motor_weakness1-1......................ppt

Tttt

1. Approach to Motor Weakness
Dr Rashmi Kumar
Professor, Pediatrics
KGMU

2. Pathways
Types of weakness
Upper motor 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:
•Compare 2 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’
•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

10. 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
 

11. 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 reflexesLost (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 Common Pathway

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 NMJ M
 
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-sudden
Hemorrhagic- 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 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

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 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

22. 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

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, ischemiastroke
•-
        
porencephaly
• Diplegia
•-
        
prematurity periventricular leukomalacia
• Dyskinetic – kernicterus, circulatory failure, asphyxia
 Ataxic – often due to unrecognized cerebellar malformation
• 

24. MANAGEMENT
Multidisciplinary approach with involvement of
neurologist, physiotherapist, speech therapist,
occupational therapist
Drugs to reduce tone , appliances