Biomedical subjects
Publications and source records attributed to W W Orrison.
An autosomal recessive disorder characterized by intrauterine growth retardation, postnatal retardation, microcephaly, sparse hair, toe syndactyly, and characteristic facial appearance is now recognized as the Dubowitz syndrome. Five addition additional cases of the Dubowitz syndrome are reported, including 2 with documented vascular abnormalities.
In 1952, Cogan introduced the term "congenital ocular motor apraxia" (COA) to describe an abnormality of eye movements characterized by absent or defective voluntary horizontal gaze. Since his original description, there have been few subsequent reports of this disorder. A ten-year review of clinical records from the University of Wisconsin Hospitals disclosed eight patients with COA. In two patients subjected to neuroradiologic testing, agenesis of the corpus callosum was detected. Voluntary horizontal gaze appears to be a learned phenomenon, and defective interhemispheric transfer of visual information may be important in the pathogenesis of COA.
During the past two years we studied six infants with subdural collections of fluid. All patients had macrocrania and excessive transillumination of the head. Rapid head growth was common but five patients were otherwise asymptomatic. Subdural taps performed on five children confirmed the presence of abnormal fluid over the cerebral convexities. Subdural fluid in four patients was compatible with effusion and in another with a hematoma. Computerized tomographic evaluation of all infants showed ventricular enlargement, wide cerebral sulci, decreased density in the anterior temporal regions, large sylvian cisterns, prominent interhemispheric fissures, and decreased density over the cerebral convexities. The CT findings resembled cerebral atrophy but psychomotor development and neurologic examinations have been norma.
Pontine myelinolysis can be suspected clinically on the basis of the following criteria: (1) Electrolyte disturbance manifested mainly by hyponatremia; (2) progressive neurologic deficits resulting in a "locked-in" syndrome; (3) usually, but not necessarily, alcohol abuse; and (4) frequent iatrogenic precipitation of the syndrome by inappropriate rehydration of patients at risk. A major pathophysiologic mechanism for this disorder seems to be the anatomic grid structure of the base of the pons, which is more vulnerable to edema than the cerebral hemispheres. Treatment should be focused on rapid reversal of electrolyte imbalance and judicious use of dehydrating agents. Early diagnosis and treatment might reverse an otherwise malignant syndrome.
During the past 2 years six infants were seen at University of Wisconsin Hospitals (UWH) with subdural hematomas (effusions). This communication describes the abnormalities found on computerized tomographic (CT) evaluation of the six infants.
Three unusual cases of fatal meningitis secondary to undetected bacterial psoas abscess occurred at this institution over an 11-year period. All three patients had suffered chronic debilitating disorders before the abscess formation. The superimposed variable clinical presentations led to the initial diagnosis of a progressing cerebrovascular accident in one case, herniated nucleus pulposus at the L3-4 level in another, and osteomyelitis of the hip joint in the third. Analysis of these cases revealed that before the meningeal dissemination, all of the patients had shown evidence of intraabdominal pathology with positive psoas signs. Diagnostic and therapeutic guidelines are discussed.
We describe a simple, inexpensive pressure dressing which supplements manual pressure and may be applied quickly and easily following femoral arterial puncture for angiography. This technique has been used on several thousand patients without complications.
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We studied 11 patients undergoing a routine lumbar puncture to determine if there were cerebrospinal fluid leaks at the puncture site and whether the maximum volume of leakage correlates with a lumbar puncture headache. Patients completed a headache questionnaire before and after the lumbar puncture. Limited magnetic resonance imaging of the lumbar spine was obtained 8 to 36 hours after the lumbar puncture and two patients also had later imaging. In a blinded fashion, the largest diameter of cerebrospinal fluid leakage into the paraspinous area was determined from T2 weighted magnetic resonance images and the maximum possible fluid volume was calculated. Six patients had a small cerebrospinal fluid leakage (< 10 mL), two had a medium leakage (10 to 110 mL), and three had a large leakage (> 110 mL). The volume of cerebrospinal fluid leakage did not correlate with occurrence of a lumbar puncture headache. The study demonstrates that cerebrospinal fluid usually leaks into the paraspinous area after a lumbar puncture, but the volume of escaped fluid does not correlate with a lumbar puncture headache.
The authors successfully used magnetoencephalography and MR data to localize the sensorimotor cortex in two patients prior to neurosurgery; preoperative localization influenced surgical management.
Twenty-three subjects from two family groups with the adrenoleukodystrophy (ALD)-adrenomyeloneuropathy (AMN) complex were examined with MR imaging at 1.5 T to determine the presence and extent of brain and spinal cord abnormalities. Nineteen individuals were identified as having ALD or AMN, or as having carrier status on the basis of pedigree analysis and/or evaluation of serum very-long-chain fatty acids. In addition to the expected intracranial white matter changes for this disorder, decreased spinal cord diameter was found in seven (30%) of the 23 subjects. In three of these cases, atrophy was limited to the thoracic spinal cord, while atrophy of both the cervical and thoracic cord was identified in four patients. Two patients who did not have MR imaging of the spine were found to have spinal cord atrophy at autopsy. The finding of decreased spinal cord diameter on MR examinations in individuals who are heterozygous for ALD-AMN, in patients with ALD or AMN, and in asymptomatic ALD-AMN patients may represent a new anatomic marker for the variable clinical presentations of this condition. In addition to cranial MR examination, MR imaging of the spine may be indicated in patients with suspected ALD or AMN, or in women with carrier status.
Magnetoencephalography (MEG) monitors magnetic field amplitudes, which are time averages of evoked neuronal responses. This method can detect magnetic fields emanating from the brain and localize the neuronal source. The location of somatosensory neuronal sources for voluntary right thumb and right index finger flexions were determined in four normal volunteers by using a seven-sensor neuromagnetometer inside a magnetically shielded room. These neuronal sources were then identified on the individual's respective CT or MR scans, and correlation was accomplished by geometric calculations, direct cranial measurement, and surface marker identification. Specific functional magnetic fields were located over the appropriate sensory motor cortex; however, there was considerable variation in the exact site. Magnetoencephalography combined with CT and MR may improve localization of normal and abnormal neurologic function.
CT and MR imaging showed basal ganglia calcification that appeared as high signal intensity on T1-weighted images of a patient with pseudohypoparathyroidism. MR imaging of an experimental model of calcium phosphate suspensions showed a signal similar to that seen in the patient. Additionally, T1 and T2 relaxation times of the solutions were measured and showed decreases in both parameters with increasing calcium phosphate concentrations. Intracranial calcification can appear as high signal intensity on T1-weighted images. An experimental model shows that the calcium salt decreases the T1 of surrounding water. Therefore, calcium, and possibly other elements, may induce paramagnetic susceptibility effects.
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