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THE HE DIAGRAM makers have provided two schemes for the connections through the medial longitudinal fasciculus (MLF) to explain the MLF syndrome in man. Some authorities depict a wiring diagram with internuclear axons running ipsilaterally in the MLF from the 6th to the 3rd nerve nucleus,1 while other authorities depict a decussation at the 6th nerve level to run in the contralateral MLF.2 In the macaque monkey the problem has been resolved.3,4The internuclear MLF fibers decussate at the 6th nerve level to run contralaterally. Thus, unilateral MLF lesions cause ipsilateral paralysis of the adducting eye and contralateral horizontal nystagmus in the abducting eye. The situation in man has been obscure because of the lack of suitable clinicopathologic material. In the few anatomically studied cases the clinical picture was beclouded by multiple signs, and the anatomic correlation was beclouded by multiple or extensive lesions.5-7 The present case is considered especially valuable because the patient showed a pure MLF syndrome clin¬ ically and only a single significant lesion patho-anatomically. Report of a CaseA 62-year-old white woman with rheumatic mitral stenosis and insufficiency and proven Strepto¬ coccus viridans endocarditis was admitted to Indi¬ ana University Medical Center for treatment. Ten days later, she suddenly had nausea, vomiting, and double vision. She had no other neurological symp¬ toms. The results of a neurological examination the next day were entirely within normal limits except for the following : On left lateral gaze the left eye displayed monocular horizontal nystagmus but full abduction ; the right eye did not adduct on this movement, although it did in convergence.There was no other disturbance of ocular move¬ ments, no ptosis, and no pupillary abnormality. The cerebrospinal fluid was normal. Thus, the only neurological deficit was the syndrome of the right MLF. Seven days after its inception, the syndrome disappeared, and the extraocular movements were entirely normal. She died with congestive heart failure 16 days after onset of the MLF syndrome.Pathologic Findings.-The heart showed stenosis of the mitral and aortic valves and chronic endo¬ carditis of the right and left atria. The only gross brain lesion was in the rostral pontine tegmentum just caudal to the trochlear nerve decussation. The brain stem was embedded in paraffin and serially sectioned from the level of the mamillary bodies to the first cervical segment. All sections were mounted and alternately stained with cresyl violet and impregnated with a modification of Hortega's silver carbonate method for neurites.8 Multiple samples of the cerebrum and cerebellum were simi¬ larly stained.Microscopically, the tegmental lesion measured 2.5 mm in greatest diameter (Fig 1 and 2). It occupied the entire medial three fourths of the right medial longitudinal fasciculus, the adjacent nucleus compactas suprafascicularis, and extended somewhat ventrolaterally to encroach slightly on the dorsomedial fibers of the central tegmental tract. ...
THE HE DIAGRAM makers have provided two schemes for the connections through the medial longitudinal fasciculus (MLF) to explain the MLF syndrome in man. Some authorities depict a wiring diagram with internuclear axons running ipsilaterally in the MLF from the 6th to the 3rd nerve nucleus,1 while other authorities depict a decussation at the 6th nerve level to run in the contralateral MLF.2 In the macaque monkey the problem has been resolved.3,4The internuclear MLF fibers decussate at the 6th nerve level to run contralaterally. Thus, unilateral MLF lesions cause ipsilateral paralysis of the adducting eye and contralateral horizontal nystagmus in the abducting eye. The situation in man has been obscure because of the lack of suitable clinicopathologic material. In the few anatomically studied cases the clinical picture was beclouded by multiple signs, and the anatomic correlation was beclouded by multiple or extensive lesions.5-7 The present case is considered especially valuable because the patient showed a pure MLF syndrome clin¬ ically and only a single significant lesion patho-anatomically. Report of a CaseA 62-year-old white woman with rheumatic mitral stenosis and insufficiency and proven Strepto¬ coccus viridans endocarditis was admitted to Indi¬ ana University Medical Center for treatment. Ten days later, she suddenly had nausea, vomiting, and double vision. She had no other neurological symp¬ toms. The results of a neurological examination the next day were entirely within normal limits except for the following : On left lateral gaze the left eye displayed monocular horizontal nystagmus but full abduction ; the right eye did not adduct on this movement, although it did in convergence.There was no other disturbance of ocular move¬ ments, no ptosis, and no pupillary abnormality. The cerebrospinal fluid was normal. Thus, the only neurological deficit was the syndrome of the right MLF. Seven days after its inception, the syndrome disappeared, and the extraocular movements were entirely normal. She died with congestive heart failure 16 days after onset of the MLF syndrome.Pathologic Findings.-The heart showed stenosis of the mitral and aortic valves and chronic endo¬ carditis of the right and left atria. The only gross brain lesion was in the rostral pontine tegmentum just caudal to the trochlear nerve decussation. The brain stem was embedded in paraffin and serially sectioned from the level of the mamillary bodies to the first cervical segment. All sections were mounted and alternately stained with cresyl violet and impregnated with a modification of Hortega's silver carbonate method for neurites.8 Multiple samples of the cerebrum and cerebellum were simi¬ larly stained.Microscopically, the tegmental lesion measured 2.5 mm in greatest diameter (Fig 1 and 2). It occupied the entire medial three fourths of the right medial longitudinal fasciculus, the adjacent nucleus compactas suprafascicularis, and extended somewhat ventrolaterally to encroach slightly on the dorsomedial fibers of the central tegmental tract. ...
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