CT with no contrasting medium was
performed. Normal images of the brain and the
cerebellum with no detectable dislocations in the
ventricular system were required for the inclusion
of a patient in the study. All the CT images were
examined by one and the same physician.

On 3rd to 4th day after trauma, by means of
“self-estimation sleep form” patients described
their wake/sleep status, replying to 12 questions
connected with the pattern of sleep after trauma,
day sleepiness and naps. They compared it with the
quality of sleep before MHT.

On the 5th to 11th day after the trauma,
polygraphic examinations were carried out on the
Medelec-2 MC apparatus between 9.00-10.00 p.m.
and 5.00-6.00 a.m. Standard technique
polygraphic record and the criteria of visual
scoring of somnogram stages according to
Rechtsschaffen and Kales [2,14] were applied.
Sleep was evaluated on the basis of the somnogram
of the second night (the first night was considered
as adaptation night). The same procedure of sleep
examination was applied in control group after a
normal activity during a week before the
examination.

The data concerning sleep EEG were computer
processed, mean values and standards deviations
for 17 parameters were calculated. Students t-test
was used for the statistical analysis of the results.
P<0.01 was adopted as significant difference.

Results

Patient’s characteristics

According to history data 18 patients (54.5%)
suffered injuiy from fights, nine (27.3%) from car
accidents and six (18.2%) from fall. Eleven of
them (33.3%) were only confused or lost
consciousness for less than dozen or so seconds.
Twelve patients (36.4%) lost consciousness for 1 to

20 minutes and ten patients lost consciousness for
30 to 60 minutes.

Retrograde amnesia (RA) occurred in every
patient and lasted up to a few minutes after trauma.
Posttraumatic amnesia (PTA) appeared in every
patient as well, but the time of duration was up to 6
hours. Data concerning RA and PTA have only
approximate value, because in 27 cases memory
improved before admission to the hospital.

On the admission to the Clinic (first-third day
after the trauma) the patients complained of a
number of symptoms which disappeared after a few
days. The complaints included headaches,
dizziness, daytime drowsiness, nausea, and emesis.
Headaches of mild and moderate intensity (not
requiring any regular medication) as well as
irritation and anxiety episodes were the longest
lasting symptoms (6 subjects (18.2%) complained
of them for 14 days after the trauma).

According to the CGS, 25 (75.8%) patients
were scored 15 points and 8 (24.2%) patients were
scored 14 points. In the latter group, one point was
subtracted from the highest score because the
patients were able to open their eyes on demand.

Self-estimation sleep form.

All patients had no sleep disturbances and even
naps before head trauma. According to the form
results (table I) 22 subjects had different sleep
abnormalities day sleepiness and naps after MHT.
Five of them (gray mark on the table) had
excessive sleep disturbances and woke up with the
feeling of fatigue.

Polysomnography

Results of patients’ sleep examinations are
shown in the table II. They are compared with the
results of control group. Statistical analysis
revealed a reduction of sleep cycle length
(p=0.001) in patients. However an increase of cycle
number (p=0.009) during a whole sleep period in
subjects after MHT, caused that total amount of
NREM sleep is similar in both groups. Another
difference found in NREM sleep between two
groups is decrease of stage 2 of sleep in patients
(p=01). Analysing REM stage we observed
shortening of REM sleep latency (p=0.0001).

Polygrafic registration of sleep in patients took
place between 4 to 11 days after trauma. In 19 of
them from 4 th to 6 th day and in 14 from 8 th to 11 th
day after MHT. Statistical analysis showed no
difference between two estimated groups.

12-3

As it is demonstrated in table I patients had
some complaints connected with disturbances in
wake - sleep cycle. Significant sleep differences
were found in group of patients who, apart from
other complaints, notified feeling of fatigue.
However because of a small number of this group
we should be careful in making a conclusion.

Discussion

Traumatic injury is mainly caused by
displacement of intracranial structures in relation
to the skull bones. A shift of these structures
towards the trauma site creates a negative pressure
which results in the formation of a vacuum on the
opposite side of the brain. The vacuum sucks in gas
bubbles to the cerebral cortex capillaries and
breaks down small blood vessels and nervous tissue
(the so-called cavitation phenomenon) [2]. After
injury focal and diffuse pathological changes
occur. MHT is mainly characterized by diffuse
changes like diffuse axonal injury (DAI), diffuse
microvascular damage (DMD) and delayed
secondary injury (DSI). DSI is caused by an
uncontrolled vicious cycle of biochemical events at
cellular level set in motion by the trauma. DSI has
come to be recognized as a major contributor to the
ultimate tissue loss after MHT. The complex of
pathological processes lead to necrosis and/or
apoptosis of nerve cells [6,9].

Exposure to the linear acceleration forces
brings about the most pronounced changes in the
deep structures of the brain. Angular acceleration
damages mainly the cerebral cortex of, particularly
frontal and temporal lobes. - in which centres
responsible for human behaviour, memory,
cognitive and learning ability are found [18].
Experimental research works revealed that some
cerebral structures, located in frontal and temporal
lobes as well, are involved in creation of final
sleep-wake status picture [10]. Thus behavioral and
cognitive abnormalities are often found in patients
with MHT.

History of sleep disorders is one of factors
affecting a quality of shift work. Traumatic brain
injury can affect even temporary, activity of
systems responsible for wake-sleep cycle. EEG
sleep pattern of comatose patients after head
trauma was the evidence of changed function of
those systems [8]. Prigantano at al. [12] obtained
single polysomnograms in a group of 10 subjects

who had complains of disturbed sleep after closed
injury. All of these patients had been comatose for
at least 24 hours. The head-injured patients had
less stage 1 sleep and a greater number of
awakenings.

This research work has revealed that even after
MHT, in early period after trauma, changes of
sleep architecture can be observed. Decrease of
stage 2 sleep is difficult to explain. It could be the
result of affected function of structures (located in
frontal and temporal lobes) involved in NREM
sleep generating. In patients with diagnosed
Alzheimer Disease (AD) pathological changes are
especially found in frontal and temporal lobes.
EEG sleep pattern of these patients disclosed poor
biological efficiency and disturbances of REM
stage [17].

Domzal et al. [3] discovered in their study that
patients after MHT had a decrease of spindles
activity - EEG elements found in NREM sleep
pattern. Diminishing of spindle number results in
reduction of stage 2 sleep. System consisting of
reticular formation, thalamus and cerebral cortex is
responsible for creation of spindles [11,13,16].
That is why affection of connections between these
structures is thought as essential factor causing
decrease of stage2 sleep.

REM stage changes found in examined group
may depend on affected function of centres located
in cerebral hemispheres. Neurons generating REM
stage are found in structures of brain stem but
different cerebral nuclei influence on the final
shape of this part of sleep [4,5,15,19].

REM sleep is thought to be responsible for
brain metabolic regeneration [7]. Shortening of
REM stage latency, duration of sleep cycle, and
increase of cycle number could be the result of
acceleration of the process.

Conclusions:

1. MHT affects a sleep architecture in early
period after trauma.

2. Polysomnography is a sensitive tool in
discovering of sleep changes developing after
MHT. It could help to improve clinical patient
estimation and usefulness to perform shift
work.

12-5

Table II

EEG sleep pattern of patients after mild head trauma versus control group.

Parameters of EEG sleep pattern

Significance
I^liffetence ' ' 5

Record time (min)

474.9

8.6

476.3

2.5

p=0.25

Time of sleep (min)

439.1

25.8

433.4

33.1

p=0.45

Total sleep time (min)

433.2

32.5

426.1

33.7

p=0.40

Wakefulness in sleep (%)

1.4

3.0

1.7

2.1

V5339HHB

Stage I (%)

6.4

5.9

6.1

3.8

Tsxmmm

Stage 2 (%)

wvm

H'- : "M

— ■

1B1111I 1

fa3H

Stage 3 (%)

11.0

3.8

11.7

3.1

p=0.42 |

Stage 4 (%)

4.4

4.1

5.5

4.6

i zrnmm

Stage 3+4 (%)

15.4

6.9

17.3

6.0

p=0.25 j

Total NEEM sleep (%)

77.5

4.7

74.8

4.6

15

Stage REM (%)

22.5

4.7

25.2

4.6

p=0.03

Sleep latency (min)

35.2

24.0

42.8

32.7

p=0.29 i

Stage 3,4 latency (min)

13.1

5.6

17.3

17.1

REM stage latency (min)

88.9

lllll'iJilM:

54.1

p=0 0001

Number of sleep cycles

4.0

mmmmm

B—

p=0.009

Number of awakenings

2.0

2.8

2.6

2.4

p=0.37

Mean length of cycle (min)

108.7

ira»

HUB

5ft ' 13.9:111

p=0.001

Sleep efficiency (%)

91.3

6.3

89.4

7.0

RSEEHHHH

Sleep maintenance (%)

98.6

3.0

98.3

2.2

msamm

References

1. Adams J.H., Graham D.I., Scott G. et aL:
Brain damage in fatal non-missile injury. J.
Clin. Pathol. 1980, 33:1132-1145;

2. American Electroencephalographic Society:
Guideline Fifteen: Guideline for Poligraphic
Assessment of Sleep - Related Disorders
(Polysomnography). J. Clin. Neurophysiol.
1994; 11:116-124;

3. Domzal T., Deczyriska I., Gawlik L.,

Ligezinska B.: Badania nad zmian^

reaktywnosci bioelektrycznej mozgu na
barbiturany pod wplywem urazu glo\vy.
Neurol. Neurochir. Pol. 1968, 2: 683-690;

4. Gadea-Ciria M.: Cerebellar control of
activity of the feline oculomotor system
during paradoxical sleep. Exp. Neurol.
1976, 51:263-265;

5. Gadea-Ciria M.: Tele-encephalic versus
cerebellar control upon ponto-geniculo-
occipital waves during paradoxical sleep in
the cat. Experientia 1976, 32:889-890;

6. Graham D.I., McIntosh T.K.:
Neuropathology of Brain Injury in:
Neurology and Trauma, red. R.W.Evans,
W.B. Saunders Comp., Philadelphia, 1996,
53-90;

7. Hartman E.: Functions of sleep, in
Jovanovic U.J. (red.): The nature of sleep.
G. Fisher Verlag Stuttgart 1973; 238-250;

8. Kowatch R.A.: Sleep and head injury.
Psychiatric Medicine 1989, 7, 37-41;

9. Malejczyk J., Gorski A.: Editoral review:
Apoptosis and its role in immunity.
Apoptosis 1996; 1:227-230;

10. Lucas E.A., Sterman M.B.: Effect of
forebrain lesion on the polycyclic sleep-
wake cycle and sleep- wake patterns in the
cat. Exp. Neurol. 1975; 368-373;

11. Petsche H., Pockberger H., Rappelsberger
P.: On the search for the sources of the
electroencephalogram. Neuroscience 1984,
11:1-27;

12-6

12. Prigantano G.P., Stahl M.L., Orr W.C. et
al.: Sleep and dreaming disturbances in
closed head injury patients. J. Neurol.
Neurosurg. Psychiat. 1982, 45, 78-80;

13. Ray W.J., Cole H.W.: EEG alpha activity
reflects attentional demands and beta
activity reflects emotional and cognitive
processes. Science 1985, 228:750-752;

14. Rechtschaffen A., Kales A.: A manual of
standardised terminology, techniques and
scoring system for sleep stages of human
subjects. Brain Information / Brain
Research Institute, Los Angeles 1968;

15. Siegel J.M.: Brainstem mechanisms

generating REM sleep, in Kryger M.H.,
Roth T., Dement W. (red.) Principles and
Practice of Sleep Medicine sec.edit.
Philadelphia, W.B. Saunders Comp., 1994,
125-144;

16. Steriade M., Domich L., Oakson G.,
Deschenes M.: The deafferented reticular
thalamic nucleus generates spindle
rhythmicity. J. Neurophysiol. 1987, 57:260-
273;

17. Vitiello M.V., Prinz P.N., Williams D.E. et
al..: Sleep disturbances in patients with
mild-stage Alzheimer’s disease. J. Gerontol.
1990; 45:M131-M138;

18. Walker A.E.: The Physiological Basis of
Concussion: 50 years later. J. Neurosurg.
1994, 81:493-494;

19. Webster H.H., Jones BE.: Neurotoxic
lesions of the dorsolateral mesencephalic
tegmentum cholinergic cell area in the cat:
Effects upon sleep-waking states. Brain Res.
1988, 458:285-302;