Muscular Weakness (Paresis and Paralysis)

How to Cite This Chapter: Oczkowski W, Bodzioch M. Muscular Weakness (Paresis and Paralysis). McMaster Textbook of Internal Medicine. Kraków: Medycyna Praktyczna. Accessed May 22, 2024.
Last Updated: November 4, 2021
Last Reviewed: November 4, 2021
Chapter Information

Definition and PathogenesisTop

Muscular weakness is one of the most common neurologic presentations.

Paresis is a reduction in muscle strength with a limited range of voluntary movement. Paralysis (-plegia) is a complete inability to perform any movement.

Dysfunction may be of the upper motor neurons (cerebral motor cortex, subcortical structures, brainstem, and corticospinal tracts) or lower motor neurons (motor nuclei of the cranial nerves or motor neurons of the ventral horn of the spinal cord; or peripheral nerve, muscle, or neuromuscular junction). Clinically, any dysfunction above the motor neurons in the brainstem or spinal cord is termed upper motor neuron weakness or spastic weakness and any dysfunction at the motor neurons or below, including the nerve, muscle, or neuromuscular junction, is termed lower motor neuron weakness or flaccid weakness (Table 1).

1. Spastic weakness: Upper motor neuron dysfunction. Commonly caused by stroke (ischemic or hemorrhagic), mass lesions (tumor, abscess), demyelination, or trauma. Acute upper motor neuron dysfunction (eg, stroke, traumatic spinal cord injury) may initially present as flaccid paresis.

2. Flaccid weakness: Lower motor neuron dysfunction. Caused by neuropathy (Guillain-Barré syndrome, heavy metal poisoning, adverse effects of drugs [vincristine, isoniazid], neuropathy in patients with autoimmune diseases or diabetes, acute intermittent porphyria, nerve compression, critical illness myopathy, critical illness neuropathy), neuromuscular junction disorders (myasthenia gravis, botulism, effects of muscle relaxants, organophosphate poisoning), or muscle disorders (inflammatory myopathy: polymyositis, inclusion body myositis, dermatomyositis), muscular dystrophy, electrolyte abnormalities (among others, periodic paralysis in patients with hypokalemia or hyperkalemia, hypomagnesemia, hypercalcemia).

3. Concomitant spastic and flaccid weakness: Caused by amyotrophic lateral sclerosis, transverse myelitis, multiple sclerosis, and other diseases of the spinal cord (spastic weakness below the level of injury caused by disruption of the corticospinal tract; flaccid weakness at the level of injury due to destruction of the motor cells of the ventral horns). Vitamin B12 deficiency can present with spastic weakness due to dysfunction of the corticospinal tracts of the spinal cord and flaccid weakness due to dysfunction of the peripheral nerves (areflexic weakness with bilateral Babinski signs).


1. History and physical examination: The nervous system is distributed throughout the body and therefore weakness on its own cannot accurately define the location of the dysfunction (eg, weakness in a leg could be due to a peripheral nerve injury or stroke affecting the cortical neurons controlling the leg). However, the pattern of weakness can help localize the abnormality:

1) In patients with muscular weakness in the arms and legs, assess the pattern of weakness and if there are upper or lower motor neuron signs:

a) Quadriparesis (all 4 limbs affected) suggests cervical cord injury (upper motor neuron signs) or Guillain-Barré syndrome (lower motor neuron signs).

b) Hemiparesis (affecting the upper and lower limbs on the same side of the body) suggests injury at the contralateral brainstem level or higher in the neuraxis.

c) Paraparesis (paresis of the lower limbs only) suggests thoracic or lumbar spinal cord injury.

d) Monoparesis (only one limb affected) suggests injury to peripheral nerves or peripheral nerve plexus unless there are upper motor neuron signs.

2) In patients with weakness of the muscles of the head and neck, evaluate distribution and severity:

a) Eye movement abnormalities: Injury to cranial nerves III, IV, VI.

b) Weakness of the muscles of mastication: Trigeminal nerve injury.

c) Weakness of the facial muscles: Weakness of the entire half of the face with inability to close the eye suggests a peripheral facial nerve injury such as Bell palsy. Weakness of the lower part of the face and a relatively preserved ability to close the eye suggests contralateral upper motor neuron dysfunction above the level of the facial nerve nucleus in the brainstem, such as stroke.

d) Dysphagia, dysphonia: Vagus nerve injury (vocal cord) or glossopharyngeal nerve injury (palate).

e) Weakness of the sternocleidomastoid and trapezius muscles: Accessory nerve injury.

f) Weakness of the muscles of the tongue: Injury to the hypoglossal nerve.

3) Pathognomonic signs can accurately identify the neurologic localization. Aphasia, agnosia, neglect, hemianopsia, and changes in cognition or behavior can only occur as a result of cortical hemispheric dysfunction. A cranial nerve abnormality as above with a contralateral limb paresis can only occur as a result of a brainstem dysfunction. A sensory level across the trunk can only occur as a result of a spinal cord dysfunction (see Sensory Disturbances).

4) Establish the circumstances in which the weakness has occurred (acute, subacute, or gradual onset); stroke is sudden, mass lesions and demyelination are subacute, neuropathy can have gradual onset. Establish the associated clinical features, such as history of trauma, fever, previous stroke or transient ischemic attack, and other medical conditions, to identify the possible pathophysiology of the neurologic disturbances.

5) Combination of predominant pure motor proximal muscle weakness with relative preservation of reflexes may direct attention to myopathy.

2. Diagnostic studies: Diagnostic tests depend on the presumed neurologic localization and pathophysiology. Blood tests are performed in the case of toxic exposure, metabolic disturbances, or suspected myopathy (see Polymyositis and Dermatomyositis). Imaging studies (computed tomography [CT], magnetic resonance imaging [MRI]) are used in the case of brain or spinal cord injury; electrophysiologic studies (EPSs) (nerve conduction, electromyography), in the case of nerve or muscle dysfunction; and lumbar puncture, in the case of infection.


Table 1.27-1. Manifestations of upper and lower motor neuron dysfunction


Upper motor neuron

Lower motor neuron


Often hemiparetic pattern

Often proximal in muscular weakness and distal in peripheral nerve weakness

Tendon reflexes


Reduced or absent

Clonus (eg, foot clonus)



Pathologic signs

Present (Babinski sign)a


Muscle atrophy

Absent; secondary atrophy possible due to lack of use of weak muscles

Develops relatively rapidly

Muscle tone

Increased (spastic)

Normal or reduced (flaccid)

Abdominal skin reflexes



Pathologic movements (eg, chorea)





Occasionally present

a Babinski sign: dorsiflexion (extension) of the big toe on scratching the sole of the foot (with a blunt object moved along the outer aspect of the foot from the heel towards the front and the big toe).

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