Paroxysmal alteration in neurological

function (i.e., behavioral, motor, or

autonomic function).

A signal of neurological disease:

Most distinctive indicator ofneurological problem innewborn period

1.PathophysiologicaL.

2.Etiological.

3. Classification acc. to age of onset

4. Clinical.

1.Epileptic seizures: originates from corticalneurons and are associated withcorresponding EEG seizure activity.

2.Non-epileptic seizures: initiated in the sub-cortical area and are not usuallyassociated with EEG changes.

Common causes:1. Hypoxic ischemic encephalopathy: the most

common cause represent 25-40% ofneonatal seizures.

2. Focal ischemic injury:2nd most commoncause esp. in FT it’s cause still unclear.

3. Intracranial Hge:10% of causes of seizures itmay be subarachnoid, subdural,periventricular or intraventricular hge.

4.Transient metabolic disturbance:5% of seizures Hypoglycemia.(<40 mg/dl in 1st 24 hr and

<50 after 24 hr) Hypocalcemia. Hypo or hypernatremia. Pyridoxine dependence. Hypomagnesemia

5.CNS infection:5% of seizures Meningitis Sepsis TORCH

1.Inborn error of metabolism: Aminoacidopathies

Organic aciduria

Peroxisomal disorders

Disorder of glucose transport (GLUT-1 deficiency)

2.Congenital brain anomalies: Cerebral dysgenesis

Neurological disorders (Sterge –Weber syndrome

-tuberous sclerosis)

3.Epileptic syndromes

4.Maternal drug withdrawal: Herion, barbiturates, cocaine.

5.Kernictrus.

6.Drug toxicity.

7.CNS trauma.

8.Polythythemia.

9.Hydrocephalus

10.Folinic acid responsive seizures

Benign Familial Neonatal Convulsions (BFNC):

1. Occur in otherwise well infants on day 2 or 3of life, family history usually unreported

2. Seizures may be focal clonic or tonic usuallyasymmetrical ,resolve after variable periodwithin 6 months

3. Developmental outcome is normal, but 5-10% may have later non febrile convulsions

Benign Idiopathic Neonatal Seizures (BINS or Fifth-day fits):

Suddenly appear on day 4-6 of life

Often with frequent seizures leading to statusepilepticus

Seizures are initially focal clonic often withapnea .tonic seizures are not expected in thisdisorder

Seizures often cease within 2 weeks

The etiology is not known

Early myoclonic encephalopathy (EME):

Usually present in the first few days of life

Focal motor seizures and myoclonus, which may be subtle and erratic and usually affect the face and limbs. tonic convulsions appear late in this disease

Seizures are very refractory to ttt

EEG ccc by brust-supression pattern may be seen during sleep

It is often associated with underlying metabolic disorder

Development is severely affected and may infant die ,often within their first year

Early infantile epileptic encephalopathy (Ohtahara syndrome):

Usually associated with very refractoryepilepsy.

It is ccc by early onset of tonic spasms alongwith focal motor seizures. Myoclonus is rarein the early stages

EEG show a burst suppression pattern

Usually associated with structural lesions

Developmental prognosis is very poor

Accompanied by infantile spasms

In the first 24 hr

HIE

Sepsis\meningitis

Metabolic

Pyridoxine dep(min-3days)

Drug withdrawal.

Intracranial Hge.

local anesthetic intoxication

Intrauterine infection.

Cerebral trauma.

Cerebral infection.

Within 24-72 hr: Sepsis\meningitis. In PT :IVH In FT: infarction,

venous thrombosis. Metabolic problems

late onset. Cerebral dysgenesis. Inborn metabolic

errors. Maternal substance

abuse Subdural Hge

1. Subtle

2. Tonic

3. Clonic

4. Myoclonic

5. Autonomic

They are not clearly tonic ,clonic,or myoclonic

More common in PT than in FT

EEG changes in PT > FT

They consist of :

1.Tonic horizontal deviation of the eyes with orwithout jerking: eyelid blinking or fluttering

2.Sucking ,smacking or drooling

3.swimming,rowing or pedaling movement

4.Apneic spells: must be accompanied with

EEG changes to be differentiated from non-convulsive apneas (due to sepsis ,lung disease,or metabolic abnormality).

N.B. convulsive apnea is usually preceded oraccompanied by other subtle manifestations.

In PT apnea is less likely to be a manifestationof seizures

More common in FT>PT

Commonly associated with EEG changes

2 types:

Focal clonic: well localized ,rhythmic, biphasicwith a fast contraction and slow relaxationmovement involving the face and upper orlower extremities on one side of the body orthe neck or trunk on one side of the body,infants are usually not unconscious during orafter the seizures.

Multi focal: several body parts in a sequentialfashion(LT arm followed by RT leg jerking)

Occur 1ry in PT Focal seizures: sustained posturing of a limb,

asymmetric posturing of the trunk or neck ,orboth, this usually associated with EEGchanges

Generalized seizures: most commonly ,theseoccur with tonic extension of both upper andlower extremities (as in decerebrateposturing) but may occur with tonic flexion ofthe upper extremities (as in decorticateposturing. It is uncommon to see EEG seizuredisorder

Seen both in FT and PT

CCC by single or multiple synchronous jerks

Focal seizures: involves the flexor muscles ofUL and not commonly associated with EEGactivity

Multifocal: exhibit asynchronous twitching ofseveral parts of the body and are notcommonly associated with EEG activity

Generalized: present with bilateral jerks offlexion of UL and sometimes LL .they arecommonly associated with EEG activity

Such as apnea, often associated with tachycardia rather than bradycardia (particularly in term

1.Jitterness: Symmetrical rapid fine movements of the hands

and feet not jerky. Stimulus sensitive: it can be initiated by sudden

movement or noise. Contain movements with low amplitude & high

frequency No abnormal eye movements No autonomic changes Movements cease with passive flexion or when

grasped EEG is normal

2.Benign myoclonic activity: Benign isolated jerky non-repetitive

movements of an extremity or other part ofthe body occur mainly during sleep.

Family history:Positive family history of neonatal seizures isusually obtained in cases of metabolic errors andbenign familial neonatal convulsions. Maternal drug history :in cases of narcotic

withdrawal syndrome. Delivery:1. regarding maternal anesthesia2. the mode and nature of delivery3. the fetal intrapartum status4. the resuscitative measures used ,Apgar score5. Information regarding maternal infections

during pregnancy

1.A thorough general examination: Gestational age.

Vital signs: temp, BP, HR, RR. Presence of skin lesions. Presence of HSM.2.Neurological examination: Level of consciousness, AF level, HC Cranial nerves Motor functions Primary neonatal reflexes

Sensory functions

Eye exam :pupillary size, reaction to light,extraoccular movement, Fundus exam forretinal Hge, chorioretinitis.

Changes in muscle tone

3.Seizure pattern:

The site of onset

Spread

Nature

Duration

Level of consciousness.

Initial Work-Up

Blood gas and check blood glucose

Basic metabolic panel (serum glucose ,serum

electrolytes; sodium, potassium, calcium total and

ionized, magnesium, BUN, creatinine)

CBC with differential, (blood,urine,and CSF culture

and sensitivity), TORCH screen

LP

Coagulation studies

Urine drug screen

Studies for inborn error : ammonia ,lactate, AA in urine

Cranial ultrasound: detect perventricularand intraventricular Hge

Cranial CT: diagnose subarachnoid orsubdural Hge,congenital malformation andcerebral infarction

MRI: diagnose cerebral infarction

Routine EEG: normal in 1/3 of cases video EEG better

The first step in treatment is to identify andtreat the underlying cause

ABC to ensure oxygenation and ventilation andcorrect any metabolic acidosis and check RBS.

Hypoglycemia: (D10W) 2-4 ml/kg IV bolusfollowed by continuous IV infusion

If no hypoglycemia start Phenobarbital: 20 mg/kg IV loading dose

given slowly over 10-15 min consideradditional dose : 5-10 mg /kg IV to a max of40 mg / kg

Maintenance dose :3-5 mg/kg/day/12hr Side effects: sedation, respiratory depression

If baby still convulsing

Start phenytoin loading 15-20 mg/kg IV slowly over 10-15 min then

maintenance 4-8mg /kg /day /12-8hrs IV (up to 8 mg/kg/dose/8 to 12 hr after one week of age)

flush IV with saline before and after administration

It is highly unstable in any iv solution, and avoid using in central lines because of risk of precipitation

Side effects: cardiac arrhythmias, hypotension

If still convulsing:

Midazolam (dormicum): loading dose 0.15mg/kg IV over at least 5 min then 0.06-0.4mg/kg/hr infusion.

Side effects: respiratory depression ,respiratoryarrest, (severe hypotension and seizures ifgiven rapidly).

Diazepam(valium): 0.1- 0.3 mg/kg IV aninfusion rate of 0.3mg/kg/hr

Lorazepam:0.05-0.1 mg /kg /ds/8-12hr IV slow push

can be repeated 4-6 times over 24 hr

If the baby still convulsing

High dose phenobarbital (>30mg/kg to achieve serum level >60mic/ml)

Pentobarbital:10 mg/kg IV then 1mg/kg/hr

Thiopental:10mg/kg then 2-4mg/kg/hr

Midazolam: 0.2 mg/kg, then 0.1 to 0.4 mg/kg per hour

Clonazepam: 0.1 mg/kg

Lidocaine: 2 mg/kg, then 6 mg/kg per hour Paraldehde:200-400mg/kg IV over 2hrs in

D5 then 16mg/kg/hr

Newer drugs:

Oral carbamazepine(10mg/kg initially then followed by 15-20 mg/kg/day)

Valproic acid :10-25mg/kg, then 20mg/kg/day/8hr

Vigabatrin:50mg/kg/day/12hr up to 200mg/kg/day

Lamotrigin :12.5mg in 2doses

Toprimate:3mg/kg/day

Levetiracetam:10mg/kg/day/12hr

Hypocalcemia: Calcium gluconate 10%, 1- 2ml/kgIV bolus (slow) (dilute 1:1 D 5%)

Dose :100-200mg/kg of 10% IV over 1-3minutes, followed by maintenance(50 mg/kg/6h)

Hypomagnesemia: Magnesium sulfate 50%, 0.25ml/kg IV bolus (slow)

Dose : 25-250mg/kg/dose.

HIE: usually in 1st 6-8 hrs after birth1. Careful observation for seizures +supportive ttt2. Prophylactic phenobarbital within 6 hrs3. Fluid restriction to 60 ml/kg fup UOP and

electrolytes4. If seizures occurred ttt started

Pyridoxine(B6): 50-100mg IV with EEG monitoring seizures will subside within min then oral form is given as maintenance 50-100mg/day every 24 hr

TTT with folinic acid in refractory cases to anticonvulsants and pyridoxine start with 2.5mg /12hr for 24-48hr up to 8mg/kg/day

TTT of hypo or hypernatremia

TTT of infection: start with empiric broad spectrum anti- biotic till cultures results.

Increase fluids or partial exchange in TTT of polythycemia

Critical determinant factors:

Neonatal neurological examination

Cause of the neonatal seizures

EEG pattern

The major predictors:

1. Underlying etiology

2. EEG finding

3. Neurological exam finding

4. Neuroimaging finding

The best prognosis in:

1. Hypocalcaemia

2. Pyridoxine dependency

3. Subarachnoid hge

The worst prognosis:

1. Brain malformation

2. Severe IVH

3. Prolonged or persistant hypoglycemia

4. Hypoxia

Sequelae can include :

1. Chronic seizures

2. MR

3. CP