Plegias

Central plegias are classified according to the affected limb:

• Monoplegia
  The complete paralysis affects only one limb, e.g. monoplegia of one arm.

• Paraplegia
  Both legs are completely paralysed; upper limbs (arms) are not affected.

• Hemiplegia
  Arm and leg of one side of the body are completely paralysed.

• Quadriplegia (tetraplegia)
  It involves a complete paralysis of all four limbs (arms and legs), and control over the torso and head is impaired.

In the case of central damage, the paralysis always affects the side opposite to the affected cerebral hemisphere. This means that damage to the right cerebral hemisphere paralyses the left side of the body and vice versa.

Causes of a plegia

Muscle paralysis is caused by damage along the course of the afferent nerve (upper or lower motor neuron). The nerve may be damaged, for example, by bleeding, infarction, inflammation, excessive pressure, or cuts. The conditions which may cause plegias are, for example:

• Stroke
• Traumatic brain injury
• Infantile cerebral palsy (early childhood brain damage)
• Multiple sclerosis
• Tetraplegia
• Herniated disc
• Carpal tunnel syndrome
• Tumours

Especially in the case of central causes, it is rare that only complete plegias, i.e. complete paralyses, occur. In most cases, the clinical presentation is a combination of complete paralyses (plegias) and incomplete paralyses (pareses), as is the case, for example, in tetraplegia with incomplete paralysis (Swiss Paraplegics Association 2012).

Diagnosis: plegia

Imaging techniques such as CT or MRI are used to diagnose a potential central plegia.

Paralyses are evaluated by testing the muscle strength. The clinical testing of muscle strength is carried out via assessments. The most common is the assessment with the help of the Medical Research Council (MRC), where 0 points represent a plegia.

If peripheral nerve damage is suspected, nerve or muscle information can be obtained by measuring nerve conduction velocity (NCV or electroneurography/ENG).

Electromyography (EMG), whereby needle electrodes are stuck into the muscle, enables the computer evaluation to provide an even more precise statement about the muscle condition of patients with injury-related atrophy (muscle wasting).

If clinical symptoms suggest a central cause of plegia, computed tomography (CT) or magnetic resonance imaging (MRI) may provide more information about the damage.

Progress of a plegia

The lack of contraction in the muscle due to the paralysis causes a reduction of muscle mass (atrophy) over time. It also causes abnormalities of the connective tissue (fibrosis) in muscle fibres and increased fat deposits.

Due to the lack of control by the brain in the case of central damage, patients with plegias often also develop spasticity (increased muscle tension) in the course of healing. For example, children with infantile cerebral palsy often have spastic monoplegia, paraplegia, hemiplegia or quadriplegia (tetraplegia). The spasticity in turn causes limited joint mobility, which may result in joint stiffness (contractures).

Rehabilitation for a plegia

In the case of complete paralysis, the cause cannot be corrected by classic physiotherapy, since the paralysed muscle can no longer be activated by the patient himself. This is why therapy with targeted functional electrical stimulation has proven successful. Special current waveforms combined with long pulse duration and low frequencies can address the muscle directly and cause it to contract. This may prevent muscle wasting and abnormalities of connective tissue (Kern et al. 2010), and can support nerve regeneration (Gordon et al. 2016).

Spasticity and joint stiffness, which occur after central paralyses, can be treated by a physiotherapist by means of stretching under weight and active movement exercises. In some cases, spasticity is also treated with botulinum toxin (Botox) injections into the affected spastic muscle groups. The targeted effect of the Botox neurotoxin can be improved by combining it with functional electrical stimulation (Cotoi et al. 2018).