PALSY Definition amp Epidemiology A group of non progressive disorders of movement and posture caused by abnormal development or damage to parts of brain that control muscle movements ID: 576149
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Slide1
CEREBRAL
PALSYSlide2
Definition & Epidemiology
A group of
non progressive
disorders of movement and posture caused by
abnormal development
or
damage
to parts of brain that control muscle movements.
Prevalence
2-2.5/1000 live birth
Its more common in
Prematures
and twinsSlide3
Risk factors
Prenatal & Perinatal
Low socioeconomic situation
Prematurity
IUGR/VLBW
Maternal
seizure disordersHormone Therapy :Thyroid- Estrogen or progesteronePregnancy complicationsMaternal FeverHyperbilirubinemiaAsphyxiaCongenital malformationsAcquired(post neonatal) (10%)MeningitisHead TraumaStroke
50% of CPs have-not any detectable risk factorSlide4
Diagnosis
Children with CP usually present with delay in reaching early developmental milestones and diagnosed
up to 18 month
by
Asymmetric movement
Spasticity
HypotoniaSometimes there are many co morbidities as:SeizureLearning disordersBehavioral disordersSensory disordersSlide5
Classification of CP based on Type of disability
Spastic
:
The most common type (70-80%)-Upper
motor pyramidal-At least two of these:
Abnormal movement pattern Hyper tonicity Pathologic reflexesDyskinetic: 10-15% of Cases - Abnormal motor pattern+ uncontrolled and repetitive motionAtaxic:Less than 5%-Cerebelluar injury-abnormal posture-movement nad or muscular disproportion
Dystonic:
Hypokinesia
-Hypotonia
Chorea-
Atetoide
:
Hyperkinesia
-Hypotonia
Mixed:
10-15% cases-Complications
are more common as sensory involvement-Seizure-Slide6
Classification of CP based on
anatomic involvement
Hemiplegia
Diplegia
: More severe in lower extremities
Quadriplegia:
Lower and upper extremitiesSlide7
Therapy
Physiotherapy
Botolinum Toxin
Baclofen pomp
(intratechal)
Anticonvulsants
……Slide8
Floppy babySlide9
The Floppy infants Presenting features
Hypotonia
Posture(Frog leg)
Range of motion
Diminished resistant to passive movement
(Scarf sign-Pull to sit)
Delayed in Motor milestonesSlide10
Diagnostic Studies
Perform complete Physical examination
Upper motor neuron lesion
Lower motor neuron lesion
Undescending
testis-High arc palate- Hypo mobility in uterine
Head CT Head MRI Electromyogram (EMG) Nerve Conduction Studies Look for SepsisSlide11Slide12
Causes of Floppy Infant Syndrome
Central nervous system
Perinatal asphyxia
Encephalopathy
Kernicterus
Cerebral palsy (atonic type)
Intracranial hemorrhageChromosomal anomalies Inborn errors of metabolismSpinal cord lesionsAnterior horn cell disease werdnig HoffmanPoliomyelitisPeripheral nervousAcute polyneuropathy
Familial
dysautonomia
Congenital sensory neuropathy
Myoneural
junction
Neonatal myasthenia gravis
Infantile botulism
Following antibiotic therapy. Slide13
Causes of Floppy Infant Syndrome(
Cnt)
Muscles
Muscular dystrophies
Congenital
myotonic
dystrophiesCongenital myopathies PolymyositisGlycogen storage disease Arthrogryposis multiplex congenitalMiscellaneous Protein energy malnutritionRicketsPrader willi syndrome
Malabsorption
syndromes
Ehler-Danlos
syndrome
Cutis
laxa
CretinismSlide14
Classification
Hypotonia with weakness
Neuromuscular disorders
Hypotonia without weakness
CNS
Metabolic
ChromosomalSlide15
Differentiating Features of a Floppy Infant according to Site of Involvement
Site of involvement
Extent to weakness
Proximal vs. distal weakness
Face
Arms
Legs
Central
-
+
+
> or =
Anterior horn cell
+
++++
++++
> or =
Peripheral nerve
-
+++
+++
<
Neuromuscular
junction
+++
+++
+++
=
Muscles
Variable
++
+
>Slide16
Differentiating Features of a Floppy Infant according to Site of Involvement
(Contd.)
Site of involvement
Deep tendon reflexes
EMG
Muscle biopsy
Central
Normal or increased
Normal
Normal
Anterior horn cell
Absent
Fasciculation / fibrillation
Denervation
pattern
Peripheral nerve
Decreased
Fibrillation
Denervation
pattern
Neuromuscular junction
Normal
Decremental / incremental
Normal
Muscle
Decreased
Short duration small amplitude potential
Characteristic Slide17
Diagnostic Studies
Labs: initial
Serum electrolytes
Serum Calcium
Serum Glucose
Creatine
Phosphokinase (CPK) Toxic scanBlood Culture Lumbar Puncture with Cerebrospinal Fluid Examination Thyroid Function TestsLabs: Test as indicated Toxicology screen Serum Ammonia and Venous pH Serum amino acids Urine amino acids and organic acid Karyotype
TORCH Virus Screening Slide18
Neurology Chapter of IAPSlide19Slide20
Neurology Chapter of IAP