Membership of the Royal College of Paediatrics and Child Health (MRCPCH) Neurology, Development, Behaviour and Mental Health Syllabus

Neurology, Development, Behaviour and Mental Health syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Neurology, Development, Behaviour and Mental Health in Membership of the Royal College of Paediatrics and Child Health (MRCPCH), not a summary of it.

1. 1

   Neurology

   6 topics

   • Epilepsy and seizure classification
     • Seizure types and syndromes
     • Antiepileptic drug selection
   • Headache and raised intracranial pressure
   • Neuromuscular disorders
     • Duchenne muscular dystrophy
     • Spinal muscular atrophy
   • Cerebral palsy and movement disorders
   • Neurocutaneous syndromes
   • Acute encephalopathy and stroke
2. 2

   Child Development and Disability

   5 topics

   • Normal developmental milestones
     • Gross motor, fine motor, speech and social domains
     • Red flags and developmental delay
   • Global developmental delay and learning disability
   • Hearing and vision assessment
   • Coordination and motor difficulties
   • Multidisciplinary and transition care
3. 3

   Neurodevelopmental and Behavioural Disorders

   5 topics

   • Autism spectrum disorder
     • Recognition and diagnostic pathway
   • Attention deficit hyperactivity disorder
   • Tic disorders
   • Sleep problems and behavioural management
   • Feeding and toileting difficulties
4. 4

   Child and Adolescent Mental Health

   5 topics

   • Anxiety and mood disorders
   • Self-harm and suicidal behaviour
   • Eating disorders
     • Anorexia, bulimia and medical complications
   • Somatic symptom and functional disorders
   • Adolescent health and risk-taking behaviour

Neurology, Development, Behaviour and Mental Health flashcards for Membership of the Royal College of Paediatrics and Child Health (MRCPCH)

18 of 51 cards from the Neurology, Development, Behaviour and Mental Health deck — real questions with worked answers.

1. What is the definition of epilepsy (operational/clinical)?

   A disorder of the brain characterised by an enduring predisposition to generate epileptic seizures. Operationally diagnosed after $\geq 2$ unprovoked seizures more than 24 hours apart, OR one unprovoked seizure with a recurrence risk $\geq 60\%$, OR diagnosis of an epilepsy syndrome.

2. In the ILAE classification, what are the two main categories of seizure onset and their key features?

   Focal onset (originates in one hemisphere; subdivided into aware vs impaired awareness, motor vs non-motor) and generalised onset (engages both hemispheres from the start; includes tonic-clonic, absence, myoclonic, tonic, atonic). A third category is unknown onset.

3. What are the typical EEG and clinical features of childhood absence epilepsy?

   Onset 4-10 years; brief (5-10 s) episodes of staring and impaired awareness with no aura or post-ictal phase, often provoked by hyperventilation. EEG shows generalised 3 Hz spike-and-wave discharges. First-line treatment is ethosuximide or sodium valproate.

4. What defines a febrile seizure, and what distinguishes a complex from a simple febrile seizure?

   A seizure with fever (usually $>38^{\circ}\mathrm{C}$) in a child aged 6 months to 6 years without CNS infection or metabolic cause. Simple: generalised, lasts $<15$ min, no recurrence within 24 h. Complex: focal, prolonged ($>15$ min), or recurs within 24 h.

5. What is the definition of status epilepticus and the immediate first-line drug treatment?

   A seizure lasting $\geq 5$ minutes, or recurrent seizures without recovery of consciousness between them. First-line treatment is a benzodiazepine (e.g. IV lorazepam, or buccal midazolam/rectal diazepam if no IV access), repeated once after 5-10 min if no response.

6. What are the clinical and EEG features of infantile spasms (West syndrome)?

   Onset typically 3-12 months; clusters of brief flexion/extension (salaam) spasms, developmental regression. EEG shows hypsarrhythmia (chaotic high-amplitude slow waves with multifocal spikes). Treatment: vigabatrin and/or high-dose steroids (ACTH/prednisolone). Vigabatrin is first-line in tuberous sclerosis.

7. What is the typical presentation of benign rolandic epilepsy (self-limited epilepsy with centrotemporal spikes)?

   Onset 3-10 years; nocturnal focal seizures with unilateral facial/oropharyngeal twitching, drooling, speech arrest, preserved awareness, sometimes secondary generalisation. EEG shows centrotemporal spikes. Usually remits by adolescence; often no treatment needed.

8. List red-flag features of headache suggesting raised intracranial pressure in a child.

   Headache worse on lying down/waking, worse with cough/straining/Valsalva, associated vomiting, visual disturbance, papilloedema, new focal neurology, change in personality/behaviour, increasing head circumference (infants), and morning symptoms. These warrant urgent neuroimaging.

9. What is the Cushing's triad and what does it indicate?

   Hypertension (widening pulse pressure), bradycardia, and irregular/abnormal respiration. It is a late sign of dangerously raised intracranial pressure and impending brain herniation, requiring emergency intervention.

10. What is idiopathic intracranial hypertension (IIH) and how is it diagnosed and managed?

    Raised ICP without a mass lesion or hydrocephalus, with normal CSF composition. Presents with headache, papilloedema, visual obscurations, and possibly 6th nerve palsy. Diagnosed by raised CSF opening pressure with normal imaging. Managed with acetazolamide, weight loss, and treatment to protect vision.

11. What is the inheritance pattern and underlying defect in Duchenne muscular dystrophy?

    X-linked recessive; caused by mutations (often deletions) in the dystrophin gene leading to absent dystrophin. Boys present age 3-5 with proximal weakness, Gower's sign, calf pseudohypertrophy, and markedly raised creatine kinase. Confirmed by genetic testing/muscle biopsy.

12. What is Gower's sign and what does it indicate?

    A child uses their hands to 'walk up' their own legs to rise from the floor, indicating proximal (pelvic girdle) muscle weakness. It is classically seen in Duchenne muscular dystrophy and other myopathies.

13. What is the genetic basis and classification of spinal muscular atrophy (SMA)?

    Autosomal recessive degeneration of anterior horn cells due to SMN1 gene mutation. Type 1 (Werdnig-Hoffmann): onset $<6$ months, never sits, severe hypotonia, poor prognosis. Type 2: sits but never walks. Type 3 (Kugelberg-Welander): walks then weakens. Treatable with nusinersen/gene therapy.

14. How is cerebral palsy defined?

    A group of permanent, non-progressive disorders of movement and posture causing activity limitation, attributed to a non-progressive disturbance in the developing fetal or infant brain. Although the lesion is static, clinical manifestations may change as the child grows.

15. Describe the main motor subtypes of cerebral palsy.

    Spastic (most common, ~70-80%; further classified as hemiplegia, diplegia, or quadriplegia), dyskinetic (dystonic/choreoathetoid, often from kernicterus or asphyxia), ataxic (cerebellar, with hypotonia and incoordination), and mixed.

16. What classification system grades gross motor function in cerebral palsy?

    The Gross Motor Function Classification System (GMFCS), levels I-V. Level I = walks without limitations; Level V = transported in a wheelchair with severe limitations in head/trunk control. It predicts mobility outcomes and guides management.

17. What are the diagnostic features of tuberous sclerosis?

    Autosomal dominant (TSC1/TSC2 genes). Skin: ash-leaf macules (Wood's lamp), shagreen patches, facial angiofibromas, periungual fibromas. CNS: cortical tubers, subependymal nodules, SEGA, infantile spasms. Plus cardiac rhabdomyomas and renal angiomyolipomas.

18. Compare neurofibromatosis type 1 and type 2.

    NF1 (chromosome 17, neurofibromin): $\geq 6$ café-au-lait macules, axillary/inguinal freckling, neurofibromas, Lisch nodules, optic glioma, bony lesions. NF2 (chromosome 22, merlin): bilateral vestibular schwannomas (acoustic neuromas), meningiomas, cataracts; fewer skin findings.

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