:Paroxysmal disorders Abrupt onset of a clinical episode

:Paroxysmal disorders Abrupt onset of a clinical episode that tends to be stereotyped and repetitive , lasts seconds or minutes (rarely hours ), .and ends abruptly :Definition of seizure transient and abruptly disturbance of cerebral function(impaired consciousness, abnormal motor activity, sensory disturbances or autonomic dysfunction) caused by excessive or over synchronized .cerebral neuronal discharges Differential diagnosis of Paroxysmal

:disorders Seizures Migraine TIA Syncope Breath holding spells Paroxysmal Vertigo hypoglycemia

Tics Pseudo seizures Night terrors Narcolepsy Paroxysmal torticollis Paroxysmal dystonia Seizures ocurr in 10% of children. Less than one third of seizures in .children are caused by epilepsy Epilepsy is the occurrence of two or more unprovoked seizures at an interval > 24 hours

Provokeing factors : fever ,infection, syncope, hypoxia, toxins, head trauma, stress,fatigue, cardiac arrhythmias Epileptic syndromes classification Age of onset Etiology Seizure type

Cognitive development Neurologic exam ,CT prognosis Janz syndrom West syndrom

Lennox-Gastaut syn. BPEC LKS Benign neonatal convulsion Clinical Seizure classification Partial (Only a portion of the brain) - Simple (Normal consciousness) - Complex (Impaired consciousness)

Generalized (Both hemispheres are involved) Type of Seizure Classification Partial (Focal Seizures) : 40-60 % of epilepsy of childhood Simple partial Simple with motor signs Simple with sensory signs Autonomic: abdominal epilepsy

Psychic :dj vu,fear, Complex partial : psychomotor seizures or temporal lobe epilepsy or limbic Classification Generalized Seizures Absence Seizures (Petit mal) Tonic/Clonic (Grand mal) Atonic Seizures (Drop attacks) Myoclonic Seizures Clonic tonic : Simple Partial seizures The most common form : motor activity

SPS arise from a anatomic specific focus. Location and direction of spread of the seizure focus determine clinical symptomology. Spread of partial seizure to the whole brain produced GTCS. (secondry generalization ). Only pshycic or autonomic symptoms can be difficult to diagnosis. SPS : 10 -20 sec Uncinate seizure : ( ( ( ( ) )

Gelastic seizure : spells of uncontrolled laugher hypothalamic tumors Versive seizure : lip smacking : anterior temporal lobe Macropsia , Micropsia, vertigo: posterior temporal lobe Autonomic :fever ,tachycardia ,shivering and increased GI motility Limbic seizure :dream like state and bizarre psychic abnormalities

CPS Aura:in one third (epigastric discomfort, vague unpleasant feeling , fear) Automatisms: in 50-75 % in infant :alimentary , in child:behavioral EEG: Spike or sharp in anterior temporal Neuroimaging: abnormal in 50-80% tumor, AVM, MTS, cortical dysplasia,focal atrophy, gliosis, infarction There may be a brief blank stare or a sudden cessation or pause in activity. Goals of epilepsy treatment Indication for start of AEDs

Control of seizures Minimal adverse events Good patient compliance AEDs suppress but do not cure seizures 80% of patients have control of seizures 60% seizure free, 20% drastically reducing with treatment Main aim is monotherapy Significant improvement in only 10 % of patients with second drug : Choosing AEDs Seizure type & Epileptic syndrome Pharmacokinetic profile Medical history , interactions/potential for future

problems Efficacy Expected adverse effects Cost Start at low dosage , gradually increase until seizure control or side effect threshold Never abruptly stop medications Principles of antiepileptic drugs Pharmacokinetics : What thetreatment body does to drug ( absorption , distribution, metabolism, elimination ) Pharmacodynamics : What the drug does to body ( study of biochemical and physiologic effects of drug) Toxicology

When a total daily dose is increased , sufficient time (about 5 t 1/2) should be allowed for the serum drug level to reach a new steady-state level Withdrawal may be considered after seizure- free period of 2-3 or more years. Relapse rate after withdrawn AEDS : 20 -40 % Treatment of generalized Seizures GTCS: First choice : valproate Second : CBZ , PHT , TPM , LMC , Pb CLZ , PRM , Zonisamide

Absence : First choice :Valproate , ethoxysuximide , LMC Second choice : TPM, Levetiracetam , Zoni Myoclonic : First : Valproate Second : LMC , CLZ, Levetiracetam , Zoni Carbamazepine may exacerbate absence and myoclonic seizures Partial Onset Seizures First-line drugs are carbamazepine and phenytoin. PHT rarely used as first-line agent in children because of toxicity. Carbamazepine : an acceptable first drug Gabapentine is another option

Adjunctive (add-on) therapy : oxacarbamazepine , LMC, TPM, VPA , Pb, PRM , felbamate, levetiracetam , tiagabine, zonisamide WHO recommends Pb as choice treatment of partial & TCG seizures in countries with restricted resources . Treatment of partial seizure Carbamazepine : drowsiness, dizziness, diplopia ,SIADH (hyponatremia ) ,aplastic anemia , agranulocytosis Phenytoin : gingival hyperplasia , hirsutism ,rickets , SLE, ataxia, coarse face, nystagmus, psudolymphoma, Stevens Johnson syndrome

Benign focal epilepsy or rolandic epilepsy or : BPEC Age of onset : 5-10 years 16% of all afebrile seizure in <15 years 50-75 % occur during sleep(20 % only one seizure) Somatosensory aura around the face and mouth and then focal motor (face and then ipsilateral exterimity ) ,and finialy secondry generalized. Good prognosis and normal CT,IQ,N.E EEG :spike in centrotemporal Treat: CBZ in frequent seizures for 2 yr

Landau-Kleffner syndrome or :Acquired Epileptic Aphasia Onset age :early childhood (4-7 yr) Cortical auditory deficit and language disability Seizure in 80% (partial and generalized) EEG :highly epileptiform during sleep CT or MRI :normal Prognosis :not good Treat :Nav, clobazam, steroid ,IVIG Rasmussen encephalitis: chronic , progressive focal inflammation of the brain of unknown origin

Usual age of onset :6-10 yr Nonspevific viral disease focal persistent motor activity (epilepsia partialis continiua ) hemiplegia and cognitive deterioriation. EEG:focal spike and slow wave activity Imaging :initially normal and then show atrophy in the involved area Prognosis :progressive and lethal Hemispherectomy for seizure eradication and prevention of cognitive deterioration but with permanent hemiparesis Absence seizures

In 6-20% of epileptic children No aura, no postictal,no loss of tone Age: 4-6 yr NE & imaging :normal A brief loss of enviroment awareness and starig or eye fluttering or simple automatism such as head bobbing &lip smacking EEG: 3cps spike and wave

Seizures provoked by HV & flashing light 40-50% have generalized seizures(60%before absence & 40% after the onset of absence. Treatment : Ethosuximide ,valproate clonazepam as alternative Differentiating of absence from CPS 1.The automatism of CPS are more

complicated (repetitive swallowing, picking of the hands or walking in nonpurposeful circles 2.postictal confusion in CPS 3. Absence provoked by hyperventilation 4.CPS last few minutes ,absence :few sec 5.absence :dozens per day but patients with CPS rarely have more than one or two seizures in day EEG Often referred as behavior problem, Poor school marks; disruptive behavior :Side effects of drugs

Valproate :pancreatitis, drowsiness, tremor , alopecia, weight gain, fatal liver failure (Reye-like syndrome ) in <2yr Ethosuximide : nausea ,lethargy, hiccups ,SLE, Stevens Johnson syndrome ; blood dyscrasia Clonazepam :ataxia, lethargy, blood dyscrasia ,depression, salivation Myoclonus:a lightning-like jerk of part of the body Epileptic: EEG shows epileptiform discharges during the jerk. Nonepileptic :may originate in the B.G ,BS, or spinal cord.

Benign: sleep myoclonus Serious pathology Underlying illness produce myoclonic epilepsy: - developmental or static progressive Juvenile myoclonic epilepsy or Janz : syndrom Onset age : 12-16 yr (adolesenct ) AD ( chromosome 6) Myoclonus in the morning with or without generalized clonic and absence seizure .

N.E is normal. EEG : 4-6 / SWD Treat : valproic acid for lifelong :Infantile spasms or west syndrome

Age : 3-8 month , 86 % onset of seizures : < 1yr Forms : mix , flexor , extensor spasms occur in drowsiness state. Repeated clusters occur each day. EEG : hypsarrhythmia ( HVSW, spikes, polyspike and disorganized background) Poor prognosis Classification : cryptogenic (40% ) symptomatic :TS is the most common 40 % of cryptogenic have a good intellectual. Very Poor intellectual prognosis in symptomatic Treat : ACTH , cortone ( irritability , swelling ,hypertension , glycosuria, severe infection ) benzodiazepines , valproate

Etiologies of infantile spasms Methabolic : PKU, Congenital infections : MSUD, biotinidase toxo, CMV, syphilis deficiency ,NKH, hypoglycemia , B6 dependency, lipidosis, Encephalopathies: postasphyxia CNS dysgenesia : posttraumatic polymicrogyria, posthemorragic lissencephaly, Down

postinfections syndrome, postimmunization Neurocutaneous : )pertusis ( tuberous scerosis,. Etiology of seizures Perinatal conditions : CNS malformation, hemorrhage, HIE, congenital infection, trauma

Metabolic conditions: hypoglycemia,hypocalcemia,B6 deficiency hypomagnesemia, hypo or hypernatremia , storage disease, degenerative , Reye syndrome Poisoning : lead , cocaine, cyanide , co, pesticide, strychnine drugs : Etiology of seizures Neurocutaneous

syndromes : Tuberous sclerosis , NF, Systemic disorders : vasculitis ( CNS or systemic ) SLE hypertensive encephalopathy renal failure hepatic encephalopathy Infection: Other : trauma , tumor, idiopathic , familial Over-the-counter drugs, illicit substances herbal preparations, can precipitate seizure

Laboratory evaluation of seizures CBC Glucose, ca,mg,p Na,K,Bun,Cr Toxicology CSF EEG Imaging metabolic Neuroimaging : Neonatal seizure Focal seizure

focal EEG Focal neurologic finding Neurodevelopmental delay Dysmorphic face Breath holding spells In 5 % of children, rare in <6mo and >5-8 yr, 80% <18mo all in <3yr, Cyanotic BHS :crying,prolonged expiratory apnea,cyanosis,UWG,tonic-clonic movement treat: reassurance, piracetam, ferrous Pallid BHS: painful stimuli,asystole, pallor, bradycardia, opisthotonos ,seizure treat: atropine , less benign than cyanotic

:Fever and seizure 1. CNS infection 2. Epilepsy triggered by fever 3. Febrile seizure F.C occur in 2- 4 % of children. AD (choromosome 19 & 8) 50 % in 1-2 yr , 93% in < 3 yr URI, roseola, AOM are the most common causes of F.C. Recurrent F.C : first FC in <1yr 50 % first FC in >1yr 28 %

10 % of children have 3 or more recurrence Febrile Seizures Fever of over 38.5C (even 37.8) Age range of 6 mo to 7 yr No infection of the CNS or electrolyte abnormality No previous non-febrile seizure or neonatal seizure Simple:

Generalized Less than 15 minutes One in 24h Complex: Focal Over 15 minutes More than one in 24h Focal neurologic sign in postictal state Risk factors of recurrence of FC Positive family history of FC prophylaxis of recurrent FC in < 1 yr FC:

Oral diazepam at the Seizure with T< 40 degree onset of each febrile illness Seizure with Prolong anticonvulsant : fever <1 hour pb or Nav Complex FC Risk of epilepsy in FC Abnormal neurologic examination or development Positive family history of epilepsy

Complex FC FC in < 1 yr Recurrent FC Seizure with T< 40 degree prophylaxis : Prolong anticonvulsant : pb or Nav Meningitis AND FC LP .1 .2 .3

.4 . .1 48 .2 .3 .4

Routine laboratory testing in epileptic patients Routine laboratory testing is not cost effective or necessary with the exception of felbamate, which is associated with a relatively high risk of aplastic anemia and requires close laboratory monitoring. Vomiting (symptom of hepatotoxicity or pancreatitis), prolonged unexplained fever, easy bruising, extreme fatigue or lethargy, flu-like symptoms, worsening of seizures, change in mental status, and abdominal pain should lead to further investigations Many idiosyncratic reactions of AEDs (Stevens- Johnson syndrome, TEN, serum sickness , pancreatitis) are not predicted by presymptomatic blood test abnormalities Patients taking AEDs should be monitored for emergence or worsening of suicidal ideation or depression.

Adverse effects of new AEDs AED Serious Adverse Events Nonserious Adverse Events Gabapentin None Weight gain, peripheral edema,

behavioral changes* Lamotrigine Rash, including Stevens Tics* and insomnia Johnson and toxic epidermal necrolysis (increased risk for children, also more common with concomitant valproate use and reduced with slow titration); hypersensitivity reactions, including risk of hepatic and renal failure, DIC, and arthritis

AED Serious Adverse Events Nonserious Adverse Events Levetiracetam None Irritability behavior change

Oxcarbazepine Hyponatremia (more common in elderly), rash None Tiagabine Stupor or spike wave stupor Weakness Topiramate

Nephrolithiasis, open angle glaucoma, hypohidrosis (predominantly children) Metabolic acidosis, weight loss, language dysfunction Zonisamide Rash, renal calculi, hypohidrosis (predominantly children)

Irritability, photosensitivity, weight loss Status epilepticus Definition :as a seizure that lasts for 30 minutes or longer or is repeated frequently so as consciousness not regained between seizures Seizure lasting more than five minutes has a high risk of lasting 30 minutes and treatment delay is associated with delayed treatment response. In 1.3 to 16% of epileptic patients. Mortality: 2.7 - 20 percent

SE occurs in 1.3 to 16% of epileptic patients Mortality: 2.7 - 20 percent Incidence rates, causes, and prognosis vary substantially by age Most in the first year of life Febrile SE is the most common etiology 60 % of children are neurologically healthy .prior to the first episode of SE

. What the common complications of status epilepticus ? Reduction of CPP Hyper/hypotension Dysrhythmeia, CHF, Apnea, Aspiration Non cardiogenic pulmonary edema, Rhabdomyolysis, Hypo/hyperglycemia Status epilepticus classification Clinical

Simple partial Complex partial Generalized convulsive Generalized non-convulsive Etiologic Symptomatic ( acute or remote) Idiopathic Reactive : Prolong FC Subtypes of status epilepticus Symptomatic :

- acute brain injury : ( 25 % of children ) CNS infections , electrolyte disorder, acute anoxia - congenital malformation or previous brain injury ( in 10 % of children ) -other : hypoglycemia , hypocalcemia, poisoning,Reye ,lead, frontal tumor, Prolonged FC: most common cause in <3yr Idiopathic : sudden cessation of AED : Pathophysiology excessive excitatory neurotransmitters : glutamate , aspartate , acetylcholine

Ineffectiveness of inhibition : GABA Neuronal loss with every episode, particularly if prolonged :Complication

Hypoxemia and acidosis Hyperglycemia & hypoglycemia Hyper tension & hypotension IICP and cerebral herniation Hyperpyrexia Hyperkalemia Myoglobinuria Non cardiogenic pulmonary edema Leukocytosis(60%) CSF pleocytosis(13%)

Risk Factors Partial seizures with clustering Focal background EEG abnormalities Secondary generalized Partial seizures Generalized abnormalities on neuroimaging Younger age of epilepsy (1 year or less) at onset Symptomatic etiology of epilepsy Occurrence of SE as the first seizure Management

Assess respiratory & circulatory status & maintenance of an adequate airway and o2 therapy , cardiac & BP monitoring, pulse oximetry A rapid history & neurologic exam: to determine classification & etiology Establishment of IV line and obtain blood samples : CBC, glucose , Ca ,P , Mg , Cr, ABG, LFT, Na, K . Toxic and metabolic screens ,AED level, blood culture,in some patients Correction of metabolic abnormalities: hypoglycemia Management

Neuroimaging: after stabilization of patient , especially in a patient with focal neurologic signs EEG for background activity evaluation : as soon as possible after the seizure stops, ideally in 1-2 hour If the patient has not regained a relatively normal mental state within a few hours after SE has stopped, an EEG should be performed to evaluate the possibility of subclinical seizures. :Drugs Oral or IM medication (Pb, Pht, VPA , OXCBZ , Levetiracetam) : in partial seizures or brief generalized motor seizures have

stopped before the child arrives in the emergency department, which are short in duration, or the child is conscious despite multiple seizures. If IV access is delayed or impossible, many AEDs can be given by alternative routes : interosseous , IM, rectal , intranasal Missed medication Paradoxical effects Nonprescription medications : over-the-counter drugs , illicit substances, herbal preparations Some AEDs commonly used to treat SE may . worsen seizures caused by illicit drugs In SE is induced by cocaine, other local anesthetics,

theophyliine , lindane treatment with benzodiazepines is recommended ( not phenytoin ) Benzodiazepines: :Drugs Diazepam : 0.3mg/kg, 2mg/min, Max :10mg duration of anticonvulsant effect <20 minutes first choice in outside of emergency department is not considered first-line therapy for SE(less efficacy and more respiratory depression) Lorazepam : Effective duration of action : 4-6 hours

IV-rectal , 0.5 - 2 mg/min , Max: 4mg <12 yr : 0.1 mg/kg >12yr : 0.05 mg/kg Midazolam : IV, IM, rectal , nasal ,oral 0.15-0.2mg/kg Antiepileptic Drugs Phenytoin: IV,15-30 mg/kg each time 10mg/kg , 1mg/kg/min or Fosphenytoin (IV-IM,15-20 mg/kg , 3mg/kg/min) with monitoring of HR and BP and avoiding of venous extravasations Side effects :

hypotension ,arrhythmias, local pain and injury, venous thrombosis and purple glove syndrome (edema, discoloration ,and pain in distal extremity to the site of infusion) Phenobarbital : IV-IM-SC, 15-20mg/kg , 2mg/kg/min Side effects : sedation, respiratory depression IV Lidocaine: (1 - 2 mg/kg ,once or twice) is one of the second-line drugs in SE treatment with favorable properties of prompt responses, less alteration of consciousness and respiratory depression

Valproic acid : 20-40 mg/kg IV(diluted 1:1 with normal saline or DW 5% ) over 5 to 10 minutes can be used as a second or third-line treatment. Refractory status epilepticus is defined as ongoing seizures despite the use of two first-line drugs, usually a benzodiazepine plus either phenytoin or phenobarbital, or which continues for > 60-90 minutes in spite of adequate treatment Admit in P-ICU treatment of cerebral edema

Drugs in

refractory SE Pentobarbital : 5-15 mg/kg stat , and 0.5-5 mg/kg/h in stable hemodynamic Side effects: hypotension , pulmonary edema, ileus, delayed neurologic recovery Midazolam:0/15-0/2mg/kg stat, 1-5 g/ kg /min Propofol:1-3mg/kg stat, 2-10mg/kg/h , should not be used in children on the ketogenic diet Adverse effects: bradycardia , apnea, hypotension , hypertriglyceridemia , acidosis , rhabdomyolysis IV valproic acid : 15-20mg/kg in 1-5 min, 5mg/kg/h lidocaine drip

Paraldehyde General anesthesia Topiramate Neonatal seizures 1.subtle :the most common forms apnea, eye deviation ,tongue thrusting, eye blinking,staring,bicycling,fluctuation of vital sign, sialorrhea,pedaling movements 2.Focal or generalized tonic :sustained posturing of limbs or trunk 3.focal or multifocal clonic: repetitive,rhythmic contraction of muscles of limbs,face, or trunk 4. Focal or generalized myoclonic: arrhythmic contraction of muscles of limbs,

face, or trunk Etiology of neonatal seizures HIE :the most common cause in full term, occur 12- 24 hours after birth asphyxia Hypoglycemia Hypocalcemia Hypomagnesemia Hypo or hypernatremia Congenital brain malformation IVH :between 1 and 3 days of age in preterm

Vit B6 dependency Injection of local anesthetic agents into fetal scalp (transient bradycardia,fixed mydriasis) in lab. room Sepsis:after 5 days Drug withdrawal IEM :lethargy,acidosis, FH of infant death SAH: sudden onset on days1-3,short duration ,do not recur

Benign idiopathic neonatal seizure or fifth day fits In 5 % of fullterm neonate Seizure in 4- 6 days Multifocal clonic seizure Duration of seizures : 24 hours Prognosis : good Mental development : normal

Benign familial neonatal seizure AD , choromosom 20 Generalized clonic seizures occurring toward the end of first week of life (2-3 ) 10- 20 times in a day Outlook : favorable Seizures stop in 6 months of age. Response to treat is variable. Differentiate of seizure from :jitteriness or tremulousness Jit are sensory dependent, elicited by stimuli,interrupted by holding the limb Jit is fine &rapid, seizure is coarse,fast and

slow clonic activity Abnormal eye movement in seizure Autonomic abnormality ( increased in BP or PR ) in seizure Jit ocurr in crying or examining jit : IDM, after asphyxia,infants with narcotic withdrawal Treatment of neonatal seizure Treat of specific cause: Hypoglycemia Hypocalcemia, Hypomagnesemia, hypo or hypernatremia and B6 deficiency In the absence of an indentifiable cause ,pb 20 40 mg/Kg and then dilantin 10 -20 mg/Kg od diazepam 0.1- 0.2 mg/Kg followed by one of the

two longer- acting drugs Prognosis : dependent to underlying cause Imitators of epilepsy : Nonepileptic paroxysmal disorders Paroxysmal disorders Abrupt onset of a clinical episode that tends to be stereotyped and repetitive , lasts seconds or minutes (rarely hours) , and ends abruptly 25 % of patients referred to epilepsy clinic don't have epilepsy & recognition is important:

to avoid unnecessary treatment to institute the correct treatment when required ... ... ...

Nonepileptic paroxysmal events Neonate : Infants : Apnea

Syncope (BHS ,) Benign myoclonus of infancy Shuddering attacks Sandifer syndrome Paroxysmal torticollis of infancy Extrapyamidal drug reaction Benign paroxysmal vertigo Spasmus nutans Opsoclonus-myoclonus Masturbation Jitteriness Sleep myoclonus Hyperkplexia

Nonepileptic paroxysmal events Children Adolescents and young adults BHS Vasovagal syncope Migraine Vasovagal syncope Migraine Daydreaming

Tic disorders Sleep disorders Paroxysmal dyskinesia Tic disorders Hemifacial spasm Stiff person syndrome Pseudoseizures Episodic rage Staring spells Sleep disorders BPV Masturbation Movement disorder

In neonate Apneic seizure : if is accompanied by abnormal eye movement, mouth movement , in BP or HR Jitteriness : elicited by stimuli, interrupted by holding the limb Jit is fine &rapid, seizure is coarse, fast and slow clonic activity Abnormal eye movement in seizure Autonomic abnormality in seizure Jit occur in crying or examining Severe jitteriness : IDM, HIE, narcotic withdrawal, hypocalcemia, hypoglycemia Benign neonatal sleep myoclonus

Bilateral, symmetric myoclonic jerks of the arms and/or legs, during non-REM sleep in the first few weeks of life and resolve by 2-3months Absence of autonomic disturbances EEG , neurologic exam & development : normal Sleep myoclonus will cease when the baby is aroused Neonates with severe cerebral dysfunction can also have myoclonic jerks, but these typically occur with a stimulus, or upon wakening or falling asleep Syncope An abrupt loss of consciousness due to sudden in cerebral perfusion ( brief tonic contraction in muscles of

face , trunk, extremities in 50 % or UWG ) Causes : vasovagal (painful procedures, blood drawing warm setting),cardiac arrhythmia, HV & panic attack , Reflex syncope (micturition or cough, carotid sinus hypersensitivity) Predisposing situation , accompanying pallor, nausa , perspiration , prodromal lightheadedness and visual changes, lack of postictal state , short duration EEG : transient slowing in attack , CPK in seizure Tilt table testing can provoke vasovagal syncope Breath-holding spells In 5 % of children, rare in <6mo and >5-8 yr 80% <18mo , all in <3yr

Iron deficiency is more prevalent in BHS A positive FH is present in 20-35% An autosomal dominant trait in some families The two clinical types of BHS: Cyanotic Pallid Family members and individual children can demonstrate both types, usually one predominates Cyanotic BHS Crying, prolonged expiratory apnea, cyanosis, UWG, followed by limpness and loss of consciousness Decorticate or decerebrate posture in prolong BHS A few children have generalized tonic or clonic seizures

prolonged postictal unconsciousness 15 -25 % have multiple episodes daily ,most children hav one to six spells per week Treat : reassurance Ferrous sulphate :5-6 mg/kg/ day Piracetam, a GABA-derivative Pallid BHS It is less common than the cyanotic variety The event is caused by cardiac bradycardia Occur after a minor fall or blow to the head or upper body, then child stops breathing and becomes pale, diaphoretic, and limp May followed by opisthotonos, incontinence & low

amplitude clonus , confusion or sleepy for several minutes afterward. Treat: in severe attacks with prolonged, severe bradycardia or asystole, atropine and cardiac pacing Benign myoclonus of infancy Known as benign nonepileptic infantile spasms Clusters of spasms at mealtime at 3-8 months Clusters increase in intensity and severity over weeks or months and then remit spontaneously at two to three years of age EEG, neurologic exam , development : normal An anticonvulsant is not indicated Without subsequent epilepsy

Masturbation In girls ( 2 mo 3 yr ) , in boredom or stress Episodes of tonic posturing with copulatory movements without manual stimulation of genitalia Suddenly flushed & perspires , may grunt & breathe irregularly without loss of consciousness Persists for a few minutes ( rarely hours ) Search for evidence of sexual abuse or abnormality of perineum Subside by 3 yr of age No specific therapy is required

Sandifer syndrome Intermittent paroxysmal spells of generalized stiffening & opisthotonic posturing with feedings (within 30 minutes following a meal) in infants due to gastroesophageal reflux These spells may be associated with apnea,

staring, and minimal jerking of the extremities Can be seen in normal children or children with hypotonia and tracheomalacia Treatment of GER reduces the frequency and severity of attacks. Benign paroxysmal torticollis in infancy Periodically, head tilts to one side, with the face rotated toward the opposite side with pallor , agitation & vomiting , begin and end suddenly, with a duration between a few hours and a few days. The child is alert and responsive during an attack. Episodes usually first occur in the first 3 months of life and resolving by the age of 3 years

EEG, neurologic exam , development : normal, A FH of migraines is common , may develop migraine later in life Benign paroxysmal vertigo (BPV) In toddlers ,sudden attacks of ataxia, nystagmus, diaphoresis, nausea, and vomiting , without altered consciousness, the child appears frightened and pale Episodes : <1minute,clusters: daily for several days then remitting for several weeks & recurring again Usually resolves by 3-5yr, may develop migraine several years later BPV remains a diagnosis of exclusion. Treat in clusters of attacks :

Diphenhydramine 5mg/kg/day PO, IM ,IV, rectal Shuddering attacks Brief episodes a rapid tremor of the head, shoulder, and trunk as "shiver" from a chill in 4-6 mo Episodes last a few seconds, can occur multiple times a day (100 times ) and occur with feeding ,or when child is excited or distressed They never occur during sleep and virtually never when being held and cuddled EEG ,Neurologic exam , development: normal FH of benign essential tremor exists

The spells spontaneously resolve by the second decade without treatment Nonepileptic staring spells or pseudoabsences In MR, ADHD, autism & in normal children Spells in boredom or inactive (watching TV or sitting in a class) Staring interrupted by tactile or vocal stimulation (bu usually not hand-waving ) HV in young children :blow out imaginary candles In HV , Video-EEG show generalized HVSW in the healthy child, but no epileptiform activity. An inexperienced electroencephalographer may

confuse this striking slow activity, "build-up" with the paroxysmal activity of an absence seizure. Dystonia An abnormal posture due to sustained contraction of both the agonist and antagonist muscle groups A dystonic posture may be generalized or focal: examples include opisthotonic posturing, torticollis, oculogyric crisis , facial spasm A common etiology of dystonia in infants is an acute reaction to drugs such as : metoclopramide ,phenothiazines , haloperidol In infants : generalized

In children: face and trunk

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