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SEIZURES IN CHILDREN
Rashmi Kumar Prof Head
Pediatrics
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APPROACH TO
DEVELOPMENTAL
DELAY PROF RASHMI
KUMAR DEPARTMENT
Kumar Oynamak
KUMAR OYNAMAK 1
Kumar Oynamak Para
Approach to Motor Weakness Dr Rashmi
Kumar Professor, Pediatrics KGMU
CNS Infections RASHMI
KUMAR Importance
Invasion of brain
Pathways Types of weakness Upper motor
neuron Lower motor neuron Localization of
lesion Patterns of weakness monoplegia
hemiplegia paraplegia quadriplegia diplegia
Cerebral palsy
Introduction to
Pediatrics Rashmi
Kumar Prof Head
Pediatrics
DENGUE FEVER DHF
Prof Rashmi Kumar
Department of
MOTOR WEAKNESS: • Types & pattern •
Anatomical localization • Etiology
History • Onset • Course • H/o fever • H/o
seizures • Developmental milestones
Examination • Young child - ‘observation’ •
Older child - ‘play’ § § § § Gait & Posture
Muscle mass Tone Power Coordination
Abnormal movements ReXexes –superZcial
& deep
Examination: Posture – – Frog leg
Scissoring
Decerebrate/decorticate/ophisthotonus
Others Gait – – Foot drop Circumduction
Limp Waddling
Examination: Muscle mass: • Compare 2
sides • Measure in relation to Zxed points • in
lower motor neuron • Slightly in upper motor
neuron Muscle Tone • in LMN, cerebellar
lesions • in UMN • physiological in newborn •
frog leg position/scissoring Muscle power •
maximum strength maybe impossible to test
in uncooperative children • normal strength
in pure cerebellar/basal ganglia lesions
Infant/toddler: ‘observation’ • deZnite hand
preference before 2 yrs suspicious •
hemiplegic arm Xexed at elbow, movement,
Zsting with thumb adduction • asymmetric
developmental reXexes • lift with hands
under arms • traction
Older child: Quick assessment • hold arms
over head • walk on heels & toes • get up
from Xoor • run • hop on 1 foot • press arms
against wall • squeeze Znger • circumduction
of thumb • formal testing
Types of motor weakness: • above anterior
horn cell – UMN • below – LMN (Znal
common pathway) UMN LMN M mass
Slightly dt disuse · severely M tone spastic
Xaccid M power Distribution Individual Mm
never affected Individual Mm maybe
affected DTRs lost Babinski absent
SuperZcial reXexes Lost (maybe regained
later) lost
Localisation of lesion: UMN MOTOR
CORTEX: • u/l weakness of opposite distal
hand, leg or lower face • proximal muscles
mb transiently weak • seizures mb+ • gaze
palsies (area 8 inv) • aphasia (Brocas area –
left side) • cranial nerves, trunk muscles not
affected dt b/l innervation Internal Capsule: •
• dense hemiplegia dystonia Midbrain • •
‘crossed’ paralysis ipsilateral IIIrd nerve +
contralateral hemiplegia Pons • • • ‘crossed’
paralysis ipsilateral Vith/VIIth nerve palsy +
contralateral hemiplegia Involvement of
reticular activating system – altered
consciousness
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Localisation of lesion : UMN Medulla •
‘crossed’ paralysis • ipsilateral XII th nerve
palsy + contralateral hemiplegia •
Involvement of reticular activating system –
altered consciousness Spinal cord • LMN
signs at level of lesion • UMN signs below
Acute destructive lesions of UMN hypotonia
All cranial nerves have b/l representation
except part of VII & XII
The Final Common Pathway
Localisation of lesion: LMN Spinal Cord
lesion: • • • LMN signs at level of lesion +
UMN signs below Acute lesions spinal shock
recovery in few weeks Bladder & bowel
involvement Anterior horn cell/ventral
root/plexus lesions: • • Weakness in speciZc
myotomes Slow degeneration of anterior
horn cells fasciculations Peripheral Nerves: •
• Single nerve lesion mononeuritis –
weakness in distribution Polyneuritis: – –
Distal weakness Early loss of reXexes – may
not correlate with degree of weakness
Neuromuscular junction: • Prediliction for
ocular/pharyngeal or proximal muscles •
ReXexes lost late in affected muscles
Muscle: • Proximal weakness • Deep reXexes
maybe but elicitable • Myotonia in some
LEVEL SC PN NMJ M Weakness ++ +/- +
DTRs - (early) (late) Distribution upper level
distal ocular+ proximal or patchy pharyngeal
fasciculations + - (in chronic degenerative
disorder) tone NCV n n EMG Zbrillations , ,
fatigue pattern BSAPP amplitude of MUP
Patterns of Weakness: • MONOPLEGIA –
weakness of a limb • Lesion often cortical,
vascular in etiology • Sometimes, peripheral
n lesion • • HEMIPLEGIA – weakness of
upper & lower limbs on same side • Usually
UMN • Lesion at cortex, internal capsule •
Sometimes, brain stem/SC lesions Signs: •
hand preference before 2 yrs of age •
circumduction gait • asymmetrical reXexes •
hemiplegic hand kept Xexed at elbow, Zsted
with adducted thum Causes: • Hemiplegic
cerebral palsy Migraine • Todds palsy
Abscess • Tumour Granuloma • Trauma
Vascular - Stroke : Sudden onset -- > gradual
recovery
Stroke in Childhood Ischemic-sudden
Hemorrhagic- severe headache, s/o ICT,
meningeal signs Infections – PM, TBM, NCC,
tuberculoma, VE, abscess o Vascular – AV
malformation, aneurysm Hypertension
Bleeding diatheses Vit K deZciency Cardiac
– CHD, RHD, SABE o Collagen vascular
disorders – SLE, PAN, APS o Hematologic –
Sickle cell disease, leukemia, dehydration,
iron deZciency, hypercoagulable states, o
Metabolic Idiopathic - 'acute infantile
hemiplegia' mb dt trauma to internal carotid
PARAPLEGIA: Weakness of both lower limbs
• Lesion in SC or PN (polyneuritis) • UMN
type – lesion in SC. If acute may spinal
shock • LMN type - - lesion in lower SC eg.
myelomeningocele - spinal shock stage -
polyneuritis eg GBS, post diptheretic palsy -
NM junction - Muscle
SPINAL CORD LESIONS: • I Compressive •
Acute – trauma, epidural abscess • Chronic
–tumour, vertebral disease, syringomyelia,
arachnoiditis • • II Non compressive • Acute
– TM, hematomyelia, infarction, infections,
post infectious • Chronic – degenerative • -
spinocerebellar degenerations • -spinal
muscular atrophy • -motor neuron disease • -
subacute combined degeneration Chronic
lesions may present acutely dt secondary
vascular changes
QUADRIPLEGIA- weakness of all 4 limbs ·
Deep coma · Lesions of brain stem Upper SC
UMN signs · Polyneuritis All causes of
paraplegia Craniovertebral malformations
DIPLEGIA- weakness of both arms or both
legs • Cerebral diplegia – a form of CP seen
in premature babies
Cerebral Palsy: • MOTOR defect due to non
progressive cerebral disorder acquired in
early life • 2/1000 • Maybe associated with
MR, seizures, hyperactivity etc. • • ETIOLOGY:
• Prenatal- radiation, drugs, infections,
malformations • Natal – LBW, trauma,
asphyxia, ischemia • Post natal –
kernicterus, neonatal illness, hypoglycemia,
CNS infections • No cause found in ¼
Cerebral Palsy: • • • • • DIAGNOSIS: Delayed
motor development Abnormal persistence of
developmental reXexes Feeding problems
TYPES: Spastic quadriplegia - most common
- severe disability, MR - pseudobulbar palsy
feeding problems - extrapyramidal signs -
multicystic encephalomalacia Hemiplegia -
related to perinatal events – PIH, ischemia
stroke - porencephaly Diplegia - prematurity
periventricular leukomalacia ·Dyskinetic –
kernicterus, circulatory failure, asphyxia ·
Ataxic – often due to unrecognized
cerebellar malformation
MANAGEMENT Multidisciplinary approach
with involvement of neurologist,
physiotherapist, speech therapist,
occupational therapist Drugs to reduce tone ,
appliances
Report
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