Seizures occur more often in the neonatal period than at any other time of life; during this period, they most often occur within the first week of life. Reported incidence ranges from 1.5 to 5.5 per 1000 in newborns and may be even higher in premature infants. Most neonatal seizures (approximately 85%) are acute provoked seizures (previously called acute symptomatic seizures), occurring as a consequence of a specific identifiable etiology.

Importantly, neonatal seizures are not generalized but focal (either unifocal or multifocal).

Most neonatal seizures are electrographic-only, characterized by the presence of an electrographic seizure on EEG that has no overt clinical manifestations.

Electrographic-only seizures were previously termed "subclinical" or "silent" seizures. A preverbal infant cannot communicate sensory phenomena associated with seizures (e.g., a visual change associated with an occipital seizure or a sense of déjà vu due to a temporal lobe seizure), and unless the seizure originates in or migrates to the motor cortex, there will generally not be a clear abnormal movement. 

An infant with electroclinical seizures may have resolution of the clinical seizure with treatment but persistent electrographic-only seizures (electro-clinical uncoupling).

Focal clonic seizures can be differentiated from tremor or clonus by restraint of movement. Tremor or clonus can be stopped by restraint, though clonic seizure activity cannot, and muscle twitching can still be felt in the restrained limb.

Myoclonic seizures are distinguished from clonic seizures by the regular rate of repetition of clonic seizures, and the fact that myoclonic seizures are nonrepetitive and erratic.

neonates may experience normal physiologic myoclonus during active sleep (the precursor of REM sleep). Myoclonus may also occur during non-REM sleep and has been referred to as benign neonatal myoclonus.

Common causes of acute provoked seizure in neonates.

Treatment algorithm of neonatal seizures

Treatment algorithm of neonatal seizure unresponsive to anti-convulsants

باختصار، رگعه بفيتامين B6, نفسه pyridoxine.

وإذا ما فاد، رگعه بالمركب الفعال من B6, نفسه PLP.

وإذا ما فاد رگعه بـ folic acid analogue, اللي هو Leucovorin.

وإذا ما فاد رگعه بـ B7, نفسه الـ Biotin.

ليش هالموضوع مهم كلش؟
لأن مرات يجيك طفل مولود قبل ساعتين كلشي ما بيه بس فجأة يدخل بنوبة صرع ما تستجيب لأي دوة تنطيه. بس بمجرد ما تنطيه شي تافه مثل فيتامين B6 تلكاها توقفت والطفل رجع طبيعي، لأن عنده وحدة من عشرات الأمراض النادرة اللي نسميها inborn errors of metabolism

يكلك هواي أطفال مُصابين بأمراض الأيض الوراثية (inborn errors of metabolism) اللي هواي منها نكدر نعالجها بشي بسيط مثل حبوب فيتامين ونظام غذائي خاص، يتم تشخيصهم خطأً على أنهم يعانون من cerebral palsy وأمراض ثانية خطيرة مالها أي علاج... ببساطة لأن أمراض الأيض الوراثية نادرة وعادةً ما تخطر على بال الطبيب.

بهالمناسبة، على حد قول دكتور الأعصاب مالتنا، يكول إذا شفت عائلة بيها ثنين أطفال عدهم CP معناها التشخيص خطأ، لأن الـ CP مو وراثي ولما تشوف حالتين بنفس العائلة عدهم نفس المرض، فغالبًا هذا مرض وراثي مثل أمراض الأيض الوراثية وغيرها.

Asphyxia is defined as the marked impairment of gas exchange leading, if prolonged, to progressive hypoxemia, hypercapnia, and significant metabolic acidosis. 

Cyanocobalamin cannot cross the blood-brain barrier, while mythelcobalamin can. This is why you should use the latter (not the former) for neuropathy caused by B12-deficiency.

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ITP, TTP, HUS, & DIC as they present in investigations