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Similar to Approach to motor weakness
Approach to motor weakness
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- 2. Pathways Types of weakness Uppermotor neuron Lower motor neuron Localization of lesion Patterns of weakness monoplegia hemiplegia paraplegia quadriplegia diplegia Cerebral palsy
- 4. MOTOR WEAKNESS: • Types& pattern • Anatomical localization • Etiology
- 5. History • Onset • Course •H/o fever • H/o seizures • Developmental milestones
- 6. Examination • Young child- ‘observation’ • Older child - ‘play’ Gait & Posture Muscle mass Tone Power Coordination Abnormal movements Reflexes –superficial & deep
- 7. Examination: Posture – Frog leg –Scissoring – Decerebrate/decorticate/ophisthotonus – Others Gait – Foot drop – Circumduction – Limp – Waddling
- 8. Examination: Muscle mass: • Compare2 sides • Measure in relation to fixed 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
- 9. Infant/toddler: ‘observation’ • definitehand preference before 2 yrs suspicious • hemiplegic arm flexed at elbow, movement, fisting with thumb adduction • asymmetric developmental reflexes • lift with hands under arms • traction
- 10. Older child: Quickassessment • hold arms over head • walk on heels & toes • get up from floor • run • hop on 1 foot • press arms against wall • squeeze finger • circumduction of thumb • formal testing
- 11. Types of motorweakness: • above anterior horn cell – UMN • below – LMN (final common pathway) UMN LMN M mass Slightly dt disuse · severely M tone spastic flaccid M power Distribution Individual Mm never affected Individual Mm maybe affected DTRs lost Babinski absent Superficial reflexes Lost (maybe regained later) lost
- 12. 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
- 13. 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
- 14. The Final CommonPathway
- 15. 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 specific myotomes • Slow degeneration of anterior horn cells fasciculations Peripheral Nerves: • Single nerve lesion mononeuritis –weakness in distribution • Polyneuritis: – Distal weakness – Early loss of reflexes – may not correlate with degree of weakness Neuromuscular junction: • Prediliction for ocular/pharyngeal or proximal muscles • Reflexes lost late in affected muscles Muscle: • Proximal weakness • Deep reflexes maybe but elicitable • Myotonia in some
- 16. LEVEL SC PN NMJM Weakness ++ +/- +/- + DTRs - - - (early) (late) Distribution upper level distal ocular+ proximal or patchy pharyngeal fasciculations + - - - (in chronic degenerative disorder) tone NCV n n n EMG fibrillations ,, fatigue pattern BSAPP amplitude of MUP
- 17. 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 reflexes • hemiplegic hand kept flexed at elbow, fisted with adducted thum Causes: • Hemiplegic cerebral palsy • Todds palsy Tumour • Trauma Migraine Abscess Granuloma Vascular - Stroke :Sudden onset -- > gradual recovery
- 18. Stroke in Childhood Ischemic-suddenHemorrhagic- severe headache, s/o ICT, meningeal signs Infections – PM, TBM, NCC, tuberculoma, VE, abscess o Cardiac – CHD, RHD, SABE o Collagen vascular disorders – SLE, PAN, APS o Hematologic – Sickle cell disease,leukemia, dehydration, iron deficiency, hypercoagulable states, o Metabolic Idiopathic - 'acute infantile hemiplegia' - mb dt trauma to internal carotid Vascular – AV malformation, aneurysm Hypertension Bleeding diatheses Vit K deficiency
- 19. PARAPLEGIA: Weakness ofboth 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
- 20. 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
- 21. QUADRIPLEGIA- weakness ofall 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
- 22. Cerebral Palsy: • MOTORdefect 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
- 23. Cerebral Palsy: • DIAGNOSIS: •Delayed motor development • Abnormal persistence of developmental reflexes • Feeding problems • TYPES: • Spastic • quadriplegia • - most common • - severe disability, MR • - pseudobulbar palsy feeding problems • - extrapyramidal signs • - multicystic encephalomalacia • Hemiplegia • - related to perinatal events – PIH, ischemiastroke • - porencephaly • Diplegia • - prematurity periventricular leukomalacia • ·Dyskinetic – kernicterus, circulatory failure, asphyxia · Ataxic – often due to unrecognized cerebellar malformation
- 24. MANAGEMENT Multidisciplinary approach withinvolvement of neurologist, physiotherapist, speech therapist, occupational therapist Drugs to reduce tone , appliances
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