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David Fairman and Gilbert Horrax

our opinion, therefore, the above terms, namely, oxycephaly, brachycephaly and scaphocephaly, represent the only logical nomenclature for the various types of craniostenosis. The neurologic symptoms are dependent upon the degree of contraction of the skull. The craniostenosis is decompensated when the patient develops chronic increased intracranial pressure as evidenced by headache, vomiting, papilledema, failing vision and convulsive seizures. Optic atrophy with blindness and psychic disturbances may also occur. An extremely striking feature of craniostenosis

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Caries Cranii A. C. de Vet July 1949 6 4 269 278 10.3171/jns.1949.6.4.0269 Description of a Skin Galvanometer that Gives a Graphic Record of Activity in the Sympathetic Nervous System Curt P. Richter Frederick G. Whelan July 1949 6 4 279 284 10.3171/jns.1949.6.4.0279 Cerebral Hemispherectomy Eric Bell Jr. Louis J. Karnosh July 1949 6 4 285 293 10.3171/jns.1949.6.4.0285 Traumatic Subdural Hematoma—Acute, Subacute and Chronic Francis Echlin July 1949 6 4 294 303 10.3171/jns.1949.6.4.0294 The Use of Dry

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Traumatic Subdural Hematoma—Acute, Subacute and Chronic

An Analysis of Seventy Operated Cases

Francis Echlin

I n the past it has been common practice to class all subdural hematomas as acute or chronic. Acuteness has been estimated on the basis of elapsed time from the injury, or on the degree of associated brain damage. According to one classification, all hematomas that cause death or come to operation before the 21st day after a cranio-cerebral injury are described as acute (Kennedy and Wortis 9 ). In another classification, cases of subdural hematoma that still show unhealed or acute brain injury are placed in the acute group, the others being classed as chronic

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Craniostenosis

With Notes on a Modified Operation for the Brachycephalic Form

David Fairman and Gilbert Horrax

all the sutures the result is a high peaked skull (oxycephaly). Other changes in the skull may also appear. The anterior fossa becomes short, with its floor oblique, and the orbit becomes shallow, with prominence of the eyes. Craniostenosis is compensated when a compensatory growth of the skull occurs at the open sutures. Since this is the only evidence of this condition, a markedly abnormal shape of the head results which must be corroborated by the roentgenologic findings. Craniostenosis is decompensated when the patient develops chronic increased intracranial

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Dean H. Echols and Frederick C. Rehfeldt

another attempt was made to explore the 5th disk without success but the entire 5th root was severed. The patient still had some sciatic pain 3 months later when he returned to work. After 3 months of heavy labor he “reinjured” his back, became incapacitated, and made a settlement with the insurance company. Later he went to work in a shipyard in California and again became incapacitated. He was last seen by Dr. Carl Rand in Los Angeles in June 1943. At that time he was having a mild attack of sciatica. This is certainly a case of chronic recurrent sciatica due to

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Everett O. Jeffreys and Richard H. Ames

time to time diplopia, vertigo, and scotomata. Examination . The patient was alert, cooperative, and in no acute distress. Positive findings were: bilateral chronic papilledema, weakness of the external rectus muscle on the right, generalized muscular hypotonia with depression of the tendon reflexes, and marked ataxia. Routine blood and urine studies were within normal limits. Blood serology was negative. Skull films were normal. Visual acuity was 20/40 in each eye. Visual fields showed minimal generalized constriction with gross enlargement of the blind spots

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John E. Scarff

I n 1936 I described a specific epileptic syndrome favorably affected by lysis of anomalous Pacchionian granulations and made a preliminary report of 3 cases. 3 The present paper consists of a follow up of these original cases, with a report on 17 additional ones. The essential features of this specific epileptic syndrome are: 1. Early onset . Convulsions usually begin during the first or second decade, suggesting a congenital lesion. 2. Chronicity . The cases here reported average more than 11 years in duration. 3. Focal convulsions

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Aidan A. Raney, R. B. Raney and C. R. Hunter

P ublished reports indicate considerable variance in opinion on the subject of etiology of chronic posttraumatic headache, although it is generally attributed to an intracranial process. There is accumulated evidence that cervical intervertebral disc pathology is often responsible. Therefore, it seems appropriate to survey pertinent clinical and experimental observations related to this interesting subject. THEORIES ON ETIOLOGY A. Intracranial Structures . The effect of trauma of the intracranial structures is often assumed to be responsible for chronic

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Metastasizing Cerebellar Tumors Robert P. Barden Frederic H. Lewey November 1949 6 6 439 449 10.3171/jns.1949.6.6.0439 Protruded Lumbar Intervertebral Discs B. M. Shinners W. B. Hamby November 1949 6 6 450 457 10.3171/jns.1949.6.6.0450 Chronic Posttraumatic Headache and the Syndrome of Cervical Disc Lesion Following Head Trauma Aidan A. Raney R. B. Raney C. R. Hunter November 1949 6 6 458 465 10.3171/jns.1949.6.6.0458 Transient Hemiplegia Associated with Cerebral Angiography (Diodrast) J. G. Chusid

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W. McK. Craig and Gilbert Horrax

in its more chronic phase may be confused with other types of lesions of the retina; in this instance it simulated tuberculous choroidoretinitis with periphlebitis. Only with the development of cerebellar symptoms and intracranial hypertension was the retinal lesion suspected of being von Hippel's disease. Case 2. Meager cerebellar symptomatology. Dilated ventricular system by ventriculography. Disclosure and complete removal of hemangiomas in both cerebellar hemispheres . E.F., aged 18, was referred to the Lahey Clinic and admitted to the New England Deaconess