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

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