Symmetrical decrease in reflexes (areflexia): causes, symptoms, diagnosis

In itself, the presence or absence of deep reflexes is not of functional significance: a persistent loss, for example, of the Achilles reflex during remission with a herniated intervertebral disc does not in any way break the gait and rapid flexion-extension movements of the foot. Nevertheless, the symmetrical prolapse of reflexes indicates that the patient has or had previously had a lesion of the peripheral nervous system. Therefore, in such cases, a thorough neurological and general clinical examination is necessary. Symmetric lowering of reflexes from the legs, from the hands and lowering of the reflex from the masticatory muscles (the only clinically verified deep reflex of cranial localization) all require the same diagnostic approaches.

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The main causes of symmetric areflexion:

I. Polineuropathy:

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

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

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

IV. Spinocerebellar ataxia (atrophy).

V. Eddie Syndrome.

VI. Spinal dorsalis (Tabes dorsalis).

VII. Disease of the motor neuron.

I. Polineuropathy

The most common cause of areflexia is polyneuropathy. All variants of acute polyneuropathy can hardly escape the doctor's attention, since in these cases muscle weakness and (or) sensitivity disorders on the involved limbs or trunk develops. Therefore, the problem is not to identify the patient's polyneuropathy as such, but to determine its etiology.

OVDP (Guillain-Barre syndrome)

There are clear diagnostic criteria for Guillain-Barre syndrome, the most important of which are: acute or subacute onset; prevalence of motor function disorders over sensitivity disorders; an ascending spread of symptoms with a gradual involvement of proximal (limb-belt) muscles, abdominal muscles, trunk and respiratory muscles; frequent development of bilateral paralysis of facial muscles; increase in the level of protein with a normal number of cells, slowing the rate of excitation along the nerves. Violations in the electrical activity of the heart muscle are possible.

The survey, in particular - serological, aimed at identifying a specific cause, is absolutely necessary. The most frequent etiologic factors are viral infections (Epstein-Barr virus, type B epidemic hepatitis virus), immunopathies, or other hematologic disorders. The latter should be borne in mind when atypical clinical manifestations, for example - with a high degree of sensitive disorders, with a descending type of development of symptoms or with an increase in cytosis in the cerebrospinal fluid. The rare causes of acute polyneuropathy also include alcoholism with severe metabolic disturbances and vitamin B1 deficiency, nodular periarteritis, subsequently, usually proceeding in the form of chronic polyneuropathy.

Chronic polyneuropathies

Chronic polyneuropathy can remain unnoticed for a long time, because the patient does not make any characteristic complaints or takes seriously his symptoms. In such a situation, the symptoms should be actively detected in a neurological study.

Many patients suffering from diabetes mellitus have a decrease or loss of achilles and / or knee reflexes, slight atrophy of the calf muscles and muscles of the anterior surface of the tibia is observed; with the rear bending of the fingers, a short extensor of the toes may not be palpable in the region of the dorsolateral part of the foot directly near the lateral ankles. Often reduced or absent vibration sensitivity in the area of the thumb of the foot or ankle. When determining the speed of conduction along the nerves, a widespread delay in the movement of motor and sensory fibers is revealed, which indicates secondary myelinopathy.

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

A complete examination of a patient whose subclinical polyneuropathy does not fit into any of the categories listed above (which is often the case) takes a long time, is expensive and often ineffective.

Below is a list of some rare causes of polyneuropathy:

• kidney failure;
• paraneoplastic polyneuropathy, rheumatoid
• arthritis or systemic lupus erythematosus;
• porphyria;
• deficiency of vitamins (В1, В6, В12);
• exogenous intoxication (for example, lead, thallium, arsenic).

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

It is extremely important to identify vitamin B12 deficiency as the cause of areflexia, since this condition is potentially curable. Such a diagnosis is very likely if the patient has a detailed picture of the combined degeneration of the spinal cord, that is, there are muscle weakness, areflexia, sensitive disorders such as "gloves" and "socks", violations of deep sensitivity in combination with Babinsky's symptom indicating the interest of the pyramidal tract . Often, somatic symptoms of achilic gastritis, characteristic changes in the mucous tongue (Hunter's glossitis: "scalded tongue", "lacquered tongue"), manifestations of asthenic syndrome are often revealed.

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

There are congenital degenerative diseases, which today are united under the name of hereditary motor-sensory neuropathy (NSMN). The variant, known as "Charcot-Marie-Toot's disease", can have a very mild course and manifest itself as an incomplete picture - the patient only has a delicacy and a slight deformation of the foot (the so-called "hollow foot").

The diagnosis is established without difficulty, if we take into account the dissociation between the expressed symptoms (absence of reflexes, a marked decrease in nerve conduction velocities) and the almost complete absence of active complaints, as well as the absence of signs of denervation with needle EMG. The most informative can be a survey of close relatives of the patient, who, as a rule, reveal the same clinical features.

IV. Spinocerebellar ataxia (degeneration)

Similar arguments apply to spinocerebellar ataxia - another large group of hereditary degenerative diseases. The leading syndrome is a slowly onset and slowly but steadily progressing cerebellar ataxia. Reflexes are often absent. A family history may not contain any valuable information. Relying on the results of neuroimaging methods of investigation does not follow: even in the case of very pronounced ataxia, the atrophy of the cerebellum is not always revealed. Methods of genetic diagnosis, if available, can sometimes help diagnosis.

V. Eddie Syndrome

If there is severe anisocoria, and a larger pupil does not respond to light, convergence with accommodation, or reacts slowly, one should keep in mind the possibility that this case is a so-called "tonic pupil"; if this reveals areflexia - the patient may have Eddie's syndrome. Sometimes the patient himself finds pupil disorders in himself: he may experience increased sensitivity to bright light due to a lack of narrowing of the pupil in response to light stimulation; possible blurred vision when reading or viewing small items at close range, which is due to the lack of rapid accommodation. Some patients, when examining themselves in the mirror, simply find out that "one eye looks unusual." It is also possible incomplete Eddie syndrome (loss of reflexes without pupillary disorders or characteristic pupil disorders without changes in reflexes).

Anisocoria and the absence of photoreactions poses a question to the doctor about the possibility of neurosyphilis, since the patient also shows areflexia. However, serological studies are negative, and ophthalmological research indicates the safety, 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 a denervational hypersensitivity to it, which can be easily checked by instillation of a diluted solution of the cholinergic drug into the eyes: a rapid contraction of the affected pupil occurs, while the intact (not hypersensitive) pupil does not narrow.

VI. Dorsal articulation

Sometimes, when examining the patient, the leading symptom of which are pupillary disorders, are areflexia. In bilateral miosis with a slightly modified pupil shape (deviation from the round shape) and lack of reactions to light, while the reactions to convergence are preserved with accommodation (Arjil-Robertson's symptom), a very likely diagnosis may be dorsal. In this case, serological examination of the cerebrospinal fluid and blood should establish whether the patient has an active specific (syphilitic) infectious process - in this case, penicillin therapy is required, or the disease is in the inactive phase - then there is no need for antibiotic therapy. The same reasoning is applicable if the pupils are wide, there is a slight anisocoria, and the photoreactions are changed in the same way as described above.

VII. Motor neuron disease

In rare cases, the leading manifestation of motor neuron disease is the loss of reflexes from the legs. The diagnosis is made in accordance with the following criteria: the presence of only motor disturbances (sensitivity is not violated), fasciculation in the interested (i.e., paretic) muscles, as well as in uninvolved muscles, diffuse signs of denervation according to EMG data at safe or almost safe rates of conduction nerves.