🧠 Cerebral Palsy - Viva Questions & Examiner Answers
1. Definition, Etiology & Pathogenesis of Cerebral Palsy
| Viva Question / Counter-Question | Model Examiner-Grade Answer |
|---|---|
| What is the consensus definition of Cerebral Palsy (Rosenbaum et al., 2007)? | Cerebral palsy (CP) describes a group of permanent disorders of the development of movement and posture, causing activity limitation, that are attributed to non-progressive disturbances that occurred in the developing fetal or infant brain (up to 2–3 years of age). The motor disorders of CP are often accompanied by disturbances of sensation, perception, cognition, communication, behavior, epilepsy, and secondary musculoskeletal problems. |
| Counter-Question: What are the top perinatal and antenatal risk factors for Cerebral Palsy? | • Prematurity & Low Birth Weight ($<32\text{ weeks, } <1500\text{ g}$): Leading cause of Spastic Diplegia due to Periventricular Leukomalacia (PVL). • Term Birth Asphyxia (HIE): Accounts for only $10-15\%$ of total CP cases; causes Spastic Quadriplegia or Dyskinetic CP (Basal ganglia / thalamic injury). • Maternal Chorioamnionitis & TORCH infections: Cytokine storm triggering fetal brain injury. • Neonatal Hyperbilirubinemia (Kernicterus): Causes Dyskinetic (Choreoathetoid) CP with sensorineural hearing loss. |
| Counter-Question: What is Periventricular Leukomalacia (PVL) and why does it preferentially cause Spastic Diplegia? | VIVA TRAP: In preterm infants ($24-32\text{ weeks}$), the periventricular white matter adjacent to the lateral ventricles is a vascular watershed zone highly susceptible to ischemia and excitotoxicity. The descending corticospinal fibers serving the lower limbs (leg fibers) lie closest to the lateral ventricular wall; hence, PVL damages lower extremity fibers far more than upper extremity fibers, creating the classic Spastic Diplegia phenotype. |
2. Classification Systems: SCPE, GMFCS & MACS
| Viva Question / Counter-Question | Model Examiner-Grade Answer |
|---|---|
| Describe the Surveillance of Cerebral Palsy in Europe (SCPE) Classification. | SCPE classifies CP into 3 major groups based on predominant neuromotor characteristics: 1. Spastic CP (80-85%): Characterized by hypertonia, clasp-knife spasticity, hyperreflexia, clonus, and positive Babinski sign. Subdivided into: • Bilateral Spastic: Diplegic (Legs $>$ Arms) or Quadriplegic (All 4 limbs equally/severely involved $\pm$ bulbar). • Unilateral Spastic (Hemiplegic): One side of body involved (Arm $>$ Leg). 2. Dyskinetic CP (10-15%): Involuntary, uncontrolled, recurring movements. Subdivided into Choreoathetoid and Dystonic CP. 3. Ataxic CP (5%): Incoordination, wide-based gait, intention tremor, hypotonia. (Mixed CP is coded by the predominant subtype). |
| Counter-Question: What is the Gross Motor Function Classification System (GMFCS)? | A 5-level functional classification based on self-initiated movement in children aged 2–18 years: • Level I: Walks without limitations; climbs stairs without rails; speed and coordination limited. • Level II: Walks with limitations; holds handrails on stairs; minimal ability to run/jump. • Level III: Walks using a hand-held mobility device (crutches/walker); wheeled mobility for long distances. • Level IV: Self-mobility with limitations; uses powered wheelchair or transported in manual wheelchair. • Level V: Severely limited self-mobility; transported in manual wheelchair; lacks head and trunk postural control. |
| Counter-Question: What are MACS, EDACS, and CFCS? | • MACS (Manual Ability Classification System): Grades how children handle everyday objects in daily activities (Levels I to V). • EDACS (Eating & Drinking Ability Classification System): Assesses safety and efficiency of eating/drinking (Levels I to V). • CFCS (Communication Function Classification System): Assesses everyday communication effectiveness. |
3. Clinical Signs & Primitive Reflex Evaluation
| Viva Question / Counter-Question | Model Examiner-Grade Answer |
|---|---|
| What is the significance of persistent primitive reflexes in diagnosing CP? | In normal infants, primitive brainstem and spinal reflexes disappear by $3-6$ months as cortical inhibition matures. In CP, failure of corticospinal maturation causes pathological persistence and obligatoriness of primitive reflexes: 1. ATNR (Asymmetric Tonic Neck Reflex): Persistent $>6$ months or obligatory at any age prevents rolling, midline hand play, and causes scoliosis/hip dislocation. 2. STNR (Symmetric Tonic Neck Reflex): Neck extension causes arm extension + leg flexion; prevents 4-point crawling. 3. TLR (Tonic Labyrinthine Reflex): Prevents rolling and sitting. 4. Moro Reflex: Persistent $>6$ months indicates delayed CNS maturation. 5. Delayed Parachute Response: Protective extension of arms should appear by $8-9$ months; absence indicates severe motor disability. |
| Counter-Question: What is the earliest bedside sign of Unilateral Spastic CP (Hemiplegia) in an infant? | VIVA TRAP: Early hand preference (handedness) before 18–24 months of age is ALWAYS pathological. Normal infants are ambidextrous until 18–24 months. An infant who consistently reaches for toys exclusively with one hand before 1 year has hemiparesis of the contralateral hand. Persistent fisting with a cortical thumb beyond 3 months is another critical early marker. |
| Counter-Question: How do you elicit the "Scissoring Sign" and what muscles cause it? | Hold the infant vertically suspended by the axillae. In CP, excessive spasticity of the Hip Adductor muscles (Adductor Longus, Brevis, Magnus, and Gracilis) causes the lower extremities to cross over each other like scissors with plantarflexed/equinus feet. |
4. Tone Assessment: Modified Ashworth vs. Modified Tardieu Scale
| Viva Question / Counter-Question | Model Examiner-Grade Answer |
|---|---|
| How does the Modified Tardieu Scale differentiate Dynamic Spasticity from Fixed Muscle Contracture? | The Modified Tardieu Scale tests resistance to passive stretch at two distinct velocities: 1. $V1$ (Slow velocity): Full passive range of motion is measured without eliciting stretch reflex $\rightarrow$ Yields Angle $R2$. 2. $V3$ (Fast velocity / drop test): Fast stretch is applied to elicit the dynamic stretch reflex "catch" $\rightarrow$ Yields Angle $R1$. Clinical Value: • Large Dynamic Range ($R2 - R1 > 20^\circ$): Indicates Dynamic Spasticity, which will respond dramatically to Botox injection or oral Baclofen. • Small Dynamic Range ($R2 - R1 < 10^\circ$ with small $R2$): Indicates Fixed Musculoskeletal Contracture, requiring orthopedic surgical lengthening. |
| Counter-Question: What is the Modified Ashworth Scale (MAS) and its grades? | • Grade 0: No increase in muscle tone. • Grade 1: Slight increase; catch and release or minimal resistance at end of ROM. • Grade 1+: Slight increase; catch followed by minimal resistance throughout remainder ($<50\%$) of ROM. • Grade 2: Marked increase in tone through most of ROM, but affected part easily moved. • Grade 3: Considerable increase in tone; passive movement difficult. • Grade 4: Affected part rigid in flexion or extension. |
5. Comprehensive Management of Cerebral Palsy
| Viva Question / Counter-Question | Model Examiner-Grade Answer |
|---|---|
| What is the stepwise algorithm for managing spasticity in Cerebral Palsy? | 1. Physical & Occupational Therapy: Daily passive stretching, positioning, orthotics (AFOs to prevent equinus deformity). 2. Oral Antispasticity Pharmacotherapy (Generalized Spasticity): • Baclofen ($GABA_B$ agonist): $0.5-1.5\text{ mg/kg/day}$ divided TID. • Tizanidine ($\alpha_2$ adrenergic agonist): $0.1-0.2\text{ mg/kg/day}$. • Trihexyphenidyl: First-line for associated dystonia. 3. Focal Spasticity: Intramuscular Botulinum Toxin A (Botox) ($3-6\text{ units/kg}$ per muscle, max $300-400\text{ units}$ total), lasts 3–6 months. 4. Severe Refractory Spasticity: Intrathecal Baclofen Pump (ITB) or Selective Dorsal Rhizotomy (SDR) (surgical transection of $30-50\%$ of sensory nerve rootlets $L1-S1$). 5. Fixed Contractures: Orthopedic Single-Event Multilevel Surgery (SEMLS). |
| Counter-Question: How do you manage nutritional failure and drooling in a child with CP? | • Nutrition / Dysphagia: Video-fluoroscopic Swallow Study (VFSS); calorie-dense pureed feeds; upright feeding chair ($90^\circ$ hip-knee flexion with chin tuck); early placement of Percutaneous Endoscopic Gastrostomy (PEG) tube if oral feeding time $>3-4\text{ hours/day}$ or recurrent aspiration. • Sialorrhea (Drooling): Oral Glycopyrrolate ($0.02-0.04\text{ mg/kg}$ BID/TID) or Trihexyphenidyl; Submandibular gland Botulinum toxin injection; surgical submandibular duct relocation in severe refractory cases. |
6. High-Yield VIVA TRAPs & Common Pitfalls
| Viva Question / Counter-Question | Model Examiner-Grade Answer |
|---|---|
| VIVA TRAP: The examiner asks: "Is Cerebral Palsy hereditary, and can it recur in the next pregnancy?" | NO. Classic Cerebral Palsy is an acquired, non-hereditary static encephalopathy resulting from perinatal, antenatal, or postnatal brain injury. The recurrence risk in subsequent pregnancies is generally baseline ($<1\%$). However, if a family has multiple affected siblings with "CP-like" features without perinatal risk factors, you must suspect a Mendelian neurometabolic mimic (e.g., Hereditary Spastic Paraplegia, Dopa-Responsive Dystonia, Glutaric Aciduria, Arginase deficiency). |
| VIVA TRAP: "A 1-year-old child presents with hypotonia, head lag, and brisk knee jerks with extensor plantars. Is this CP?" | YES. This represents the Hypotonic / Atonic Phase of Cerebral Palsy (often preceding the development of overt spasticity). In lower motor neuron hypotonia (e.g., SMA), deep tendon reflexes are absent; whereas in cerebral hypotonia (central CP), DTRs are brisk and plantars are extensor. |
| VIVA TRAP: "Why is muscle biopsy or nerve conduction study unnecessary in classic CP?" | Because CP is a pathology of the upper motor neuron / central cerebral cortex and white matter tracts, not of the peripheral nerve or muscle. Diagnostic confirmation is achieved via detailed history and Contrast MRI Brain (which reveals PVL, multicystic encephalomalacia, or basal ganglia gliosis in $>85\%$ of cases). |
| VIVA TRAP: "Can a child outgrow Cerebral Palsy?" | The underlying brain injury is permanent and static; however, clinical manifestations evolve as the nervous system matures. With aggressive multidisciplinary physical therapy, early spasticity control, and neurodevelopmental training, functional capability can improve, but the baseline lesion remains. |