[The medullary compression syndrome caused by a metastatic process in the cervical spine].
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Biomedical subjects
Publications and source records attributed to F Gjerris.
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Motor disturbances in 16 patients with normal-pressure hydrocephalus were assessed by quantitative registration of handwriting, fine movements of the hand, hand tremor, postural instability, and gait. Tremor intensity was measured using an accelerometer and electronic integration of the accelerometer curves. Postural instability was measured on a computer-assisted force-plate, and computerized analysis of gait was made using an instrumented treadmill. Severe disturbances in motor performance in the upper extremities and postural stability were found. The gait of the hydrocephalic patients was characterized by a very low speed, short steps, ataxia (especially in the vertical direction), and high energy consumption. After shunt operation, significant improvement was found in motor performance in the upper extremities and postural stability, and gait ataxia decreased in all patients to values within the 95% confidence interval of age-matched controls.
In 15 patients fulfilling conventional diagnostic criteria for pseudotumor cerebri, anterior and posterior pituitary functions were examined. Eight of 12 female patients with pseudotumor were grossly overweight. Except for a subnormal response of growth hormone level to insulin-induced hypoglycemia in four patients, no major disturbances were found in pituitary, gonadal, thyroid, or adrenal functions. Vasopressin concentration in the cerebrospinal fluid was increased in patients with pseudotumor, whereas cerebrospinal fluid concentration of estrogens was below detection limit.
Forty patients who had normal-pressure hydrocephalus were examined neuropsychologically before and 12 months after a ventriculoatrial shunt operation. Comparison of the preoperative and postoperative test results showed that cognitive functions improved in 16 patients, were unchanged in 19, and deteriorated in 5. Moreover, we found that the outcome of the operation depended on patient selection criteria. When three or more of the following preoperative signs were present (known cause, short history, low cerebrospinal fluid outflow, small sulci and/or periventricular hypodensity indicated by computed tomography), an improvement in cognitive function was seen in 80% of the patients after a shunt operation.
The Plastimed epidural pressure sensor was evaluated in 35 patients, twenty-eight of whom were suffering from head injury. In seven patients simultaneous intraventricular pressure measurements were obtained. The epidural pressure sensor was only functioning satisfactorily in approximately 2/3 of the patients, while it was malfunctioning or not functioning in the remainder. In seven comparable IVP/EDP studies significant differences up to 25 mm Hg were noted. In three patients IVP was greater than EDP. In two patients the opposite was true. No significant complications were observed. These unsatisfactory results have made us abandon the technique and resort to intraventricular or subarachnoidal pressure measurements.
In a series of 20 consecutive patients with pseudotumor cerebri, five patients had a protracted course of the disease with complaints of persistent disturbances in learning and memory functions. Neuropsychological examination disclosed a light general intellectual impairment with most marked disturbances in verbal tests. After intensive medical treatment or ventriculo-atrial shunt operation, psychological re-examination showed improvement in the test results in accordance with the improvement of the patients' occupational and social situation. Cognitive dysfunction can be the result of a prolonged course of benign intracranial hypertension, and the term "benign" may be misleading in these cases. However, the intellectual impairment, even when long-standing, seems to be reversible in most patients after medical or surgical measures to lower the intracranial pressure.
Head injury in children is very common. Mostly the trauma is slight and the child improves without defects. Even after severe injuries, which can be fatal for an adult, many children will survive in a good condition. Prediction of survival and of quality of life after severe head injuries can be difficult. Predictors of a bad outcome are: low age, initial low grade of coma, abnormal motor responses, fixed pupils, abnormal eye movements, very high ICP, presence of diffuse cerebral edema or intracranial hematoma and obliteration of basal cisters on CT scans. Many children surviving a severe diffuse head injury will be mentally retarded or show behavioural changes.
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Pattern reversal visual evoked potentials in 13 patients with pseudotumor cerebri were significantly delayed (99 +/- 7.3 ms [mean +/- SD]) compared with the findings in 20 normal subjects (94 +/- 2.7 ms), although only four patients had latencies outside the normal range. There was, however, a significant correlation between the intracranial pressure and the latency of visual evoked potentials. After medical treatment of the intracranial hypertension, visual evoked potential latencies decreased in patients who recovered and in whom the papilledema disappeared. In one patient with progressive visual failure, the visual evoked potentials were abnormal before disturbances of visual fields and visual acuity were evident. Repeated examinations of visual evoked potentials might be of value in patients with pseudotumor cerebri to ensure neurosurgical intervention in due time to prevent visual loss in patients with impending optic nerve atrophy.
Intracranial pressure, conductance to cerebrospinal fluid outflow, and cerebral blood flow were investigated in 14 patients with benign intracranial hypertension (pseudotumor cerebri). Intracranial pressure was increased in 9 patients (20 to 30 mm Hg), borderline in 4 patients (15 to 18 mm Hg), and normal in 1 patient (8 mm Hg). Six patients had plateau waves, and all had B waves in more than 50% of the monitored time. Conductance to cerebrospinal fluid outflow, measured by a lumbo-lumbar perfusion method, was significantly reduced: 0.042 ml X mm Hg-1 X min-1 (+/- 0.004 [SEM]; normal, more than 0.080 ml X mm Hg-1 X min-1). Cerebral blood flow was measured by xenon 133 inhalation and single photon emission computer tomography. Mean hemispheric flow was normal in all cases, averaging 59 +/- 9 ml X 100 gm-1 X min-1. Only 2 patients showed focal low-flow areas. Thus, a disturbance of cerebrospinal fluid circulation seems to be of pathogenetic significance in benign intracranial hypertension.
Four patients aged 11, 11, 8 and 18 years, shunted in early childhood for hydrocephalus, were followed in the outpatient clinic for severe headache from 3 months to 2 years. The headache lasted for days and up to a week, was usually severe, and was often followed by screaming attacks or aggressive behavior. In all patients repeated computed tomography disclosed a normal ventricular system or slit ventricles. The intracranial pressure (ICP) was measured in all four patients and showed an increased intracranial steady-state pressure between 20-50 mmHg, plateau waves and, in two of the patients, a very high intracranial pulse-pressure amplitude. At operation all patients had dysfunction of the shunt (most often of the distal end). In three patients ICP monitoring post-operatively showed normal intracranial pressure without any abnormal increments from the normal steady-state pressure. Thus, severe headache can be the only symptom of long-standing shunt dysfunction, even without ventricular dilation. In shunted hydrocephalic children complaining of headaches, ICP measurement is highly recommended.
The response of plasma and ventricular cerebrospinal fluid vasopressin concentration to short-time induced intracranial hypertension was studied in 8 patients with hydrocephalus, defined as ventricular enlargement on computerized tomography. In connection with measurement of conductance to cerebrospinal fluid outflow, the concentration of vasopressin in plasma and cerebrospinal fluid was measured during perfusion at a low (less than 10 mmHg) and at a high (greater than 20 mmHg) intraventricular pressure level. Mean plasma vasopressin concentration was increased from 2.4 +/- 0.4 pg/ml (SEM) during perfusion at the low pressure level to 4.2 +/- 0.8 pg/ml (p less than 0.01) at the high pressure level. The cerebrospinal fluid concentrations of vasopressin at the low and high intraventricular pressure were 1.2 +/- 0.1 pg/ml and 1.7 +/- 0.2 pg/ml (p less than 0.05), respectively. However, only half of the patients responded to the increase in intraventricular pressure with an increase in cerebrospinal fluid vasopressin concentration exceeding 50%. The results of the present study suggest that an increase in the intracranial pressure might be a stimulus for vasopressin release in both the blood and the cerebrospinal fluid.
The concentration of glial fibrillary acidic protein (GFAP) in lumbar cerebrospinal fluid (CSF) was measured in 12 patients with normal pressure hydrocephalus (NPH) 11 patients with primary degenerative dementia (PDD), 8 patients with various other neurological diseases, and 18 patients without signs of organic nervous disease (controls). Mean CSF GFAP concentration was significantly higher in NPH patients: 96 +/- 23 ng/ml (SEM) when compared with PDD patients: 8.2 +/- 1.9 ng/ml (P less than 0.01), or with controls: 4.3 +/- 0.7 ng/ml (P less than 0.01). Only 2 NPH patients had a GFAP concentration within the range of the control group (2-14 ng GFAP/ml CSF). No significant differences were found between the PDD patients and the control group, or between the group of patients with other neurological diseases and the control group. In addition, a rostro-caudal gradient of GFAP in CSF could be demonstrated. In 6 NPH and 2 PDD patients both ventricular and lumbar CSF samples were investigated. In all cases the ventricular GFAP concentration was higher than the lumbar concentration. The difference was statistically significant (P less than 0.01). Our results suggest that determination of CSF GFAP concentration might be of diagnostic value in discrimination between NPH patients and patients with enlarged ventricles associated with degenerative brain disease.
The variation in vasopressin concentrations of ventricular cerebrospinal fluid and plasma throughout a 24-h period was studied in 10 patients with hydrocephalus. In 6 control patients, the diurnal variation in plasma vasopressin concentrations was studied. Vasopressin concentrations were determined by radioimmunoassay in plasma and in extracted and unextracted cerebrospinal fluid. Cortisol and osmolality in plasma were also measured. Vasopressin concentrations measured in extracted cerebrospinal fluid showed only small intra- and interindividual variation, while the corresponding values for unextracted cerebrospinal fluid were 2-5-fold higher and showed more variation. Plasma vasopressin concentrations varied considerably throughout the 24-h period in the individual hydrocephalic patient and between the patients. The pattern of variation was inconstant with no circadian rhythm, and the variation was not related to any changes in plasma osmolality, blood pressure or intracranial pressure. In some of the patients, the normal diurnal pattern of variation in plasma cortisol was broken, however, without a relation to the observed fluctuations in vasopressin concentrations. The abnormal variation of plasma vasopressin and cortisol was considered to reflect stress in connection with the intracranial pressure monitoring procedure. In the control patients, plasma vasopressin showed only small variations and plasma cortisol showed a normal diurnal rhythm. It is concluded that cerebrospinal fluid vasopressin concentration in patients with hydrocephalus is very constant throughout the day, even when plasma vasopressin concentrations show marked episodic increases. Thus, a circadian rhythm in the cerebrospinal fluid vasopressin concentration, as reported in several animal species, could not be confirmed in these patients.
In a prospective study twenty patients with benign intracranial hypertension, 15 females and five males with mean age 34 years (range 12-61 years), were followed up from 12 to 61 months (mean 22 months). Initially all patients showed marked papilledema, normal visual acuity, considerable enlargement of the blind spot area, and significantly delayed pattern reversal visual evoked potentials. During medical treatment eleven patients showed within 3-6 months a rapidly regression and normalization of papilledema, blind spot area, and visual evoked potentials. Eight patients continued in showing papilledema including disc gliosis, enlargement of blind spot area, and pathological visual evoked potentials. One patient developed optic nerve atrophy. The results indicated that repeated examinations of visual evoked potentials, when suspect of threatening visual loss has come up (papilledema, increased blind spot area, and field defects), might increase the change of diagnose of an optic nerve atrophy as early as possible.
The authors report a prospective, randomized 18-month study on the effect of prophylactic antibiotic treatment in 152 hydrocephalic patients in whom clean shunt operations or revisions were done. The treated group received methicillin (totally 200 mg/kg) divided into six i.v. doses during 24 hours starting at the induction of anesthesia. Patients allergic to penicillin received erythromycin instead. Seventy-nine patients received antibiotics, and 73 (the control group) received none. All patients were followed at least 6 months after operation or to their death. Eleven patients developed signs of infection, giving an overall infection rate of 7.2%; however, the infection occurred less than 1 month after the operation in only half of these. Six of the patients had septicemia, 4 had peritonitis, and 1 had meningitis. In the treated group, the infection rate was 8.9%; in the control group, the rate was 5.5%. There was no statistically significant difference. The prophylactic antibiotic regimen in this investigation did not reduce the infection rate connected with cerebrospinal fluid shunting procedures.
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Cerebrospinal fluid and plasma vasopressin were measured in patients with cerebral disorders associated with varying levels of elevated intracranial pressure. The mean cerebrospinal fluid vasopressin concentration was significantly increased in patients with pseudotumor cerebri (2.0 +/- 0.2 [SEM] pg/ml), intracranial tumor (2.3 +/- 0.4 pg/ml), and intracranial hemorrhage (1.9 +/- 0.3 pg/ml) compared with control patients (1.2 +/- 0.1 pg/ml). A significant relationship was found between intracranial pressure and the cerebrospinal fluid vasopressin concentration within all groups of patients and in the whole sample as well (r = 0.79; p less than 0.001). In the groups of patients with intracranial tumor, hydrocephalus, and intracranial hemorrhage, some individuals showed plasma vasopressin concentrations inappropriate to the corresponding plasma osmolality, but no relationship was found between intracranial pressure and plasma vasopressin concentration. It is suggested that increased intracranial pressure is a stimulus to centrally released vasopressin. The clinical importance of increased cerebrospinal fluid vasopressin concentrations is still not known.