ACUTE ACQUIRED COMITANT NONACCOMMODATIVE ESOTROPIA IN CHILDHOOD

A. PUTTEMAN, H. DECONINCK

E. DE NIJS, J. SELLIER

CHU ST-PIERRE BRUXELLES

UZ BRUSSEL

UZ GENT

ACUTE ACQUIRED COMITANT NONACCOMMODATIVE ESOTROPIA

DOES NOT RULE OUT SERIOUS UNDERLYING NEUROLOGIC PROBLEMS

TYPES OF ACUTE COMITANT ESOTROPIA

  SWAN TYPE AFTER OCCLUSION INDEPENDENT OF REFRACTION ERROR   FRANCESCHETTI TYPE STARTS BETWEEN 8M AND 3 YEARS LATE TYPE STARTS BETWEEN 3 YEARS AND 8 YEARS

INTERMITTENT AND VARIABLE THAN CONSTANT ACUTE DIPLOPIA MILD HYPEROPIA NORMAL AC/A SOME DECOMPENSATED MONOFIXATION

TYPES OF ACUTE COMITANT ESOTROPIA

BIELSCHOWSKY TYPE

MODERATE MYOPIA

DIVERGENCE INSUFFICIENCY

TYPES OF ACUTE COMITANT ESOTROPIA

HOYT AND GOOD

VARIOUS DEGREES OF MYOPIA

EQUAL DEVIATIONS AT DISTANCE AND NEAR

ARNOLD CHIARI TYPE 1

  CONGENITAL DISPLACEMENT CEREBELLAR TONSILS 5 MM BELOW THE FORAMEN MAGNUM INTO UPPER CERVICAL CANAL

  VOLUMETRICALLY SMALL POSTERIOR CRANIAL FOSSA

  > 2 ½ YEARS OLD   MOSTLY SECOND AND THIRD DECADE   DIPLOPIA   DIVERGENCE INSUFFICIENCY PATTERN   NYSTAGMUS   A PATERN IF HYDROCEPHALUS

ARNOLD CHIARI TYPE 1

BRAIN TUMORS

PEDIATRIC PATIENTS

50% POSTERIOR FOSSA

  INTERMITTENT COMITANT ESOTROPIA

  BECOMING CONSTANT

CAN BE THE ONLY SIGN

DIPLOPIA IS NOT ALWAYS PRESENT

BRAIN TUMORS

  SMALL V PATTERN A PATTERN ONLY IF HYDROCEPHALUS

DIVERGENCE INSUFFICIENCY LACK OF MOTOR AND SENSORY FUSION

BEFORE AND AFTER SURGERY SOMETIMES NORMAL MOTOR AND SENSORY FUSION SEARCH FOR NYSTAGMUS IN ABDUCTION

  EOG (saccades)

BRAIN TUMORS

  CEREBELLUM

  BRAIN STEM

  SELLAR REGION

  CORPUS CALLOSUM

BRAIN TUMORS

BRAIN TUMORS

  T OF CEREBELLUM ARE MOST COMMON   CEREBELLAR MEDULOBLASTOMA CEREBELLAR ASTROCYTOMA

LONG PERIOD BEFORE NEURO DYSFUNCTION HYDROCEPHALUS ASK FOR MOTOR INSTABILITY AND

CLUMSINESS SOMETIMES 17 TO 28 MONTHS BETWEEN

AACE AND START OF NEURO DYSFUNCTION

BRAIN TUMORS

T OF BRAIN STEM PONTINE GLIOMA

SHORT PERIOD BEFORE NEURO DYSFUNCTION

VI, VII PALSY, GAZE PALSY, HEMIPARESIS

DIVERGENCE PARESIS WITH NORMAL FUSION

IS POSSIBLE

POSSIBLE MECHANISMS FOR AACE

LENNERSTRAND DISTURBANCE IN THE VERGENCE MECHANISMS

WITH NEURONAL LOCALIZATION TO THE MESENCEPHALON BY COMPRESSION

MILHORAT CHANGES IN THE CEREBROSPINAL FLUID

DYNAMICS

POSSIBLE MECHANISMS FOR AACE

OTHERS INCREASED INTRACRANIAL PRESSURE MAY

CAUSE ISSCHEMIA OF BRAINSTEM AND HYPOTHALAMUS

INJURY TO SUPRANUCLEAR MESENCEPHALIC STRUCTURES WHICH CONTROL EYE MOUVEMENTS

INFRANUCLEAR INSULTS( BEST PROGNOSIS FOR FUSION)

SPREAD OF COMITANCE AFTER MILD VI NERVE PALSIES

MYASTHENIA GRAVIS

  PEDIATRIC PATIENTS

  COMITANT ESOTROPIA OR EXOTROPIA CAN BE THE ONLY SIGN FOR MONTHS

  SOMETIMES RESOLVE AND RECUR MONTHS LATER

  ALWAYS NORMAL MOTOR AND SENSORY FUSION

DEMYELINATING DISEASE

  PERIAQUEDUCTAL GRAY MATTER IN THE MIDBRAIN

PRESENTATION

  1. PONTINE GLIOBLASTOMA

FEMALE 4 YEARS OLD CHANGES BEHAVIOUR AACE: Et 12°, MODERATE HYPEROPIA FAMILIAL HISTORY OF SQUINT Et 5°WITH GLASSES NEUROLOGICAL SIGNS VI,VII

HEMIPARESIS AFTER 3 MONTHS NORMAL EYEFUNDUS

PRESENTATION

2. BRAIN STEM GLIOMA

MALE 2 YEARS OLD AACE ESOTROPIA AND V PATTERN 01.1991 OPERATED IN 08.1991 AND 20.03.1993 MICROSTRABISMUS NEUROLOGICAL SIGNS: DIFFICULTIES AT SCHOOL

11.01.98 BRAIN STEM GLIOMA

PRESENTATION

3. BRAINSTEM GLIOMA

MONOCULAR ELEVATION DEFICIENCY INFANCY

7 YEARS OLD OPERATION WITH GOOD RESULT

2 YEARS LATER MRI AFTER HEAD TRAUMA

PONTINE GLIOMA

NO OTHER NEUROLOGIC SIGNS

TUMOR STABLE LOW GRADE GLIOMA

CONCLUSION

  ACUTE COMITANT ESOTROPIA AND DIPLOPIA

  DIVERGENCE INSUFFICIENCY

  MOTOR AND SENSORY FUSION LOSS

  NYSTAGMUS IN LATERAL GAZE

  ABSENCE OF REFRACTIVE ERROR

  ABSENCE OF FAMILIAL STRABISMUS

  OTHER CLINICAL SIGNS

ALWAYS CLOSE FOLLOW UP