- Nonketotic hyperglycemia-related epileptic seizures
- Post-ictal Physiology: Adding Blood Pressure to the Equation
- Seizures and Blood Pressure
- Seizures Not Caused by Epilepsy
- Nonepileptic Seizures
- Diagnosing Nonepileptic Seizures
- Treating Nonepileptic Seizures
- Community Forum
- Endocrine Abstracts
- Neuroscientists’ discovery could bring relief to epilepsy sufferers; Computational model of epileptic seizures at molecular level
- Anorexia Side Effects: Causes of Seizures
- Seizures and Epilepsy in Children
- What is epilepsy in children?
- Focal (partial) seizures
- Generalized seizure
- What causes a seizure in a child?
- What are the symptoms of a seizure in a child?
- How are seizures diagnosed in a child?
- How are seizures treated in a child?
- How can I help my child live with epilepsy?
- When should I call my child’s healthcare provider?
- Key points about epilepsy and seizures in children
Abnormal glucose levels, whether too high or too low, can cause seizures. The problem is especially pertinent to individuals with diabetes, whose blood glucose levels can fluctuate widely over the course of a day, as a result of intercurrent illness, variations in insulin levels, or other metabolic factors. Clinical studies show that adults with hyperglycemia have an increased predisposition to experiencing seizures. Experimental studies, both in vivo and in vitro, suggest that a threshold glucose concentration is necessary to support synaptic transmission. Conversely, it appears that elevated extracellular glucose is associated with neuronal hyperexcitability, indicating that glucose balance is necessary for normal neurotransmission. The importance of glucose balance has been identified in studies demonstrating that hyperglycemia exacerbates ischemia-induced brain damage, whereas fasting-induced hypoglycemia protects against this neurotoxicity. The present study, by Schwechter and co-workers, hypothesizes that the reduction of extracellular glucose could ameliorate seizure activity by decreasing neuronal excitability.
First, Schwechter et al. examined the relation between extracellular glucose levels and seizure susceptibility in adult rats in vivo. They tested the hypothesis that elevated glucose is proconvulsant in the flurothyl model of generalized seizures (flurothyl is a gaseous convulsant capable of inducing seizures by inhalation). Hyperglycemia was induced in two ways: (a) streptozocin (STZ) administration, which reliably produces hyperglycemia and simulates diabetes; and (b) short-term intraperitoneal injection of 20% glucose to create a condition of nonketotic hyperglycemia independent of diabetes. A variety of well-chosen controls were used to compare outcomes. The three groups comprising “nondiabetic controls” included rats injected with the STZ vehicle, STZ-injected rats that did not develop diabetes, and rats that received no injection but otherwise were handled identically to the other animals. A final comparison group consisted of rats that underwent a 24-hour fast and thus were hypoglycemic.
Testing with flurothyl demonstrated a negative correlation between blood glucose level and clonic seizure threshold—with STZ-induced diabetic rats having significantly lower seizure thresholds than did nondiabetic controls. Fasted, hypoglycemic rats had the highest thresholds. To control for other metabolic or hormonal effects resulting from STZ injection, an additional group of rats was injected with 20% glucose, 30 minutes before flurothyl testing, and then were compared with saline-injected controls. Again, the hyperglycemic rats had significantly lower thresholds for clonic flurothyl seizures, suggesting that hyperglycemia itself is proconvulsant, in both diabetic and normal rats. Furthermore, no damage to hippocampal neurons was seen in any of the experimental conditions, as assessed by Fluro-Jade and silver stain techniques, suggesting that neither STZ or elevated glucose causes structural neuronal injury.
Next, Schwechter and colleagues evaluated the effects of elevated extracellular glucose on epileptiform activity in vitro. Slices of entorhinal cortex–hippocampus were exposed to a Mg2+-free extracellular medium, causing epileptiform bursts for which amplitude and frequency can be measured and compared under different experimental conditions. In Mg2+-free medium with 10 mM extracellular glucose (i.e., the usual glucose concentration used in slice experiments), typical epileptiform discharges occurred. When the glucose was increased to 20 mM, epileptiform burst frequency did not change; however, the burst amplitudes increased significantly, suggesting enhanced neuronal firing. The effect was reversed when the glucose was switched back to 10 mM. In addition, no epileptiform discharges were seen in normal cerebral spinal fluid (CSF), that is 2 mM Mg2+, plus a 20 mM glucose solution. As a caveat—consider the fact that nearly all brain-slice electrophysiology experiments have used a CSF-glucose concentration of 10 mM, rather than the physiologic concentration, which is closer to 5 mM. The conventionally accepted practice of using the higher-glucose-level solutions is based on empiric experience, showing that the synaptic viability of slices is optimized with the higher concentration (1).
This well-designed study confirms previous work with several animal models of diabetes, which show a reduction in seizure threshold. The important new finding from Schwechter and colleagues is that hyperglycemia, itself, is proconvulsant. How can elevated glucose enhance seizure susceptibility? The answer to this crucial question regarding the mechanism of action awaits further research, as the mechanism per se is not addressed in this report. However, one clue to the answer might be gleaned from the authors’s observation that hypoglycemia was associated with a higher seizure threshold. Other studies have indicated that restricting calories, thus inducing hypoglycemia, in the epilepsy-prone EL mouse also reduces seizure susceptibility (2). With any model that induces hypoglycemia, the role of ketosis must be excluded, as ketones themselves can affect seizure threshold (3). Moreover, multiple other mechanisms could explain hypoglycemia- and hyperglycemia-induced alterations of neuronal excitability. Furthermore, the effects of age on glucose balance and neuronal excitability must be delineated, as children with diabetes tend to develop seizures with hypoglycemia rather than with hyperglycemia. In addition to clarifying further the relation between hyperglycemia and seizures, Schwechter et al. highlight the link between metabolism and neuronal excitability and emphasize the need for further research on the long-term effects of hyperglycemia on various aspects of brain function (4).
Focal seizures (also known as partial seizure) induced by hyperglycemia were first reported by Maccario et al in 1965 . They were often encountered in clinical practice and characterized by hyperglycemia without keto-acidosis. Seizure control associated with resolution of the hyperglycemia was usually used to manage the partial seizures . Many studies have described this clinical syndrome . In recent years, clinical reports gradually increased about NKH-related epileptic seizures, which are considered one of the major neurological complications of diabetes . It indicates an unsatisfactory blood glucose control if NKH-related epileptic seizures occur .
For patients with seizures as main manifestations, especially those without a history of diabetes, the initial diagnosis would often be neurology-related. If conventional antiepileptic treatment is applied, the results would be more harmful than beneficial, and in few ill cases, increased mortality might be observed. The possible explanations include: (1) these patients are more frequently accompanied with unconsciousness and seizures. The preferred drugs, such as diazepam and phenobarbital that ends epileptic episode, often aggravated the unconscious patients by causing respiration inhibition, making the disease more complicated and affecting the subsequent diagnosis and treatment; (2) treatment of intractable seizures uses anti-epilepsy medicine that involves multi-combination of mannitol, corticosteroids and other drugs to reduce brain edema; however, the risk factors of the focal seizure disease are high-blood glucose, high permeability and intracellular dehydration. These drugs will inevitably aggravate the patient’s condition; (3) NKH: featured with reduction of brain γ-aminobutyric acid content, and therefore diazepam and phenobarbital actually decreased the antiepileptic effect; (4) Since glucose saline injection is commonly used as intravenous drugs in the absence of insulin, it might worsen the condition. The disease tend to cause seizures in some patients without diabetes history, and therefore it is more difficult to catch the attention, and more likely to be misdiagnosed.
Diabetes is the most common cause of the seizures in patients with low blood glucose. The subsequent unconsciousness with ketosis acidosis and NKH coma are more common in clinical practice; however, high blood glucose can also lead to seizures, even status epilepticus without awareness. Careful analysis the patients who had epilepsy, accompanied with occasional onset of unconsciousness in this group, first found significantly increased biochemical blood glucose levels, leading to the exclusion of the possibility of hypoglycemia. Diabetes can be complicated by acidosis or ketosis ketotic hyperosmolar coma. As their urine ketone was negative, the possibility of ketosis acidosis could next be ruled out. Blood biochemistry showed that their glucose, sodium, and potassium, were only slightly elevated, and so was the blood urea nitrogen content in plasma osmolality values inferred, which was less than 350 mOsm/L, nonketotic diabetic hyperosmolar coma was also excluded. Therefore, NKH-related epileptic seizures should be next considered. The seizures pathogenesis caused by this disease is still controversial, as some people think that the main pathogenesis is the lack of insulin. Among the patients, insulin levels are sufficient to inhibit the free fatty acid metabolism and the subsequent ketoacidosis, but not enough to transport glucose into the cells . High blood glucose levels increase the levels of urine glucose, causing osmotic diuresis effect and progressive dehydration, which would in turn increase the incidence of this disease. Some people believe that the possible mechanisms include high blood glucose, high plasma osmolality and γ- aminobutyric acid (GABA) levels, and low focal cerebral ischemia . Specific mechanisms also include: (1) osmotic changes. Hyperglycemia causes significant and rapid increase of intracellular osmotic pressure, leading to nerve cell dehydration, and changes in enzyme activity and brain cell energy metabolism. Membrane ion pump function is impaired, causing the loss of intracellular potassium and the subsequent sodium accumulation, which destroys the membrane potential and the stability of cell depolarization, ultimately resulting in seizures . (2) in vivo biochemical changes in metabolism. Citric acid cycle is inhibited in vivo in the patients with this disease, whereas GABA metabolism is increased, causing the increased brain energy consumption, and the reduced seizure threshold . In contrast, seizures are less frequent in ketoacidosis patients, as ketosis acidosis increases intracellular activities of glutamate and tryptophan decarboxylase, leading to the increased content of brain inhibitory neurotransmitter GABA. GABA is related to the rapid changes of synaptic sensitivities by binding to the neurons, which then increases the permeability of chloride ions. Under such conditions, the membrane potential is maintained at a stable resting potential level and the excitatory synaptic reactivities are weakened so that the epilepsy is prevented. This is also an alternative way to prove that the GABA contents decrease in NKH-related epileptic seizures patients. (3) brain cell energy deficiency. Because of the diabetic hyperglycemia, plasma fibrinogen significantly increases, red blood cell and platelet aggregate, and blood is in a hypercoagulable state. In addition, the aggravation of existing diabetes microcirculation and small artery hyalinization, the dysfunction of endothelial cells, and damages of cerebral blood flow autoregulation, decrease regional cerebral blood flow, causing hypoxic-ischemic damages and functional changes in cortical cells, which are “epilepsy cells”. Such cells are sensitive to the metabolic disorders, high blood glucose condition especially is likely to cause seizures (4) immune abnormalities: the presence of glutamic acid decarboxylase autoantibodies in both type 1 diabetes and epilepsy. Peltola, et al studied 51 cases of refractory epilepsy and found that these patients were autoantibody positive, with antibody titers similar to that in patients with type 1 diabetes, suggesting that intrinsic link might exist between them Their results supported the idea that immune dysfunction was involved in the hyperglycemia-related epilepsy (5) studies suggest that NKH-related seizures might be linked to the brain barrier damage caused by long-term high blood glucose . However, most of patients do not have seizures even if their blood glucose levels are high as the high levels of blood glucose are not the only factor for epilepsy. Other factors include individual health status and genetic factors . In 1968, Maccario et al. first reported that NKH and partial seizures co-existed, which were featured with high blood glucose, absence of ketosis, consciousness, and partial seizures. Tiamkao et al. , based on a retrospective analysis of 2 l partial NKH-related seizures patients, found that the average blood glucose level was 32.6 l mmol/L(16.11 ~ 61.33 mmol/L), and mean plasma osmolality was 302 mOsm/L (288-323 mOsm/L). When the seizure was under control, the average of blood sugar level was 11.3 mmol/L (4.11-21.67 mmol/L).
This paper reported eight cases with EEG showing spikes, slow waves, and scattered sharp slow waves. In previously published reports, EEG results of patients with NKH-related epileptic seizures have shown normal waves or spikes, sharp slow or high amplitude slow waves . Therefore, EEG is not very valuable in diagnosis of the disease. Imaging is not specific, either. This group mostly showed the normal imaging results, or age-related abnormalities such as old lacunar infarction, brain atrophy, and white matter demyelination, similar to most of the previous studies . However, some studies described a transient change in head MRI in a patient with NKH-induced seizures, that is, the reversible and Flair weighted hyperintense cortex, and low signal of white matter. He also displayed cytotoxic edema. Its mechanism was unclear. Possibly, the cortical ischemia seizures and angioedema, caused aggregation and deposition of iron radicals . Some scholars believe that these changes result from the damages in blood-brain barrier caused by long-term high levels of blood sugar .
This article summarized the following clinical features of NKH-related epileptic seizures: (1) common in the elderly (2) with or without a previous history of diabetes and epilepsy (3). Seizures were always accompanied with a rapid rise in blood glucose. Plasma osmolality may be normal or slightly elevated, but not to the diagnostic criteria for diabetes hypertonic (4) urine ketone negative (5). Seizures could not be effectively alleviated by antiepileptic drugs alone. Application of insulin to correct hyperglycemia and metabolic disorders ended the seizures (6) seizure-related lesions were not detected in the head imaging tests (7). If blood glucose was under control, epilepsy did not occur any more. Analysis from the clinical effectiveness showed that the primary treatment for the NKH-related epileptic seizures included early, active, and rational rehydration and insulin hypoglycemic therapy, while closely monitoring blood glucose. Such treatments are key to the success of salvage therapy among these patients. Phenytoin-induced insulin resistance can inhibit the release of insulin, and therefore increase the possibility of NKH-related seizures. Diazepam increase the opening frequency of GABA-mediated chloride ion channel. Phenobarbital extended the start time of GABA-mediated chloride channel, by reducing the brain GABA levels among the patients with NKH-related seizures, Therefore, the stability and antiepileptic effects of phenobarbital and Diazepam decline which explained why conventional antiepileptic drugs in those patients with epilepsy were not marketly effective. Antiepileptic drugs preferred include carbamazepine, clonazepam diazepam and other anti-epileptic drugs as they do not affect the levels of blood glucose. Long-term use of anti-epileptic drugs is not necessary. If blood glucose and the seizures are well controlled, anti-epileptic drugs can be discontinued gradually. Smooth phasing out the anti-epileptic drugs among the patients in the present study did not cause the recurrence.
In short, NKH-related epileptic seizures has low occurrence rate in clinical practice. Epilepsy is often the first symptom. Compared with other diseases presenting clinical manifestations of epilepsy, they are not specific, and tend to be misdiagnosed. Therefore, early recognition of this clinical syndrome and other seizure causes as well as early phase identification is critical, because the condition can be corrected by adjusting blood glucose level plus rapid rehydration. The disease pathogenesis is not entirely clear. In order to clarify the clinical features and pathogenesis of this disease, further research should be carried out in the imaging and electrophysiological aspects.
Post-ictal Physiology: Adding Blood Pressure to the Equation
Recent studies examining the effects of seizures on cardiac and respiratory function have shown that a seizure can often impact cardiopulmonary function in ways that can be dangerous in the right setting.
Seizures in people undergoing video-EEG monitoring, including both focal (also called partial) and secondarily generalized tonic-clonic seizures, can lead to impaired breathing, depressed arousal reflexes, and heart instability. The clinical data suggests that autonomic and respiratory dysfunction following seizures, especially tonic-clonic seizures, is critical to mechanisms of sudden unexpected death in epilepsy (SUDEP).
Seizures and Blood Pressure
Little is known about the impact of seizures on blood pressure, which is vital to maintaining an adequate quantity and supply of blood (known as perfusion) to the brain and the heart. New advances in non-invasive continuous measurement of blood pressure has made it feasible to record blood pressure around the time of seizures.
Bozorgi et al. reported a case of a woman with refractory epilepsy who had a generalized tonic-clonic seizure while undergoing video-EEG monitoring with simultaneous non-invasive blood pressure recording. Immediately after the seizure, she had a significant drop in systemic blood pressure lasting more than 1 minute.
More recently, Hempel et al. performed a prospective systematic assessment of blood pressure during and after seizures in 37 patients. They found that:
- Focal seizures, with or without impaired awareness, were associated with a seizure-related rise in systemic blood pressure with a parallel increase in heart rate.
- The time course of the blood pressure and heart rate changes were similar and proportional to the severity and duration of focal seizures.
- On the other hand, in secondarily generalized tonic-clonic seizures there was a dissociation between heart rate and blood pressure changes. In a few seizures, there was a post-seizure decrease in blood pressure but most seizures had increases in blood pressure that normalized quickly. On the other hand, heart rate remained elevated for a long time after a tonic-clonic seizure.
- The authors speculate that this mismatch between post-ictal heart rate and blood pressure changes reflect an autonomic failure that could limit the adequate supply of oxygen to the brain and heart following a seizure.
- New studies of seizure-related blood pressure changes provide an additional piece of the puzzle in understanding how tonic-clonic seizures can trigger deadly heart, brain, and breathing dysfunction in cases of SUDEP and may provide a new target for intervention.
Seizures Not Caused by Epilepsy
From the outside, nonepileptic seizures look like epilepsy, but the hallmark electrical brain activity of epilepsy isn’t found on the diagnostic tests. Nonepileptic seizures are also known as nonepileptic attack disorder, psychogenic nonepileptic seizures (PNES), dissociative seizures, conversion seizures, and pseudoseizures. (3)
It is estimated that 5 to 20 percent of people diagnosed with epilepsy may actually have nonepileptic seizures. Among people diagnosed with intractable seizures (seizures that aren’t responding well to treatment) who seek inpatient epilepsy monitoring, 25 to 40 percent are later diagnosed with PNES.
PNES is believed to be a type of disorder called a “conversion” disorder. Conversion disorders are physical symptoms that don’t have an underlying physical cause. Instead, the symptoms are caused by a psychological conflict.
Diagnosing Nonepileptic Seizures
The diagnostic test called a video EEG (electroencephalogram) is the common way to determine whether seizures are psychogenic (arising from the psyche). A video camera captures the features of the person’s seizures; meanwhile, an EEG captures readings of the person’s electrical brain waves. The two can later be compared side by side to see if there is a correlation between the seizure activity and the brain wave activity.
EEGs are not foolproof, however. Approximately 15 to 33 percent of focal seizures — which are epileptic seizures — are too deep in the brain or cover too small an area of the brain to be perceived by EEG electrodes. Additionally, movement from tonic-clonic seizures can obscure EEG results. What’s more, some people may have both epileptic seizures and PNES.
Treating Nonepileptic Seizures
The recommended treatment for PNES is psychotherapy, particularly cognitive behavioral therapy. Other recommended therapies include interpersonal therapy and group therapy.
Because nonepileptic seizures are believed to be similar to post-traumatic stress disorder (PTSD), some people have found that the medications and treatment approaches for PTSD are helpful in treating their seizures. The treatment called eye movement desensitization and reprocessing has been found to be helpful in PTSD and in nonepileptic seizures, but not in epilepsy.
Clinicians are often careful how they deliver a diagnosis of PNES because it can sound like telling someone they are crazy. Not only are people with PNES not crazy but their seizures are real and disabling.
Because PNES seizures have a different cause and treatment from epileptic seizures, getting a PNES diagnosis can help guide a person toward more helpful and less toxic treatment than epilepsy treatment.
Syncope is the most common “non-epileptic” cause of altered consciousness. The two main types are reflex (vasovagal) and orthostatic syncope. Less common but more serious causes include cardiac and central nervous system syncope.
Reflex (vasovagal) syncope
This is caused by exaggerated but normal cardiovascular reflexes, and so occurs in otherwise healthy individuals, mainly children and young adults.
Table 1 shows characteristics distinguishing vasovagal syncope from epileptic seizures.
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Clinical distinction of reflex (vasovagal) syncope from seizures
Triggers include prolonged standing (school assembly), rising from lying (bathroom at night), hot crowded environments (restaurant), emotional trauma, and pain (doctor’s surgery). Prodromal symptoms (presyncope) developing over 1–5 minutes include light headedness, nausea, sweating, palpitation, greying or blacking of vision, muffled hearing, and feeling distant.
A witness may describe pallor, sweating, and cold skin. Muscle tone is flaccid sometimes with a few uncoordinated clonic jerks occurring after the fall. A common error is to label syncope as a seizure, given a witness account of shaking (convulsive syncope).2 Incontinence and injury are uncommon and lateral tongue biting rare. Recovery is usually rapid and without confusion.
The mechanism is complex. Venous return falls when blood pools in either the legs (prolonged standing) or the splanchnic vessels (increased vagal tone—for example, response to seeing blood). Cardiac output therefore falls, but the blood pressure is maintained initially by sympathetically induced peripheral vasoconstriction. The Bezold-Jarisch reflex is initiated when vigorous cardiac contractions stimulate ventricular wall mechanoreceptors, exciting 5-hydroxytryptamine (5-HT, serotonin) mediated vagal afferents, falsely “suggesting” an overfilled heart. The resulting surge in vagus activity and reduced sympathetic tone, despite the falling blood pressure, set up a vicious cycle of bradycardia, falling peripheral resistance, and abrupt circulatory collapse. In addition, cerebral vasoconstriction preceding the circulatory collapse explains presyncope preceding major falls in blood pressure.
The history usually gives the diagnosis. An electrocardiogram (ECG) is indicated if syncope occurs with exercise, when lying, or with palpitation (see cardiac syncope below). Significant falls in postural blood pressure rarely happen in outpatients; indeed, blood pressure usually shows the normal initial rise on standing. Tilt table testing (60° tilt for 45 minutes) (fig 1A) is therefore important if there is diagnostic doubt.3 It is highly sensitive (< 90%) and specific (70%) for a syncopal tendency. Measures to induce syncope—for example, with isoprenaline—provoke syncope more rapidly but with lowered specificity.
Heart rate and blood pressure changes during tilt table testing in (A) vasovagal and (B) orthostatic syncope.
An explanation and postural advice—head down or lie flat at symptom onset, or rise slowly from lying—is often sufficient. Behavioural psychotherapy and systematic desensitisation may help with specific triggers—for example, seeing blood. Medications include β blockers4 to limit vigorous cardiac contractions, salt loading or fludrocortisone to prevent cardiac underfilling, or selective serotonin reuptake inhibitors to modulate vagal brainstem reflexes. Dual chamber cardiac pacing may help in severe (malignant) vasovagal syncope: maintaining the heart rate despite falling blood pressure may not prevent syncope, but allows presyncopal symptoms (and evasive action) to occur.
Orthostatic syncope (autonomic failure)
People with autonomic dysfunction lose their normal vasoconstriction response to a postural fall in blood pressure. Syncope occurs within seconds or minutes of becoming upright, especially when rising and after meals. Unlike in reflex vasovagal syncope, the skin stays warm, the pulse rate is unchanged despite the fall in blood pressure, and sweating is absent.
Autonomic dysfunction may relate to autonomic neuropathy (for example, old age, diabetes, alcohol, amyloidosis) or complex autonomic failure (multiple system atrophy). Medications such as antihypertensives, phenothiazines, tricyclic antidepressants, anti-parkinsonian treatments, and diuretics worsen the problem.
Lying and standing blood pressure (postural drop without pulse rate change) provides the diagnosis. Other autonomic function tests (blood pressure and pulse rate during hyperventilation or Valsalva manoeuvre) and tilt table testing also help (fig 1B). Exclusion of anaemia or hyponatraemia is important.
Management includes withdrawing provoking medications and avoiding certain situations, such as prolonged standing, large meals, and alcohol. Head-up tilt at night may help. Fludrocortisone acetate (50–200 μg daily) is the usual first line medication.
Cardiac syncope results from either rhythm (electrical) or structural (“plumbing”) disorders, and is potentially life threatening. Some sudden unexplained epilepsy deaths are undoubtedly misdiagnosed cardiac syncope. Syncope occurs from any posture (arrhythmogenic syncope is common in bed), during exertion or emotion. Syncope during exercise requires urgent exclusion of a cardiac cause, though most turn out to be reflex vasovagal syncope.
Rapid tachycardia reduces cardiac output through incomplete diastolic ventricular filling. Palpitation occurs during and between attacks. Supraventricular tachycardias are common, often benign, and usually not associated with structural heart disease; ventricular tachycardias are more serious, often occurring with heart disease.
Wolff-Parkinson-White syndrome (short PR interval and delta wave) predisposes to “re-entry tachycardias” through an abnormal short circuit, the bundle of Kent. The related Lown-Ganong-Levine syndrome shows a short PR interval but no delta wave.
Inherited long QT syndromes are potassium or chloride channel disorders giving variable refractoriness between adjacent cardiac myofibrils.5 Resulting “micro re-entry” phenomena provoke “torsades de pointes”, a potentially fatal ventricular tachyarrhythmia where the QRS axis rotates repeatedly through 360°. The main genetic syndromes are Romano-Ward (autosomal dominant) and the Jervell and Lange-Neilsen syndrome (autosomal recessive, more severe, and with deafness). Recurrent syncope develops, particularly on rising. Typically patients fall, lie still, and then convulse. The risk of sudden death lends urgency to family screening.
Acquired QT changes predisposing to arrhythmia are common. Shortening occurs with digoxin, hyperthermia, and hypercalcaemia; lengthening occurs with some antiarrhythmics, antihistamines, and with ischaemic heart disease.
Chronic bradycardia—for example, complete heart block—reduces cardiac output, impairing the cerebral circulation; patients develop fatigue as well as syncope.
Carotid sinus hypersensitivity is a common cause of sinus arrest and “drop attacks”.6 This is found in 10–20% of people over 60 years, particularly men, of whom about 20% present with syncope attributable to carotid pressure (for example, tight collar, head turning, etc). Diagnostic carotid sinus massage is performed with the patient supine (repeated upright if suspicion is strong), under ECG and blood pressure monitoring. Each carotid is massaged for < 15 seconds (leaving > 15 seconds between sides). Positive responses are either cardioinhibitory (sinus pause > 3 seconds), vasodepressor (blood pressure fall > 50 mm Hg), or mixed. The risks include prolonged asystole, transient or permanent neurological deficit, and sudden death.
Other causes of reflex bradycardic syncope are the Valsalva manoeuvre (for example, cough or trumpeter’s syncope), swallowing (often with glossopharyngeal neuralgia), or micturition.
Structural cardiac causes
Left ventricular outflow tract obstruction (aortic stenosis, hypertrophic obstructive cardiomyopathy) and left ventricular underfilling (mitral stenosis, atrial myxoma) reduce stroke volume. Cardiac pump failure (cardiomyopathy, ischaemic heart disease, arrhythmogenic right ventricular dysplasia (ARVD)) also reduces cardiac output. In each case, however, syncope is principally vasovagal, the vigorous ventricular contractions giving increased vagal tone.
ARVD is autosomal dominant and may present as sudden death. The diagnosis is difficult without a family history since ECG abnormalities (inverted T waves in V2–V4) occur in only 70%, and the patchy right ventricular wall fibrosis may be missed on endocardial biopsy.
Central nervous system (CNS) syncope
There are several patterns of CNS syncope:
▸ Intermittent obstructive hydrocephalus (third ventricular cyst, Chiari malformation) typically presents as “pressure” headache building over several seconds before losing consciousness. The potential result is sudden death. ▸ Concussive (immediate post-traumatic) seizures occur within seconds of an acute head injury. They are non-epileptic, show no typical EEG changes, and do not predict later epilepsy. ▸ Autonomic dysreflexia may follow complete spinal cord lesions. Loss of autonomic blood pressure control allows intermittent massive hypertension, sometimes sufficient to alter consciousness. ▸ Diencephalic attacks following diffuse brain insults (head injury, hypoxic encephalopathy) manifest as intermittent hypertension, sweating, tachycardia, and even loss of consciousness.
I’m newly diagnosed with seizures, had the first of three on February 21st, 2015. It was a normal work day for me, with a normal amount of stress for my job (hotel management) and a headache. Some misplaced glasses, brief confusion, burning tongue and oddly bruised arm turned into a night in the ER – the only information that we’ve attributed the incident to was low potassium at the time, and the ER doc giving me a fowl tasting “shot” to boost my level. My current neurologist doesn’t care to explore anything further other than meds for the rest of my life, and I’m waiting on an appointment with a larger more skilled facility out of the area.
Just wondering if anyone has had any seizures related to vitamin deficiencies, specifically potassium. I have also had a gastric bypass in 2005 and no prior issues until this year. I’m not a heavy drinker, no recreational drug use – although I did have a high caffeine intake daily and very erratic sleep schedule due to my responsibilities, but I’m just looking for….answers…help….understanding???
Introduction: We present 3 cases of the same severe electrolyte imbalance presenting with acute neurological symptoms.
Case descriptions: Case A, a 48 year old lady with severe CREST syndrome presented with prolonged vomiting and diarrhoea. Initial investigations showed: Sodium 141 mmol/l, Potassium 3.2 mmol/l, Creatinine 53 mmol/l, Glucose 4.3 mmol/l, Haemoglobin 13.9 g/dl, Albumin 38 g/l. 2 days after admission she developed seizures. Case B, a 75 year old residential home resident with Addisons disease who was admitted with an infection-precipitated Addisonian crisis, with increasing frailty during her 3 week in-patient stay, became acutely confused, drowsy and developed a seizure with temporary respiratory arrest. Baseline investigations: Sodium 143 mmol/l, Potassium 3.2 mmol/l, Creatinine 124 mmol/l, Glucose 5.3 mmol/l, Haemoglobin 11 g/dl, Albumin 30 g/l. Case C, a 42 year old man with hypoparathyroidism and poor adherence to alpha-calcidol was admitted with several self-limiting seizures. Baseline investigations: Sodium 140 mmol/l, Potassium 3.3 mmol/l, Creatinine 110 mmol/l, Glucose 4.8 mmol/l.
All 3 cases were found to have low calcium and magnesium levels.
Case A: 1.4 mmol/l and 0.2 mmol/l, Case B: 1.63 mmol/l and 0.28 mmol/l, Case C: 1.5 mmol/l and 0.25 mmol/l, respectively.
Discussion: Interestingly, the baseline blood tests were virtually normal, apart from the slightly low potassium. Despite these reassuringly normal baseline tests, the history of prolonged vomiting and diarrhoea (A) and prolonged poor nutrition (B) could have prompted an earlier full electrolyte screen. The history of poor adherence to medication (C) allowed prompt diagnosis of the hypocalcaemia and hypomagnesaemia.
Conclusion: These cases demonstrate the need to consider metabolic causes in acute neurological disturbances. They emphasise that patients with prolonged hospital stays with poor oral intake and patients with a prolonged history of possible decreased gastro-intestinal absorption and excess gut losses, as in severe diarrhoea, warrant a full electrolyte screen, including calcium and magnesium.
Neuroscientists’ discovery could bring relief to epilepsy sufferers; Computational model of epileptic seizures at molecular level
Neurons, the basic building blocks of the nervous system, are cells that transmit information by electrical and chemical signaling. During epileptic seizures, which generally last from a few seconds to minutes and terminate spontaneously, the concentrations of ions both inside the neuron and the space outside the neuron change due to abnormal ion flow to and from neurons through ion “channels” — tiny gateways that are embedded to the surface of the neuron.
Ordinarily, intracellular (inside the cell) sodium concentration is low compared to extracellular sodium (the reverse is true of potassium). During seizure, however, there is a buildup of intracellular sodium, with sodium ions moving into neurons from the extracellular space, and potassium ions doing the opposite.
To understand exactly how neurons function during epileptic seizures, Maxim Bazhenov, an associate professor of cell biology and neuroscience, and Giri P. Krishnan, a postdoctoral researcher in his lab, developed and used realistic computer simulations in their analyses and found that while there is a progressive and slow increase in intracellular sodium during seizure, it is this accumulation of intracellular sodium that leads to the termination of the seizure.
“According to our model, sodium concentration reaches a maximum just before the seizure terminates,” Bazhenov said. “After seizure initiation, this intracellular sodium buildup is required to terminate the seizure.”
The researchers’ computational model simulates the cortical network. (The cortex is the outer layer of the cerebrum of the mammalian brain. A sheet of neural tissue, it is often referred to as gray matter.) The model simulates neurons, connections between neurons, variable extracellular and intracellular concentrations for sodium and potassium ions and variable intracellular concentrations for chloride and calcium ions.
Bazhenov explained that conventional antiepileptic drugs are commonly designed to target various sodium channels in order to reduce their activity.
“These drugs essentially slow down the intracellular build-up of sodium, but this only prolongs seizure duration,” he said. “This is because seizure duration is affected by the rate of intracellular sodium accumulation — the slower this rate, the longer the seizure duration.”
According to Bazhenov, targeting the sodium channels is not the best approach for drugs to take. He explained that even for drugs to increase the activity of the sodium channels (in order to reduce seizure duration) there is an undesirable effect: seizures become more likely.
“The drugs ought to be targeting other ion channels, such as those responsible for the buildup of intracellular chloride,” he advises. “According to our model, restricting the chloride increase would lead to a faster termination of seizure and can even make seizures impossible.”
Bazhenov and Krishnan’s model also shows that the occurrence of seizures depends critically on the activity of ionic “pumps” — structures that are also embedded to the surface of neurons. These pumps help remove the sodium and chloride ions from inside the neurons and critically influence their concentrations in the brain.
Study results appear in the June 15 issue of The Journal of Neuroscience.
The research was supported by a grant to Bazhenov from the National Institutes of Health.
Epilepsy is a chronic neurological condition characterized by recurrent seizures — involuntary changes in body movement or function, sensation, awareness or behavior. The seizures are caused by abnormally excited electrical signals in the brain. It is estimated that about 10 percent of people will experience a seizure some time during their lifetime; about 3 percent will have had a diagnosis of epilepsy by age 80. Epilepsy cannot be transmitted from person to person. No definite cause for epilepsy has been identified.
The autonomic mechanisms involved in neurogenic paroxysmal hypertension are not understood. We present the first demonstration of the precise haemodynamic and autonomic changes during a complex partial seizure.
A 50 year old headmaster was investigated for an 8 year history of recurrent absence attacks, stereotyped in nature and of sudden onset, each lasting about half a minute. He became pale, sweaty, and mentally withdrawn but did not fall down. Recovery was rapid and associated with transient headache. Previous neurological investigations, including repeated EEG and MRI, were negative. Electrocardiographic Holter monitoring disclosed only sinus bradycardia so he underwent head up tilt testing to exclude vasovagal syncope. Intra-arterial blood pressure and ECG were recorded continuously. Microneurography needles were positioned in the peroneal nerve of the right leg for recording efferent postganglionic MNSA.1 This technique allows beat to beat monitoring and quantification of MNSA (bursts/min) which controls vascular tone in skeletal muscle. MNSA in turn is modulated by changes in blood pressure via the baroreflexes. Blood pressure is normally maintained during head up tilt by increased MNSA and vasocontriction.2
The patient showed normal blood pressure, heart rate, and MNSA responses to tilt initially, but after 10 minutes, he suddenly became pale, sweaty, and withdrawn for about 30 seconds. No loss of muscle tone was seen and he later confirmed that this was a typical absence attack. Coinciding with the onset of his symptoms, MNSA increased briefly for 3 seconds associated with a sudden increase in blood pressure from 138/95 to 222/150 mm Hg over 10 seconds. Heart rate simultaneously increased from 65 to 98 bpm (fig 1). Over the next 20 seconds,blood pressure and heart rate decreased and there was a major burst of MNSA followed by reciprocal oscillation of blood pressure with MNSA (0.1Hz) as blood pressure reached normal levels. During recovery, he complained of his usual transitory headache. Venous noradrenaline (norepinephrine) concentrations were 1650 pmol/l and 5250 pmol/l before tilt and during recovery respectively. Normal values in our laboratory before and after 10 minutes of tilt are 456 (SD 50) and 705 (SD 74) pmol/l.3 His absence symptoms could not be reproduced by rapidly increasing blood pressure to similar values (250/120 mm Hg for 30 seconds) with an intravenous bolus of epinephrine (100 μg). One week later, an EEG during a similar absence attack showed sharp waves arising from the left frontoparietal area (fig 2). Subsequent continuous EEG and blood pressure monitoring confirmed that focal seizure activity was simultaneous with paroxysmal hypertension. Studies with MRI showed hippocampal atrophy consistent with the diagnosis of complex partial seizure disorder. His absences were abolished with 400 mg carbamazepine daily and he has remained free of symptoms for 6 months.
A 2 minute recording of blood pressure (BP), muscle nerve sympathetic activity (MNSA), and heart rate (ECG) during an absence attack after 10 minutes of head up tilt. At 30 seconds there was sudden mental withdrawal and a rapid increase in MNSA* followed by a severe and paroxysmal increase in blood pressure and heart rate. As blood decreased, MNSA increased and when blood pressure normalised there was a marked baseline shift in MNSA‡. During recovery, blood pressure and MNSA oscillated reciprocally (0.1 Hz)†.
EEG recording obtained during light sleep showing sharp waves arising maximally in the left frontotemporal area. The montage consists of four sets of channels running anterior to posterior recorded from the right parasagittal, left parasagittal, right temporal, and left temporal areas respectively.
This is the first demonstration of paroxysmal neurogenic hypertension triggered by a seizure in a patient with complex partial seizure. The diagnosis of complex partial seizure was supported by the following: focal EEG changes during a subsequent absence seizure; no reproduction of absence symptoms during drug induced paroxysmal hypertension; characteristic hippocampal atrophy on MRI4; and complete response to anticonvulsant drugs. Other possible diagnoses including brain stem tumour, phaeochromocytoma, and renal artery stenosis were excluded by appropriate imaging and neurohormonal analysis. Pseudoseizures were excluded on the basis of the EEG findings and the rapid response to treatment. Although rapid increases in MNSA and heart rate have been found during panic attacks, paroxysmal hypertension and loss of consciousness are not consistent features.5
The paroxysm consisted of simultaneous hypertension and tachycardia associated with sweating and facial pallor during the absence attack. We suggest that this is secondary to a generalised increase in sympathetic activity causing vasoconstriction and increased cardiac output. This is supported by (a) increased MNSA and heart rate despite progressive rise in blood pressure; (b) symptomatic blood pressure overshoot; (c) noradrenaline increased to over seven times the normal tilt levels; (d) prominent low frequency (0.1Hz) oscillations in blood pressure and MNSA during recovery.2 These low frequency oscillations (0.1 Hz) are thought to be secondary to changes in brain stem sympathetic activity separate from the effects of respiration, which are generally of a higher frequency (0.2 Hz). We emphasise that the initial increase in MNSA occurred when blood pressure was increasing and so was not baroreflex mediated as would be expected for respiratory or normal brain stem low frequency oscillations.
We hypothesise that this generalised increase in sympathetic activity is permitted by a transient interruption of baroreflex feedback inhibition during the seizure. We think that this is a unique recording of transient baroreflex failure characterised by a rapid and generalised increase in sympathetic activity, overriding the baroreflex afferents in the brain stem. It has long been suspected that paroxysmal hypertension occurs in complex partial seizures but to date, ambulatory monitoring has only demonstrated changes in heart rate.6Ambulatory beat to beat blood pressure monitoring would allow closer study of this phenomenon and its possible relation to sudden cardiac death in epileptic patients. Finally, this a good example of an episodic medical condition which may be very difficult to diagnose. Occasionally, when an episode is seen fortuitously in the laboratory, we may identify pathophysiology previously suspected but not actually seen.
We are grateful for the advice of Dr M Hurrell and Dr GJ Carroll and the technical assistance of Mrs J Sutherland. The figures were prepared by the Department of Medical Illustration, Christchurch Hospital.
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(1998) MR in temporal lobe epilepsy: adults with pathological confirmation. Am J Neuroradiol 19:19–27.
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(1998) Sympathetic activity in patients with panic disorder at rest, under laboratory mental stress, and during panic attacks. Arch Gen Psychiatry 55:511–520.
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Hypertension is associated with a 2.5-fold increased risk for developing epilepsy in older age, and this risk may be mitigated with hypertension treatment, according to study results presented at the American Epilepsy Society 2019 Annual Meeting, held in Baltimore, Maryland from December 6 to 10.
While stroke is a known cause for epilepsy in older age, recent studies have attempted to explore the association between vascular risk factors and epilepsy. The goal of the current study was to explore the association between modifiable vascular risk factors – including hypertension, diabetes mellitus, smoking, and hyperlipidemia – and epilepsy among patients aged ≥45 years.
The researchers reviewed data on 2986 participants (mean age 58, 48% male) of the offspring cohort who attended Framingham Heart Study exam 5 between 1991 and 1995.
During a follow-up period of 1-25 years (mean 19.2 years) there were 55 cases of new-onset epilepsy.
The researchers identified an association between history of cardiovascular disease and atrial fibrillation with epilepsy, but this was not statistically significant.
“Our results offer further evidence that hypertension, a vascular risk factor which is highly prevalent in the general population, increases 2.5-fold the risk developing epilepsy in older age, even in the absence of a clinical stroke,” concluded the researchers.
Stefanidou M, Himali J, Devinsky O, Beiser A, Seshadri S, Friedman D. Vascular risk factors as predictors of epilepsy in older age: The Framingham Heart Study. Presented at: The American Epilepsy Society 2019 Annual Meeting; December 6-10, 2019; Baltimore, MD. Abstract 2.386.
By The Recovery Village Updated on09/15/19
Anorexia nervosa is an eating disorder that can lead to numerous health issues. Side effects of anorexia can be unexpected, including the development of seizures. Someone who has anorexia may experience seizures, even if they do not have epilepsy or an epileptic condition.
Anorexia Side Effects: Causes of Seizures
Anorexia can cause seizures for several different reasons, including from:
- Dehydration: Dehydration occurs when the body does not get enough fluids. Many people who have anorexia starve themselves, don’t drink enough water, abuse laxative drugs and force themselves to vomit. All of these behaviors can deplete the body of necessary fluids and cause dehydration. When the body is dehydrated, the kidneys and heart can fail and seizures can occur.
- Malnutrition: A person who has anorexia does not eat a balanced diet and therefore does not give their body the nutrition it needs. Chronic malnutrition from irregular eating habits, including eating too little or eating unhealthy foods, can lead to fainting and seizures.
- Refeeding syndrome: People who have anorexia may experience instances of refeeding syndrome. This syndrome happens when someone who has been starving quickly eats many calories. Refeeding syndrome can send the body into shock, causing irregular breathing, heart failure and seizures.
- Medications: Some antidepressant medications can cause seizures in people who have anorexia. Given that most drug side effects are listed, including the risk of seizure, it’s up to the person to decide whether the benefits outweigh the risk of seizures.
Not everyone who has anorexia will experience seizures, but seizures are a severe side effect that should not be taken lightly. Professional anorexia treatment can lower a person’s risk of seizure and other potentially life-threatening side effects of anorexia.
Misra M, Shulman D, Weiss A. “Anorexia.” J Clin Endocrinol Metab, May 1, 2013. Accessed February 20, 2019.
Seizures and Epilepsy in Children
What is epilepsy in children?
Epilepsy is a brain condition that causes a child to have seizures. It is one of the most common disorders of the nervous system. It affects children and adults of all races and ethnic backgrounds.
The brain consists of nerve cells that communicate with each other through electrical activity. A seizure occurs when one or more parts of the brain has a burst of abnormal electrical signals that interrupt normal brain signals. Anything that interrupts the normal connections between nerve cells in the brain can cause a seizure. This includes a high fever, high or low blood sugar, alcohol or drug withdrawal, or a brain concussion. But when a child has 2 or more seizures with no known cause, this is diagnosed as epilepsy.
There are different types of seizures. The type of seizure depends on which part and how much of the brain is affected and what happens during the seizure. The 2 main categories of epileptic seizures are focal (partial) seizure and generalized seizure.
Focal (partial) seizures
Focal seizures take place when abnormal electrical brain function occurs in one or more areas of one side of the brain. Before a focal seizure, your child may have an aura, or signs that a seizure is about to occur. This is more common with a complex focal seizure. The most common aura involves feelings, such as deja vu, impending doom, fear, or euphoria. Or your child may have visual changes, hearing abnormalities, or changes in sense of smell. The 2 types of focal seizures are:
Simple focal seizure. The symptoms depend on which area of the brain is affected. If the abnormal electrical brain function is in the part of the brain involved with vision (occipital lobe), your child’s sight may be altered. More often, muscles are affected. The seizure activity is limited to an isolated muscle group. For example, it may only include the fingers, or larger muscles in the arms and legs. Your child may also have sweating, nausea, or become pale. Your child won’t lose consciousness in this type of seizure.
Complex focal seizure. This type of seizure often occurs in the area of the brain that controls emotion and memory function (temporal lobe). Your child will likely lose consciousness. This may not mean he or she will pass out. Your child may just stop being aware of what’s going on around him or her. Your child may look awake, but have a variety of unusual behaviors. These may range from gagging, lip smacking, running, screaming, crying, or laughing. Your child may be tired or sleepy after the seizure. This is called the postictal period.
A generalized seizure occurs in both sides of the brain. Your child will lose consciousness and be tired after the seizure (postictal state). Types of generalized seizures include:
Absence seizure . This is also called petit mal seizure. This seizure causes a brief changed state of consciousness and staring. Your child will likely maintain posture. His or her mouth or face may twitch or eyes may blink rapidly. The seizure usually lasts no longer than 30 seconds. When the seizure is over, your child may not recall what just occurred. He or she may go on with activities as though nothing happened. These seizures may occur several times a day. This type of seizure is sometimes mistaken for a learning or behavioral problem. Absence seizures almost always start between ages 4 to 12.
Atonic seizure. This is also called a drop attack. With an atonic seizure, your child has a sudden loss of muscle tone and may fall from a standing position or suddenly drop his or her head. During the seizure, your child will be limp and unresponsive.
Generalized tonic-clonic seizure (GTC). This is also called grand mal seizure. The classic form of this kind of seizure has 5 distinct phases. Your child’s body, arms, and legs will flex (contract), extend (straighten out), and tremor (shake). This is followed by contraction and relaxation of the muscles (clonic period) and the postictal period. During the postictal period, your child may be sleepy. He or she may have problems with vision or speech, and may have a bad headache, fatigue, or body aches. Not all of these phases occur in everyone with this type of seizure.
Myoclonic seizure. This type of seizure causes quick movements or sudden jerking of a group of muscles. These seizures tend to occur in clusters. This means that they may occur several times a day, or for several days in a row.
What causes a seizure in a child?
A seizure can be caused by many things. These can include:
An imbalance of nerve-signaling brain chemicals (neurotransmitters)
Brain damage from illness or injury
A seizure may be caused by a combination of these. In most cases, the cause of a seizure can’t be found.
What are the symptoms of a seizure in a child?
Your child’s symptoms depend on the type of seizure. General symptoms or warning signs of a seizure can include:
Jerking movements of the arms and legs
Stiffening of the body
Loss of consciousness
Breathing problems or stopping breathing
Loss of bowel or bladder control
Falling suddenly for no apparent reason, especially when associated with loss of consciousness
Not responding to noise or words for brief periods
Appearing confused or in a haze
Nodding head rhythmically, when associated with loss of awareness or consciousness
Periods of rapid eye blinking and staring
During the seizure, your child’s lips may become tinted blue and his or her breathing may not be normal. After the seizure, your child may be sleepy or confused.
The symptoms of a seizure may be like those of other health conditions. Make sure your child sees his or her healthcare provider for a diagnosis.
How are seizures diagnosed in a child?
The healthcare provider will ask about your child’s symptoms and health history. You’ll be asked about other factors that may have caused your child’s seizure, such as:
Recent fever or infection
Congenital health conditions
Your child may also have:
A neurological exam
Blood tests to check for problems in blood sugar and other factors
Imaging tests of the brain, such as an MRI or CT scan
Electroencephalogram , to test the electrical activity in your child’s brain
Lumbar puncture (spinal tap) , to measure the pressure in the brain and spinal canal and test the cerebral spinal fluid for infection or other problems
How are seizures treated in a child?
The goal of treatment is to control, stop, or reduce how often seizures occur. Treatment is most often done with medicine. Many types of medicines used to treat seizures and epilepsy. Your child’s healthcare provider will need to identify the type of seizure your child is having. Medicines are selected based on the type of seizure, age of the child, side effects, cost, and ease of use. Medicines used at home are usually taken by mouth as capsules, tablets, sprinkles, or syrup. Some medicines can be given into the rectum or in the nose. If your child is in the hospital with seizures, medicine may be given by injection or intravenously by vein (IV).
It is important to give your child medicine on time and as prescribed. The dose may need to be adjusted for the best seizure control. All medicines can have side effects. Talk with your child’s healthcare provider about possible side effects. If your child has side effects, talk to the healthcare provider. Do not stop giving medicine to your child. This can cause more or worse seizures.
While your child is taking medicine, he or she may need tests to see how well the medicine is working. You may have:
Blood tests. Your child may need blood tests often to check the level of medicine in his or her body. Based on this level, the healthcare provider may change the dose of medicine. Your child may also have blood tests to check the effects of the medicine on his or her other organs.
Urine tests. Your child’s urine may be tested to see how his or her body is reacting to the medicine.
Electroencephalogram (EEG). An EEG is a procedure that records the brain’s electrical activity. This is done by attaching electrodes to the scalp. This test is done to see how medicine is helping the electrical problems in your child’s brain.
Your child may not need medicine for life. Some children are taken off medicine if they have had no seizures for 1 to 2 years. This will be determined by your child’s healthcare provider.
If medicine doesn’t work well enough for your child to control seizures or your child has problems with side effects, the healthcare provider may advise other types of treatment. Your child may be treated with any of the below:
A ketogenic diet is a type of diet is very high in fat, and very low in carbohydrates. Enough protein is included to help promote growth. The diet causes the body to make ketones. These are chemicals made from the breakdown of body fat. The brain and heart work normally with ketones as an energy source. This special diet must be strictly followed. Too many carbohydrates can stop ketosis. Researchers aren’t sure why the diet works. But some children become seizure-free when put on the diet. The diet doesn’t work for every child.
Vagus nerve stimulation (VNS)
This treatment sends small pulses of energy to the brain from one of the vagus nerves. This is a pair of large nerves in the neck. If your child is age 12 or older and has partial seizures that are not controlled well with medicine, VNS may be an option. VNS is done by surgically placing a small battery into the chest wall. Small wires are then attached to the battery and placed under the skin and around one of the vagus nerves. The battery is then programmed to send energy impulses every few minutes to the brain. When your child feels a seizure coming on, he or she may activate the impulses by holding a small magnet over the battery. In many cases, this will help to stop the seizure. VNS can have side effects such as hoarse voice, pain in the throat, or change in voice.
Surgery may be done to remove the part of the brain where the seizures are occurring. Or the surgery helps to stop the spread of the bad electrical currents through the brain. Surgery may be an option if your child’s seizures are hard to control and always start in one part of the brain that doesn’t affect speech, memory, or vision. Surgery for epilepsy seizures is very complex. It is done by a specialized surgical team. Your child may be awake during the surgery. The brain itself does not feel pain. If your child is awake and able to follow commands, the surgeons are better able to check areas of his or her brain during the procedure. Surgery is not an option for everyone with seizures.
How can I help my child live with epilepsy?
You can help your child with epilepsy manage his or her health. Make sure to:
If age-appropriate, make sure your child understands the type of seizure he or she has, and the type of medicine that is needed.
Know the dose, time, and side effects of all medicines. Give your child medicine exactly as directed.
Talk with your child’s healthcare provider before giving your child other medicines. Medicines for seizures can interact with many other medicines. This can cause the medicines to not work well, or cause side effects.
Help your child avoid anything that may trigger a seizure. Make sure your child gets enough sleep, as lack of sleep can trigger a seizure.
Make sure your child visits his or her healthcare provider regularly. Have your child tested as often as needed.
Keep in mind that your child may not need medicine for life. Talk with the healthcare provider if your child has had no seizures for 1 to 2 years.
If your child’s seizures are controlled well, you may not need many restrictions on activities. Make sure your child wears a helmet for sports such as skating, hockey, and bike riding. Make sure your child has adult supervision while swimming.
When should I call my child’s healthcare provider?
Call the healthcare provider if:
Your child’s symptoms get worse or do not get better
Your child has side effects from medicine
Key points about epilepsy and seizures in children
A seizure occurs when one or more parts of the brain has a burst of abnormal electrical signals that interrupt normal signals
There are many types of seizures. Each can cause different kinds of symptoms. These range from slight body movements to loss of consciousness and convulsions.
Epilepsy is when a person has 2 or more seizures with no known cause.
Epilepsy is treated with medicine. In some cases, it may be treated with VNS or surgery.
It’s important to avoid anything that triggers seizures. This includes lack of sleep.