Diabetes insipidus and blindness caused by a suprasellar tumor: Pieter Pauw's observations from the 16th century.

Tumors in the suprasellar region may cause both visual and endocrinologic symptoms. This association, well known to modern physicians, was established during the 19th century. However, we have identified a 16th-century autopsy report, written by the Dutch professor of anatomy Pieter Pauw (1564-1617), which describes an 18-year-old girl who developed marked polyuria and subsequently became totally blind from a cystic tumor compressing the optic chiasm. Based on prevailing theories on the nature of diabetes, Pauw attributed the disease to the kidneys. Undoubtedly, however, his lucid report is the earliest known account of diabetes insipidus caused by an arachnoid cyst, the Rathke cleft cyst, or craniopharyngioma in the region of the pouch of Rathke. The description also gives insights into the role of anatomic dissections in late 16th-century northern Europe.

Interstitial chemotherapy with carmustine-loaded polymers for high-grade gliomas: a randomized double-blind study.

OBJECTIVE: To find out the effect of carmustine (bischloroethyl-nitrosourea) combined with a biodegradable polymer in the treatment of malignant (Grades III and IV) gliomas, applied locally, at the time of the primary operation. METHODS: Prospective, randomized double-blind study of an active treatment group versus a placebo group. Conducted at the Departments of Neurosurgery of the University Hospitals of Helsinki, Tampere, and Turku in Finland and Trondheim in Norway. The study consisted of 32 patients (16 in each treatment group) enrolled between March 23, 1992, and March 19, 1993. The study was planned to include 100 patients but had to be terminated prematurely, because the drug that was being used had become unobtainable. The main outcome measures included the survival times of patients after the operations and the application of an active drug or placebo. RESULTS: The median time from surgery to death was 58.1 weeks for the active treatment group versus 39.9 weeks for the placebo group (P = 0.012). For 27 patients with Grade IV tumors, the corresponding times were 39.9 weeks for the placebo group and 53.3 weeks for the active treatment group (P = 0.008). At the end of the study, six patients were still alive, five of whom belonged to the active treatment group. CONCLUSION: Carmustine applied locally in a biodegradable polymer at the time of primary operation, seems to have a favorable effect on the life span of patients with high-grade gliomas.

Long-term outcome after removal of spinal schwannoma: a clinicopathological study of 187 cases.

Are spinal schwannomas as benign as we think? To what extent do patients recover? Are patients prone to develop late complications such as cystic myelopathy or symptomatic spinal deformity? Is their life expectancy compromised? In an effort to answer these questions, the authors analyzed the long-term outcome for 187 patients from one neurosurgical department with surgically treated spinal schwannoma. Median follow-up period was 12.9 years (2454 patient years). One-fifth of the patients considered themselves free of symptoms at follow-up examination. The most common late complaint was local pain (46%), followed by radiating pain (43%), paraparesis (31%), radicular deficit (28%), sensory deficit due to a spinal cord lesion (27%), and difficulty voiding (19%). Late complications occurred in 21% of the patient population, including cystic myelopathy (2%), spinal arachnoiditis (6%), spinal deformity (6%), and troublesome pain (7%). Life expectancy of the patients corresponded to that of the general population.

Long-term outcome after removal of spinal neurofibroma.

Spinal neurofibromas are uncommon, comprising approximately 3% of all spinal tumors. They occur both sporadically and in association with neurofibromatosis 1 (NF1; von Recklinghausen's disease). This study presents the clinical characteristics of 32 patients who underwent surgery for symptomatic spinal neurofibromas. Twenty-two of these patients showed clinical signs of NF1. The patients were typically younger (median age 31 years) than those with spinal schwannomas. The tumors were located mainly in the cervical region and tended to grow both extra- and intradurally. Patients with NF1 were prone to develop new spinal neurofibromas. A life-table analysis showed a reduced survival rate for these patients compared to that of the general population.

Prediction of psychosocial recovery after head injury with cognitive tests and neurobehavioral ratings.

A series of 53 patients was studied using a battery of tests and a neurobehavioral rating scale on average 4 months after closed-head injury (CHI). Social outcome was assessed 1 year after injury by interviewing a family member. The results supported the hypothesis that tests of flexibility and programming rather than tests of cognitive skills predict psychosocial recovery after CHI. Spatial Learning with Self-Set Goals and Sorting were measures of flexibility and programming. Contrary to expectation, word fluency performance was unrelated to these measures, but was associated with conventional intelligence tests, which did not predict psychosocial recovery. Cognition/Energy deficit on the Neurobehavioral Rating Scale and increased age were useful predictors of poor psychosocial outcome, whereas computed tomography findings or the Glasgow Coma Score were weakly related to the outcome indices. Evidently, cognitive flexibility and mental programming are very important psychological prerequisites of social recovery after CHI.

Treatment of spontaneous intracerebral and intracerebellar hemorrhages.

Most primary intracerebral and intracerebellar hemorrhages are hypertensive, and the most common site is the basal ganglion. In typical basal ganglia hematoma, surgery offers no benefit, and such patients should be treated conservatively. Surgery is not indicated in pontine hematomas either. Cerebellar hematomas may block the circulation of the cerebrospinal fluid and cause an acute life-threatening hydrocephalus; therefore such hematomas should be operated on. Subcortical hematomas, which are usually not associated with hypertension and may be due to tumor or vascular malformation, should as a rule be operated on. Carotid angiography is necessary for most supratentorial hematomas to exclude the presence of aneurysm or arteriovenous malformation. Secondary hematomas from ruptured arterial aneurysm should be operated on as urgently as traumatic intracranial hematomas if the patient's level of consciousness is deteriorating and if there is severe neurological deficit. Hematomas due to arteriovenous malformation must sometimes be evacuated as an emergency measure if the patient is unconscious, and the malformation should be excised if technically possible. The operation should preferably be postponed to the second week after the bleeding if the patient's level of consciousness is not deteriorating, since the malformation is more easily excised after the brain edema has subsided. Hematomas associated with anticoagulant treatment should be evacuated if the hematoma is expansive and if the patient is unconscious or somnolent but the results are not very good. Hematomas of hemophiliacs should be evacuated, and these patients need an appropriate replacement therapy.

Natural history of unruptured intracranial aneurysms: a long-term follow-up study.

To investigate the natural history of unruptured aneurysms and predictive risk factors determining subsequent rupture, the authors followed 142 patients with 181 unruptured aneurysms until death or subarachnoid hemorrhage intervened, or for at least 10 years after the unruptured aneurysm was diagnosed. Six patients had a symptomatic aneurysm, five had an incidentally discovered aneurysm, and 131 had multiple aneurysms, of which the ruptured lesion was clipped at the beginning of the follow-up study. The median follow-up time was 13.9 years (range 0.8 to 30.0 years). During 1944 patient-years of follow-up study there were 27 first episodes of hemorrhage from a previously unruptured aneurysm, giving an average annual rupture incidence of 1.4%. Fourteen of these bleeding episodes were fatal. The cumulative rate of bleeding was 10% at 10 years, 26% at 20 years, and 32% at 30 years after the diagnosis. The only predictor for the rupture was the size of the aneurysm (p = 0.036). However, in patients with multiple aneurysms (the main subgroup) the only variable that tended to predict rupture was the age of the patient: risk of rupture was inversely associated with age (p = 0.080). The median diameter of the aneurysms was 4 mm at the beginning of the follow-up period, both in those with and those without a later hemorrhage. During the angiographic monitoring period, a ruptured aneurysm significantly (p < 0.001) increased in size in 17 patients with hemorrhage but aneurysms did not increase significantly in 14 patients without hemorrhage. In addition, a new aneurysm was found in six of 31 patients. The authors conclude that an unruptured aneurysm should be operated on, irrespective of its size, if it is technically possible and the patient's age and concurrent diseases are not contraindications to surgery.

Cognitive test performances related to early and late computed tomography findings after closed-head injury.

Computed tomography (CT) findings from early (less than 24 hours) and late scan (6 months) after closed-head injury (CHI) were compared to cognitive test scores obtained on an average of 4 months after injury in a consecutive series of 53 patients. The presence of parenchymal lesion was associated with poor test results, indicating cognitive inflexibility and disinhibition of routine response tendencies in novel tasks. These deficits have previously been found to be related in particular to frontal-lobe dysfunction, but the present study did not support the hypothesis that frontal lesion is the principal cause of this impairment in CHI. Parenchymal lesions in the right and left hemisphere were associated with spatial and verbal deficits, respectively. Ventricular enlargement in the late CT was related to cognitive inefficiency, both being strongly associated with age. The results suggest that parenchymal lesion in the early CT is an indicator of diffuse axonal injury, which results in cognitive inflexibility during recovery.

Effect of intrathecal fibrinolytic therapy on clot lysis and vasospasm in patients with aneurysmal subarachnoid hemorrhage.

A prospective series of 30 patients with a single, angiographically verified aneurysmal subarachnoid hemorrhage (SAH) was studied for the effect of intrathecal thrombolytic therapy with recombinant tissue plasminogen activator (rt-PA) on outcome, angiographic vasospasm, and computerized tomography (CT) findings after surgery. The patients included fulfilled the following criteria: operation was performed by Day 3 after the hemorrhage, CT showed only blood in the basal cisterns, and the patient had a single aneurysm or multiple aneurysms that could be treated surgically at the same operation. The patients were divided into groups of 10, with patients receiving 3, 10, or 13 mg of rt-PA in a single intracisternal injection at the end of the operation. There were no differences between the treatment groups in overall outcome. One patient from the 3-mg rt-PA group developed a postoperative intracerebral hemorrhage, and one patient from the 10-mg rt-PA group had a postoperative epidural hematoma. There was one death in the 13-mg rt-PA group that was caused by inclusion of a segment of pericallosal artery in the clip. In all treatment groups a reduction was observed in the amount of blood seen on the postoperative CT scans compared to the preoperative CT scans. The reduction in SAH grade between the 10-mg and 13-mg rt-PA groups was significant (p less than 0.05). The difference in the severity of angiographic vasospasm between the 3-mg and 13-mg rt-PA groups was also significant (p less than 0.05).

Angiographic vasospasm and release of platelet thromboxane after subarachnoid hemorrhage.

We studied adenosine diphosphate-induced platelet aggregation and the associated release of thromboxane B2 in 49 patients with subarachnoid hemorrhage in relation to angiographic vasospasm. Postoperative cerebral angiography was performed less than or equal to 3 (median 1) days after surgery for an aneurysm 5-14 days after subarachnoid hemorrhage. Correspondingly, one sample from each patient was taken within 24 hours either before or after angiography. The occurrence of severe as well as diffuse, moderate, or severe angiographic vasospasm was associated with the presence of delayed cerebral ischemia (p less than 0.05). Patients with diffuse angiographic vasospasm had significantly higher (p less than 0.05) values for thromboxane B2 release than the others, even after adjustment by the clinical grades on admission and before surgery, the timing of surgery, the time from subarachnoid hemorrhage to angiography and blood sampling, and nimodipine therapy. Severe and diffuse angiographic vasospasm were also associated with poor outcome at 1 year (p less than 0.05). Our results suggest that augmented release of platelet thromboxane may be involved in the pathogenesis of vasospasm in large cerebral arteries.

Risks factors for cerebral infarction in good-grade patients after aneurysmal subarachnoid hemorrhage and surgery: a prospective study.

A prospective series of 265 patients with aneurysmal subarachnoid hemorrhage (SAH) of Grades I to III (Hunt and Hess classification) upon admission were evaluated as to neurological outcome and computerized tomography (CT) findings 1 to 3 years (mean 1.4 years) after the SAH and surgery. A total of 73 patients underwent acute surgery (within 72 hours after the bleed: Days 0 to 3), 86 were operated on subacutely (between Days 4 and 7), and 91 had late surgery (on Day 8 or later). Fifteen patients died before surgery was undertaken and another 20 patients died during the follow-up period. A total of 104 patients received nimodipine and the rest of the patients received either placebo (109 patients) or no medication (52 patients). A logistical regression analysis revealed the following prognostic factors for cerebral infarction, in order of importance: the amount of blood on the primary CT scan; postoperative angiographic vasospasm; the timing of the operation; and a history of hypertension. The use of nimodipine was associated with a significant reduction of cerebral infarcts visualized by CT scanning in patients who received intermediate or late surgery. In patients who underwent acute surgery no significant difference between the incidence of cerebral infarcts was observed.

Long-term effects of nimodipine on cerebral infarcts and outcome after aneurysmal subarachnoid hemorrhage and surgery.

A total of 213 patients with verified aneurysmal subarachnoid hemorrhage (SAH) of Grades I to III (Hunt and Hess classification) were enrolled in a double-blind placebo-controlled trial to determine the effect of intravenous nimodipine on delayed ischemic deterioration and computerized tomography (CT)-visualized infarcts after SAH and surgery. The administration of the drug or matching placebo was started immediately after the radiological diagnosis of a ruptured aneurysm had been made. Of the 213 patients enrolled in the study, 58 were operated on early (within 72 hours after the bleed: Days 0 to 3), 69 were operated on subacutely (between Days 4 and 7), and 74 had late surgery (on Day 8 or later). Eleven patients died before surgery was undertaken and one was not operated on. A follow-up examination with CT scanning, performed 1 to 3 years after the SAH (mean 1.4 years), revealed no significant differences in the overall outcome between the groups. However, nimodipine treatment was associated with a significantly lower incidence of deaths caused by delayed cerebral ischemia (p = 0.01) and significantly lower occurrence of cerebral infarcts visualized by CT scanning in the whole population (p = 0.05), especially in patients without an associated intracerebral hemorrhage on admission CT scan (p = 0.03).

Social outcome related to cognitive performance and computed tomographic findings after surgery for a ruptured intracranial aneurysm.

A series of 83 patients was examined with a battery of cognitive tests, a clinical interview, and computed tomography 1 year after surgery for a ruptured intracranial aneurysm. Disability on the Glasgow Outcome Scale (33%), failure to return to work (25%), impaired social relations (25%), and subjective or clinical mental impairment (56%) were found to be related to each other and to poor performance on cognitive tests, especially to verbal impairments in patients with left lateral infarctions and to memory deficits and cognitive inflexibility in patients with frontal medial infarctions. Furthermore, cognitive deficits and poor outcome were associated with diffuse brain damage. Depression and anxiety were unrelated to test performances, but were frequently reported by patients with right lateral infarctions.

Cognitive deficits related to computed tomographic findings after surgery for a ruptured intracranial aneurysm.

A consecutive series of 118 patients operated on for ruptured intracranial arterial aneurysms was studied. Ninety-six of them could be adequately examined with a battery of psychological tests and computed tomographic scans 1 year after a subarachnoid hemorrhage. Seventeen orthopedic control patients with no history of brain damage were also tested. The pattern of cognitive deficits was strongly related to the findings on the computed tomographic scans. Patients with left lateral infarctions had deficits on performances requiring verbal efficiency, including memory and classification tasks, whereas patients who had right lateral infarctions were poor on a visuoconstructional task (the copying of Rey's Figure). These deficits were pronounced when lateral infarction was associated with diffuse brain damage. Patients with frontal medial infarctions had low scores on memory tests; the inefficiency in verbal fluency, categorical reasoning, and memory was related to diffuse brain damage. The patients who had no infarctions did not differ significantly from the control group. Cognitive impairments after left lateral and frontal medial infarctions, as well as diffuse brain damage, correlated with the Glasgow Outcome Scale.

The treatment of spontaneous intracerebral hemorrhage. A prospective randomized trial of surgical and conservative treatment.

In a prospective study, 52 patients with a spontaneous supratentorial intracerebral hematoma (ICH) were randomly assigned to receive emergency surgery or conservative treatment within 48 hours after the bleed. Patients with a decreased level of consciousness and/or a severe neurological deficit were admitted to the study. The overall mortality rate at 6 months was 42%: 10 (38%) of the 26 patients in the conservative group and 12 (46%) of the 26 in the surgical group. Six (20%) of the 30 survivors at 6 months were able to conduct their activities of daily living independently: five (31%) of the 16 patients in the conservative group and one (7%) of the 14 in the operative group. These differences are not statistically significant. The mortality rate of semicomatose or stuporous patients (Glasgow Coma Scale score 7 to 10) was statistically significantly lower in the surgical group (none of the four patients) than in the conservative group (four of five patients) (p less than 0.05); however, all surviving patients in this subgroup were severely disabled. The study suggests that surgical treatment of this category of patients with ICH does not offer any definite advantage over conservative treatment. In semicomatose or stuporous patients, surgery may improve the length of survival, but the quality of life remains poor.

Ruptured intracranial arterial aneurysms of children and adolescents. Surgical and total management results.

Sixteen children and adolescents under 20 years of age were treated at the Neurosurgical Department of Helsinki University Central Hospital between 1977 and 1986. These children represent 1.2% of the total 1,346 patients with aneurysm. Fourteen patients with Hunt and Hess grades I-III were operated on without surgical mortality or morbidity. Eight aneurysms were at the carotid bifurcation and six at the anterior communicating artery. One patient was grade IV and one grade V. Both died before operation. The hospital management mortality was 2 out of 16 or 12.5%. Seven patients of that age group within our area of responsibility died of a ruptured aneurysm during the years before patients were referred for neurosurgical treatment. Thus, the total mortality was 9 of 23 patients or 39%. Assuming transfer without delay to the neurosurgical clinic, operation within the first few days of bleeding, and no surgical mortality, the theoretical minimum mortality would be 22%.