LETTERS
benefit from an aripiprazole-olanzapine combination.
Jan Thone
References

1. Fleischhacker WW: Aripiprazole. Expert
Opin on Pharmacotherapy 2005; 6:2091–
2101
2. Duggal HS, and Mendhekar DN: Highdose aripiprazole in treatment-resistant
schizophrenia. J Clin. Psychiatry 2006;
67:674–675
3. Ramaswamy S, Vijay D, William M. et
al: Aripiprazole possibly worsens psychosis. Int. Clin. Psychopharmacol 2004;
19:45–48
4. Yokoi F, Gründner G, Biziere K, et al:
Dopamine D2 and D3 receptor occupancy in normal humans treated with
the antipsychotic drug aripiprazole
(OPC 14597): a study using positron
emission tomography and [11C] raclopide. Neuropsychopharmacology 2002;
27:248–259

MELAS Presented With
Status Epilepticus and
Anton-Babinski Syndrome;
Value of ADC Mapping in
MELAS

and bilateral sensorineural deafness. In past medical history, she
had a sudden hearing loss 2 years
ago. A conventional hearing aid
had been given. However, a clear
diagnosis was not established.
The CBC, metabolic parameters
and hormone levels were normal.
EEG showed diffuse slowing of
bioelectrical activity without any
epileptiform discharge. T1 and T2
weighted MRI revealed an hyperintense area on right temporooccipital region. Diffusion-weighted
images (DWI) showed diffusion restriction in same area. Intravenous
mannitol was initiated with suspicion of edema secondary to an ischemic infarction. The patient became oriented on the second day,
but fluctuations in mental status
continued in first week. Generalized
seizures also occurred, but its duration and frequency decreased with

carbamazepine. Echocardiogram
and carotid-vertebral Doppler ultrasounds were normal. She was discharged with antiaggregant and
antiepileptic treatment.
Control MRI revealed prominent
decrease in size of hyperintense
area on right temporo-occipital region, but also formation of a new
one on left occipital lobe at the end
of first month. DWI revealed diffusion restriction in same area. Different from other brain regions, apparent diffusion coefficient (ADC)
values were increased in that area
(Figure 1). She was hospitalized
again. MR spectroscopy showed severely elevated lactate and reduced
N-acetylaspartate, glutamate, myoinositol, total creatine concentrations in these lesions. The serum
level of lactic acid was detected as
2000 mg/dl (normal: 20–40 mg/dl).
EMG showed pathological myo-

FIGURE 1.

SIR: Mitochondrial encephalomyopathy, lactic acidosis with strokelike episodes (MELAS) is a mitochondrial disorder and an
important diagnostic consideration
in young patients with nonhemorrhagic stroke.1 We report on a patient with MELAS presented with
status epilepticus, and developed
Anton-Babinski syndrome during
the follow-up.
Case Report
A 38-year-old female admitted to us
with prolonged (about 20 minutes)
generalized tonic-clonic seizures.
They continued after intravenous 20
mg diazepam, but ceased with intravenous phenytoin infusion (20
mg/kg). Neurological examination
revealed moderate left hemiparesis

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J Neuropsychiatry Clin Neurosci 19:4, Fall 2007

LETTERS
pathic patterns, and nerve conduction velocities were normal. High
doses of vitamins and antioxidants
were introduced with the diagnosis
of MELAS. EEG again revealed
only diffuse slowing of bioelectrical
activity excluding the nonconvulsive seizures. Although she denied
it, she was suspected to have blindness during EEG procedure. After a
detailed neuro-ophthalmologic examination, she was detected to have
cortical blindness. DWI revealed
diffusion restriction in a large area
on left occipito-temporal region
which could underlie Anton-Babinski syndrome. Hyperglycemia (140–
220 mg/dl) was also detected at
15th day, and insulin treatment was
initiated. She died after a cardiac
arrest despite the resuscitation 2
days later.
Comment
The current knowledge about MELAS in the literature is indispensable especially for establishing an
early diagnosis. Diagnostic radiological approaches are important issues in differential diagnosis of MELAS and ischemic stroke. This
report clearly illustrates the value of
ADC mapping and serial imaging
for reaching the MELAS diagnosis
in earlier episodes. Acute ischemic
infarction with cytotoxic edema is
characterized by decreased diffusion and ADC values which can
also occur in MELAS.2–4 But it was
recently revealed that MELAS lesions could have increased ADC
values demonstrating vasogenic
edema.5 Therefore, the DWI and
ADC values of this case were in accord with the latter one. Although
it could not be excluded in opposite
states, MELAS must be highly suspected when restricted diffusion in
an area combined with increased
ADC values.
Anton-Babinski syndrome is a
well-known manifestation of
strokes in posterior circulation. This

is the first case of MELAS to develop Anton-Babinski syndrome reported in the literature. A clinician
must be careful in MELAS patients
to notice the formation of new lesions, and should differentiate this
entity from other confusional states.
Murat Alemdar, M.D.
Department of Neurology, Faculty of Medicine, University of
Kocaeli, Kocaeli, Turkey.
Pervin Iseri, M.D.
Department of Neurology, Faculty of Medicine, University of
Kocaeli, Kocaeli, Turkey.
Macit Selekler, M.D.
Department of Neurology, Faculty of Medicine, University of
Kocaeli, Kocaeli, Turkey.
Faik Budak, M.D.
Department of Neurology, Faculty of Medicine, University of
Kocaeli, Kocaeli, Turkey.
Ali Demirci, M.D.
Department of Radiology, Faculty of Medicine, University of
Kocaeli, Kocaeli, Turkey
Sezer Sener Komsuoglu, M.D.
Department of Neurology, Faculty of Medicine, University of
Kocaeli, Kocaeli, Turkey.
References

1. Pavlakis SG, Phillips PC, DiMauro S, et
al: Mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike
episodes: a distinctive clinical syndrome. Ann Neurol 1984;16:481–488
2. Chien D, Kwong KK, Gress DR, et al:
MR diffusion imaging of cerebral infarction in humans. AJNR 1992; 13:1097–
1102
3. Iizuka T, Sakai F, Kan. S, et al: Slowly
progressive spread of the stroke-like lesions in melas. Neurology 2003;
61:1238–1244
4. Wang XY, Noguchi K, Takashima S, et
al: Serial diffusion-weighted imaging in
a patient with melas and presumed
cytotoxic oedema. Neuroradiology 2003;
45:640–643
5. Kolb SJ, Costello F, Lee AG, et al: Distinguishing ischemic stroke from the
stroke-like lesions of melas using apparent diffusion coefficient mapping. J Neurol Sci 2003; 216:11–15

J Neuropsychiatry Clin Neurosci 19:4, Fall 2007

Acute Hypertensive Crisis
May Be a Risk Factor for
Alzheimer’s Disease
Induction and Progression
SIR: Epidemiological studies have
shown that Alzheimer disease is a
preventable disease and protective
strategies relating to dietary supplements, life style, avoiding environmental toxins, and in some cases
medication, have the capacity to reduce Alzheimer’s risk by 50% or
more.1 Increasing evidence show
that reactive oxygen species production, which is one of the main
causes of neurodegenerative diseases as Alzheimer, is increased in
patients with hypertension.2,3
The role of hypertension in Alzheimer disease has been studied,4
but the effect of hypertensive crises
has not yet been clearly demonstrated.
Poulet et al.5 have explored the effect of acute-induced hypertensive
conditions on cerebral oxidative
stress using a mouse model of transverse aortic coarctation between the
two carotid arteries, which acutely
imposes a dramatic increase in
blood pressure on the right brain
hemisphere. The results show that
hypertension acutely induced by
aortic coarctation induces a breaking
of the blood-brain barrier and reactive astrocytosis through hyperperfusion, and evokes trigger factors of
neurodegeneration such as oxidative
stress and inflammation.
We propose that acute hypertensive states including pheochromocytoma and acute postoperative hypertension may be risk factors for
induction and progression of Alzheimer disease. Surely this opinion needs
to be examined in clinical trials.
Shahriar Gharibzadeh
Neuromuscular Systems Laboratory, Faculty of Biomedical
Engineering, Amirkabir University of Technology, Tehran, Iran

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