Increased tactile sensitivity (hyperesthesia) is characterized by heightened perception when exposed to stimuli. It is observed in mononeuropathy, polyneuropathy, ganglionitis, ganglioneuritis, causalgia, erythromelalgia, meningeal syndrome, and some other neurological, rheumatic and infectious diseases. The cause is determined by the results of the conversation, neurological examination, electromyography, cerebral MRI, laboratory tests and other studies. Treatment includes analgesics, antimicrobial agents, antispasmodics, ganglion blockers, and other drugs. Conduct physiotherapy. In some cases, operations are performed.
An increase in tactile sensitivity is detected when the threshold for the perception of various non-specific stimuli is lowered: touch, friction, temperature changes, etc. When the peripheral nervous system is affected, it is usually combined with other sensory disorders: paresthesia, allodynia, dysesthesia. It develops in the initial stages of the disease, subsequently replaced by hypesthesia or anesthesia.
In patients with CNS pathologies, it often occurs acutely, supplemented by cerebral and focal manifestations, signs of intoxication or cerebrovascular accident. In rheumatic and orthopedic diseases, it appears in the area above the lesion. It is caused by edema, inflammation, constant re-irritation of nerve endings.
Why does tactile sensitivity increase?
Diseases of the peripheral nerves
Tactile hyperesthesia is characteristic of Charlin's syndrome, accompanied by painful paroxysms in the orbital area and nearby areas. Attacks are provoked by food intake, pressure on the wing of the nose, last up to 1 hour, are supplemented by lacrimation, photophobia, blepharospasm, and increased skin sensitivity. The symptom is also observed in trigeminal neuralgia, in which there are paroxysmal short-term, but very intense pains in half of the face.
The development of tactile hyperesthesia is also possible with other mononeuropathy, however, with damage to peripheral nerves in the limbs, this manifestation rarely plays a significant role in the clinical picture of the disease. Increased tactile sensitivity can be observed at the initial stage of polyneuropathies, combined with other sensory disorders, muscle weakness, autonomic dysfunction.
Typically symmetrical involvement of the distal extremities with subsequent spread of symptoms in the proximal direction. The cause of hyperesthesia is such polyneuropathies as:
- Toxic: alcohol, when taking drugs, exposure to occupational hazards;
- Primary inflammatory: multifocal sensory and motor polyneuropathy, with Guillain-Barré and Fisher syndromes;
- Secondary inflammatory: with systemic vasculitis, Sjögren's disease, SLE, viral hepatitis C, HIV infection, oncological diseases (sarcoidosis, hepatocellular carcinoma, etc.).
- Metabolic: in diabetes mellitus, hypothyroidism, severe pathologies of the kidneys and liver.
ganglionitis, ganglioneuritis
The main manifestation of ganglionitis and ganglioneuritis is diffuse burning pain with indistinct localization, spreading beyond the innervation zone of the affected node. Painful sensations are provoked by strong emotions, weather changes, food intake. Does not increase with movement. Complemented by paresthesia, hypesthesia or hyperesthesia, vasomotor disorders.
The clinical picture is determined by the location of the ganglion. With cervical ganglioneuritis, ophthalmic manifestations, paresis of the larynx, pain in the arm and upper half of the chest are possible. With the involvement of the upper thoracic nodes, cardialgia, tachycardia, shortness of breath are noted, with damage to the lower thoracic and lumbar nodes - visceral disorders, itching of the genital organs, dysuria.
Vegetative ganglionitis of the head includes neuralgia of the ear, submandibular and sublingual nodes. With herpes zoster involving the crankshaft, Ramsey-Hunt syndrome may develop, which is manifested by pain in the auricle and paresis of the facial nerve. With ganglionitis of the pterygopalatine node, signs of trigeminal neuralgia are determined.
Increased tactile sensitivity
Causalgia
This pathological condition occurs after injuries, most often fractures and gunshot wounds. At the initial stage, a patient with causalgia is concerned about prolonged burning pains that develop without external influence or on contact with minor stimuli (for example, touch), which decrease when immersed in water or applying wet bandages. Along with increased tactile sensitivity, hyperpathy, allodynia and hyperalgesia are noted. Vegetative and trophic disorders are revealed. Over time, dystrophic changes in muscles, paresis and contractures are formed.
erythromelalgia
The main manifestation of erythromelalgia are attacks of baking or burning pain lasting from several hours to several minutes, supplemented by edema and hyperemia. First, the big toe suffers, then both feet are involved in the process, sometimes the hands, less often the perineum, ears and nose. In the future, paroxysms become more frequent, hyperesthesia, hyperpathia, paresthesia are found. Trophic and vascular disorders progress.
meningeal syndrome
It occurs when the meninges are damaged, provoked by infections, injuries, toxic effects and other causes. Includes characteristic pain manifestations, increased muscle tone and hyperesthesia. Along with hypersensitivity, light and sound fear are observed. The patient takes a typical posture (on his side, with his head thrown back, arms and legs bent). The cause of the development of meningeal syndrome are:
- Serous meningitis. Often accompanied by symptoms of SARS. Manifests acutely with intense headache, intoxication and fever. Drowsiness, slight stupor, strabismus, diplopia can be determined.
- Purulent meningitis. It is provoked by meningococcal infection, other bacterial pathogens. Along with chills, fever and hyperthermia, disturbances of consciousness, delirium, psychomotor agitation, and sometimes convulsions are detected. Specific symptoms are more pronounced than in the serous form. There are signs of damage to certain cranial nerves.
- Meningoencephalitis. Specific and general nonspecific manifestations are complemented by severe disorders of consciousness. With an unfavorable development of events, a coma is possible. The clinical picture resembles purulent meningitis, but focal symptoms are more diverse, may include hemiparesis, hyperkinesis, vestibular ataxia, cerebellar disorders.
- tuberculous meningitis. Unlike other forms, there is a prodrome lasting 1-2 weeks, including apathy, irritability, cephalalgia, weakness. Then comes a sharp deterioration with the appearance of meningeal symptoms. In the terminal stage, paresis and paralysis are formed, breathing and heart rhythm are disturbed.
- Meningitis in children. Patients become whiny, capricious. Meningeal, cerebral and general infectious manifestations are found. Seizures often occur. Disturbances of consciousness, hyperkinesis, hemiparesis, oculomotor disorders are possible.
Other reasons
Other diseases and pathological conditions in which increased tactile sensitivity is determined include:
- Neurological diseases: migraine stroke, aneurysms of cerebral vessels, primary and metastatic brain tumors.
- Rheumatological and orthopedic problems: arthritis of various origins, Schinz's disease, epicondylitis of the elbow joint.
- Traumatic injuries: electrical injury (lightning strike), condition during the recovery period after burns.
- Infectious pathologies: pappataci fever.
Diagnostics
The neurologist is engaged in establishing the etiology of tactile hyperesthesia. Patients with provoking somatic diseases and injuries are referred for a consultation with the relevant specialists: therapist, endocrinologist, traumatologist. The doctor finds out when hypersensitivity first appeared, with what symptoms it was combined, how the disease developed over time. The diagnostic program provides for the following manipulations:
- Neurological examination. To determine the presence and zone of tactile hyperesthesia, special tests are carried out (touch, pressure, movement). In addition, the technique provides for the detection of other sensory disorders, the study of reflexes and muscle strength.
- Electrophysiological methods. Electromyography and electroneurography help to establish the localization, prevalence and severity of damage, the severity of the pathological process. Studies are used to differentiate damage to the peripheral nerves and the central nervous system. They are reused during the treatment process to evaluate the effectiveness of therapeutic measures.
- visualization techniques. Brain MRI is performed for meningitis, tumors, aneurysms. MR angiography is indicative of diseases of the intracerebral vessels. CT of the skull is informative when excluding nerve compression in the bone canal as the cause of trigeminal neuralgia. For arthritis and epicondylitis, x-rays or CT scans of the joints are recommended.
- Laboratory tests. Fibromyalgia is characterized by a decrease in the amount of serotonin in the blood. To establish the etiology of polyneuropathies, genetic tests, antibody tests, biochemical blood tests for sugar, pancreatic hormones, liver enzymes, urea and creatinine may be required. The causative agent of meningitis is determined according to PCR or CSF culture.
Tactile Sensitivity Test
Treatment
Conservative therapy
Depending on the cause of increased skin sensitivity, the following therapeutic measures are carried out:
- Fibromyalgia. Recommended painkillers, anticonvulsants, antidepressants. Locally perform irrigation with anesthetics and therapeutic blockade. Carry out exercise therapy, biofeedback therapy, acupuncture. With an increased tendency to negative experiences, concomitant mental disorders, psychotherapy is indicated.
- Polyneuropathy. If possible, etiopathogenetic therapy is carried out: selection of an adequate insulin therapy regimen, administration of hormonal drugs, etc. Specific treatment of inflammatory neuropathies has not been developed, the administration of human immunoglobulin, extracorporeal detoxification is required. To alleviate symptoms, all patients with multiple nerve damage are prescribed neurotrophic drugs and vitamin preparations.
- Ganglionitis, ganglioneuritis. Pain is relieved with analgesics. In severe cases, novocaine is administered intravenously. To combat infectious agents, antiviral and antibacterial agents are used. With an increase in the activity of the sympathetic department of the National Assembly, antipsychotics, antispasmodics, anticholinergics and ganglionic blockers are recommended, with a decrease, cholinomimetics are used. UVR, diadynamic therapy, mud applications, drug electrophoresis are effective.
- Causalgia. The treatment regimen includes anti-inflammatory drugs, narcotic and non-narcotic analgesics, anticonvulsants, anxiolytics, antidepressants. Perform therapeutic blockades. As part of physiotherapy, electroanalgesia, electrophoresis with analgesics, amplipulse therapy, kinesiotherapy (exercise therapy, hydrokinesiotherapy, with paresis - passive gymnastics) are performed.
- Erythromelalgia. For the relief of paroxysms, vasoconstrictors are administered. To eliminate puffiness, antihistamines are used, novocaine blockades are carried out. The complex therapy program includes medicines to strengthen the vascular wall, reflexology, foot baths, therapeutic mud, darsonvalization.
- meningeal syndrome. Urgent hospitalization required. To eliminate the pathogen, depending on the etiology, broad-spectrum antibiotics, antiviral or antifungal agents are prescribed. Carry out detoxification. For the prevention of cerebral edema, diuretics and glucocorticosteroids are administered. Symptomatic therapy is carried out using antipyretics, anticonvulsants, antiemetics, antihypertensive drugs.
Surgery
Patients with tactile hyperesthesia on the background of ganglioneuritis, erythromelalgia and causalgia undergo sympathectomy. Cerebral tumors are excised using open and minimally invasive techniques. With cerebral edema against the background of meningitis, external ventricular drainage or decompressive craniotomy is performed to relieve increased intracranial pressure.