Approach to Motor Weakness
Dr Rashmi Kumar
Professor, Pediatrics
KGMU
Pathways
Types of weakness
Upper motor neuron
Lower motor neuron
Localization of lesion
Patterns of weakness
monoplegia
hemiplegia
paraplegia
quadriplegia
diplegia
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 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’
• 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
·
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
severely  
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
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 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
Weakness
DTRs
Distribution
fasciculations
tone
NCV
EMG
SC
PN
NMJ
M
++
+/-
+/-
+
(early)
(late)

distal
ocular+ proximal
pharyngeal
-
upper level
or patchy
+
(in chronic degenerative
disorder)


n

fibrillations
,,
 amplitude of MUP
-
-


n
n
fatigue pattern BSAPP
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
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
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
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 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 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
MANAGEMENT
Multidisciplinary approach with involvement of
neurologist, physiotherapist, speech therapist,
occupational therapist
Drugs to reduce tone , appliances