Exam Abnormalities

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Exam Abnormalities

• Part III

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Cerebellar Dysfunction

• Ataxia of limbs and gait, dysmetria,
  dysdiadochokinesis
• Vertigo, nystagmus
• Hypotonia
• Sensation not affected
• Normal or decreased DTRs

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Other Abnormalities

• Tremor (intention/dysmetria)
• During purposeful movements
• Decreased muscle tone deep tendon reflexes on
  affected side
• Ataxia (awkwardness of posture, gait and speech)
  - truncal, appendicular
• DD intoxication, loss of position sense

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Ataxia

• In ataxia due to loss of position sense, vision
  compensates for the sensory loss
• Positive Romberg Test
• In cerebellar ataxia, the patient has difficulty
  standing with feet together whether eyes are open
  or closed

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Basal Ganglia Thalamus

• Extrapyramidal signs
• Bradykinesia, shuffling gait, masked facies,
  rigidity
• Movement disorder
• Chorea, athetosis, tremor
• Unilateral or bilateral
• Sensation not affected
• DTRs normal or decreased

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Disorder of Muscle Tone- Paratonia

• Location both hemispheres, usually in the
  frontal lobes
• Gegenhalten (holding against sudden increase in
  tone making passive motion more difficult),
  mitgehen (sudden loss of tone that increases the
  ease of passive motion)
• Common cause dementia

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Disorder of Muscle Tone-Spasticity

• Location corticospinal tract UMN
• Hypertonia (increased muscle tone)
• Rate-dependent - greater tone with rapid passive
  movement, may give way suddenly (clasp-knife
  resistance)
• Greater tone at extremes of movement
• Common cause stroke- late or chronic

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Loss of Higher Control

• Decorticate posturing (flexed upper and extended
  lower extremity due to intact rubrospinal
  pathways)
• Decerebrate posturing (4-limb extension due to
  intact vestibulospinal tracts/loss of rubrospinal
  tracts)
• Opisthotonos
• Abnormal tonic neck reflexes

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Disorder of Muscle Tone-Flaccidity

• Location LMN at any point from anterior horn
  cell to peripheral nerves
• Hypotonia (loss of muscle tone)
• Limb is loose or floppy, may be hyper-extensible
  or flail-like
• Causes Guillain-Barré syndrome initial phase of
  SCI (spinal shock) or stroke PNS disease,
  cerebellar disease

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Changes in Tone

• With acute UMN lesions, flaccid paralysis with
  decreased tone and decreased reflexes is replaced
  in hours to weeks with increased tone and
  hyperreflexia

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Tone Abnormalities

• Spasticity increased resistance commonly worse
  at extremes of range
• Lead-pipe rigidity resistance that persists
  throughout range in both directions

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Spinal Cord Injury

• Sensory level (dermatomal) on trunk at lesion
  level, tract damage sensory loss below
• Loss of reflexes at involved cord level,
  hyperactivity below that level
• Weakness may involve both legs or all limbs (when
  damage is bilateral)
• Bowel and bladder signs, Babinski signs, leg
  spasticity, autonomic nervous system dysfunction

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Syringomyelia

• Expanded spinal cord central canal
• Loss of pain and temperature sensation (crossing
  spinothalamic fibers in the anterior commissure)
• Dissociated sensory loss (preservation of light
  touch)

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Anterior Spinal Artery

• Occlusion causes stroke in anterior two-thirds of
  the spinal cord
• Dense motor deficits
• Loss of pain and temperature sensation (preserved
  dorsal columns supplied by the posterior spinal
  arteries)

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Brown-Sequard

• Spinal cord syndrome typically due to injury -
  of loss to pain/temperature below the lesion,
  with loss to touch, pressure, position and
  vibration on the opposite side of the body

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Strength Abnormalities

• UMN weakness, hyperreflexia, increased tone no
  atrophy or fasciculations
• Disuse or deconditioning can reduce bulk by 1/3rd
• LMN weakness, atrophy, hyporeflexia,
  fasciculations (if denervation is active),
  decreased tone

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Central (UMN) Weakness

• Weakness greater in extensors of upper
  extremities, flexors of lower extremities
  (stroke or MS causing hemiplegia) supination
  weaker than pronation in the upper extremity
• vs. Extensor weakness in PNS disease Radial
  nerve damage

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Sensory Abnormalities

• Sensation to vibration is often the first
  sensation to be lost in a peripheral neuropathy
• Also lost in posterior column disease
• Vitamin B12 deficiency, tertiary syphilis
• Loss of position sense, like vibration, suggests
  posterior column disease or a lesion of the
  peripheral nerve or root

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Sensory Alterations

• Patients with sensory disturbances from diabetes,
  vitamin deficiency or neurotoxin damage can
  report loss of sensation, paresthesias (pins and
  needles sensation), or dysesthesias (pain) in the
  hands and feet (stocking-glove distribution)

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Other Sensory Terms

• Analgesia absence of pain sensation
• Hypalgesia decreased sensitivity
• Hyperalgesia increased sensitivity
• Anesthesia absence of touch sensation
• Hypesthesia decreased sensitivity
• Hyperesthesia increased sensitivity

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Sensory Loss

• Disturbance of cortical sensory function (intact
  primary modalities) indicates parietal lobe
  involvement
• Lesion(s) causing disturbance(s) of primary
  sensation may be along the pathways from the
  receptors in the skin/muscles/joints/tendons to
  the sensory cortex (cerebrum)

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Reflex Abnormalities

• Hyperactive Reflexes suggest CNS disease
  sustained clonus confirms it
• Reflexes may be diminished or absent when
  sensation is lost, when the rele-vant spinal
  segments are damaged, or when the peripheral
  nerves are damaged
• Muscle NMJ disease also may decrease

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Abnormal Reflexes

• Sustained clonus, spread, crossed adduction,
  clavicular-biceps, inverted radial reflexes,
  and/or Hoffmans sign signify hyperreflexia

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Clonus

• Clonus continued rapid flexion and extension
• A sharp downward displacement of the patella in
  the extended knee may elicit patellar clonus

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Babinskis Sign

• Abnormal extensor plantar response
• Scratch lateral aspect of foot
• Great toe extends, other toes fan
• Stereotypical/similar each time
• Distinguish from normal voluntary withdrawal
  reaction when too much pressure is applied
  (tickling)
• Normal in children younger than 2yrs

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Reflexes Clinical Pearls

• Children young adults tend to have brisk
  reflexes, especially if cold or anxious
• Augmentation/reinforcement may help to elicit
  reflexes when difficult to obtain (gritting
  teeth, making a fist)
• Frontal lobe release signs imply bilateral damage
  (grasp, suck, snout)

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Grasping
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Infants Cry

• Shrill or high-pitched increased ICP, infants
  born to narcotic-addict
• Hoarse hypocalcemia, congenital hypothyroidism
• Stridor upper airway obstruction, small larynx,
  tracheomalacia
• Absence of cry severe illness, vocal cord
  paralysis, profound brain damage

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Hearing Problems

• Parents impression of their babys auditory
  acuity usually is correct
• Hearing defects associated with LBW (lt1500
  grams), anoxia, treatment with ototoxic Rx
  (aminoglycoside antibiotics), exchange
  transfusion, congenital infection meningitis,
  hyperbilirubinemia

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Dysmorphism
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Sturge-Weber Syndrome

• Port wine stain affects the skin innervated by
  the ophthalmic portion of CN V
• Vascular network of the meninges ocular orbit
  also may be affected
• May see seizures, hemiparesis, mental
  retardation, glaucoma

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Sturge-Weber
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Head Circumference

• Delayed premature closure of the sutures
  (microcephaly)
• Familial, chromosomal abnormalities, congenital
  infections, maternal metabolic disorders,
  neurologic insults
• Too rapid macrocephaly
• Hydrocephalus, brain tumor, subdural

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Hydrocephaly

• Bulging anterior fontanelle
• Setting sun sign
• May be seen briefly in some normal newborns

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Fontanelle Abnormalities

• Increased ICP bulging fontanelle
• Obstructed CSF
• Infection, neoplasm
• Decreased ICP de-pressed fontanelle
• Dehydration
• Large posterior fon-tanelle hypothyroid

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Craniosynostosis

• Premature closure of one or more of the cranial
  sutures
• Saggital suture long, narrow head
• Parietal bones do not grow laterally to their
  full extent

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Plagiocephaly

• Asymmetry of the cranial vault
• Flattening of the occiput on the depen-dent side
  prominent frontal region on the opposite side
  (infant constantly lies on one side)
• Torticollis from injury to the SCM at birth, in
  the mentally physically handicapped in
  understimulated infants

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Postural Abnormalities

• Predominant extension of the extremities
• Constant turning of the head to one side
• Marked extension of the head, stiff-ness of the
  neck extension of the arms legs
  (opisthotonus)
• Intracranial infection or hemorrhage

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Abnormal Eye Movements

• Divergent strabismus (laterally deviated eyes) or
  alternating convergent strabismus persisting
  beyond 6 months or becoming unilateral sooner,
  may indicate ocular muscle weakness or diminished
  visual acuity

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Nonparalytic Strabismus

• Imbalance in ocular muscle tone
• May be hereditary and usually appears early in
  childhood

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Congenital Hemiplegia

• Unilaterally absent or diminished movement of an
  extremity
• Abnormal posturing
• Reflexes muscle tone may be normal

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Sensory Abnormalities

• Absence of withdrawal when a painful stimulus is
  applied to an extremity (flicking palm or sole
  with your finger) indicates anesthesia or
  paralysis
• Change in facial expression or cry changes
  without withdrawal paralysis
• Spinal cord lesion extremity withdraws
  reflexively no change in cry or facial expression

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Reflex Abnormalities

• Asymmetries or sustained clonus CNS disease
• Absence of automatisms in the neonate or
  persistence beyond their expected time of
  disappearance may indicate severe CNS dysfunction
  (suck or rooting reflexes)

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Abnormal Moro Reflex

• Persistence beyond 6 months is conclusive
  evidence of neurologic disease
• Asymmetrical upper extremity response
• Hemiparesis, injury to the brachial plexus or
  fracture of the clavicle or humerus
• Absence in one or both legs
• Low spinal injury, congenital hip dislocation

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Clues to CNS Disease

• Abnormal localized neurologic findings
• Failure to elicit expected infantile automatisms,
  late persistence of infantile automatisms, or
  re-emergence of vanished infantile automatisms
• Delays in reaching developmental milestones

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Other Clues

• Asymmetrical movements of the arms or legs at any
  time signal possibility of CNS or PNS deficits,
  birth injuries or congenital anomalies
• By 4 days after birth, tremors at rest signal CNS
  disease
• Hyperirritability in an infant implies
  encephalopathy

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Spastic Diplegias

• Variable dystonic spasms followed by hypotonia
  early in infancy
• Persistent clenched fists coupled with scissoring
  after the first few months
• Most common pattern of cerebral palsy in children
  born prematurely
• Usually from periventricular leukomalacia, from
  hypoxic-ischemic encephalopathy

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Cerebral Palsy

• Motor impairment from birth or shortly after
  (prenatal or perinatal)
• Spasticity, hypotonia, ataxia, dyskinesia
• Dyskinesia in the absence of spasticity suggests
  an underlying inborn error of metabolism
• Nonprogressive(static encephalopathy)
• More common in low weight, preterm

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Mental Retardation

• IQ lt 70
• Mild IQ 55-70 moderate 45-55 severe 25-50
• Family history of borderline IQ or mild
  retardation, genetic abnormality, inborn error of
  metabolism, infection, toxic exposure

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Autism Spectrum

• Autism impaired sociability, verbal non-verbal
  communication skills, restricted activities and
  interests stereotyped behaviors, rigid
  routines, failure to empathize or share with
  others
• Pervasive developmental disorders
• Full autism criteria not met

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Learning Disabilities

• Affect one or more cognitive skills reading
  (dyslexia), motor function (dysgraphia,
  dyspraxia), attention deficit disorder with or
  without hyper-activity (ADD or ADHD)