chapter 5 handouts

8/8/2019 Chapter 5 Handouts

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Motor Deficits

Examination: Muscle Tone:

Assessment: Observation of extremities @ rest Palpation of the muscle belly Determination of resistance to passive stretch &

movement


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Motor Deficits


H ypertonia: Spasticity: inc tone

Arms: Flexors > ExtensorsLegs: Flexors < Extensors

C lasp-Knife Phenomenond/t an UMN lesion; e.g. stroke


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Motor Deficits


H ypertonia: Rigidity: inc resistance to passive movement

L ead-Pipe Rigidity AKA C og-Wheeld/t extra-pyramidal dysfunction lesion of the basal

ganglia; e.g. Parkinsons


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Motor Deficits


H ypotonia: excessive floppiness d/t reduced resistanceto passive movement

Distal portion of the extremity is easily waved H yperextension of the joints is possible

Muscle appears flat & less firm d/t LMN lesion or a primary muscle disorder i.e. NMJ

disorder


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Motor Deficits


Paratonia: t h e patient is unable to relax w h en 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


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Motor Deficits

Examination: Muscle Power:

Dysfunction in muscle power can result from an UMN or LMN lesionDistribution of weakness distinguishes between an UMNor LMN lesion

UMN: Arms: Ext/Abd > Flex/AddLegs: Ext/Abd < Flex/Add

LMN: affects only t h e supplied muscles


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Motor Deficits


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 lesionProximal Distribution: myopat h ic disorder Distal Distribution: LMN disturbance


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Motor Deficits


Assessment: General Terminology:

Monoplegia/MonoparesisH emiplegia/ H emiparesis

Paraplegias/ParaparesisQuadriplegia/Quadriparesis


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Motor Deficits


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 Trace0 No contraction


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Motor Deficits

Examination: C oordination:

Mainly controlled by the cerebellumTests:

Finger to Nose H eel Shin Rapid Supination/pronation


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Motor Deficits

Examination: C oordination:

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


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Motor Deficits

Examination:

Tendon Reflexes: Areflexia: lost or depressed reflexH yperreflexia:

Occurs w/ an UMN lesion C lonus: a series of rythmic reflex after stretch of the

muscle Sustained C lonus: 3-4 beats - pathological


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Motor Deficits

Examination:

Tendon Reflexes:Reflex Asymmetry:

L ateralized Asymmetries:UMN Lesion BriskLMN Lesion Depressed

F ocal Reflex: Assoc w/ NR, Plexus, or PN lesions, e.g. unilateralloss of the Knee-Jerk

L oss of Distal Reflex:Polyneuropathies

Proximal reflexes are preserved


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Motor Deficits

Examination:

Tendon Reflexes:Pathological Reflexes:

Babinski: dorsiflexion of great toe & toe flaringd/t an UMN lesion involving the contralateral motor cortex or corticospinal tract


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Motor Deficits

Examination:

G ait: 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


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Motor Deficits

Examination:

G ait:Circumducted Gait:

Unilateral One leg swings around when walking while the ipsilateral

arm is flex and adducted

d/t corticospinal lesionsScissor-Like Gait:

Bilateral Knees are close together and the legs move in a scissor-

like motion

d/t corticospinal lesions


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Motor Deficits

Examination:

G ait: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 Parkinsons signs


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Motor Deficits

Examination:

G ait:Festinating Gait:

d/t an extra-pyramidal lesion Parkinsons 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


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Motor Deficits

Clinical Correlation

Upper Motor Neuron LesionsWeakness/ParalysisSpasticityH yper-reflexia+ BabinskisLittle to no atrophy


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Motor Deficits


Lower Motor Neuron LesionsWeakness/ParalysisH ypotoniaH ypo-reflexia or AreflexiaMuscle Wasting & fasciculation


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Motor Deficits


Cerebellar DysfunctionH ypotoniaH ypo-reflexia or Pendular DTRs

AtaxiaGait DisturbanceImbalance

Assoc Eye movement disordersDysarthria


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Motor Deficits


Neuromuscular Transmission DisordersWeaknessNormal or Reduced ToneNormal or H ypo-reflexiaNo sensory changes


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Motor Deficits


Myopathic DisordersWeaknessNo muscle atrophy or wastingNo change in DTRs until advanced stagesNo sensory changes


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Motor Deficits

Spinal Cord Disorders Cord lesions can lead to motor, sensory, or sphincter

disturbances and changes in muscle toneMotor:

Above C5: ipsilateral h emiparesis or bilateral quadriparesis Lower Cervical: UE only partially involved Below T1: L E only involved

Sensory Posterior Columns: ipsilateral loss of position & vibratory

sensations Spinothalamic Tracts: contralateral loss of pain & temp


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Motor Deficits

Spinal Cord Disorders Cord lesions can lead to motor, sensory, or sphincter

disturbances and changes in muscle toneSphincter

Conus Medullaris Syndrome: d/t T12 compression injury Cauda Equina Syndrome: d/t N R compression below L 1

Muscle Tone: Spasticity is common w/ UMN lesions and occur below the level

of the lesion in pts w/ myelopathies


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Motor Deficits

Traumatic Myelopathy

Total Cord Transection:Immediate & permanent paralysis & loss of sensationbelow the level of the lesionReflexes: absent initially but return over timeProgression

Acute Stage: Spinal Shock S/s more like LMN lesion Weeks After: S/s more like U MN lesion

C linical Pearl Flexor or Extensor Spasms of the Legs


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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


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Motor Deficits

Demyelinating Myelopathies

Role of MyelinProvides insulation for axonsNecessary for conductionComposed of tightly wrapped lipid bilayersFormed by Schwann cells in the PNSFormed by Oligodendrocytes in the CNS


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Motor Deficits


Multiple SclerosisOne of the most Neurological Disorders300,000 pts in the USH ighest incidence in ages 20-40Female predilection by 2xThere is increase in the incidence of the MS with thegreater distance away from the equator


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Motor Deficits


Multiple SclerosisPathology:

Inflammatory relapsing or progressive disorder of CNSwhite matter

Cause: idiopathic


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Motor Deficits


Multiple SclerosisClinical Features

Sensory symptoms: M C manifestationN umbnessParest h esias

Dysest h esiasHyperest h esiasS ensory C ord S yndromeUseless Hand S yndrome


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Motor Deficits



Pyramidal Tract Dysfunction

Visual Disturbance:

O ptic N euritis

Cerebellar Dysfunction:Dysdiadoc h okinesia


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Motor Deficits



MiscellaneousSymptoms fluctuate & are made worse by exercise or elevation of body temperature

Urinary DifficultiesConstipationCognitive Disorders

Affect DisordersFatigue


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Motor Deficits


Multiple SclerosisCourse

Relapsing-Remitting: 85% 2o Progressive: 85% after 25 yrs 1o Progressive: 10%

Progressive-Relapsing: Rare


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Motor Deficits


Multiple SclerosisDiagnosis 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 clinicalattack

2. 2 Clinical episodes, but only 1 lesion


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Motor Deficits

Cervical Spondylosis

Accumulation of degenerative changes in thecervical spine, which become clinically relevantwhen they cause pain or neurologicaldysfunction

Degenerative Changes:

Loss of disc heightBulging or herniationOsteophyte & hypertrophic changes of facetsH ypertrophy of the LF


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Motor Deficits


PathophysiologyDistorted & flattened spinal cordsDemyelination of Lateral & Posterior ColumnsCentral Gray Matter


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Motor Deficits


Clinical FeaturesOnset of S/S is usually insidiousCN Exam WNLUpper Extremity CROM

NP & Radiculopathy Mild weakness, brisk reflexes w/ myelopathy If NR involvement:


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Motor Deficits


Clinical FeaturesLower Extremity: Weakness Common Spastic Tone Sensory Loss

Bowel & Bladder dysfunction uncommon


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Motor Deficits

Cord Tumors

ClassificationIntramedullary: M ake up 10% Ependymomas: M C Gliomas

Extramedullary: M ake up 9 0%

Neurofibromas Meningiomas


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Motor Deficits

Cord Tumors

Clinical FeaturesSigns: Localized spinal tendorness LMN deficits if ant roots are involved Dermatomal sensory changes w/ post root involvement

UMN LesionsSymptoms: (Table 5-9) Pain Motor Dysfunction Sensory Disturbance

Sphincter Dysfunction


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Motor Deficits

Anterior H orn Cell Disorders

Characterized by LMN S/S Motor Neuron Disease in Adults

Onset 30-60 yoa w/ a male predilectionClassification Progressive Bulbar Palsy Pseudobulbar Palsy Progressive Spinal Muscular Atrophy Primary Lateral Sclerosis Amyotrophic Lateral Sclerosis


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Motor Deficits


Motor Neuron Disease in AdultsClassification Progressive Bulbar Palsy

Bulbar ( brainstem) paralysis predominatesCN dysfunction

Death w/I 1-3 yrs Pseudobulbar Palsy

d/t an UMN Lesion RareLower CN dysfunction


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Motor Deficits


Motor Neuron Disease in AdultsClassification Progressive Spinal Muscular Atrophy

LMN disorder primarilyProgression occurs from the UE LE - generalized

Primary Lateral SclerosisPure UMN disorder Rare

Amyotrophic Lateral Sclerosis AKA Lou Gerigs DiseaseMixed UMN & LMN disorder


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Motor Deficits

Nerve Root Lesion

Lumbar Disk ProlapseLBP & Radiculopathy in L5 & S1Decreased L-ROMParaspinal Muscle H ypertonicity

Cervical Disk ProlapseNP & Radiculopathy in the armsInc pain w/ C-ROMLateral HerniationC entral Herniation


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Motor Deficits

Traumatic Avulsion of Nerve Roots

Erb-Duchenne Paralysis: Avulsion of C5/C6Causes: birth & traumaClinical Features Loss of shoulder abduction & elbow flexion

Klumpkes Paralysis: Avulsion of C8/T1Causes: fall & grabClinical Features Wasting of intrinsic muscles of the hand


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Motor Deficits

Traumatic Avulsion of Nerve Roots

Cervical Rib Syndrome: C8/T1 InvolvementClinical Features Similar to Klumpkes Paralysis Weakness & wasting of the intrinsic muscles of the

hands

Pain & numbness in the hands


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Motor Deficits

Myasthenia Gravis

PathophysiologyBlock of Ach receptors Associated Conditions

Thymic Tumor ThyrotoxicosisRheumatoid ArthritisDisseminated Lupus Erythematosis


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Motor Deficits

Myasthenia Gravis

Clinical FeaturesInsidious onsetFluctuating weaknessPredilection for: EOM, Muscles of Mastication, FacialMuscles, Pharyngeal & Laryngeal muscles

Ptosis & Diplopia w/ normal pupilsRespiratory TroubleMild AtrophyNormal sensory modalities & DTRsCoexisting Thymoma


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Motor Deficits

Myasthenic Syndrome: AKA L ambert-Eaton Syndrome

Pathophysiology Assoc w/ Tumor Cross reaction of tumor antibodies w/ voltage gated Ca 2+channels

Clinical FeaturesProximal muscle weakness & EOM sparedDry mouth & Constipation

DiagnosisEMG: response

Serology: auto-antibodies to Ca2+

channels


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Motor Deficits

Muscular Dystophy

DuchennesM C type & X-linked recessive w/ a male predilectionOnset by 5 yoa (3-7 yoa) & Severely disabled byadolescenceDeath in the 30s

Clinical Features Early: toe walking, waddling gait, inability to run Later: Pronounced proximal muscle weakness, Gowers Sign,

Pseudohypertrophy of calves, Mental retardation, Serum CKlevels , Absent dystophin


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Motor Deficits

Muscular Dystophy

BeckersX-linked recessiveOnset by 11 yoaDeath by the 40sClinical Features Similar pattern of muscle weakness to Duchennes No cardiac or mental retardation CK levels are high, but not as high Dystrophin levels are WNL

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