J. Hamer

Prognosis of oculomotor palsy in patients with aneurysms of the posterior communicating artery.

SummaryIn patients with symptomatic aneurysms of the posterior communicating artery, the prognosis of oculomotor palsy mainly depends on the interval between the onset of palsy and the time of operation, and furthermore on the degree of preoperative deficit and the development of the cranial nerve lesion. The incidence of ultimately complete or incomplete palsy is the same in cases with subarachnoid haemorrhage and without rupture (“warning symptom”). In many cases, an initially incomplete paresis develops to a complete ocular palsy within eight days. Ptosis is generally the first symptom, and it frequently shows the earliest recovery of all other disturbed oculomotor functions after surgery. Full recovery of oculomotor palsy occurs usually only in those patients who undergo early clipping of an aneurysm,i.e. mainly within 10 days after onset of ocular palsy. Complete restitution after carotid ligation is possible, but rare. In cases with full recovery, restitution occurs mostly within three months, sometimes even within a few weeks. An improvement in oculomotor palsy is still possible after a year, but ultimately in these patients recovery remains always more or less incomplete. Incomplete restitution of a third cranial nerve lesion is very often associated with aberrant regeneration and subsequent synkinetic ocular movement. The restitution of the single ocular muscle functions shows a fairly constant course: the levator palpebrae muscle and the M. rectus medialis show rapid recovery. The parasympathetic fibres follow next, but normal function of elevation and depression of the ocular bulb (M. rectus sup., M. obliquues inf. and M. rectus inf.) is often delayed.

The Effect of Stepwise Arterial Hypotension on Blood Flow and Oxidative Metabolism of the Brain

SummaryWith the Kety-Schmidt-technique in ten dogs anaesthetized with 0.5% halothane, blood flow and oxidative metabolism of the brain were studied during stepwise lowering of CPP due to arterial hypotension at 71 and 41 torr. CBF remained constant (65.6 and 64.1 ml/100 g min) when CPP dropped from 98 to 71 torr, but at a CPP of 41 torr CBF fell to 32.2 ml/100 g min, i. e. to about 50% of the resting value. The CMR-oxygen did not change (4.20 and 4.38 ml/100 g min) when CPP was reduced from about 100 to about 70 torr, but decreased to 2.90 ml/100 g min, i. e. about 70% of the resting value in deep arterial hypotension.The uptake of glucose changed from 4.62 to 6.19 mg/100 g min as well as the output of CO2 and lactate (from 4.64 to 6.57 ml/100 g min and from 0.33 to 1.62 mg/100 g min) when CPP was decreased to 71 torr. It could be demonstrated that at this CPP range the oxidative metabolism was unchanged. It was assumed that the increased uptake of glucose was only to form lactate, and that this non-hypoxic lactate production was responsible for the elevated CO2 release. At a CPP range of 41 torr the metabolic rates of glucose and CO2 decreased to 3.33 mg/100 g min and to 3.37 ml/100 g min, respectively, while the output of lactate remained relatively high (1.14 mg/100 g min). These findings support the assumption that at a CPP range of 41 torr the oxidative metabolism of the brain becomes insufficient. All findings demonstrate close interactions between cerebral flow blood and oxidative brain metabolism in arterial hypotension. In deep arterial hypotension respiratory acidosis has an effect on CBF. The increase of CBF is accompanied by an improvement of CMR-oxygen but not of CMR-glucose. Although CMR-lactate is reduced, the lactate/glucose index remains high.

Diagnosis by computerized tomography of intradural dermoid with spontaneous rupture of the cyst.

SummaryTwo cases of para and suprasellar dermoid cysts are presented. The specific CT findings for this tumour are demonstrated: very low absorption values below minus 40 EMI units, variable densities in the cyst content, shell-like annular calcifications, and absent central enhancement effect. Spontaneous perforation of the cyst with dissemination of dermoid material into the CSF spaces is shown. The differential diagnosis from other low density lesions (epidermoid, cystic craniopharyngioma, arachnoid cyst) is discussed.

Cerebral blood flow and oxidative brain metabolism during and after moderate and profound arterial hypoxaemia.

SummaryIn anaesthetized artificially ventilated dogs, the effect of graded arterial hypoxaemia on cerebral blood flow (CBF) and on the oxidative carbohydrate metabolism of the brain was tested. It is shown that the hypoxic vasodilatory influence on cerebral vessels is present even atmoderate systemic hypoxaemia, provided that PaCO2 is kept within normal limits. At PaO2 of about 50 Torr, CBF increased from 56.6 to 89.7 ml/100 g/min. With increasing cerebral hyperaemia (CBF increased to 110.9 ml/100 g/min, at PaO2 of 30 Torr), CMRO2 (4.2 ml/100 g/min) was not significantly raised above its normal level (4.7 ml/100 g/min) even with profound arterial hypoxaemia. This shows that CMRO2 levels are poor indices of hypoxic hypoxia. A disproportionately high increase in cerebral glucose uptake (CMR glucose levels rose from 4.4 to 10.4 mg/100 g/min) and enhanced cerebral glycolysis (CMR lactate changed from 0.2 to 1.6 mg/100 g/min) at moderately reduced PaO2 (50 Torr) indicated early metabolic changes which became more marked with further falls in arterial oxygen tension. However, 60 minutes after restoration of a normal PaO2 level, CBF and brain metabolism were found to have completely recovered. It is concluded that a short period of profound systemic hypoxaemia does not produce long lasting metabolic and circulatory disorders of the brain provided the cerebral perfusion pressure does not vary, and is kept at normal levels.

Cerebral blood flow and cerebral metabolism in acute increase of intracranial pressure

SummaryThe effects of a stepwise acute increase of intracranial cerebrospinal fluid pressure on cerebral blood flow, cerebral arteriovenous differences of oxygen and glucose and on the output of lactate were studied in anaesthetized normoventilated normoxic dogs. Intracranial hypertension was produced by infusing mock-CSF into the cisterna magna. Mean arterial blood pressure was kept at a constant level throughout the experimental investigations. At a cerebral perfusion pressure of about 70 mm Hg, CBF and the cerebral metabolic rates of oxygen and glucose were not significantly changed. However, further reduction in the cerebral perfusion pressure to below 40 mm Hg, was accompanied by a statistically significant decrease of CBF and a deterioration of the oxidative metabolism. Glucose uptake was particularly disturbed by raised intracranial pressure. Increased cerebral output of lactate and low CMRO2 indicated raised glycolysis. But (V-A)lactate was also increased at a relatively moderate reduction of the cerebral perfusion pressure, when autoregulation was still effective and CMRO2 unchanged. The data are discussed in context with similar experimental results recently published by other investigators.

Cerebral glucose and energy metabolism, cerebral oxygen consumption, and blood flow in arterial hypoxaemia.

SummaryThe influence of moderately reduced arterial oxygen tension (aPO2 of about 45 Torr) on the metabolism and the blood flow of the brain was tested in 20 anaesthetized, artificially ventilated normotensive, normocapnic beagle dogs. It is demonstrated that the decrease in systemic oxygen delivery to the brain is countered by an appropriate increase in flow (CBF being 60.3 ml/100 g min at normoxia and 84.5 mg/100 g min m hypoxaemia) which maintained the cerebral oxygen consumption unchanged (CMRO2 3.80 versus 3.32 ml/100 g min). The cortical tissue content of energy-rich phosphates such as ATP, ADP, AMP, and phosphocreatine was also found to be unaltered. Neuropathological examinations excluded any hypoxic cell damage. This reactive vasodilatory reaction of the cerebral vessels is apparently a sensitive regulatory process which protects the brain against marked oxygen lack. However, a normal carbohydrate metabolism is not restored by this cerebrovascular mechanism. For, significantly increased CMRlactate (0.32 versus 1.46 ml/100 g min) indicated raised cerebral glycolysis, and the tissue metabolites of glucose suggested an increased glycolytic flux in the brain. It is concluded that in moderate arterial hypoxaemia, which is not uncommon in clinical practice, cerebral blood flow plays an effective homeostatic role in preventing a disturbance of the energy metabolism of the brain.

Effects of arterial hypoxaemia, hypercapnia, and changes in cerebral perfusion pressure on mean cerebrospinal fluid and sagittal sinus pressure

SummaryIn 20 anaesthetised, artificially ventilated dogs the influence of arterial hypoxaemia, hypercapnia, and decreased systemic arterial blood pressure on mean cerebrospinal fluid pressure and on the pressure in the superior sagittal sinus was studied. Below a PaO2 of 40 Torr and above a PaCO2 of 70 Torr, CSFP was significantly increased. The pressure rise in the torcular, however, was only moderate. Simultaneous CBF measurements showed marked cerebral hyperaemia to be the essential cause of the increase in CSFP. In deep normovolaemic arterial hypotension (MABP below 50 mm Hg), CSFP and SSP were significantly decreased. CBF fell sharply by about 50% compared to the resting values. In arterial normotension and under normocapnic-normoxic conditions, a pressure difference of about 3 mm Hg existed between CSFP and SSP. This pressure difference increased in hypoxia and hypercapnia and fell in arterial hypotension below the “opening-pressure” of the arachnoid villi. An artificially induced rise of CSFP in another 5 experimental animals was reflected to a minor degree in the torcular pressure. However, during rapid reduction of raised intracranial pressure, a transient, but marked pressure rise occurred in the torcular, persisting as long as systemic arterial blood pressure was increased (Cushing response). This is explained by post-compression cerebral hyperaemia and by the undamped transmission of the hypertensive arterial pressure to the dilated cerebral vessels. The origin of the rapid CSF pulse waves was studied in simultaneous recordings of intracranial CSF, cerebral venous, systemic arterial and central venous pressure, and it was shown that the height of CSFP is dependent on MABP, whereas the contour of the CSF pulse waves is shaped by rapid changes of cerebral blood volume in the post-capillary cerebral vascular bed.

Small angioma of the choroid plexus as a cause of primary intraventricular haemorrhage

SummaryA case of primary intraventricular haematoma due to rupture of an angioma of the choroid plexus is presented. Special emphasis is laid on early diagnosis by CT scan and angiography and on a deliberate two-stage surgical procedure. The literature on this rare type of cerebral vascular malformation is reviewed.

The value of spinal computed tomography in diagnosis of herniated lumbar discs

SummaryIn this study the diagnostic value and topographical accuracy of spinal computed tomography (CT) in the preoperative diagnosis of lumbar disc herniations were tested in 36 patients with surgically proven herniated discs. All patients also underwent metrizamide myelography. CT findings and myelograms were compared and correlated with the surgical observations. Especially in demonstrating exact diagnosis (lateral or more medial protrusion), and in showing the extent of upward or downward displacement of free disc material, CT provides valuable preoperative information. As a non-invasive diagnostic procedure, spinal CT scan may replace lumbar myelography in many patients with radicular lumbar pain.

The significance of cerebral vasospasm with regard to early and delayed aneurysmal surgery. Preliminary results of early surgery.

SummaryThe time course and clinical significance of cerebral vasospasm at various intervals from aneurysmal haemorrhage is discussed with regard to timing of surgery. Very early operation,i.e., within the first 3 days after bleeding, is advisable in patients with clinical grade I or II and without concomitant diffuse vasospasm.