patients in each group the findings suggest that any
screening which is presently being done is based
predominantly on the patient's age rather than clinical
assessment.
We do not seek to criticise general practitioners in
this regard; many will have had little or no formal
training in otoscopy since undergraduate days. A
recent survey showed that roughly one sixth of vocational training schemes included ear, nose, and throat
attachments, and only a quarter of these included full
time six month posts.6 For the Royal National Institute
for the Deaf to suggest that general practitioners
wishing to provide hearing aid services based in their
own practices might receive "supplementary training
which could be organised during a single or two days"'
is frankly naive. The suggestion that screening
should be performed by the dispenser is unacceptable,
and were general practitioners to delegate in this
manner they would almost certainly carry ultimate
legal responsibility.

1 Royal National Institute for the Deaf. Hearing aids-the case for change.
London: RNID, 1988.
2 Spitzer RL, Cohen J, Fleiss JI, Enidicott J. Qtiantification of agrecmelnt in
psychiatric diagnosis. Arch Gen Psschiatrs 1967;17:83-7.
3 Hardcastle PF, son Haacke N, Murray JAM. Obscrver variation itt clittical
examination of the nasal airway. Clin Osolarvngol 1984:10:3-7.
4 Johnson J, Grover B, Martin MA. .A surves' of National Health Service hearilg aid
services. London: Royal National Institute for the Deaf, 1984.
5 Anonymous. Authority blitz cnds queue for hearing aids. Hospital D)otor
1989;9:(18):6.
6 Rivron RI', Clayton MI. Ear, nose, and throat teaching. Clin Otolarvngol
1988;13: 133-8.

(Accepted 30 Mas 1989)

Lesson ofthe Week
Multiple forms of epileptic attack secondary to a small chronic
subdural haematoma
S C Jones, J M Bamford, J Heath, N Bradey, R V Heatley
Comparatively rare
manifestations of
epilepsy may be the
presenting features of a
subdural haematoma

St James's University

Hospital, Leeds LS9 7TF
S C Jones, MRCP, registrar in
medicine
J M Bamford, MRCP, senior
registrar in neurology
J Heath, MRCP, senior
registrar in clinical
neurophysiology
N Bradey, MRCP, senior
registrar in neuroradiology
R V Heatley, MRCP, senior
lecturer in medicine
Correspondence to: Dr S C
Jones, Pinderfields General
Hospital, Wakefield
WF1 4DG.
?r.Atedj 1989;299:439-41

BMJ

VOLUME 299

Since the introduction of computed tomography (CT)
small or asymptomatic chronic subdural haematomas
have been recognised with increasing frequency,
though their detection may depend on the use of
contrast enhancing agents.' Patients with chronic
subdural haematoma commonly present with headache, disturbances of higher cerebral function such as
personality change and confusion, or features of raised
intracranial pressure. Hemiparesis, with dysphasia if
the lesion is over the dominant hemisphere, is the most
frequent focal neurological deficit. Epilepsy is traditionally thought of as a rare presenting feature.) We
describe a patient in whom several different forms of
epilepsy were the only clinical manifestations of a very
small chronic subdural haematoma.

Case history
A 75 year old man was admitted after a witnessed
tonic-clonic convulsion. Over the previous two weeks
he had suffered three episodes of sudden, complete
inability to speak, during which he remained fully
conscious without any abnormal movements being
noted. Each episode lasted about five minutes. He
was seen by his general practitioner, who diagnosed
transient ischaemic attacks but did not prescribe
aspirin. The patient denied headache, and neither he
nor his family could recall any recent head injury. He
12 AUGUST 1989

was taking chlorpropamide for maturity onset diabetes
but there was no previous history of epilepsy or
cerebrovascular disease. He had never had an excessive
alcohol intake. Full neurological examination on
admission showed nothing abnormal, and in particular
there was no disturbance of higher cerebral function.
Blood glucose, electrolyte, and calcium concentrations
remained normal throughout.
Over the next 24 hours attacks were witnessed
during which the patient would become vacant and his
head and eyes would deviate to the right. His right arm
would then become elevated with external rotation
of the shoulder followed by alternating flexion and
extension at the elbow while the wrist remained flexed
and the fingers extended and abducted. These attacks
would last between five and 60 seconds and were
followed by a variable period of confusion. They could
occur several times an hour, often without complete
recovery of consciousness in between. During periods
of full consciousness, however, no neurological deficit
could be detected. An attack could be terminated with
intravenous diazepam, which would continue to act for
about 30 minutes. He was given a loading dose of
intravenous phenytoin followed by conventional oral
doses.
About 48 hours after admission a further change was
noted, in that he was continuously confused with a
fluctuating level of consciousness. On occasions he
439

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Hearing loss is not a diagnosis; rather it is a
symptom, and patients require careful assessment.
The Royal National Institute for the Deaf proposes
that hearing aid dispensers should perform this
function. Failure to recognise and further investigate
asymmetric sensorineural hearing loss or unilateral
glue ear may lead to neglect of serious disease such as
acoustic neuroma or postnasal carcinoma. Though the
incidence of such diseases is low, even the small sample
of 100 patients in this study included seven who
warranted further investigation to exclude such conditions. Recognising glue ear and other middle ear
abnormalities, which may be amenable to surgical
correction, requires skill in otoscopy. Our results
suggest that otoscopy performed by general practitioners may miss abnormalities in a considerable
number of patients. As a result of inadequate assessment some patients may be denied the option of
surgical treatment.
Comparison of the group referred specifically for the
provision of a hearing aid with the group referred for
assessment suggests that general practitioners already
perform some screening and in many cases assess their
patients' needs correctly. The group referred for a
hearing aid contained a higher proportion of patients
who required an aid (46/54) compared with those
referred for assessment (23/46). Similarly a greater
proportion of patients referred for assessment had
hearing loss amenable to surgery. The kappa values for
interobserver agreement (table II), however, were
substantially different for each group, showing much
poorer agreement in the group referred for hearing
aids. When viewed alongside the age distribution of

($jI
100mV

I
ls

I_

A,<

S *--N * - . * a, x,

FIG I-Eight channels of electroencephalogram and one of electrocardiogram recorded during period of
complex partial status epilepticus showing epileptiform discharges predominantly in left hemisphere and
abnormally slow background rhythms

FIG 2-Contrast enhanced
computed tomogram showing
thin rim of subdural haematoma
(arrowed) with effacement of
sulci but no compression of
ventricular system

440

further seizures. He was discharged without any focal
neurological deficit and with normal higher cerebral
function. A follow up electroencephalogram showed a
normal background of alpha and beta rhythms devoid
of "epileptic" activity. The patient remained free of
seizures while taking phenytoin for over six months.
Discussion
Though computed tomography has made detecting
chronic subdural haematomas much easier, we may
have to rely on subtle abnormalities such as the
effacement of sulci to detect very small collections.
Contrast enhancement may help to delineate some of
these smaller collections, particularly when they
are isodense with respect to the brain.' This should
always be performed in patients with refractory partial
seizures, as a considerable proportion will have underlying structural disease.3 Though small subdural
collections may be seen as incidental in computed
tomograms and cause no ill effects, it seems likely that
in our patient the collection was responsible for the
epileptic focus in view of the focal nature of the seizures
and the lateralised abnormality in the electroencephalogram. Whether the resolution of the epilepsy
was directly attributable to the removal of the haematoma is debatable, as possibly the combined anticonvulsant regimen may have suppressed the seizures
at about the same time as the surgery. We, however,
think that the change from status epilepticus that was
responding poorly to multiple drug treatment to
complete control of seizures with a single anticonvulsant supports the decision to operate in this
case. Though the patient was receiving chlorpropamide, we had no evidence to suggest that hypoglycaemia was contributory.
Seizures are thought to be a rare presenting feature
of chronic subdural haematoma,2 though Luxon and
Harrison, who reported epilepsy or loss of consciousness as an initial symptom in 6% of their cases,
suggested that this traditional viewpoint should be
questioned.4 It is our impression that when they do
occur there is usually a large haematoma and there is
interictal evidence of a focal neurological deficit. One
previous report described simple partial seizures as the
sole manifestation of a chronic subdural haematoma,
and the authors made the point that such episodes
might easily be mistaken for transient ischaemic
attacks.5 Our case is of interest because there were four
distinct manifestations of the seizure disorder, two of
which might not be recognised immediately as being
due to epilepsy.
The first manifestation of neurological dysfunction
was that of loss of speech with preservation of consciousness and no abnormal motor activity. There
has been debate about the pathogenetic mechanisms
underlying this clinical picture and those of other
''transient neurological deficits," a term preferred to
transient ischaemic attack in this setting. Ross thought
that a focal seizure discharge would be a reasonable
explanation for such attacks,6 but Melamed et al
suggested that other mechanisms were more likely,
including intermittent compression of surrounding
vessels, spreading cortical depression of the type
associated with migraine after mechanical stimulation
of the cortex, and even coexistent thromboembolic
transient ischaemic attack.7 Moster et al noted that
aphasia was the most frequent presenting symptom of
these transient neurological deficits, though suggested
that repeated small haemorrhages into the haematoma
might be responsible.8
The subsequent clinical course in our patient
suggests that the episodes of loss of speech were the
first manifestation of epilepsy. It is possible that the
chronic subdural haematoma caused a small area of

BMJ VOLUME 299

12 AUGUST 1989

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s_~-\fQ%A

would respond to simple commands but otherwise
muttered incoherently. Signs of motor automatism
such as rubbing his body and attacks of exaggerated
blinking were noted. During this period the electroencephalogram contained background rhythms
dominated by theta and delta activity with recurring
epileptiform discharges in the left hemisphere (fig 1).
As before, intravenous diazepam stopped the muttering and signs of automatism temporarily, though
adding oral clonazepam did not prolong control.
As the earlier seizures had a focal motor component,
routine computed tomography had been requested,
but in view of the fluctuating level of consciousness
an emergency non-contrast scan was performed.
This did not show any obvious localised collection,
shift of the midline, or ventricular distortion. At
that stage the cerebrospinal fluid was normal. After
review by the neuroradiologists, however, a contrast
enhanced study disclosed a small subdural collection
over the left frontotemporal region (fig 2).
Further attempts were made to control the seizures
including adding carbamazepine but the pattern persisted for a further 48 hours. At that point, five days
after admission, we thought that neurosurgical intervention was indicated despite the apparently small
volume of the haematoma. At operation only a few
millilitres of thick, changed blood was found and
removed. Nevertheless, the patient did not suffer any

later in his illness showed continuing seizure activity at
a time when his clinical state was very similar to that
described above. Williamson et al, using implantcd
depth electrodes, reported that complex partial status
epilepticus tended to occur with foci outside the
temporal lobe and that the frontal lobe was frequently
affected.' 2Their patients had symptoms very similar to
those in our case.
It is important to recognise that these comparatively
rare forms of epilepsy may be the presenting feature of
a chronic subdural haematoma. Loss of speech may be
treated erroneously as a thromboembolic transient
ischaemic attack by using potentially detrimental
drugs, and the confusional state caused by the complex
partial status epilepticus may be attributed to coexistent but less treatable disorders in elderly patients.
In our case the previous clear cut epileptic episodes had
led us to suspect that the symptoms were due to
epilepsy, but patients may present with such an
episode as their first manifestation of epilepsy."
Though a fluctuating level of consciousness with a
chronic subdural haematoma is most likely to be
due to raised intracranial pressure, if the collection is
small or the fluctuation persists after drainage of the
haematoma the possibility of complex partial status
epilepticus should be considered.
1 Tsai FY, Huprich JE, Segall ID, Teal JS. The contrast-enhanced CT scan in
the diagnosis of isodense subdural hematoma. 7 Neurosuirg 1979;50:64-9.
2 Walton JN, ed. Stibdural haematoma. In: Brain's diseases ofthe/ nervous s.ystert.
8th ed. Oxford: Oxford Universitv Press, 1981:395-7.
3 Robb P. Focal epilcpsy: the prohlein, prcvalence, anid contrrihbting factors. In:
Purpura DP, Penry JK, Waltcr RD, eds. Advances itn neuroloug. Vol 8. Ncss
York: Raven Press, 1975:1 1-22.
4 Ltuxon LM, Harrison \1JG. Chronic suLbdural hacmatoma. 2 d7
Md
1979;48:43-53.
5 Hilt DC, Alexander GE. Jacksonian somatoscnsory scizures as the solc
manifestation ot'chronic subdural liematoma. Arch Neurol 1982;39:786.
6 Ross RT. Transicnt tumor attacks. Arch Neurol 1983;40:633-6.
7 Melamed E, I av S, Reches A, Sahar A. Chronic stibdtiral hematoma
simulating transicnt cerebral ischemic attacks. J Neuirosurg 1975;42:101-3.
8 Moster ML, Johnston DE, Rcinmuth OM. Chronic subdtiral hematoma with
transient neurological deficits: a review of 15 cases. Ann Neurol 1983;14:
539-42.
9 Sandercock P. Aspirin for strokes and transient ischaemic attacks. BrAl
M 7
1988;297:995-6.
10 Rasmussen T. Surgery of frontal lobe epilcpsy. In: Ptirpura DI', Penry JK,
Walter RD, eds. Advances in neurology. Vol 8. New Y'ork: Ravcn Plress,

1975:197-205.
11 Ballenger CE, Kinig D)W, Gallaghcr BB. IPartial complex stattis epilcpticus.

Neurology 1983;33:1545-52.
12 Williamson PD, Spencer DD, Spencer SS, Novcvy RA, Mattson RH.
Complex partial status epileptictis: a depth-elecvtiride stiidy. Ann Nseurol

1985;18:647-54.

(Accepted4.May 1989)

MATERIA PARAMEDICA
A ray of sunshine for old ladies: a tip for the geriatricians?
"They die like flies," said the GP. This was in the 1930s, and she was
referring to infantile gastroenteritis in general practice. The condition was
highly infective and could kill several children in a large family. An
outbreak in hospital could be equally frightening, causing deaths in
children admitted for other conditions. Intravenous drip infusions and
antibacterial drugs had not been invented.
Ten years later I was a "general" physician at St Giles's Hospital in north
Camberwell. In that capacity I was deemed to be a specialist in all branches
of medicine, which then comprised paediatrics, inter alia, and the giving of
anaesthetics. Treatment had scarcelyr advanced in the meantime, but the
importance of isolation was better understood. There were, however, no
facilities for isolating these tiny patients. How was I to protect the other
children in the ward?
The plan I adopted was to isolate the child with gastroenteritis by
removing all the other children. There was room for one cot in each female
ward, and a child was moved to the centre aisle between the rows of beds in

BMJ

VOLUME 299

12 AUGUST 1989

the old "Nightingale" wards. I had a hunch that children were less
susceptible to adults' germs than to those that more specifically affected
children. At all events, no child who was thus transferred-picked up an
infection.
Most remarkable and unexpected was the effect of a child's presence on
the patients. Many of these ladies were elderly, and some were senile,
taking no apparent interest in their surroundings. One bv one they came to
the cot side and took their turn at baby talk. The whole ward became a
livelier, happier place, with conversation drifting to and fro. I have no
doubt that each child also benefited from the affectionate attention
received. Graham Hunter, a former geriatrician, describes the electrifying
effect on elderlv patients of visits from members of his staff who brought
their newborn babies.' Perhaps there is a lesson here.
BERNARD J FREEI)MAN
1 Hunter GM. Pci-sonal view. 13rJlI d' 1985:290:1511.

441

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cortical thrombophlebitis, but we would not have
expected such transient, repetitive, or stereotyped
attacks to arise from the purely ischaemic effects of
such a lesion. It seems unlikely that there was any
appreciable displacement of adjacent vessels because of
the very small volume of the haematoma, and the
tempo of the attacks would be more rapid than we
should expect from spreading cortical depression. We
cannot exclude thromboembolic transient ischaemic
attacks as a cause but note that the patient did not
have any attacks postoperatively. That the general
practitioner diagnosed the episodes of loss of speech as
transient ischaemic attacks is noteworthy at a time
when antihaemostatic drugs are being prescribed
routinely for any episode which is thought to be due to
transient cerebral ischaemia.9 This emphasises that the
negative symptom of loss of speech might be due to
epilepsy and that there may be an underlying lesion
such as a chronic subdural haematoma which, at least
theoretically, might be made worse by some drugs.
The next two manifestations of epilepsy in our
patient were a generalised convulsion and then
complex partial seizures with a prominent focal motor
component. These second forms of attacks were very
similar to those described by Rasmussen, which he
correlated with lesions in the medial aspect of the
intermediate frontal lobe and supplementary motor
strip. ' The clinical and electroencephalographic
findings during the days before surgery would fulfil the
criteria for non-convulsive complex partial status
epilepticus.
Ballenger et al, in a review of published work, noted
that two distinct forms of complex partial status
epilepticus could be recognised," and both were seen
in our patient. In one group the patients have recurrent
partial complex seizures. They are usually unresponsive, and adversive or tonic motor phenomena with
stereotyped automatism are often noted. In the
interictal phase there is improvement in responsiveness but incomplete return to normality. In the other
group the patients have continuous complex partial
activity in their electroencephalograms. Clinically
the patients show quite pronounced fluctuations in
response to verbal stimuli and their responsiveness
varies from a mild confusional state in which simple
commands can be obeyed to complete unresponsiveness. Stereotyped non-purposeful automatism is rare.
Though our patient did not have continuous electroencephalographic monitoring, a standard recording