Arachnoiditis is an autoimmune inflammatory lesion of the arachnoid membrane of the brain, leading to the formation of adhesions and cysts in it. Clinically, arachnoiditis is manifested by cerebrospinal hypertension, asthenic or neurasthenic syndromes, as well as focal symptoms (damage to cranial nerves, pyramidal disorders, cerebellar disorders), depending on the predominant localization of the process. The diagnosis is established on the basis of anamnesis, assessment of the neurological and mental status of the patient, data from Echo-EG, EEG, lumbar puncture, ophthalmological and otolaryngological examination, MRI and CT of the brain, CT cisternography. Disease is treated mainly with complex drug therapy, including anti-inflammatory, dehydration, antiallergic, antiepileptic, resorbing and neuroprotective drugs.
ICD 10
G00 Bacterial meningitis, not classified elsewhere
General information
To date, neurology distinguishes between true arachnoiditis, which has an autoimmune genesis, and residual conditions caused by fibrous changes in the arachnoid membrane after a traumatic brain injury or neuroinfection (neurosyphilis, brucellosis, botulism, tuberculosis, etc.). In the first case, arachnoiditis is diffuse and has a progressive or intermittent course, in the second case it often has a local character and is not accompanied by a progressive course. Among organic lesions of the central nervous system, true arachnoiditis accounts for up to 5% of cases. Disease is most often observed among children and young people under the age of 40. Men get sick 2 times more often than women.
Causes
In approximately 55-60% of patients, pathology is associated with a previously transmitted infectious disease.
Viral infections:
- influenza
- viral meningitis
- meningoencephalitis
- chickenpox
- cytomegalovirus infection
- measles, etc.
Chronic purulent foci in the skull:
- periodontitis
- sinusitis
- tonsillitis
- otitis media
- mastoiditis
In 30%, arachnoiditis is a consequence of a traumatic brain injury, most often a subarachnoid hemorrhage or brain contusion, although the likelihood of arachnoiditis does not depend on the severity of the injuries.
In 10-15% of cases, arachnoiditis does not have a well-established etiology.
Predisposing factors to the development of arachnoiditis are chronic fatigue, various intoxications (including alcoholism), heavy physical labor in adverse climatic conditions, frequent acute respiratory infections, repeated injuries, regardless of their localization.
Pathogenesis
The arachnoid membrane is located between the dura and soft meninges. It is not fused with them, but fits snugly to the soft meninges in places where the latter covers the convex surface of the brain convolutions. Unlike the soft meninges, the arachnoid does not enter the cerebral gyrus and subarachnoid spaces filled with cerebrospinal fluid are formed under it in this area. These spaces communicate with each other and with the cavity of the IV ventricle. Outflow of cerebrospinal fluid from the cranial cavity occurs from the subarachnoid spaces through the granulations of the arachnoid membrane, as well as through the perineural and perivascular slits.
Under the influence of various etiofactors, antibodies to its own spider membrane begin to be produced in the body, causing its autoimmune inflammation — arachnoiditis. Disease is accompanied by thickening and clouding of the arachnoid membrane, the formation of connective tissue adhesions and cystic extensions in it. Adhesions, the formation of which is characterized by arachnoiditis, lead to obliteration of the indicated pathways of cerebrospinal fluid outflow with the development of hydrocephalus and cerebrospinal hypertension crises, causing the occurrence of cerebral symptoms. The focal symptoms accompanying arachnoiditis are associated with irritating effects and involvement of the underlying brain structures in the adhesive process.
Classification
In clinical practice, arachnoiditis is classified by localization. Cerebral and spinal arachnoiditis are isolated. The first, in turn, is divided into convexital, basilar and arachnoiditis of the posterior cranial fossa, although such a separation is not always possible with the diffuse nature of the process. According to the peculiarities of pathogenesis and morphological changes, arachnoiditis is divided into adhesive, adhesive-cystic and cystic.
Symptoms
The clinical picture unfolds after a significant period of time from the influence of the factor that caused it. This time is due to the ongoing autoimmune processes and may differ depending on what exactly caused arachnoiditis. So, after the flu, arachnoiditis manifests itself after 3-12 months, and after a traumatic brain injury in an average of 1-2 years. In typical cases, arachnoiditis is characterized by a gradual, barely noticeable onset with the appearance and increase of symptoms characteristic of asthenia or neurasthenia: increased fatigue, weakness, sleep disorders, irritability, increased emotional lability. Against this background, the appearance of epileptic seizures is possible. Over time, the general cerebral and local (focal) symptoms accompanying arachnoiditis begin to manifest.
General cerebral symptoms
The general cerebral symptoms are caused by a violation of cerebrospinal fluid dynamics and in most cases is manifested by a cerebrospinal hypertension syndrome. In 80% of cases, patients with arachnoiditis complain of a fairly intense bursting headache, most pronounced in the morning and aggravated by coughing, straining, physical exertion. Increased intracranial pressure is also associated with soreness when moving the eyeballs, a feeling of pressure on the eyes, nausea, vomiting.
Arachnoiditis is often accompanied by tinnitus, hearing loss and non-systemic dizziness, which requires the exclusion of ear diseases in the patient (cochlear neuritis, chronic otitis media, adhesive otitis, labyrinthitis). Excessive sensory excitability (poor tolerance of harsh sounds, noise, bright light), vegetative disorders and vegetative crises typical of vegetative-vascular dystonia may occur.
Arachnoiditis is often accompanied by a periodic sharp aggravation of cerebrospinal fluid disorders, which is clinically manifested in the form of a cerebrospinal fluid crisis — a sudden attack of intense headache with nausea, dizziness and vomiting. Such attacks can occur up to 1-2 times a month (arachnoiditis with rare crises), 3-4 times a month (arachnoiditis with medium-frequency crises) and more than 4 times a month (arachnoiditis with frequent crises). Depending on the severity of the symptoms, cerebrospinal fluid crises are divided into mild, moderate and severe. Severe cerebrospinal fluid crisis can last up to 2 days, accompanied by general weakness and repeated vomiting.
Focal symptoms
The focal symptoms of arachnoiditis may be different depending on its predominant localization.
Convexital arachnoiditis can manifest itself as mild to moderate disorders of motor activity and sensitivity in one or both extremities on the opposite side. In 35%, arachnoiditis of this localization is accompanied by epileptic seizures. Usually there is a polymorphism of epiprimes. Along with primary and secondary generalized psychomotor simple and complex seizures are observed. After an attack, a temporary neurological deficit may occur.
Basilar arachnoiditis can be widespread or localized mainly in the optic chiasmal region, anterior or middle cranial fossa. His clinic is mainly due to the defeat of the cranial nerves located at the base of the brain I, III and IV pairs. Signs of pyramidal insufficiency may occur. Arachnoiditis of the anterior cranial fossa often occurs with impaired memory and attention, a decrease in mental performance. Opto-chiasmal arachnoiditis is characterized by a progressive decrease in visual acuity and narrowing of visual fields. These changes are most often bilateral in nature. Opto-chiasmal arachnoiditis may be accompanied by a lesion of the pituitary gland located in this area and lead to the appearance of an endocrine exchange syndrome similar to the manifestations of pituitary adenoma.
Arachnoiditis of the posterior cranial fossa often has a severe course, similar to brain tumors of this localization. Arachnoiditis of the bridge-cerebellar angle, as a rule, begins to manifest itself as a lesion of the auditory nerve. However, it is possible to start with trigeminal neuralgia. Then there are symptoms of central neuritis of the facial nerve. With arachnoiditis of the large cistern, a pronounced cerebrospinal hypertension syndrome with severe cerebrospinal fluid crises comes to the fore. Cerebellar disorders are characteristic: coordination disorders, nystagmus and cerebellar ataxia. Arachnoiditis in the area of the large cistern can be complicated by the development of occlusive hydrocephalus and the formation of a syringomyelitic cyst.
Diagnostics
A neurologist can establish true arachnoiditis only after a comprehensive examination of the patient and a comparison of anamnestic data, the results of a neurological examination and instrumental studies. When collecting anamnesis, attention is paid to the gradual development of the symptoms of the disease and their progressive nature, recent infections or traumatic brain injuries. The study of the neurological status makes it possible to identify disorders on the part of the cranial nerves, to determine focal neurological deficits, psycho-emotional and mnestic disorders.
Skull x-ray in the diagnosis is an uninformative study. It can reveal only signs of long-existing intracranial hypertension: finger depressions, osteoporosis of the back of the Turkish saddle. The presence of hydrocephalus can be judged by the Echo-EG data. With the help of EEG in patients with convexital arachnoiditis, focal irrigation and epileptic activity are detected.
Patients with suspected arachnoiditis must necessarily be examined by an ophthalmologist. In half of the patients with arachnoiditis of the posterior cranial fossa, during ophthalmoscopy, congestion in the area of the optic nerve disc is noted. Opto-chiasmal arachnoiditis is characterized by a concentric or bitemporal narrowing of the visual fields detected during perimetry, as well as the presence of central cattle.
Hearing disorders and noise in the ear are the reason for consulting an otolaryngologist. The type and degree of hearing loss are determined using threshold audiometry. To determine the level of damage to the auditory analyzer, electrocochleography, the study of auditory evoked potentials, acoustic impedance measurement are performed.
CT and MRI of the brain make it possible to identify morphological changes that accompany arachnoiditis (adhesions, the presence of cysts, atrophic changes), determine the nature and degree of hydrocephalus, exclude volumetric processes (hematoma, tumor, brain abscess). Changes in the shape of the subarachnoid spaces can be detected during CT cisternography.
Lumbar puncture allows you to get accurate information about the size of intracranial pressure. A study of the cerebrospinal fluid with active arachnoiditis usually reveals an increase in protein to 0.6 g / l and the number of cells, as well as an increased content of neurotransmitters (for example. serotonin). It helps differentiate arachnoiditis from other cerebral diseases.
Treatment
Arachnoiditis therapy is usually performed in a hospital. It depends on the etiology and degree of activity of the disease. The scheme of drug treatment of patients with arachnoiditis may include:
- anti—inflammatory therapy with glucocorticosteroid drugs (methylprednisolone, prednisolone), absorbants (hyaluronidase, quinine iodosmutate, pyrogenal)
- antiepileptic drugs (carbamazepine, levetiracetam, etc.)
- dehydration drugs (depending on the degree of increase in intracranial pressure – mannitol, acetazolamide, furosemide)
- neuroprotectors and metabolites (piracetam, meldonium , ginkgo biloba, brain hydrolysate pigs, etc.)
- anti-allergic medications (clemastine, loratadine, mebhydroline, hifenadine)
- psychotropic drugs (antidepressants, tranquilizers, sedatives).
A mandatory moment in the treatment of arachnoiditis is the rehabilitation of existing foci of purulent infection (otitis, sinusitis, etc.).
Severe opto-chaotic form or arachnoiditis of the posterior cranial fossa in the case of progressive vision loss or occlusive hydrocephalus are indications for surgical treatment. The operation may consist in restoring the patency of the main cerebrospinal tract, removing cysts or disconnecting adhesions, leading to compression of nearby brain structures. In order to reduce hydrocephalus in arachnoiditis, it is possible to use shunting operations aimed at creating alternative ways of outflow of cerebrospinal fluid: cystoperitoneal, ventriculoperitoneal or lumboperitoneal shunting.
