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Abdominal epilepsy: An uncommon of non-convulsive status epilepticus

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To recognize abdominal epilepsy in adults. Case report. Case 1: A 21-year-old woman with DM type I presented with a 2-month history involving four episodes of severe abdominal pain and vomiting, each of which lasted four to five days. She had a recurrence every two weeks. The EEG revealed 'spike and wave ' and she was started an intravenous phenytoin that resolved the symptoms. Case 2: A 20-year-old woman with DM type I was admitted with a 2-month history of recurring severe left upper quadrant pain associated with occasional nausea but no vomiting. She experienced two more episodes of generalized tonic-clonic seizures and was treated with 300 mg phenytoin given orally The abdominal pains gradually subsided and she was symptom-free within two days. An EEG showed frequent sharp waves. She was treated with 10 mg intravenous diazepam and her symptoms and sharp waves disappeared within two minutes. Case 3: A 46-year-old man with DM type I was admitted with a four-month history of recurring severe epigastric pain and vomiting. His physical examination, laboratory tests, and extensive investigation for a primary GI disorder revealed nothing unusual. The EEG revealed spike and wave and he was treated with intravenous AED (phenytoin) loading after which the symptoms disappeared. Physicians should consider abdominal epilepsy in diabetics with recurrent, intractable abdominal pain in whom extensive investigations for primary gastrointestinal (GI) disorders are unremarkable.
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998 J Med Assoc Thai Vol. 94 No. 8 2011
Correspondence to:
Tiamkao S, Division of Neurology, Department of Medicine,
Faculty of Medicine, Khon Kaen University, Khon Kaen 40002,
Thailand.
Phone: 043-363-664, Fax: 043-374-542
E-mail: somtia@kku.ac.th
Abdominal Epilepsy: An Uncommon of
Non-Convulsive Status Epilepticus
Somsak Tiamkao MD*,
Thongchai Pratipanawatr MD**, Suthipun Jitpimolmard MD*
* Division of Neurology, Deparment of Medicine, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand
** Division of Endocrinology, Deparment of Medicine, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand
Objective: To recognize abdominal epilepsy in adults.
Material and Method: Case report.
Results: Case 1: A 21-year-old woman with DM type I presented with a 2-month history involving four episodes of severe
abdominal pain and vomiting, each of which lasted four to five days. She had a recurrence every two weeks. The EEG
revealed ‘spike and wave’ and she was started an intravenous phenytoin that resolved the symptoms. Case 2: A 20-year-old
woman with DM type I was admitted with a 2-month history of recurring severe left upper quadrant pain associated with
occasional nausea but no vomiting. She experienced two more episodes of generalized tonic-clonic seizures and was treated
with 300 mg phenytoin given orally. The abdominal pains gradually subsided and she was symptom-free within two days. An
EEG showed frequent sharp waves. She was treated with 10 mg intravenous diazepam and her symptoms and sharp waves
disappeared within two minutes. Case 3: A 46-year-old man with DM type I was admitted with a four-month history of
recurring severe epigastric pain and vomiting. His physical examination, laboratory tests, and extensive investigation for a
primary GI disorder revealed nothing unusual. The EEG revealed spike and wave and he was treated with intravenous AED
(phenytoin) loading after which the symptoms disappeared.
Conclusion: Physicians should consider abdominal epilepsy in diabetics with recurrent, intractable abdominal pain in whom
extensive investigations for primary gastrointestinal (GI) disorders are unremarkable.
Keywords: Abdominal epilepsy, Non-convulsive status epilepticus, Abdominal pain
Abdominal epilepsy is an uncommon cause
of gastrointestinal complaints in adults. Such were first
reported in 1868 by Trousseau, in a boy with paroxysmal
attacks of abdominal pain, vomiting, giddiness, pallor,
who later developed grand mal attacks(1). Most reported
cases are in children and adolescents. Abdominal
epilepsy is usually treated with an antiepileptic drug
(AED). Clinical manifestations include abdominal pain,
most commonly sharp or colicky (86%), nausea and/or
vomiting (28%), diarrhea (5%), and bloating (3%)(2).
The site of abdominal pain is most commonly peri-
umbilical or in the upper abdomen. Many patients
have associated disturbances of consciousness and
an abnormal electroencephalogram (EEG). Although
the abdominal symptoms may be similar to those of
irritable bowel syndrome, they may be distinguished
from the latter by the occurrence of altered
consciousness during the attacks, tiredness after
an attack and/or by an EEG positive for epileptic
waveform. This unusual cause for abdominal pain
should be considered in patients with abdominal
symptoms who do not respond to the usual
treatment.
The authors’ objective was to present
three cases reports of diabetic patients who suffered
from abdominal pain for several months before being
diagnosed with abdominal epilepsy.
Case Report
Case 1
A 21-year-old woman with DM type I
presented with a two-month history characterized by
four episodes of severe abdominal pain and vomiting,
each of which persisted for four to five days. During
Case Report
J Med Assoc Thai 2011; 94 (8): 998-1001
Full text. e-Journal: http://www.mat.or.th/journal
J Med Assoc Thai Vol. 94 No. 8 2011 999
each attack, she could not eat and needed to have
stomach contents (1,500 cc/day) removed with a
nasogastric tube.
Her physical examination, laboratory tests and
extensive evaluation for a primary GI disorder were
unremarkable (including stool exams for ova and
parasites, abdominal ultrasound, routine blood exams,
such as liver, pancreas, renal function, upper and long
GI study, and gastro scope).
She had a recurrence every two weeks. An
EEG during an attack revealed a spike and wave at
both temporal lobes (Fig. 1). She was then started
on intravenous phenytoin, which abolished the
symptoms, then the her brain MRI was normal.
Case 2
A 20-year-old woman with DM type I was
admitted with a two-month history of recurring severe
left upper quadrant pain associated with occasional
nausea but no vomiting. The abdominal pains were
associated with chest discomfort and dizziness. She
experienced two episodes of generalized tonic-clonic
seizures (GTCs) and was treated with phenytoin
(300 mg) orally. The abdominal pain gradually
subsided and she was symptom-free within two days.
Notwithstanding, three weeks later, she developed an
episode of severe abdominal pain and an EEG showed
diffuse frequent sharp waves (Fig. 2). She was treated
with intravenous diazepam (10 mg) and her symptoms
and sharp waves disappeared within two minutes.
A subsequent brain MRI was normal.
Case 3
A 46-year-old man with DM type I was
admitted with a four-month history of recurring severe
epigastric pain and vomiting. His physical examination,
laboratory tests and extensive investigation for a
primary GI disorder revealed normal findings. He
had recurrent episodes monthly. An EEG revealed
spike and wave, so he was treated with intravenous
phenytoin loading and the symptoms disappeared. His
brain MRI was normal.
Discussion
Non-convulsive status epilepticus (NCSE)
refers to prolonged seizure activity in the absence of
major motor signs(3). The four major types of NCSE
are absence status epilepticus, simple partial status
epilepticus (SPSE) without motor features, complex
partial status epilepticus (CPSE) and status epilepticus
in coma including subtle status epilepticus.
NCSE is described as a change in behavior
and/or mental processes from baseline associated
with continuous epileptic-form discharges on the
EEG. Nonetheless, there is no universally-accepted
definition of NCSE. Some suggested definitions
include different components such as clinical changes
that usually incorporate impaired consciousness,
ictal EEG abnormalities, and response to treatment.
Therefore, saying, the definition must not exclusively
rely on EEG changes because no single pattern can be
regarded as pathognomonic. A positive electro clinical
response to acute AED treatment may be helpful in
the diagnostic process, but ‘no response’ does not
exclude its diagnosis.
Abdominal sensations commonly herald the
onset of a motor seizure. This so-called abdominal
aura, which may include sensations such as pain,
nausea, gassiness and hunger, is the most common
aura in epilepsy, especially temporal lobe epilepsy.
However, gastrointestinal signs and symptoms may be
the primary or only manifestation of seizures hence,
abdominal epilepsy.
Fig. 1 An EEG revealed a spike and wave at both temporal
lobes
Fig. 2 An EEG showed diffuse frequent sharp waves
1000 J Med Assoc Thai Vol. 94 No. 8 2011
The diagnostic criteria for abdominal
epilepsy include (1) paroxysmal gastrointestinal
complaints unexplained by complete evaluation
(including laboratory tests, radiographic imaging,
and endoscopy), (2) symptoms of a CNS disturbance,
(3) an abnormal EEG with findings specific for a
seizure disorder and (4) a sustained abolition of
symptoms with AED(2). The diagnosis of abdominal
epilepsy begins with eliciting a history typical for
the syndrome, namely paroxysmal and brief episodes
of abdominal pain or other gastrointestinal symptoms.
The presence of associated neurological symptoms
including convulsions, impaired consciousness, and
other sensory phenomenon, is an important clue and
should be elicited when considering the diagnosis,
albeit neurological symptoms may not be present with
every episode.
An appropriate evaluation including
physical and neurological examination, laboratory
studies, endoscopy, and abdominal imaging, usually
with computed tomography and ultrasound, should
be performed to exclude other more common
etiologies. Then, when none is found, or the history is
still suggestive, an EEG should be performed to look
for abnormalities specific to epilepsy. These so-called
interictal, epileptiform discharges (IEDs) comprise
paroxysmal spikes and/or sharp waves. There are no
studies on the sensitivity of EEG for this condition
and but a few from case series showing the range of
positive EEGs (29-55%). An EEG recorded during an
event can be normal, even if there is no associated
convulsion or impairment of consciousness(4).
How seizures induce abdominal sensations
has been studied but the etiology is still unclear.
Stimulation of the temporal lobe structures, including
sensations, hippocampus, and insular cortex, has been
shown to induce abdominal sensations, including
nausea, hunger and ‘funny feelings’, in humans(2).
Some researchers have postulated that abdominal
symptoms could result from true visceral stimuli
which, through connections to the brain, could induce
seizures(5). The first case usually developed symptoms
of dyspepsia, nausea/ vomiting or diarrhea and then
followed with abdominal epilepsy. Most cases of
abdominal epilepsy are of temporal lobe origin(5)
although several cases have also been traced to
parietal lobe lesions(6). An EEG of the first case found
spike and wave at both temporal lobes (Fig. 1).
Treatment usually starts with an AED,
typically phenytoin. Importantly, no controlled trials
have been published regarding treatment of abdominal
epilepsy. Moreover, while helpful for confirming a
diagnosis of abdominal epilepsy, a response to therapy
alone is not diagnostic. Therefore, AED therapy may
improve many non-epileptic causes of abdominal pain,
either by its sedating effect or as a placebo.
Hyperglycemia may present with seizures,
visual hallucination, abnormal movement (chorea,
hemiballism) and coma in severe cases of hyper-
glycemia(7,8). Hyperglycemia induced seizure are
usually focal seizures(8) and epilepsia partialis
continua(EPC)(9). Seizures are more common in
non-ketotic compared to ketotic hyperglycemia.
Keto-acidosis decrease neuronal excitability by
increasing level of GABA(10). Tiamkao S(11) reported
21 patients with non-ketotic hyperglycemic induced
seizures (NKHS), EPC were found in 80%. NKHS
usually controlled with insulin therapy, lowering the
plasma glucose less than 200 mg/dL usually controls
NKHS and no AED is need(11,12). All of the three cases
in the present report had underlying DM type I, treated
with insulin therapy. All of admissions, their plasma
glucose level were higher than 500 mg/dL and no
metabolic acidosis. All of patients need to control
plasma glucose and IV AED for control abdominal
epilepsy. All three cases had a history of high plasma
glucose, which precipitated abdominal epilepsy.
All three of our patients had recurrent
episodes of severe abdominal pain, each episode
lasting for 4-5 days. All GI investigations and blood
tests were unremarkable and an EEG during an attack
showed abnormal findings specific for a seizure disorder.
Sustained abolition of symptoms was achieved with
AED. Since all of the clinical manifestations were
compatible with NCSE(3), the presented patients were
diagnosed with abdominal epilepsy.
Conclusion
Physicians should consider abdominal
epilepsy in diabetic patients with recurrent, intractable
abdominal pain and in whom extensive investigations
of primary GI disorder were unremarkable.
Acknowledgement
The authors wish to thank Mr. Bryan
Roderick Hamman for assistance with the English-
language presentation of the manuscript.
Potential conflicts of interest
The authors wish to thank the Faculty of
Medicine, Khon Kaen University, for support of our
research.
J Med Assoc Thai Vol. 94 No. 8 2011 1001
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โรคลมชกชนดปวดทอง: ภาวะชกตอเนื่องชนดไมกระตกที่พบไม่บ่อย
สมศกดิ์ เทยมเก่า, ธงชัย ประฏภาณวตร, สุทธิพันธ จิตพมลมาศ
วัตถุประสงค์: ทราบถึงโรคลมชักชนิดปวดท้องในผู้ใหญ
วัสดุและวิธีการ: รายงานผู้ป่วย
ผลการศกษา: รายที่ 1 ผู้หญงอาย 21 ปี ป่วยเปนโรคเบาหวานชนดที่ 1 มีประวัติปวดทองอยางแรงรวมกบอาเจยน
4 ครั้งในระยะเวลา 2 เดือน อาการแต่ละครั้งนาน 4-5 วัน ผู้ป่วยมีอาการเป็นซ้ำทุก 2 สัปดาห์ ผลการตรวจ
คลื่นไฟฟ้าสมองพบ spike และ wave ได้รับการรักษาด้วยยาฟีนัยโตอินฉีดเข้าทางหลอดเลือดดำและอาการหายไป
รายที่ 2 ผู้ป่วยหญงอาย 20 ปี ป่วยเปนโรคเบาหวานชนดที่ 1 รับไว้รักษาในโรงพยาบาลดวยประวัติปวดบรเวณชองทอง
ด้านซ้ายบนเป็นซ้ำ บางครั้งมีอาการคลื่นไส้แต่ไม่อาเจียน ผู้ป่วยเคยชักแบบเกร็งกระตุกทั้งตัว 2 ครั้ง และรักษาด้วย
ยาฟีนัยโตอิน 300 มก./วัน ชนิดรับประทาน อาการปวดท้องค่อย ลดลง และหายภายใน 2 วัน ผลการตรวจ
คลื่นไฟฟ้าสมองพบคลื่นสมองลักษณะ sharp wave บ่อย ผู้ป่วยรักษาด้วยยาไดอะซีแพมชนิดฉีดเข้าทาง
หลอดเลือดดำ อาการ และคลื่นสมองลักษณะ sharp wave หายไปภายใน 2 นาที รายที่ 3 ผู้ป่วยอายุ 46 ปี
ป่วยเป็นโรคเบาหวานชนิดที่ 1 รับไว้รักษาในโรงพยาบาลดวยประวัติ ปวดบรเวณลิ้นปี่อยางแรง และอาเจียนซ้ำ
ตรวจร่างกาย ผลการตรวจทางห้องปฏิบัติการและการตรวจเฉพาะโรคทางระบบทางเดินอาหาร ไม่พบความผิดปกต
ผลการตรวจคลื่นไฟฟ้าสมองพบ spike และ wave ผู้ป่วยได้รับการรักษาด้วยยากันชักฟีนัยโตอินฉีดเข้าทาง
หลอดเลือดดำแบบโถม หลังจากนั้นอาการปวดบริเวณลิ้นปี่หาย
สรุป: แพทย์ควรคิดถึงโรคลมชักชนิดปวดท้องในผู้ป่วยโรคเบาหวานมีอาการปวดท้องซ้ำ ไม่ตอบสนองต่อการรักษา
และได้รับการตรวจทางห้องปฏิบัติการโรคทางเดินอาหารไม่พบความผิดปกต
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... An important advantage of MEG over EEG is the absence of the smearing effect. Magnetic fields in MEG are significantly less affected by electrical conductivity of the brain surrounding tissue than electrical fields Table 2. Common semiologic features with lateralizing and localizing values (18,20,26,29,32,33) in EEG (40) . MEG coregistered with MRI can facilitate the relationship between functional and structural domains (41) . ...
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To study the factors predictive for seizure control in non-ketotic hyperglycemic induced seizures (NKHS). We studied 21 patients who were clinically diagnosed as NKHS at Khon Kaen University hospital, Thailand. Multiple linear regression analysis was used to identify the factors predictive for seizure control. Most patients had no previous history of diabetes and presented with repetitive partial seizures. The mean number of seizure attacks was 45 times prior to admission. The average duration to terminate seizure was 36 hours and significantly predicted by frequency of seizures (estimate 0.9, p value 0.013). Frequency of seizures is the only predictive factor for the success of seizure control in NKHS.
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Purpose: Ictal pain is a rare symptom of seizures. Epileptic pain may be experienced unilaterally (lateral/peripheral), cephalically, or in the abdomen. Painful seizures have been associated with seizure origin in both the parietal and the temporal lobes. We report on the different types of epileptic pain and discuss its etiology and possible localizing value. Methods: We reviewed the records of patients referred to our epilepsy program over the last 6 years. Eight (1.4%) of 573 patients had pain as an early prominent symptom of their seizures. Results: Pain was predominantly unilateral in three patients, cephalic in two, and abdominal in three patients. Seizure onset was in or involving the parietal lobe in all patients, and when the painful symptoms were lateralized, they were contralateral to the side of seizure origin. Parietal lobe seizure origin was determined by both intracranial EEG recording and neuroimaging [magnetic resonance imaging (MRI), ictal single photon emission computed tomography (SPECT)] in five patients, and by both scalp EEG and neuroimaging in three patients. Conclusions: We conclude that ictal pain is a rare symptom of parietal lobe seizure origin with lateralizing potential.
Article
Coma and other neurologic abnormalities are present in patients with either diabetic ketoacidosis (DKA) or nonketotic coma (NKC), and the cause of such phenomena are not known. Patients with NKC also manifest seizures and focal neurologic changes. Treatment of diabetic coma with insulin may induce cerebral edema by as yet undefined mechanism(s). In patients with DKA, cerebral oxygen utilization is impaired, and there is hyperviscosity of the blood. A substantial part of the brain's energy source is derived from ketones, which in themselves can depress sensorium. Extracellular hyperosomolality is present, which may also contribute to the genesis of coma. In addition, most ketoacidotic patients have associated medical conditions, which may further impair consciousness. Biochemical changes in the brains of animals with DKA include impairment of both phosphofructokinase activity and pyruvate oxidation, and accumulation of citrate. The net effect upon sensorium in ketoacidotic patients probably represents the interaction of most of the above factors and differs markedly among individuals. Patients with NKC manifest not only depression of sensorium, but also focal motor seizures, hemiparesis, and other neurologic changes, such as aphasia, hypereflexia, sensory defects, autonomic changes, and brainstem dysfunction. Most of the aforementioned changes revert to normal after correction of hyperosomolality. Gamma amino butyric acid, which has been shown to elevate the seizure threshold, is normal in brains of ketoacidotic animals, but may be low in nonketotic coma. Also, hyperosomolality per se may produce seizures. Cerebral edema may complicate the treatment of either DKA or NKC. The available experimental evidence suggests that many of the commonly held theories for the production of such brain swelling probably do not occur. There is no breakdown of the sodium pump, sorbitol or fructose do not accumulate in brain, and brain glucose is only about 25 percent of that in plasma; Cerebral edema is probably produced largely by a direct action of insulin on brain at a time when plasma glucose is approaching normal values. Cerebral edema can thus theoretically be avoided by stopping insulin when plasma glucose has been lowered to values approaching normal.
Article
This report reviews the gastrointestinal and central nervous system complaints and clinical course in 10 adult patients with abdominal epilepsy. Abdominal symptoms included paroxysmal pain, nausea, bloating, and diarrhea. Nervous system manifestations included dizziness, headache, confusion, syncope and transient blindness. Each patient had specific electroencephalographic abnormalities of a temporal lobe seizure disorder. Anti-convulsant therapy has resulted in the sustained abolition of symptoms in each case.
Article
Epilepsia partialis continua (EPC) is a rare epileptic syndrome, observed in various cortical lesions and also in metabolic disorders. We report the case of a 57-year-old patient with EPC as the first manifestation of hyperosmolar non-ketotic hyperglycaemia (NKH) of diabetes mellitus. Computed tomography (CT) and magnetic resonance imaging (MRI) were normal. Initial laboratory data revealing serum glucose 1540 mg/dl, and serum osmolality 391 mOsm/l confirmed the diagnosis. Electroencephalography (EEG) showed ictal discharges in the ipsilateral hemisphere during focal seizures. Seizures are resistant to anticonvulsant treatment and respond best to insulin and rehydration. Focal motor seizures or EPC are commonly a symptom of NKH in the elderly patients. We recommend that in such cases a metabolic disorder such as diabetes mellitus be ruled out.