Tumefactive multiple sclerosis

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Tumefactive multiple sclerosis
AFIP-00405558-Glioblastoma-Radiology.jpg
An example of a ring-enhancement around a lesion in gliobastoma. In tumefactive multiple sclerosis, the ring-enhancement is open, not forming a complete ring.

Tumefactive multiple sclerosis is a condition in which the central nervous system of a person has multiple demyelinating lesions with atypical characteristics for those of standard multiple sclerosis (MS). It is called tumefactive as the lesions are "tumor-like" and they mimic tumors clinically, radiologically and sometimes pathologically. [1]

Contents

These atypical lesion characteristics include a large intracranial lesion of size greater than 2.0 cm with a mass effect, edema and an open ring enhancement. A mass effect is the effect of a mass on its surroundings, for example, exerting pressure on the surrounding brain matter. Edema is the build-up of fluid within the brain tissue. Usually, the ring enhancement is directed toward the cortical surface. [2] The tumefactive lesion may mimic a malignant glioma or cerebral abscess causing complications during the diagnosis of tumefactive MS. T2-hypointense rim and incomplete ring enhancement of the lesions on post-gadolinium T1- weighted imaging on brain MRI enable accurate diagnosis of TDL [3]

Normally a tumefactive demyelinating lesion appears together with smaller disseminated lesions separated in time and space, yielding a diagnosis of Multiple Sclerosis. Hence the name "tumefactive multiple sclerosis". When the demyelinating lesion appears alone it has been termed solitary sclerosis. [4] [5] [6] These cases belong to a multiple sclerosis borderline and there is currently no universal agreement on how they should be considered.

Tumefactive multiple sclerosis is a demyelinating and inflammatory disease. Myelination of the axons are highly important for signalling as this improves the speed of conduction of action potentials from one axon to the next. This is done through the formation of high-resistance, low-conductance myelin sheaths around the axons by specific cells called oligodendrocytes. As such, the demyelination process affects the communication between neurons and this consequently affects the neural pathways they control. Depending on where the demyelination takes place and its severity, patients with tumefactive MS have different clinical symptoms. [7]

Signs and symptoms

Symptoms of standard MS consist of both sensory and motor symptoms. The more common symptoms include spasticity, visual loss, difficulty in walking and paresthesia which is a feeling of tickling or numbness of the skin. [8] but symptoms of tumefactive MS are not so clear. They often mimic a variety of other diseases including ischemic stroke, peroneal nerve palsy and intracranial neurologic disease.[ citation needed ]

Subjects have been reported to suffer from a decreased motor control resulting in a 'foot drop', [9] or significantly reduced leg movement. [10] In other cases closer mimicking strokes, subjects may suffer from confusion, dizziness, and weakness in one side of the face. [11] Symptoms also can mimic a neoplasm with symptoms such as headaches, aphasia, and/ or seizures.[13]

There are some differences with normal MS symptoms.

Spasticity is not as prevalent in tumefactive cases, because in standard MS it is caused by demyelination or inflammation in the motor areas of the brain or the spinal cord. [8] This upper motor neuron syndrome appears when motor control of skeletal muscles is affected due to damage to the efferent motor pathways. Spasticity is an involuntary muscle movement like an exaggerated stretch reflex, which is when a muscle overcompensates and contracts too much in response to the muscle being stretched. It is believed that spasticity is the result of the lack of inhibitory control on the muscles, an effect of neuronal damage. [12]

Visual loss or disturbances are also different. In standard MS, they are a result of inflammation of the optic nerve, known as optic neuritis. The effects of optic neuritis can be loss of color perception and worsening vision. Vision loss usually starts off centrally in one eye and may lead to complete loss of vision after a period of time. [8]

The possible cognitive dysfunction is also rare in tumefactive cases. MS patients may show signs of cognitive impairment where there is a reduction in the speed of information processing, a weaker short-term memory and a difficulty in learning new concepts. [13] This cognitive impairment is associated with the loss of brain tissue, known as brain atrophy which is a result of the demyelination process in MS. [14]

About fatigue: most MS patients experience fatigue and this could be a direct result of the disease, depression or sleep disturbances due to MS. It is not clearly understood how MS results in physical fatigue but it is known that the repetitive usage of the same neural pathways results in nerve fiber fatigue that could cause neurological symptoms. Such repeated usage of neural pathways include continuous reading which may result in temporary vision failure. [8]

Evolution

Some reports indicate that an initial tumefactive lesion can evolve to various pathological entities: multiple sclerosis (the most common), Balo's concentric sclerosis, Schilder's disease and acute disseminated encephalomyelitis [15]

Course

Usually tumefactive demyelination is monophasic, but cases with recurrence have been reported [16]

Cause

The pathology of the tumefactive demyelinating lesion (TDL) is heterogeneous. [17] Several conditions can produce tumefactive lesions. This is known because in some special cases the etiology can be identified. For example, there are some cases of NMO, misidentified as MS and treated with interferon-beta by mistake. Some of these patients developed tumefactive lesions. [18] [19] Anyway, it is important to have into account that NMO itself can also produce them [20] [21]

Some other cases have been found related to viral infection, [22] some others related to NMOSD, [23] others could be paraneoplastic, [24] [25] Also some cases could be related to hormonal treatments [26]

Other possible cause are immunomodulatory combinations. In particular, it has been found that switching from standard MS therapies to fingolimod can trigger tumefactive lesions in some MS patients [27] [28] [29] [30] While standard multiple sclerosis process has an autoimmune response after the breach of the blood–brain barrier, in tumefactive MS things do not process in the same way, and demyelinating lesions do not always show antibody damage. Subjects with tumefactive multiple sclerosis display elevated levels of choline (Cho)/creatine ratio and increased lactate which is associated with demylinating diseases. Cases also display oligoclonal bands in the cerebrospinal fluid. [11]

The disease is heterogeneous and the lesions do not always comply with the requirements for multiple sclerosis diagnosis (dissemination in time and space). In these cases it is only possible to speak about tumefactive demyelination (TD). [31]

In general, it is accepted that the two main causes of pseudo-tumoral lesions are Marburg multiple sclerosis and acute disseminated encephalomyelitis (ADEM). [32] Tumefactive demyelination of the spinal cord is rare but it has been reported [33]

Damage is not confined to the demyelinating area. Wallerian degeneration outside the lesions has been reported. [34]

In general, during the acute phase, the plaques of lesions were characterized by massive demyelination with relatively axonal preservation associated with reactive astrocytosis and infiltration of macrophages. In plaques of chronic lesions, demyelinated lesions with relative axonal preservation and sharply defined margins were major findings. And myelin-laden macrophages accumulate at the edges of plaques and stay inactive [35]

Diagnosis

Diagnosis of tumefactive MS is commonly carried out using magnetic resonance imaging (MRI) and proton MR spectroscopy (H-MRS). Diagnosis is difficult as tumefactive MS may mimic the clinical and MRI characteristics of a glioma or a cerebral abscess. However, as compared to tumors and abscesses, tumefactive lesions have an open-ring enhancement as opposed to a complete ring enhancement. [1] Even with this information, multiple imaging technologies have to be used together with biochemical tests for accurate diagnosis of tumefactive MS. [36]

Tumefactive demyelination is distinguished from tumor by the presence of multiple lesions, absence of cortical involvement, and decrease in lesion size or detection of new lesions on serial imaging [37] Tumefactive lesions can appear in the spinal cord, making the diagnosis even more difficult. [38]

Magnetic resonance imaging

MRI diagnosis is based on lesions that are disseminated in time and space, meaning that there are multiple episodes and consisting of more than one area. [39] There are two kinds of MRI used in the diagnosis of tumefactive MS, T1-weighted imaging and T2-weighted imaging. Using T1-weighted imaging, the lesions are displayed with low signal intensity, meaning that the lesions appear darker than the rest of the brain. Using T2-weighted imaging, the lesions appear with high signal intensity, meaning that the lesions appear white and brighter than the rest of the brain. When T1-weighted imaging is contrast-enhanced through the addition of gadolinium, the open ring enhancement can be viewed as a white ring around the lesion. [40] A more specific MRI, Fluid attenuation inversion recovery (FLAIR) MRI show the signal intensity of the brain. Subjects with tumefactive multiple sclerosis may see a reduction of diffusion of the white matter in the affected area of the brain. [11]

Proton MR spectroscopy

Proton (H+) MR spectroscopy (H-MRS) identifies biochemical changes in the brain such as the quantity of metabolic products of neural tissue including choline, creatine, N-acetylaspartate (NAA), mobile lipids and lactic acid.[ citation needed ]

When demyelination is occurring, there is breakdown of cell membranes resulting in an increase in the level of choline. NAA is specific to neurons and thus, a reduction in NAA concentration indicates neuronal or axonal dysfunction. As such, the levels of choline and NAA can be measured to determine if there is demyelination activity and inflammation in the brain.[ citation needed ]

Usually, the ratio of choline to NAA is used as biomarker [41] being higher in gliomas than in TDLs or MS lesions [42]

Treatment

Typical tumefactive lesions have been found to be responsive to corticosteroids because of their immunosuppressive and anti-inflammatory properties. They restore the blood–brain barrier and induce cell death of T-cells. [13]

No standard treatment exists, but practitioners seem to apply intravenous corticosteroids, followed by plasmapheresis and cyclophosphamide in non-responsive cases [43]

Plasmapheresis has been reported to work even in the absence of response to corticosteroids [44]

Disease-modifying agents

Pharmacologic treatments for MS include immunomodulators and immunosuppressants which reduce the frequency and severity of relapses by about 35% and reduce the lesion growth. [45] Unfortunately they are mainly tested for RRMS and its effect in tumefactive lesions is unknown. The main ones are Interferon beta (IFN-beta), Glatiramer acetate and Mitoxantrone [ citation needed ]

Plasma exchange has been reported to work at least in some cases [46]

Treatment of symptoms

Due to the wide range of symptoms experienced by people with MS, the treatment for each MS patient varies depending on the extent of the symptoms.

Spasticity

The treatment of spasticity ranges from physical activity to medication. Physical activity includes stretching, aerobic exercises and relaxation techniques. Currently, there is little understanding as to why these physical activities aid in relieving spasticity. Medical treatments include baclofen, diazepam and dantrolene which is a muscle-relaxant. Dantrolene has many side effects and as such, it is usually not the first choice in treatment of spasticity. The side effects include dizziness, nausea and weakness. [13]

Fatigue

Fatigue is a common symptom and affects the daily life of individuals with MS. Changes in lifestyle are usually recommended to reduce fatigue. These include taking frequent naps and implementing exercise. MS patients who smoke are also advised to stop. Pharmacological treatment include anti-depressants and caffeine. Aspirin has also been experimented with and from clinical trial data, MS patients preferred using aspirin as compared to the placebo in the test. One hypothesis is that aspirin has an effect on the hypothalamus and can affect the perception of fatigue through altering the release of neurotransmitters and the autonomic responses. [13]

Cognitive dysfunction

There are no approved drugs for the treatment of cognitive dysfunction, however, some treatments have shown an association with improvements in cognitive function. One such treatment is Ginkgo biloba , is a herb commonly used by patients with Alzheimer's disease. [13]

Epidemiology

Approximately 2 million people in the world suffer from multiple sclerosis [47] Tumefactive multiple sclerosis cases make up 1 to 2 of every 1000 multiple sclerosis cases. This means that only around 2000 people in the world suffer of tumefactive MS. Of those cases, there is a higher percentage of females affected than males. The median age of onset is 37 years. [36]

As in general MS, there are differences for gender, ethnicity and geographic location. Based on epidemiological studies, there are about 3 times more female MS patients than male patients, indicating a possibility of an increased risk due to hormones. Among different ethnic groups, MS is the most common among Caucasians and seems to have a greater incidence at latitudes above 40° as compared to at the equator. While these associations have been made, it is still unclear how they result in an increased risk of MS onset. [48]

Solitary sclerosis

Normally a tumefactive demyelinating lesion appears together with smaller disseminated lesions. Hence the name "tumefactive multiple sclerosis". When the demyelinating lesion appears alone it has been termed "solitary sclerosis"[ citation needed ]

This variant was first proposed (2012) by Mayo Clinic researches. [4] though it was also reported by other groups more or less at the same time. [49] [50] It is defined as isolated demyelinating lesions which produce a progressive myelopathy similar to primary progressive MS, [51] [52] [53] and is currently considered inside the Tumefactive Multiple sclerosis. [5] Some groups have reported some kind of response of this variant to biotin [54]

solitary pontine lesion

Syndrome consisting in solitary lesions uniformly located along the trigeminal pontine pathway, producing trigeminal neuralgia (TN). They present similar clinical features than MS-TN but with a single pontine lesion. [55]

MOG antibody‐associated demyelinating pseudotumor

Main article: anti-MOG associated encephalomyelitis

Some anti-MOG cases satisfy the MS requirements (lesions disseminated in time and space) and are therefore traditionally considered MS cases. After the discovery of the anti-MOG disease this classification is into revision. [56]

See also

Related Research Articles

<span class="mw-page-title-main">Acute disseminated encephalomyelitis</span> Autoimmune disease

Acute disseminated encephalomyelitis (ADEM), or acute demyelinating encephalomyelitis, is a rare autoimmune disease marked by a sudden, widespread attack of inflammation in the brain and spinal cord. As well as causing the brain and spinal cord to become inflamed, ADEM also attacks the nerves of the central nervous system and damages their myelin insulation, which, as a result, destroys the white matter. The cause is often a trigger such as from viral infection or vaccinations.

<span class="mw-page-title-main">Optic neuritis</span> Inflammation of the optic nerve

Optic neuritis describes any condition that causes inflammation of the optic nerve; it may be associated with demyelinating diseases, or infectious or inflammatory processes.

<span class="mw-page-title-main">Multiple sclerosis</span> Disease that damages the myelin sheaths around nerves

Multiple sclerosis (MS) is an autoimmune disease in which the insulating covers of nerve cells in the brain and spinal cord are damaged. Being a demyelinating disease, MS disrupts the ability of parts of the nervous system to transmit signals, resulting in a range of signs and symptoms, including physical, mental, and sometimes psychiatric problems. Symptoms include double vision, vision loss, eye pain, muscle weakness, and loss of sensation or coordination. MS takes several forms, with new symptoms either occurring in isolated attacks or building up over time. In relapsing forms of MS, between attacks, symptoms may disappear completely, although some permanent neurological problems often remain, especially as the disease advances. In progressive forms of MS, bodily function slowly deteriorates once symptoms manifest and will steadily worsen if left untreated.

<span class="mw-page-title-main">Demyelinating disease</span> Any neurological disease in which the myelin sheath of neurons is damaged

A demyelinating disease refers to any disease affecting the nervous system where the myelin sheath surrounding neurons is damaged. This damage disrupts the transmission of signals through the affected nerves, resulting in a decrease in their conduction ability. Consequently, this reduction in conduction can lead to deficiencies in sensation, movement, cognition, or other functions depending on the nerves affected.

Neuromyelitis optica spectrum disorders (NMOSD) are a spectrum of autoimmune diseases characterized by acute inflammation of the optic nerve and the spinal cord (myelitis). Episodes of ON and myelitis can be simultaneous or successive. A relapsing disease course is common, especially in untreated patients.

<span class="mw-page-title-main">Uhthoff's phenomenon</span> Worsening of neurologic symptoms in multiple sclerosis caused by heat

Uhthoff's phenomenon is the worsening of neurologic symptoms in multiple sclerosis (MS) and other demyelinating diseases when the body is overheated. This may occur due to hot weather, exercise, fever, saunas, hot tubs, hot baths, and hot food and drink. Increased temperature slows nerve conduction, but the exact mechanism remains unknown. With an increased body temperature, nerve impulses are either blocked or slowed in a damaged nerve. Once the body temperature is normalized, signs and symptoms typically reverse.

<span class="mw-page-title-main">McDonald criteria</span>

The McDonald criteria are diagnostic criteria for multiple sclerosis (MS). These criteria are named after neurologist W. Ian McDonald who directed an international panel in association with the National Multiple Sclerosis Society (NMSS) of America and recommended revised diagnostic criteria for MS in April 2001. These new criteria intended to replace the Poser criteria and the older Schumacher criteria. They have undergone revisions in 2005, 2010 and 2017.

Experimental autoimmune encephalomyelitis, sometimes experimental allergic encephalomyelitis (EAE), is an animal model of brain inflammation. It is an inflammatory demyelinating disease of the central nervous system (CNS). It is mostly used with rodents and is widely studied as an animal model of the human CNS demyelinating diseases, including multiple sclerosis (MS) and acute disseminated encephalomyelitis (ADEM). EAE is also the prototype for T-cell-mediated autoimmune disease in general.

<span class="mw-page-title-main">Pathophysiology of multiple sclerosis</span>

Multiple sclerosis is an inflammatory demyelinating disease of the CNS in which activated immune cells invade the central nervous system and cause inflammation, neurodegeneration, and tissue damage. The underlying cause is currently unknown. Current research in neuropathology, neuroimmunology, neurobiology, and neuroimaging, together with clinical neurology, provide support for the notion that MS is not a single disease but rather a spectrum.

<span class="mw-page-title-main">Lesional demyelinations of the central nervous system</span>

Multiple sclerosis and other demyelinating diseases of the central nervous system (CNS) produce lesions and glial scars or scleroses. They present different shapes and histological findings according to the underlying condition that produces them.

Inflammatory demyelinating diseases (IDDs), sometimes called Idiopathic (IIDDs) due to the unknown etiology of some of them, are a heterogenous group of demyelinating diseases - conditions that cause damage to myelin, the protective sheath of nerve fibers - that occur against the background of an acute or chronic inflammatory process. IDDs share characteristics with and are often grouped together under Multiple Sclerosis. They are sometimes considered different diseases from Multiple Sclerosis, but considered by others to form a spectrum differing only in terms of chronicity, severity, and clinical course.

<span class="mw-page-title-main">Balo concentric sclerosis</span> Medical condition

Baló's concentric sclerosis is a disease in which the white matter of the brain appears damaged in concentric layers, leaving the axis cylinder intact. It was described by József Mátyás Baló who initially named it "leuko-encephalitis periaxialis concentrica" from the previous definition, and it is currently considered one of the borderline forms of multiple sclerosis.

<span class="mw-page-title-main">Marburg acute multiple sclerosis</span> Medical condition

Marburg acute multiple sclerosis, also known as Marburg multiple sclerosis or acute fulminant multiple sclerosis, is considered one of the multiple sclerosis borderline diseases, which is a collection of diseases classified by some as MS variants and by others as different diseases. Other diseases in this group are neuromyelitis optica (NMO), Balo concentric sclerosis, and Schilder's disease. The graver course is one form of malignant multiple sclerosis, with patients reaching a significant level of disability in less than five years from their first symptoms, often in a matter of months.

Research in multiple sclerosis may find new pathways to interact with the disease, improve function, curtail attacks, or limit the progression of the underlying disease. Many treatments already in clinical trials involve drugs that are used in other diseases or medications that have not been designed specifically for multiple sclerosis. There are also trials involving the combination of drugs that are already in use for multiple sclerosis. Finally, there are also many basic investigations that try to understand the disease better and in the future may help to find new treatments.

Poser criteria are diagnostic criteria for multiple sclerosis (MS). They replaced the older Schumacher criteria, and are now considered obsolete as McDonald criteria have superseded them. Nevertheless, some of the concepts introduced have remained in MS research, like CDMS, and newer criteria are often calibrated against them. The criteria were unveiled in the Annals of Neurology in 1983 by a team led by Dr. Charles M. Poser.

<span class="mw-page-title-main">Diagnosis of multiple sclerosis</span>

Current standards for diagnosing multiple sclerosis (MS) are based on the 2018 revision of McDonald criteria. They rely on MRI detection of demyelinating lesions in the CNS, which are distributed in space (DIS) and in time (DIT). It is also a requirement that any possible known disease that produces demyelinating lesions is ruled out before applying McDonald's criteria.

<span class="mw-page-title-main">Pathology of multiple sclerosis</span> Pathologic overview

Multiple sclerosis (MS) can be pathologically defined as the presence of distributed glial scars (scleroses) in the central nervous system that must show dissemination in time (DIT) and in space (DIS) to be considered MS lesions.

MOG antibody disease (MOGAD) or MOG antibody-associated encephalomyelitis (MOG-EM) is an inflammatory demyelinating disease of the central nervous system. Serum anti-myelin oligodendrocyte glycoprotein antibodies are present in up to half of patients with an acquired demyelinating syndrome and have been described in association with a range of phenotypic presentations, including acute disseminated encephalomyelitis, optic neuritis, transverse myelitis, and neuromyelitis optica.

Radiologically isolated syndrome (RIS) is a clinical situation in which a person has white matter lesions suggestive of multiple sclerosis (MS), as shown on an MRI scan that was done for reasons unrelated to MS symptoms. The nerve lesions in these people show dissemination in space with an otherwise normal neurological examination and without historical accounts of typical MS symptoms.

Anti-AQP4 diseases, are a group of diseases characterized by auto-antibodies against aquaporin 4.

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