Indian Journal of Cerebral Palsy

ANNOTATION
Year
: 2016  |  Volume : 2  |  Issue : 1  |  Page : 3--21

Seizures in cerebral palsy


Nagabhushana Rao Potharaju 
 Former Prof. and HOD of Neurology, Osmania Medical College; Chief Neurologist/Pediatric Neurologist, Osmania General Hospital; Niloufer Hospital, Hyderabad; Kurnool Medical College/Govt. General Hospital, Kurnool, Andhra Pradesh; Short Term Consultant, Japanese Encephalitis Projects, PATH, WHO; Team Leader and Facilitator, Joint Monitoring Mission of World Health Organization and Government of India; National Expert for AES/Japanese Encephalitis, Govt. of India; Chairman, National Advisory committee on Japanese Encephalitis to Govt. of India; Chairman, Expert group of Japanese Encephalitis/Acute Encephalitis Syndrome clinical management group, Uttar Pradesh, India

Correspondence Address:
Nagabhushana Rao Potharaju
10-3-185, St. John«SQ»s Road, Secunderabad,Telangana
India




How to cite this article:
Potharaju NR. Seizures in cerebral palsy.Indian J Cereb Palsy 2016;2:3-21


How to cite this URL:
Potharaju NR. Seizures in cerebral palsy. Indian J Cereb Palsy [serial online] 2016 [cited 2017 Jul 27 ];2:3-21
Available from: http://www.ijcpjournal.org/text.asp?2016/2/1/3/188150


Full Text

 INTRODUCTION



"Cerebral palsy (CP) describes a group of permanent disorders of the development of movement and posture, causing activity limitation, which are attributed to nonprogressive disturbances that occurred in the developing fetal or infant brain. The motor disorders of CP are often accompanied by disturbances of sensation, perception, cognition, communication, and behavior, by epilepsy, and by secondary musculoskeletal problems." [1]

The addition of secondary impairments and functional limitations to the definition emphasizes the significance of understanding and communicating the effect of these co-occurring diseases, impairments, and functional limitations to parents to help them foreknow the outcomes. Although the brain damage in CP is nonprogressive, the co-occurring diseases, impairments, and functional limitations change over time resulting in the worsening of function and quality of life. [2]

In history, the two conditions, epilepsy and CP, are among the earliest syndromes recorded. [3],[4] In addition to mental defect which is common to the CP group as a whole, epilepsy is the most frequent single complication of CP. [3] Epilepsy, as similar to CP, is also not a disease but a symptom of cerebral dysfunction, and so frequently coexists in the same patient. The coexistence of two disabling conditions is a double handicap to the child and a dual challenge for the managing medical and paramedical teams.

 NEUROANATOMY AND NEUROPHYSIOLOGY



The overall number of neurons is usually finalized at birth. After birth, neurons neither divide, nor can the diseased or dead neurons be replaced. This limits the response of the central nervous system (CNS) to injury and ultimate recovery. Ultimate deficit due to prenatal damage in the brain is minimized by the presence of a higher number of neurons (which compensates partially for loss of some neurons) and neuronal and network plasticity (ability to repair itself) of the brain. This is the reason a prenatal facial palsy is better compensated than that occurring later in infancy. The development of skills, such as thinking, talking, and walking, depends on these neurons making correct connections with other relevant neurons and on myelination of the connecting axons. Human function is primarily at a subcortical level at birth, and therefore, many reflex patterns are mediated by brainstem and spinal cord mechanisms that are inhibited at predictable times as the brain axons are myelinated and connecting pathways mature during infancy. Persistence of the primitive reflexes is seen with CNS lesions or with developmental delays.

 PATHOPHYSIOLOGY OF EPILEPSIES AND ELECTROENCEPHALOGRAPHIC FINDINGS



CP etiology may predict the development of epilepsy. The larger/more critical the area damaged in the brain, the greater is the probability of developing both CP and epilepsy. Temporal and frontal lobe damage is particularly responsible for epilepsy. Severity of epilepsy is proportional to the severity of CP. [5] The incidence of epilepsy in the different groups varies depending on whether gray matter or white matter is involved and the extent of their involvement. In people with cerebral cortical lesions (gray matter is involved), the incidence of epilepsy is significantly increased. [6],[7] Cognition also depends on the gray matter. Children with cognitive impairment had a higher frequency of epilepsy than those without cognitive impairment. [8] Associated disabilities such as mental problems are much more common in children with cerebral palsy with epilepsy than in those without seizures. [9] Walking ability is an indicator of total disability load. [10] A good association exists between tetraplegia and age-dependent epileptic encephalopathy. Epilepsy most commonly affected children with spastic tetraplegia and those with mental subnormality. All children with tetraplegic cerebral palsy and about one-third of the children with other cerebral palsy types developed epilepsy. [8],[11] Children with cerebral palsy caused by gray matter damage, brain atrophy, CNS malformation, and CNS infection all showed a higher frequency of epilepsy than children with cerebral palsy of other etiologies. [8],[12] Seizures are less frequent in mild symmetric spastic diplegia and CP that is mainly athetoid. [13] Low birth weight, neonatal seizures, seizures during the 1 st year of life, and family history of epilepsy are related to significantly increased risk of epilepsy in children with cerebral palsy. [11],[12],[14] Apgar score, mode of delivery, head circumference, adjusted birth weight, gender and ethnic group, consanguineous marriage, and prematurity were not found to be risk factors in the occurrence of epilepsy in these children.

Larger/critical area damage of the brain leads to earlier presentation of CP and epilepsy. Hence, age of onset differs with the type of cerebral palsy: Children with tetraplegic cerebral palsy had an earlier onset of epilepsy than children with other cerebral palsy types. [8] Almost 50% of the epileptic children had their first seizure within the first 12 months of life. [12]

Seizures and epilepsy can be the result of inherited or acquired factors or both. In pediatrics, developmental brain malformations are important, which can be focal, hemispheric, or generalized. Epileptogenesis may be due to abnormal cell proliferation or differentiation (tuberous sclerosis, focal cortical dysplasia, and hemimegalencephaly), or abnormal neuronal migration (lissencephaly, subcortical band heterotopias, and periventricular nodular heterotopias), or abnormal cortical organization (polymicrogyria and schizencephaly). Few of the malformations are genetic such as lissencephaly, tuberous sclerosis, bilateral periventricular nodular heterotopia, and subcortical band heterotopia. Most of the malformations have associated neurologic deficits and have diagnostic magnetic resonance imaging (MRI) findings.

West and Lennox-Gastaut syndromes

Hypsarrhythmia predominates in the occipital areas around 6 months of age, because at that age, occipital area undergoes major maturation. The epileptiform activity prevents normal maturation and gnosic functions. Furthermore, this activity disinhibits subcortical areas resulting in generation of paroxysmal motor activity, the "epileptic spasms" (including infantile spasms). Supratentorial myelination occurs within the first 2 years of life. This results in generalization of paroxysmal activity generating the slow spike-and-wave pattern of Lennox-Gastaut syndrome.

Idiopathic generalized epilepsy

Between 4 and 8 years of age, thalamic and prerolandic cortical hyperexcitability creates a thalamic-cortical slow-wave loop whose 3 Hz rhythmicity affects the rolandic strip generating generalized myoclonus. Myoclonus can be the only manifestation in infancy (1-2 years) (myoclonic epilepsy in infancy) or adolescence (juvenile myoclonic epilepsy). From 2 to 5 years of age, this slow-wave loop interacts with age-related excitability of the frontal lobe producing myoclonic-astatic seizures with drop attacks. The late stage of this epilepsy syndrome presents as a combination of atypical absences, tonic seizure, and slow spike-waves, a pattern seen in both Lennox-Gastaut syndrome and epilepsy with myoclonic-astatic seizures because they share frontal lobe hyperexcitability.

Status epilepticus

During status epilepticus, the brain requires more adenosine triphosphate (ATP) than can be synthesized by the tissues from the accessible oxygen and glucose. A deficiency of ATP, phosphocreatine, and glucose causes secondary hypoxia, lactate accumulation, and acidosis, resulting in progressive brain tissue injury and destruction.

 SEIZURES AND EPILEPSY IN CEREBRAL PALSY



Seizures are paroxysmal disturbances in cerebral functioning caused by an abnormal, excessive, hypersynchronous discharge of cortical neurons. The epilepsies are a group of conditions characterized by recurrent unprovoked seizures and are an expression of an underlying brain disorder. A remote symptomatic seizure is a seizure that occurs later than 1 week following a disorder that is known to increase the risk of developing epilepsy. It can present many years after a brain insult (such as perinatal hypoxia and brain injury). The most common acquired causes of epilepsy in young infants are perinatal hypoxia/asphyxia, perinatal intracranial trauma, metabolic disturbances, congenital malformations of the brain, and infection.

 PREVENTION OF CEREBRAL PALSY AND EPILEPSY



0Antenatal measures for prevention of cerebral palsy and epilepsy

Maternal illnesses

0Children of mothers who had illnesses during pregnancy have 1.6 times higher probability of developing epilepsy. [15] Maternal immune system, maternal infections, or factors related to maternal immune function play a role in the observed associations between maternal infections before pregnancy and cerebral diseases, including CP in the offspring. [16]

Macrolide antibiotics (like azithromycin)

An increased risk of CP or epilepsy is associated with macrolide prescribing in pregnancy. [17] There is no association with other antibiotics. [17]

Role of magnesium in eclampsia

Magnesium is the first-line drug for the treatment of eclampsia in pregnant women. Approximately 1000 people per annum of CP in the United States could be prevented if magnesium was consistently used during labor. [18]

Neonatal preventive measures

Magnesium sulfate in preterm newborns and head cooling during or after resuscitation at birth may reduce brain damage and risk of CP. [19],[20]

 EPIDEMIOLOGY OF EPILEPSY IN CEREBRAL PALSY



Epilepsy occurs in 25-45% of children with cerebral palsy. [21],[22] First seizures occur during the 1 st year of life in 70% of the children with epilepsy and cerebral palsy. The risk of epilepsy is highest among children with dyskinetic cerebral palsy or bilateral spastic cerebral palsy who are unable to walk unaided and lowest among those with bilateral spastic cerebral palsy who can walk unaided. Children with atonic-diplegic, dystonic, tetraplegic, and hemiplegic cerebral palsy had a higher incidence of epilepsy (87.5%, 87.1%, 56.5%, and 42%, respectively). [23] Both the prevalence and incidence of epilepsy in individuals with CP continue to fall with time. [8],[14]

 SEIZURE TYPES IN CEREBRAL PALSY



All types of epileptic seizures [Figure 1] are seen in children with cerebral palsy [Table 1]. [5],[24],[25] In general, focal-onset seizures (often with secondary generalization) predominate in children with unilateral spastic (hemiplegic) or bilateral spastic (diplegic) cerebral palsy [8],[12],[14],[26] whereas epilepsy in other motor subtypes of cerebral palsy is characterized by multiple types of generalized seizure in the same patient. [8],[14] These include generalized tonic-clonic, tonic, atonic, absence, and atypical absence seizures. Infantile spasms occur in some infants, particularly in those with microcephaly and spastic quadriplegic or atonic CP. [13] Lennox-Gastaut syndrome is particularly frequent. [5],[14] In children with cerebral palsy, deep white matter injuries (periventricular leukomalacia) are not associated with West syndrome; therefore, spasms are unusual in premature infants.{Figure 1}{Table 1}

 EPILEPTIC ENCEPHALOPATHIES



They are severe brain diseases of early life with progressive cerebral dysfunction that manifests with (1) usually multi-form and intractable seizures, (2) electroencephalography (EEG) abnormalities, (3) usually progressive behavioral, cognitive and neurological deficits, and (4) occasionally early death. Ictal (seizure) and electrical (EEG) epileptogenic activity during brain maturation are responsible for the progressive cognitive and neuropsychological deterioration. This age-related epileptogenic reaction of the immature brain varies significantly with the stage of brain maturity at the time of insult. As the child grows, the seizure and EEG evolve from one age-related stage to another, namely, from burst-suppression (seen in neonates) to hypsarrhythmia (seen in infants) and then to slow generalized spike-wave discharges (seen in early childhood). All epileptic encephalopathies have a tendency to subside or even halt in adolescence but frequently with serious neurocognitive deficits.

A number of age-related epileptic syndromes relate to maturational events in brain circuits or ion channels. One syndrome can have different etiologies and prognoses. In the classification of the International League Against Epilepsy, age-related epileptic encephalopathy syndromes that are recognized include early myoclonic encephalopathy and Ohtahara syndrome in the neonatal period, West syndrome and Dravet syndrome in infancy, Lennox-Gastaut syndrome, Landau-Kleffner syndrome, and epilepsy with continuous spike-waves during slow-wave sleep in childhood and adolescence. Most of these syndromes result from the sodium channel-encoding gene mutations. [27]

 RISK FACTORS FOR EPILEPSY IN CHILDREN WITH CEREBRAL PALSY



Risk factors for epilepsy in early childhood are neonatal seizures, complex febrile seizures (CFSs), infections, head trauma, vascular malformations, brain tumors, parasitic infections, stroke, inflammatory and autoimmune disorders, and limbic encephalitis.

 ACUTE SYMPTOMATIC SEIZURES



Seizures can result from specific precipitants such as fever in young children (febrile convulsions); infections, structural or inflammatory lesions, soon after stroke; metabolic disturbances (hypoglycemia, hyperglycemia, hyponatremia, hypocalcemia, hypomagnesemia, and uremia); drug abuse (cocaine in excess), abrupt drug withdrawal (benzodiazepines, baclofen, and barbiturates); or acute head injury. These seizures are termed acute symptomatic seizures. Following such seizures, the chance of an unprovoked seizure is usually quite low and so the person would not be considered as having epilepsy. Metabolic and toxic causes are unlikely to cause chronic epilepsy.

Febrile seizures in cerebral palsy

When a seizure occurs in a febrile cerebral palsy infant, differential diagnosis includes (1) infection of the nervous system, (2) CFS [Table 1], (3) seizure of a seizure disorder precipitated by fever, and (4) simple febrile seizure (SFS) [Table 1].

Risk factors for first febrile seizure

A history of febrile seizure (FS) in a first-degree or higher relative seems to be the factor with the strongest prediction power. [28] Other risk factors include preexisting developmental delays, day-care attendance, stay in the neonatal nursery for more than 28 days, and various viral infections. [28] Risk of FS is increased by associated iron deficiency. [29] Associations with zinc remain unclear at the moment.

Vaccinations-related febrile seizure

FS after vaccinations is similar to FS due to other causes. [30] The illness course and risk of hospitalization are similar between vaccination-related and other illness-related FS. [31] . Postvaccination FS is rare and often occurs within the first 3 days after administration of live attenuated vaccines. Concomitant multivaccination increases the risk of developing FS. [32] . After the initial seizure, the risk of subsequent seizures and neurodevelopmental affection does not increase. None of the routine vaccinations is currently contraindicated in children with FS. Antipyretics can be prescribed at the time of some potentially pyrexic vaccinations for children at risk of FS. [33]

Risk factors for recurrent febrile seizure

They include (1) FS onset before the age of 1 year, (2) duration of fever <1 hour before seizure onset, (3) fever of 38-39°C (100.4-102.2°F) at the time of the seizure, (4) CFS, (5) low serum sodium, (6) positive personal and family history of FS, (7) family history of epilepsy, (8) daycare, and (9) male gender. Recurrence risk is 12% if there are no risk factors, 25-50% with one risk factor, 50-59% with two risk factors, and 73-100% with three or more risk factors. An FS of long duration does not increase the risk of recurrence but does increase the risk of recurrence of a prolonged FS. Antipyretics decrease the discomfort caused by fever but do not reduce the risk of a recurrent FS because the seizure occurs when the temperature is rising or falling.

Risk factors for the development of epilepsy after febrile seizure

They are (1) CFS - increase the risk 3.6 times, (2) age at the onset of FS beyond the 3 rd year of life - increases the risk 3.8 times, (3) positive family history of epilepsy - increases the risk 7.3 times, and (4) multiple episodes of FS about 10 times. Focality at the first and the second FS recurrence increased the risk of epilepsy about 9.7 and 11.7 times, respectively.

Indications for antiepileptic drug prophylaxis of febrile seizure

In view of the benign nature, antiepileptic drug (AED) prophylaxis for SFS is usually unnecessary. There is no definitive evidence that anticonvulsant prophylaxis for SFS prevents the development of unprovoked seizures. AED prophylaxis is considered in following situations: (1) Family history of epilepsy and recurrent FS (both simple or complex), (2) CFS, (3) significant reaction of family or social disturbance caused by the seizures, (4) child had status epilepticus, (5) respiratory compromise during the seizure, and (6) FS recurring in <3 months. AED prophylaxis: Phenobarbital, 3-5 mg/kg orally daily. [34] Side effects include attention-deficit/hyperactivity disorder (ADHD) and depressed cognition and learning. Valproic acid or divalproex, 30 mg/kg orally divided into two doses daily. Side effects include thrombocytopenia and may provoke acute liver dysfunction in a patient younger than 2 years.

 SEIZURE PRECIPITANTS



Most common seizure precipitants are emotional stress, sleep deprivation, fatigue, fever or illness, flickering light, and menstruation (catamenial epilepsy). Many medications such as tricyclic antidepressants, bupropion, various antipsychotics, CNS stimulants, fluoroquinolone antibiotics, older antihistaminics, meperidine, and tramadol reduce the seizure threshold. Hyperventilation is well known to precipitate generalized absence seizures. It can also precipitate other seizure types to a much lesser extent. [35] Breakthrough seizures occur with missing any of the AEDs. Carbamazepine and oxcarbazepine result in more severe seizures upon abrupt withdrawal. [36] A precipitation of seizures in relation to the menstrual cycle is called catamenial epilepsy. The most frequent pattern of clustering of seizures is peri-menstrual (3 days before to 3 days after the onset of the period). The mechanism of catamenial epilepsy is probably related to the opposite effects of estradiol and progesterone on the seizure threshold. Estradiol is a proconvulsant whereas progesterone is an anticonvulsant. Progesterone therapy is considered when catamenial epilepsy does not respond to AEDs.

Sleep and seizures

Certain types of seizures typically manifest during sleep, for example, benign focal epilepsy of childhood with rolandic spikes, benign focal epilepsy with occipital paroxysms in EEG, nocturnal frontal lobe epilepsy, juvenile myoclonic epilepsy, tonic seizure as a component of Lennox-Gastaut syndrome, childhood occipital epilepsy, generalized tonic-clonic seizures on awakening, nocturnal temporal lobe epilepsy, Landau-Kleffner syndrome, and continuous spike-and-wave discharges during nonrapid eye movement sleep.

 DIFFERENTIAL DIAGNOSIS OF EPILEPSY



Since CP is a static encephalopathy (brain damage is static), with proper medical management, there must be some improvement, though the speed of improvement could vary. Sometimes, phases of rapid growth in CP may briefly make it appear progressive. Every attempt to find an underlying cause for CP must be made. Metabolic and genetic evaluation should be considered if there is a family history of childhood neurologic disease, if there is episodic or progressive deterioration and if no etiology can be determined. If the disability worsens in spite of thorough care, progressive encephalopathies (such as trauma, deficiencies, inborn errors of metabolism (IEM), neurodegenerations, and poisonings) must be considered. A small fraction of people with cerebral palsy may, in fact, have a slowly progressive but treatable condition, for example, glucose transporter (GLUT) deficiency [37] and serine-deficiency disorders. [38] Neurodegenerations that can be misdiagnosed as CP include Friedreich ataxia, ataxia-telangiectasia, metabolic and mitochondrial diseases associated with spasticity, and metachromatic leukodystrophy.

Epilepsy must be considered in the differential diagnosis of any unexplained worsening of the motor disorder in CP, sudden falls, a cognitive decline or a decrease in alertness. Nonconvulsive status epilepticus (NCSE) or electrical status epilepticus of slow sleep must be excluded if necessary. The misdiagnosis of other paroxysmal disorders as epilepsy compounds the error leading to the diagnosis of "refractory" seizures and misuse of polytherapy of AEDs. Nonepileptic paroxysmal events must be positively identified to manage them appropriately. Children with cerebral palsy can present with various types of paroxysmal attacks (such as syncope, paroxysmal motor disorders, behavioral and psychogenic events, or parasomnias) that may be seen in children without cerebral palsy. The progression of the attacks must be carefully reviewed. Eyewitness accounts, videos taken with mobile devices can be very useful for accurate diagnosis. Complicating the issue, nonepileptic attacks are often seen in children who have epileptic seizures. This is especially true in children with cerebral palsy: Certain paroxysmal motor phenomena, such as repetitive sleep starts (hypnagogic or hypnic jerks, are bilateral, sometimes asymmetric, usually single, brief body jerks that coincide with the sleep onset) in bilateral spastic CP (quadriplegia) or status dystonicus in baclofen withdrawal, [39] present similarly to seizures and pose diagnostic challenges if proper history is not taken. Hallucination also may occur if baclofen is discontinued abruptly.

Differential diagnosis of aura

Some children may have a difficult-to-describe feeling (prodrome) that a seizure may occur. Epilepsy prodromes may last hours or even days and have to be distinguished from auras. Epilepsy auras are characteristically short in duration, lasting seconds to few minutes. Aura, like focal seizures, is contralateral to the hemisphere involved in seizure activity. Seizures are more frequent and shorter in duration than transient ischemic attacks (TIAs). Finally, postictal weakness can occur in one limb. The aura in migraine typically lasts 5-60 min due to spreading cortical depression (characteristic of migraine) resulting from a slow depolarization spreading with a speed of 3 mm/min. The aura takes 10-20 min to spread from the initial point to their maximal distribution. This is slower than the spread of a sensory seizure and sensory symptoms associated with TIA. Another useful distinction is that the visual aura in migraine is a scintillating scotoma or fortification spectrum whereas colored circles are seen in occipital lobe seizures. The visual aura of migraine is perceived with the eyes closed or opened because it is a positive phenomenon. Migraine and epilepsy have a greater overlap than would be expected by chance. The prevalence of each is increased in the presence of the other. Aura of syncope lasts longer than that of epilepsy. Syncope is due to gradual failure of cerebral perfusion with a reduction oxygen supply to the brain. Syncope is a symptom complex consisting of lightheadedness, giddiness, visual blurring, tinnitus, muscle weakness, and gastrointestinal symptoms. The child is pale and feels cold and "sweaty." Loss of consciousness generally is gradual allowing the child to protect itself from falling and injury. Factors precipitating a simple faint are emotional stress, prolonged standing, unpleasant visual stimuli, or pain.

Other nonepileptic paroxysmal events to be considered in the differential diagnosis

They are breath-holding attacks, tics (Tourette syndrome), parasomnias (night terrors, sleep talking, walking, "sit-ups"), nightmares, migraine, benign nocturnal myoclonus, shuddering, gastroesophageal reflux (Sandifer syndrome), infantile masturbation/gratification movements, conversion reaction/psychogenic nonepileptic seizures, temper tantrums and rage attacks, benign paroxysmal vertigo, staring spells, TIA, rage attacks, and panic attacks.

 DIAGNOSIS



History

Developmental milestones must be recorded. In people with cerebral palsy and mental retardation, the diagnosis of epilepsy presents unique difficulties because of lack of accurate history. Description of children's own experiences before, during and after the episode if they are articulate enough, eyewitness account of the episode, history from caregiver concerning remote injuries to the nervous system, progressive neurologic symptoms, or intercurrent illness must be elicited.

Physical examination

Physical examination between seizures may show evidence of CP. Children should be examined carefully for focal or lateralizing neurologic signs. Assessment of development, mental status, and genetic disorders must be done.

Laboratory studies

Initial investigations should include complete blood count, serum glucose, electrolytes, creatinine, calcium, magnesium, and liver function tests to exclude various causes of seizures and to provide a baseline for subsequent monitoring of long-term effects of treatment. A peripheral blood smear for malarial parasite must be considered. A cerebrospinal fluid (CSF) analysis is necessary if infection is suspected. Meningeal irritation may not be obvious in infants <1 year, in the postictal period or if pretreated with antibiotics. CSF is must in all infants <6 months of age who present with fever and seizure, or if the child is ill-appearing or at any age if there are clinical signs or symptoms of meningitis. Lumbar puncture (LP) is optional in a child 6-12 months of age who has not received Haemophilus influenzae Type B and Streptococcus pneumoniae immunizations or whose immunization status is unknown or has been pretreated with antibiotics. In febrile status epilepticus without any CNS infection, a nontraumatic LP infrequently shows CSF pleocytosis (96% have <3 nucleated cells in the CSF), and the CSF protein and glucose are normal. Historical information can frequently guide the need for metabolic tests. Urine toxicology is necessary when illicit drug use is suspected. For refractory seizures, CSF analysis may provide evidence of underlying IEM such as pediatric neurotransmitter disorders (e.g., dopa-responsive dystonia), reduced serine levels (serine-deficiency disorders), [38] or low CSF glucose concentration (hypoglycorrhachia) which can be caused by GLUT1 deficiency. [40] Depending on associated symptoms, a complete metabolic workup or genetic testing, or both, may be performed to explore the possibility of deficiency or malabsorption. [41]

Electroencephalography

Forty percent of children with epilepsy have a normal EEG. If the child has first SFS and is neurologically otherwise normal, an EEG is unnecessary.

Improving the success rate of electroencephalography

Hyperventilation brings out abnormalities in petit mal. Sleep-deprived EEG is superior to a routine EEG and an EEG with medication-induced sleep. [42] In generalized epilepsy, a morning EEG is preferable to an afternoon EEG. [43] Special techniques (e.g., prolonged monitoring with telemetry, special anatomic electrode placements) can sometimes help overcome the standard EEG limitations of sample time and inaccessible areas of the cerebral cortex. Prolonged EEG-video monitoring is expensive and reserved for recurrent episodes with atypical manifestations, a nondiagnostic EEG or AED-refractory episodes.

An EEG must be interpreted along with clinical and neuroimaging findings and the diagnosis must not rest on the EEG alone. EEG can confirm the diagnosis, help classify the epilepsy as generalized or focal, and help diagnose the specific syndrome in some persons. The EEG is usually abnormal in CP. [14] Generalized or focal slowing are extremely common in children with cerebral palsy, whether or not they have a history of seizures. Children with cerebral palsy generally display ictal or interictal EEG findings characteristic of a range of electroclinical epilepsy syndromes, including hypsarrhythmia with infantile spasms, generalized polyspike discharges associated with myoclonic jerks, [26] or even centrotemporal spikes associated with rolandic seizures. An epileptiform EEG is associated with an increased risk of seizure recurrence. If untreated, the risk of recurrence was increased by a factor of 1.54. [44]

Electroencephalography abnormality without clinical seizure

Interictal epileptiform discharges (IEDs), although more frequent in those with epilepsy, also occur in those who do not have seizures. [14] In a significant number of cerebral palsy children, IEDs are obtained in their EEG even in the absence of clinical epilepsy. All that spikes may not be fits. No evidence supports AED treatment of incidentally detected IEDs in persons without seizures, either for the prevention of subsequent epilepsy or for improving behavior or cognition. [45] The prognostic significance of IEDs in patients without seizures requires additional studies, particularly for children with as cerebral palsy, autism spectrum disorder or ADHD, which predispose them to epilepsy development. [46],[47] However, a few trials aimed at treating IEDs in autistic patients without epilepsy and in children with behavior problems have yielded favorable results. Based on these studies, one author proposed inclusion of EEG investigation in the management protocol of cerebral palsy children and treatment of IEDs (when detected even in the absence of clinical epilepsy) for a better outcome in their prognosis. [48]

Neuroimaging

MRI is the method of choice in the diagnosis of both epilepsy and CP. MRI shows the underlying brain damage in 85% patients. Recognizing the lesion (1) confirms that the deficit will be permanent, but nongenetic and nonprogressive and (2) explains the neurologic deficits like motor disability, epilepsy, severe learning difficulties, or visual deficits. MRI is either normal or nonspecific <2 years of age due to ongoing myelination. If it is normal, later progressive genetic disease must be excluded. MRI scans are especially useful if there is a progression of neurologic deficit, a history of neurologic insult, an asymmetry of neurologic findings or focal seizures, dysgenesis is present in other parts of the body or postictal encephalopathy persists too long. A structural abnormality avoids the necessity for expensive metabolic testing. Coronal MRI scans detect mesial temporal sclerosis, a lesion in the hippocampus in chronic temporal lobe epilepsy; ictal positron emission tomography (PET) using fludeoxyglucose F18, interictal PET using a-methyl-l-tryptophan, single-photon emission computerized tomography, functional MRI, and magnetoencephalography may help delineation of the nature of epileptogenic cortex or the underlying lesion and distinguish it from the normal cortex.

 TREATMENT



Drug treatment

Patients/parents must be fully informed of the management plans. Progressive epileptic encephalopathies (like West syndrome, Lennox-Gastaut syndrome, etc.) have to be controlled at the earliest to minimize brain damage. In the presence of CP, the recurrence rate is considerably higher. Treatment is not usually started after a single seizure unless a seizure is associated with a neurological deficit, abnormal EEG (such as the presence of 3 cps spike and wave), or a progressive neurological disorder. Treatment halves the risk of further seizures. Compliance can be improved by limiting to a minimum number of daily doses. All patients must be warned about the dangers of abrupt cessation of AED and must be advised to take the missed dose at the earliest opportunity if they forget a dose or vomit a dose. Recurrent seizures or status epilepticus may result if drugs are taken erratically.

Choice of medication

The principles of drug therapy in children with cerebral palsy and epilepsy are the same as those for children with epilepsy in general. The type of seizure, epilepsy syndrome, age, gender, cost, the side effect profile of the medicine being considered, interactions with other possible medications, and associated comorbidities guide the selection of AEDs. About half of all patients with a new diagnosis of epilepsy will be seizure-free with the first AED prescribed. [49] In general, carbamazepine or lamotrigine should be the first-line AEDs for focal-onset seizures, and valproate for generalized seizures. [50] A guide to AED selection by seizure type is summarized in [Table 2]. The dose of the selected drug is progressively increased until seizures are controlled or side effects prevent the further increase. If seizures continue despite treatment at the maximal tolerated dose, a second drug is added, and the dose is gradually increased depending on tolerance; the first drug is then gradually withdrawn. In most patients with seizures of a single type, satisfactory control can be achieved with a single AED. Treatment with two AEDs may further reduce seizure frequency or severity but frequently at the cost of increased side effects. Combination therapy (polytherapy) should be attempted only after at least two adequate sequential trials of single agents have failed. Although seizures in most children are controlled by one medication, the epileptic pattern and clinical course may require more than one drug to control the seizures. [51] Treatment with more than two AEDs is almost always not useful unless there are seizures of different types. Polytherapy was commonly used in children with spastic tetraplegia 59.5%. [14] Failure to control epilepsy with adequate trials of two drugs meets criteria for treatment-resistant epilepsy, and surgery must be considered. [52] [Table 2] shows commonly used AEDs.{Table 2}

Relationship of antiepileptic drug selection with age and sex

Tolerance profiles differ in children and adults, and they influence the risk/benefit ratio for particular AEDs. Behavioral adverse effects due to levetiracetam, serious rashes due to lamotrigine, and oligohidrosis due to zonisamide and topiramate are more frequent in children whereas hyponatremia due to oxcarbazepine and aplastic anemia due to felbamate are less likely. Valproate-induced liver failure and Reye syndrome are more likely in children younger than 2 years of age. Some AEDs reduce the efficiency of oral contraception in women. Valproate is contraindicated in women of child-bearing age for two extremely important reasons: Higher risk of congenital malformations in the fetus and increased risk of polycystic ovaries and hyperandrogenism. [53]

The use of antiepileptic drugs in patients without renal or hepatic disease

Routine blood tests before and after starting AEDs for avoiding or detecting early adverse effects, although recommended by manufacturers, are not cost-effective and are discouraged by NICE. However, human leukocyte antigen testing of individuals of certain races, particularly those of Chinese origin, before treatment with carbamazepine to avoid Stevens-Johnson syndrome, must be considered.

The use of antiepileptic drugs in patients with renal or hepatic disease

It is not uncommon in clinical practice. Because the liver and kidney are the main organs concerned in the elimination of many drugs, their dysfunction can delay the elimination of the parent drug or an active metabolite that can lead to accumulation and clinical toxicity. They can as well affect the distribution, protein binding, and metabolism of a drug. Renal failure significantly reduces the protein binding of anionic acidic drugs such as phenytoin and valproate causing difficulties for the interpretation of values of total serum concentrations. In addition, dialysis can modify the pharmacokinetics or remove significant quantities of the AEDs. AEDs that are eliminated intact by the kidneys or undergo negligible metabolism include vigabatrin, topiramate, gabapentin, and pregabalin when used as monotherapy. AEDs eliminated mainly by biotransformation are valproate, carbamazepine, phenytoin, rufinamide, and tiagabine. AEDs eliminated by a combination of biotransformation in liver and renal excretion are oxcarbazepine, eslicarbazepine, levetiracetam, lacosamide, zonisamide, phenobarbital, primidone, felbamate, ezogabine/retigabine, and ethosuximide. AEDs in the latter group have to be used carefully in patients with either liver or renal failure. AEDs that are extracted by hemodialysis include levetiracetam, gabapentin, lacosamide, pregabalin, ethosuximide, and topiramate. The use of AEDs in the presence of hepatic or renal disease is complicated and requires reasonable knowledge with their pharmacokinetics. To optimize clinical outcomes of these patients, frequent monitoring of serum concentrations and reviews are required. [54] For example, periodic tests of hepatic function may be necessary if valproic acid, carbamazepine or felbamate is used, and serial blood counts are important with carbamazepine, ethosuxumide or felbamate.

Drug interactions

They must be considered if the patient is getting other drugs. Trihexyphenidyl reduces the serum levels of valproate. Reduction in gastrointestinal motility by trihexyphenidyl may have impaired the absorption of sodium valproate, resulting in suboptimal serum concentrations. [55]

Monitoring blood levels of antiepileptic drugs

The concentration range for an AED is a guide based on population data, and there are many patients who are seizure-free at a lower level or require a higher level for seizure control. Dosing should therefore, be guided by clinical response. Routine blood monitoring is not recommended if dose is stable, seizures are controlled, and no side effects are noted. Increasing the dose of drugs in a child who is seizure-free to achieve a "therapeutic" level does not decrease the chance of relapse but increases the chance of side effects. There are certain circumstances where monitoring may be undertaken: (1) detection of noncompliance, (2) suspected toxicity, (3) adjustment of phenytoin dose (because of its nonlinear kinetics of metabolism), (4) managing pharmacokinetic interactions, and (5) managing situations that affect drug levels, such as concomitant illnesses or concomitant drugs such as trihexyphenidyl with valproate.

Evaluation of drug-resistant seizures and epilepsy

When seizures are drug resistant, the diagnosis of epilepsy and the AEDs selected must be reassessed. Potentially preventable factors include sleep deprivation, poor compliance with AEDs, the use of concomitant medications such as cephalosporins that can reduce the seizure threshold, alcohol/drug abuse, or abuse of caffeine. Video-EEG recordings can capture characteristic episodes for definitive diagnosis.

Discontinuation of medication

Withdrawing AEDs must be done with the agreement of the patient after discussion of the risks and benefits. After 2 years of seizure freedom, seizure recurrence risk without AED withdrawal over the next 2 years is 20% and 40% with AED withdrawal. The risk depends on clinical circumstances and the longer the period of seizure freedom, the greater the chance of successful AED withdrawal. Discontinuation of AEDs in children with cerebral palsy must be considered after patients have been seizure-free for at least 2 years. [56] Unfortunately, there is no way of predicting which patients will have a relapse after tapering AED although seizure recurrence is more likely in patients who initially did not respond to therapy, those with seizures having focal features or of multiple types, and those with persisting EEG abnormalities. Dose reduction must be gradual (over weeks or months), and if on polytherapy, drugs should be withdrawn one at a time. If seizures recur, treatment is reinstituted with the previously effective drug regimen. During the process of withdrawal, if seizure recurs, the AED dose must be reversed to the last dose change and seek medical advice at the earliest.

Surgical treatment

Patients with seizures refractory to AEDs may be considered for operative treatment. Surgical resection is most effective when there is a single well-defined seizure focus, especially in the temporal lobe. Other operative interventions include partial or complete severing of the corpus callosum for intractable generalized epilepsy. Bilateral deep-brain stimulation of the anterior thalamus for medically refractory focal-onset seizures and electrical stimulation of other cortical and subcortical targets may be considered. Epilepsy surgery should not be pursued for patients who are noncompliant with medications and brief, subjective, focal sensory seizures (i.e., isolated auras) since these seizures often persist after epilepsy surgery.

Vagal nerve stimulation

Children with intractable epilepsy have shown some benefit from using a vagal nerve stimulator. [57] This treatment for adolescents and adults with medically refractory focal seizures provides another approach for patients who are not fit for surgery. The mechanism of action is unknown. Adverse effects consist of transient hoarseness during stimulus delivery.

Hyperbaric oxygen therapy

Hyperbaric oxygen therapy is not recommended due to lack of efficacy, risk for adverse effects, and high-cost. [58],[59]

Ketogenic diet

Ketogenic diet (KD) may be effective as a supplement treatment for epilepsy that is difficult to control with AEDs or have intolerable side effects. The goal is to maintain a state of ketosis, which reduces seizure frequency and severity for difficult-to-control seizures in children. Seizure reduction may occur within 5-14 days of starting the diet and generally within 6 months. KD may be unpalatable and difficult to follow, especially if the child can access other foods. Carbohydrates may be added by 5 g increments after 3-6 months if seizures are controlled, and ketosis is maintained. The mechanisms are not completely understood, but enhanced ATP production, mitochondrial respiration, and reduced reactive oxygen species formation may alter the dynamics of excitatory and inhibitory neurotransmitter systems within the brain resulting in neuroprotection and seizure control. Side effects can include lethargy, acidosis, renal stones, gastrointestinal distress, hypoglycemia, dehydration, and poor growth. Most side effects are treatable. [60-64]

Stem cell therapy

Stem cells present a ray of hope in the dark. A population of "stem cells" with mitotic potential is present in the subventricular zone and beneath the hippocampal dentate gyrus. Since they can be induced to mature as neurons, they have created substantial interest to regenerate the damaged adult brain. [65] Transplanted stem cells have an augmented risk of neoplastic (cancerous) transformation, however. [66] Published cell transplant experiments conducted so far in humans suggest probable safety, but efficacy has to be still confirmed on a large scale. A small-scale study published in a peer-reviewed journal showed that SB623 stem cells were safe and associated with improvement in clinical outcome end-points at 12 months in 16 adults who completed the study. [67]

 BONE HEALTH IN CEREBRAL PALSY WITH EPILEPSY



Children with disabilities that limit mobility are at increased risk for osteoporosis. CP and epilepsy, which are both chronic disorders that frequently coexist, are predictors of muscular and skeletal compromise. Care must be taken for promoting and achieving optimal bone health in children with these disabilities and screening patients who are at risk of sustaining fractures. [68]

 Educational, Social, and Environmental Approaches



Epilepsy management includes not only control of seizures but also management of numerous psychosocial challenges. The diagnosis of epilepsy in the child with cerebral palsy should readjust the rehabilitation measures if necessary but never stopped. Epilepsy and CP make a difficult situation in classrooms. Fits disrupt the class and education of all other students. In children with cerebral palsy, epilepsy is associated with a higher prevalence of problems with cognition [69],[70] and behavior. [56] Children with unilateral cerebral palsy (hemiplegia) and epilepsy did not demonstrate improvement over time in verbal intelligence quotient (IQ) shown by those with cerebral palsy but without seizures, [69],[70] suggesting that active epilepsy may have an adverse effect on neural plasticity.

Educational difficulties are frequent in children with epilepsy, [71] and probably the high prevalence of comorbid cognitive, [72] behavioral, and psychiatric [56],[69],[70] problems among this population are a major contributing factor. Other, more general interventions in the school setting would include education about epilepsy for teachers and peers, to decrease the stigma attached to epilepsy, and to prevent a child being excluded from activities unnecessarily.

Low academic achievement is more common than academic underachievement (achievement below that expected on the basis of IQ scores), and it is not clear if rates of academic underachievement are significantly higher than in the general population. [71] In contrast, children with cerebral palsy maintain their full-scale IQ scores but develop cognitive weaknesses in aspects of performance IQ with time. [70],[73] Thus, the child with cerebral palsy and epilepsy has a complex and evolving neuropsychological profile, and benefits from regular assessment to guide specific educational intervention.

People with a learning disability often have multiple seizure types. Rare childhood epilepsy syndromes such as Lennox-Gastaut and Dravet syndrome are overrepresented in adults with a learning disability. Learning and behavioral side effects are of great concern for all individuals with learning disability and epilepsy. Using psychology and other services may be necessary. AED treatment does not change the ultimate prognosis in terms of the likelihood of seizure remission and treating with AEDs to avoid behavioral and learning problems is tricky given the neurobehavioral side effects of AEDs except in epileptic encephalopathies where rapid control of seizures increases the likelihood of remission and limits the development of behavioral and learning problems.

 STATUS EPILEPTICUS



Status epilepticus is any seizure continuing for 30 min or more, or recurrent seizures for >30 min during which the patient does not regain consciousness. Serial seizures are seizures with recovery of consciousness between the attacks.

Convulsive status epilepticus (CSE)

CSE occurs in 14-47% of children who have both cerebral palsy and epilepsy. [8],[14] Poor compliance to the AED regimen is the most common cause; other causes include intracranial infection or neoplasms, metabolic disorders, and drug overdose.

Nonconvulsive status epilepticus

Here, status epilepticus presents without motor activity but with confusion, a fluctuating abnormal mental status, impaired responsiveness and automatism. EEG confirms the diagnosis. The treatment approach outlined above for convulsive status epilepticus applies to any type of status epilepticus although intravenous anesthesia is usually not necessary. There is usually no necessity for intensive care. Steroids may be helpful in diseases such as Landau-Kleffner syndrome or epileptic encephalopathy with continuous spike and waves during sleep. The prognosis is reflected by the underlying cause rather than continuing seizures. Certain medications such as carbamazepine, tiagabine, baclofen, and some antibiotics such as cephalosporins have been associated with provocation of NCSE. Abrupt withdrawal of medications such as benzodiazepines, valproate, and lamotrigine can also cause NCSE.

 Obstructive Sleep Apnea (OSA)



OSA must be looked for in all children with cerebral palsy, especially in those with more severe cerebral palsy and those with epilepsy. [74]

 PROGNOSIS



To simplify a complicated process, a generalization is necessary. CP associated with a higher rate of epilepsy implies more gray matter involvement. Associated MR indicates still more gray matter destruction. The more the gray matter damaged, the worse is the outcome. The prognosis of childhood epilepsy is related to etiology and epilepsy syndrome; [75] in particular, drug resistance is associated with structural abnormality on brain imaging and onset of epilepsy earlier than 1 year of age. Children with cerebral palsy and epilepsy due to structural abnormality are, thus, at an increased risk of drug resistance and continuing seizures. Early onset (within the 1 st year) epileptic encephalopathies have the worst prognosis; the risk of developing epileptic encephalopathies is highest in a child with cerebral palsy and early-onset seizures. [76] A large proportion of children with cerebral palsy and epilepsy achieve good seizure control on their first or second AED, and most of the seizure-related morbidities depend on those who continue to have seizures. This latter group is estimated at 13-23% in children with epilepsy overall whereas it is 25-50% in children with epilepsy and cerebral palsy. [14] Among those with cerebral palsy, children with an underlying etiology of developmental anomalies or CNS infections are likely to have a poor prognosis [8] as are children with quadriplegia. [14]

Prognosis of epilepsy

The prognosis of epilepsy is not related to the type of CP. [6] The prognosis for epilepsy depends on many factors. Earlier age of onset, coexisting factors, epileptic encephalopathies, usage of AEDs with more side effects, and failure of treatment carry a poor prognosis. In general, the outcome of seizures in children with cerebral palsy is poor, requiring long course of AEDs, polytherapy with multiple AEDs because of higher incidence of refractory seizures and repeated hospital admissions for SE. [5],[14] Many children become seizure-free or have sustained remission of seizures after starting AEDs. [77] Total control of seizures was achieved in 65.2% of the patients with cerebral palsy and epilepsy; seizures may be worse in spastic hemiplegia with a postnatal etiology than in patients with prenatal or perinatal causes.

Neonatal seizures

Survivors of neonatal seizures face an exceptionally high risk for CP often with mental retardation and CP epilepsy. CP was identified in 37% and developmental delay in 34%, and 21% had epilepsy at 24 months of follow-up. [78] In children with neonatal seizures, the long-term disability and mortality are worse in premature newborns than in term newborns. However, the etiology of the seizures is the primary determinant of prognosis. [79]

Intelligence quotient (IQ)

Epilepsy can impose an additional handicap when it is refractory to treatment, or if anticonvulsant drug doses cause sedation that further impairs learning and socialization. Despite the prognosis of seizures, epilepsy is a major prognostic factor for the presence of mental retardation. Intellectual disability is more frequent in cerebral palsy children with seizures than in those without seizures, and severe intellectual disability is more probable in those with multiple types of seizure. [8],[80] A low IQ is frequent in most of the children with epilepsy and children with tetraplegia have significantly lower IQ than other groups. [8],[13],[80] The occurrence of epilepsy, mainly in children with hemiplegia and diplegia is associated with worse mental capacities. [81] In spastic cerebral palsy, the patients with epilepsy showed more severe intellectual disabilities. [6] Regardless of the prognosis of seizures, epilepsy was a major prognostic factor to the presence of mental retardation.

Cognitive deficits

They tend to be worse in children with seizures. This is because of more gray matter destruction.

Behavioral problems

They are common in children with cerebral palsy, and even more when epilepsy is present. [56]

Seizure response to antiepileptic drug

Factors associated with a seizure-free period of 1 year or more in epileptic children with cerebral palsy were normal intelligence, single seizure type, monotherapy, and spastic diplegia. Epilepsy is often severe and difficult to control particularly in children with mental retardation. [82] The presence of quadriparesis, mental retardation, and myoclonic seizures was predictive of poor response to AEDs. [83]

Motor function

The occurrence of epilepsy in children with cerebral palsy is associated with worse motor function. The occurrence of epilepsy in CP is associated with limitations in conscious motor functions. [81] Regardless of the prognosis of seizures, epilepsy was a major prognostic factor for the motor development of children with cerebral palsy.

Quality of life

Children with epilepsy do not perceive any important difference in quality of life compared to children with cerebral palsy or children in the general population. [84] Mothers of children with cerebral palsy and epilepsy have a poorer quality of life than mothers of children with cerebral palsy without epilepsy. [85]

Seizure recurrence risk

The risk of a relapse in persons with cerebral palsy is high. [5] 75.3% were seizure-free for >3 years and could discontinue therapy whereas 24.7% were still on AEDs. 13.4% relapsed after a 3-year seizure-free period on discontinuation of AEDs. Total control of seizures could be achieved in 65.2%. CP etiology may predict the outcome of epilepsy as children with cerebral palsy caused by CNS malformation, CNS infection, and gray matter damage all had a less chance of becoming seizure-free. [8] A history of previous neurologic insult (remote symptomatic) as in CP was associated with a 2.5-fold increased risk of recurrence. Treatment with anticonvulsant medication was not associated with a decrease in recurrence risks. AED discontinuation in patients with spastic hemiparesis is significantly more likely to lead to seizure relapse than in children of other cerebral palsy types, but no other factor is yet known to increase the chance of relapse.

 CAUSES OF DEATH



Standardized mortality ratios ranged from 7 to 50 in CP with epilepsy. [86] Deaths in epilepsy are related to seizures themselves or the underlying cause of epilepsy. Seizure-related deaths are due to status epilepticus, drowning (and other accidents) caused by seizures, and sudden unexplained death in epilepsy (SUDEP). [86] The mechanisms responsible for SUDEP may be cardiac or respiratory. Ictal bradycardia or ictal asystole occurs with temporal lobe epilepsy. Ictal apnea and hypoxia are common. [87] Prolonged, generalized EEG suppression (>80 s) probably due to profound postictal cerebral dysfunction quadruples the odds of SUDEP. [88] Patients with AED-resistant epilepsy are at high risk for SUDEP and have to be informed about this potential complication. Treatment-related deaths due to drug reactions are preventable by being vigilant.

 Information for Paramedical Staff/Teachers/Parents



Parents must be provided prognostic information in a "parent-friendly" language to facilitate their understanding and acceptance of information. [2],[89],[90] They must look out for (1) sudden change in the behavior, (2) sudden crying or running to the mother without a reason, (this may be an aura of a seizure), and (3) if video recording of the episode can be done using at least a mobile phone, epilepsy diagnosis and treatment would be much better.

CP with epilepsy requires a multi-dimensional approach. Epilepsy, because of the electrical disturbance, results in dysfunction of the brain with frequent episodes affecting the cognitive abilities, behavior, and attention. In addition, the crises are frequently an excuse for the child to stop going to school. Proper management of epilepsy minimizes or eliminates impairment of cognitive and executive functions (such as regulation and control of impulse, expect consequences, focus attention, control emotion, permit flexibility, plan, and monitor results). Executive functions are the last of the cognitive functions to mature, and they depend on an extensive interconnectivity of the prefrontal cortex with other parts of the brain. Damage to the prefrontal cortex results in sluggish information processing and a reduction in sustained attention performance.

There is a necessity to combine the active restoration of motor deficit with antiepileptic treatment. Epilepsy treatment leads frequently to stop the restoration process resulting in aggravation of patient's motor disability. [91]

 THE ADULT WITH CEREBRAL PALSY AND EPILEPSY



Epilepsy accounts for a high proportion of morbidity and mortality in adults with cerebral palsy. [92],[93] Adults with cerebral palsy are unlikely to present with new-onset epilepsy. However, those who persist with seizures into adulthood usually have refractory epilepsy with associated intellectual disability. Cerebral palsy with epilepsy and cognitive impairment was associated with failure to live independently as an adult. [94] This suggests that the continued involvement of a is essential. The range of services that are necessary for the care of adults with cerebral palsy and epilepsy is wide, and they should receive proper assessment, treatment, and services.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

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