Flashcards in this deck (40)

• What is the effect on voluntary movement in a lower motor neuron (LMN) lesion?

  • Localized ipsilateral flaccid paralysis of a muscle or group of muscles supplied by the affected nerves.
  lmn motor
• What are the effects on reflexes, muscle tone, and muscle bulk in an LMN lesion?

  • Reflexes: decreased or lost (hyporeflexia or areflexia)
  • Tone: hypotonia or atonia (flaccidity)
  • Muscle bulk: marked atrophy due to loss of activity and loss of trophic effects

  
  reflexes atrophy
• What are fasciculations and what causes them?

  • Definition: Jerky, visible contractions of groups of muscle fibers.
  • Can be: felt and seen
  • Cause: Pathologic discharge of spinal motor neurons
  lmn fasciculation neurology
• What are fibrillations and what causes them?

  • Definition: Fine, irregular contractions of individual fibers, detectable electrophysiologically but invisible to the eye.
  • Cause: Denervation hypersensitivity of denervated muscles to circulating acetylcholine

  
  lmn fibrillation neurology
• What is the typical pattern of paralysis after an upper motor neuron lesion above the medulla?

  • Generalized contralateral paralysis of half of the body (contralateral hemiplegia)
  neurology motor
• After 2 weeks following an upper motor neuron lesion, which improvements occur and what gait does the patient use?

  • Improvement: gross movements of axial and proximal limb muscles improve (not regeneration)
  • Permanent loss: fine movements of distal muscles
  • Gait: circumduction
  • Cause: intact ipsilateral corticospinal fibers terminating on medial a cells mediate gross movements
  recovery gait
• What characterizes clasp-knife spasticity in upper motor neuron lesions?

  • Initial high resistance to passive stretch followed by sudden loss of resistance due to activation of an oversensitive Golgi tendon organ

  
  neurology spasticity umn
• What is clonus and where is it commonly tested?

  • Repeated cycles of stretch–inverse stretch reflex in a hyperreflexic muscle; commonly tested as patellar clonus (knee) and ankle clonus (ankle)

  
  neurology reflexes umn
• Why does an affected muscle show minimal (disuse) atrophy in an upper motor neuron lesion?

  • Because voluntary activity is lost while reflex activity is exaggerated
  • Trophic effects on muscle metabolism are preserved since the lower motor neuron supply is intact
  neurology umn atrophy
• What are the key contrasting features of chronic UMNL versus LMNL regarding laterality, muscle tone, reflexes, clonus, and atrophy?

  • Chronic UMNL: Contralateral; spastic paralysis; increased tone; hyperreflexia; clonus present; disuse atrophy on long term
  • LMNL: Ipsilateral; flaccid paralysis; decreased tone; hyporeflexia; clonus absent; immediate denervation atrophy
  neurology umn lmn reflexes
• What are the facial findings in an upper motor neuron lesion of the corticobulbar tract?

  • Upper face is spared
  • Lower face is affected
  • Contralateral effects
  umn facial
• What are the facial findings in a lower motor neuron facial nerve lesion (facial palsy)?

  • Upper face is affected
  • Lower face is affected
  • Ipsilateral effects

  
  lmn facial
• Examine the photograph:

  Which side shows facial paralysis and what are the visible signs?

  • Left-sided facial paralysis
  • Drooping mouth
  • Partially closed eye
  neurology facial motor
• Examine the photograph:

  Which side shows facial paralysis and what are the visible signs?

  • Right-sided facial paralysis
  • Drooping mouth
  • Inability to close the eye
  neurology facial motor
• What is muscle tone and which muscles does it mainly affect?

  • Muscle tone: a state of sub-tetanic continuous contraction of skeletal muscle caused by the static component of the stretch reflex.
  • Mainly affects antigravity muscles (flexors of upper limbs; extensors of lower limbs; neck and trunk extensors; elevators of lower jaw).
  tone antigravity physiology
• Name the two major types of hypertonia and one key clinical difference between them.

  • Spasticity: initial resistance followed by sudden release (clasp-knife); caused by upper motor neuron lesion.
  • Rigidity: maintained resistance throughout movement (lead-pipe or cog-wheel); associated with lesion in substantia nigra.

  
  hypertonia spasticity rigidity
• Compare the site of lesion and upper limb posture in decorticate versus decerebrate posturing.

  • Decorticate: lesion in the upper midbrain (above superior colliculus); upper limbs flexed and adducted
  • Decerebrate: lesion in lower midbrain (between colliculi) or upper pons; upper limbs extended

  
  posturing localization neurology
• List the main causes of hypotonia (flaccidity) from loss of excitatory supraspinal control of static muscle stretch reflex.

  • Neocerebellar (cerebellar) lesions
  • Chorea
  • Lower motor neuron lesion (e.g., tabes dorsalis, polyneuritis, myasthenia gravis)
  • Acute stage of upper motor neuron lesion
  • Lesion of area 4
  • Increased serum Ca++ level
  hypotonia causes motor
• What is mononeuropathy and what are its main effects?

  • Definition: Lesion of a peripheral nerve.
  • Effects: Loss of all sensations in the area supplied by the affected nerve and motor affection in muscles innervated by that nerve.
  mononeuropathy peripheral
• What is polyneuropathy and what are common acquired causes?

  • Definition: Lesion of multiple peripheral nerves that supply the distal parts of upper and lower limbs.
  • Acquired causes: Metabolic disorders (e.g. Diabetes mellites), Physical injury (trauma) to nerves, Tumors, Toxins, Autoimmune responses, Nutritional deficiencies (e.g. vitamin B12), Alcoholism, Vascular.

  
  polyneuropathy peripheral
• What are the sequential sensory changes in peripheral parts (hands and feet)?

  • Numbness, tingling, pricking sensations (paresthesia)
  • Then, hypoesthesia (diminished all sensations)
  • Then, anesthesia (loss of all sensations)
  • Distribution: gloves and stockings sensory loss

  
  sensory peripheral
• What are the motor features of a lower motor neuron lesion (LMNL) in peripheral limbs?

  • Muscle weakness (paresis)
  • Then, paralysis of muscles
  • Loss of reflexes of muscles
  • Muscle wasting (atrophy)
  motor lmn
• What is syringomyelia and which spinal segments are commonly affected?

  • Definition: A cyst or glial tissue/fluid accumulation that enlarges and causes cavitation around the central canal of the spinal cord.
  • Common segments: Cervical (may extend to thoracic and medulla oblongata).
  syringomyelia spinalcord definition
• What are the characteristic sensory, motor, and autonomic effects of a central cord (syringomyelia) lesion?

  • Sensory: Bilateral loss of pain and temperature in a 'jacket/cape' distribution due to damage to crossing spinothalamic fibers; dorsal column touch preserved (dissociated sensory loss).
  • Motor: LMN signs from anterior horn cell damage; UMN signs from corticospinal tract damage.
  • Autonomic: Lateral horn damage causing autonomic dysfunction, commonly Horner's syndrome.

  
  syringomyelia sensory motor autonomic
• What is Tabes Dorsalis and its common cause?

  • Tabes Dorsalis: atrophy of dorsal roots of the spinal cord central to the DRG, commonly affecting lumbosacral segments
  • Cause: a complication of neurosyphilis
  neurology tabes neurosyphilis
• What are the key sensory and motor consequences of late-stage Tabes Dorsalis?

  • Sensory: loss of all sensations in affected dermatomes; first lost = vibration; last lost = slow pain
  • Coordination: sensory ataxia requiring vision; stamping (steppage) gait
  • Motor: decreased or absent reflexes from deafferentation
  tabes sensory reflexes
• What clinical features define an Argyll-Robertson pupil?

  • Loss of pupillary light reflex
  • Pupil size and near response preserved
  neuro ophthalmology pupils
• What are the main motor and sensory deficits in Brown-Séquard (hemisection) syndrome?

  • At the level: LMN flaccid paralysis with loss of reflexes; loss of all sensations in the affected dermatome
  • Below the level: Ipsilateral UMN spastic paralysis and loss of dorsal column sensations; contralateral loss of spinothalamic sensations

  
  neuro spinal brown-sequard
• Name common causes of complete transection of the spinal cord.

  • Gunshot injuries
  • Dislocation of spine
  • Vascular accident
  spinalcord causes
• What are the sensory and voluntary motor effects of complete spinal cord transection, and how does lesion level affect paralysis?

  • Sensory: complete, permanent loss of all sensations below lesion (damaged sensory tracts lack neurilemma).
  • Voluntary motor: complete, permanent loss of voluntary movements below lesion (paralysis).
  • Level examples:
  • Above C5: fatal (respiratory failure).
  • Below C5 (cervical): quadriplegia; diaphragmatic breathing.
  • Mid-thoracic: paraplegia; upper limbs intact.
  spinalcord effects
• What is the definition of spinal shock?

  • Complete loss of all reflexes below the level of the lesion.
  neurology spinalshock
• What are the key manifestations of spinal shock?

  • Loss of stretch reflex, atonia, areflexia, flaccid muscles
  • Loss of flexor withdrawal and superficial reflexes
  • Loss of autonomic reflexes causing bladder/rectum retention and overflow dribbling
  • Loss of vasomotor tone with hypotension
  • Cyanosed, cold, dry paralyzed limbs; bedsores; muscle atrophy; bone demineralization with hypercalcemia
  neurology manifestations
• What routine care measures reduce the risk of complications during the stage of spinal shock?

  • Physiotherapy to prevent muscle atrophy
  • Antibiotics to resist infections of bedsores
  • Frequent mobilization in bed to avoid bed sores
  • Good nutrition
  • Urinary catheter and rectal enema

  
  spinalshock care bedsores
• What serious outcome can result from inappropriate care during the stage of spinal shock?

  Severe bedsores and urinary tract infections can cause toxemia that depresses CNS functions, including vital centers, which may lead to death.
  spinalshock complications toxemia
• Name one mechanism that can cause recovery of reflex excitability after spinal shock.

  • Development of denervation hypersensitivity by remaining spinal neurons, enabling them to respond to afferent stimulation
  spinal reflexes
• How does bladder function behave during recovery of reflexes after spinal shock?

  • Automatic bladder evacuation similar to infants: fills to about 150 ml then reflexive evacuation without voluntary control
  spinal autonomic
• What stimuli can elicit the mass reflex after spinal cord injury and what are its main immediate responses?

  • Stimuli: scratching skin over lower limbs or anterior abdominal wall
  • Immediate responses: spasm of flexor muscles in both limbs; evacuation of rectum and bladder; profuse sweating below lesion; contraction of abdominal muscles; erection; elevation of ABP
  neuro spinalcord massreflex
• What mechanisms explain the mass reflex, and what later motor changes may follow?

  • Mechanisms: denervation hypersensitivity; release from inhibitory gamma motor neurons; increased spinal collaterals causing irradiation and reverberation
  • Later changes: increased extensor tone (paraplegia in extension); flexor withdrawal with crossed extensor reflex; return of infantile reflexes (grasp, positive Babinski)
  mechanism spasticity neurophysiology
• What is the primary cause of Thalamic (E-) syndrome?

  • Hematoma or thrombosis of the thalamo-geniculate artery
  thalamus etiology neurology
• What are the main immediate and delayed sensory manifestations of Thalamic (E-) syndrome?

  • Immediate: Crossed hemi-anesthesia; secondary hyperalgesia; sensory ataxia
  • Delayed: Crude sensation recovery with poor localization; fine sensation never recovers; secondary hyperalgesia; paroxysmal pain attacks; thalamic hyperpathia; emotional disturbances; motor ataxia
  thalamus sensory clinical