By Niels 1. Low, M.D., and Sidney Carter, M.D.
Neurological Institute, Presbyterian hospital of New York and Department of Neurology,
College of Physicians and Surgeons, Columbia University
Dr. Low was a United Cerebral Palsy Fellow in pediatric neurology.
PRESENT ADDRESS: (N.L.L.) Department of Pediatrics, University of Utah, 1940 South Second East, Salt Lake City 15, Utah.
MULTIPLE
SCLEROSIS
IN CHILDREN
24
T
HE PURPOSE of this paper is to report 7 cases of multiple sclerosis recently seen at the Neurological Institute in New York,in order to remind pediatricians that this
condition, while uncommon, silould be con-sidered in differential diagnosis in children
with neurological symptoms.
Multiple sclerosis has been considered to be so uncommon in childhood that little mention is made of it in textbooks or in the pediatric literature. Some of the newest and
fllOst commonly used pediatric textbooksl
mention multiple sclerosis in only a
sen-tence or not at all. Ford’s book2 Oil pediatric
neurology gives no details, and, in
Brenne-manns Practice of Pediatrics, Ford states that “rare instances may appear before
)uberty, but it is doubtful whether the typi-cal clinical picture ever develops at this age.” Tile standard neurological texts men-tion the disease in the pediatric age group
only briefly. Wilson’ reported 2 examples in
9-year-old girls, and in 1107 cases of mul-tiple sclerosis in the literature found an
mci-dence of 2.2 per cent below the age of 10
years. He emphasized that “actual proof is
often missing and in many the diagnosis can
reasonably be challenged.” Merritt5 finds
multiple sclerosis “uncommon” before the
age of 10; Buchanan6 mentions “a few reports of this disease in childhood”; Grinker and BucyT state that “cases have been recognized as early as 10 years”; Schaltenbrand5 described it as rare in child-hood. Nielsen9 recognizes that it “can occur at any age from infancy to senility” but warns also, correctly, that “there must be evidence of more than one lesion” and also “evidence of progression such as ex-acerbations and remissions.”
In the older literature on the subject, one
finds among prepuberal children some pa-tients with a typical course but others that are very questionable or definitely not ac-ceptable for inclusion. A 9-year-old boy de-scribed by WestphaP#{176} is such an example of a premature report that was withdrawn 1 year later by the same author” because the patient was shown to ilave died of a thalamic tumor. In our judgment it is
un-likely that another boy he reported had multiple sclerosis either. Eichhorst12 was the first author to describe a child with mul-tiple sclerosis proven at necropsy. That child was admitted at 8 years of age and
iliS mother had also died of the same
(hiS-ease. The youngest documented case is one presented by NobeP3 in Vienna in Decem-ber, 1911. This patient subsequently came to necropsy in June, 1912, at the age of 2%
years. His main clinical manifestations were
spasticity, ataxia and partial optic atrophy. The proved instance of multiple sclerosis in mother and child reported by Eichhorst raises the question of the frequency of familial occurrence. Although “it is un-usual for the disease to affect siblings or to
appear in successive generations”6 there are additional reports. Among them are the adult cases in 2 families reported by
Reyn-olds” and a brother and sister reported by
Spiegel and Keschner;15 1 was necropsied. Wilson4’ P- 173 has seen 2 undoubted familial
cases and quotes others. The most extensive reviews on the familial incidence of the dis-ease are tiloSe by Pratt et al.16 and by Mackay.7
Sidney Carter and co-workers18 found no patients under the age of 16 years among
1773 cases and added 197 personal
observa-tions, he reported 4 children below the age of 15 years, the youngest being 7 years old.
Klaussner,20 Jehliffehl and Morawitz22
to-gether reported 14 children under 10 years old and 5 children between 11 and 15 years out of a total of 268 cases, but these 3 authors gave no detailed case reports, just the statistics. McIntyre and McIntyre23 pre-sented the life charts of 55 patients with multiple sclerosis beginning with the first attack, and found 3 typical cases with an onset before the age of 15 years. A fourth
case within that age group, whose first
attack was described as hysteria, was not adequately documented. Muller24 studied 810 cases of multiple sclerosis in an effort to find a relation between age of onset and the course of the disease. Three of these pa-tients developed the first symptoms be-tween 5 and 9 years, and 43 cases between 10 and 14 years. The only conclusion was that patients whose disease -started after the age of 25 years were likely to have a more rapid course than those whose first symp-toms appeared before that age. H. R. Carter25 reported typical childhood cases observed at tile Neurological Institute in New York during an 11-year period; the
youngest case had the first attack at 9 years
of age. Bouduelle et 26 reported a classi-cal case which certainly cannot be chal-lenged in spite of the fact that there was no necropsy. This patient had numerous at-tacks from the age of 7 years. He had left optic neuritis in 1942, paresis of the right lower extremity for 2 to 3 weeks in 1947, paresis of the left lower extremity for 3 months and of the right lateral rectus mus-cle for 5 months in April, 1951, dysmetria, disturbances of gait and reflexes and absent vibration sense in October, 1951, diplopia and ataxia in 1952, and repeated exacerba-tions and remissions between 1952 and
1954.
CASE REPORTS
The first 3 patients are children who have
already had remissions and exacerbations
of manifestations relating to several parts
of the central nervous system; the other 4
children have had only 1 attack of a neurological condition \vilicil is suggestive
of multiple sclerosis, but recurrences have not as yet been observed.
Like most authors we have included at-tacks of retrobulbar neuritis as episodes of multiple sclerosis. Seguin27 apparently was
the first to report the simultaneous occur-rence of optic neuritis and spinal cord
symptoms but regarded it as a coincidence.
Erb2 recognized this concurrence as a
defi-nite syndrome, and Devic29 emphasized, in a discussion of 16 such cases with 4
fatali-ties, that the disseminated foci should be
regarded as an acute stage of multiple
sclerosis.
Case 1
Linda F. (229348), born July 6, 1946, normal
delivery, full-term, walked unassisted at 15 months, normal intelligence.
July, 1952: Episode of rash and fever
fol-bowed by marked drowsiness and some
head-ache for several days.
August, 1952: Fever with undue drowsiness
and tremor for a few days; 1 week later
para-plegia with bladder and l)owel incontinence developed. She had recovered fully by
Sep-tember 19.
September 22, 1952: Sudden onset of stupor,
aphasia and dysphagia with full recovery
with-in 2 weeks.
January, 1953: Right hemiparesis with right
Babinski sign, full recovery within 1 month.
March, 1953: Uncomplicated mumps.
April, 1953: Uncomplicated chicken pox.
February :3, 1955: Developed complete
blindness over a 12-hour period. Reaction to light returned after 4 days and vision was said
to have returned to normal within 3 weeks.
May 9, 1955: Hospitalized with history of
left hemiplegia for 10 days and severe vertigo
for 1 week.
Physical examination revealed an alert and
intelligent girl with considerable discomfort because of vertigo on the slightest movement of the head; mild left hemiparesis and slight
ataxia of the arm and leg on the left. The
optic discs were flat and slightly pale. The
deep tendon reflexes in the arms were 2+ on
3+ and ankle jerks 4+ bilaterally. The plantar response was flexor on the right, and
extensor (Babinski’s sign) on the left. The blood count was normal, urine contained many
leukocytes. The cerebrospinal fluid was under a pressure of 160 mm. of water; it contained
6 lymphocytes’mm., 39 mg./100 ml. of pro-tern, 7 per cent of which was gamma globulin.
Serology of the blood and spinal fluid was
negative. Roentgenograms of the chest and skull were normal. She was discharged on May
20, 1955, the vertigo and hemiparesis were
improved.
COMMENT: Over a 3-year period this child
had episodes of tremor, paraplegia, aphasia,
stupor, right hemiplegia, left hemiplegia, blind-ness and vertigo with complete and partial
re-missions. This case fulfills all clinical criteria of
multiple sclerosis.
Case 2
Louis M. (217731), born January 5, 1948, normal full-term delivery, sat at 6 months, walked unassisted at 12 months.
February 14, 1955: Seen in outpatient clinic
with complaints of pain in legs, limping and
dysuria for 10 days. He also had had
pares-thesias of the soles of the feet and abdominal
pain 10 days before the visit. On examination he was found normal except for the reflexes which were as follows: ankle jerks 4+
bilaterally; left abdominal and scrotal reflexes
2+ , right upper abdominal 1 + , right
bover abdominal variable, right cremasteric
absent; bilaterally positive Babinski. Roent-genograms of dorsolumbar spine were normal.
Blood examination showed slight hypochromic
anemia. Urine normal. Sedimentation rate 6
mm./hour. Mantoux negative.
March 2, 1955: Marked urinary frequency,
normal gait, bilateral ankle clonus, bilateral
Babinski, intact sensation, urine normal.
March 9, 1955: Urinary frequency lessened;
ankle jerks 3+ right, 4+ left, Babinski hi-laterally positive.
March 28, 1955: Hospitalized. General
ex-amination normal. The deep tendon reflexes in
the arms were 2+ bilaterally, knee jerks were
3+, abdominal reflexes unchanged since 2/14/55, Babinski bilaterally positive. Patient
was myopic with visualacuity 20/40-2 bilateral,
correctible to normal. Optic discs normal. Urine
normal, containing no porphyrins; blood NPN 34, blood sugar 89 mg./100 ml. Cerebrospinal
fluid: pressure and dynamics were normal, 1 cell, 20 mg./100 ml. protein, 6 per cent of
which was gamma globulin; serology negative.
Discharged April, 1955.
April 16, 1955: Readmitted to hospital
be-cause of ataxia, weakness of the left lower
extremity, blurring of vision and urinary
in-continence. Examination revealed considerable ataxia to all tests and moderate spasticity, more on the left than on the right side. Biceps, triceps, radial and ankle reflexes were 4 +,
knee jerks 3 + , the Babinski reflex was positive on both sides. There was nystagmus on right lateral and on upward gaze, the uvula deviated to the left. Roentgenograms of skull, blood count and urine examinations were normal. Three days after the second admission the pa-tient was markedly improved, walking around
the ward with little ataxia and a slight facial
weakness. He was discharged on April 21,
1955.
May 4, 1955: Clinic visit: no complaints, no
ataxia, normal gait in spite of bilateral ankle clonus and Babinski.
June 29, 1955: Clinic visit: Bilateral
Babin-ski, intermittent urinary frequency, rare incon-tinence and occasional dysuria. Normal deep tendon reflexes; no clonus.
COMMENT: This patient had one episode
of dysuria, pain and paresthesias in feet and
bilateral extensor toe signs; 2 months later he
had a second episode consisting of ataxia, blurring of vision and weakness in the left leg with marked improvement. These episodes would be difficult to explain by any other
diag-nosis than multiple sclerosis.
Case 3
Michael De T. (215534), born July 18, 1950.
Normal full-term delivery; normal
develop-ment; measles at 18 months; asthma since 2 years of age.
October, 1954: Patient was pushed off a
3-foot ledge and immediately following there was loss of vision; the local physican found mild spasticity of the left side % hour after the accident. Twelve hours later there was complete left hemiplegia. Patient’s vision re-turned to normal and the left hemiplegia dis-appeared within 10 clays. Lumbar puncture was said to have revealed a normal fluid.
January 13, 1955: Sudden right hemiplegia
and complete aphasia.
Examina-27
tion revealed a mild right spastic hemiplegia and great difficulty in naming objects; the speech improved considerably within a few
days. All deep tendon reflexes were 3+ and
symmetrical, plantar responses were normal. There was unsustained nystagmus on gaze to the left. The fundi were normal. Roentgen-ograms of skull and chest were normal. Lumbar puncture on 1/28/55: initial pressure 180 mm. of water; 1 cell, 21 mg./100 ml. protein,
70 mg./100 ml. sugar, negative serology.
Blood count, urine, bleeding time and platelets were normal. Electroencephalogram : diffuse
slowing and depression of voltage on the left side. The patient was much improved at time of discharge on February 1, 1955.
March 23, 1955: Clinically normal.
March 30, 1955: Electroencephalogram
“much improved.”
May 18 1955: Clinically normal.
COMMENT: This child has had episodes of
right and left hemiplegia respectively several months apart. All other examinations were normal. Because blood was not found in the cerebrospinal fluid, it is very unlikely that the attacks were caused by trauma. These episodes with full recovery are consistent with a diag-nosis of multiple sclerosis.
Case 4
John 0. S. (215651), born July 22, 1949.
Full-term normal delivery. Chicken pox and measles, 1951; tonsil- and adenoidectomy, 1952.
January 1, 1955: Upper respiratory infection
with fever.
January 8, 1955: Weakness and unsteadiness
in legs were noted by parents and was con-firmed by referring physician.
January 9, 1955: Onset of dysuria and
in-voluntary urination.
February 1, 1955: Hospitalized. Examination
showed the patient to have unsteady gait. Finger to nose test was performed very poorly on the left; deep tendon reflexes and abdominal and cremasteric reflexes were 2+ bilaterally,
plantar response normal on right and extensor
on the left side. Position sense was impaired in both feet and there was nystagmus on right
lateral gaze. The fundi appeared normal.
Roentgenograms of the skull and spine were normal. Spinal fluid examination revealed a pressure of 130 mm. of water, 2 cells, 31 mg.,’
100 ml. protein, 11 per cent of which was
gamma globulin, 61 mg./100 ml. sugar,
serol-ogy and colloidal gold negative. Blood count was normal. The urine showed a few
leuko-cytes with E. coli and B. proteus on culture.
February 8, 1955: Discharged fully
re-covered.
March 30, 1955: Clinically normal.
COMMENT: Neurological disease with py-ramidal and cerebellar signs with full recovery
and so far no recurrence. No evidence of tremor or other disease could be established, making
the diagnosis of multiple sclerosis quite likely.
Case 5
Alfred T. (947832), born September 28, 1946. Full-term normal birth and normal early
development; fractured right radius and ulna
ill 1949 from falling out of a first-story window.
Had measles and chicken pox, tonsil- and
adenoidectomy in 1950.
May 28, 1954: Hospitalized with a history
of staggering gait for 8 days; slurred speech
for 4 days; clumsy hands, right more than left, for 4 days. Physical examination: wide based,
ataxic gait, tended to turn toward right side; was generally hypotonic; adiadochokinesis right
more than left; slurred speech; fundi normal.
Blood pressure 128/90; blood count and throat
culture were normal. Urine contained a few
leukocytes. Blood NPN 24, sugar 106 mg./100
ml., serum potassium 4.8 mEq./1.;
sedimenta-tion rate 8 mm./hour; serology negative.
Cere-brospinal fluid: 1 cell, 25 mg./100 ml. protein, 9 per cent of which was gamma globulin; sugar
80 mg./100 ml.; initial pressure 150 mm. of
water; colloidal gold and serology negative.
Roentgenograms of chest normal, of skull shows
right maxillary sinusitis. Heterophile antibody
titer 1:16, cold agglutinins 1 :32, plasma CO2
and chlorides normal. Blood: type A, Rho D
p05.
June 9, 1954: Ventriculogram unsuccessful.
Pneumoencephalogram normal with fourth ventricle well visualized.
June 24, 1954: Marked improvement; no
nystagmus, speech better, less ataxia.
July 6, 1954: Walks well by himself;
dis-charged.
September 2, 1954: Readmitted to hospital
with a history that the patient’s walking had
deteriorated during the last 2 weeks, that he
was drooling clay and night and had been
ataxia of trunk and extremities and had marked
intention tremor and scanning speech. Normal deep tendon and abdominal reflexes; negative
Babinski; normal optic funchi and slow vertical iiystagmus iii both eyes. Skull roentgenograms showed no evidence of increased intracranial
pressure. Cerebrospinal fluid : initial pressure
90 mm. of water, 1- cell, 30 mg/100 ml.
pro-tein, 8 per cent of which was gamma globulin, 79/ 100 ml. sugar. Electroencephalogram on
9//3/54 reported as diffusely slow, and on 9/10/54 as improved.
September 14, 1954: Second
pneumoen-cephalogram normal.
September 18, 1954: Discharged
consider-ai)ly improved.
April 20, 1955: “Slow improvement” since
last fall.
April 27, 1955: Refraction 20/30 on.
May 4, 1955: Normal fundi.
June 1, 1955: Slight alternating strabismus,
slight ataxia, no nystagmus; no pyramidal tract signs.
COMMENT: This patient had cerebellar signs which improved slowly. A diagnosis of neo-plasm is extremely unlikely with 2 normal pneumoencephabograms and normal optic discs.
Heredodegenerative disease of the cerebellum
is also very unlikely l)ecause of repeated
im-provement and absence of family history. This
could be a case of multiple sclerosis.
Case 6
Christopher W. (877120), born January 3,
1944. Full-term normal delivery; walked alone at 15 months, talked at 2 years. Tonsillitis,
1949; measles, 1950; chicken pox, 1951.
September 7, 1952: Hospitalized following
sudden onset of dizziness and diplopia of a
few hours’ duration. Physical examination:
normal tendon and abdominal reflexes, normal
optic fundi, right external squint, diplopia in
all directions except extreme right lateral gaze
and a coarse rotatory nystagmus. Cerebrospinal
fluid: 9/8/52, revealed an initial pressure of 180 mm. of water, 20 lymphocytes, 73 mg./
100 ml. sugar, 707 mg./100 ml. chlorides, 31
mg./100 ml. protein, 4 per cent of which was gamma globulin; the serology was negative and
colloidal gold curve was normal.
September 9, 1952: Dizziness disappeared.
September 10, 1952: Normal audiometrics,
roentgenograms of skull and chest were normal.
September 11, 1952: Nystagmus
disap-September 14, 1952: Function of right
medial rectus normal; caloric tests normal.
Cerebrospinal fluid 9/15/52 showed 56
lymphocytes, 32 mg./100 ml. protein and 55
mg./100 ml. sugar.
September 18, 1952: Discharged from the
hospital.
October 1, 1952: Clinic visit: Normal, no
strabismus.
May 13, 1953: Clinically well.
COMMENT: This patient had an acute disease
affecting oculomotor function and causing a cellular reaction in the spinal fluid. He had
either some form of encephalitis or a first
at-tack of multiple sclerosis.
Case 7
Michael
J.
T. (220883), born January 29, 1944, full-term by cesarean section because ofbreech presentation. Normal development;
un-complicated mumps, measles and chicken pox;
broken wrist, 1951.
February 23, 1955: Sudden inability to see
the blackboard in school. Refraction by school
nurse that day showed 20/100 o.d., 20/30 os.
March 2, 1955: Refracted by ophthalmologist
20/200 o.d., 20/30 o.s.
March 14, 15, 16, 1955: Examined in the
Pediatric, Eye and Neurology Clinics. General examination normal; blood count and urine
normal, roentgenograms of skull and special
views of optic foramina were normal. Full
visual fields with 5 mm. test object, normal
optic discs, vessels and maculae; acuity 20/
50 + 2 o.d., 20/20 - 4 0.5., flO improvement
with lenses. No abnormal findings on
neuro-logical examination.
June 29, 1955: Patient asymptomatic. Visual
acuity 20/20 o.u. Normal neurobogicahly.
COMMENT: This apparently was an attack of retrobulbar neuritis. There were no other
ab-normal findings during this episode. Only ob-servation over many years can tell us whether he ever will have other evidence attributable
to multiple sclerosis.
COMMENT
criterion of remission and exacerbation of the manifestations is also essential but the
disease may be suspected before an exacer-bation has occurred after all other expiana-tions for the clinical picture have been reasonably well excluded. Retrospective study of patients show that many years may elapse between the first and subsequent acute episodes. Without post-mortem cx-anlinations establishment of the diagnosis is based on clinical judgment alone, and can often be challenged. However, the nature of the disease is such that children Witil
multiple sclerosis will seldom die before
adulthood.
SUMMARY
Reference to textbooks on pediatrics and
neurology, individual case reports and
re-view articles on multiple sclerosis showed that multiple sclerosis can occur in child-hood in typical form and has been occa-sionally confirmed by necropsy.
During the past year 3 children were seen at the Neurological Institute in New York in whom the diagnosis of multiple sclerosis seemed reasonably certain. Four
additional patients are presented in whom
that diagnosis was suspected. In the latter group years of observation will be required for confirmation of the diagnosis.
REFERENCES
1. a) Nelson, W. E., editor: Textbook of
Pedi-atrics, 6th Ed. Philadelphia, Saunders,
1954.
b) Holt, L. E., Jr., and McIntosh, R., cdi-tors: Holt Pediatrics, 12th Ed. New
York, Appleton, 1953.
c) Fanconi, G., and Wablgren, A., editors: Lehrbuch der P#{228}diatrie, 3rd Ed. Basel, Schwabe, 1954.
2. Ford, F. R.: Diseases of the Nervous
Sys-tem in Infancy, Childhood and Adoles-cence, 3rd Ed. Springfield, Thomas,
1952.
3. Ford, F. R.: In Brennemann’s Practice of
Pediatrics, vol. IV, edited by McQuarrie,
I. Hagerstown, Prior, chap. XVI1, p. 21.
4. Wilson, S. A. K.: Neurology, 2nd Ed.
Baltimore, Williams & Wilkins, 1955. 5. Merritt, H. H.: Textbook of Neurology.
Philadelphia, Lea, 1955.
6. Buchanan, D. : The demyelinating diseases,
ill Baker, A. B. : Clinical Neurology, Vol.
2. New York, Harper, 1955, pp.
1075-1107.
7. Grinker, R. R., and Bucy, P. C. :
Neurol-ogv, 4th Ed. Springfield, Thomas, 1949.
8. Schaltenbrand, G. : Lehrbuch der Neu-rologie in 2 Teilen. Die Nervenkrank-heiten. Stuttgart, Thieme, 1951. 9. Nielsen,
J.
M. : A Textbook of ClinicalNeurology, 3rd Ed. New York, Hoeber,
1951.
10. Westphal, A. : Ueber multiple Sklerose bei zwei Knaben. Charit#{233}-Ann., 13:459, 1888.
11. Westphal, A.: Em Irrthum in der Diagnose bei einem 9 jahrigen Knaben, der das Krankheitsbild einer multiplen Sclerose
darbot. Charit#{233}-Ann., 14:367, 1889. 12. Eichhorst, H. : Ueber infantile und
heredi-tare multiple Sklerose. Virchow’s Arch.
path.Anat., 146:173, 1896.
13. Nobel, E. : Histobogischer Befund in einem Fahle von akuter multipler Sklerose.
Wien. med. Wchnschr., 62:2632, 1912. 14. Reynolds, E. S. : Some cases of familial
disseminated sclerosis. Brain, 27 : 163,
1904.
15. Spiegel, L. A., and Keschner, M. : Familial multiple sclerosis. Arch. Neurol. & Psychiat., 50:706, 1943.
16. Pratt, R. T. C., Compston, N. D., and McAlpine, D. : The familial incidence of disseminated sclerosis and its
sig-nificance. Brain, 74:191, 1951.
17. Mackay, R. P. : The familial occurrence of multiple sclerosis and its implications. A. Res. Nerv. & Ment. Dis., Proc., 28:
150, 1950.
18. Carter, S., Sciarra, D., and Merritt, H. H.
The course of multiple sclerosis as dc.
termined by autopsy proven cases. A. Res. Nerv. & Ment. Dis., Proc., 28:471.
1950.
19. Wechsler, I. S. : Statistics of niultiple sclerosis. A. Res. Nerv. & Ment. Dis.,
Proc., 2:27, 1921.
20. Klausner, I. : Em Beitrag zur Aethiologie
der multiplen Skierose. Arch. Psychiat.,
34:841, 1901.
21. Jebliffe, S. E. : Multiple sclerosis; its oc-currence and etiology.
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Nerv. & Ment. Dis., 31:446, 1904.22. Morawitz, P.: Zur Kenntnie der multiplen Sklerose. Deutsches Arch. klin. Med.,
82:151, 1904.
23. McIntyre, H. D., and McIntyre, A. P.:
Prognosis of multiple sclerosis. Arch.
Neurol. & Psychiat., 50:431, 1943.
dis-seminated sclerosis in relation to the age of onset. Arch. Neurol. & Psychiat., 66:
561, 1951.
25. Carter, H. H. : Multiple sclerosis in child-hood. Am.
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Dis. Child., 71:138, 1946. 26. Bonduelle, M., Bouygues, P., and Sallou,C. : La scl#{233}rose en plaques chez l’enfant. Presse med., 62:563, 1954.
27. Seguin, E. C. : On the coincidence of optic
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Nerv. & Ment. Dis., 5:177, 1880. 28. Erb, W. : Ueber das Zusammenvorkommenvon Neuritis optica und Myelitis suba-cuta. Arch. Psychiat., 10: 146, 1879.
29. Devic, E.: My#{233}lite aigue dorso-lombaire
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SUMMARIO
IN INTERLINGUA
Sclerosis Multiplice in Juveniles
Sclerosis multiplice es considerate como
in-commun in juveniles. Es presentate un revista
del casos reportate in le litteratura. Es
repor-tate septe casos additional de juveniles con
Prest111Ptive sclerosis multiplice. Le diagnose (lepeiidbe dcl demonstration do manifestationes
de plus iue Un lesion in be s’stcma nervose
central. Exacerbationes e remissiones es tractos
characteristic de sclerosis multiplice. Sin illos be diagnose non pote esser conformate, ben
que on pote suspicer lo ante que un
exacerba-tion ha occurrite. Confirmation del diagnose es rarmente obtenibile in juveniles proque le
natura del morbo permitte generalmente le
superviventia del patiente usque al etate adulte. Es presentate un reporto complete del
usual combinationes de symptomas. Le reporto es illustrate per be historias clinic de septe
individuos. Ii es possibile que be morbo es plus commun que lo que on ha generalmente
sus-picite, e caute observationes a bonge durantia
un precondition pro determinar he ver
