The acute traumatic central cord syndrome (ATCCS) is commonly stated to result from an injury which affects primarily the center of the spinal cord and is frequently hemorrhagic. To test the validity of this widely disseminated hypothesis, the magnetic resonance images [MRI] of 11 consecutive cases of ATCCS caused by closed injury to the spine were analyzed and correlated with the gross pathological and histological features of 3 cervical spinal cords obtained at post mortem from patients with ATCCS, including 2 of patients studied by MRI. The MRI studies were performed acutely (18 h to 2 days after injury) in 7 patients and subacutely (3-10 days after injury) in 4. Ten of the 11 patients had pre-existing spondylosis and/or canal stenosis. The 11th suffered a cervical fracture. All patients exhibited hyperintense signal within the parenchyma of the cervical spinal cord on gradient echo MRI. None showed MRI features characteristic of hemorrhage on T1-weighted spin echo or T2-weighted gradient echo studies. Gross and histological examination of the necropsy specimens showed no evidence of blood or blood products within the cord parenchyma: the primary finding was diffuse disruption of axons, especially within the lateral columns of the cervical cord in the region occupied by the corticospinal tracts. The central gray matter was intact. In patients with ATCCS, the predominant loss of motor function in the distal muscles of the upper limbs may reflect the importance of the corticospinal tract for hand and finger function in the primate. In this study, the MRI and pathological observations indicate that ATCCS is predominantly a white matter injury and that intramedullary hemorrhage is not a necessary feature of the syndrome; indeed, it is probably an uncommon event in ATCCS. We suggest that the most common mechanism of injury in ATCCS may be direct compression of the cervical spinal cord by buckling of the ligamenta flava into an already narrowed cervical spinal canal; this would explain the predominance of axonal injury in the white matter of the lateral columns.
We propose a system for staging nasopharyngeal angiofibromas based on clinical evaluation and computerized tomography. Twenty-three patients with this pathologic diagnosis have been managed at the University of Miami/Jackson Memorial Medical Center in the past two decades. In 13 patients, the clinical diagnosis was confirmed by transnasal biopsy as a minor outpatient procedure. This avoided unnecessary diagnostic studies, shortened the hospital stay, and expedited treatment. Computerized tomography has replaced conventional x-ray studies and routine tomography, although angiography is still necessary for proper evaluation of larger tumors. Stage groupings recommended on the basis of this experience are stage I--tumor confined to nasopharynx; stage II--tumor extending into nasal cavity and/or sphenoid sinus; stage III--tumor extending into one or more of the following: antrum, ethmoid sinus, pterygomaxillary and infratemporal fossae, orbit, and/or cheek; and stage IV--tumor extending into cranial cavity. Surgical excision is recommended for stages I, II, and III. Stage IV tumors require surgical resection and/or radiation therapy with the possible addition of hormonal therapy.
Findings on cranial magnetic resonance (MR) images were correlated with known histopathologic findings in 42 patients with tuberous sclerosis (TS), 17 of whom received gadopentetate dimeglumine, to extend the range of signs on MR images. Four neuroradiologists recorded the number, sites, configurations, and relative signal intensities of intracranial abnormalities. White matter lesions, found in 39 patients (93%), showed four distinct patterns: (a) straight or curvilinear bands extending radially from the ventricle through the cerebral mantle toward the cortex, (b) wedge-shaped lesions, (c) nonspecific conglomerate foci, and (d) cerebellar radial bands. It is concluded that cortical tubers, white matter lesions, subependymal nodules, and sub-ependymal giant cell astrocytomas (SGCAs) may be enhanced after administration of gadopenetetate dimeglumine. Enhancement of a TS lesion does not indicate neoplastic transformation into SGCA. Imaging surveillance every 12 months appears indicated during the peak ages (8-18 years) of occurrence of SGCA. The appearance of white matter lesions supports the theory that the cerebral lesions of TS may be caused by disordered migration of dysgenetic cells.
Evaluation of intracranial and intraspinal CSF flow was accomplished by the use of cardiac gated gradient echo magnetic resonance (MR) technique. Normal patterns of pulsatile flow within the ventricles, cisterns and cervical subarachnoid space were established by this technique and these observations were compared to prior description of CSF flow. With systole there is downward (caudal) flow of CSF in the aqueduct of Sylvius, the foramen of Magendie, the basal cisterns and the dorsal and ventral subarachnoid spaces while during diastole, upward (cranial) flow of CSF in these same structures is seen. The relationships between the cardiac cycle and the CSF pulsations are demonstrated on both magnitude reconstruction and phase reconstruction MR images. Calculations of actual fluid velocity within CSF containing spaces can be obtained from the phase reconstruction images and holds promise for a more accurate analysis of CSF flow. In conditions which result in alterations of flow, cine MR dramatically shows either obstruction or excessively turbulent flow within the CSF pathways. The site of obstructed flow whether in the third ventricle, aqueduct, fourth ventricle, or subarachnoid space can be appreciated by changes in or absence of the normal hypointense signal. Cystic cord lesions such as congenital syringohydromyelia and posttraumatic spinal cord cysts may show pulsatile flow of CSF, a fact which can relate to progressive enlargement of these cysts. The distinction between myelomalacia and cyst formation in the cord is facilitated by the technique. Although the use of cine MR for the analysis of CSF flow is in its infancy, our experience indicates that this technique is useful in a wide range of pathological conditions including, but not limited to, conditions resulting in hydrocephalus or cystic cord lesions.
Infection in the marrow of the temporal, occipital, and sphenoid bones is an uncommon, but increasing occurrence. It is usually secondary to infections beginning in the external auditory canal and is caused almost uniformly by the gram negative Pseudomonas aeruginosa bacteria. Technetium and gallium scintigraphy help in the early detection of such infections while CT scans demonstrate dissolution of bone in well-developed cases. Headache is the predominant symptom. Dysphagia, hoarseness, and aspiration herald the inevitable march of cranial nerves. We have diagnosed and treated 17 cases of osteomyelitis of the skull base. Although the total mortality rate is 53%, it is now a curable disease. Six of our last 8 patients remain alive, although 1 is still under treatment. Treatment is medical and requires the long-term concomitant intravenous administration of an aminoglycoside and a broad spectrum semisynthetic penicillin effective against the causative organism.
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