Multiple Sclerosis

Multiple Sclerosis

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Multiple sclerosis
Multiple Sclerosis is a demyelinating disease cause a widespread degeneration of the central nervous system (CNS) which gradually results in severe neurological deficits. The disease is characterized by remissions and relapse, erratic onset and duration is flare up acutely. Each relapse may involve different area in white matter in central nervous system (CNS) .

There is may involve in genetic and environmental factor, which may cause immunologically mediated inflammatory response with CNS . The immune response in mediating tissue damage, and the extent to which these change are the cause or consequence of myelin injury, remain too established. Exposure to other viral illness such as measles, mumps, and rubella rather late in childhood may be a factor in those who are at risk of developing the disease. The further evidence of genetic susceptibility is provided by epidemiological studies within and between ethnic. The risk is raise group for offspring and for sibling of affected persons. Other than that, environment may be relatively more protective. Age is also a factor in immigration populations. Dean (1967) said the multiple sclerosis is higher for who migrated as adults rather than as children. Furthermore, the multiple sclerosis does not have a single cause . A new episode of demyelination is more likely to occur following a viral infection but no single agent has implicated.

Demyelination is a disintegrated of the myelin sheath cause by an inflammatory and destruction process, the axon being partly or completely denuded. The features of multiple sclerosis lesions are perivascular inflammation followed by myelin depletion, oligodendrocytes loss and astroglial proliferation. The initial stage characterized by the accumulation of inflammatory cells, lymphocytes and monocytes around venules within the CNS. Inflammation may cause a function block in conduction through myelinated axons. Next, there is active destruction of the oligodendrocyte and its myelin sheath as a result of contact with macrophanges and microglia . This followed by depletion of oligodendrocytes in which denuded axons re seen within the lesion. Finally, the lesion heals by scar formation dependent upon astrocytic reactivity, producing hardened patches or plaques from which the disease gets its name. the most common side of plaques are in the boundary grey matter in the cerebellum, cerebellar white matter, optic nerves, cervical portion of spinal cord and brain stem.

Multiple sclerosis Diagnostic Criteria
Numerous different diagnostic criteria have been proposed over the year. The criteria that colleagues formulated in 1965 was define of relapses worsening symptom lasting longer than 24 hours and separated by 1 month is still used in practice and research protocols today.

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The stated strict age cutoffs are now known to be inappropriate. In modern era, MRI allows both pediatric and late onset multiple sclerosis to be more easily differentiated from etiologies that are more common in these age groups . The predictive MRI features were subsequently use to develop the most recent diagnostic criteria, known as McDonald criteria and subsequently revised and adapted in 2005. In the McDonald criteria, the authors used Barkhof MRI criteria, as a modified by Tintore to DIS. The Barkhof or Tintore criteria have the advantages of a high specificity by decreasing the chance that T2- weighted hypertensive not secondary to demyelination (e.g, ischemic, unidentified bright object) will be erroneously labeled as multiple sclerosis. The 2001 McDonald criteria dor DIT were designed to prevent misdiagnosis of patient with acute disseminated encephalomyelitis (ADEM), who can develop new MRI lesions for up to 3 months after symptom onset without the development of new clinical deficits.

Clinically symptoms
Cognitive and affective symptoms
Multiple sclerosis may have a intentional deficits, both visual and auditory including memory disorder. If the deficits more severe and prevalent in patient with the progressive form of the disease than in the relapsing disease (Beatty et al. 1989) .
Mostly personality changes, preference and attitudes tend to accompany impairments in focusing attention and distractability (Lazek 1995). Usually, therapist may be able to observe the patient may more tend to depression. Their feeling may mentally block, of dissatisfaction with themselves and diminished spontaneity of action (Lezak 1995). Emotional distress may also see in the multiple sclerosis patient due to experiencing increasing severity of symptom .

Special sense
Visual pathway involvement is very common in multiple sclerosis disease. In early stage of disease, patient may experience of progressively blurring of vision, then later stage patient may losing sight in one eye or suffering double vision.
Sensory motor impairment
Multiple sclerosis usually affects both or one limbs. The patient may experience of heaviness and clumsiness. This sign may depend on which site may affect cerebellum, upper motor lesion or corticospinal damage. Each of the sites may appear different type of symptom. Multiple sclerosis patient may have a spasticity impairment. Altered sensation occurs at some stage in almost every individuals of multiple sclerosis (sinkjaer and colleagues 1993) .

Differential diagnosis:
Postinfections Encephalomyelitis
• Postinfections encephalomyelitis is a subacute syndrome which is caused by autoimmune response to a viral infection. Clinically most of client may complaint of acute or subacute onset difficulty in walking, confusion on their daily task, disorientation, problems with bladder or bowel control, reduce of muscle power or complaint of easily fatigue, and other symptom. Abnormalities consistent with demyelinating lesions can see o MRI images. This condition may or may not be monophysic, in chronic case, patient may require a proper treatment.
Primary Central nervous system Vasculatis
• Mostly, this may result in syndrome resembling Multiple sclerosis. Therapist can identify the symptoms includes severe headache, confusion and sudden stroke like episode. We may can seen high level of protein in CSF, as well as high erythrocyte sedimentation rate. Patient may have abnormal angiogram of cerebral vessels. Antinuclear or anti phospholipid antibodies may be present.

Lyme disease
• This type of symptom known to cause intermittent neurologic events. Some of the most frequent problems include Bell’s palsy, nonspecific symptom of numbness, fatigue and amnesia. CSF findings may resemble those found in the Multiple sclerosis, the MRI may show a white matter disease. History of tick bites, rashes and arthalgia should be sought after. This desease must be screen by using a MRI to detect the sugar level which present in cerebro spinal fluid.

Systemic Lupus Erytheatosus
• This type of symptom may cause multiple neurologic pathology such as optic abnormalities, encephalopathy, tranverse myelitis, strokes. As a physical therapist, we needs to look for systemic abnormalities, such as elevated erythrocyte sedimentation rate. Sometimes occasions lupus erythematosus and Multiple Sclerosis may be found in the same patient .

Tropical Spastic Paraparesis
• Tropical spastic paraparesis is a retroviral disease caused by HTLV-1 virus. It is uncommonly in the continental United States, but may be seen infrequently in patients who resided for some time around the Caribean Sea Basin. The major clinical manifestations are progressive spastic paraparesis or generalized white matter disease .

Behcet syndrome
• This sigh is very similar to Multiple sclerosis. However, the main distinguishing features of this condition are oral and genital ulcers, and uveitis, as well as possible involvement of lungs, joint, intestines and heart. This group of patients may present with either lower lim paresis, atrophy of calf and tongue muscle, impairment of balance, cerebellar ataxia or cerebral venous thrombosis .

Sarcoidosis and sjogren syndrome
• This is one of the syndrome may show lesions on MRI that resemble those found in Multiple Sclerosis. This may affect a multiple organ systems and have different from Multiple Sclerosis. A chest X-ray may show granulomatous disease of the lungs and meningeal enhancement is seen in patient with CNS involvement. Oligoclonal bands and IgG are raised in CSF of patient with sarcoidosis. Central nervous system may involve and the course of the disease may show sriking similarity to Multiple Sclerosis. Angiotensin converting enzyme determination may be elevated in either serum or CSF but is not reliably abnormal .

Deficiency of vitamin B-12 in Multiple sclerosis
• The patient who deficiency of Vitamins B-12 and tertiary syphilis may result in dorsum column abnormalities and dementia. The two conditions need to be ruled out when patients present with the above mentioned symptoms as their chief complaints .

Leukodystrophies in Adulthood
• Leukodystrophies of adulthood (metachromatic leukodystropy, krabbe’s disease, adrenal leukodystrophy), show large areas of involvement on the MRI scan where no normal white can be found .

Hereditary Degenerative Disorders
• Multiple sclerosis may associated with Hereditary disorder (olivopontocererallar, spinocerebellar degeneration,) initially may resemble chronic progressive multiple sclerosis. However, we cannot identify the characteristic of white matter on MRI and the CSF is normal in these patients .

Progressive Multifocal Leukoencephalopathy
• This is the result taken from the MRI in progressive multifocal leukoencephalopathy in immune compromised patients (frequently in patients who diagnos with AIDS) other disease of multiple sclerosis .

Pain pathway abnormalities
• Pain and other uncomfortable sensory syndromes may constitute the initial symptom in multiple sclerosis. Due to the prevalence of neuropathic and idiopathic pain syndrome in the general population, distinguishing multiple sclerosis related pain from others conditions may present a challenge .
• Certain pain syndrome is may feel by patient in Multiple sclerosis than others. Terminology neuralgia occurs uncommonly in Multiple sclerosis and may be clinically indistinguishable from idiopathic trigeminal pain. Clues to a possible demyelinating etiology include younger age of onset (less than 40 years) and bilateral symptom pain may be the heralding symptom of Multiple sclerosis, in most cases it develops later in the disease course.
• Pain syndrome associated with Multiple sclerosis :
o Pseudoradicular pain
o Lhermitte sign
o Paroxysmal spasms

o Trigeminal neuralgia
o Migraine

• Lhermitte sign;
o The sensation of radiating electrical sensation elicited by neck flexion, can be painful or disconceting to patients.
o Lhermitte sign may be caused by multiple conditions affecting the cervical spinal cord.
o Cervical stenosis with or without cord compression, extrinsic and extrinsic spinal tumor, spinal cavernous angioma, and B12 deficiency have all been associated with Lhermitte sign .

• Tonic spasm;
o Paroxysmal may attacks of involuntary muscle contraction that frequent migrate into adjacent parts of the body and may cause intense discomfort. They seldom intense constitute the initial presentation of demyelination disease, but not occur in small percentage population of Multiple sclerosis over the disease course .
o Cereberal infarction involving the corticospinal tract have also ben associated with tonic spasms.
o Unpleasant headache may aoccur in the multiple sclerosis people more commonly than in the general population but only limited evidence suggests multiple sclerosis may present as a migraine disorder. Magraineurs may have a brain MRI performed because of headache, and identify of hypertensities onT2- weighted scans will identified .

Psychiatric and cognitive presentations
• Depression and progressive amnesia appear to be the most common features of such a presentation, but less common symptom such asmania, aphasia, and overall personality changes may occurs .
• Differential diagnosis of cognitive and behavioral syndrome with abnormal Magnetic resonance imaging:
o Metachromatic leukodystrophy and Adrenoleukodystrophy
o Apart from that, Viral encephalitis or herpes simplex virus also involved
o Postinfection encephalitis and Multiple sclerosis
o Patient who have a past history of HIV ,Lupus cerebritis and Progressive multifocal leukoencephalopathy may also can identify with MRI.
o Some of the result may show Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy may apper in the MRI

Optic neuritis
• The incidence of MRI abnormalities in children with ON is than less in adults, which, when coupled with clinical experience, suggest that the rate of progression to Multiple sclerosis in children with isolated ON may well be less than that in adults. MRI was a strong predictor, the 5 years there was increasing of Multiple sclerosis by 18% in patient with no brain MRI lesion and 51% in patients with three or more lesions .
• There is two type of optic neuritis
1. Inflammatory optic neuritis: is also known as idiopathic inflammatory demyelinating disease, acute disseminated demyelinating disease and neuromyelitis optica
o Parainfectious optic neuritic is cause by a viral which known as adenovirus, coxsackievirus, cytomegalovirus, epstien-Barr Virus, hepatitis A, hepatitis B, HVI, measles, mumps, herpes zoster simplex.
o Bacteria like Borrelia burgdorferi, bortonella henselae, troponema pallidum and mycobacterium tuberculosis may cause inflammation of optic neuritis.

2. Optic neuropathies
o Vascular is due to lack of blood supply to optic neuropathy, other cell arthritis, nonarteritic anterior ischemic optic neuropathy
o Posterior ischemic optic neuropathy which cause by infection of herpes zoster virus, cytomegalovirus, t. pallidum, B. henselae, Mycobacterium tuberculosis, T. gondlii, T. canis, Cryptococcus.
o The optic neuropathies may also cause by hereditary such as leber’s heditary optic neuropathy, other mitochondrial disorders traumatic.
3. Other ophthalmologic disorder is a anterior segment disease, corneal trauma or inflammation, acute angel closure glaucoma
o The retinal disease like retinitis pigmentosa, cone rod dystrophy, central serous retinopathy, and melanoma associated retinopathy, recoverin associated retinopathy.

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