Intracranial Manifestations Research Articles

Posterior fossa plasmacytoma: Computed tomographic findings

A patient with multiple myeloma developed neurological symptoms consistent with an expanding intracranial lesion. The CT scan showed evidence of a posterior fossa mass. This was pathologically confirmed to be a plasmacytoma. There was no CT or pathological evidence of bone involvement. When the neurological symptoms developed, there was no systemic evidence of recurrence of the myeloma. The intracranial manifestations of multiple myeloma are reviewed. The CT findings and differential diagnosis of the plasmacytoma are reviewed.

Moyamoya disease associated with renovascular hypertension

Findings at the autopsy of a 7-year-old Japanese girl with moyamoya disease associated with renovascular hypertension are reported. There was disruption of a saccular aneurysm located at the junction of the left posterior cerebral and the posterior communicating arteries. Intimal thickening of carotid, coronary, and renal arteries, similar to findings in cases of intimal hyperplasia of fibromuscular dysplasia, was observed. These findings indicate that moyamoya disease may actually be an intracranial manifestation in a systemic arterial disorder.

Acquired immunodeficiency syndrome: cerebral computed tomographic manifestations.

CT examination of the central nervous system was performed in 19 patients with acquired immunodeficiency syndrome (AIDS). Eighteen patients were homosexuals, and five drug abusers. Parenchymal and meningeal inflammations were seen in patients with intracranial manifestations of the disease. The most common demonstrable lesion in the parenchyma was toxoplasmosis, which produced ring enhancement, solid enhancement, and nonenhancing focal edema. The most common meningeal inflammation was cryptococcosis, which was diagnosed by examination of the cerebrospinal fluid and did not show specific CT changes. It is concluded that toxoplasmosis and cryptococcosis should be the first diagnostic consideration in patients with neurologic findings who have a history of homosexuality and/or intravenous drug abuse and previous unusual infections or anergy. A delayed contrast scan, single or double dose, appears to be the most accurate method of outlining the total extent of disease thereby helping to locate the best biopsy site for pretreatment diagnosis. Empirical institution of toxoplasmosis therapy is recommended in those cases in which CT findings are consistent with toxoplasmosis and the biopsy shows only nonspecific encephalitis. A biopsy of every parenchymal lesion is not considered necessary.

Cerebrospinal fluid pressure-gradients in spina bifida cystica, with special reference to the Arnold-Chiari malformation and aqueductal stenosis.

Ten infants with spina bifida cystica were investigated during life by simultaneous ventricular and intraspinal CSF pressure recordings, and 11 post-mortem specimens were studied by means of crystic resin castings of the ventricles. The results indicate marked pressure differentials between the lateral ventricles and intraspinal CSF pathways, which contribute to the moulding of the Arnold-Chiari malformation as a sliding hernia. Similar pressure differentials may exist at the incisura, with moulding of tissues producing blockage of the aqueduct and the subarachnoid pathways. A valvular action was demonstrated, in which baseline pressure differences were exaggerated by the infant's straining (e.g. crying, sucking), and it seems that complete dissociation between the two pressures may develop as a result of periods of partial dissociation. Removal of the meningocele sac increased the peaks in recordings of intraspinal pressure produced by straining. If it is carried out when there is a valvular effect, it seems that it will hasten the onset of established ventriculo-spinal pressure dissociation and uncompensated hydrocephalus by leading to impaction of the Arnold-Chiari malformation in the foramen magnum. The results indicate that even after birth the CSF pathways of babies with spina bifida cystica are in a plastic and changeable condition, with competition between constricting and distending forces. The demonstration that pressures tend to be low in the spine and to become lower before exacerbation of hydrocephalus suggests that all the intracranial manifestations of spina bifida cystica may be due to low intraspinal pressure, which results from initial failure of the neural tube to close during embryogenesis.

Neurofibromatosis complicated by intracranial tumors.

Four cases of neurofibromatosis complicated by intracranial tumors are reported. Case 1 showed an intracranial neurofibromatosis while the other three cases contained gliomas in various stages of malignancy.Japanese autopsy records for 11 years from 1958 to 1968 were investigated from a statistical point of view. Meningiomas and neurinomas associated with neurofibromatosis show an earlier peak of age distribution than that of those tumors without neurofibromatosis. There is no different age distribution between gliomas related to neurofibromatosis and the ones not related to it.These facts suggest that both neurinomas and meningiomas associated with neurofibromatosis are intracranial manifestations of neurofibromatosis perse, while complicated gliomas are thought to be an incidental neoplasm, probably associated with transformation of disoriented neuroglial rests.

Continuous pressure monitoring in experimental obstructive hydrocephalus. II. The origin of undulating ventricular waves and periodic respirations.

Mayer waves and undulating ventricular waves were produced in hydrocephalic and nonhydrocephalic animals. Carotid sinus stimulation resulted in an increase in both wave forms, whereas carotid sinus denervation resulted in their diminution. The reflex pathway involved in the production of the waves constitutes a feedback mechanism between carotid sinus, the peripheral proprioceptor, and medullary vasomotor center. The ventricular fluid pressure wave forms are the intracranial manifestations of passively transmitted changes occurring in the systemic circulation secondary to dysfunction of the brain stem.

Radiation therapy for intracranial lymphoma.

Although lymphoma is seen frequently in an active radiotherapy department, intracranial manifestations attributed to the disorder are rare (2). Histologic proof of such involvement is reported even less frequently. In one-third of the patients with clinical symptoms of intracranial lymphoma, no histologic evidence of involvement could be demonstrated at surgical exploration or postmortem examination (6, 7). In the absence of histologic confirmation, it is difficult to judge the effect of treatment or the course of the disease. Long-term survival in intracranial lymphoma has been considered nonexistent (5, 7). Recent evidence to the contrary led us to review the experience in the Division of Radiotherapy of the Columbia-Presbyterian Medical Center and New York Neurological Institute in an attempt to determine the course of disease more accurately. Present Experience Twenty-four histologically verified cases of intracranial lymphoma (lymphosarcoma, reticulum-cell sarcoma, mixed lympho-reticulum-cell sarcoma...

CRANIAL AND INTRACRANIAL LESIONS IN NEUROFIBROMATOSIS

CRANIAL AND INTRACRANIAL LESIONS IN NEUROFIBROMATOSISKENDRICK C. DAVIDSON, M.D.Audio Available | Share

Intracranial calcification in children following tuberculous meningitis.

From the analysis of 40 cases of intracranial calcification following tuberculous meningitis, we may draw the following conclusions: 1. Intracranial calcification and other residual manifestations occur more frequently with serious forms of tuberculous meningitis, in cases with late diagnosis and delayed institution of therapy. 2. So far there is no good reason to state that there is a correlation between the development of intracranial calcification and the methods of treatment. 3. Intracranial calcification can develop after tuberculous meningitis in children of various ages and independently from other local forms of tuberculosis. 4. X-ray examination of the skull of children with a history of tuberculous meningitis reveals important pathological changes of scientific and practical interest.

Intracranial manifestations in two cases of systemic rheumatoid disease.

Meningeal and intracranial vascular lesions were observed in two cases of rheumatoid arthritis. Granulomas of the meninges were present and histologically identical with subcutaneous rheumatoid nodules. Arteritis similar to that occasionally seen in systemic rheumatoid disease was found in all types of intracranial vessels. Lesiones vascular meningee e intracranial esseva observate in duo casos de arthritis rheumatoide. Granulomas del meninges esseva presente e histologicamente identic con subcutanee nodulos rheumatoide. Arteritis simile a illo incontrate a vices in systemic morbo rheumatoide esseva observate in omne typos de vaso intracranial.

Recognition and Treatment of Intracranial Manifestations of Leukemia

One of the prime objectives in the therapy of acute childhood leukemia is to maintain the patient symptom-free and capable of enjoying normal activity. The development of neurologic complications poses a serious threat to this aim. Leukemia involving the central nervous system may be manifested by symptoms and signs of meningeal irritation and increased intracranial pressure, seizures, and/or cranial nerve palsies. Not infrequently patients who have had no symptoms or signs of central nervous system involvement during life may at necropsy be found to have widespread infiltrative lesions involving the meninges and brain. Since orally administered antimetabolites apparently do not penetrate the blood-cerebrospinal fluid barrier in sufficient concentrations to prevent or control such complications, therapy in the past has included steroids and irradiation to the skull. The beneficial effects of these modes of therapy may be quite short in duration. 1 Recently, Burchenal and co-workers 2 described a dramatic beneficial

Symptoms and signs referable to the basal ganglia in brain tumor.

CEREBRAL tumor is not generally considered a cause of extrapyramidal signs and symptoms, and it has been stated by Kinnier Wilson1and others2that neoplastic involvement of the basal ganglia is often asymptomatic. Focal neurologic signs are not usually observed until the internal capsule is involved. The relevant literature consists largely of individual case reports. It is the purpose of this paper to describe a series of 12 cases of intracranial tumor and manifestations indicating involvement of the extrapyramidal system and to review the pertinent literature. In 1923 Parker3described the case of a 12-year-old boy with a clinical picture of Parkinsonism who was found to have a tumor involving both thalami. Moersch4in 1928 reported the case of a man aged 28 with Parkinsonian facies and gait and a tremor of the left upper extremity who recovered completely after the removal of a right parasagittal

Periphlebitis Retinalis Associated with Intracranial Manifestations

Periphlebitis Retinalis Associated with Intracranial Manifestations

ASTROCYTOSIS ARACHNOIDEAE CEREBELLI

Bizarre intracranial manifestations of von Recklinghausen's neurofibromatosis have been described frequently. The present case is a unique example of one of the peculiar lesions of this kaleidoscopic disease. REPORT OF A CASE R. N. L., a 16 year old girl, was admitted to the University of Chicago Clinics, to the service of Dr. A. Kenyon, on Aug. 6, 1939. She complained of severe headache during most of her life, aggravated recently and associated with nausea and vomiting, awkwardness and clumsiness for twelve years, urinary frequency and incontinence all her life and mental retardation. The patient was an only child of parents who separated when she was 4 years old. Both parents were in good health, and the family history was irrelevant except that the patient's maternal aunt and grandmother had multiple small tumors all over their bodies (neurofibromatosis?). In her early teens the patient's head became so large that her

Spheno-Occipital Chordoma

Intracranial neoplasms originating from the vestiges of the notochord in the basisphenoid have been recognized since the time of Virchow, but they are decidedly uncommon. Mabrey (1), in a painstaking review of the literature through 1934, found only 47 cases of intracranial chordoma recorded. Since the appearance of his article approximately 24 additional cases have been reported. The subject of the present paper is one of a series of neoplasms of the central nervous system previously studied by the author (2). This tumor furnishes confirmation of former histological observations and also a few unusual features of interest. Report of Case The patient was a white woman thirty-five years of age, whose history up to her last illness showed nothing relevant. About two years before admission to the Boston City Hospital she began to be troubled with headache. This gradually increased in severity, and was complicated in the course of time first by fainting attacks and subsequently by increasing ataxia. For these disorders the patient was admitted for observation on the Neurological Service. Localizing symptoms and signs of increased intracranial pressure were not then apparent, and for a while she was regarded as a victim of one of the protean forms of multiple disseminated sclerosis. As time passed, however, no remission appeared, and the intracranial manifestations tended progressively to dominate the picture. It was decided, therefore, to explore the posterior fossa on the chance that a removable tumor might be found. Accordingly a suboccipital craniotomy was done. The floor of the fourth ventricle was found crowded up against the cerebellum, and the brain stem rotated some 30 degrees to the right. No tumor was visible, and since it was evident that the tumor, if any, was inoperable, and the patient9s condition was precarious, operation was limited to suboccipital decompression. She did not regain consciousness and died the following day.