Farishta and Shaik UJP 2015, 04 (01): Page 60-65

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Universal Journal of Pharmacy

Review Article
ISSN 2320-303X

Take Research to New Heights

UNDERSTANDING SEIZURES IN DIABETES

Farishta Faraz1*, Shaik Abdul Suhale2
1

Assistant Professor, Department of Internal Medicine, Mediciti institute of Medical sciences, Hyderabad, India
2
Registrar, Internal Medicine, Mediciti institute of Medical sciences, Hyderabad, India

Received 06-12-2014; Revised 04-01-2015; Accepted 02-02-2015

ABSTRACT
In diabetic patients, abnormal blood glucose levels may be associated with exacerbation of focal seizures.
Hyperglycemia leads to hyperexcitability of the neurons that make up the central nervous system, including the brain.
With the brain's overexcited imbalance, hyperglycemic seizures can be triggered. Hypoglycemia reduces the activity of
neurons in the brain ,which in turn reduces the activity across synapses ,the microscopic spaces in between neurons
that propagate the brains activities and preserve bodily function, thus leading to a seizure. Impaired activity across
synapses may lead to seizures. In the clinical setting, hypoglycemic seizures occur most commonly in individuals with
poorly regulated type 1 diabetes mellitus, especially at times of altered insulin availability or function. In children, 75%
of hypoglycemic seizures occur at night, which is the most vulnerable period for hypoglycemia, since sleep blunts the
counter regulatory responses to hypoglycemia. In young children, there is concern that severe hypoglycemic events can
cause permanent neurologic sequelae. It is therefore critical to know how long hypoglycemia can be tolerated before a
severe hypoglycemic event (seizure or coma) occurs. Recording of blood glucose levels before, during, or after seizures
rarely occurs. Without this information, it is difficult to determine whether hypoglycemia was the cause of the seizure.
Focal seizures associated with nonketotic hyperosmolar hyperglycemia are refractory to anticonvulsant treatment and
respond best to insulin and rehydration. It is difficult to establish a clear cause-and-effect relationship between
hypoglycemia and seizures in the diabetic population. In the future, continuous glucose monitoring (CGM) technology
may aid in the diagnosis.
Keywords: Diabetes, Seizures, Hypoglycemia, Hyperglycemia, Neuron, Brain.

INTRODUCTION
Diabetes mellitus (DM) is the most common metabolic
and endocrine disease, defined by World Health
Organization as a syndrome consisting of a group of
metabolic
entities
characterized
by
chronic
hyperglycemia as the result of inadequate insulin
resistance and/or resistance to its biological effect1. An
epileptic seizure (or fits) is defined as a transient
symptom of abnormal excessive or synchronous
neuronal activity in the brain2. About 4% of people will
have an unprovoked seizure by the age of 80 and
chance of experiencing a second seizure is between
38% and 40%3. Seizures are categorized into generalized
and focal (or partial) types, depending upon whether
they arise deep within thalamocortical circuits, or from
a specific site (or focus) within the brain, respectively.
*Corresponding author:
Dr. FARAZ FARISHTA,
Assistant professor,Department of Internal Medicine,
Mediciti institute of Medical sciences Hyderabad, India.

Etiology of Seizures can vary from high fevers, viral

infections of the brain, head injuries, drug reactions or
insulin shock. Mixed signals from brain cells cause
seizures which are similar to those caused by a head
injury or a high fever.
Health care providers and patients have become aware
of the relationship between insulin, seizures and
coma4. Seizures are a common complication of
endocrine disease, either as a result of general
biochemical and metabolic abnormalities, or as a
specific syndrome related to the primary disease
process5. Hyperglycemia (high blood sugar) or
hypoglycemia (low blood glucose <3.9 mmol/L) can
cause seizures, which could lead to coma, convulsion,
or death if untreated6.
It is critical to know how long hypoglycemia can be
tolerated before a severe hypoglycemic event (seizure
or coma) occurs7. There is a paucity of data to support
whether it is absolute serum levels of glucose or rather
rapid changes that are more important for
epileptogenesis. Anticonvulsants used at doses that
control seizures in other disorders, often seem

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Farishta and Shaik UJP 2015, 04 (01): Page 60-65

ineffective in treating seizures resulting from hypo- or
hyperglycemia5.
Clinical studies in diabetic patients have yielded varied
results, episodes of severe hypoglycemia have been
shown to alter brain structure and are reported to
cause significant cognitive damage in many, but not all
studies.8 Medical literature on the prevalence of
diabetes along with seizures is scarce. This article will
explore the features of seizures in diabetes mellitus,
including their incidence, prevalence, potential
underlying mechanisms that lead to seizures among
diabetic patient, treatment, and clinical evidence
available for this association.
Prevalence of seizures in diabetes mellitus
Hypoglycemia is the most prevalent clinical
complication in diabetic patients on insulin treatment
and continues to be the limiting factor in the glycemic
management of diabetes. Since severe hypoglycemia
affects 40% of insulin-treated people with diabetes,
concern regarding the hazardous potential for severe
hypoglycemia to cause brain damage continues to be
a very real barrier in striving to fully realize the
benefits associated with intensive glycemic control8.
Seizures have been reported to occur in 7-20% of all
diabetic patients. In the clinical setting, hypoglycemic
seizures occur most commonly in individuals with
poorly regulated type 1 diabetes mellitus (T1DM),
especially at times of altered insulin availability or
function. Hypoglycemic seizures also occur frequently
in infants of diabetic mothers and in newborns with
asphyxia, sepsis, congenital heart disease, and a
variety of hereditary metabolic disorders and
endocrinopathies9.
In children, 75% of hypoglycemic seizures occur at
night. Among patients with T1DM, there is a 6% lifetime
risk of dead-in-bed, which may in part be a result of
severe nocturnal hypoglycemia.7 In young children,
there is also concern that severe hypoglycemic events
can cause permanent neurologic sequelae.
The Diabetes Control and Complications Trial reported
the frequency of hypoglycemic loss of consciousness
events in patients with T1DM. In the studys intensive
therapy group, loss of consciousness events occurred at
a rate of 16.3 episodes per 100 patient-years, which
falls within the range of other reports4.
A study conducted by Ramakrishnan and Appleton
(2010) in the Paediatric Diabetes Clinic at Alder Hey
Childrens Hospital, UK, evaluated the prevalence of
epilepsy in 285 T1DM children below 16 years of age.
The prevalence of epilepsy in diabetic children was
found to be 21/100 (6 out of 285 children had
epilepsy), which was 6 times greater than the
prevalence in the general population of children in the
UK10.
Schober et al (2011)11 estimated the prevalence of
epilepsy and possible risk factors in children and
adolescents with DM. They conducted an observational

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cohort study, based on the Diabetes Patienten
Verlaufsdokumentation (DPV) database, including data
from 45,851 patients (52% male) with T1DM, aged
between 13.9 4.3 years (mean SD) and duration of
diabetes mellitus 5.4 4.2 years. The database was
searched for the concomitant diagnosis of epilepsy or
epileptic convulsions and for antiepileptic medication.
A total of 705 patients with epilepsy were identified,
giving a prevalence of 15.5 of 1000. Patients with
epilepsy were younger at onset of DM and shorter than
patients without epilepsy, and their weight and body
mass index were comparable. No difference could be
demonstrated for metabolic control, type of insulin
treatment, insulin dose, and prevalence of B-cell
specific autoantibodies. The frequency of severe
hypoglycemia was lower in patients treated with
antiepileptic medication. The risk for diabetic
ketoacidosis (DKA) was almost double in patients with
epilepsy compared with patients with T1DM alone
(P < 0.01). Children and adolescents with diabetes
mellitus show an increased prevalence of epileptic
seizures. For unknown reasons, there is an association
between epilepsy and diabetic ketoacidosis in children
with T1DM11.
Causes for diabetic seizures
In diabetic patients increase or decrease in blood sugar
levels can be attributed of different reasons, and these
fluctuations in blood sugar levels are primary cause of
seizures in these patients. With majority of episodes
occurring at night when the blood sugar levels are low.
Hypoglycemia can also be the result of pancreatic islet
cell dysfunction such as islet cell hyperplasia or
insulinoma. In such cases the seizures present during
the night or early morning are resistant to conventional
antiepileptic treatment5.
The long-term regulation of cerebral energy substrates
undoubtedly involves glycogen storage and release,
during acute seizures resulting from hypoglycemia, the
brains energy needs might be unmet, leading to the
adverse consequences for seizure susceptibility and
cognition9.
Glucose transport across the blood brain barrier is
reduced during seizures and therefore, it is assumed
that tissue hypermetabolism during the ictus is
independent of the plasma glucose level. It is unclear if
this presumed energy substrate deficiency may prolong
the seizures5.
Pathophysiology of hypoglycemic seizures
Glucose is known to play a critical role in brain
functions because it represents the main source of
metabolic energy generation. Hypoglycemic episodes,
particularly at night, are known to be a common
problem in patients with insulin-treated diabetes12.
Glutamic acid decarboxylase (GAD) is the enzyme that
catalyzes the conversion of glutamic acid into -aminobutyric acid (GABA),
one of the classical
neurotransmitters with neuroinhibitory function. GAD is

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present only in GABAnergic neurons, but also in
pancreatic -cells, testis, liver, kidney, and adrenal
glands. AntiGAD antibodies are now considered to be a
marker of T1DM, since they can be found in the sera of
the majority of individuals with preclinical and early
phase T1DM13.
The mechanisms underlying the epileptic phenomena
during hypoglycemia have not yet been fully
understood, however, experimental studies suggest
that the loss of high-energy substrates for the
tricarboxylic acid cycle may cause a neurotransmitter
imbalance that result in a massive release of excitatory
amino acids and possible subsequent excitotoxic
effects. Consequently, hypoglycemia may, on the one
hand, induce epileptic symptomatic seizures and, on
the other, predispose to the development of
epileptogenic processes12.
Symptoms of diabetic seizures
Seizures are the most common presenting neurological
symptoms of hypoglycemia at any age. Hypoglycemic
seizures usually occur at a serum glucose level of less
than 40 mg/dL.
The symptoms of diabetic seizures are similar to the
symptoms of epileptic or other types of seizures.6
Symptoms could be as faint as staring into space or
blinking, or as strong as violent convulsions6. Seizures
can range from mild to severe. Mild seizures may take
place and end in a matter of seconds. Severe seizures
may involve uncontrollable muscle spasms, rigidity, loss
of consciousness, loss of bladder and bowel control,
and in some cases, breathing that stops temporarily.6
A diabetic person experiencing seizures may have any
of the following symptoms5,6: muscles may twitch, jerk,
or slowly become rigid (clonic seizures); can, but do
not always causes violent convulsions; loss of muscle
tone (tonic seizures); can affect involuntary body
movement and function (clonic seizures); alter
sensation, awareness or behaviour; body parts can
become numb; tachycardia, palpitations, nervousness,
dizziness;
nausea;
sweating;
fatigue;
hunger,
headache; tremor, and brief loss of memory. These
symptoms may be followed by a change in mental
status, focal neurological signs, seizures, and coma5. A
diabetic person experiencing grand mal seizures could
call out, pass out, fall down, and injure themselves6.
Clinical evidence
Although there have been some reports of the
frequency of insulin-induced unconsciousness events,
validating the formal relationship in a clinical setting
may be difficult for several reasons4.Insulin induced
unconsciousness sometimes
can mimic a seizure
activity.
The association between T1DM and epilepsy is unclear
and requires more definitive epidemiologic analysis,
despite the fact that antibodies to glutamic acid
decarboxylase may provide a link between the two
conditions14.

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Hypoglycemia-induced Seizures
Hypoglycemia, common in diabetic patients treated
with insulin, can induce various neurological
disturbances. Of these, seizures are the most common
acute symptom, mainly of the generalized tonic-clonic
type, with focal events only exceptionally being
reported and documented. The relationship between
hypoglycemia and epileptic phenomena is complex and
has not yet been fully understood. Hypoglycemia can
modify cortical excitability by determining an
imbalance between excitation and inhibition; some
brain structures, such as the temporal lobe and
hippocampus, appear to be particularly susceptible to
this insult12.
Seizure caused by hypoglycemia is a benign and curable
situation, but it may be fatal if unrecognized.15 CNS
complications of diabetes mellitus increase with the
severity and chronicity of disease. Most seizures result
from severe metabolic abnormalities associated with
Nonketotic Hyperosmolar Hyperglycemia (NHH), DKA,
hyperglycemia, or from increase in cerebrovascular
disease from diabetes16.
Hypoglycemia can occur at anytime during the night,
most typically around 3 am. Undetected night time
hypoglycemia can lead to seizures and convulsions but
it is important to remember that not all seizures result
in convulsions. Two indications that a person has had a
severe night time episode of hypoglycemia (whether or
not seizures were involved) include waking with a high
fasting blood glucose level (Somogyi, or Rebound
Effect) and morning headache, and being drenched in
sweat.
Hart and Frier (1998)17 retrospectively analyzed the
clinical features of patients with acute hypoglycemia
admitted to the hospital with hypoglycemia in a large
teaching institution in a 12-month period. Of 51
patients, 41 had diabetes mellitus and the other had
hypoglycemia.
Neurological
manifestations
of
hypoglycemia were the main reason for hospital
admission, and 11 events (20%) had precipitant
convulsions. Patients who require hospital admission
for treatment of hypoglycemia have a high incidence of
neurological manifestations, a high rate of mental
illness and other medical disorders, and may represent
a high-risk subgroup with a poor long-term prognosis.17
Recently, continuous glucose monitoring (CGM)
technology has allowed researchers to capture data
furthering the understanding of hypoglycemia-induced
seizures. The capturing of these seizure events on CGM
suggests that several factors, including nocturnal
timing, sleep status, and preceding duration of
hypoglycemia, may be necessary to create the clinical
event of a hypoglycemic seizure4.
Hyperglycemia-induced Seizures
The importance of glucose balance has been identified
in
studies
demonstrating
that
hyperglycemia
exacerbates ischemia-induced brain damage9.

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It is common practice to measure blood sugar content
in patients with acute episodes of convulsions.
However, very few reports deal with blood glucose
levels during fits in infancy. One study found raised
values (from 117 to 296 mg/100 mL) in 6 out of 12
children examined during or immediately after a febrile
convulsion. It appears that the hyperglycemia during a
convulsive episode is due to stress, is of short duration,
and probably has no pathological significance. It may
be important to bear in mind because of its possible
effects on the glucose level of the cerebrospinal fluid18.
Epileptic seizures or insulinoma in diabetes
Insulinoma, a rare neuroendocrine neoplasm deriving
mainly from pancreatic islet cells can secrete insulin in
short bursts and cause fluctuation of blood glucose
level correspondingly, and then the patients will have
intermittent neuroglycopenic symptoms, such as
conscious disorder, abnormal behavior, psychiatric
symptoms, or convulsion. Therefore, it is sometimes
misdiagnosed as epileptic seizures. Hypoglycemia can
activate focal abnormality in electroencephalography
(EEG) in epileptic who have an old lesion in the cortex.
The EEG for hypoglycemia usually shows diffuse or focal
slowing and enhanced response to hyperventilation.
However, the EEG in some patients with insulinoma
showed focal slowing (over the left mesial temporal
lobe) and later generalized spikes and sharp waves as
well as slow waves. An EEG slowing caused by
hypoglycemia represents an inhibitory state and
adaptive hypometabolism of the brain; additionally,
epileptiform discharges could reflect disarrangement of
neuronal excitation and inhibition as a result of
selective neuronal vulnerability to neuroglycopenic
damage. Various experimental studies confirmed that
severe hypoglycemia is able to induce spontaneous
synchronic discharges in vitro and in vivo, thus even
generate a hypermetabolic state and further deplete
the brain energy reserve. This seizure-like event cannot
be blocked by the common antiepileptic drugs15.
Diabetic ketoacidosis and epileptic seizures
Diabetic ketoacidosis, an acute complication of
diabetes mellitus, is characterized by the triad of
hyperglycemia, ketosis, and metabolic acidosis. DKA is
an emergency situation, can complicate mainly T1DM,
and hospitalization of the patient is necessary for
immediate treatment19. The American Diabetes
Association estimates that 5-25% of children with newly
diagnosed type 2 diabetes mellitus have DKA20.
There is a lower incidence of seizures in ketotic
hyperglycemia compared with NHH. Ketosis itself has
an anticonvulsant action due to intracellular acidosis
which is known to increase GAD activity leading to
enhanced GABA synthesis5,21. Ketogenic diets in
patients with intractable epilepsy are thought to be
effective through a similar mechanism5.
In the presence of hyperglycemia, GABA metabolism is
increased and the levels of this important inhibitory

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neurotransmitter may be depressed resulting in a
reduction of seizure threshold. Focal reduction in blood
flow may be important and is known to occur in
hyperglycemia but even when this was severe enough
to cause cerebral infarction focal seizures occurred
only when blood glucose was high21.
Nonketotic hyperosmolar hyperglycemia and focal
seizures
Nonketotic Hyperosmolar Hyperglycemia is one of the
most serious acute complications of diabetes, with
significant morbidity and mortality. It is characterized
by usually extreme hyperglycemia (> 600 mg/dL
[33.3 mmol/L),
hyperosmolality,
and
profound
dehydration, without significant ketoacidosis.
Focal seizures in adults may indicate diabetes mellitus.
Recurrent focal motor seizure was the first
manifestation of NHH of diabetes mellitus. The seizures
were characterized by stereotypical tonic changes in
body posture and arrest of speech that have been
associated with supplementary motor area seizures22.
In NHH, seizures occur early in hyperglycemia, when
the osmolality is only modestly increased, with minimal
reduction in sodium levels, and usually when
consciousness is preserved5. In general, 6% of the NHH
cases present with focal motor seizures, and 25% of
NHH patients eventually develop seizures5. Seizures
related to NHH may occasionally have strange features:
reflex seizures, speech arrest or have a visual
component, or transient subcortical T2 and fluid
attenuated inversion recovery hypointensity due to the
accumulation of free radical and iron deposition.
Focal seizures associated with NHH are refractory to
anticonvulsant treatment and respond best to insulin
and rehydration. The occurrence of focal seizures in a
middle aged to elderly patient should signal the
possibility of diabetes mellitus22.
Recognition of the link between this unusual form of
focal epilepsy and NHH would help in the early
diagnosis and treatment of the serious underlying
metabolic disturbance22.
Correlation between epileptic seizures and diabetes
mellitus during and after stroke
Epilepsy can occur as the first symptom of stroke
(associated seizure) during the acute stroke phase
(early epileptic seizure) within 2 weeks of the stroke
onset or as a consequence of stroke after 14 days or
later (late epileptic seizures). A retrospective study
conducted by Aljbegovi (2002)1 evaluated the impact
of diabetes on the onset of stroke and of the early/late
epileptic seizures in 7001 stroke patients. Of 114
patients with epileptic seizures, 34 (29.8%) had
diabetes mellitus (7.9% type 1 and 20.2% type 2): 19
with early seizures (3 with type 1 and 12 with type 2)
and 15 with late seizures (3 with type 1 and 11 with
type 2). The mean duration of diabetes after stroke in
patients with late and early seizures was 10 years and
14.7 years,
respectively.
Hyperglycemia
was

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significantly more common in the group of patients
with early seizures than in the group with late seizures
(60.9%). Diabetes mellitus was found to be a significant
risk factor for the onset of stroke as well as for the
occurrence of early epileptic seizures during stroke
(P< 0.1). In diabetics with stroke, hyperglycemia is a
significant factor that can lead to the occurrence of
early epileptic seizures1.
Relevance of electroencephalography in diabetic
seizures
The EEG is more responsive to acute hypoglycemia than
hyperglycemia. Generalized seizures with high voltage
spike activity, as well as focal discharges, can be seen
in metabolic disorders causing acute hypoglycemia,
such as insulinomas23. In severe hyperglycemia,
pronounced slowing is typical although focal
abnormalities can be seen. Exaggerated response to
hyperventilation and accentuation of underlying
interictal patterns can be seen during hypoglycemia.
The EEG changes in hypoglycemia are nonspecific. A
study performed by Bjrgaas and colleagues (1998)24
recorded quantitative EEG in 19 diabetic children
(mean age 14.2 [SD 1.4] years, mean HbA1c 9.8 [SD
1.2]%) and 17 nondiabetic children (mean age 14.3
[SD 1.1] years) exposed to a gradual reduction in serum
glucose. At specific serum glucose level of 4 mmoL,
diabetic children displayed significantly more EEG
deterioration during hypoglycemia than nondiabetic
children. This suggests that seizure thresholds may be
lower in diabetic patients, and factors other than
absolute serum glucose levels are responsible for the
seizures24.
Seizure management in diabetes mellitus
Hypoglycemia should be in the differential diagnosis of
any individual with seizures. Because diabetes is a
condition that typically uses hypoglycemia-causing
agents (insulin and oral hypoglycemic agents in the
sulfonylurea and meglitinide drug classes), it is
important to be aware that seizures in this population
could be iatrogenic4.
In seizing patients, particularly those taking insulin,
sulfonylureas, or meglitinides, hypoglycemia-induced
seizure should be considered. If clinically appropriate,
a seizing patient should be administered glucose as a
possible remedy4.
To prevent serious events such as seizures, glucose
sensors must both detect hypoglycemia and provide a
sufficiently robust alarm to awaken the patient or some
other member of the household7. It is difficult to
establish a clear cause-and-effect relationship between
hypoglycemia and seizures in the diabetic population.
In the future, CGM technology may aid in the
diagnosis4. If a person shows any of the symptoms of
diabetic seizure, then immediately seek medical help.
In case of hypoglycemia (low blood sugar), honey or
syrup can be placed inside the gums or glucose
injection can be given to raise blood sugar levels. In

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case of hyperglycemia (high blood sugar), insulin
injections can be given to lower blood sugar levels.6
A diabetic person having a seizure can fall, bang their
bodies against objects or bite their tongues. Acute
seizures should be controlled, seizure prophylaxis with
antiepileptics should be instituted, and any causative
factors, including biochemical/metabolic abnormalities
and the primary disease process, should be corrected.5
It is important to measure antiGAD antibodies in
cerebrospinal fluid in case of T1DM whenever
accompanied by neurological disorders, such as seizure,
ataxia, rigidity, or painful spasms.13 Prompt treatment
of hypoglycemic seizures may help avert those
complications,
possibly
in
conjunction
with
neuroprotective agents that work independently of
glycogen (eg, NMDA receptor antagonists, GABA
receptor agonists)9.
Patients and caregivers must know how to avoid
seizures and to recognize their signs so that proper
immediate assistance is provided.

CONCLUSION
The potential cognitive consequences of severe
hypoglycemia, including coma and seizure, are a key
concern for clinicians, patients, and families. Diabetes
increases the risk of seizures. The magnitude of this
problem will continue to expand as the prevalence of
diabetes increases worldwide, thus presenting
numerous challenges for the future. There needs to be
greater awareness of the association of NHH and focal
epilepsy. If not recognized the diagnosis of diabetes
mellitus may be missed and the patient subjected to
unnecessary
investigations
and
inappropriate
treatment. Seizures in chronic diabetic patients
with/out comorbid conditions such as stroke, seizures
or other metabolic problems and antiepileptic drugs
effect on diabetes in general illustrates the importance
of appropriate education of patients with diabetes and
the techniques to prevent hypoglycaemia and needs
further evaluation and research. Self-report of severe
hypoglycaemia is an important prognostic indicator that
should be included in the clinical assessment of each
patient with diabetes. There is also need to undertake
more studies to correlate the blood and cerebrospinal
fluid glucose levels in convulsive episodes.

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Source of support: Nil, Conflict of interest: None Declared

Universal Journal of Pharmacy, 04(01), Jan-Feb 2015

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