Journal of Neurology, Neurosurgery, and Psychiatry, 1977, 40, 932-935

Short report

Mesial temporal haemorrhage, consequence of
status epilepticus
P. NOEL, A. CORNIL, P. CHAI LLY, AND
J. FLAMENT-DURAND
From the Departments of Medicine and Pathology, Universite Libre de Bruxelles, Brussels, Belgium

S U M M A R Y A 52 year old woman developed a severe encephalopathy with status epilepticus
of six days duration in the terminal course of an acute hepatitis associated with hyperammonaemia and hyperventilation. Acute haemorrhagic lesions were observed in the brain, involving
symmetrically both amygdala and cornu Ammonis. The sequential occurrence of these lesions
with status epilepticus are discussed in the light of data from the literature.
Numerous reports have delineated the pathological
findings in status epilepticus (Fowler, 1957; Scholz,
1959; Norman, 1964): ischaemic lesions and glial
reactions are observed in selectively vulnerable
regions. These lesions are commonly held to be
the consequence and not the cause of the convulsive status (Meldrum, 1976). However, in a
number of cases, this relation cannot be ascertained, particularly when the pathological findings
reveal old gliotic hippocampal lesions. They could
precede and be responsible for the initiation of

The day before the final admission, she complained of headache and vomited repeatedly. A
few hours later, she was found obtunded with recurrent generalised convulsions. The medical
history was unremarkable. She had never presented epileptic fits nor indulged in alcoholism.
On admission, the rectal temperature was
38.20C, the pulse rate 100/min, the blood pressure
120/70 mmHg, and the respiratory rate 40/min.
She was unconscious and reacted to painful stimuli
by semi-purposeful movements. No jaundice or
convulsions.
rash were present. Coarse rales were audible
In the case reported here, the unusual character throughout both lungs. The heart and abdomen
of the lesions leaves no doubt about the sequence were normal. There was prominent acrocyanosis
of events: they are acute and secondary to the with peripheral vasoconstriction and unpalpable
status epilepticus.
arteries. Eye movements were full, with spontaneous roving movements. The right pupil was 2 mm
Case report
wide, the left pupil 4 mm; they both reacted to
light. The ocular fundi and the cranial nerves were
A 52 year old woman was admitted for treatment normal. The deep reflexes were present with a flexor
of coma and convulsive seizures. One month plantar reaction. Treatment consisted of tracheal
earlier she had been admitted to another hospital intubation, assisted ventilation, rehydration, phenofor pyrexia and exertion dyspnoea. The physical barbitone, phenytoin, dexamethasone, and ampiexamination was normal except for a slight py- cillin. The urine was normal. The haematocrit was
rexia. Liver biopsy showed no pathological altera- 29.7%, the white cell count was 11 300 per mm3
tions. She was discharged without further with 90% neutrophils, 6% lymphocytes, 2% monoinvestigations.
cytes and 2% metamyelocytes. The platelet count
was 340 000 per mm3. The urea nitrogen was
0.72 g/l, the glucose 1.82 g/l, the bilirubin 0.031
Address for reprint requests: Dr J. Flament-Durand, Department of
g/l and the protein 7.1 g/l (albumin 40.5%, alphaPathology, Faculty of Medicine, rue aux Laines 97, B-1000 Brussels,
1 globulins 5.5%, alpha-2 globulins 8%, beta
Belgium.
globulins 6.4%, and gamma globulins 38.6%). The
Accepted 21 March 1977
932

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Mesial temporal haemorrhage, consequence of status epilepticus

933

glutamic oxalacetic transaminase (SGOT) level in the inflammatory lesions. The liver was small,
was 1650 IU/1, the glutamic pyruvic transaminase weighing 975 g, soft and yellow, presenting a
620 IU/i. The serum sodium level was 138 mmol, smooth surface. Histological examination revealed
potassium 3.9 mmol, chloride 95 mmol, and large areas of necrosis, steatosis of some hepatocalcium 4.3 mmol/l. There were no LE cells. The cytes, phagocytosis of lipofuscin granules by Kupprothrombin time was 21% of normal. A spinal ffer cells, slight fibrosis of the portal vessels, and
tap was performed. The opening pressure was 12 biliary stasis. Histolytic changes were prominent,
mmH,O; the fluid was clear. The CSF protein possibly due to the hyperthermia presented by the
content was 0.42 g/l and there were no cells.
patient a few days before death. The heart, spleen,
On the second day, she presented numerous and kidneys were unremarkable.
generalised seizures which were refractory to treatOn macroscopic examination, the brain apment by intravenous diazepam and clonazepam.
peared normal. The arteries forming the circle of
On the third day the patient reacted to painful Willis were of normal aspect and anatomical constimuli by decerebrate posturing. The pupils were figuration. There was no temporal herniation and
equal and reacted sluggishly to light. The deep re- the mammillary bodies were of normal size. On
flexes were hyperactive in the four limbs with a coronal section, symmetrical lesions with a strikbilateral Babinski sign.
ing haemorrhagic character were seen, involving
On the fourth day, seizures were permanent, the anterior white commissure, the amygdala, and
interrupted only by short periods of total hypo- the cornu Ammonis (Fig. 2). Histological examtonia. Mucosal and cutaneous jaundice was promi- ination of these areas confirmed haemorrhagic
nent. The serum bilirubin was 0.10 g/l. A spinal necrosis of recent character, without any microtap revealed clear CSF with 3.20 g/l protein, and glial or astrocytic reactions. In one of the
154 red cells/ml. A brain Te scan and carotid Ammon's horns, in addition to these haemorrhagic
angiography disclosed no abnormal feature.
lesions, a small solitary mycotic abscess was obOn the fifth day, the patient did not react to served. The inflammatory infiltration consisted of
stimuli. The pupil reflexes were still present. The polynuclear cells and the same filamentous fungi
seizures were lateralised either to the right or to as those seen in the lungs were observed. This
the left limbs. The EEG disclosed diffuse poly- lesion was minute and well demarcated. Scattered
morphic slow waves (Fig. 1). A generalised seizure ischaemic lesions were seen in the Purkinje cells
was recorded, initiated by spike activity on the and the temporal neurones. The hypothalamus,
right side. The temperature rose to 41 0C. The brainstem, and basal ganglia were intact.
patient died on her sixth day in hospital.
Discussion
PATHOLOGY

Visceral necropsy showed congestion and oedema
of both lungs and foci of bronchopneumonia, confirmed by histological examination which, in addition, showed the presence of filamentous fungi

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This patient presented a severe encephalopathy
with status epilepticus of six days duration. It was
associated with an acute, probably viral, hepatitis
assessed by evidence of liver necrosis, hyperam-

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monaemia, and hyperventilation. The usual signs
of hepatic coma were absent, notably the asterixis
and extrapyramidal syndrome, but convulsions
were prominent which are rarely seen in the
absence of an associated alcohol withdrawal syndrome (Adams and Foley, 1953). Encephalomyelitis was described in the early stage of viral
hepatitis (Thorling, 1950; Friedlander, 1956). It
was characterised by altered state of consciousness
and various neurological deficits but convulsions
were only reported in children. By contrast, severe
seizures are common with acute encephalopathy
associated with the fatty liver degeneration described in children (Reye et al., 1963) and attributed
to unspecified virus or toxins. In this latter syndrome, death would result from the increased
intracranial pressure and uncal herniation, rather
than from the hepatic insufficiency (Kindt et al.,
1975).
However, the necropsy findings in our case are
not consistent with this diagnosis. The liver
showed discrete steatosis and large areas of
necrosis with incipient portal fibrosis confirming
an acute hepatitis. Death resulted from intractable
convulsive status, but no evidence of uncal herniation was apparent. Haemorrhagic infarction was
found in the Ammon's horn and amygdala. The
distribution is comparable to the 'mesial temporal
sclerosis' observed in 50-70% of patients with
longstanding epilepsy (Sano and Malamud, 1953;
Falconer et al., 1964; Falconer, 1974) though the
exact relationship between both findings has been
much debated.

Experimental evidence has been presented that
mesial temporal sclerosis may be produced by
prolonged seizures. Meldrum et al. (1973a,b) provided a primate model of hippocampal sclerosis
induced by epileptic activity. Sustained generalised
seizures triggered by intravenous bicuculline were
shown to induce ischaemic changes in the
Ammon's horns, the amygdala, thalamus, Purkinje
cells, and the 3rd and 4th layers of the cortex.
The incidence of these ischaemic cell changes was
related to the total duration of seizure activity.
The distribution of the damage, with the emphasis
on the hippocampus and the almost invariable
sparing of the calcarine cortex (Ounsted et al.,
1966) is different from that which usually results
from an obstruction of the posterior cerebral
artery, which rules out an uncal herniation
secondary to an increased supratentorial pressure.
It may be postulated that the hippocampal lesions
result from coincidence of systemic hypoxia,
hypoglycaemia, arterial hypotension and hyperthermia, and local vascular factors (Brierley et al.,
1971).
Of significance could be the close relation between the hippocampus and the free edge of the
cerebellar tentorium. Indeed the Ammon's horn
is irrigated by a long collateral branch of the
posterior cerebral artery quoted by Lindenberg
(1955) as the Uchimura artery, after its first description (1928). In cerebral oedema accompanying
status epilepticus, this artery could be squeezed
between the brainstem and the free edge of the
tentorium, thus producing selective ischaemic

Mesial temporal haemorrhage, consequence of status epilepticus

changes in the Sommer's sector and the terminal
plate of the hippocampus. Simultaneous involvement of the Ammon's horn and the amygdala has
already been reported by Meyer et al. (1955) in
status epilepticus and could imply additional
interference with the blood supply in the territory
of the anterior choroidal arteries.
The scarring of the hippocampal lesions could
eventually lead to secondary temporal seizures,
accounting for the gliotic sclerosis commonly
seen in the temporal lobes of patients with longstanding epilepsy.
In our patient, status epilepticus lasted for six
days which is sufficient to induce cerebral damage
(Scholz, 1959). The liver insufficiency and defective coagulation mechanisms probably account for
the unusual haemorrhagic character of the lesions.
In any case, this peculiarity clearly underlines an
acute lesion of recent onset, thus secondary and
not primary to the convulsive status. By comparison with the accepted denomination of mesial
temporal sclerosis, this lesion complex could be
called mesial temporal haemorrhage.
The cause of the status epilepticus remains unclear. In the encephalitis complicating hepatitis
previously quoted (Friedlander, 1956) the only
pathological finding was cerebral venous congestion without inflammatory infiltration. It cannot
be ruled out that the fungal abscess found in one
Ammon's horn could have been a critical factor
in initiating the convulsive seizures, though such
parasitic complications are by no means rare in
fatal hepatic disease and usually go unnoticed
until necropsy.
References

Adams, R. D., and Foley, J. M. (1953). The neurological disorder associated with liver disease.
Research Publications, Association for Research
in Nervous and Mental Diseases, 32, 198-237.
Brierley, J. B., Brown, A. W., and Meldrum, B. S.
(1971). The nature and time course of the neuronal
alterations resulting from oligaemia and hypoglycaemia in the brain of Macaca mulata. Brain
Research, 25, 483-499.
Falconer, M. A. (1974). Mesial temporal (Ammon's
horn) sclerosis as a common cause of epilepsy.
Aetiology, treatment and prevention. Lancet, 2,
767-770.
Falconer, M. A.. Serafetinides. E. A., and Corsellis,
J. A. N. (1964). Etiology and pathogenesis of tem-

935

poral lobe epilepsy. A rchives of iN\eurology
(Chicago), 10, 233-248.
Fowler, M. (1957). Brain damage after febrile convulsions. Archives of Disease in Childhood, 32, 6776.
Friedlander, W. J. (1956). Neurological signs and
symptoms as a prodrome to virus hepatitis.
Neurology (Minneapolis), 6, 574-579.
Kindt, G., Waldman, J., Kohl, S., Baublis, J., and
Tucker, R. T. (1975). Intracranial pressure in Reye
syndrome. Journal of the A merican Aledical
Association. 231, 822-825.
Lindenberg, R. (1955). Compression of brain arteries
as pathogenetic factor for tissue necrosis and their
area of predilection. Journal of Neuropathology and
Experimental Neurology, 14, 223-243.
Meldrum, B. S. (1976). Neuropathology and pathophysiolegy. In A Textbook of Epilepsy. Edited by
J. Laidlaw and A. Richens, pp. 314-354. Churchill
Livingstone: Edinburgh, London, New York.
Meldrum, B. S.. and Horton, R. W. (1973a). Physiology of status epilepticus in primates. Archives of
Neurology (Chicago), 28, 1-10.
Meldrum, B. S., and Brierley, J. B. (1973b). Prolonged
epileptic seizures in primates. Archives of Neurology
(Chicago), 28, 10-17.
Meyer. A., Beck, E., and Shepherd, M. (1955). Lesions
in brain following status epilepticus. Journal of
Neurology, Neurosurgery, and Psychiatry, 18, 24-33.
Norman, R. M. (1964). The neuropathology of status
epilepticus. Medical Science Law, 4, 46-51.
Ounsted, C., Lindsay, J.. and Norman, R. (1966).
Biological factors in temporal lobe epilepsy. Clinics
in Developmental Medicine, Vol. 22. William
Heinemann Medical Books: London.
Reye, R. D. K., Morgan, G., and Baral. J. (1963).
Encephalopathy and fatty degeneration of the
viscera: a disease entity in childhood. Lancet, 2,
749-752.
Sano, K., and Malamud, N. (1953). Clinical significance of sclerosis of the cornu Ammonis. A rchives
of Neurology and Psychiatry (Chicago), 70, 4053.
Scholz, W. (1959). The contribution of pathoanatomical research to the problem of epilepsy.
Epilepsia, 1, 36-55.
Thorling, L. (1950). Neurological complications in
acute infectious hepatitis. Acta Medica Scandinavica. 137, 322-334.
Uchimura, J. (1928). Uber die Gafaszversorgung des
Ammonshornes. Zeitschrift fiur die Gesamte Neurologie und Psychiatrie, 112, 1-19.
Uchimura. J. (1928). Zur Pathogenesis der ortlich
elektiven Ammonshorn Erkrankung. Zeitschrift
fiir die Gesamte Neurologie und Psychiatrie, 114,

567-601.