Weakness

Published on 10/04/2015 by admin

Filed under Neurology

Last modified 22/04/2025

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Weakness

Weakness is a common symptom and a commonly elicited sign on neurological examination. Weakness arises from lesions at every level of the nervous system. This produces:

different types of weakness reflecting the element of the nervous system that is impaired (Fig. 1)

different distributions of weakness reflecting the way in which the nervous system is organized.

Fig. 1 Sites of lesions and resulting weakness.

As with all neurology, the time course of the development of the weakness, which comes from the history, is most important in understanding its aetiology. Sometimes patients complain of weakness when they mean something else, for example fatigue. Similarly, other abnormalities can be mistaken for weakness on examination (Box 1).

Box 1 Weakness that is not there

Patients may appear weak when they are not, if:

they do not understand what you want them to do (altered higher function)

they are slow to initiate movements (bradykinesia as in Parkinson’s disease)

they are not sure where their affected limb is (with marked loss of proprioception)

the movement produces pain (arthritis).

Type and distribution of weakness (Table 1)

Upper motor neurone weakness

Lesions to the brain, brain stem and spinal cord produce upper motor neurone signs:

Increased tone (spasticity).

Brisk reflexes.

Extensor plantars.

Table 1 Types of weakness and possible causes

Weakness	Possible causes
Hemiplegia	Stroke Multiple sclerosis Tumour Subdural haematoma Trauma

Brain stem syndrome

Multiple sclerosis

Spinal cord syndrome

Multiple sclerosis

Cauda equina syndrome

Inflammatory lesion

Neuropathy See pages 102–105

They produce a pyramidal distribution of weakness which particularly affects the extensors in the arms and flexors in the legs. With severe pyramidal weakness, the position assumed is flexed arms and extended legs.

It may not be possible to elicit the plantar response with a severe weakness. Muscles can thin in longstanding upper motor neurone lesions reflecting inactivity.

The distribution of the weakness reflects the site of the lesion (Fig. 2). Broadly speaking, hemisphere or brain stem lesions produce contralateral weakness affecting a combination of the face, arm or leg depending on the site. There are usually other signs, either with disturbance of higher function speech or cranial nerve signs or sensory signs, to help locate the lesion.

Fig. 2 Distribution of weakness.

Spinal cord lesions either produce unilateral or, more commonly, bilateral lesions below the level of other lesions. There are usually sensory signs to help in localization.

Lower motor neurone lesions

Lesions of the lower motor neurone, anterior horn cell nerve root or peripheral nerve produce lower motor neurone signs:

Wasting – this takes weeks to develop.

Loss of reflexes.

Muscles that are wasting may develop fasciculations – spontaneous discharge of motor units.

The distribution reflects the pattern of lower motor neurone involvement. A generalized neuropathy can produce generalized weakness, though a distal weakness is more common (p. 102). Nerve root lesions and peripheral nerve lesions produce changes within the distribution of the nerve or root (pp. 82, 106). Usually there are associated sensory signs.

One important pattern of lower motor neurone weakness is the weakness of both legs, particularly of recent onset. This reflects a cauda equina lesion. This is usually associated with sensory and sphincter signs (p. 83).

Anterior horn cell disease produces prominent wasting and fasciculation with normal sensation. Some conditions produce upper and lower motor neurone signs. These include cervical and spine disease where spinal cord compression produces upper motor neurone signs, and where root compression produces lower motor neurone signs. There are usually associated sensory signs (pp. 80–84). Motor neurone disease (amyotrophic lateral sclerosis; ALS) produces a mixture of upper motor and lower motor neurone signs without sensory loss (p. 108).

Neuromuscular junction weakness (p. 110)

This is uncommon and is usually due to myasthenia gravis. It is characterized by prominent, variable and fatiguable weakness. Muscle bulk, tone and reflexes are normal. Ocular muscles, bulbar muscles, neck, trunk and the small muscles of the hand are particularly affected. There are no sensory impairments.

Muscle weakness

This can usually be distinguished from lower motor neurone weakness as there is less muscle wasting, with preserved reflexes until there is severe weakness. Sensation is normal.

Muscle disease produces weakness in several distributions. Indeed, this pattern of distribution has founded the basis of clinical classification (p. 112). However, most commonly it produces proximal limb weakness.

Non-neurologically determined weakness

This is the most difficult type of weakness to assess. This can reflect limitation because of pain, for example arthritis. However, with encouragement, full power can usually be sustained, even if only briefly.

Non-neurologically determined weakness usually has a collapsing quality where the patient gives way suddenly. The distribution is very variable and does not conform to anatomical boundaries. The difficulty is greatest with elaborated weakness, where there is neurologically determined weakness but its assessment is distorted by super-added non-organic weakness. Muscle bulk, tone, reflexes and plantar responses are all normal in non-organic weakness.

Weakness

The pattern of weakness, the muscle tone and reflex changes allow the level of the nervous system producing the weakness to be identified.

There are five types of weakness: upper motor neurone, lower motor neurone, neuromuscular junction, muscle and non-organic.

Altered proprioception, inattention or bradykinesia in extrapyramidal disease can all masquerade as weakness.

The time course of the onset suggests the likely pathology.

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