The Neuromuscular System and Spinal Cord

Abstract

Muscle tone, strength and movements are the product of a complex process orchestrated by the motor system, an elaborate network of multiple, hierarchically organized loops: the motor cortex (initiation of voluntary movement), lateral and medial descending motor tracts (conduction), basal ganglia (modulation), cerebellum (coordination), spinal cord (conduction and modulation), peripheral nerves (conduction), neuromuscular junction (signal transmission) and muscle (movement). The first or upper motor neuron originates from the primary motor cortex (precentral gyrus) and connects to the second or lower motor neuron in the spinal cord at the level of the respective spinal nerve roots.

Clinical Practices

Box 1 Characteristic Signs and Symptoms of Peripheral Neuropathy

• Absence of brain or spinal cord lesions as a cause of neurological deficits.

• Lower extremities more affected than upper extremities.

• Often asymmetrical (exception: “hand-and-glove” pattern in diabetic neuropathy).

• Often associated with decreased sensation (epicritic sensation impaired first).

• Paraesthesias and neuropathic pain are common.

• Rarely presents with acute weakness.

• Muscle tone and muscle stretch reflexes may be reduced.

• Dermatomal pattern of deficits suggests lesions of one peripheral nerve.

• Involvement of several peripheral nerves suggests plexus lesion.

• Chronic neuropathies often associated with trophic changes of the skin, hair and nails.

Box 2 Evaluating an Epidural Block and Recognizing Complications of Neuroaxial Anaesthesia/Analgesia

Assessing the adequacy of epidural analgesia:

• (Epidural) Analgesia is adequate if the patient feels mild or no pain. This does not require impaired temperature sensation. (NB: In these cases it is reasonable to reduce or stop the epidural infusion and review the patient later.)

• Ask the patient to take a deep breath and cough. Adequate epidural analgesia allows patients to do so without feeling pain or grimacing (watch the patient’s face!).

• Determine the level of epidural analgesia by the level of altered temperature sensation on both sides (e.g. using a wet and cold gauze or cold spray).

• For adequate analgesia, appropriate epidural segments must be covered:

  • Upper abdominal surgery (incl. oesophageal surgery): up to Th4–Th6

  • Lower abdominal surgery: up to Th6–Th8

  • Hip surgery: up to Th10

  • Lower extremity surgery: up to L1

  • Perineal surgery: S2–S5

Clinical signs of a high neuroaxial (epidural or spinal) block:

• Vasodilatory arterial hypotension (arterial hypotension with adequate peripheral perfusion and absence of skin mottling)

• (Relative) bradycardia

• Paraesthesia in small fingers

• Respiratory depression/difficulties to breath

• Impaired consciousness

Clinical signs of local anaesthetic toxicity:

• Light-headedness

• Perioral paraesthesias

• Metallic taste

• Confusion/agitation

• Seizures

• Tachypnoea

• Arterial hypotension

• Bradycardia

• Impaired consciousness

• Respiratory and/or cardiac arrest

Clinical signs of an epidural haematoma:

• An epidural haematoma occurs mostly on insertion or after removal of epidural catheter.

• Sudden localized back pain or radicular dermatomal pain.

• Paraesthesias.

• Early neurological deficits: paraesthesias and bowel and bladder dysfunction.

• Late neurological deficits: motor and sensory deficits.

Clinical signs of postdural puncture headache:

• Onset within 3 days after dural puncture

• Pulsating frontal and/or occipital headache radiating to the neck and shoulders

• Reported as “searing and spreading like hot metal”

• Pain exacerbated by head movements and upright position

• Nausea and vomiting

• Vertigo

• Hearing loss and tinnitus

• Cranial nerve VI palsy

Clinical signs of epidural abscess:

• May occur delayed after epidural catheter removal

• Fever

• Infection at the (former) insertion site (e.g. pus)

• Localized back pain or radicular dermatomal pain

• Early neurological deficits: paraesthesias and bowel and bladder dysfunction

• Late neurological deficits: motor and sensory deficits

Box 3 Distinguishing Common Causes of Neuromuscular Weakness in the Critically Ill

	ICU-acquired weakness	Guillain-Barré syndrome	Myasthenia gravis	Lambert-Eaton syndrome
Cardinal sign/symptom	Symmetrical weakness with absent or reduced muscle stretch reflexes following a period (e.g. 1–2 weeks) of critical illness	Progressive, ascending, symmetrical weakness with absent or reduced muscle stretch reflexes	Fluctuating skeletal muscle weakness (tiring) including ocular symptoms (ptosis and/or diplopia)	Slowly progressive, symmetrical muscle weakness
Distribution of muscular weakness	Legs more affected than arms, spares cranial nerves	Usually starts distally, predominantly in legs	Proximal, arms more often affected than legs	Proximal, affects arms and legs
Paraesthesias	Rare	Frequent (up to 80%)	Absent	Absent, but pain, cramps and uncomfortable muscular sensations may occur
Autonomic dysfunction	Rare	Frequent	Rare	Frequent, but mostly confined to sluggish pupillary light reflex and xerostomia
Specific comments	Starts after the onset of critical illness, often results in difficulties to wean a patient off the ventilator	Usually causes critical illness and rarely complicates critical illness	Progressive weakness after vigorous, brief muscle activation, improvement of ptosis after application of ice on the eyelid	Improvement of muscle strength and reflex responses after vigorous, brief muscle activation (e.g. 15 s of max. isometric muscle contraction)