Arq Neuropsiquiatr 2008;66(1):101-103

HEMIPARESIS AND LATERALIZED CORTICAL LESIONS
ASSOCIATED TO SEVERE HYPOGLYCEMIA
Marcus Sabry Azar Batista1, Kelson James Silva Almeida2,
Marcelo Cunha Avelino3, Luciana Marinho Viana Borges3
Severe hypoglycemia may occur as a complication of
insulin therapy or as a consequence of accidental or suicidal insulin injections1. It may result in a variety of neurological symptoms such as focal deficits, epileptic crisis, coma state and death. There is a relative rarity of reports about hypoglycemic-induced brain lesions2. In newborns, the parieto-occipital region is the most affected3.
In adults, there is a greater variability, with reports of lesions in basal ganglia, hippocampus, temporal and occipital gray matter, insula cortex, corona radiata and splenium of the corpus callosum1,4.
The aim of this study is to report the case of a patient presenting coma, with left hemiparesis and brain lesions detected by computerized tomography scan (CT)
and conventional magnetic resonance imaging (MRI). He
had insulin-dependent diabetes mellitus and had a record
of severe hypoglycemic episode.
CASE
A 31-year-old male, insulin-dependent diabetic patient, which
left his home after a family brawl, at about 8 o’clock p.m when
he had a capillary glycemia, which resulted 212 mg%. He was met
unconscious in the morning by his wife at a car, near their home,
with many empty flasks and syringes of insulin. The last register
of glycaemia in the dosimeter was 34 mg%, at about 3 o’clock a.m.
He was taken to the hospital by the urgency medical care
service. On admission, he showed stable vital signs and capillary
glycemia of 82 mg%. On neurological examination, the patient
was comatose and with left hemiparesis. He was submitted to
orotracheal intubation, mechanical ventilation and supportive
care. A cerebral computerized tomography (CT) scan showed a
slight parietal high-density area and MRI (Figure) showed cortical lesions with hypointensity and hyperintensity in T1- and T2weighted images, respectively, affecting the insula bilaterally,
but more evident on the right side, the hippocampus (more accentuated on the right side), the medial part of frontal lobe, bilaterally but more accentuated on the right side, and the parietal lobe, almost exclusively on the right side.

Figure. MRI showing cortical lesions with hyperintensity and hypointensity in T2- (A) and T1- (B) weighted images, respectively.

Hemiparesia e lesões corticais lateralizadas associadas à hipoglicemia grave
1

Neurology Professor of the Federal University of Piauí, Piauí PI, Brazil (UFPI); 2Medical School Student, UFPI. Getúlio Vargas Hospital; 3Radiologist,
Prontomed Hospital, Teresina PI, Brazil.
Received 27 July 2007, received in final form 8 October 2007. Accepted 28 November 2007.
Dr. Marcus Sabry Azar Batista – Rua Olavo Bilac 1737 - 64001-020 Teresina PI - Brasil. E-mail: marcussabry@uol.com.br
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Batista et al.

He evolved with progressive recovery of consciousness after a week, regaining temporospatial orientation gradually. The
patient keeps memory for new facts and he has been slowly recovering the memory for events previous to the episode. He fully recovered from left hemiparesis. After three months of follow up, he did not return to his professional activity (teacher in
a university) but he has been increasingly remembering a portion of the content of the subject he teaches. This study was approved by the Local Ethical Committee (Prontomed Hospital) after the informed consent by the patient.

DISCUSSION
Hypoglycemia in diabetic patients can occur because
of dietetic errors, alcohol abuse, excessive physical effort
or error in the dose of hypoglycemic drug, especially in
elderly patients. Severe hypoglycemia, on the other hand,
occurs when the insulin is used inadequately, because of
an accident or suicidal or homicidal intentions1,2.
In newborns, hypoglycemia is the most common metabolic disorder, and there are many reports describing
hypoglycemia-induced brain injury in this phase of life3.
Neonatal hypoglycemia can result in long-term disabilities
like epilepsy and visual impairment. The injuries include
the parietal region frequently, but mainly the occipital
region. The explanation for this selective vulnerability of
occipital lobes in neonates is a regional deficit in expression and function of the glucose membrane transporter
proteins3.
In adults, differently from neonates, the severe hypoglycemia can result in injuries with a bigger variability of
brain regions1, like in basal ganglia, hippocampus, insula,
frontal regions and corpus callosum. Usually, patients are
in coma or with respiratory failure; in the clinical outcome, entire disappearance of clinical features and even
death have been reported due to hypoglycemic encephalopathy, deep memory loss and persistent vegetative
state1,4,5. Hemiparesis is a rare and/or under-diagnosed
clinical manifestation of hypoglycemia6,7.
Dealing with a patient with acute onset of hemiparesis and coma, the possibility of stroke is the most probable4,8. In spite of this, patients with severe hypoglycemia
usually have a normal glycemia at admission, which may
delay the accurate recognition of etiology situation. Furthermore, diabetes mellitus is common among patients
with vascular brain disease. In these circumstances, the
clinical evolution and the MRI pictures can help in the
differentiation between stroke and hemiparesis resultant
of severe hypoglycemia.
In the hypoglycemic encephalopathy a reversion of
brain lesions is more likely to take place than in stroke.
Aoki et al. described reversible abnormalities in diffusionweighted MRI 10 days after glucose infusion9. In fact, as
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the reversible brain-imaging abnormalities and hemiparesis caused by hypoglycemia can mimic a transient
ischemic attack or stroke10, the determination of blood
glucose levels, the effects of its infusion and the comparison of MRI images on the day of admission to one taken
several days after glucose infusion can be useful tools to
make differential diagnosis9.
The mechanisms that explain the neuronal damage
during hypoglycemic episodes involves cytotoxic oedema,
shrinkage of the extracellular space and failure of ionic
pumps of the cell membrane after energy depletion 4,8.
Additionally, it is developed a tissue alkalosis for ammonia formation from the deamination of amino acids and
consumption of metabolic acids. The opposite occurs in
regions of brain infarction where it is observed intracellular acidosis4,8.
Another considerable hypothesis is the disruption of
protein synthesis in the superficial layers of the cortex,
in the basal ganglia, and hippocampus 1,9. On the other
hand, the cerebellum and brain stem are less affected by
this mechanism because they have effective strategies to
transport glucose9. Hypoperfusion in injured areas of the
cortex may occur for the selective regional loss of autoregulation in the cortex after hypoglycemia1. Another possibility is the occurrence of changes in blood-brain barrier
induced by hypoglycemia resulting in brain oedema11.
Mori et al. described the post-mortem examination
in a patient with hypoglycemic encephalopathy that had
evidence of high-intensity areas in brain white matter on
diffusion weighted MRI. More than cortical laminar necrosis, neuronal necrosis in hippocampus and dentate gyrus
(lesions compatibles with the brain injury induced by hypoglycemia), they observed that the cerebral white matter exhibited severe loss of myelin and that its axons had
reactive astrocytosis and macrophage infiltration12.
Others neuroimaging techniques such as positron
emission tomography (PET), functional magnetic resonance imaging (f-MRI) and diffusion weighted MRI can
provide maps of blood flow/oxygenation changes during
the neuronal activity and the manner in which these are
modulated by physiological factor, such as blood glucose
level1,13,14.
Anderson et al. induced a hypoglycemic state in ten
healthy patients and studied, by the f-MRI that contrasted
in dependence of blood oxygen level, the signs changes
in visual cortex after passive visual stimulation. They observed that during moderate hypoglycemia, this method
showed a reduced activity in the considered cortical area
and they suggested also that in other regions of cortex,
the variations in signal on f-MRI could reveal the regional
vulnerability of the brain to hypoglycemia13.

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Batista et al.

Arq Neuropsiquiatr 2008;66(1)

It is reported that radiological findings caused by hypoglycemia can have time-related changes. Maekawa et al.
evidenced lesions on diffusion weighted MRI at the cortex
of the bilateral posterior lobes and hippocampus in a patient with severe hypoglycemia; these lesions were sustained for 7 days after the severe hypoglycemic episode.
In the sequence, these findings lessened and disappeared
at the fourteenth day after the insult. It is important to
comment that at the day of images’ reversion, the patient
started opening his eyes in response to calling15.
The analysis of the brain images’ changes after a severe
hypoglycemic episode can be useful to predict the prognosis. Mainly the f-MRI can predict the patient’s evolution
for its sensitivity to detect the cytotoxic damage9. It has
been described that the most patients with lesions on
conventional MRI have a poor functional prognosis14. Basal ganglia involvement is also correlated with poor clinical outcome5. Nevertheless, it has been suggested that
lesions in this region can be a result of the association of
hypoglycemia with hypoxia1.
We supposed that the preservation of occipital cortex in our patient could have occurred for the absence of
luminous stimulation in the place where the event happened; the impairment of parietal cortex and pre-motors
areas can reflect the active regions during hypoglycemia.
This article contributes for the evaluation of severe
hypoglycemia-induced changes in CT and MRI and for the
understanding of selective susceptibility of cortical areas
to severe hypoglycemia. For the early recognition and intervention, we consider essential to remember that severe
hypoglycemia can be a possible cause of coma state and
focal signs, to favor a differential diagnosis with a pos-

sible stroke, especially in insulin-dependent patients or
in those cases in which intentional insulin injection was
suspected.
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