Motor Deficits

Refer to Chapter 5 of
Clinical Neurology
Textbook
Motor Deficits

 Regulation of motor activity is controlled by

the:
– Pyramidal Systems
– Extra-pyramidal Systems
– Lower Motor Neuron (LMN)
Motor Deficits

 Pyramidal Systems
– Consists of fibers that descend from the cerebral
cortex through the internal capsule, across the
medullary pyramid, crossing & descending in
the lateral corticospinal tract on the
contralateral side and synapsing w/ a LMN in the
cord
Motor Deficits

 Extra-Pyramidal Systems
– Involves all other descending influences on the
LMN
– It originates primarily in the basal ganglia & the
cerebellum
Motor Deficits

 Lower Motor Neuron

– Contain motor fibers, which make up the CN &
PN
– Disturbance in fcn @ any point in the PNS can
result in dysfunction in motor activity
Motor Deficits

 HPI:
– Onset:
 Abrupt – vascular disturbance; e.g. stroke
 Subacute (Dys – Wks) – neoplastic, infective, or
inflammatory disorder
 Slow (Mnths – Yrs) – hereditary, degenerative,
endocrinological, or neoplastic disorder
Motor Deficits

 HPI:
– Course of Development:
 Progressive Deficits
 Episodic
 Rapid Fluctuation
Motor Deficits

 Examination:
– The examination process should be systematic
and sequential
– Muscle Appearance:
 Atrophy
 Pseudohypertrophy
Motor Deficits

 Examination:
– Muscle Appearance:
 Fasciculation: spontaneous muscle contractions of
individual motor units, which cause visible irregular
“twitches” over the surface of the muscle
Motor Deficits

 Examination:
– Muscle Tone:
 The resistance of muscle to passive movement of a joint
 Dependent upon:
– Degree of muscle contraction
– Mechanical properties of the muscle & CT
Motor Deficits

 Examination:
– Muscle Tone:
 Assessment:
– Observation of extremities @ rest
– Palpation of the muscle belly
– Determination of resistance to passive stretch &
movement
Motor Deficits

 Examination:
– Muscle Tone:
 Hypertonia:
– Spasticity: inc tone
 Arms: Flexors > Extensors

 Legs: Flexors < Extensors

 Clasp-Knife Phenomenon

 d/t an UMN lesion; e.g. stroke

Motor Deficits

 Examination:
– Muscle Tone:
 Hypertonia:
– Rigidity: inc resistance to passive movement
 Lead-Pipe Rigidity AKA Cog-Wheel

 d/t extra-pyramidal dysfunction – lesion of the basal

ganglia; e.g. Parkinson’s

Motor Deficits

 Examination:
– Muscle Tone:
 Hypotonia: excessive floppiness d/t reduced resistance
to passive movement
– Distal portion of the extremity is easily waved
– Hyperextension of the joints is possible
– Muscle appears flat & less firm
– d/t LMN lesion or a primary muscle disorder i.e. NMJ
disorder
Motor Deficits

 Examination:
– Muscle Tone:
 Paratonia: the patient is unable to relax when asked, pt
will move limb in passive movement even after being
told not to
– d/t frontal lobe or diffuse cerebral disease, i.e. UMN lesion
Motor Deficits

 Examination:
– Muscle Power:
 Dysfunction in muscle power can result from an UMN or
LMN lesion
 Distribution of weakness distinguishes between an UMN
or LMN lesion
– UMN:
 Arms: Ext/Abd > Flex/Add

 Legs: Ext/Abd < Flex/Add

– LMN: affects only the supplied muscles

Motor Deficits

 Examination:
– Muscle Power:
 Assessment:
– Select the muscles most likely to be involved from the
case hx
– In general: motor deficits or weakness in all limbs which is
not assoc w/ an UMN lesion
 Proximal Distribution: myopathic disorder

 Distal Distribution: LMN disturbance

Motor Deficits

 Examination:
– Muscle Power:
 Assessment:
– General Terminology:
 Monoplegia/Monoparesis

 Hemiplegia/Hemiparesis

 Paraplegias/Paraparesis

 Quadriplegia/Quadriparesis
Motor Deficits

 Examination:
– Muscle Power:
 Assessment:
– Grading (Table 5-3):
 +5 – Normal

 +4 – Active movement vs gravity & resistance

 +3 – Active movement vs gravity, no resistance

 +2 – Active movement when gravity is eliminated

 +1 – Trace

 0 – No contraction
Motor Deficits

 Examination:
– Coordination:
 Mainly controlled by the cerebellum
 Tests:
– Finger to Nose
– Heel – Shin
– Rapid Supination/pronation
Motor Deficits

 Examination:
– Coordination:
 Pyramidal Lesions:
– Fine voluntary movements are performed more slowly
 Cerebellar Lesions:
– The main complaint is incoordination; there is little else
revealed by exam
– Rate, rhythm, & amplitude of movement are irregular
 Loss of Sensation:
– Coordination improves with visual input
Motor Deficits

 Examination:
– Tendon Reflexes:
 Areflexia: lost or depressed reflex
 Hyperreflexia:
– Occurs w/ an UMN lesion
– Clonus: a series of rythmic reflex after stretch of the
muscle
– Sustained Clonus: 3-4 beats - pathological
Motor Deficits

 Examination:
– Tendon Reflexes:
 Reflex Asymmetry:
– Lateralized Asymmetries:
 UMN Lesion – Brisk

 LMN Lesion – Depressed

– Focal Reflex:
 Assoc w/ NR, Plexus, or PN lesions, e.g. unilateral loss of the

Knee-Jerk
– Loss of Distal Reflex:
 Polyneuropathies

 Proximal reflexes are preserved

Motor Deficits

 Examination:
– Tendon Reflexes:
 Pathological Reflexes:
– Babinski: dorsiflexion of great toe & toe flaring
 d/t an UMN lesion involving the contralateral motor

cortex or corticospinal tract

Motor Deficits

 Examination:
– Gait: see web links for videos of gaits
 Apraxic Gait:
– d/t disturbances in frontal lobe fcn
– No weakness or incoordination
– Pt is unable to stand unsupported or to walk properly
Motor Deficits

 Examination:
– Gait:
 Circumducted Gait:
– Unilateral
– One leg swings around when walking while the ipsilateral arm is flex
and adducted
– d/t corticospinal lesions
 Scissor-Like Gait:
– Bilateral
– Knees are close together and the legs move in a scissor-like motion
– d/t corticospinal lesions
Motor Deficits

 Examination:
– Gait:
 Marche a petit pas Gait:
– Often mistaken for a Parkisonian gait
– Short, shuffling steps, w/ hesitation in starting or turning
– Wide-base
– Preserved arm swing
– Cognitive impairment
– Absent any Parkinson’s signs
Motor Deficits

 Examination:
– Gait:
 Festinating Gait:
– d/t an extra-pyramidal lesion
– Parkinson’s disease
 Steppage Gait:
– d/t impaired sensation, i.e. proprioception
 Foot Drop or Waddling Gait:
– d/t ant horn cell, PN, or striated muscles lesion
Motor Deficits

 Clinical Correlation
– Upper Motor Neuron Lesions
 Weakness/Paralysis
 Spasticity
 Hyper-reflexia
 + Babinski’s
 Little to no atrophy
Motor Deficits

 Clinical Correlation
– Lower Motor Neuron Lesions
 Weakness/Paralysis
 Hypotonia
 Hypo-reflexia or Areflexia
 Muscle Wasting & fasciculation
Motor Deficits

 Clinical Correlation
– Cerebellar Dysfunction
 Hypotonia
 Hypo-reflexia or Pendular DTR’s
 Ataxia
 Gait Disturbance
 Imbalance
 Assoc Eye movement disorders
 Dysarthria
Motor Deficits

 Clinical Correlation
– Neuromuscular Transmission Disorders
 Weakness
 Normal or Reduced Tone
 Normal or Hypo-reflexia
 No sensory changes
Motor Deficits

 Clinical Correlation
– Myopathic Disorders
 Weakness
 No muscle atrophy or wasting
 No change in DTR’s until advanced stages
 No sensory changes
Motor Deficits

 Spinal Cord Disorders

– Cord lesions can lead to motor, sensory, or sphincter
disturbances and changes in muscle tone
 Motor:
– Above C5: ipsilateral hemiparesis or bilateral quadriparesis
– Lower Cervical: UE only partially involved
– Below T1: LE only involved
 Sensory
– Posterior Columns: ipsilateral loss of position & vibratory
sensations
– Spinothalamic Tracts: contralateral loss of pain & temp
Motor Deficits

 Spinal Cord Disorders

– Cord lesions can lead to motor, sensory, or sphincter
disturbances and changes in muscle tone
 Sphincter
– Conus Medullaris Syndrome: d/t T12 compression injury
– Cauda Equina Syndrome: d/t NR compression below L1
 Muscle Tone:
– Spasticity is common w/ UMN lesions and occur below the level
of the lesion in pt’s w/ myelopathies
Motor Deficits

 Traumatic Myelopathy
– Total Cord Transection:
 Immediate & permanent paralysis & loss of sensation
below the level of the lesion
 Reflexes: absent initially but return over time
 Progression
– Acute Stage: “Spinal Shock” – S/s more like LMN lesion
– Weeks After: S/s more like UMN lesion
 Clinical Pearl

– Flexor or Extensor Spasms of the Legs

Motor Deficits

 Traumatic Myelopathy
– Total Cord Transection:
 Whiplash
– Can cause focal cord lesions which result in ischemia
– Bilateral brachial plexus paresis
– Sensory disturbances can be present as well
Motor Deficits

 Demyelinating Myelopathies
– Role of Myelin
 Provides insulation for axons
 Necessary for conduction
 Composed of tightly wrapped lipid bilayers
 Formed by Schwann cells in the PNS
 Formed by Oligodendrocytes in the CNS
Motor Deficits

 Demyelinating Myelopathies
– Multiple Sclerosis
 One of the most Neurological Disorders
 300,000 pts in the US
 Highest incidence in ages 20-40
 Female predilection by 2x
 There is increase in the incidence of the MS with the
greater distance away from the equator
Motor Deficits

 Demyelinating Myelopathies
– Multiple Sclerosis
 Pathology:
– Inflammatory relapsing or progressive disorder of CNS
white matter
 Cause: idiopathic
Motor Deficits

 Demyelinating Myelopathies
– Multiple Sclerosis
 Clinical Features
– Sensory symptoms: MC manifestation
 Numbness

 Paresthesias

 Dysesthesias

 Hyperesthesias

 Sensory Cord Syndrome

 Useless Hand Syndrome

Motor Deficits

 Demyelinating Myelopathies
– Multiple Sclerosis
 Clinical Features
– Pyramidal Tract Dysfunction

– Visual Disturbance:
 Optic Neuritis

– Cerebellar Dysfunction:
 Dysdiadochokinesia
Motor Deficits

 Demyelinating Myelopathies
– Multiple Sclerosis
 Clinical Features
– Miscellaneous
 Symptoms fluctuate & are made worse by exercise or

elevation of body temperature

 Urinary Difficulties

 Constipation

 Cognitive Disorders

 Affect Disorders

 Fatigue
Motor Deficits

 Demyelinating Myelopathies
– Multiple Sclerosis
 Course
– Relapsing-Remitting: 85%
– 2o Progressive: 85% after 25 yrs
– 1o Progressive: 10%
– Progressive-Relapsing: Rare
Motor Deficits

 Demyelinating Myelopathies
– Multiple Sclerosis
 Diagnosis
– Requires evidence of @ least 2 different regions of the
CNS white matter being affected @ different times
– Clinical Definite
 Relapsing-Remitting course & signs of at least 2
lesions involving different regions of white matter
– Probable
1. Multifocal white matter disease, but only one clinical
attack
2. 2 Clinical episodes, but only 1 lesion
Motor Deficits

 Cervical Spondylosis
– Accumulation of degenerative changes in the
cervical spine, which become clinically relevant
when they cause pain or neurological
dysfunction
– Degenerative Changes:
 Loss of disc height
 Bulging or herniation
 Osteophyte & hypertrophic changes of facets
 Hypertrophy of the LF
Motor Deficits

 Cervical Spondylosis
– Pathophysiology
 Distorted & flattened spinal cords
 Demyelination of Lateral & Posterior Columns
 Central Gray Matter
Motor Deficits

 Cervical Spondylosis
– Clinical Features
 Onset of S/S is usually insidious
 CN Exam WNL
 Upper Extremity
– ↓ CROM
– NP & Radiculopathy
– Mild weakness, brisk reflexes w/ myelopathy
– If NR involvement:
Motor Deficits

 Cervical Spondylosis
– Clinical Features
 Lower Extremity:
– Weakness Common
– Spastic Tone
– Sensory Loss
 Bowel & Bladder dysfunction uncommon
Motor Deficits

 Cord Tumors
– Classification
 Intramedullary: Make up 10%
– Ependymomas: MC
– Gliomas
 Extramedullary: Make up 90%
– Neurofibromas
– Meningiomas
Motor Deficits

 Cord Tumors
– Clinical Features
 Signs:
– Localized spinal tendorness
– LMN deficits if ant roots are involved
– Dermatomal sensory changes w/ post root involvement
– UMN Lesions
 Symptoms: (Table 5-9)
– Pain
– Motor Dysfunction
– Sensory Disturbance
– Sphincter Dysfunction
Motor Deficits

 Anterior Horn Cell Disorders

– Characterized by LMN S/S
– Motor Neuron Disease in Adults
 Onset 30-60 yoa w/ a male predilection
 Classification
– Progressive Bulbar Palsy
– Pseudobulbar Palsy
– Progressive Spinal Muscular Atrophy
– Primary Lateral Sclerosis
– Amyotrophic Lateral Sclerosis
Motor Deficits

 Anterior Horn Cell Disorders

– Motor Neuron Disease in Adults
 Classification
– Progressive Bulbar Palsy
 Bulbar (brainstem) paralysis predominates
 CN dysfunction
 Death w/I 1-3 yrs
– Pseudobulbar Palsy
 d/t an UMN Lesion – Rare
 Lower CN dysfunction
Motor Deficits

 Anterior Horn Cell Disorders

– Motor Neuron Disease in Adults
 Classification
– Progressive Spinal Muscular Atrophy
 LMN disorder primarily
 Progression occurs from the UE – LE - generalized
– Primary Lateral Sclerosis
 Pure UMN disorder – Rare
– Amyotrophic Lateral Sclerosis
 AKA Lou Gerig’s Disease
 Mixed UMN & LMN disorder
Motor Deficits

 Nerve Root Lesion

– Lumbar Disk Prolapse
 LBP & Radiculopathy in L5 & S1
 Decreased L-ROM
 Paraspinal Muscle Hypertonicity
– Cervical Disk Prolapse
 NP & Radiculopathy in the arms
 Inc pain w/ C-ROM
 Lateral Herniation
 Central Herniation
Motor Deficits

 Traumatic Avulsion of Nerve Roots

– Erb-Duchenne Paralysis: Avulsion of C5/C6
 Causes: birth & trauma
 Clinical Features
– Loss of shoulder abduction & elbow flexion
– Klumpke’s Paralysis: Avulsion of C8/T1
 Causes: fall & grab
 Clinical Features
– Wasting of intrinsic muscles of the hand
Motor Deficits

 Traumatic Avulsion of Nerve Roots

– Cervical Rib Syndrome: C8/T1 Involvement
 Clinical Features
– Similar to Klumpke’s Paralysis
– Weakness & wasting of the intrinsic muscles of the
hands
– Pain & numbness in the hands
Motor Deficits

 Myasthenia Gravis
– Pathophysiology
 Block of Ach receptors
– Associated Conditions
 Thymic Tumor
 Thyrotoxicosis
 Rheumatoid Arthritis
 Disseminated Lupus Erythematosis
Motor Deficits

 Myasthenia Gravis
– Clinical Features
 Insidious onset
 Fluctuating weakness
 Predilection for: EOM, Muscles of Mastication, Facial Muscles,
Pharyngeal & Laryngeal muscles
 Ptosis & Diplopia w/ normal pupils
 Respiratory Trouble
 Mild Atrophy
 Normal sensory modalities & DTR’s
 Coexisting Thymoma
Motor Deficits

 Myasthenic Syndrome: AKA Lambert-Eaton Syndrome

– Pathophysiology
 Assoc w/ Tumor
 Cross reaction of tumor antibodies w/ voltage gated Ca2+ channels
– Clinical Features
 Proximal muscle weakness & EOM spared
 Dry mouth & Constipation
– Diagnosis
 EMG: ↑ response
 Serology: auto-antibodies to Ca2+ channels
Motor Deficits

 Muscular Dystophy
– Duchenne’s
 MC type & X-linked recessive w/ a male predilection
 Onset by 5 yoa (3-7 yoa) & Severely disabled by
adolescence
 Death in the 30’s
 Clinical Features
– Early: toe walking, waddling gait, inability to run
– Later: Pronounced proximal muscle weakness, Gower’s Sign,
Pseudohypertrophy of calves, Mental retardation, Serum CK
levels ↑, Absent dystophin
Motor Deficits

 Muscular Dystophy
– Becker’s
 X-linked recessive
 Onset by 11 yoa
 Death by the 40’s
 Clinical Features
– Similar pattern of muscle weakness to Duchenne’s
– No cardiac or mental retardation
– CK levels are high, but not as high
– Dystrophin levels are WNL