Muscle weakness (paresis)

Muscle weakness is an objective symptom expressed in a decrease in the strength of skeletal muscles, or a subjective sensation described as increased fatigue. The causes of this phenomenon are extremely diverse and usually include structural damage at any of the levels of signal transmission along the nerve pathways, damage to myoneural synapses, muscle fibers. Diagnostics is carried out by means of neuroimaging, neurophysiological procedures, laboratory methods. Treatment involves conservative and surgical correction.

Muscle weakness and rapid muscle fatigue are among the most common symptoms with which neurological medical care is sought. There are objective and subjective criteria to determine the presence of a pathological condition. When talking about weakness, they usually mean a decrease in muscular strength, but patients often complain of general fatigue or difficulty in moving in certain areas of the body.

Weakness may be present in individual muscles, affect many groups or the entire body. It occurs suddenly or increases gradually, is noted periodically or persists constantly. In paretic limbs, muscle tone changes, reflexes become animated or weakened. Depending on the origin and localization of the pathological focus, the clinical picture is supplemented by other symptoms.

Classification
Muscle weakness is caused by a wide range of pathologies. It can be common (widespread) or local. The first implies a state of increased fatigue while maintaining muscular strength. In the second case, a violation of the pathways of the nerve impulse from the central nervous system to certain muscles is detected. At the same time, it is important to understand the level of lesion for topical diagnostics:

Central motor neuron: motor cortex, corticospinal and corticobulbar tracts.
Peripheral motor neuron: anterior horns of the spinal cord, roots, nerves.
Neuromuscular synapse.
Muscles.
If the central or peripheral motor neurons are involved, paresis with a decrease in muscle strength is noted. According to the degree of severity, they can be mild, moderate, deep or take on the character of paralysis (complete lack of movement). Traditionally, paresis is systematized taking into account the localization of the lesion and clinical features. In neurology , the following classification is generally accepted:

Central (spastic). Due to the elimination of the inhibitory effect of the cortex on the spinal cord, muscle tone and reflexes increase, pathological signs and synkinesia occur.
Peripheral (sluggish). The defeat of the peripheral motor neuron leads to a rupture of the reflex arc, which is accompanied by hypotension and hyporeflexia, muscle atrophy, fascicular twitching are noticeable during examination.
Mixed. A combination of spastic paresis below the lesion level due to interruption of the corticospinal tract and peripheral, due to a pathological process in the anterior cord of the spinal cord.
Psychogenic paresis is singled out separately, which occur without organic causes with complete preservation of the conductive pathways of the brain and spinal cord. Their development is associated with a violation of the functions of higher nervous activity. The involvement of individual limbs in the process is essential for diagnosis, therefore, several types of paresis are distinguished in the clinic of nervous diseases:

Monoparesis. Weakness is observed in one limb.
Biparesis. It is divided into hemiparesis, in which the arm and leg suffer from one side, and paraparesis involving symmetrical limbs – upper or lower.
Triparesis. Muscle strength is reduced in three limbs (a combination of hemi- and paraparesis).
Tetraparesis. Motor disorders cover both arms and legs.
Based on the prevalence, there is a weakness of some muscles (for example, fingers or facial), whole groups (flexors, extensors) or departments (distal, proximal). It should be understood that the term “paresis” is used not only when describing the work of skeletal muscles, but also applied to some internal organs (intestines, bladder).

Why does muscle weakness occur
Causes of weakness in the limbs
Considering the origin of skeletal muscle weakness, it is worth separating the concept of paresis associated with damage to nerve pathways and symptoms caused by defects in synaptic transmission, muscle damage. Often we are talking about blockade or increased destruction of acetylcholine, primary or secondary muscle pathology, reflex syndromes. Among the most well – known causes of weakness are the following:

Myasthenia gravis.
Myasthenic syndromes: Lambert-Eaton syndrome associated with slow closure of ion channels, familial infantile myasthenia gravis.
Hereditary paroxysmal myoplegia: hyper-, hypo- and normokalemic, Andersen-Tavil syndrome.
Infections: botulism, tick-borne encephalitis.
Endocrine pathology: hyper- and hypothyroidism, Conn’s syndrome, Addison’s disease.
Myopathies: inflammatory (acute myositis, polymyositis, dermatomyositis), metabolic (including accumulation diseases), mitochondrial.
Muscular dystrophy: progressive (Duchenne, Becker, Emery-Dreyfus), non-progressive (myotubular myopathy).
Diseases of the musculoskeletal system: arthrosis, tendinitis, injuries.
Vascular pathology: obliterating endarteritis, varicose veins of the lower extremities, Takayasu disease.
Poisoning: organophosphate compounds, carbon monoxide, cyanides, aromatic hydrocarbons (toluene, benzene), plants (hemlock), nicotine, cocaine.
Taking medications: D-penicillamine, antibiotics, antitumor agents, statins, cortisone, colchicine, chloroquine.
Weakness in the muscles of the whole body is provoked by various systemic diseases, intoxication. It is noted for acute and chronic infections, autoimmune pathology, malignant tumors. Low motor activity in the elderly, during immobilization, prolonged bed rest are common causes of widespread limb weakness.

Causes of facial muscle weakness
Facial muscles are innervated by the facial nerve (VII pair). Any pathology that disrupts the conduction of an impulse along the motor fibers – from the corticonuclear pathway to the peripheral part – can cause muscle weakness. It is also worth considering the direct defeat of the muscles themselves. The following conditions are present in the list of probable pathologies:

Neuritis of the facial nerve (Bell’s palsy).
Facial-shoulder myodystrophy of Landuzi-Dezherin.
Degenerative diseases: progressive bulbar paralysis, syringobulbia.
Tumors: the base of the skull (Garcin syndrome), the bridge of the cerebellar angle, the temporal bone and the middle ear.
Hemorrhages and infarctions of the Varoliev bridge area.
Congenital anomalies: Chiari malformation, Klippel-Feil syndrome.
Infections: herpetic ganglionitis of the knee node (Ramsey-Hunt syndrome), polioencephalitis, Lyme disease, syphilis.
Meningitis: bacterial, tuberculous, fungal.
Systemic pathology: sarcoidosis, nodular periarteritis, Behcet’s disease.
The consequence of injuries, operations on the face, installation of a cochlear implant.
The effect of chemotherapy drugs.
The facial nerve is often damaged by inflammatory processes in the ear and parotid salivary gland. Compression or rupture of its fibers is observed in TBI with a fracture of the base of the skull. The risk of facial nerve paresis increases in the elderly, with prolonged smoking experience, the presence of concomitant pathology (diabetes mellitus, hypertension).

Causes of paresis
The upper or first neuron of the motor pathway begins in the motor cortex of the precentral gyrus, goes as part of the pyramidal tract through the inner capsule and trunk, ending in the anterior horns of the spinal cord. There, the impulse is transmitted to the second motor neuron, the axons of which make up the roots and peripheral nerves. Damage to these structures at any length is accompanied by paresis, which is characteristic of various pathologies of the nervous system:

Strokes: hemorrhagic, ischemic, subarachnoid hemorrhage.
Tumors and traumatic brain injuries.
Demyelinating diseases: leukodystrophy, multiple sclerosis, Devik’s opticomyelitis.
Motor neuron diseases: amyotrophic lateral sclerosis, spinocerebellar and bulbospinal atrophy.
Cerebral palsy.
Neurodegenerative processes: Wilson-Konovalov disease, Strumpel, Refsum.
Myelopathies: compression, spinal cord ischemia, transverse myelitis.
Peripheral nerve damage: polyneuropathies (metabolic, toxic, hereditary), tunnel syndromes, plexopathies.
Acute polyradiculoneuritis: diphtheria, Guillain-Barre syndrome, Landry ascending paralysis.
Infections: polio, meningococcal meningoencephalitis, rabies.
Vertebrogenic pathology: intervertebral hernias, osteochondrosis, scoliosis.
Intoxication: nerve poisons, salts of heavy metals (thallium, lead, arsenic).
Violation of spinal conduction is often caused by spinal cord injuries, which entail compression, ischemic damage, edema of nervous tissue. There are also direct wounds – gunshot wounds, bone fragments in fractures. Usually, the cervical region is susceptible to such injuries, the thoracic and lumbar are affected much less often. With concussion of the brain tissue, the changes are transient in nature, in other cases they are more persistent.

Metastatic tumors (with lung, breast or prostate cancer) become a common cause of compression of the spinal cord, lymphoma, myeloma, epidural hematomas are less common. When weakness appears in the arms or legs, tuberculous spondylitis, rheumatoid arthritis with subluxation of the atlantoaxial joint, spinal vascular malformations are excluded.

Diagnostics
During a clinical examination, true weakness in the muscles with a decrease in strength is distinguished from increased fatigue as a subjective sign. In the anamnesis, information is found out about the intensity and rate of development of the symptom, the presence of additional signs. During the neurological examination, the doctor determines muscle strength (in points), the volume of active and passive movements, reflexes. To find out the cause of muscle weakness, additional studies are prescribed:

Blood test. If infection is suspected, the hemogram gives an idea of the leukocyte formula, ESR. Biochemical analysis allows you to identify electrolyte and hormonal disorders, the presence of antibodies to the pathogen. Toxicological examination shows the content of toxic substances in the blood.
Lumbar puncture. Cerebrospinal fluid is taken for examination to exclude subarachnoid hemorrhages, infectious and inflammatory diseases of the brain and membranes. The pressure of the cerebrospinal fluid is assessed for volumetric processes (tumors, abscesses, hematomas).

Radiography. Radiography of the spine is the first study prescribed for spinal injuries. Standard images do not show fractures of the dentoid process or the lower cervical segment, which requires the appointment of special radiographs and the use of other imaging techniques.
Tomography. When the central nervous system is affected, MRI is considered the main method of neuroimaging. The method is highly informative in the pathology of the posterior cranial fossa, inflammation of the meninges, myelopathy. CT of the brain is more suitable for patients with fractures of the base of the skull, in the acute period of stroke.
Myelography. It is a radiopaque examination of the central canal of the spinal cord. The procedure is performed for herniated intervertebral discs, spinal injuries, tumors. The technique shows any obstacles to normal cerebrospinal fluid dynamics.
Electroneuromyography. The lesion of nerve trunks and fibers requires a functional study with an analysis of the conductivity of the impulse to the muscles, allows you to assess the speed of signal transmission, localization of damage, the ability of muscles to contract.
If muscle weakness is accompanied by systemic disorders, ultrasound of the kidneys and adrenal glands, thyroid and parathyroid glands are included in the examination plan. In case of vascular disorders, ultrasound and angiography are performed. The search for a malignant tumor may require radioisotope scintigraphy. Given the variety of reasons, a neurologist has to carry out a thorough differential diagnosis with the involvement of related specialists.
Treatment of paresis
Help before diagnosis
A pronounced local or general muscle weakness that has arisen sharply is a reason to seek medical help. In acute conditions associated with a direct threat to life, urgent measures are necessary. Suspected craniocerebral and spinal injuries require immobilization of the cervical spine with a head holder or collar, patients with probable spinal injury are transported on a rigid stretcher.

In case of serious injuries with paresis of the respiratory muscles, hemorrhagic stroke, resuscitation measures are necessary – ventilation with intubation, indirect heart massage. At the prehospital stage, blood pressure is stabilized, brain edema is combated, vomiting and convulsions are stopped. Undifferentiated stroke treatment involves the use of neuroprotectors.

Conservative therapy
Reducing muscle strength requires a comprehensive solution aimed at eliminating the cause of motor dysfunction, restoring lost abilities. The basis of the conservative strategy is drug therapy, selected in accordance with clinical expediency. Taking into account the causes and mechanisms of the development of weakness, the following drugs may be prescribed:

Neuroprotectors. They are used for strokes (ischemic, hemorrhagic), the consequences of TBI, myelopathies. The main directions of neuroprotection are represented by antioxidant protection, inhibition of local inflammation (cytokine antagonists), improvement of trophic (nootropics, choline, carnitine preparations), blood circulation (nimodipine, vinpocetine).
Immunosuppressors. Treatment of myasthenia gravis is carried out with immunosuppressants (azathioprine, cyclosporine), immunoglobulins. Interferons, monoclonal antibodies, and glucocorticoids are used to suppress autoimmune reactions in patients with multiple sclerosis. The latter are also used as replacement therapy for Addison’s disease, for cerebral edema, and root syndrome.
Antimicrobial. Therapy of neuroinfections of bacterial origin requires the appointment of antibiotics. In tick-borne encephalitis, specific immunoglobulins are indicated, botulism is treated with the introduction of antitoxic serum. In addition to etiotropic therapy for acute infections, detoxification agents are prescribed.

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