Tetraparesis : Causes, Symptoms, Diagnosis & Treatment

Last Updated: 21/09/2022

Tetraparesis is observed in injuries, neoplasms, inflammatory, vascular, demyelinating diseases of the central, less often - peripheral nervous system. The cause of the development of tetraparesis is established according to complaints, anamnesis data, physical examination, neurological examination, instrumental and laboratory methods. Treatment regimens include neuroprotectors, immunosuppressants, antimicrobials, vascular agents, surgical interventions, and complex rehabilitation measures.

Characteristics of tetraparesis

Tetraparesis is manifested by a decrease in muscle strength or the absence of movements in the arms and legs at the same time. It is combined with disorders of pelvic functions, sensory disturbances in the trunk and limbs, weakness of the respiratory muscles is possible. It can be flaccid (peripheral), spastic (central), or mixed. For flaccid tetraparesis, a decrease in reflexes and muscle tone, muscle atrophy are typical.

With central paresis, deep reflexes are increased, superficial ones are reduced, pathological signs, synkinesis are revealed. Muscle tone is increased, hypotrophy is absent. The severity of tetraparesis is assessed in points from to 5, where - total paralysis, 5 - fully preserved muscle strength and range of motion. The affected area in the spinal cord is localized at the level of the cervical spine, in the brain it extends to both hemispheres or covers the underlying structures on both sides.

Why does tetraparesis occur?

Spinal cord injury

The cause of tetraparesis in spinal cord injury is compression or destruction of the nervous tissue, ischemia, and hemorrhage. The condition is detected with fractures, dislocations, fracture-dislocations, open wounds. First, the phenomena of flaccid paresis are detected, later - spastic. Pathology can be observed with injuries such as:

  • Concussion of the spinal cord. The decrease in muscle strength is slight or moderate, is transient.
  • Spinal injury. Typically, a combination of functional and organic disorders, in the long term, residual effects of varying severity are likely.
  • compression myelopathy. Occurs due to edema, compression by a hematoma or solid structures. It can be acute, early, late.
  • anatomical break. Crushing or rupture of the spinal cord is observed with gunshot fractures, injury by bone fragments.
  • Circulatory disorders. They develop against the background of hemorrhages in the spinal cord and intershell space, damage to the main vessels.

In the acute period, the real severity of disorders is often difficult to assess due to spinal shock, in which movements, sensitivity and reflexes below the injury site are completely lost due to transmarginal inhibition. The shock resembles a picture of a total rupture of the spinal cord, however, in the subsequent movements are gradually restored, a residual neurological deficit is formed, due to areas of uncompensated tissue destruction.



Vascular pathologies

Violations of the spinal circulation with the development of tetraparesis occur due to congenital (hypoplasia) and acquired (embolism, thrombosis, atherosclerosis) vascular diseases involved in the blood supply to the spinal cord. In some patients, they are caused by compression by tumors, inflammatory infiltrates, and enlarged lymph nodes. Sometimes they form as a result of iatrogenic injuries, against the background of hemorrhagic diathesis or infectious vasculitis.

In spinal stroke, tetraparesis occurs acutely within minutes or hours. Particularly dangerous are foci of ischemia and hemorrhage at the C1-C4 level, often accompanied by respiratory disorders. If the underlying segments are affected, tetraparesis or tetraplegia is noted with a decrease in tone in the muscles of the arms and an increase in the muscles of the legs, spontaneous breathing is preserved.

With transient disorders of the spinal circulation, myelogenous intermittent claudication, sudden weakness in the limbs with or without loss of consciousness when the head is thrown back are detected. Against the background of transient disorders, persistent progressive tetraparesis is gradually formed.

Circulatory disorders in arteriovenous malformations of the spinal cord can also be acute (apoplexy form) or gradually developing (paralytic form). The clinical picture in the first case corresponds to a hemorrhagic stroke. In the second category of patients, a progressive or intermittent course is observed. The appearance of symptoms of tetraparesis may be preceded by radicular syndrome.

Inflammatory pathologies

Half of the cases of myelitis of the cervical spine are caused by infectious lesions of the spinal cord with mycoplasmas, herpes simplex virus, cytomegalovirus, spirochete pallidum, borrelia, meningococci. Sometimes myelitis is complicated by osteomyelitis of the spine. The remaining cases of the disease are associated with damage to the nervous tissue by neurotropic poisons, the development of inflammation against the background of injuries. Along with the phenomena of tetraparesis, intoxication syndrome and general hyperthermia are observed.

Poliomyelitis is caused by enteroviruses. Tetraparesis is less common than paraparesis and is found in the spinal variant of the disease. Muscle weakness occurs a few days after the onset of general infectious symptoms. Along with the muscles of the limbs, the diaphragm, muscles of the face and torso may be involved in the process. It is possible to damage the centers of regulation of vital functions in the medulla oblongata. The recovery period lasts about a year, contractures, deformities, persistent flaccid paralysis are observed at the end.

Acute radiculoneuropathy in neuroAIDS is manifested by flaccid tetraparesis, bulbar disorders, paresis of the facial nerve. Symptoms increase over several days or weeks, then stabilize and subside after another 2-4 weeks. Limb functions are fully restored in 70% of patients. In 15% of cases, pronounced residual neurological disorders are detected.

Progressive rubella panencephalitis develops as a result of intrauterine infection or persistence of the virus in the body after rubella. It is characterized by a chronic course with a gradual increase in manifestations: cognitive impairment, cerebellar ataxia, pyramidal symptoms. Spastic tetraparesis is formed at stage 2 of the disease, subsequently aggravated, chaining patients to bed.

Cerebral palsy

Tetraparesis manifests various forms of cerebral palsy, including the most common spastic diplegia. With this type of disease, hypertonicity is observed, with a predominant lesion of the lower extremities. A striking sign is the typical position of the legs: the hips are turned inward, the knees are pressed to each other, the shins are connected or crossed. There are pseudobulbar paralysis, strabismus, hearing loss. Hyperkinesis is possible.

In addition, tetraparesis is detected in double hemiplegia, mixed forms of pathology. Double hemiplegia is the most severe variant of cerebral palsy with total muscle rigidity, inability to move, independently hold the head, and minimal self-care. In mixed forms, variable symptoms are determined.

Autoimmune diseases

For opticomyelitis, bilateral damage to the optic nerves is typical in combination with tetraparesis or lower paraparesis. The phenomena of myelitis precede the development of neuritis. An intermittent course is more often observed. Lambert-Eaton syndrome is diagnosed in patients with malignant neoplasms, autoimmune diseases, and is formed on the basis of autoimmune reactions. The weakness of the muscles of the thighs, the pelvic girdle predominates.

Hereditary pathologies

Signs of tetraparesis are detected in a number of hereditary diseases:

  • Leukodystrophy. Spastic tetraparesis develops with metachromatic leukodystrophy and Alexander's disease, which debut in childhood, less often at a young age. In children with an early childhood variant of Krabbe's disease, symptoms are detected in the first six months of life, and death occurs by the age of one.
  • Sphingomyelinosis. In type A Niemann-Pick disease, hepatosplenomegaly and lymphadenopathy are diagnosed already in infancy. Muscle spasticity is formed in the second year of life. Children die from respiratory and cardiac disorders.
  • Phenylketonuria. Spastic tetraparesis is determined in type 3 disease. Pathology manifests itself in 2-6 months. Accompanied by lethargy or hyperactivity, vomiting, the appearance of a specific smell of skin and urine.
  • Amavrotic idiocy. Decreased activity, loss of motor skills are the first symptoms of early childhood amaurotic idiocy. In the future, the violations progress, severe tetraparesis is formed.
  • Kennedy's bulbospinal amyotrophy. Initial manifestations are detected after 4 years, flaccid paresis with a predominant lesion of the proximal segments of the extremities is detected after 10-2 years from the onset of the disease.

Volumetric formations

Tetraparesis is caused by benign and malignant neoplasms. Craniospinal tumors are simultaneously located in the upper spinal segments and the caudal brain, are primary or metastatic. They are characterized by a combination of cerebral, focal, spinal symptoms. Hemiparesis or upper paraparesis are noted, which then transform into tetraparesis.

Tumors of the spinal cord are extramedullary (meningiomas, neuromas, neuroblastomas, myelomas, chondrosarcomas, lipomas) or intramedullary (gliomas). For extramedullary neoplasms, a sequential change from radicular syndrome to Brown-Sequard syndrome and then to total tetraparesis is typical. Intramedullary neoplasias manifest sensory disturbances, then cause tetraparesis, then radicular syndrome.

Brain compression

Tetraparesis can develop against the background of compression of the nervous tissue by intracerebral tumors and neoplasms of the membranes, post-traumatic hematomas, hemorrhages in hemorrhagic stroke, abscesses, cerebral cysts. The clinical picture is variable, depending on the volume, localization, and rate of development of the pathological process. Meningeal symptoms, cerebral and focal symptoms, respiratory and circulatory disorders are revealed.


In patients with hereditary, autoimmune, toxic, metabolic polyneuropathies, flaccid symmetrical tetraparesis is found with predominant involvement of the distal extremities. Weakness of the proximal muscle groups is less common and is formed due to acquired demyelinating polyneuropathies. With Guillain-Barré syndrome and the severe course of some other varieties of the disease, weakness of the respiratory muscles can be detected.

Other pathologies

In amyotrophic lateral sclerosis, asymmetric upper flaccid paraparesis and lower spastic paraparesis, bulbar syndrome, pyramidal symptoms are noted. The sequence of occurrence of manifestations is determined by the form of the disease. In multiple sclerosis, spastic tetraparesis is less common than lower paraparesis. It is supplemented with dysfunctions of the pelvic organs, sensory disorders, signs of damage to the cranial nerves, cerebellar and pyramidal tracts.

Other pathologies with the possible development of tetraparesis include Chiari anomaly, basilar impression. Sometimes limb weakness becomes a complication of vertebrogenic pathologies (osteochondrosis, intervertebral hernia, spondylolisthesis), tuberculous spondylitis, C1 subluxation in rheumatoid arthritis. Unsharply expressed phenomena of tetraparesis are found against the background of rapidly worsening hypokalemia, for example, in patients with acute renal failure. Hysterical neurosis stands apart, in which the organic basis of tetraparesis is absent.




The cause of tetraparesis is determined by a neurologist. The specialist establishes the time and circumstances of the onset of the violation, the rate of development of the symptom, the presence of other signs. The purpose of the neurological examination is to determine muscle strength, the volume of active and passive movements, the study of reflexes. To clarify the diagnosis, the following procedures are carried out:

  • Radiography . Radiography of the skull and spine - basic techniques for craniocerebral and spinal cord injuries. Confirm dislocations, fractures, displacement of solid structures.
  • Tomography . CT and MRI are prescribed to clarify the data obtained during radiography, to identify pathological processes that are not detected in conventional images. Informative for injuries, tumors, hemorrhages, myelopathy, inflammatory lesions.
  • Myelography. Contrasting the central spinal canal allows you to determine the obstacles to the circulation of CSF. The method is indicated for neoplasms, spinal injuries, herniated discs.
  • Electroneuromyography. This functional technique makes it possible to assess the conduction of nerve impulses to skeletal muscles, to establish the localization of damage, and the contractility of the muscles.
  • Lumbar puncture. The procedure is performed to study the pressure of the cerebrospinal fluid during volumetric processes, the subsequent analysis of cerebrospinal fluid in inflammatory pathologies and subarachnoid hemorrhages.
  • Laboratory tests . Informative for hereditary diseases with metabolic disorders (phenylketonuria, lipoidosis), inflammatory and autoimmune diseases.


Help at the prehospital stage

Sudden tetraparesis is a reason for the immediate call of an ambulance. The neck of the victim with a spinal or craniocerebral injury is fixed with a head holder. A patient with a spinal injury is placed on a rigid stretcher. If necessary, resuscitation is carried out: the patient is transferred to a ventilator, an indirect heart massage is performed. Drugs are administered to stabilize blood pressure, stimulate cardiac activity.

Conservative therapy

The treatment of tetraparesis is complex, including the impact on the cause of the pathology, the relief of concomitant symptoms, and the restoration of motor capabilities. Drug therapy is carried out using drugs of the following groups:

  • Neuroprotectors . Indicated for patients with myelopathies, consequences of TBI, strokes.
  • Immunosuppressors . Effective in autoimmune processes, multiple sclerosis. Hormonal agents are effective in radicular syndrome, cerebral edema.
  • Antimicrobial . Depending on the etiology of the inflammatory process, specific immunoglobulins, antiviral drugs, and antibiotics are included in the treatment regimen.
  • Detoxification . Necessary for tetraparesis of toxic origin, acute infections. Additionally, extracorporeal techniques are used.
  • Vascular . For vascular lesions, antiplatelet agents, venotonics, and vasoactive drugs are used.
  • Others . In pathologies accompanied by tetraparesis, NSAIDs, cholinesterase inhibitors, B vitamins are prescribed.

In the recovery period, non-drug measures come to the fore. To improve motor functions, exercise therapy, massage, physiotherapy, mechanotherapy, kinesiotherapy are carried out. According to indications, orthopedic correction is carried out.


Taking into account the etiology of tetraparesis, patients perform the following surgical interventions:

  • Traumatic injuries : resection of the Urban wedge, vertebroplasty, interbody fusion, intervertebral fixation with cages, fixation of C2 tooth with screws, fixation with plates.
  • Circulatory disorders : embolization of aneurysms and AVMs of the spinal cord.
  • Neoplasms : removal of intramedullary tumors, excision of meningiomas, neurinomas, ependymas.
  • Compression of brain tissue : drainage of abscesses, evacuation of hematomas, removal of neoplasia.

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