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Neurological Lyme Disease

 

Neurological Lyme Disease

Lyme disease is caused by a bacterium, Borrelia burgdorferi, and rarely Borrelia mayonii, that is spread to people by the bite of an infected tick. The majority of patients who have Lyme disease develop a rash around the bite site. The rash may be hot to the touch and vary in size, shape, and color, but it will usually appear as a "bull's-eye" (a red ring with a clear center).

However, some people will not develop the rash, making Lyme disease difficult to identify because its symptoms and indications are similar to those of many other illnesses.

The initial stage of Lyme disease can start anywhere from 7 to 14 days (or even 30 days) after an infected tick bite, with flu-like symptoms such as fever, chills, swollen lymph nodes, headaches, lethargy, muscular aches, and joint pain.

Lyme disease is an infectious disease that affects multiple organ systems. After the skin and joints, the nervous system is the third most commonly implicated organ system, accounting for 10%-15% of infected individuals in both Europe and the United States. Numbness, discomfort, weakness, facial nerve paralysis, vision problems, and meningitis can occur. Symptoms such as fever, stiff neck, and severe headache are the most common neurological sequelae in the second stage of Lyme disease.

Reduced attention, irritability, memory and sleep disturbances, and nerve damage in the arms and legs are some of the other issues that may not manifest for weeks, months, or years after a tick bite.

Radiculoneuritis is diagnosed less frequently in the United States than meningitis or facial palsy, and these symptoms can occur alone or in combination.

Regardless of the duration of the infection and the clinical manifestations, appropriate antimicrobial treatment and other therapies resulted in a microbiologic cure in the vast majority of patients.

The diagnosis of Lyme disease in the neurological system is based on the following factors:

  • The clinical disorder should include objective evidence of both nervous system disease and Lyme disease.
  • Laboratory testing (positive Lyme serologies and antibodies with or without positive cerebrospinal fluid [CSF] Lyme antibodies) should support the diagnosis because the disease is transmitted exclusively by Ixodes tick bites.

 

Manifestations of neurological Lyme disease

The most common neurological manifestations of Lyme disease include (they can occur alone or in combination):

  • Meningitis
  • Paralysis of the facial nerve
  • Radiculoneuritis

 

Meningitis

The most prevalent type of nervous system involvement is lymphocytic or monocytic meningitis, which can occur alone or in conjunction with cranial nerve or spinal nerve root involvement. Meningitis commonly develops several weeks to months after a tick bite and is the initial symptom of Lyme disease. Meningitis rarely manifests itself months or years after the initial infection.

Approximately 2% of Lyme disease cases confirmed by the Centers for Disease Control and Prevention (CDC) in the United States had isolated meningitis.

Clinical presentation: Symptomatic lymphocytic or monocytic meningitis caused by Lyme disease is nearly identical to any viral meningitis in terms of headache, fever, photosensitivity, and neck stiffness. According to studies in children, it has a slightly slower start than viral meningitis, taking a few days longer between the first symptom and clinical presentation.

Evaluation and diagnosis: CSF and serum testing are required in the examination of any patient suspected of having acute meningitis.

If there is a clinical suspicion of elevated intracranial pressure (especially papilledema) or parenchymal brain involvement with focal neurologic symptoms or changes in mental status, neuroimaging is required.

Serologic or antibody testing: Patients who may have Lyme disease should be tested for antibodies to Borrelia burgdorferi. Serologic testing is very sensitive and specific for the diagnosis of Lyme disease, with the exception of atypical patients who show neurologic signs within 4-6 weeks of infection.

Analyses of the CSF: A CSF examination is required in a patient with a clinical presentation suggesting acute meningitis to rule out potentially harmful microorganisms and, if feasible, pinpoint the causal agent. CSF studies include cell counts and differentials, protein and glucose concentrations, Gram staining, and bacterial cultures, among other things. It's also a good idea to get tested for syphilis, as syphilis also has neurological manifestations.

Treatment and prognosis of meningitis: When a patient has meningitis caused by an unknown pathogen, empiric antibiotic therapy is usually started right away, even before definite test results are available. The treatment for Lyme disease might be changed once the disease has been identified. Antibiotic regimens for Lyme disease are useful in treating meningitis caused by Lyme disease.

The majority of patients respond well to treatment. Even without therapy, Lyme meningitis is usually self-limiting. In most cases, a second lumbar puncture is unnecessary. While antibodies usually decrease slowly after effective therapy, reporting a decrease in CSF pleocytosis can be useful if there are concerns about treatment efficacy.

 

Paralysis of the facial nerves

The seventh (facial) nerve palsy was reported in 9% of patients confirmed with Lyme disease in the United States by the CDC. It usually appears early in the course of an infection (e.g., weeks to several months after the tick bite). Acute facial nerve palsy usually develops months or years after the initial illness. Lyme facial palsy and Lyme meningitis are frequently reported together.

Clinical presentation: Facial palsy caused by Lyme disease has a similar clinical appearance to idiopathic Bell's palsy, with a fast start of unilateral facial paralysis (developing over hours to a day or two); some individuals have bilateral involvement, either concurrently or in rapid succession.

Several symptoms, including an inability to close the eye completely on the affected side, decreased tearing, dryness of the eyes which can later cause watering of the eyes because of irritation or inflammation, drooping of the affected side's mouth, taste perception that may be altered, slurring of speech, drooling, earache, or pain behind the ear, are observed.

If there is a chance that a patient with facial nerve palsy has been exposed to Lyme disease, the condition should be suspected and examined. On the basis of serologies, one-quarter of cases of facial nerve palsy in an endemic location were likely caused by Lyme disease in the summer.

Evaluation and diagnosis: Serological or antibody testing is recommended in the following cases: a young individual who has visited an endemic region and an adult in an endemic location from spring until fall. Except in children with Lyme disease, facial nerve palsy is uncommon in young children.

Anti-B. burgdorferi antibody concentrations in the blood of most patients are relatively high, with a prominent immunoglobulin M (IgM) component, either alone or in conjunction with an enhanced IgG response.

It's up for debate whether to test CSF in individuals with facial nerve palsy and suspected Lyme disease. Associated meningitis is prevalent; however, it usually has no effect on treatment. A CSF study may not be necessary in patients with typical (isolated) facial nerve palsy and a positive serology indicating Lyme infection.

Idiopathic Bell's palsy (facial nerve paralysis of unknown cause) is identified in patients with isolated facial palsy and negative serology.

Treatment and prognosis of facial nerve paralysis: A proper antibiotic treatment for facial nerve palsy caused by Lyme disease is required. An antibiotic treatment of isolated facial nerve palsy is indicated largely to prevent future complications of disseminated Lyme disease, as antibiotic medication may not have a significant effect on the facial palsy's outcome.

The majority of patients with Lyme facial palsy heal on their own. In one study, the median recovery period was 26 days (range: 1-270 days). Patients with bilateral (both sides) illnesses may have a worse prognosis.

 

Radiculoneuritis

Radiculoneuritis is inflammation of one or more roots of the spinal nerves. The main symptom is pain, usually in the chest (thoracic) or abdominal region. It can last for many weeks if left untreated.

Lyme radiculoneuritis is found in 3% of Lyme disease cases confirmed by the CDC in the United States. Although this usually appears quite early in the infection (within weeks to a few months), there may be a delay of several months.

Painful radiculoneuritis appears to be a more prevalent manifestation of nervous system Lyme in Europe, though this could be because of differences in recognition of the condition rather than genuine incidence. The phrase "Garin-Bujadoux-Bannwarth syndrome" (or "Bannwarth syndrome") has been used to describe a constellation of painful radiculoneuritis.

Clinical presentation: Patients commonly experience radicular discomfort or pain in one or more dermatomes, usually in the chest and abdominal area. The pain is often belt-like and worsens at night. Sensory impairments (decreased sensation), motor weakness, and/or reflex abnormalities are also observed.

Evaluation and diagnosis: Neurologic localization is the first step in the diagnostic process. Nerve conduction investigations and electromyography are not required, although they can help confirm the diagnosis of polyradiculopathy in patients who have an unclear clinical examination.

In endemic places, Lyme should be suspected in a patient with polyradicular signs and symptoms who appears in the late spring through autumn months and does not have an evident mechanical precipitant to their symptoms. Serologic testing for Lyme disease, which is very sensitive and specific for Lyme disease and establishes the diagnosis, should be performed on such patients.

In some patients, additional testing is necessary to rule out other possibilities in the differential diagnosis:

When structural or mechanical entities are suspected, a magnetic resonance imaging (MRI) with gadolinium contrast of the affected nerve root level is indicated.

Segmental spinal cord involvement at the same level as the afflicted nerve root has been recorded in several European (and a few American) patients with Bannwarth syndrome.

Lumbar puncture: Whether to acquire CSF is a point of contention; however, it is likely unnecessary in patients with positive Lyme serology if no other etiology is suspected. Inflammatory CSF is common in patients with polyradiculitis, but it has little effect on treatment. Lyme antibodies have been found in the CSF but not in the blood of a small number of individuals, mostly in Europe.

Treatment and prognosis of radiculoneuritis: Antibiotic regimens for treating B. burgdorferi infection are helpful in treating radiculoneuritis. In observational studies, most patients improve during the first 4 weeks of antibiotic therapy. Medications to suppress pain and inflammation can provide symptomatic relief. Painful radiculoneuritis will also resolve if left untreated, but it will take longer.

 

Neurological manifestations that are less common:

Though less common, the following neurological manifestations are seen in Lyme disease:

Multiple cranial neuropathies:

While facial nerve involvement accounts for around 80% of all Lyme disease-related cranial neuropathies, other cranial nerves can be affected as well.

Multiple cranial neuropathies can co-occur, either concurrently or sequentially, just as facial nerve palsies can be bilateral. Diplopia, vertigo, facial numbness, and other symptoms have been observed when nerves innervating the extraocular muscles, the vestibulocochlear nerve, occasionally the trigeminal nerve, and infrequently the lower cranial nerves are involved.

Optic neuritis:

Optic neuritis (inflammation of the second cranial nerve) is thought to occur infrequently. Intracranial hypertension, papilledema, and optic nerve symptoms are common in patients with meningitis. Contrast-enhanced MRI is commonly used in the evaluation of cranial neuropathy to rule out vascular, structural, or inflammatory problems.

When a patient arrives with unexplained cranial neuropathy, serologic testing for Lyme disease should be pursued, especially if they live in an endemic location and are present during the spring and fall months.

Lyme encephalomyelitis:

Inflammatory encephalomyelitis linked to Lyme disease has been noted in a small number of patients in Europe and the United States. This condition was once thought to affect one in a million people at risk each year; however, this number is likely to be significantly smaller currently.

It has been described as a disease symptom that appears both early and late. Lyme encephalomyelitis is a genuine neuraxis infection, indicating that it affects the entire nervous system. It can look like multiple sclerosis on the surface, with inflammatory parenchymal abnormalities on MRI and inflammatory alterations in the CSF, including increased total immunoglobulin production and oligoclonal bands.

Patients with encephalomyelitis have multifocal central nervous system (CNS) symptoms that appear suddenly or gradually.

Intracranial hypertension:

Lyme disease is associated with a clinical state comparable to pseudotumor cerebri or idiopathic intracranial hypertension (IIH), which occurs more frequently in adolescents than adults. In contrast to IIH, when the CSF profile is normal, nearly all of the documented instances had inflammatory CSF, implying that the increased intracranial pressure is the result of meningitis.

The symptoms and potential consequences are the same regardless of the method, including compression of the cranial nerves, with a particular threat to the optic nerves and vision. Patients appear with headaches and papilledema (swelling of the optic nerve head because of transmitted increased intracranial pressure).

Many patients recover in days or weeks with antibiotic treatment, although others' symptoms can last longer.

Other types of peripheral nerve involvement:

This may occur with Lyme disease and likely reflect various forms of mononeuropathy multiplex, though they are less prevalent than cranial neuropathy and radiculoneuritis. Although Lyme disease has been linked to rare cases of demyelinating neuropathies, these are so uncommon that they are most likely coincidental.

Patients may develop an acute mononeuropathy, affecting a single nerve or nerve root early in the illness. Patients with an untreated infection may develop what is known as a confluent mononeuropathy multiplex later on. This illness manifests as a distal polyneuropathy with distal (stocking-glove) sensory loss and weakening, and it appears to be caused by the involvement of numerous tiny nerve branches.

Encephalopathy:

In early investigations, many patients with active Lyme disease reported weariness, cognitive slowness, and memory problems. These symptoms, on the other hand, are vague and are common co-morbidities of many inflammatory and other systemic illnesses. Patients with cognitive deficits, memory problems, or mental problems are evaluated independently.

Chronic Lyme disease and posttreatment Lyme disease syndrome:

The term "chronic Lyme disease" can indicate various things to different people, and it can include post-Lyme disease symptoms as well as other illnesses and symptom complexes.

"Posttreatment Lyme disease syndrome" or "posttreatment Lyme disease symptoms" refers to a group of symptoms that are widespread in the general population. While patients frequently report problems with memory and cognition, this symptom complex is not linked to an active or earlier B. burgdorferi infection of the neurological system.

 

What is Lyme disease brain fog?

Some of the negative effects of Lyme disease include memory loss, confusion, difficulty formulating words and thoughts, difficulty concentrating, and personality changes. These symptoms usually develop later in the disease and are mild. This is commonly expressed as "brain fog".

More than one in ten people with Lyme disease who are successfully treated with antibiotics endure chronic, sometimes debilitating, and poorly understood fatigue and brain fog symptoms that can last for years after the illness is treated.

The brain fog caused by Lyme disease is multifaceted and associated with inflammation. It is never related to the disease-causing brain damage.

Slow thinking, as well as difficulties concentrating, remembering, or mentally focusing, affects practically everyone with an active inflammatory condition to some degree. These are the adverse effects of chemicals that the body produces in reaction to infection or inflammation. Once the infection or inflammation is gone, these adverse effects will go away.

Lyme disease infections can cause inflammation in the blood vessels of the brain and nerve roots from the brain to the spinal cord and degradation of the myelin coating that protects nerves. It can obstruct thought, focus, communication, and memory.

There are two different types of brain fog. You can have one or both categories at any given time.

Type 1 brain fog makes you feel like your mind is clouded or obscured. It is caused by an accumulation of inflammatory molecules such as cytokines, mold, yeast, and other toxins.

Type 2 brain fog leads to poor focus, short-term memory issues, and a lack of order.

A doctor can diagnose brain fog and design a treatment plan to help you feel better. Type 2 will be taken care of if type 1 is taken care of. To improve brain fog, it's critical to minimize inflammation and take steps to eliminate infection with the appropriate antibiotics prescribed.

 

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