Neuropathology 2010; 30, 76–83

Cas e Rep o r t

neup_1039

doi:10.1111/j.1440-1789.2009.01039.x

76..83

Morel’s laminar sclerosis showing apraxia of
speech: Distribution of cortical lesions in
an autopsy case
Zen Kobayashi,1,2 Kuniaki Tsuchiya,2,3 Mafuyu Takahashi,4 Osamu Yokota,2,5 Kazuhiro Taki,6
Hideki Ishizu,7 Tetsuaki Arai,2 Haruhiko Akiyama2 and Hidehiro Mizusawa1
1

Department of Neurology and Neurological Science, Graduate School, Tokyo Medical and Dental University, Tokyo,
2
Tokyo Institute of Psychiatry, Tokyo, 3Department of Laboratory Medicine and Pathology, Tokyo Metropolitan
Matsuzawa Hospital, Tokyo, 4Department of Neurology, Ohme Municipal General Hospital, Tokyo, 5Department of
Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama,
6
Department of Pathology, Musashino Redcross Hospital, Tokyo and 7Department of Laboratory Medicine, Zikei
Institute of Psychiatry, Okayama, Japan

A 57-year old man with chronic alcoholism presented with
apraxia of speech and disturbance of consciousness.
He had a history of gastrectomy and had been drinking
alcohol. The symptoms improved with administration of
thiamine, but he later developed diarrhea and delirium,
and died approximately 40 days after the onset. Autopsy
findings were consistent with Wernicke’s encephalopathy
and pellagra encephalopathy. Furthermore, laminar cortical necrosis with vacuoles and astrocytosis was found in the
second and third layers of the bilateral frontal cortices,
suggesting Morel’s laminar sclerosis. The lesions were
mainly located in the bilateral primary motor cortices.
Involvement of the lower part of the left primary motor
cortex may be associated with apraxia of speech in our
case.
Key words: apraxia of speech, Morel’s laminar sclerosis,
pellagra encephalopathy, primary motor cortex, Wernicke’s encephalopathy.

paper.1 This time, we have added the description of the
clinical course, pathological findings, distribution of the cortical lesions, and review of the literature regarding Morel’s
laminar sclerosis, and discuss matters related to clinical
practice.
The term Morel’s laminar sclerosis was derived from the
publication by Morel in 1939 describing unusual pathological changes in four alcoholics, taking the form of spongiform change and gliosis of the cerebral cortex, mostly
confined to the third layer.2 Although some reports
described patients with Morel’s laminar sclerosis,3–6 the
information regarding clinical and pathological findings
has been limited.
Apraxia of speech (AOS) is caused by disturbance of
motor programming of articulation, and is classically distinguished from Broca’s aphasia by the preservation of the
ability to write language.7 Here, we report a patient presenting with AOS, and having histological findings indicating Morel’s laminar sclerosis, as well as Wernicke’s
encephalopathy and pellagra encephalopathy.

INTRODUCTION
A brief summary of the clinicopathological features of this
case was previously reported in this journal as “Neuropathology Education” by Tsuchiya, one of the authors of this

Correspondence: Zen Kobayashi, MD, Tokyo Institute of Psychiatry,
2-1-8 Kamikitazawa, Setagaya-ku, Tokyo 156-8585, Japan. Email: zen@
bg7.so-net.ne.jp
Received 17 March 2009; revised 7 May 2009 and accepted 10 May
2009; published online 25 June 2009.

© 2009 Japanese Society of Neuropathology

CASE REPORT
The patient was a 57-year-old Japanese man, who had been
living alone. After the publication of the previous paper,1
we found that the patient had been drinking 80–100 g of
alcohol per day (The duration was unclear.). Past history
included diabetes mellitus, foot necrosis, angina pectoris,
and gastric cancer. Because of these diseases, coronary
artery bypass graft (at age 51), digital amputation (at age
55), and total gastrectomy (at age 55) were performed. Five

Morel’s laminar sclerosis
days before admission, his brother had contact with the
patient by telephone, and the patient had been normal. On
the day of admission, an acquaintance visited him and
found him lying near his bed. He opened his eyes, but could
not speak. On admission, body temperature was 36.0°C,
blood pressure 136/115 mmHg, and heart rate 101 beats/
min. General examination showed severe emaciation and
surgical scars on the chest and abdomen. The palpebral
conjunctiva was anemic. The second and third digits of the
right foot had been amputated. On neurological examination, consciousness disturbance (easy arousal after normal
calling), and hyporeflexia in the four extremities were
demonstrated. He could not speak, but comprehension
of spoken language was normal. Tongue protrusion was
impossible. External ocular movement was normal. There
was no motor paralysis in the face or limbs. Ataxia of the
upper limbs was not apparent, while that of the lower limbs
and trunk could not be examined. Blood test showed a
white blood cell (WBC) of 7100/mm3 (normal range: 4000–
9000), red blood cell (RBC) 237 ¥ 104/mm3 (normal range:
430–570 ¥ 104), platelet count (Plt) 14.9 ¥ 104/mm3 (normal
range: 15–35 ¥ 104), total protein 6.3 g/dL (normal range:
6.5–8.0), urea nitrogen 41.6 mg/dL (normal range 8–20),
creatinine 0.7 mg/dL (normal range: 0.6–1.2), aspartate
aminotransferase (AST) 58 IU/L (normal range: < 35),
alanine aminotransferase (ALT) 45 IU/L (normal range:
< 40), blood sugar 180 mg/dL, and C-reactive protein
0.9 mg/dL. Brain CT demonstrated mild atrophy at the
bilateral frontal and temporal lobes. Although blood thiamine was not measured, the diagnosis of Wernicke’s
encephalopathy was suspected based on the history of gastrectomy and drinking alcohol. Hydration with administration of thiamine was initiated, but niacin was not given.
Consciousness disturbance gradually improved, but
anterograde and retrograde amnesia, and time disorientation became evident. At that time, we found that his
written language was normal, although the disturbance in
speech output was not completely resolved. Diarrhea was
also seen after the initiation of oral intake, but he was
transferred to another hospital 30 days after admission.
Thereafter, he developed delirium and convulsion, and
was transferred back to our hospital 6 days later. He
died on the same day. Artificial ventilation was not administered throughout the course. Autopsy was limited to the
brain.
The brain weighed 1130 g after fixation. Macroscopically,
bilateral mamillary bodies and inferior colliculi appeared
gray. There were no abnormalities in the thalamus or cerebral cortex (Fig. 1). Atherosclerotic changes of the middle
cerebral arteries and basilar artery were mild. Brain tissue
samples were fixed post mortem with 10% formalin and
embedded in paraffin. Ten-mm-thick hemispheric sections
were prepared at the plane of the left frontal lobe (the most
© 2009 Japanese Society of Neuropathology

77

Fig. 1 (a,c) Grayish discoloration in the bilateral mamillary
bodies (a, arrows) and inferior colliculi (c, arrowheads). (b) At the
level of the upper midbrain. There are no macroscopic abnormalities in the periaqueductal gray matter, thalamus or cerebral
cortex.

anterior section), left amygdala, bilateral mamillary bodies,
left pulvinar nucleus, and right occipital lobe.The sections of
upper and lower portions of the midbrain, upper and middle
portions of the pons, upper, middle, and lower portions of
the medulla oblongata, and bilateral cerebellum were also
prepared.These sections were stained with HE, KB, Bodian,
and Gallyas method, and anti-glial fibrillary acidic protein
(GFAP) (rabbit, polyclonal, Dako, Glostrup, Denmark,
1:1000). Reticulin silver stain was also performed to visualize the capillaries.
Microscopic examination demonstrated necrotic foci
with many vacuoles, accompanied by proliferation of
macrophages and astrocytes, and capillary proliferation in
the bilateral mamillary bodies and left inferior colliculi
(Figs 2,3). Pinpoint hemorrhages were seen in the right
mamillary body (Fig. 2c) and bilateral inferior colliculi.
Neurons were relatively preserved in the lesion (Fig. 2d).
Periaqueductal gray matter and oculomotor nucleus were
not involved. In the thalamus, neuronal loss with astrocytosis was obvious in the bilateral mediodorsal nuclei, anterior nuclei (Fig. 3c), and left pulvinar nuclei. In the bilateral
inferior olivary nucleus, patchy neuronal loss (Fig. 3d) with
astrocytosis was evident. There were no abnormalities in
the hypoglossal nucleus or cerebellum. These findings
suggested the diagnosis of Wernicke’s encephalopathy. In
addition, central chromatolysis of the neurons without
astrocytic or microglial changes was evident in the Betz

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Z Kobayashi et al.

a

b

c

d

e

cells (Fig. 3e), pontine nucleus (Fig. 3f), left abducens
nucleus, and bilateral cuneate nucleus, indicating pellagra
encephalopathy. Furthermore, laminar cortical necrosis
with vacuoles and astrocytosis was found in the second and
third layers of the bilateral frontal cortices (Fig. 4). The
vacuoles were partly seen in the first layer. The distribution
of cortical lesions is shown in Figure 5. The lesions were
mainly located in the bilateral primary motor cortices. On
the left side, the lower part of the primary motor cortex was
involved. The deep layers of the cortex were preserved.
Neither thrombi nor atherosclerotic changes were
observed in the vessels adjacent to the lesions. Alzheimer’s
type-II astrocytes were absent in the cerebral cortex and
basal ganglia. There were no ischemic changes in the hippocampal pyramidal cells or cerebellar Purkinje cells. The
Braak stage of neurofibrillary tangles was stage I. There
were no Lewy bodies or Pick bodies. In other words, cortical changes cannot be explained by ischemia, hypoxia,
hepatocerebral degeneration, or neurodegenerative
diseases.

Fig. 2 (a) and (b) are serial sections. (a)
Necrotic lesions in the right mamillary
body. Bar = 500 mm. (b) Astrocytosis and
central necrosis. Bar = 500 mm. (c) Many
vacuoles and hemorrhages (arrow) in the
right mamillary body. Bar = 100 mm. (d)
Relative preservation of the neurons
(arrows) in the right mamillary body.
Bar = 50 mm. (e) Capillary proliferation in
the right mamillary body. Bar = 50 mm. (a)
KB stain, (b) GFAP stain, (c, d) HE stain,
(e) Reticulin silver stain.

DISCUSSION
Clinically, our patient presented with AOS that improved
after the administration of thiamine. He also developed
diarrhea and delirium probably associated with pellagra.
At autopsy, the diagnosis of Wernicke’s encephalopathy
and pellagra encephalopathy was confirmed. Furthermore,
laminar cortical necrosis with vacuoles and astrocytosis
was found in the second and third layers of the bilateral
frontal cortices, suggesting Morel’s laminar sclerosis.
Thiamine deficiency, which is considered a cause of Wernicke’s encephalopathy, damages the mamillary bodies,
medial thalamus, and periaqueductal gray matter. Other
areas that are sometimes affected include the corpora
quadrigemina, reticular formation of the midbrain, pontine
tegmentum, superior vermis of the cerebellum,8 and inferior olivary nucleus.9 Observed lesions include loosening of
the neuropil and vascular changes such as hemorrhage,
capillary proliferation/dilatation, and endothelial swelling
in the mamillary bodies and the subependymal structures
© 2009 Japanese Society of Neuropathology

Morel’s laminar sclerosis

Fig. 3 (a) and (b) are serial sections.
(a,b) Central necrosis with astrocytosis (a)
and capillary proliferation (b) in the left
inferior colliculi. Bar = 200 mm. (c) Astrocytosis in the mediodorsal nucleus (indicated with M) and anterior nucleus
(indicated with A) of the right thalamus,
with sparing of the lateral nucleus (indicated with L). Bar = 500 mm. (d) Patchy
neuronal loss in the right inferior olivary
nucleus (arrowhead). Bar = 200 mm. (e)
Central chromatolysis of the Betz cell
(arrowhead) and a normal Betz cell
(arrow). Bar = 50 mm. (f) Central chromatolysis of the neurons in the pontine
nucleus. Bar = 50 mm. (a, c) GFAP stain,
(b) Reticulin silver stain, (d–f) KB stain.

79

a

b

c

d

e

f

along the aqueduct and fourth ventricle.9,10 In the thalamus
and inferior olivary nucleus, by contrast, neuronal loss is
demonstrated with sparing of the neuropil and capillaries.9
The distribution of lesions is associated with abundant
thiamine-related glucose and oxygen metabolism.11 Most
surgical procedures that include gastrectomy, gastrojejunostomy, colectomy, gastric bypass surgery are risk factors
for the development of Wernicke’s encephalopathy.8
Various CNS disorders are seen in patients with
Wernicke’s encephalopathy. They include MarchiafavaBignami disease,6 pellagra encephalopathy,12 and
Morel’s laminar sclerosis.5 To date, pathomechanisms of
Marchiafava-Bignami disease or Morel’s laminar sclerosis
have not been fully understood, although direct intoxication of alcohol or thiamine deficiency is considered to
cause these diseases, while pellagra is thought to be caused
by niacin deficiency.
Pellagra is classically characterized by a triad of dermatitis, diarrhea and dementia (or derilium), but dermatitis
and diarrhea are often lacking.13 Coexistence of Wernicke’s
encephalopathy or Marchiafava-Bignami disease makes
© 2009 Japanese Society of Neuropathology

the diagnosis of pellagra difficult. Based on the alcoholic
background, thiamine therapy is started in most patients,
but niacin is rarely started. Furthermore, antagonism
between thiamine and niacin had also been suggested. The
metabolic demands from a relative excess of thiamine may
increase the requirements for pyridine coenzymes, nicotinamide adenine dinucleotide (NAD) and nicotinamide
adenine dinucleotide phosphate (NADP). These require
niacin as a cofactor. Serudaru et al. reported a case of
a “late-onset” pellagra encephalopathy in an alcoholic
patient who deteriorated after thiamine therapy.13 This case
and our case suggested that multiple vitamin therapy
should be started when treating undiagnosed encephalopathies in patients with chronic alcoholism.
Pellagra encephalopathy presents with various symptoms such as dementia (or derilium), hypertonus, and
myoclonus.13 Serudaru et al. reported that hypertonus and
myoclonus were associated with lesions of pontine nucleus
and cerebellar dentate nucleus, respectively,13 but correlation between the symptoms and brain lesions has
not been fully established. Histopathologically, pellagra

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Z Kobayashi et al.

a

b

c

d

e

f

g

Fig. 4 (a) and (b) are serial sections. (a,b) Laminar cortical necrosis with vacuoles (a) and astrocytosis (b) in the second and third layers
of the left primary motor cortex, with some vacuoles in the first layer (a). Bar = 500 mm. The arrowhead in (a) indicates a Betz cell located
in the fifth layer. Inset shows this Betz cell. Bar = 50 mm.The area surrounded by the rectangle in (a) is shown in (d). (c) Normally, astrocytes
are present only in the first layer of the cerebral cortex (the left postcentral gyrus of the patient). Bar = 500 mm. (d) Neuronal loss in the
second and third layers. Bar = 200 mm. (e) There are no abnormalities in the second and third layers of the left postcentral gyrus.
Bar = 200 mm. (f), (g) Another cortical lesion. Bar = 200 mm. (a), (d–f) HE stain, (b, c, g) GFAP stain.

© 2009 Japanese Society of Neuropathology

Morel’s laminar sclerosis

81

Fig. 5 The primary motor cortices where
Betz cells were seen are depicted with
lines. The distribution of laminar cortical
necrosis with vacuoles and astrocytosis is
shown in red. The lesions were mainly
located in the bilateral primary motor cortices. On the left side, the lower part of
the primary motor cortex was involved
(arrows).

encephalopathy is characterized by central chromatolysis
of the neurons in the pontine nucleus, where they are constant, in the cerebellar dentate nuclei, nuclei of cranial
nerves, gracile and cuneate nuclei, and Betz cells.14 The
central chromatolysis in pellagra is thought to be not a
retrograde change but a primary cytoplasmic change.14
Morel’s laminar sclerosis was derived from the publication by Morel describing unusual pathological changes in
four alcoholics, demonstrating spongiform change and
astrocytosis seen extensively and symmetrically in the
cerebral cortex, mostly confined to the third layer.2 The
review of Morel’s laminar sclerosis published by Okeda
et al. in 19765 described 21 cases of Morel’s laminar sclerosis, in which Marchiafava-Bignami disease was seen in 17
cases (81%), and Wernicke’s encephalopathy was seen in
six cases (30%). They reported that Morel’s laminar sclerosis was not seen in the occipital lobe. In their own case,
laminar astrocytosis was seen in the third layer of the
frontal, parietal, and temporal cortex. Spongiform changes
were observed in the adjacent second layer. The lesions
were severe in the middle and inferior frontal gyri.5 Since
1976, three papers have reported patients with Morel’s
laminar sclerosis in the English language literature.3,4,6
Naeije et al. reported that the lesions selectively involved
the third and fourth layers of the cortex. Characteristic
© 2009 Japanese Society of Neuropathology

changes were neuronal loss, capillary proliferation with
thickened endothelia, proliferation of microglial cells, and
swollen astrocytes.3 Okeda et al. reported that the cerebral
cortex presented extensive laminar astrocytosis and/or
laminar neuronal loss accompanied by capillary proliferation in the middle layers of the frontal and parietal cortices
in case 2.4 Sato et al. reported that the cerebral cortices
showed mild neuronal loss and proliferation of astrocytes,
particularly in the third layer.6
Recently, by application of MRI, cortical involvement in
patients with Wernicke’s encephalopathy or MarchiafavaBignami disease has been increasingly reported.11,15–22
Interestingly, the primary motor cortex was involved in
most of these cases while the description regarding focal
neurological signs was absent. In other words, the regions
around the primary motor cortex seem to be sometimes
mildly involved in these diseases. Although these reports
did not include detailed histological findings, the cortical
lesions may reflect Morel’s laminar sclerosis17 or hepatocerebral degeneration.23
To date, clinicopathological correlation in Morel’s
laminar sclerosis has rarely been reported, probably
because consciousness disturbance due to concomitant
Wernicke’s encephalopathy or Marchiafava-Bignami
disease masks the symptoms. In our case, spontaneous

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Z Kobayashi et al.

speech was impossible on admission, but comprehension
of spoken language was good. After the disappearance of
consciousness disturbance, we found that the written language was normal, even though the disturbance in speech
output was not completely resolved. Although neuropsychological tests were not performed in detail, we considered that his speech disturbance was AOS. The concept of
AOS has been controversial and is sometimes called pure
anarthrica24 or aphemia.7,25 AOS is caused by disturbance
of motor programming of articulation, and is classically
distinguished from Broca’s aphasia by the preservation of
ability to write language.7 The differentiation of AOS from
dysarthria is also sometimes difficult. In our case, tongue
protrusion was impossible, but speech disturbance was significantly worse than expected. Although AOS has been
reported to be caused by brain lesions involving various
areas,7,24–27 one of the responsible areas is the lower part of
the left primary motor cortex.25,27
In conclusion, we report a patient with Morel’s laminar
sclerosis in whom AOS was seen. Involvement of the lower
part of the left primary motor cortex may be associated
with AOS in our case.

ACKNOWLEDGMENT
The authors thank Dr Satoru Ishibashi (Department of
Neurology and Neurological Science, Graduate School,
Tokyo Medical and Dental University) for help for the
production of the manuscript, and Ms Hiromi Kondo
(Tokyo Institute of Psychiatry) for excellent technical
assistance. This work was supported by a grant-in-aid for
scientific research from the Ministry of Education, Culture,
Sports, Science and Technology (14570957) and a research
grant from the Zikei Institute of Psychiatry.

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