Clinical Features of Guillain-Barre¢ Syndrome (McLeod, ND)
- Paresthesias in the hands and feet
- Back pain in approximately 30% of cases
- Depressed or absent tendon reflexes
- Progressive symmetrical weakness of the limbs
- Cranial nerves are affected (especially the facial nerves) in approximately 50% of cases
- Progression to peak disability in four weeks
Symptoms of Guillain-Barre¢ can range from mild to extreme. In mild cases, the patient may only have slight weakness in walking, requiring a cane or crutches. In the more extreme cases the weakness may progress to the point where the patient is almost totally paralyzed, possibly requiring mechanical ventilation. Ascending motor weakness can develop over 2-4 weeks, and can be acute or sub acute. This is followed by a gradual recovery period that could last weeks to many months. Most people will have complete recovery from even the most severe cases of GBS, but there are some patients that continue to have some residual weakness.
The main complaint is of weakness that varies widely in severity in different patients and often has a proximal emphasis and symmetric distribution. It usually begins in the legs, spreading to a variable extent but frequently involves the arms and often one or both sides of the face. Back pain is present in approximately 1/3 of GBS cases. The muscles of respiration or deglutition may also be affected. Cranial nerve deficits can be presented either alone or associated with limb weakness. Deep tendon reflexes are usually absent, while pupils and eyelids are often spared.
The paresis, weakness, and pain follow an ascending pathway, ultimately involving the upper extremities and the cranial nerves. Signs and symptoms are symmetrical and may or may not include a sensory component. Paraesthesias are initially described as tingling, prickling, pins-and-needles sensations followed later by needlelike and burning sensations.
Sensory nerves tell us about our surroundings; whether we are hurt; or if something is smooth or rough, hot or cold. Sensory symptoms are less common, but distal paresthesias and dysethesias are common. Neuropathy or radicular pain is present in many patients. The sensory disruptions are thought to be related to ectopic activity from damaged inhibitory neurons. Gradually muscle pain is experienced in the large muscles, such as the thighs, back and shoulders. Stiffness and cramping pain or deep aching muscle pain is common. As the sensory nerves are attacked the patient experiences loss or reduction of the sense of touch, or abnormal sensations such as burning, tingling, pins and needles, ants under the skin sensation or vibrations, and numbness.
Motor nerves control movement and damage to them results in partially or completely blocked signals. The body is affected when the damaged nerve loses its ability to function normally, resulting in reduced movement or coordination. The patient experiences this as a communication breakdown between what he wants to do and his ability to do it.
Autonomic nerves control the inner organs whose function is normally carried out automatically, such as secretion of hormones, heartbeat, urination, breathing, and vision. These functions may be disrupted resulting in arrhythmia, unstable blood pressure, blurred or double vision, dizziness, fainting spells, inability to regulate the body temperature, difficulty breathing, reduced ability to control the functions of the stomach, and digestive system. Loss of weight, vomiting after meals, reduced function of various glands, incontinence, and impotency may be seen. Autonomic disturbances are also common, may be severe, and are sometimes life threatening such as tachycardia, and pulmonary dysfunction. Other symptoms may occur such as sweating, facial flushing and impaired sphincter control. Cardiac dysrhythmias, abnormal hemodynamic response to drugs, and pupil dysfunction are common signs and symptoms of autonomic dysfunction.
Acute ventilatory failure is a common and devastating complication explained by the loss of motor innervation to skeletal muscles of the chest and diaphragm. With decreased inspiratory and expiratory capacities, coughing becomes ineffective, and the airway is compromised, leading to hypoxia, atelectasis, pneumonia, and aspiration. Aspiration occurs as a direct result of weakened laryngeal and glottis musculature. Airway obstruction occurs as a result of tongue and retropharyngeal weakness. Alveolar hypoventilation, along with impaired carbon dioxide levels also may occur. The patient is put at great risk, since the clinical signs of impaired respiratory function, such as hypercarbia, occur well before impaired respiratory function occurs. This is why it is important that serial measurements of respiratory parameters, including respiratory rate and pattern, (observing for paradoxical breathing and frequent changes in muscle use or use of accessory muscles) are completed along with frequent tidal volume, and vital capacity checks (McLeod, ND).
Possible life threatening symptoms of GBS that require close monitoring (McLeod, ND):
- Difficulty breathing (dyspnea) or taking deep breaths, breathlessness (SOB)
- Drooling, difficulty swallowing (dysphagia)
- Fainting spells (syncope)
Etiologies of other rapidly progressive weakness of muscles (McLeod, ND):
- Transverse myelitis
- Myasthenia Gravis
- Poliomyelitis
- Acquired hypokalemia
- Periodic paralysis
- Botulism
Other etiologies of Acute Polyneuritis (McLeod, ND):
- HIV
- Acute Intermittent Porphyria
- Vitamin B deficiencies
- Heavy metals and other toxins
- Lymphoma, Carcinoma
- Lyme disease
- Vasculitis
- Diphtheria
- Diabetes
