approach to motor weakness dr rashmi kumar professor, pediatrics kgmu
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Approach to Motor Weakness
Dr Rashmi Kumar
Professor, Pediatrics
KGMU
PathwaysTypes of weakness
Upper motor neuronLower motor neuron
Localization of lesionPatterns of weakness
monoplegiahemiplegiaparaplegiaquadriplegiadiplegia
Cerebral palsy
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 Reflexes –superficial & 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 fixed points in lower motor neuron• Slightly in upper motor neuronMuscle Tone in LMN, cerebellar lesions in UMN• physiological in newborn• frog leg position/scissoringMuscle power• maximum strength maybe impossible to test in uncooperative
children• normal strength in pure cerebellar/basal ganglia lesions
Infant/toddler: ‘observation’• definite hand preference before 2 yrs
suspicious• hemiplegic arm flexed at elbow,
movement, fisting with thumb adduction• asymmetric developmental reflexes• lift with hands under arms• traction
Older child: Quick assessment• 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
Types of motor weakness:• 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
Localisation of lesion: UMNMOTOR 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
Localisation of lesion : UMNMedulla• ‘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 hypotoniaAll cranial nerves have b/l representation except
part of VII & XII
The Final Common Pathway
Localisation of lesion: LMNSpinal 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
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 nEMG fibrillations ,, 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 reflexes• hemiplegic hand kept flexed at elbow, fisted with adducted thum Causes:• Hemiplegic cerebral palsy• Todds palsy Tumour• Trauma
MigraineAbscessGranulomaVascular - Stroke :Sudden onset -- > gradual recovery
Stroke in ChildhoodIschemic-sudden Hemorrhagic- severe headache, s/o
ICT, meningeal signsInfections – 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
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 paraplegiaCraniovertebral 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 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
•
MANAGEMENTMultidisciplinary approach with involvement of
neurologist, physiotherapist, speech therapist, occupational therapist
Drugs to reduce tone , appliances
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