Abstract
The gastrointestinal system communicates with the brain by way of vagus nerve fibers and the gut-brain axis. There is a well-known relationship between autoimmune diseases and epileptogenesis, and this may explain the involvement of gut microbiota in the course of epilepsy. Many seizures which are described, depending the severity and/or duration, as benign or epilepsy may be related and based on gastrointestinal origin. Epilepsy and related neurological symptoms may alert the clinician to additional life-threatening conditions and complications during the course of gastrointestinal system-based chronic disease such as inflammatory bowel disease and celiac disease. Since the gut is the only part of inner body exposed to environment, novel therapeutic options that target gut microbiata may be promising in many diseases including epilepsy.
Keywords
- autoimmune
- electrolyte
- epilepsy
- gastrointestinal
- gut
1. Introduction
The enteric nervous system (ENS), located in the wall of the bowel, is also known as the “second brain.” The ENS exhibits a wide similarity to the brain, both structurally and functionally. Its neuronal structure is not cemented by collagen and Schwann cells but by glial astrocytes of the central nervous system (CNS). It has similar complex functions to the brain and contains various neurotransmitters [1]. The gastrointestinal system communicates with the brain through vagus nerve fibers and the gut-brain axis. The interaction between the CNS and ENS is known as the gut-brain axis. This axis is mainly regulated by gut microbiota and related neurotransmitters such as 5-hydroxytryptamine (5-HT), also known as serotonin [2]. The common features in terms of function between the ENS and the CNS are reflected in the context of disorder, in that gastrointestinal dysfunction may be seen in neurological diseases, and neurological dysfunction may become evident in gastrointestinal disease processes [3]. Painful abdominal cramping, nausea, and cyclical vomiting syndrome are related to childhood epilepsy, and also in adults, abdominal symptoms are usually associated with idiopathic complex partial or secondary generalized seizures [4]. The ketogenic diet has beneficial effects on intractable seizures, and has been shown to affect the gut microbiota [5]. The gut microbiota and the immune system are interrelated [6]. Gut bacteria balance affects the development of autoimmune disorders. For instance, changing the balance of
2. GI disorders could be accompanied by epilepsy or seizures
The child was previously healthy.
Nonfebrile convulsions accompanied by mild gastroenteritis, possible mild dehydration, absence of apparent acid intoxication, and electrolyte imbalance.
Convulsions mainly occurring during winter, and the gastroenteritis may persist for 1–5 days.
Convulsions may manifest as single or multiple episodes of generalized tonic-clonic seizure (GTCS).
Normal interictal electroencephalogram (EEG).
Normal serum electrolytes, serum glucose, and cerebrospinal fluid (CSF) with stool antigen test positive for rotavirus.
Favorable prognosis with rare relapse and unimpeded development.
CwG is primarily caused by rotavirus, norovirus, sapovirus, adenovirus, and coxsakie virus. Convulsions usually occur between the first and sixth day after the initial symptoms of gastroenteritis. The principal agent determined in cases of CwG is rotavirus. The mechanisms involved in CwG are still unknown [27]. Since CwG only appears in early childhood, it has been hypothesized to be related to the immature nervous system, similarly to febrile convulsions. Rotavirus can directly reach the central nervous system and cause cerebropathy, encephalitis, or convulsions [28]. Children with CwG do not require antiepileptic treatment. CWG has a short and benign course, with most episodes ending within 24 hours. Acute treatment with antiepileptic should be considered in patients with two or more convulsions [29]. Bacterial agents such as
There are four diagnostic criteria for AE in the context of noninflammatory, neoplastic, metabolic, or anatomic abnormalities.
These are:
Otherwise unexplained, paroxysmal gastrointestinal complaints.
Symptoms arising from CNS disturbance.
An abnormal EEG with findings specific for a seizure disorder.
Improvement with anticonvulsant medication.
The most important differential for AE is abdominal migraine. In patients presenting with headache, it is very difficult to differentiate AE and abdominal migraine because symptoms usually overlap. Duration of the symptoms may be used to differentiate the two; being longer in migraine than in AE [36]. EEG is usually abnormal in AE and may confirm the diagnosis of AE. There is no recommended special AED therapy for abdominal epilepsy. Most of the patients may respond to single-drug therapy [37].
3. Gastrointestinal problems associated with antiepileptic drugs
AEDs have a relatively narrow therapeutic index, and their adverse effects can impact on any organ or system. Some 10–30% of patients with epilepsy discontinue their first prescribed AED due to adverse effects and intolerance [43]. Many AEDs cause gastrointestinal side effects. Multi-AEDs in particular may increase the potential side effects in intractable seizures. The most common AED-related side effects are vomiting and nausea [44]. Some important adverse gastrointestinal side effects of AEDs are mentioned below.
Felbamate and
4. Conclusions
Gastrointestinal system manifestations may be a milestone of many neurological diseases, including epilepsy and benign seizures. Epilepsy and related neurological symptoms may alert the clinician to the presence of additional life-threatening conditions and complications during the course of gastrointestinal-based chronic disease such as inflammatory bowel disease and celiac disease. Since the gut is the only part of inner body exposed to environment, novel therapeutic options that target gut microbiata may be promising in many diseases including epilepsy.
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