﻿WEBVTT

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[HF4088 Multiple sclerosis 1967, Length: 00:26:25, Color, Sound.

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This Beta SP was duplicated from a 16mm answer print by Bono Film & Video, Inc

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for the National Library of Medicine, February, 2010.]

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[Dark, then film leader and countdown]

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[This film has been aquired for distribution by the National Medical Audiovisual Center]

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[Narrator:] The patient with multiple sclerosis staggers down a long road,

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weaving between despair on the one side and hope on the other.

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The doctor who must guide this patient is faced with a disorder in which the diagnosis

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is a gamble of odds and probabilities.

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The etiology is hidden in a jungle of clues and the therapy stirs a broth of heated dispute.

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It is hoped that this film will enable the practitioner and the student to better understand

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this elusive disease.

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[The National Multiple Sclerosis Society presents]

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[Multiple Sclerosis]

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[supervised by The Division of Neurology of The The School of Medicine,

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University of California at Los Angeles]

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[Narrator:] This is a...at 19, she had a two-week episode of burning and hypersensitivity

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of the right arm.

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A second episode occurred nine months later, beginning with sharp pains in the right forehead

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and scalp, then numbness and tingling in the right fingers and toes, ascending in three days

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to include the entire right side below the neck.

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After one month, these symptoms had almost cleared, but she then developed loss of vision

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in the left eye over a three-day period, followed in two weeks by blurring of vision in the right eye

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with pain on movement of the eyes.

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At this time, she also noted a tingling down the back, on bending the head forward.

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On examination at the peak of this attack, she could only count fingers with the left eye,

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and the visual field showed a huge scotoma involving the central region and the area around the blind spot.

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On the right, visual acuity was 20 over 40 and field-testing showed a scotoma involving the area

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around the blind spot and the entire inferior nasal quadrant, but sparing central vision.

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The optic discs appeared normal.

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These findings of optic neuritis gradually disappeared over the next two months.

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In the four years since then, she has remained well, except for one persistent symptom.

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[Patient:] When I bend my neck down, I get an electric shock sensation that extends

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from my neck down my back, through my legs.

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[Narrator:] This electric shock-like sensation on flexion of the neck is called Lhermitte's sign

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and is considered a manifestation of posterior column damage in the cervical spinal cord.

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This is a 43-year-old sales manager for a dairy company.

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At 33, he had an episode of left-sided numbness and weakness, unsteady walk, and double vision,

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with complete recovery in six months.

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At 36, he developed slurred speech, difficulty focusing his eyes, clumsiness of the left arm and leg,

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hypersensitivity of the right side of the body, and Lhermitte's sign.

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He improved after one month but was left with permanent residual.

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This stayed the same for the next four years, then slowly worsened.

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Ten years after onset, he demonstrates the following:

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His eye movements are impaired in all directions of gaze.

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When he looks to the sides, the in-turning eye is paralyzed.

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The out-turning eye shows horizontal nystagmus.

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There is weakness of upward gaze, left more than right, and vertical nystagmus

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on upward and downward gaze.

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This disconjugate gaze difficulty is called internuclear ophthalmoplegia.

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It represents damage to the median longitudinal fasciculus, a tract that runs through

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the dorsal portion of the brain stem on each side of the midline.

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Bilateral internuclear ophthalmoplegia is considered by many authorities

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to be pathognomonic of multiple sclerosis.

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His speech shows dysarthria characterized by jerky rhythm and slurring.

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[Patient 2:] On July 24th, 1858, after consulting friends about the proposal, Abraham Lincoln,

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the Republican candidate for senator, challenged his Democratic opponent, the incumbent,

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Stephen A. Douglas, to divide time and address the same audience during the present canva...

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[Narrator:] Testing of his hands shows good coordination on the right.

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But on the left, there is a tremor of the outstretched hand accentuated

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by performing any accuracy test.

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There is also inability to perform rapid alternating movements with this hand.

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These signs represent the ataxia of cerebellar disease.

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Testing of his legs reveals the weakness on the left.

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[The doctor examines the way each leg reacts to stretches.]

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There is ankle clonus on the left.

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There are bilateral upgoing toes on plantar stimulation.

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These signs are indicative of damage to the pyramidal tract somewhere between

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the cerebral cortex and the lumbar cord.

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This is a 23-year-old insurance company clerk.

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Beginning at age 18, she has had one episode each year.

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The first attack consisted of buzzing and decreased hearing in the left ear, double vision,

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and impaired balance, with complete recovery in six weeks.

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The second attack included left-sided tinnitus and hearing loss, staggering walk, double vision,

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slurred speech, tingling in the right hand, and numbness in both legs below the knees.

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After six months, these symptoms improved, but she was left with permanent nystagmus

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and ataxia.

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Her third attack began with pain and foggy vision in the right eye, reaching a peak in one month,

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at which time the visual acuity was 20 over 30, and the visual fields showed a scotoma adjacent

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to the macular region.

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This paracentral scotoma of optic neuritis remitted in another month.

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A right oculomotor nerve palsy lasting five weeks constituted the fourth attack.

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She is now in her fifth attack with symptoms of vertigo, slurred speech, double vision,

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staggering gait, and numbness in the right hand.

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Examination of eye movements reveals coarse horizontal nystagmus on lateral gaze,

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vertical nystagmus on gaze up and down.

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A rhythmic head tremor may also be seen.

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This represents damage to vestibular pathways.

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When she holds out the left hand, there is a flapping tremor at the wrist,

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intensified by performance of the finger-to-nose test.

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This is independent of whether the eyes are open or closed.

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It represents the intention tremor of cerebellar disease.

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The right hand exhibits searching movements of the fingers when the eyes are closed,

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and hesitancy on the finger-to-nose test, which is not present when the eyes are open,

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indicating position sense loss due to posterior column damage in the spinal cord.

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Her gait is weaving and lurching because of ataxia in the legs.

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She has bilateral ankle clonus.

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And Babinski signs as a result of pyramidal tract damage.

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This is a 41-year-old housewife and mother whose first symptoms occurred at age 30,

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when she developed weakness of the left leg.

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At 33, she had nystagmus and an ataxic gait.

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Since 35, both legs have become progressively weaker and stiffer.

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There have been no remissions.

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After 11 years, she shows the following.

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Testing of eye movements demonstrates bilateral internuclear ophthalmoplegia,

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with weakness of the adducting eye and jerking of the abducting eye on gaze to each side.

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There is a mild intention tremor of both hands, representing damage to the cerebellar system.

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Babinski signs are present bilaterally.

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Both legs show spasticity and weakness, the left more than the right.

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The patellar reflexes are hyperactive bilaterally.

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This spastic paraparesis with hyperactive and pathological reflexes denotes pyramidal tract

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damage in the spinal cord.

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This is a 41-year-old schoolteacher whose symptoms began at age 31 when he developed

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difficulty focusing his eyes with apparent movement of objects upon which he would fix.

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This represented nystagmus.

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It occurred intermittently for one year, then disappeared.

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At 33, he noted intermittent balance difficulty and weakness of the legs.

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At 34, incoordination of the hands and feet.

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At 36, his left leg and arm became weak and have remained so ever since.

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After ten years, he shows the following.

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There is mild ataxia of all four limbs on coordination testing.

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This is more prominent on the left.

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A slight head tremor occurs intermittently with effort.

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[The doctor watches the way the patient's wrists and ankles tremble as he attempts to stretch.]

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Spasticity in the left arm and leg is demonstrated when he walks.

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The left arm does not swing, and the left leg is used stiffly.

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[The patient walks around to demostrate the difference in the way each leg works.]

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The reflexes are hyperactive everywhere.

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[The patient's reflexes are tested in various parts of his body.]

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Hoffmann signs are present bilaterally.

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There are bilateral Babinski signs.

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This patient's findings indicate damage to the pyramidal tract and the cerebellar system

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bilaterally, most likely in the brain stem.

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Multiple sclerosis can be diagnosed with certainty only at autopsy

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when a picture of patchy demyelination in the central nervous system is seen.

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The glial scars or plaques may be seen and felt on the surface of the brain or spinal cord,

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as grayish-brown, firm, translucent spots.

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All of these pictures are from one patient, a 24-year-old lady with a four-year history

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of multiple sclerosis.

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Here on the pons is a large, brown, sclerotic plaque with two smaller lesions above it.

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These lesions represent a late stage in the pathological process, the demyelinated patch

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having been filled in by a scar of glial cell overgrowth.

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When cut sections of brain or cord are viewed, foci of demyelination appear as brown patches

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in the white matter.

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Cerebral foci have a predilection for the white matter immediately adjacent to the ventricles,

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especially posterior and inferior horns,

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and the white matter about the cortical and basal nuclear gray matter.

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The lesions in the cerebral hemisphere vary in size from that of a pinhead

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to several centimeters in diameter.

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Similarly, numerous areas of discoloration are found in the brain stem and cerebellum.

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Early in the plaque formation, there is perivascular inflammation.

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Then tissue is destroyed, myelin preponderantly.

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Myelin sheaths fragment into globules, fat is liberated, and macrophages ingest the fat.

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As the lesion ages, glial cells proliferate and produce fibrils, which give the older lesions

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their sclerotic appearance and make them visible to the naked eye.

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Here on a freshly cut section of the spinal cord, only a faint area of discoloration is seen

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in the posterior columns.

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When stained for myelin, the lesions appear as pale foci within the darkly staining white matter.

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Many more plaques are now apparent.

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The lesions are often far in excess of what one would've expected

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from the patient's symptoms and signs during life.

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Thus, many plaques may be clinically silent, such as this demyelinated patch

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in the optic radiation of the cerebrum.

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In fact, there is evidence that a patient may go through life with pathological demyelination

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and yet have no clinical manifestations of multiple sclerosis.

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[Louis J. Rosner:] The only relatively consistent laboratory abnormalities in multiple sclerosis

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are spinal fluid changes.

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The spinal fluid may be entirely normal.

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This occurred in 40 percent of patients in the UCLA Multiple Sclerosis Clinic.

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An elevated gamma globulin content, over 13 percent of the total protein, was found in 58 percent.

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The colloidal gold curve was abnormal, the numbers adding up to ten or more in 36 percent.

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This test is an indirect measure of relative gamma globulin elevation.

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There was an elevated protein in 35 percent, an increased white cell count in 20 percent.

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With no pathognomonic laboratory test by which to confirm the diagnosis, the doctor must rely

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on his evaluation of the history and the physical examination.

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The clinical criteria for the diagnosis of multiple sclerosis are two.

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Number one, episodic course.

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Number two, multiple symptoms and signs pointing to optic nerve, brain stem, or spinal cord.

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Optic nerve manifestations are: decreased visual acuity, central scotoma,

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or paracentral, cecocentral, or peripheral on visual field examination

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and optic atrophy on ophthalmoscopic examination.

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Brain stem manifestations include nystagmus, the disconjugate gaze difficulty known as

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internuclear ophthalmoplegia, trigeminal neuralgia, facial sensory deficit, facial weakness,

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vertigo, dysarthria, dysphagia, emotional lability, and ataxia of the head, trunk, or limbs.

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Spinal cord manifestations consist of the electric sensations on flexing the neck

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known as Lhermitte's sign, tight band feelings around the trunk called girdle sensations,

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superficial or proprioceptor sensory deficit, spastic weakness with hyperactive and pathological reflexes,

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and neurogenic bladder disorder.

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Variations in the course and in the signs define four varieties of multiple sclerosis,

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the incidence of which is as follows.

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Number one, episodic disseminated, the classical type, 78 percent.

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Number two, progressive disseminated, 15 percent.

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Number three, episodic non-disseminated, five percent.

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Number four, progressive non-disseminated, two percent.

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Returning to our five patients, it will be seen that the first three represent

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the classical type of multiple sclerosis.

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The other two, atypical types.

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The college student in the first year of her illness had intermittent sensory symptoms

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with no objective signs.

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She was considered neurotic at that time.

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Many patients in the early stages of multiple sclerosis are given the diagnosis of psychoneurosis.

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The differential can be a difficult one.

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It is recommended that multiple sclerosis be diagnosed only if there are

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documented, objective abnormalities on examination.

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When this young lady developed the scotomas of optic neuritis and the Lhermitte's sign

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of spinal cord involvement, there was objective evidence of neurological disease

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and definite evidence of dissemination.

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The spinal fluid was normal, except for an elevated gamma globulin of 20 percent.

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Then the diagnosis of multiple sclerosis could be made.

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The excellent remission further confirmed this impression.

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The sales manager began with an attack suggesting both brain stem

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and spinal cord pathology.

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With complete remission of these symptoms, multiple sclerosis was suspected,

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but other remitting conditions occurring at the cervicomedullary junction region

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were still possible.

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After a two-year interval, he developed the disconjugate gaze difficulty of brain stem disease

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and the spinal cord sign of Lhermitte.

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Now, the diagnosis of multiple sclerosis was definite on the basis of episodic course

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and disseminated signs.

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A normal spinal fluid reinforced this conclusion.

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The pretty young clerk had only brain stem manifestations with her first attack.

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Multiple sclerosis could not be diagnosed at that time, as several other diseases

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can give a similar picture with remission.

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For example, cholesteatoma in the posterior fossa.

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In the second attack, there were sensory symptoms suggestive of spinal cord involvement

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in addition to the previous brain stem signs.

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There was still the possibility of a compressive lesion at the foramen magnum.

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Only with her third attack, when signs of optic neuritis occurred,

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was dissemination unequivocal.

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The diagnosis could not be made with assurance then, until this, the third year of her illness.

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The housewife has had a progressive, non-remitting course.

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This occurs in ten to 40 percent of MS patients in different large series.

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It is more common with an older age of onset and with a spinal cord type of onset.

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With time, it became apparent that this lady had damage in both the brain stem and spinal cord,

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as evidenced by the nystagmus and ataxia on the one hand and the spastic paraparesis on the other.

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The further development of bilateral internuclear ophthalmoplegia confirms the diagnosis

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of multiple sclerosis.

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The schoolteacher initially had only nystagmus, which remitted.

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After a one-year interval, intermittent ataxia appeared.

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Subsequently, the ataxia became constant, and he developed a spastic left hemiparesis

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with bilateral hyperreflexia and pathological reflexes.

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All signs could be localized to the brain stem.

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The early remissions suggested multiple sclerosis, but the absence of

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signs of dissemination necessitated the performance of many special tests.

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The entirely normal spinal fluid was further evidence of multiple sclerosis.

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However, in this type of case, the doctor should be especially cautious in his diagnosis.

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After the diagnosis, then what?

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Although multiple sclerosis has been known for almost 100 years, its etiology and its treatment

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are still unsettled.

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One important clue is the epidemiology of the disease.

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The geographical distribution is that of a low prevalence in tropical zones

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and a high prevalence in temperate and northern zones where studies have been made.

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Certain factors commonly found to precipitate exacerbations of the disease include

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physical exhaustion, infection, surgical procedures, and emotional crises.

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This patient's most recent exacerbation was in association with an emotional crisis.

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When an attack occurs, bed rest at the beginning may decrease the duration

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and the severity of the relapse.

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Symptomatic treatment includes the use of anti-vertigo drugs, muscle relaxants,

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antispasmodics for the bladder, and physical therapy.

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Most important of all is the psychological support that the doctor can render the patient

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by giving him attention, encouragement, and hope.

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Specific treatment for multiple sclerosis must await the discovery of the cause.

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Many theories have been proposed, but none has been proved.

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Research programs are now studying the problems of precipitants in the exacerbations of MS:

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geographical factors in its incidence, the nature and function of myelin, the significance of

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anti-myelin antibodies, and the experimental demyelinating disease of animals.

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The solution to multiple sclerosis will open the door to an understanding

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of many other neurological problems.

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Speaking for the National Multiple Sclerosis Society is Dr. Augustus S. Rose,

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Professor of Neurology at the University of California, Los Angeles.

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[Dr. Augustus S. Rose:] It is generally believed that patients derive encouragement and hope

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through the effort and programs of the National Multiple Sclerosis Society.

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Not many years ago, there was comparatively little scientific and public interest in the problem

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of multiple sclerosis.

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Today, it is recognized as the leading neurological disorder of our time and a major health problem.

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A large and diversified research program is being conducted in many laboratories throughout

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the world and with promising results.

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Through research and research fellowship training grants, the National Multiple Sclerosis Society

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supports fundamental, applied, and clinical studies considered to have relationship

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to the problem of multiple sclerosis and demyelination.

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Positions and research persons at a postdoctoral level interested in these programs

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should communicate with the medical and research director of the National Multiple Sclerosis Society

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in New York City.

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[written and narrated by Louis J. Rosnerm M.D., assistant Professor of Neurology, U.C.L.A.

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in association with Augustus S. Rose, M.D., Professor of Neurology, U.C.L.A.]

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[Produced and donated to The Multiple Sclerosis Society by]

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[Rex Fleming Productions Santa Barbara, Calif.]

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[presented by the]

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[National Multiple Sclerosis Society 257 Park Avenue South New York, N.Y. 10010]