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| Demyelinative diseases of the central nervous system are characterized by |
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loss of myelin with variable loss of axons.
In contrast, infarcts, contusions, encephalitis, and other conditions destroy myelin and axons equally. |
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| The main demyelinative disease of the CNS is multiple sclerosis (MS) and its variants. Its counterpart in the peripheral nervous system is inflammatory demyelinative polyradiculoneuropathy (Guillain-Barré syndrome-GBS) and its chronic variants. |
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| autoimmune inflammatory diseases. There are also virus-induced demyelinative diseases, such as progressive multifocal leukoencephalopathy. Demyelinative diseases should be distinguished from leukodystrophies, which are inherited metabolic disorders of myelin lipids and proteins. |
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| Guillain-Barré syndrome (GBS) is a autoimmune disorder in which the body's immune system attacks part of the peripheral nervous system. The first symptoms of this disorder include varying degrees of weakness or tingling sensations in the legs. In many instances the symmetrical weakness and abnormal sensations spread to the arms and upper body. These symptoms can increase in intensity until certain muscles cannot be used at all and, when severe, the person is almost totally paralyzed. In these cases the disorder is life threatening - potentially interfering with breathing and, at times, with blood pressure or heart rate - and is considered a medical emergency. Most individuals, however, have good recovery from even the most severe cases of Guillain-Barré syndrome, although some continue to have a certain degree of weakness. |
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Guillain-Barré syndrome can affect anybody. It can strike at any age and both sexes are equally prone to the disorder. The syndrome is rare, however, afflicting only about one person in 100,000. Usually Guillain-Barré occurs a few days or weeks after the patient has had symptoms of a respiratory or gastrointestinal viral infection. Occasionally surgery will trigger the syndrome. Recently, some countries worldwide have reported an increased incidence of GBS following infection with the Zika virus. In rare instances vaccinations may increase the risk of GBS.
After the first clinical manifestations of the disease, the symptoms can progress over the course of hours, days, or weeks. Most people reach the stage of greatest weakness within the first 2 weeks after symptoms appear, and by the third week of the illness 90 percent of all patients are at their weakest. |
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In, Guillain-Barré syndrome however, the immune system starts to destroy the myelin sheath that surrounds the axons of many peripheral nerves, or even the axons themselves (axons are long, thin extensions of the nerve cells; they carry nerve signals). The myelin sheath surrounding the axon speeds up the transmission of nerve signals and allows the transmission of signals over long distances.
In diseases in which the peripheral nerves' myelin sheaths are injured or degraded, the nerves cannot transmit signals efficiently. That is why the muscles begin to lose their ability to respond to the brain's commands |
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| Lumbar puncture for cerebrospinal fluid (CSF) studies is recommended. During the acute phase of GBS, characteristic findings on CSF analysis include albuminocytologic dissociation, which is an elevation in CSF protein (>0.55 g/L) without an elevation in white blood cells. The increase in CSF protein is thought to reflect the widespread inflammation of the nerve roots. |
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In MS, the immune system attacks the protective sheath (myelin) that covers nerve fibers and causes communication problems between your brain and the rest of your body. Eventually, the disease can cause the nerves themselves to deteriorate or become permanently damaged.
Signs and symptoms of MS vary widely and depend on the amount of nerve damage and which nerves are affected. Some people with severe MS may lose the ability to walk independently or at all, while others may experience long periods of remission without any new symptoms. |
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| MS affects one in every 500 persons, women twice as frequently as men. It is more common in young adults and causes a variety of neurological deficits (visual loss, paralysis, sensory loss, ataxia, brainstem signs, psychiatric disorders, dementia). Many MS cases evolve over a long period (20-30 years) with remissions and exacerbations. Some cases have an acute, fulminant, even fatal course, and others go into a relentlessly progressive phase after a period of remissions and exacerbations.[image] |
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The pathology is characterized by multifocal lesions, the MS plaques. The usual evolution of the MS plaque is as follows: in the acute phase (active plaque), activated mononuclear cells, including lymphocytes, microglia, and macrophages destroy myelin and, to a variable degree, oligodendrocytes. Myelin debris are picked up by macrophages and degraded. At an early stage, macrophages contain myelin fragments; later, they contain proteins and lipids from chemical degradation of myelin. This evolution takes a few weeks. With time, gliosis develops, and plaques reach a burned-out stage consisting of demyelinated axons traversing glial scar tissue (inactive plaque). Remaining oligodendrocytes attempt to make new myelin. If the inflammatory process is arrested at an early phase, plaques are partially remyelinated (shadow plaque). In more advanced lesions, remyelination is ineffective because gliosis creates a barrier between the myelin producing cells and their axonal targets. The pathological process may be arrested at any time, sometimes after partial demyelination.
http://neuropathology-web.org/chapter6/chapter6aMs.html |
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| A process leading to scars in the central nervous system that involves the production of a dense fibrous network of neuroglia (supporting cells) in areas of damage. Gliosis is a prominent feature of many diseases of the central nervous system, including multiple sclerosis and stroke. After a stroke, neurons die and disappear with replacement gliosis. |
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| CSF of people with MS contains |
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The CSF of people with MS usually contains:
Elevated levels of IgG antibodies, as well as
A specific group of proteins called oligoclonal bands.
Occasionally there are also certain proteins that are the breakdown products of myelin. |
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These findings indicate an abnormal immune response within the central nervous system, meaning that the body is producing an immune response against itself.
An abnormal immune response in CSF is found in a number of other diseases, so the test is not specific for MS;
Conversely, some 5-10 percent of patients with MS never show these CSF abnormalities.
Therefore, CSF analysis by itself cannot confirm or rule out a diagnosis of MS. It must be part of the total clinical picture that takes into account the findings of the person’s history and neurologic exam as well other diagnostic procedures.
Other tests that your doctor might recommend to rule out or confirm a diagnosis of MS include:
1. blood tests
2. MRI (magnetic resonance imaging) test
3. Evoked potential test |
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| Evoked potential (EP) tests measure the electrical activity of the brain in response to stimulation of specific sensory nerve pathways. They are able to detect the slowing of electrical conduction caused by damage (demyelination) along these pathways even when the change is too subtle to be noticed by the person or to show up on neurologic examination. Because the diagnosis of MS requires evidence of demyelination in two distinct areas of the central nervous system, EP testing can help confirm the diagnosis by enabling the physician to identify a second demyelinating event that caused no clinical symptoms or was not otherwise apparent. In order to measure evoked potentials, wires are placed on the scalp overlying the areas of the brain being stimulated. The examiner then provides specific types of sensory input (e.g., sound, light or sensation), and records the responses of the person’s brain. Evoked potential testing is harmless, generally painless, and is a very sensitive technique for detecting lesions (damaged areas). |
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1. Post-lumbar puncture headache. Up to 25 percent of people who have undergone a lumbar puncture develop a headache afterward due to a leak of fluid into nearby tissues.
The headache typically starts several hours up to two days after the procedure and may be accompanied by nausea, vomiting and dizziness. The headaches are usually present when sitting or standing and resolve after lying down. Post-lumbar puncture headaches can last from a few hours to a week or more.
2. Back discomfort or pain. You may feel pain or tenderness in your lower back after the procedure. The pain might radiate down the back of your legs.
3. Bleeding. Bleeding may occur near the puncture site or, rarely, into the epidural space.
4. Brainstem herniation. Increased pressure within the skull (intracranial), due to a brain tumor or other space-occupying lesion, can lead to compression of the brainstem after a sample of cerebrospinal fluid is removed.
A computerized tomography (CT) scan or MRI prior to a lumbar puncture can be obtained to determine if there is evidence of a space-occupying lesion that results in increased intracranial pressure. This complication is uncommon. |
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| Lumbar Puncture procedures |
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[image]
https://www.youtube.com/watch?v=QoUGM4wqUU0 |
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Long vertebral column and short spinal cord
Intervertebral foramina and Spinal nerves
Innervation of the back
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| Veins in spinal Cord and Meninges |
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