Symmetric reduction of reflexes (areflexia): causes, symptoms, diagnosis

The presence or absence of deep reflexes in itself has no functional significance: persistent loss of, for example, the Achilles reflex during remission in a herniated disc does not interfere with gait or rapid flexion-extension movements of the foot. However, symmetrical loss of reflexes indicates that the patient has or has had a lesion of the peripheral nervous system. Therefore, in such cases, a thorough neurological and general clinical examination is necessary. Symmetrical decrease in reflexes from the legs, arms, and a decrease in the reflex from the masticatory muscles (the only deep reflex of cranial localization available for clinical verification) - all this requires the same diagnostic approaches.

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The main causes of symmetrical areflexia are:

I. Polyneuropathy:

1. AIDP (Guillain-Barre syndrome).
2. Chronic polyneuropathy.

II. Combined degeneration of the spinal cord (funicular myelosis).

III. Hereditary motor and sensory neuropathy (Charcot-Marie-Tooth disease) type I.

IV. Spinocerebellar ataxia (atrophy).

V. Eddie's syndrome.

VI. Tabes dorsalis.

VII. Motor neuron disease.

I. Polyneuropathy

The most common cause of areflexia is polyneuropathy. All variants of acute polyneuropathy are unlikely to escape the attention of the physician, since in these cases muscle weakness and/or sensory disturbances develop in the involved limbs or trunk. Therefore, the problem is not in identifying polyneuropathy as such in the patient, but in determining its etiology.

AIDP (Guillain-Barre syndrome)

There are clear diagnostic criteria for Guillain-Barré syndrome, the most important of which are: acute or subacute onset; predominance of motor impairment over sensory impairment; ascending spread of symptoms with gradual involvement of the proximal (limb-girdle) muscles, abdominal muscles, trunk and respiratory muscles; frequent development of bilateral paralysis of the facial muscles; increased protein levels with a normal number of cells, slowing of the rate of conduction of excitation along the nerves. Disturbances in the electrical activity of the heart muscle are possible.

An examination, in particular a serological one, aimed at identifying a specific cause, is absolutely necessary. The most common etiologic factors are viral infections (Epstein-Barr virus, epidemic hepatitis B virus), immunopathy or other hematological disorders. The latter should be taken into account in the case of atypical clinical manifestations, for example, in the case of severe sensory disorders, in the case of a descending type of symptom development or in the case of increased cytosis in the cerebrospinal fluid. Rare causes of acute polyneuropathy also include alcoholism with pronounced metabolic disorders and vitamin B1 deficiency, nodular periarteritis, which subsequently, as a rule, occurs as chronic polyneuropathy.

Chronic polyneuropathy

Chronic polyneuropathy may remain unnoticed for a long time because the patient does not present characteristic complaints or does not take the symptoms seriously. In such a situation, symptoms should be actively identified during a neurological examination.

Many patients with diabetes mellitus have decreased or absent Achilles and/or knee reflexes, mild atrophy of the calf muscles and anterior shin muscles, and the short extensor digitorum muscle in the dorsolateral foot just below the lateral malleolus may not be palpable when the toes are dorsiflexed. Vibratory sensitivity in the big toe or ankle is often decreased or absent. Nerve conduction velocity testing reveals widespread slowing of motor and sensory fibers, indicating secondary myelinopathy.

The detection of subclinical polyneuropathy in patients admitted in a delirious or confused state may indicate alcoholism as a cause of mental disorders. Chronic alcohol abuse leads to the development of polyneuropathy, clinically characterized by a decrease in deep reflexes and mild paresis of the muscles of the lower extremities, especially the extensors, and the absence of pronounced sensory disorders. Electrophysiological studies reveal an axonal nature of the lesion, which is indicated by the presence of denervation potentials in needle EMG with normal or nearly normal nerve conduction velocities.

A full examination of a patient whose subclinical polyneuropathy does not fit into any of the above categories (which is not uncommon) is time-consuming, expensive, and often inconclusive.

Below is a list of some rare causes of polyneuropathy:

• renal failure;
• paraneoplastic polyneuropathy, rheumatoid
• arthritis or systemic lupus erythematosus;
• porphyria;
• vitamin deficiency (B1, B6, B12);
• exogenous intoxication (eg, lead, thallium, arsenic).

II. Combined degeneration of the spinal cord (funicular myelosis)

It is extremely important to identify vitamin B12 deficiency as a cause of areflexia, since this condition is potentially curable. Such a diagnosis is very likely if the patient has a detailed picture of combined degeneration of the spinal cord, i.e. there is muscle weakness, areflexia, sensory disorders of the "glove" and "sock" type, disturbances of deep sensitivity in combination with Babinski's symptom, indicating the involvement of the pyramidal tract. Somatic symptoms of achylic gastritis, characteristic changes in the mucous membrane of the tongue (Hunter's glossitis: "scalded tongue", "varnished tongue"), manifestations of asthenic syndrome are often detected.

III. Hereditary motor and sensory neuropathy types I and II (Charcot-Marie-Tooth disease)

There are congenital degenerative diseases that are now grouped under the name of hereditary motor-sensory neuropathy (HMSN). The variant known as Charcot-Marie-Tooth disease can have a very mild course and manifest itself as an incomplete picture - the patient only has areflexia and a slight deformation of the foot (the so-called "hollow foot").

The diagnosis is easily established if we take into account the dissociation between the pronounced symptoms (absence of reflexes, marked decrease in nerve conduction velocities) and the almost complete absence of active complaints, as well as the absence of signs of denervation in needle EMG. The most informative may be an examination of the patient's close relatives, who, as a rule, reveal the same clinical features.

IV. Spinocerebellar ataxias (degenerations)

Similar considerations apply to the spinocerebellar ataxias, another large group of inherited degenerative diseases. The leading syndrome is a gradually onset and slowly but steadily progressive cerebellar ataxia. Reflexes are often absent. Family history may not provide any useful information. Neuroimaging studies should not be relied upon: even in cases of very severe ataxia, cerebellar atrophy is not always detected. Genetic diagnostic methods, if available, can sometimes help the diagnosis.

V. Eddie's Syndrome

If there is marked anisocoria and the larger pupil does not react to light or to convergence with accommodation, or reacts slowly, then it should be borne in mind that this is a so-called "tonic pupil"; if areflexia is detected, the patient may have Edie syndrome. Sometimes the patient himself discovers pupillary disorders: he may experience increased sensitivity to bright light due to insufficient constriction of the pupil in response to light stimulation; blurred vision is possible when reading or looking at small objects at close range, which is associated with the lack of rapid accommodation. Some patients, when looking at themselves in the mirror, simply discover that "one eye looks unusual". Incomplete Edie syndrome is also possible (loss of reflexes without pupillary disorders or characteristic pupillary disorders without changes in reflexes).

Anisocoria and the absence of photoreactions raise the question of the possibility of neurosyphilis for the physician, since the patient also has areflexia. However, serological studies are negative, and ophthalmological examination indicates the preservation, but extreme slowness, of photoreactions. The cause of this pathological condition is the degeneration of parasympathetic cells of the ciliary ganglion. Since there is parasympathetic denervation of the pupil, there is also denervation hypersensitivity, which can be easily verified by instilling a dilute solution of a cholinergic drug into the eyes: a rapid constriction of the affected pupil occurs, while the intact (non-hypersensitive) pupil does not constrict.

VI. Tabes dorsalis

Sometimes, when examining a patient whose leading symptom is pupillary disorders, areflexia is detected. In case of bilateral miosis with a slightly altered pupil shape (deviation from a round shape) and no reaction to light while maintaining reactions to convergence with accommodation (Argyll-Robertson symptom), a very likely diagnosis may be tabes dorsalis. In such a case, using serological examination of cerebrospinal fluid and blood, it is necessary to establish whether the patient has an active specific (syphilitic) infectious process - in this case, penicillin therapy is required, or whether the disease is in an inactive phase - then antibiotic therapy is not necessary. The same reasoning applies if the pupils are dilated, there is mild anisocoria, and photoreactions are altered similarly to those described above.

VII. Motor neuron disease

In rare cases, the leading manifestation of motor neuron disease is loss of reflexes in the legs. The diagnosis is made according to the following criteria: presence of only motor disturbances (sensitivity is not impaired), fasciculations in the affected (i.e., paretic) muscles, as well as in uninvolved muscles, diffuse signs of denervation according to EMG data with preserved or almost preserved nerve conduction velocities.