🧠Cerebral Palsy - Proforma

Presenting History

When evaluating a child with suspected Cerebral Palsy (CP) or Global Developmental Delay (GDD), obtain an exhaustive chronological account of the child's symptoms. Ask specific follow-up questions to determine the depth, severity, and exact nature of the complaints.

Delayed Milestones: Ask precisely which milestones are delayed (head holding, sitting, standing, walking). Inquire if the delay involves motor alone, or if language and social domains are also affected to differentiate a specific motor delay from GDD.
Abnormal Motor Patterns: Ask if the child exhibits a "commando crawl" or "bottom shuffling" (deviations from normal milestones).
Abnormal Tone (Stiffness/Floppiness): Inquire about difficulty in putting on diapers (suggests adductor spasm/scissoring). Ask about persistent fisting of hands beyond 2 months (an early marker of cortical damage). Ask if the baby feels floppy or slips through the mother's hands.
Postural & Gait Abnormalities: Ask if the child walks exclusively on their toes (suggests contractures or spasticity of calf muscles).
Involuntary Movements: Inquire about sudden stiffness or arching of the back with excessive crying when handled (suggests dystonia). Ask about writhing, choreoathetoid movements, noticing that these may only appear after 1 year of age.
Feeding & Bulbar Difficulties: Ask about difficulty in breastfeeding, trouble chewing or mixing food, spillage of water/food from the mouth, nasal regurgitation, or choking (suggests pseudobulbar palsy).
Advanced or Asymmetric Milestones: Ask if there was an early hand preference before 2 years of age (indicates contralateral hemiplegia). Ask about early weight-bearing or standing before 6 months (pseudo-standing due to spasticity).

Negative History (3C 1D Framework)

This section is critical to ascertain the etiology (Causes), define the extent of the disease (Complaints), evaluate for associated morbidity (Complications), and rule out other mimicking conditions (Differentials).

Category	Pertinent Negative Question	Rationale / Significance
Causes (Etiology)	History of maternal fever with rash and cervical lymphadenopathy during pregnancy?	Points towards intrauterine TORCH infections (e.g., Rubella), which cause microcephaly, cataracts, deafness, and CP.
Causes	History of maternal drug intake (e.g., phenytoin), alcohol, or smoking?	Phenytoin causes fetal hydantoin syndrome; alcohol causes fetal alcohol syndrome; smoking causes placental insufficiency and birth asphyxia.
Causes	History of bleeding in the third trimester or hypertension (preeclampsia)?	Predisposes the fetus to placental insufficiency, hypoxia, and birth asphyxia.
Causes	Did the baby cry immediately after birth? Was there a need for NICU admission, or history of lethargy/refusal to feed?	Helps establish perinatal insult, birth asphyxia, or neonatal encephalopathy. Even if crying was delayed, inquire about neonatal encephalopathy signs to confirm significant hypoxic insult.
Causes	History of severe jaundice requiring intervention/exchange transfusion?	High bilirubin leads to kernicterus, predisposing the child to dyskinetic/extrapyramidal CP, enamel hypoplasia, and deafness.
Causes	History of head trauma or neuroinfections (meningitis/encephalitis) in the first year of life?	Post-infectious or post-traumatic brain damage within the first year of life fits the Nelson definition of CP.
Complaints	History of loss of attained milestones (regression)?	Critical negative: CP is a non-progressive disorder. Regression strongly rules out CP and points to neurodegenerative disorders.
Complications	History of seizures or breakthrough convulsions?	Seizures are a major comorbidity, very common in spastic quadriplegia, though rare in spastic diplegia.
Complications	History of squint, lack of visual fixation, or lack of response to sound?	Visual (cataract, cortical blindness, optic atrophy) and hearing (sensorineural deafness) abnormalities are highly prevalent comorbidities in CP.
Complications	History of persistent constipation or recurrent respiratory infections?	Up to 80% of CP children have constipation due to pelvic floor spasticity, dismotility, and fiber-poor mashed diets. Recurrent pneumonias occur due to aspiration and pseudobulbar palsy.
Differentials (Mimics)	History of failure to thrive, recurrent vomiting, or abnormal urine odor?	Suggests Inborn Errors of Metabolism (IEMs), which are classic CP mimics.
Differentials	History of prolonged constipation, dry skin, and coarse voice?	Suggests Hypothyroidism. Note: Only ask this if the child has isolated GDD. If prominent motor abnormalities (fisting, scissoring) are present, hypothyroidism is unlikely.
Differentials	History of diurnal variation in symptoms (worse at night, better in morning)?	Points to Dopa-responsive dystonia, an important treatable mimic of dyskinetic CP.

Other Relevant History

Antenatal History: Maternal diabetes mellitus (risk of macrosomia, hypoglycemia, polycythemia, and strokes leading to hemiplegic CP). Maternal UTI in the third trimester (risk of prematurity and sepsis).
Natal History: Gestational age is crucial. Prematurity requires correcting the chronological age for milestones up to 2 years. Premature infants are highly prone to periventricular leukomalacia, leading classically to Spastic Diplegia, though they can develop any CP type. Mode of delivery and prolonged labor (first and second stage combined >12 hours in multipara, >18 hours in primigravida).
Developmental History: Must comprehensively cover four domains: Gross motor, Fine motor, Social/Adaptive, and Language. Calculate the Developmental Quotient (DQ) for each domain: (Developmental Age / Chronological Age) x 100. Look for dissociation of milestones; for instance, in spastic diplegia, motor domains are severely delayed while language and social milestones might be relatively preserved.
Nutritional History: Assess feeding difficulties, type of diet (mashed vs. solid), and exact caloric and protein deficits.
Immunization History: Ask about routine vaccinations. Note: Whole-cell pertussis vaccine is safe in CP and is only contraindicated in progressive neurodegenerative diseases.
Socioeconomic & KAP History: Assess via the modified Kuppuswamy scale. Document parental Knowledge, Attitude, and Practices (KAP)—do the parents understand the brain-origin of the disease, the need for chronic physiotherapy, and regular anti-epileptic compliance?.
Treatment & Rehabilitation History: For children >5 years, utilize the Gross Motor Function Classification System (GMFCS, Levels I-V) to define ambulatory status and independence. Detail the exact physiotherapy regimen (ideally 3 times a day, 10 minutes per joint, full range of motion).

History Summary

Summarize the history using a structured, academic format to present to the examiner without premature labeling. Template: "I would like to think of a non-progressive neuromotor disorder of cerebral origin, probably cerebral palsy [mention specific topographic type if clues exist, e.g., spastic diplegia], likely secondary to [mention insult, e.g., perinatal asphyxia/prematurity], associated with comorbidities like [seizures/visual impairment/constipation], with no history suggestive of regression of milestones.".

General & Head-to-Toe Examination

Vitals: Check for tachycardia or tachypnea (may indicate concurrent aspiration pneumonia or autonomic instability).
Anthropometry: Accurately measure Head Circumference (HC). Compare against the WHO 3 Standard Deviation charts. Label as Microcephaly only if HC is < -3 SD. Note: In older children (>5 years), state: "The head circumference is less than -3 SD for a 5-year-old, hence I consider it microcephaly, as head growth plateaus after 5 years". Differentiate primary (dysmorphic, receding forehead) from secondary microcephaly.
Head/Facies: Enamel hypoplasia/yellowish-greenish discoloration of teeth (points to prior severe jaundice/kernicterus).
Drooling Assessment: Grade 1 (lips), Grade 2 (chin), Grade 3 (clothes), Grade 4 (surroundings). Also note abnormal mouthing beyond 15 months of age.
Neurocutaneous Markers: Rule out neurogenetic mimics. Look for Café-au-lait macules (>5mm prepubertal, >15mm postpubertal, >6 in number), ash-leaf spots, or port-wine stains.
Spine & Posture: Inspect for severe scoliosis, bed sores, or asymmetric chest (evidence of prolonged bedridden state). Look for Windswept deformity of the hips (adducted on one side, abducted on the other).
Limbs: Measure leg length discrepancy (difference of >1 cm is significant, common in congenital hemiplegia). Look for short nails/thumbs (indicates contralateral parietal lobe damage). Elicit scissoring by suspending the child vertically by the axillae (adductor spasm).
Contractures: Check if contractures are dynamic or static (fixed). Elicit R1 (initial catch angle upon fast stretch) and R2 (maximum passive stretch angle). If R1 and R2 are different, it is a dynamic contracture (amenable to physiotherapy/Botox). If R1 equals R2, it is a static/fixed contracture.

Systemic Examination

1. Higher Mental Functions (HMF)

Assess consciousness and orientation to the mother (stranger anxiety indicates intact cognition).
Speech evaluation: Cooing, babbling, or intelligible speech. Look for pseudobulbar dysarthria (slurred syllables).
Behavioral assessment: Look for hyperactivity, irritability, or autistic traits.

2. Cranial Nerves

CN II (Optic): Assess visual tracking. Crucially, examine the fundus. If the child is blind but the fundus is strictly normal, diagnose cortical blindness (occipital lobe damage). Look for cataracts (TORCH).
CN III, IV, VI: Check for non-paralytic squint (movements present in all directions but asymmetric light reflex). Paralytic squint is rare in CP.
CN VIII: Assess hearing via distraction techniques (tuning fork/bell 90 cm away).
CN IX, X: Check for pooling of secretions and gag reflex. In CP, the lesion is upper motor neuron (pseudobulbar palsy), so the gag reflex is intact or exaggerated, differentiating it from true bulbar palsy where gag is lost.

3. Motor System (Granular Assessment)

Bulk: Observe for disuse atrophy in long-standing cases.
Tone:
- Spasticity (Pyramidal): Velocity-dependent catch. Must be described as "clasp-knife type" hypertonia.
- Dystonia (Extrapyramidal): Tone is fluctuating/same throughout. The stiffness precipitates upon handling the child and disappears in the prone position or sleep.
- Amiel Tyson Tone Assessment (<1 year old): Evaluate adductor angle, popliteal angle, scarf sign, and heel-to-ear extension.
Power: In young/uncooperative children, grade as "best observed power >3/5" if moving against gravity. In older cooperative children, detail proximal vs. distal muscle groups. Spastic CP typically shows distal weakness with specifically affected hip flexion and shoulder abduction.
Reflexes:
- Deep Tendon Reflexes (DTRs): Brisk/exaggerated in spastic CP. Note: Severe contractures may falsely mask brisk reflexes.
- Superficial Reflexes: Plantar reflex shows Babinski extensor response (UMN sign).
- Primitive Reflexes (Crucial): Must assess Moro, Grasp, Rooting, ATNR. Differentiate voluntary holding from true primitive Palmar Grasp (stroking the dorsum of the hand releases a primitive grasp; voluntary hold will not release). Persistence of Moro/ATNR beyond 6 months indicates severe cortical damage.
- Postural Reflexes: Check Landau (appears 3m, disappears 9-12m) and Parachute (appears 9m, persists for life). Delayed appearance is a hallmark of CP.
Coordination & Cerebellar Signs: Assess for nystagmus, intention tremors, or ataxia (wide-based gait) if ataxic CP is suspected.

4. Sensory System & Gait

Sensory: Tactile and pain sensation must be verified. Thalamocortical tract damage can cause sensory deficits, which critically impairs physical rehabilitation outcomes.
Gait (if ambulant): Observe for hemiplegic (circumduction), diplegic (scissoring/crouch gait), or extrapyramidal (choreoathetoid/hyperkinetic) gait patterns.

5. Anthropometric Developmental Assessment (180-Degree Flip)

If the child is <1 year developmental age, assess via the 180-degree flip:
- Supine: Quality/quantity of movement, symmetry, reaching for objects.
- Pull-to-sit: Head lag, flexor tone.
- Sitting: Rounding of back, tripod support.
- Vertical suspension: Scissoring of lower limbs.
- Ventral suspension: Posture of head relative to trunk (rag doll vs extended).
- Prone: Position of hips and head lifting.

6. Other Systems

Respiratory: Signs of recurrent aspiration/LRTI.
Cardiovascular: Congenital heart defects (suggests genetic/TORCH etiologies).
Abdomen: Hepatosplenomegaly (must rule out intrauterine infections or metabolic storage disorders).

Final Summary & Diagnosis

Clinical Summary Template: "A Age-year-old Gender child, Birth Order born to non-consanguineous parents, presenting with a history of delayed motor and mental milestones without regression, associated with features of stiffness/abnormal movements. Examination reveals microcephaly, UMN signs: e.g., spasticity, brisk reflexes, extensor plantars, and intact bulbar gag reflex, without hepatosplenomegaly or neurocutaneous markers.".

Final Diagnosis Format: State the diagnosis mapping to Topography, Severity, and Comorbidities: "Spastic Diplegia / Quadriplegia / Hemiplegia with Global Developmental Delay or Intellectual Disability if >5 years, with moderate retardation (Developmental Quotient of X%), with Primary / Secondary Microcephaly, with comorbidities including Seizures / Squint / Hearing impairment, likely secondary to Perinatal asphyxia / Prematurity / rule out cerebral malformation if no insult found. GMFCS Level I-V.".