Limb Weakness

Limb weakness results from damage to the motor system at any level from the motor cortex to muscle.

UPPER MOTOR NEURON WEAKNESS

MUSCLE TONE

Hypertonicity develops after a period (a few days or weeks) of 'neural shock'. Passive movements produce a 'clasp knife' quality, i.e. sudden 'give' towards the end of movement. Clonus - present.

MUSCLE FASCICULATION

Absent.

MUSCLE WASTING

Absent - but, in the long term, disuse atrophy results.

REFLEXES

- Tendon - exaggerated.

- Superficial - depressed or absent

(abdominal, cremasteric).

- Plantar response - extensor.

MOTOR CORTEX

Corticobulbar V t/^TK tract

MIDBRAIN

Somatotopic arrangement

DISTRIBUTION

In general, whole limb or limbs are involved, e.g. monoplegia, hemiplegia, paraplegia.

Weakness shows a PREDILECTION for certain muscle groups in a PYRAMIDAL DISTRIBUTION, i.e.

Somatotopic arrangement

PONS VII nerve

MEDULLA

X, XI, XII nerves upper limbs - extensor weakness lower limbs - flexor weakness

flexor weakness

Lateral cortico spinal tract

MOTOR CORTEX

MIDBRAIN

PONS VII nerve

MEDULLA

X, XI, XII nerves

SPINAL CORD

The anterior corticospinal tract carries only 20% of thfi descending fibres and decusssates at segmental level.

extensor weakness

Decussation

SPINAL CORD

The anterior corticospinal tract carries only 20% of thfi descending fibres and decusssates at segmental level.

This results in the 'spastic' posture with the arm and the wrist flexed and the leg extended. In upper motor neuron lesions, SKILLED movements, e.g. fastening buttons, are always more affected than unskilled movements.

N.B. Dual innervation from each hemisphere results in sparing of the upper face, muscles of mastication, the palate and tongue with a unilateral upper motor neuron lesion.

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