Where is the legion?

 Motor Problems

Upper vs Lower Motor neuron problems

  • Upper (i.e. spinal cord/brain)
    • Pyramidal Weakness
      • Flexion and pronation is stronger than extension/supination in the upper limb
      • Extension is stronger than flexion in the lower limb
    • Hyperreflexia
    • Hypertonia
      • Spasticity (velocity-dependent)- pyramidal defect
        • Noticable most in elbow extension and supination / Knee flexion
      • Rigidity (non-velocity dependent)- basal ganglia defect (most commonly)
        • Lead pipe- resistance throughout
        • Cog-wheel (rigidity + tremor)- intermittant rigidity
  • Lower
    • Weakness
      • May be of a particular nerve or root distribution

      • Lower motor neuron weakness may also be global
    • Hyporeflexia
    • Fasciculations (due to spontaneous discharge from anterior horn cells causing muscle twitch)
    • Muscle wasting (again may be myotomal or nerve distribution
Blue- UMN
Green- LMN

Lesions of the Visual system

Visual pathway and field cuts

  1. Lesion of the optic nerve- blind in one eye
  2. Lesion of the optic chiasm- bitemporal hemianopia (crossed fibres are interrupted- temporal vision)
  3. Lesion of the optic tract- homonymous hemianopia
  4. Lesion of the temporal optic radiation- upper quadrantanopia (contralateral)
  5. Lesion of the parietal optic radiation- lower quadrantanopia (contralateral)
  6. Lesion of the occipital cortex- homonymous hemianopia (with macular sparing)
    1. NB Macular sparing may occur (there is debate as to why- ?large cortical representation, ?different blood supply, ?a shift in ocular fixation)

Lesions of the Cerebellum

  • Midline lesion:
    • Disturbance of postural control.  Patient will tend to fall over when standing or sitting despite preserved limb coordination (Romberg test)
  • Unilateral hemispheric lesion
    • Disturbance of coordination in limbs.  Can result in intention tremor and unsteady gait in the absence of weakness or sensory loss.
      • NB lesions will affect the ipsilateral side of the body (in contrast with those in the motor/sensory cortex
  • Bilateral cerebellar dysfunction
    • Results in slow, slurred speech (dysarthria), bilateral incoordination of the arms and a staggering, wide based gait.

Lesions of the Brainstem

Quick review of anatomy (useful)

  • Rule of 4s
    • 4 Midline structures beginning with M
      • Motor Pathways; Medial Lemniscus System; Medial Longitudinal Fasciculus; Motor nucleus nerve (see rule 2)
    • 4 Medial Motor Nuclei
      • CN (n) where n is a divisor of 12 (i.e. 3, 4, 6, 12)
      • The rest (5, 7, 9, 10, 11) are lateral
    • 4 Side structures beginning with S
      • Spinocerebellar; Spinothalamic; Sensory nucleus and sympathetic pathways
    • Cranial nerves are split into groups of 4 with structure
      • CN I-IV are above pons; CN V-VIII are pons; CN IX-XII are medulla

Symptoms

Lesions of the Brain

Following a head injury, a 49-year old male presents with personality change, intellectual impairment and urinary incontinance.

  • This is likely to a bilateral frontal lobe lesion
    • head injury is usually to the occiput or forehead- the frontal lobe is most likely to be injured in both of these situations
    • the frontal lobe is responsible for personality and cognition.  If both sides are affected, urinary incontinence is also a symptoms.

Following a stroke, a 72-year old man has a pure expressive aphasia.

  • This is likely to be a frontal lobe (left-sided) lesion (in particular the inferior frontal gyrus)
    • An expressive (or motor) aphasia is caused by damage to Broca’s area in the inferior frontal gyrus
      • this is compared to a receptive (sensory) aphasia that occurs with damage to Wernicke’s area in the posterior part of the superior temporal gyrus
    • the damage is usually on the dominant side

A 73-year old female presents with sudden onset receptive aphasia, acalculia, agraphia and has a right sided homonymous field defect.

  • This is likely to be a left sided temporo-parietal lesion
    • As mentioned above, a receptive aphasia is caused by damage to the superior temporal gyrus
    • The dominant parietal lobe is also responsible for mathematical thinking and writing (hence the agraphia and acalculia)
    • The hemianopia is caused by interruption of the optic radiations that travel through the parietal (fibres from superior retina i.e. inferior visual field) and temporal (fibres from the inferior retina i.e. superior visual field)

An 82-year old man presents with increasing confusion, an inability to recognise familiar faces and has a left sided homonymous field defect.

  • This is likely to be a right sided temporal lesion.
    • The non-dominant temporal lobe is responsible for spacial (and particular facial) recognition.

A 77-year old female presents with sudden onsetvisual lossand is noted to have cortical blindness.  Her pupillary reflexes are normal, as is fundoscopy.  She also seems to react to intimidating visual cues.

  • Likely to be a bilateral occipital lobe lesion.

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