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Neuritis

Neuritis refers to the inflammation of one or more nerves, typically in the peripheral nervous system, which can lead to impaired nerve function and symptoms such as pain, sensory disturbances, or motor deficits.^[1]^[2] This condition arises from various etiologies, including viral or bacterial infections (such as herpes zoster or Lyme disease), traumatic injuries (mechanical, chemical, or thermal), autoimmune disorders (like Guillain-Barré syndrome or sarcoidosis), metabolic factors (such as diabetes or rapid glycemic control leading to treatment-induced neuropathy), and exposure to toxins or certain medications.^[1] Symptoms depend on the affected nerve but often manifest as burning or aching pain, heightened sensitivity to touch (allodynia), abnormal sensations (paresthesia or dysesthesia), numbness, muscle weakness, or, in cases involving cranial nerves, vertigo or vision loss.^[1] Neuritis can be classified into types such as mononeuritis (affecting a single nerve), polyneuritis (multiple nerves), or specific forms like optic neuritis or vestibular neuritis, with the latter often linked to viral triggers.^[1] Diagnosis typically involves a thorough medical history, physical examination, electromyography, nerve conduction studies, and imaging or serological tests to identify underlying causes.^[1] Treatment is tailored to the etiology and may include antiviral or antibiotic medications for infections, corticosteroids or nonsteroidal anti-inflammatory drugs to reduce inflammation, pain management with gabapentinoids or opioids, and supportive measures like physical therapy; in severe or traumatic cases, surgical intervention may be necessary.^[1] While many cases resolve with appropriate care, chronic or recurrent neuritis can lead to permanent nerve damage if untreated.^[2]

Definition and Classification

Definition

Neuritis is defined as the inflammation of one or more nerves, typically affecting the peripheral or cranial nerves and resulting in disrupted neural signaling and function.^[3] This inflammatory process primarily targets the nerve's structural components, including the axons—which are the long, slender projections of nerve cells responsible for transmitting electrical impulses—and the surrounding myelin sheath, a protective lipid-rich layer formed by specialized glial cells that insulates the axon to facilitate rapid signal conduction.^[4] When inflammation occurs, it can swell these structures, impair myelin integrity, and lead to demyelination, thereby hindering efficient nerve impulse transmission.^[2] Unlike the broader term neuropathy, which encompasses any form of peripheral nerve dysfunction or damage from various causes such as trauma, toxins, or metabolic disorders, neuritis specifically denotes inflammatory involvement, often featuring immune-mediated or infectious triggers that provoke swelling and potential demyelination of the affected nerves.^[2] This distinction highlights neuritis as a subset of neuropathic conditions where inflammation is a hallmark, though the terms are sometimes used interchangeably in clinical contexts.^[2] The term neuritis originated in the early 19th century, first appearing around 1825, derived from the Greek "neuron" meaning nerve and "-itis" denoting inflammation, initially used to describe acute inflammatory conditions of nerves before evolving to include chronic and varied presentations across peripheral, cranial, and optic nerve variants.^[5]

Classification

Neuritis is classified primarily by the anatomical location of the affected nerves and by the extent and pattern of involvement, providing a framework for identifying variants and guiding clinical evaluation. By location, neuritis can affect peripheral nerves, cranial nerves, or structures with central nervous system overlap. Peripheral neuritis involves inflammation of nerves outside the brain and spinal cord, commonly targeting those in the limbs or trunk, leading to localized or diffuse dysfunction.^[6] Cranial neuritis refers to inflammation of one or more cranial nerves, such as the facial nerve (cranial nerve VII) in cases of Bell's palsy. Optic neuritis specifically denotes inflammation of the optic nerve (cranial nerve II), which transmits visual signals from the retina to the brain and is often associated with demyelinating conditions.^[7] Vestibular neuritis involves inflammation of the vestibular portion of the eighth cranial nerve, disrupting balance and spatial orientation.^[8] By extent, classifications distinguish between involvement of single versus multiple nerves and symmetric versus asymmetric patterns. Mononeuritis affects a single peripheral nerve, resulting in focal deficits confined to its distribution. Polyneuritis, or polyneuropathy, encompasses inflammation of multiple peripheral nerves, typically in a symmetric, distal-to-proximal pattern.^[6] Mononeuritis multiplex describes asynchronous involvement of several individual peripheral nerves, often in a patchy, asymmetric manner.^[9] Ganglionitis involves inflammation of sensory nerve ganglia or roots, such as the dorsal root ganglia, potentially leading to sensory neuronopathy.^[10] Certain forms of neuritis overlap with broader syndromes characterized by widespread inflammatory processes. For instance, Guillain-Barré syndrome represents an acute form of polyneuritis with rapid-onset symmetric weakness due to immune-mediated nerve inflammation.^[11] Similarly, chronic inflammatory demyelinating polyneuropathy (CIDP) manifests as a chronic polyneuritis with progressive or relapsing nerve root and peripheral nerve involvement.^[12]

Pathophysiology

Inflammatory Processes

In immune-mediated neuritis, the inflammatory process often begins with the activation of the adaptive immune response, primarily involving CD4+ T-cells that adopt a Th1 phenotype and infiltrate peripheral nerve tissues. These T-cells produce interferon-gamma (IFN-γ), which activates macrophages to phagocytose myelin debris and release pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). This cascade leads to perivascular cuffing, characterized by the accumulation of immune cells around nerve blood vessels, and subsequent edema due to heightened vascular permeability in the endoneurium.^[13] A pivotal mechanism in this inflammation is the breakdown of the blood-nerve barrier (BNB), a specialized structure analogous to the blood-brain barrier that maintains nerve homeostasis. Inflammatory mediators like TNF-α and IL-6 disrupt tight junctions (e.g., claudin-4 and catenin alpha-1) in endoneurial microvessels, enabling the infiltration of T-cells, monocytes, and macrophages into the nerve parenchyma. This breach facilitates further release of pro-inflammatory mediators, including chemokines that amplify cellular recruitment and perpetuate the inflammatory environment. In non-immune causes, such as toxic or metabolic neuritis, inflammation may arise from direct cellular damage or oxidative stress without prominent adaptive immune involvement.^[14]^[15] Demyelinating inflammation in neuritis, as observed in conditions like experimental autoimmune neuritis (EAN), targets the myelin sheath through immune-mediated attacks involving autoantibodies against myelin components, which activate the complement system. Complement deposition recruits macrophages via C3a and C5a anaphylatoxins, promoting opsonization and membrane attack complex formation that strips myelin from axons. In axonal variants, such as those in Guillain-Barré syndrome, inflammation similarly involves T-cell and macrophage infiltration but primarily affects nerve fibers directly, with less emphasis on myelin-specific autoantibody involvement and more on anti-ganglioside antibodies.^[16]^[17] Inflammation in neuritis manifests as acute or chronic depending on the underlying trigger. Acute forms, often post-viral, exhibit rapid T-cell activation, intense cytokine storms (e.g., elevated IL-6 and TNF-α), and swift BNB disruption with prominent macrophage influx, typically peaking within days to weeks. Chronic inflammation, prevalent in autoimmune neuritis, features sustained Th1 cytokine production and persistent cellular infiltration, with anti-inflammatory cytokines like IL-10 and transforming growth factor-beta (TGF-β) emerging later to modulate but not fully resolve the process. For infectious causes, direct pathogen invasion can trigger innate immune responses leading to inflammation.^[13]^[18]

Nerve Damage Mechanisms

In neuritis, demyelination primarily manifests as segmental loss of the myelin sheath surrounding peripheral nerve axons, leading to structural disruption without initial axonal damage. This process involves the stripping of myelin by invading macrophages and the dedifferentiation of Schwann cells, resulting in vesicular degeneration and splitting of the myelin lamellae. The exposure of the axon to the extracellular environment impairs the insulation necessary for efficient nerve signaling. In metabolic or toxic neuritis, demyelination may result from impaired Schwann cell function due to oxidative stress or toxin exposure rather than immune attack.^[19] Axonal degeneration in neuritis often follows severe inflammatory insults, progressing via Wallerian degeneration where the distal axon segment breaks down into fragments after separation from the neuronal cell body. This begins within 48 hours of injury, with complete degeneration occurring by 7-11 days, accompanied by myelin ovoid formation and clearance by macrophages and Schwann cells. In demyelinating forms of neuritis, such as those seen in chronic inflammatory demyelinating polyneuropathy (CIDP), axonal loss can become secondary, observed in a majority of cases on nerve biopsy and contributing to irreversible nerve impairment.^[20]^[21] Remyelination in peripheral neuritis offers potential for partial functional recovery, driven by the regenerative capacity of Schwann cells, which proliferate to form bands of Büngner that guide axonal regrowth and subsequently wrap new, thinner myelin sheaths around repaired axons. This process contrasts with the limited remyelination in the central nervous system, where oligodendrocytes show poorer regenerative ability; in the peripheral system, repeated demyelination-remyelination cycles can lead to onion bulb formations from concentric Schwann cell layers. However, the efficiency of remyelination diminishes in chronic or severe cases, with internodal lengths remaining shorter than normal.^[20] These mechanisms culminate in functional nerve impairments, particularly the disruption of saltatory conduction, where action potentials fail to jump efficiently between nodes of Ranvier due to myelin loss, causing slowed conduction velocities or complete conduction blocks. In axonal degeneration, the loss of axonal integrity further halts signal propagation beyond the site of damage until regeneration occurs, underscoring the vulnerability of peripheral nerves to inflammatory-mediated breakdown. In traumatic neuritis, damage may involve direct axonal transection without initial inflammation.

Causes

Infectious Causes

Infectious causes of neuritis involve pathogens that directly or indirectly damage peripheral nerves, leading to inflammation and dysfunction. These infections can trigger acute or chronic neuritis through various mechanisms, including direct neural invasion, toxin production, or secondary immune responses. Common pathogens include viruses, bacteria, and other microorganisms that target the peripheral nervous system, often resulting in conditions like polyneuropathy, mononeuritis, or cranial neuritis.^[22] Viral infections are frequent contributors to neuritis, with herpes zoster virus (varicella-zoster virus, VZV) reactivation causing Ramsay Hunt syndrome, characterized by facial nerve inflammation, ear pain, and vesicular rash. This condition arises from VZV latency in the geniculate ganglion, leading to neuritis in less than 1% of herpes zoster cases. Human immunodeficiency virus (HIV) is associated with distal symmetric polyneuropathy, affecting sensory nerves and occurring in approximately 30-50% of advanced cases, primarily due to viral effects on nerve fibers and immune dysregulation. Enteroviruses, such as coxsackieviruses, can invade the peripheral nerves, causing acute flaccid myelitis-like syndromes with neuritis, particularly in children, through direct cytopathic effects.^[23]^[24]^[25] Bacterial infections also play a significant role, with Borrelia burgdorferi in Lyme disease leading to neuroborreliosis, manifesting as radiculoneuritis or cranial neuritis in 10-15% of untreated cases. This spirochete disseminates hematogenously to invade peripheral nerves, causing lymphocytic inflammation. Diphtheria, caused by Corynebacterium diphtheriae, induces toxin-mediated neuritis, where the diphtheria toxin inhibits protein synthesis in Schwann cells and neurons, resulting in demyelination and polyneuropathy weeks after initial infection.^[26]^[27] Other pathogens include Mycobacterium leprae in leprosy, which specifically targets peripheral nerves, leading to chronic granulomatous neuritis and sensory loss through intracellular invasion and immune-mediated damage. Treponema pallidum in syphilis can cause meningovascular neuritis, affecting cranial and peripheral nerves in the secondary or tertiary stages via direct spirochetal invasion.^[28]^[29] The mechanisms of infectious neuritis vary by pathogen: direct invasion occurs when microbes like VZV or Borrelia enter nerve tissues via axonal transport or hematogenous spread, causing local inflammation and cell death. Toxin production, as in diphtheria, disrupts neural function without widespread replication in nerves. Post-infectious immune responses, seen in many viral cases like vestibular neuritis—presumed viral in origin and often following upper respiratory infections—trigger autoimmune-like attacks on nerves, with viral etiology implicated in the majority of cases. For instance, vestibular neuritis has an annual incidence of 3.5-15.5 per 100,000, predominantly post-viral. These processes highlight the need for early pathogen identification to mitigate nerve damage.^[22]^[27]^[8]

Autoimmune Causes

Autoimmune causes of neuritis involve dysregulated immune responses that target peripheral or central nerve components, leading to inflammation and demyelination without direct pathogen invasion. These conditions arise from aberrant activation of the immune system, where self-reactive antibodies or T cells attack myelin sheaths or axonal structures, resulting in impaired nerve conduction and neurological deficits.^[30] Demyelinating diseases represent key autoimmune etiologies of neuritis. Multiple sclerosis (MS), a central nervous system disorder, frequently manifests as optic neuritis, affecting the optic nerve in approximately 15-20% of initial presentations, where immune-mediated inflammation causes vision loss and pain.^[31] Guillain-Barré syndrome (GBS), an acute peripheral neuropathy, primarily involves the acute inflammatory demyelinating polyneuropathy (AIDP) variant, in which immune attacks lead to rapid-onset weakness and sensory loss, often triggered by preceding infections but driven by core autoimmune mechanisms.^[32] Chronic autoimmune forms include chronic inflammatory demyelinating polyneuropathy (CIDP), which presents as relapsing-remitting or progressive symmetric weakness and sensory impairment over months to years, mediated by ongoing immune-mediated demyelination of peripheral nerves.^[33] At the molecular level, these disorders target specific neural antigens. Anti-myelin antibodies, such as anti-GQ1b immunoglobulin G in the Miller Fisher variant of GBS, bind to gangliosides on nerve membranes, disrupting neuromuscular transmission and contributing to ophthalmoplegia and ataxia.^[34] T-cell mediated damage further exacerbates demyelination in both GBS and CIDP by promoting macrophage infiltration and cytokine release that strip myelin from axons.^[35] Epidemiologically, GBS has an annual incidence of 1-2 cases per 100,000 individuals worldwide, underscoring its rarity yet significant public health impact as the leading cause of acute flaccid paralysis in non-polio settings.^[32]

Metabolic Causes

Metabolic disturbances represent a significant category of non-infectious, non-autoimmune etiologies for neuritis, primarily through nutritional deficiencies and chronic systemic conditions that impair nerve function. Vitamin B12 deficiency, often resulting from inadequate dietary intake, malabsorption due to gastrointestinal disorders, or pernicious anemia, leads to subacute combined degeneration of the spinal cord, frequently accompanied by peripheral neuropathy manifesting as paresthesias and sensory loss in the extremities.^[36] This condition arises from disrupted myelin synthesis and axonal integrity due to impaired methylation processes in nerve cells, affecting up to 30% of deficient patients with combined myeloneuropathy.^[37] Similarly, thiamine (vitamin B1) deficiency, prevalent in chronic alcoholics due to poor nutrition and impaired absorption, contributes to peripheral neuropathy characterized by distal sensory and motor deficits, though it is distinct from pure alcoholic neuropathy.^[38] Diabetes mellitus induces diabetic amyotrophy, a proximal radiculoplexus neuropathy involving acute pain, weakness, and atrophy in the thighs and hips, driven by microvasculature damage and hyperglycemia-induced oxidative stress in diabetic patients, typically those with type 2 disease.^[39]^[40]

Toxic Causes

Exposure to toxins, including heavy metals, pharmaceuticals, and alcohol, can trigger neuritis via direct neurotoxic effects or secondary metabolic disruption. Heavy metal poisoning from lead, often occupational or environmental, results in a predominantly motor neuropathy with wrist drop and abdominal pain, caused by inhibition of enzymes essential for nerve conduction and heme synthesis.^[41] Arsenic toxicity, from contaminated water or industrial sources, produces a sensory-motor axonopathy with painful paresthesias and symmetric distal weakness, stemming from mitochondrial dysfunction and oxidative damage to peripheral nerves.^[42]^[43] Certain medications, such as vincristine—a vinca alkaloid used in chemotherapy—induce dose-dependent peripheral neuropathy through microtubule disruption, leading to sensory symptoms like numbness and autonomic effects in up to 30% of treated patients.^[44] Isoniazid, an antitubercular drug, causes neuropathy by depleting pyridoxine (vitamin B6), resulting in sensory-predominant symptoms that are preventable with supplementation.^[45] Chronic alcohol consumption directly contributes to alcoholic neuropathy, featuring axonal degeneration with an inflammatory component evidenced by elevated cytokines and oxidative stress markers, affecting sensory fibers distally in heavy drinkers.^[46]

Paraneoplastic Causes

Paraneoplastic neuritis arises from remote effects of malignancy, where tumor-induced immune responses target neural tissues. It is notably associated with small-cell lung cancer (SCLC), in which anti-Hu antibodies (also known as ANNA-1) attack intracellular neuronal proteins, leading to sensory neuronopathy with subacute onset of asymmetric sensory loss, pain, and ataxia.^[47] These antibodies, present in 16-17% of SCLC patients, reflect an autoimmune cross-reactivity between tumor antigens and neuronal components, often preceding cancer diagnosis by months.^[48]

Rare Causes

Less common etiologies include trauma-induced inflammation and ischemic mechanisms. Traumatic neuritis can develop following direct nerve injury from accidents or surgery, where local inflammation and edema provoke secondary demyelination and axonal damage in affected peripheral nerves.^[40] Ischemic neuritis, as seen in vasculitic forms without primary autoimmunity, results from occlusion of vasa nervorum, causing hypoxic injury and multifocal neuropathy through reduced blood flow to nerve tissues.^[49]

Signs and Symptoms

Sensory Manifestations

Sensory manifestations are among the most common presenting features of neuritis, arising from inflammation and subsequent dysfunction of sensory nerve fibers. These symptoms vary depending on the affected nerve but typically include alterations in sensation such as pain, paresthesias, and sensory deficits within the distribution of the involved nerves.^[6] Neuropathic pain is a hallmark sensory symptom in neuritis, often described as burning, shooting, or electric shock-like sensations that follow the path of the inflamed nerve. This pain results from aberrant signaling in damaged sensory neurons and can be accompanied by allodynia, where non-painful stimuli like light touch provoke discomfort, and hyperalgesia, an exaggerated response to painful stimuli. In peripheral neuritis, such pain frequently begins distally in the extremities and may intensify at night.^[29]^[50]^[51] Paresthesias, including tingling, numbness, and the "pins and needles" sensation, commonly occur due to partial disruption of sensory nerve conduction in neuritis. These abnormal sensations often appear in a stocking-glove distribution for polyneuritis or along specific dermatomes in mononeuritis, such as the thoracic dermatomes in herpes zoster neuritis, where the rash and paresthesias align with the affected sensory ganglion.^[6]^[52]^[53] Sensory loss manifests as hypoesthesia, a reduced ability to perceive touch, temperature, or vibration, or anesthesia, complete loss of sensation, particularly in peripheral forms of neuritis affecting large-fiber sensory nerves. This deficit can lead to unnoticed injuries and is more pronounced in chronic or severe cases.^[54]^[50] In optic neuritis, sensory alterations primarily involve visual disturbances, including blurred vision, temporary vision loss in one eye, and color desaturation, where colors appear faded or grayish, often accompanied by pain on eye movement. These symptoms stem from inflammation of the optic nerve, impacting visual sensory pathways.^[7]^[19]^[55] Vestibular neuritis presents with sensory manifestations related to balance and spatial orientation, such as severe vertigo, a spinning sensation, and imbalance, without auditory involvement, due to inflammation of the vestibular nerve. These symptoms typically onset abruptly and may include oscillopsia, where the visual world seems to move.^[56]^[8]^[57]

Motor and Other Symptoms

Motor symptoms in neuritis primarily manifest as impairments in muscle function due to inflammation affecting motor nerves. Patients often experience muscle weakness or paresis, which can range from mild difficulty in initiating movements to severe paralysis, particularly in the limbs.^[54] In mononeuritis involving the peroneal nerve, this weakness commonly presents as foot drop, characterized by an inability to dorsiflex the ankle and evert the foot, leading to a steppage gait.^[58] Fasciculations, or involuntary muscle twitches, may also occur alongside painful cramps and eventual muscle atrophy if the condition persists.^[54] In polyneuritis, such as Guillain-Barré syndrome, motor involvement typically begins with symmetric weakness in the lower extremities, ascending proximally and potentially affecting respiratory muscles in severe cases.^[59] This progressive paresis can lead to significant functional limitations, including difficulty walking or standing.^[60] Autonomic symptoms arise when neuritis disrupts the involuntary nervous system, particularly in polyneuritic forms. Orthostatic hypotension, a sudden drop in blood pressure upon standing, can cause dizziness or syncope due to impaired cardiovascular regulation.^[59] Sweating abnormalities, such as anhidrosis (reduced sweating) or hyperhidrosis, reflect sympathetic nerve involvement and may contribute to temperature dysregulation.^[61] Cranial nerve involvement in neuritis can produce distinct motor deficits. Facial paralysis, as seen in Bell's palsy—a form of isolated facial neuritis—results in unilateral weakness of facial muscles, causing drooping of the mouth, inability to close the eye, and altered expressions.^[62] Bulbar neuritis may lead to dysphagia, or difficulty swallowing, due to weakness in the pharyngeal and laryngeal muscles, increasing the risk of aspiration.^[59] Systemic symptoms accompanying neuritis often include profound fatigue, stemming from overall neuromuscular exhaustion and energy demands on weakened muscles.^[54] In acute inflammatory cases, fever may occur as part of the inflammatory response, though it is more commonly associated with preceding infections.^[63]

Diagnosis

Clinical Evaluation

The clinical evaluation of neuritis begins with a detailed history to characterize the condition's onset, progression, and potential etiologies. Onset is classified as acute (hours to days, often linked to infections or toxins), subacute (days to weeks, potentially autoimmune-mediated), or chronic (months to years, suggesting metabolic or hereditary factors).^[64] Distribution is assessed as focal (single nerve, e.g., mononeuritis), multifocal (multiple nerves, as in mononeuritis multiplex), or symmetric (often distal "stocking-glove" pattern).^[65] Associated exposures are explored, including recent infections (e.g., viral or bacterial), toxin or medication history (e.g., chemotherapy, heavy metals), occupational risks, family history, and travel to endemic areas for conditions like leprosy.^[64] Physical examination focuses on neurological assessment to confirm peripheral nerve involvement. Sensory evaluation tests for loss of light touch, pinprick, vibration (using a 128-Hz tuning fork), and proprioception, typically starting distally and progressing proximally in symmetric cases.^[65] Deep tendon reflexes are checked for hypo- or areflexia, a hallmark in inflammatory forms like Guillain-Barré syndrome (GBS).^[60] Muscle strength is graded using the Medical Research Council (MRC) scale, ranging from 0 (no contraction) to 5 (normal power against full resistance), to quantify weakness, which may manifest as distal foot drop or proximal difficulty rising from a chair.^[66] Atrophy or fasciculations are noted if present, alongside gait observation for unsteadiness.^[67] Red flags indicating urgency include rapid progression of weakness (e.g., nadir within 2 weeks in GBS), asymmetry suggesting multifocal involvement, or autonomic features such as bowel or bladder dysfunction (e.g., urinary retention or constipation), which may signal severe inflammatory processes requiring immediate intervention.^[60] These findings prompt expedited referral to neurology.^[65] Differential diagnosis relies on distinguishing neuritis from central or root-level disorders. Unlike radiculopathy, which follows dermatomal patterns with back pain and preserved distal sensation beyond the root, neuritis shows length-dependent or multifocal peripheral deficits without spinal tenderness.^[67] Stroke, by contrast, presents with abrupt, unilateral central signs like hemiparesis or cortical sensory loss, rather than the gradual, bilateral peripheral progression typical of neuritis.^[64]

Ancillary Tests

Ancillary tests play a crucial role in confirming the diagnosis of neuritis, assessing its extent, and identifying underlying etiologies beyond initial clinical evaluation. These investigations provide objective evidence of nerve inflammation, demyelination, or axonal damage, helping differentiate neuritis from other neuropathies. Electrophysiological studies, including nerve conduction studies (NCS) and electromyography (EMG), are fundamental for evaluating peripheral neuritis. NCS typically reveal slowed conduction velocities and prolonged latencies in demyelinating forms, such as Guillain-Barré syndrome (GBS), indicating segmental demyelination or conduction block.^[68] EMG complements this by detecting signs of denervation, such as fibrillation potentials and reduced recruitment, particularly in axonal variants of neuritis.^[68] Imaging modalities offer visualization of nerve involvement. Magnetic resonance imaging (MRI) is highly sensitive for detecting inflammation, showing optic nerve enhancement with gadolinium in cases like multiple sclerosis-associated optic neuritis.^[69] For peripheral neuritis, high-resolution ultrasound can identify nerve swelling, enlargement, or increased vascularity, aiding in the assessment of entrapment or inflammatory conditions.^[70] Laboratory tests target specific etiologies. Cerebrospinal fluid (CSF) analysis in acute inflammatory demyelinating polyneuropathy (a form of GBS-related neuritis) often demonstrates albuminocytologic dissociation, with elevated protein levels (>400 mg/L) and normal cell counts, reflecting blood-nerve barrier disruption.^[71] Serologic testing identifies infectious causes, such as Lyme disease via Borrelia burgdorferi antibody titers or syphilis through treponemal-specific assays.^[72] Autoantibody panels detect immune-mediated neuritis, including anti-aquaporin-4 (AQP4) antibodies in neuromyelitis optica spectrum disorder-related cases or anti-ganglioside IgG (e.g., anti-GM1) in acute motor axonal neuropathy.^[73] Nerve biopsy, typically of the sural nerve, is reserved for ambiguous cases to confirm inflammation. It reveals perivascular lymphocytic infiltrates, demyelination, or vasculitic changes in conditions like chronic inflammatory demyelinating polyneuropathy or vasculitic neuritis, guiding targeted therapy.^[74]

Treatment

Supportive Measures

Supportive measures for neuritis focus on alleviating symptoms, preventing secondary complications, and promoting functional recovery without addressing the underlying etiology. These interventions are essential across various forms of neuritis, such as peripheral neuropathy or acute inflammatory types like Guillain-Barré syndrome (GBS), and typically involve a multidisciplinary approach including pharmacotherapy, rehabilitation, and vigilant monitoring.^[75]^[76] Pain management is a cornerstone of supportive care, particularly for the neuropathic pain that often accompanies neuritis. First-line agents include anticonvulsants such as gabapentin or pregabalin, which reduce neuronal excitability and have demonstrated efficacy in reducing pain intensity in conditions like diabetic neuropathy and postherpetic neuralgia, with pregabalin often showing faster onset.^[77]^[78] For milder symptoms, over-the-counter analgesics like nonsteroidal anti-inflammatory drugs (NSAIDs) may suffice, while topical treatments such as lidocaine patches or capsaicin cream provide localized relief by desensitizing nerve endings or blocking sodium channels.^[75]^[76] In severe cases, such as GBS, carbamazepine or tricyclic antidepressants like amitriptyline can be added for refractory pain.^[63] Physical therapy plays a vital role in maintaining mobility and preventing deconditioning. Tailored exercises target muscle weakness and improve coordination, with strengthening programs shown to enhance muscle power and reduce neuropathic pain in peripheral neuropathy.^[79]^[80] For vestibular neuritis, balance training through vestibular rehabilitation therapy, including gaze stabilization and habituation exercises, helps restore equilibrium and minimizes fall risk.^[57] Assistive devices like braces, canes, or orthotics may be prescribed to support gait and posture during recovery.^[75] Nutritional support is indicated when deficiencies contribute to or exacerbate neuritis symptoms. Supplementation with B vitamins, particularly vitamin B12, thiamine (B1), and pyridoxine (B6), is recommended for nutritional neuropathies, as replenishing these nutrients can halt progression and improve nerve function by supporting myelin synthesis and axonal health.^[81] A balanced diet rich in fruits, vegetables, and lean proteins further ensures adequate intake of antioxidants and micronutrients to aid nerve repair.^[75] In severe cases, such as rapidly progressive GBS, close monitoring in a hospital setting is critical to manage potential complications. Patients may require intensive care unit admission for respiratory support if vital capacity falls below 20 mL/kg or if autonomic dysfunction affects heart rate and blood pressure, with up to 22% needing mechanical ventilation within the first week.^[82] Regular assessments of muscle strength, swallowing, and cardiovascular stability guide timely interventions like physical aids or nutritional support via feeding tubes if needed.^[63]^[83]

Etiology-Specific Therapies

Etiology-specific therapies for neuritis target the underlying cause to address the root pathology and potentially halt disease progression. For infectious etiologies, antimicrobial agents are the cornerstone of treatment. In cases of herpes zoster virus (VZV)-associated neuritis, early administration of antiviral drugs such as acyclovir, valacyclovir, or famciclovir for 7 days is recommended in immunocompetent individuals to reduce viral replication and mitigate nerve damage.^[22] For Lyme disease-related neuritis caused by Borrelia burgdorferi, oral doxycycline serves as a first-line antibiotic, particularly effective in early localized disease to eradicate the spirochete and prevent persistent neuropathy.^[84] In post-infectious scenarios, such as Guillain-Barré syndrome (GBS) following an acute infection, immunomodulatory therapies like intravenous immunoglobulin (IVIG) or plasmapheresis are employed to remove autoantibodies and inflammatory mediators, with strong evidence from randomized trials demonstrating their efficacy in hastening recovery.^[85] Autoimmune-mediated neuritis requires immunosuppressive interventions to dampen aberrant immune responses. High-dose corticosteroids, typically intravenous methylprednisolone at 1 g daily for 3 days followed by an oral prednisone taper, accelerate visual recovery in optic neuritis without altering long-term outcomes, as established in the Optic Neuritis Treatment Trial.^[86] For GBS and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), both IVIG (0.4 g/kg daily for 5 days) and plasmapheresis (five exchanges over 2 weeks) are first-line options, with randomized controlled trials confirming equivalent efficacy in reducing disability and supporting nerve function.^[87] In non-infectious, non-autoimmune causes, therapies focus on toxin removal or neoplasm management. Toxin-induced neuritis, such as lead neuropathy, is treated with chelation therapy using agents like EDTA to bind and excrete heavy metals, leading to symptom resolution once exposure ceases.^[88] For paraneoplastic neuritis, the primary intervention is tumor-directed therapy, including surgery, chemotherapy, or radiation, which often stabilizes or improves neurological symptoms by eliminating the antigenic trigger.^[89] For metabolic causes, such as diabetic neuropathy, treatment emphasizes strict glycemic control to slow progression, alongside supportive pain management.^[90] For traumatic neuritis from mechanical injury, surgical interventions like nerve repair or decompression may be required in severe cases to restore function.^[19] Emerging therapies offer promise for refractory or regenerative needs. Monoclonal antibodies like rituximab, targeting CD20-positive B cells, have been investigated for refractory CIDP; a 2025 multicenter RCT found no significant benefit over placebo in preventing deterioration after IVIG discontinuation.^[91] Stem cell therapies, particularly mesenchymal stem cells, are under investigation in 2023-2025 clinical trials for promoting peripheral nerve regeneration in chronic neuritis, demonstrating enhanced axonal regrowth and remyelination in preclinical models.^[92] Optic neuritis variants warrant tailored approaches. Pulsed intravenous methylprednisolone (1 g daily for 3-5 days) is standard for acute idiopathic optic neuritis to expedite recovery.^[93] In myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) presenting as optic neuritis, high-dose intravenous corticosteroids are used acutely, but guidelines emphasize a structured oral taper (e.g., starting at 1 mg/kg prednisone with reduction over 3-6 months) to minimize relapse risk while avoiding indefinite routine steroid use, favoring steroid-sparing maintenance immunotherapy where indicated.^[94]

Prognosis and Complications

Prognostic Factors

Prognostic factors in neuritis vary by etiology and subtype, influencing the likelihood of recovery and long-term functional outcomes. In general, acute forms such as those triggered by infections tend to have better prognoses with timely intervention, while chronic or axonal variants often lead to persistent deficits if untreated. Favorable prognostic indicators include younger age, as older patients with Guillain-Barré syndrome (GBS), an acute inflammatory neuritis, experience higher rates of severe disease and residual disability.^[95] Early intervention significantly improves outcomes; for instance, rapid administration of intravenous immunoglobulin (IVIG) in GBS has reduced mortality to less than 5% and supported recovery in over 80% of cases.^[95] Acute infectious causes also correlate with higher recovery rates, with 70-80% of GBS patients achieving full or near-full recovery following treatment.^[96] Conversely, poor prognostic factors encompass axonal involvement detected on nerve conduction studies (NCS), which predicts slower recovery and greater disability in peripheral neuritis, including GBS variants. Delayed diagnosis exacerbates outcomes, particularly in chronic inflammatory demyelinating polyneuropathy (CIDP), where untreated cases can progress to wheelchair dependence in approximately 30% of patients, and even with treatment, severe disability occurs in up to 13%.^[97]^[98] Underlying malignancy further worsens prognosis, as neuropathies associated with lymphoma show rapid axonal loss, poor treatment response, and high rates of persistent deficits.^[99] Type-specific prognoses highlight these patterns: in optic neuritis, approximately 92% of patients achieve visual acuity of 20/40 or better within months, often spontaneously.^[100] In contrast, untreated CIDP typically results in progressive worsening and permanent nerve damage, while treated cases show remission or good outcomes in about 74%, emphasizing the need for ongoing therapy to prevent irreversible axonal loss.^[98] Recent 2025 data on GBS confirm improved long-term outcomes with early IVIG, with over 50% of patients reaching good functional recovery (disability score 0-1) at one year.^[101]

Potential Complications

Untreated or severe neuritis can lead to significant neurological complications, including permanent paralysis due to ongoing nerve damage and muscle weakening. In cases of brachial neuritis, for instance, the initial intense pain often progresses to persistent weakness or paralysis in the affected arm or shoulder muscles, potentially resulting in long-term functional impairment if not addressed promptly through early intervention and physical therapy.^[102] Similarly, in chronic inflammatory demyelinating polyneuropathy—a form of recurrent neuritis—permanent loss of nerve function may cause enduring weakness or paralysis in the limbs, underscoring the importance of timely immunosuppressive treatments to mitigate progression.^[103] Chronic pain syndromes represent another key neurological risk, particularly in viral-induced neuritis such as herpes zoster. Post-herpetic neuralgia, a debilitating complication, manifests as persistent burning or stabbing pain in the dermatomes affected by the initial rash, lasting months or years after resolution of the acute inflammation, and affects up to 10-18% of shingles patients over age 50. Preventive vaccination against varicella-zoster virus and early antiviral therapy during acute episodes can substantially reduce the incidence of this chronic condition.^[104] Systemically, ascending polyneuritis, exemplified by Guillain-Barré syndrome, poses a risk of respiratory failure due to diaphragmatic and intercostal muscle weakness, occurring in approximately 20-30% of cases and necessitating mechanical ventilation in up to 30% of patients. This life-threatening complication highlights the need for close monitoring of vital capacity and rapid initiation of intravenous immunoglobulin or plasmapheresis to halt ascent and prevent ventilatory collapse. Imbalance from sensory loss and motor deficits further increases the likelihood of falls, which can result in fractures or head injuries, especially in peripheral neuritis where proprioception is impaired; balance training and assistive devices are essential preventive measures.^[11]^[82]^[29] Neuritis also carries associated risks of progression to chronic neuropathy, where acute inflammation evolves into irreversible axonal degeneration and persistent sensory-motor deficits over months to years if the underlying cause—such as diabetes or autoimmune activity—remains unmanaged. In optic neuritis specifically, there is an elevated risk of developing multiple sclerosis, with a cumulative probability of 50% within 15 years, particularly in those with brain MRI lesions at onset; regular follow-up with MRI and disease-modifying therapies can help detect and avert demyelination spread.^[6]^[105] Rare complications include autonomic involvement leading to dysreflexia-like episodes in severe polyneuritic states with sympathetic overactivity, though this is more commonly linked to coexisting spinal issues, and secondary infections arising from immobility-induced pressure ulcers or unnoticed injuries in insensate areas. Prolonged bed rest in advanced cases heightens vulnerability to urinary tract infections or pneumonia, preventable through meticulous skin care, mobility aids, and prophylactic antibiotics when indicated.^[106]^[29]

References

[1]
Neuritis - an overview | ScienceDirect Topics
Neuritis is a condition caused by inflammation of a nerve or nerves secondary to injury or infection of viral or bacterial etiology.
[2]
When nerves get damaged - Harvard Health
Jul 6, 2024 · For example, neuritis means inflammation of the nerves. Many medical reference books say it is synonymous with neuropathy, although ...
[3]
Optic Neuritis - StatPearls - NCBI Bookshelf - NIH
Jan 20, 2025 · Optic neuritis is a vision-threatening disorder and often the first symptom of demyelinating diseases such as multiple sclerosis.Optic Neuritis · Toxicokinetics · Treatment / Management
[4]
Vestibular Neuronitis - StatPearls - NCBI Bookshelf - NIH
Vestibular neuritis is thought to be the result of inflammation of the vestibular portion of the eighth cranial nerve and classically presents with vertigo, ...
[5]
Neuritis | Harvard Catalyst Profiles | Harvard Catalyst
A general term indicating inflammation of a peripheral or cranial nerve. Clinical manifestation may include PAIN; PARESTHESIAS; PARESIS; or HYPESTHESIA. ... Below ...
[6]
Myelin Sheath: What It Is, Purpose & Function - Cleveland Clinic
A myelin sheath is a sleeve (sheath) that's wrapped around each nerve cell (neurons). It's a protective layer of fat (lipids) and protein that coats the main “ ...
[7]
Neuritis - Etymology, Origin & Meaning
Origin and history of neuritis "inflammation of a nerve or nerves," 1825, from Greek neuron "nerve" (see neuro-) + -itis "inflammation." Related: Neuritic. ...
[8]
Neuropathy - StatPearls - NCBI Bookshelf - NIH
Oct 15, 2022 · Peripheral neuropathies encompass disorders of peripheral nerve cells and fibers, manifesting secondary to a wide range of pathologies.Continuing Education Activity · Introduction · Pathophysiology · Evaluation
[9]
Optic neuritis - Symptoms & causes - Mayo Clinic
a bundle of nerve fibers that transmits visual information from your eye to your ...
[10]
Multiple Mononeuropathy - Neurologic Disorders - Merck Manuals
Multiple mononeuropathies are characterized by sensory disturbances and weakness in the distribution of ≥ 2 affected peripheral nerves.
[11]
Myelitis and ganglionitis, an atypical presentation of Hansen's disease
May 20, 2024 · Neuritis strictly means inflammation of the nerve, implying involvement of the host's system. Neuritis can be seen in type 1 and type 2 leprosy ...
[12]
Guillain-Barre Syndrome - StatPearls - NCBI Bookshelf - NIH
Guillain-Barré syndrome (GBS) is a rare but serious post-infectious immune-mediated neuropathy. It results from the autoimmune destruction of nerves in the ...
[13]
Chronic Inflammatory Demyelinating Polyradiculoneuropathy - NCBI
Chronic inflammatory demyelinating polyradiculoneuropathy is an immune-mediated polyneuropathy marked by nerve roots and peripheral nerve inflammation.
[14]
https://pmc.ncbi.nlm.nih.gov/articles/PMC7145763/
[15]
Biology of the Human Blood-Nerve Barrier in Health and Disease
Increased permeability of, or leukocyte trafficking at the human BNB, commonly cited as a “BNB breakdown”, has been pathologically associated with peripheral ...
[16]
Functional and Structural Changes of the Blood-Nerve-Barrier in ...
Jan 13, 2019 · Accumulating evidence suggests that breakdown of the blood-nerve barrier (BNB) plays a pivotal pathophysiological role in diabetic neuropathy.Abstract · Barriers of the Nervous System... · The Diseased Blood-Nerve...
[17]
The Role of the Complement System in Chronic Inflammatory ... - NIH
The complement system appears to play a role in promoting macrophage-mediated demyelination. Complement deposition in sural nerve biopsies, as well as signs of ...
[18]
Complement updates in optic neuritis - Frontiers
B cells and antibody-mediated complement activation contribute to astrocyte and myelin destruction. ... demyelination caused by excessive complement activation.
[19]
Inflammatory Neuropathies: Pathology, molecular markers and ...
Inflammatory neuropathies may be divided into three major disease categories: Guillain-Barré syndrome (particularly the acute inflammatory demyelinating ...
[20]
Peripheral nerve injury and myelination - PubMed Central - NIH
This review will succinctly discuss the potential therapeutic strategies in the context of myelination following peripheral neurotrauma.Missing: neuritis | Show results with:neuritis
[21]
Peripheral Nervous System Manifestations of Infectious Diseases
Three of these viruses, varicella-zoster virus (VZV), and herpes simplex virus types 1 and 2 (HSV-1 and HSV-2), are neurotropic and reside in neural ganglia.
[22]
Ramsay Hunt Syndrome - StatPearls - NCBI Bookshelf - NIH
Ramsay Hunt syndrome, also known as herpes zoster oticus, is a late complication of varicella-zoster virus infection that results in inflammation of the ...Introduction · Pathophysiology · History and Physical · Treatment / Management
[23]
HIV-related neuropathy: current perspectives - PMC - PubMed Central
Distal symmetric polyneuropathy (DSP) related to human immunodeficiency virus (HIV) is one of the most common neurologic complications of HIV, possibly ...
[24]
Arbovirus, herpesvirus, and enterovirus associated with neurological ...
Regarding viral infections, arbovirus, non-polio enterovirus (EV), and human herpesvirus (HHV) can have harmful effects, including neurological diseases and ...
[25]
Lyme Neuroborreliosis: Clinical Outcomes, Controversy ...
The Centers for Disease Control and Prevention (CDC) reports approximately 30,000 cases of Lyme disease per year but estimates that the true incidence is higher ...
[26]
Epidemics and outbreaks of peripheral nervous system disorders
Sep 10, 2020 · We describe here the three main infectious causes of epidemics that affect the peripheral nervous system: leprosy, poliomyelitis and diphtheria.The Infectious Causes · Leprosy · The Immune-Mediated Causes<|control11|><|separator|>
[27]
Neurological features of Hansen disease - PubMed Central - NIH
May 6, 2024 · Leprosy, also known as Hansen's disease, is caused by Mycobacterium leprae infection and affects mainly the skin and peripheral nervous system.
[28]
Peripheral neuropathy - Symptoms and causes - Mayo Clinic
Sep 2, 2023 · Peripheral neuropathy happens when the nerves that are located outside of the brain and spinal cord (peripheral nerves) are damaged.Diagnosis and treatment · Hypothyroidism · Anti-seizure medications
[29]
Autoimmune Disorders of the Nervous System - PubMed Central - NIH
Apr 14, 2021 · Autoimmune disorders of the nervous system may affect any part of the nervous system, including the brain and spinal cord (central nervous system, CNS) and ...
[30]
Factors associated with recovery from acute optic neuritis in patients ...
Acute optic neuritis (AON) is an inflammatory disorder of the optic nerve and the initial presenting symptom of multiple sclerosis (MS) in approximately 15% to ...<|control11|><|separator|>
[31]
Global, regional, and national burden of Guillain–Barré syndrome ...
Nov 11, 2021 · GBS occurs worldwide with an overall incidence rate of 1–2 cases per 100,000 people per year, affecting all age groups, but is slightly more ...
[32]
Deciphering immune mechanisms in chronic inflammatory ...
Feb 13, 2020 · Chronic inflammatory demyelinating polyneuropathy (CIDP) is an autoimmune disease of the peripheral nerves and nerve roots. It is the most ...
[33]
Anti‐ganglioside complex antibodies in Miller Fisher syndrome - NIH
The presence of the IgG anti‐GQ1b antibody in serum is an excellent diagnostic marker for MFS. This antibody often cross reacts with GT1a, and is ...
[34]
Pathophysiology of Chronic Inflammatory Demyelinating ... - NIH
May 14, 2020 · Chronic inflammatory demyelinating polyneuropathy (CIDP) is an acquired immune-mediated neuropathy characterized by heterogeneous clinical ...Macrophage-Induced... · Fig. 1 · Fig. 4<|control11|><|separator|>
[35]
Spinal Cord Subacute Combined Degeneration - StatPearls - NCBI
Apr 21, 2024 · It can be caused by inadequate oral intake of vitamin B12 and poor absorption of vitamin B12 due to gastrectomy, ileal resection, intake of ...
[36]
A Comprehensive Overview of Subacute Combined Degeneration
Approximately up to 30% of patients with vitamin B12 deficiency experience peripheral neuropathy, which may occur alongside SCD, resulting in myeloneuropathy ...<|separator|>
[37]
Alcoholic neuropathy is clinicopathologically distinct from thiamine ...
We concluded that pure-form of alcoholic neuropathy (ALN) was distinct from pure-form of thiamine-deficiency neuropathy (TDN).
[38]
Diabetes-Related Amyotrophy: Causes, Symptoms & Treatment
Diabetes-related amyotrophy is a rare neuromuscular condition that causes widespread pain and weakness in your hip and leg.Overview · Symptoms And Causes · Management And Treatment
[39]
Diabetic Lumbosacral Plexopathy - Medscape Reference
Aug 9, 2024 · Diabetic amyotrophy, which is distinct from other types of diabetic neuropathy, usually has its onset during or after middle age (although it ...
[40]
Heavy Metal Poisoning - Lead, Mercury, Arsenic and Cadmium
Oct 24, 2024 · Heavy metal poisoning may occur as a result of industrial exposure, air or water pollution, foods, medicines, improperly coated food containers ...
[41]
What are the Physiologic Effects of Arsenic Exposure ... - CDC Archive
Arsenic poisoning can cause peripheral neuropathy. The lesion is a sensory-motor axonopathy. The classic finding is a peripheral neuropathy involving ...
[42]
Arsenic neuropathy | MedLink Neurology
Arsenic toxicity has predominately been the result of suicidal or homicidal ingestion of massive quantities of arsenic. However, in India and Taiwan, ...
[43]
Drug-Induced Peripheral Neuropathy: A Narrative Review - PMC
Among this class of therapies, vincristine is associated with the greatest incidence of neurotoxicity, although studies have also reported DIPN in patients ...
[44]
Drug‐Induced Peripheral Neuropathy - Vilholm - Wiley Online Library
Apr 30, 2014 · Adverse drug effects associated with isoniazid are liver toxicity, nausea, enhanced epileptic tendency and peripheral neuropathy, which ...Missing: neuritis | Show results with:neuritis
[45]
Alcoholic Neuropathy - StatPearls - NCBI Bookshelf - NIH
Dec 30, 2022 · Multiple components are responsible for the development of alcoholic neuropathy. ... inflammatory markers, and oxidative stress. Go to ...
[46]
Anti-Hu antibodies in patients with small-cell lung cancer - PubMed
Purpose: Anti-Hu antibodies (HuAb) recognize antigens expressed by neurons and small-cell lung cancer (SCLC). High titers of HuAb were initially reported in ...Missing: neuritis | Show results with:neuritis
[47]
Prevalence and Meaning of Anti-Hu Antibodies in Small Cell Lung ...
Dec 1, 1999 · This case series confirms earlier reports that anti-Hu antibodies are present in the serum of 16% to 17% of SCLC patients without paraneoplastic ...Missing: neuritis | Show results with:neuritis
[48]
Vasculitic Neuropathy: Background, Pathophysiology, Etiology
Sep 24, 2024 · Necrotizing vasculitis causes neuropathy through ischemic injury to the vessels supplying the nerve. Poor collateral circulation in the nerves ...Background · Pathophysiology · Etiology · EpidemiologyMissing: trauma | Show results with:trauma
[49]
Sensory Neuropathy - StatPearls - NCBI Bookshelf - NIH
Feb 25, 2024 · One of the most distinct symptoms of sensory neuropathy is early-onset ataxia, mainly due to the disruption of the afferent neurons, which ...Introduction · Pathophysiology · Evaluation · Treatment / Management
[50]
Peripheral Neuropathy: What It Is, Symptoms & Treatment
Peripheral neuropathy refers to any condition that affects the nerves outside your brain or spinal cord.
[51]
Herpes Zoster and Postherpetic Neuralgia - PubMed Central - NIH
Jul 1, 2015 · HZ is characterized by unilateral painful vesicles in the affected sensory ganglion. · Seventy-five percent of patients with HZ experience ...
[52]
Herpes Zoster - StatPearls - NCBI Bookshelf
At the same time, the individual may experience headaches, general malaise, and photophobia. The acute eruptive phase is marked by the vesicles and the symptoms ...
[53]
Peripheral Neuropathy | National Institute of Neurological Disorders ...
Aug 7, 2024 · Peripheral neuropathy refers to the many conditions that involve damage to the peripheral nervous system.Charcot-Marie-Tooth Disease · Guillain-Barré Syndrome · Friedreich Ataxia
[54]
Optic Neuritis: Symptoms, Causes & Treatment Options
Optic neuritis (ON) is a type of neuropathy (nerve disease) that can cause eye pain and vision loss or vision changes. It happens when inflammation affects ...Overview · Symptoms And Causes · Infections
[55]
Vestibular Neuritis: Symptoms, Causes & Treatment - Cleveland Clinic
Vestibular neuritis is an inner ear disorder that causes symptoms like sudden vertigo, dizziness, nausea and vomiting.Overview · Symptoms And Causes · Management And Treatment
[56]
Current diagnosis and treatment of vestibular neuritis
This study aimed to review the etiology, epidemiology, diagnosis, and treatment of vestibular neuritis, focusing on the current diagnosis and treatment of ...<|separator|>
[57]
An Update on Peroneal Nerve Entrapment and Neuropathy
Jun 18, 2021 · Clinical presentation of CPN neuropathy includes weakness of ankle dorsiflexion, great toe extension, foot eversion, and sensory loss to the ...Missing: fasciculations | Show results with:fasciculations
[58]
Guillain-Barré Syndrome
Jan 31, 2025 · The main symptoms are weakness or paralysis of the muscles that move the eyes, problems with balance and coordination, and abnormal or no ...Missing: drop | Show results with:drop
[59]
Guillain-Barre syndrome - Symptoms and causes - Mayo Clinic
Jun 7, 2024 · Weakness and tingling in the hands and feet are usually the first symptoms. These sensations can quickly spread and may lead to paralysis. In ...Missing: drop | Show results with:drop
[60]
Autonomic neuropathy - Symptoms & causes - Mayo Clinic
Autonomic neuropathy occurs when there is damage to the nerves that control automatic body functions. It can affect blood pressure, temperature control, ...
[61]
Bell's Palsy | National Institute of Neurological Disorders and Stroke
Apr 7, 2025 · Bell's palsy is a neurological disorder that causes paralysis or weakness on one side of the face. It occurs when one of the nerves that ...
[62]
Guillain-Barré Syndrome - AAFP
Feb 1, 2013 · The most common symptoms reported before onset of GBS are fever, cough, sore throat, and other upper respiratory symptoms. Infection with ...
[63]
An Algorithm for the Evaluation of Peripheral Neuropathy - AAFP
Feb 15, 1998 · The motor examination includes a search for fasciculations or cramps, or loss of muscle bulk. Tone is normal or reduced. The pattern of weakness ...Abstract · Diagnostic Approach · History · Physical Examination
[64]
Peripheral Neuropathy: Evaluation and Differential Diagnosis - AAFP
Dec 15, 2020 · Peripheral neuropathy is idiopathic in 25% to 46% of cases. Diagnosis requires a comprehensive history, physical examination, and judicious laboratory testing.
[65]
Muscle Strength Grading - StatPearls - NCBI Bookshelf
Apr 27, 2025 · The Medical Research Council (MRC) Scale for Muscle Strength is the most widely accepted method of grading muscle strength clinically.[1] This ...
[66]
Peripheral Neuropathy - Neurologic Disorders - Merck Manuals
Peripheral neuropathy is dysfunction of one or more peripheral nerves (the part of a nerve distal to the root and plexus). It includes numerous syndromes ...
[67]
Electrodiagnostic Evaluation of Peripheral Neuropathy - NCBI - NIH
Jan 30, 2023 · Electrodiagnostic testing, which includes nerve conduction studies (NCS) and needle electromyography (EMG), can support the diagnosis of peripheral neuropathy.Missing: neuritis | Show results with:neuritis<|control11|><|separator|>
[68]
Optic Neuritis - PMC - PubMed Central
Optic neuritis is the initial presentation of multiple sclerosis in 25% of individuals. The presence of enhancing and nonenhancing brain MRI lesions meeting ...
[69]
Diagnosis of peripheral neuropathy - PMC - NIH
Jul 15, 2020 · Testing for ATTRv amyloidosis should be considered in patients presenting with the following red flags, i) origin from endemic regions ( ...
[70]
Guillain-Barre Syndrome Workup - Medscape Reference
Jul 29, 2024 · Most, but not all, patients with GBS have an elevated CSF protein level (>400 mg/L), with normal CSF cell counts. Elevated or rising protein ...Approach Considerations · Peripheral Neuropathy Workup · Serologic Studies
[71]
Diagnostic Testing of Neurologic Infections - PMC - PubMed Central
CSF evaluation displays a pleocytosis in two-thirds of patients, and the diagnosis is made with CSF VZV serology or PCR. VZV IgG levels have higher sensitivity ...
[72]
Antibodies in Autoimmune Neuropathies - Neurology.org
Aug 1, 2024 · In 50% of patients with acute motor neuropathies, anti-GM1 and anti-GD1a IgG antibodies are detected. GM1 and GD1a are expressed in both motor ...
[73]
Nerve biopsy: Current indications and decision tools - PMC
Nerve biopsy is typically required to diagnose tumors of peripheral nerve; which may be benign or malignant. The most common benign tumors are schwannoma and ...
[74]
Peripheral neuropathy - Diagnosis and treatment - Mayo Clinic
Sep 2, 2023 · Peripheral neuropathy has many possible causes. Besides a physical exam, which may include blood tests, diagnosis usually requires:Care at Mayo Clinic · Acupuncture · Doctors and departments
[75]
Peripheral Neuropathy: Differential Diagnosis and Management
Apr 1, 2010 · In the early stages of peripheral neuropathy, patients typically present with progressive symptoms, including sensory loss, numbness, and pain ...Missing: paresis | Show results with:paresis
[76]
Conventional management and current guidelines for painful ...
Most current international guidelines recommend a choice of four drugs: amitriptyline, duloxetine, pregabalin or gabapentin, as initial treatment for PDN.
[77]
Pregabalin vs. gabapentin in the treatment of neuropathic pain
Jan 7, 2025 · Pregabalin demonstrated superior and faster efficacy in alleviating neuropathic pain than gabapentin did.
[78]
Physical Therapy Guide to Peripheral Neuropathy - Choose PT
Dec 9, 2018 · Treatment by a physical therapist can help reduce symptoms of PN in some cases, and reduce the effect the symptoms have on movements and activities.What Is Peripheral Neuropathy? · How Can a Physical Therapist...
[79]
Exercise & Physical Therapy
Strengthening exercises can improve muscle strength and my reduce neuropathic pain in people with PN. Tailored workouts or PT sessions may help.
[80]
Nutritional Neuropathy Medication: Vitamins - Medscape Reference
To treat a nutritional neuropathy, replacing the deficient nutrients is necessary. This may involve administration of folate, thiamine (vitamin B 1 ) ...
[81]
Diagnosis and management of Guillain–Barré syndrome in ten steps
Sep 20, 2019 · The ten steps then cover early recognition and diagnosis of GBS, admission to the intensive care unit, treatment indication and selection, monitoring and ...
[82]
Guillain–Barré syndrome - World Health Organization (WHO)
Oct 24, 2025 · Treatment and care · GBS is potentially life-threatening. · Supportive care includes monitoring of breathing, heartbeat and blood pressure. · There ...<|separator|>
[83]
Possible Lyme Carditis with Sick Sinus Syndrome - PubMed Central
Apr 8, 2020 · For patients with early localized Lyme disease, doxycycline, amoxicillin, and cefuroxime are first line. For children younger than 8-years-old, ...Case · Fig. 1 · Discussion
[84]
Post-infectious neurological disorders - PMC - PubMed Central - NIH
Several neurological autoimmune disorders are thought to occur through post-infectious mechanisms. In this review, we discuss the proposed mechanisms ...Molecular Mimicry · Herpes Simplex Virus... · Sydenham's Chorea
[85]
A Randomized, Controlled Trial of Corticosteroids in the Treatment ...
Feb 27, 1992 · Intravenous methylprednisolone followed by oral prednisone speeds the recovery of visual loss due to optic neuritis and results in slightly better vision at ...<|separator|>
[86]
Treatment of Guillain-Barré syndrome and CIDP - PubMed
Randomized controlled trials (RCT) have shown that intravenous immunoglobulin (IVIg) and plasma exchange (PE) are effective in both GBS and CIDP.Missing: plasmapheresis | Show results with:plasmapheresis
[87]
Toxic neuropathies: a practical approach
Inorganic arsenic toxicity occurs in the settings of contaminated drinking water, agricultural (herbicides, pesticides) and occupational exposure (mining, ...
[88]
Diagnosis and Treatment of Paraneoplastic Neurologic Syndromes
Jul 31, 2023 · The hallmark of therapy is the treatment of the underlying malignancy and early immunosuppressive therapy. Symptomatic treatments can be used as ...
[89]
Rituximab versus placebo for chronic inflammatory demyelinating ...
The possible efficacy of rituximab in CIDP has been summarized in two reviews showing an improvement in >70% of the patients,11,14 and in three series of CIDP ...Introduction · Materials and methods · Results · Discussion
[90]
The Role of Stem Cells in Peripheral Nerve Regeneration
Sep 2, 2025 · Preclinical and early clinical studies demonstrate that stem cell therapies can enhance nerve regeneration, remyelination, and revascularization ...Missing: neuritis | Show results with:neuritis
[91]
Successful treatment with 5-day oral 1 g/day methylprednisolone of ...
Dec 13, 2021 · Based on the ONTT trial, the usual treatment of optic neuritis is 1 g/day of intravenous methylprednisolone for 3 days (Beck et al., 1992).
[92]
Oral corticosteroid dosage and taper duration at onset in myelin ...
Oct 16, 2024 · The optimal dose of 12.5 mg of prednisone daily in adults (0.16 mg/kg/day for children) for a minimum of 3 months at the onset of MOGAD delays ...Missing: guidelines | Show results with:guidelines
[93]
Guillain–Barré Syndrome in Older People—A Case Report and ...
Sep 18, 2025 · More than 80% of cases will fully recover, but 10% may have residual disability, with mortality estimated at 3–7%. Older age, multiple ...
[94]
Guillain-Barre Syndrome Life Expectancy and Long-term Outlook
May 27, 2025 · Statistics have shown that 70% of people with GBS eventually experience a full recovery with no negative impacts on their life expectancy.
[95]
Long term prognosis of chronic inflammatory demyelinating ... - NIH
The long term prognosis of CIDP patients was generally favourable, but 39% of patients still required immune treatments and 13% had severe disabilities.
[96]
Neuropathies associated with lymphoma - PMC - PubMed Central
Neuropathy either precedes or is the initial symptom of lymphoma. Diagnostic indicators include rapid progression with early axonal involvement, poor ...Missing: neuritis | Show results with:neuritis
[97]
Optic Neuritis in the Era of Biomarkers - Insights - Mayo Clinic Labs
Jun 3, 2019 · An improvement to 20/40 or better was seen in 92% of patients. However, not all cases improved, with 3% remaining 20/200 or worse.
[98]
Guillain-Barré Syndrome (Gbs): Natal to Fatal: Database Research ...
Feb 11, 2025 · 53.8% of patients achieved good recovery (GBS disability score 0-1) after one year. Prolonged ICU stays (>3 weeks) were common, and 64% required ...
[99]
Brachial Neuritis | Johns Hopkins Medicine
Brachial neuritis is a form of peripheral neuropathy that affects the nerves going to the chest, shoulder, arm, and hand.Missing: definition | Show results with:definition
[100]
Chronic inflammatory demyelinating polyneuropathy - MedlinePlus
Jun 13, 2024 · CIDP is a disorder that involves nerve swelling and irritation (inflammation) that leads to a loss of strength or sensation.
[101]
Postherpetic neuralgia - Symptoms and causes - Mayo Clinic
Feb 10, 2023 · It causes a burning pain in nerves and skin. The pain lasts long after the rash and blisters of shingles go away.
[102]
Multiple Sclerosis Risk after Optic Neuritis - PubMed Central - NIH
Twenty-five percent of patients with no baseline brain MRI lesions developed MS during follow-up compared with 72% of patients with one or more lesions. After ...
[103]
Guillain-Barre Syndrome - Medscape Reference
Jul 29, 2024 · Patients may also have mild limb weakness, ptosis, facial palsy, or bulbar palsy. Patients have reduced or absent sensory nerve action ...