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Biomedical subjects

N V Todd

Publications and source records attributed to N V Todd.

At least 19 recordsLinked to original sources
PubMed1992

CSF drainage in patients with posterior fossa tumours.

The management of hydrocephalus secondary to a posterior fossa tumour is controversial. We audited recent practice with a retrospective analysis of 287 consecutive patients undergoing posterior fossa exploration for tumour. 85 shunts and 112 external ventricular drains (EVD) were placed. The overall CNS infection rate in the series was 6%. There was a significantly higher (p less than 0.01) infection rate in patients who had a drainage procedure, and a trend towards higher infection rates in patients with two drainage procedures. Early infection rates with EVDs and shunts were the same (7%). One third of patients with hydrocephalus had pre-operative drainage, a third had per-operative drainage but only a quarter required a permanent shunt. The majority of patients will not require a permanent shunt and where temporary CSF diversion is required EVD is reasonable.

Adolescent↗
PubMed1991

Long-term outcome following anterior cerebral artery ligation for ruptured anterior communicating artery aneurysms.

The long-term prognosis (15 years) was determined for 17 patients who had undergone anterior cerebral artery (ACA) ligation as the sole treatment for an anterior communicating artery aneurysm. The number of early and late rebleeds was lower than expected from previously ruptured aneurysms. Late ischemia was not a major complication while late postoperative epilepsy occurred in 19% of survivors. In a review of previously published series, ACA ligation appears to have significantly reduced the rates of both early and late rebleeding. This study helps to define the late results of "conservative" operations for ruptured aneurysms.

Cerebral Angiography↗
PubMed1990

Blood-brain barrier damage in traumatic brain contusions.

Plasma proteins were used as an endogenous marker of blood-brain barrier damage in 19 patients dying with traumatic cortical contusions. Patients survived for a few hours to 31 days after head injury. Eight proteins (M WT 61-2,500 x 10(3) were demonstrated with standard immunohistochemical techniques. Proteins were not found in "control" brains or in macroscopically normal parasagittal cortex in the head injury patients. Proteins were found in all of the macroscopic contusion in all brains. Protein leakage appeared to be from the contusion itself. Protein staining around histologically normal vessels was unusual. There was a gradient of staining from the macroscopic contusion into the surrounding brain. There was a trend for staining to be most marked between 3 and 8 days survival after head injury. There was no gradient of leakage by molecular size of the protein.

Blood Proteins↗
PubMed1990

Intracerebral haematoma: aetiology and haematoma volume determine the amount and progression of brain oedema.

In a study of 182 patients with a traumatic, 'spontaneous', or aneurysmal intracerebral haematoma (ICH) a significant correlation was found between the amount of focal brain oedema seen on computed tomogram (CT) and both the aetiology and the size of the haematoma. Traumatic haematomas were associated with twice the oedema per unit volume of haematoma, and a doubling of median oedema volume on second CT (performed in 18 patients), compared to spontaneous or aneurysmal haematomas.

Brain Edema↗
PubMed1990

Norman Dott's contribution to aneurysm surgery.

Between 1926-36 Norman Dott managed 39 patients with suspected intracranial haemorrhage. During this period he established important principles of diagnosis and developed new methods for the medical and surgical treatment of aneurysmal subarachnoid haemorrhage. Dott performed the first intracranial operation to treat an aneurysm and the first angiogram to demonstrate an intracranial aneurysm. This article reviews Dott's early experiences of aneurysmal subarachnoid haemorrhage.

Cerebral Angiography↗
PubMed1990

Cerebral radiation necrosis complicating stereotactic radiosurgery for arteriovenous malformation.

A patient presented with symptoms and signs of raised intracranial pressure and increasing focal deficit 13 months after stereotactic radiosurgical treatment of an arteriovenous malformation (AVM). Computed Tomography (CT) showed a mass lesion at the site of the previous abnormality typical of radiation necrosis, but with features identical to those of a malignant neoplasm. Biopsy confirmed cerebral radiation necrosis. The radiation dose was 25 Gray to the periphery of two overlapping 14 mm collimator fields, delivered in a single dose. Treatment with steroids led to improvement in the symptoms and signs of raised intracranial pressure, but not the focal deficit. Radiation necrosis is a consequence of the large doses required to obliterate AVMs and is a limiting factor in their treatment. It is important for clinicians referring patients for stereotactic radiosurgery to be aware of this complication, and to be able to recognise and treat it.

Adult↗
PubMed1990

Aneurysm rebleeding after treatments that leave the aneurysm sac patent.

Three operations that leave the aneurysm sac patent have been used to treat ruptured intracranial aneurysms: carotid ligation, anterior cerebral artery ligation and aneurysm wrapping. The rates of early rebleeding (0-6 months) for these operations are respectively less than 10, 3.9 and 8.6%. The long-term risks of rebleeding are at least 1% per year for anterior cerebral or carotid artery ligation and 1.5% per year for wrapping. Eighty per cent of rebleeds are fatal. Most aneurysms are still seen to be patent if angiography is performed after these treatments. Should patients who have had these operations be offered aneurysm clipping?

Carotid Arteries↗
PubMed1989

Subarachnoid fat embolism complicating autologous fat grafting following translabyrinthine excision of acoustic neuroma.

A 64-year-old man had complete excision of an acoustic schwannoma via the translabyrinthine route and the mastoid cavity was packed with fat. Post-operatively there were two episodes of aseptic meningitis and CT scanning demonstrated migration of fat into the basal subarachnoid CSF spaces. This unusual complication should be recognized and differentiated from both true infective meningitis and aseptic meningitis from other causes.

Adipose Tissue↗
PubMed1989

Outcome following aneurysm wrapping: a 10-year follow-up review of clipped and wrapped aneurysms.

One hundred and eighty-one patients with single aneurysms involving the anterior circulation were treated either by wrapping (60 cases) or clipping (121 cases), and 96.1% of them were followed for 10 years. The rate of early rebleeding (less than 6 months) from wrapped aneurysms was 8.6% (confidence interval 1.4% to 15.8%) and the late rebleeding (6 months to 10 years) rate was 1.5% per annum (confidence interval 0.3% to 2.5%/yr). Wrapping an aneurysm offers some protection from rebleeding, particularly during the first 6 months when the risk of rebleeding is high.

Adolescent↗
PubMed1988

Cerebral ischaemia and surgical practice.

This review article examines the principles underlying the control of cerebral blood flow, the consequences of brain ischaemia and subsequent reperfusion and discusses the impact of brain ischaemia in a number of clinical situations of surgical importance.

Brain Ischemia↗
PubMed1987

What follows diagnosis by computed tomography of solitary brain tumour? Audit of one year's experience in South East Scotland.

The referral rate to neurosurgeons after diagnosis by computed tomography (CT) of solitary brain tumour (SBT) was audited for South East Scotland in 1985. 142 patients had SBT diagnosed by CT, but histological confirmation by biopsy or open operation was sought in only 67. Among these the CT diagnosis of glioma proved to be incorrect in 3 of 44 cases and that of solitary metastasis in 4 of 8 cases. Since CT diagnosis of SBT is not fully reliable, biopsy should be considered in all cases.

Adult↗
PubMed1986

Quantitative measurement of cerebral blood flow and cerebral blood volume after cerebral ischaemia.

CBF obtained by the hydrogen clearance technique and cerebral blood volume (CBV) calculated from the [14C]dextran space were measured in three groups of rats subjected to temporary four-vessel occlusion to produce 15 min of ischaemia, followed by 60 min of reperfusion. In the control animals, mean CBF was 93 +/- 6 ml 100 g-1 min-1, which fell to 5.5 +/- 0.5 ml 100 g-1 min-1 during ischaemia. There was a marked early postischaemic hyperaemia (262 +/- 18 ml 100 g-1 min-1), but 1 h after the onset of ischaemia, there was a significant hypoperfusion (51 +/- 3 ml 100 g-1 min-1). Mean cortical dextran space was 1.58 +/- 0.09 ml 100 g-1 prior to ischaemia. Early in reperfusion there was a significant increase in CBV (1.85 +/- 0.24 ml 100 g-1) with a decrease during the period of hypoperfusion (1.33 +/- 0.03 ml 100 g-1). Therefore, following a period of temporary ischaemia, there are commensurate changes in CBF and CBV, and alterations in the permeability-surface area product at this time may be due to variations in surface area and not necessarily permeability.

Animals↗
PubMed1986

Recirculation after cerebral ischemia. Simultaneous measurement of cerebral bloodflow, brain edema, cerebrovascular permeability and cortical EEG in the rat.

The 4-vessel occlusion rat model of cerebral ischemia was modified to permit the simultaneous measurement of cerebral blood flow (hydrogen clearance), brain edema (specific gravity), cerebrovascular permeability (14C-AIB) and electrocardiogram. Surgery was performed in one stage in the anesthetised, paralysed and ventilated rat and severe hemispheric ischemia was produced in all animals. Electrode implantation did not alter cortical specific gravity or Ki for 14C-AIB. During 4-vessel occlusion mean cortical CBF was 5.8 +/- 1.4 ml-1 100 g-1 min. and this was associated with an isoelectric ECoG; 15 min of ischemia produced a significant reduction in mean cortical specific gravity (increase in brain edema). Following 15 min ischemia, 180 min of recirculation were permitted. Post-ischemic blood flow showed an immediate hyperemia (CBF = 202 +/- 12 ml-1 100 g-1 min.) followed by hypoperfusion (CBF = 58 +/- 8 ml-1 100 g-1 min). There was an early further decrease in cortical specific gravity. Further recirculation led to a significant increase in cortical specific gravity (resolution of brain edema). The transfer constant (Ki) for 14C-AIB was not altered at any stage in recirculation. This appears to be a model of pure cytotoxic edema until 180 min recirculation after 15 min cerebral ischemia. Recirculation permitted return of cortical electrical activity.

Animals↗