Regional cerebral oxygen utilization, blood flow, and blood volume in benign intracranial hypertension studied by positron emission tomography

Using PET, we measured regional cerebral oxygen utilization, oxygen extraction, blood flow, and blood volume in five patients with benign intracranial hypertension. No significant differences in regional cerebral function were found between the patients and 15 age-matched normal controls. Cerebral decompression with a lumboperitoneal shunt produced little change in regional cerebral function in one patient studied serially. The raised CSF pressure of benign intracranial hypertension is therefore not associated with any significant deterioration in cerebral oxygen metabolism or hemodynamics.     

Computed tomographic evidence of cerebral swelling in benign intracranial hypertension.

Computed tomography of 30 patients presenting acutely with benign intracranial hypertension was compared with that of 30 normal controls matched for age and sex. Qualitative and quantitative assessments showed smaller cranial CSF spaces in the cases of benign intracranial hypertension, suggesting that cerebral swelling is involved in the pathogenesis of benign intracranial hypertension.     

Familial benign intracranial hypertension.

Three sisters with benign intracranial hypertension are reported. This is the first documentation of benign intracranial hypertension in three family members. Obesity is a striking feature in these patients as well as five of the six previously reported patients with familial benign intracranial hypertension. Pregnancy and chronic dysfunctional uterine bleeding, well known predisposing factors in this syndrome when it occurs sporadically, were present in two of the sisters. A familial metabolic defect may be responsible for the intracranial hypertension in these patients.     

EEG in benign intracranial hypertension

A retrospective study of standard EEG's obtained from 26 patients with benign intracranial hypertension was done with particular emphasis on the effect of age on the EEG findings. Abnormal EEG's were found in 10 patients, all were less than 20 years of age. Although no consistent pattern of EEG abnormality could be identified, there appears to be a difference between the immature and adult brain in the EEG response to intracranial hypertension.     

Spatial contrast sensitivity in benign intracranial hypertension.

Spatial Contrast Sensitivity (CS) was studied in 20 patients with benign intracranial hypertension (BIH). At presentation CS loss was found in 43% of the eyes, and impairment of visual acuity attributed to BIH in only 16%. Nine patients had blurred vision or visual obscurations, all of whom had abnormal CS. The clinical application of CS measurement in BIH for monitoring the progression or regression of the disease is illustrated by serial measurements in 11 patients. Progressive visual loss in longstanding papilloedema and improvement of visual function in subsiding papilloedema can occur without any change in Snellen acuity or visual field charting.     

Effect of systemic arterial blood pressure on cerebral blood flow in intracranial hypertension.

In five baboons and 11 cats cerebral ischaemia was produced either by inflating an epidural balloon and or by ligating major arteries supplying the brain. Fifteen of the animals developed intracranial hypertension after cerebral ischaemia. If ICP were high, but still significantly lower than MABP, elevation of MABP by noradrenaline infusions was accompanied by a proportional increase of ICP. However, the increase of ICP was lower than that of MABP so that CPP was raised. CBF measured by the 133Xenon clearance technique was significantly increased by arterial hypertension in eight cases. The proportional increase of CPP and CBF by elevation of arterial blood pressure was substantially greater, the lower ICP was immediately after ischaemia. There was no effect of MABP in cases in which ICP equalled MABP.     

Vitamin A induced benign intracranial hypertension.

A case of benign intracranial hypertension due to prolonged administration of a low dose of Vitamin A is described in a young male investigated as a brain tumor suspect. Computerized axial tomography showed small and symmetrical lateral ventricles which was consistent with the diagnosis. The syndrome of benign intracranial hypertension and its relationship to chronic Vitamin A toxicity is discussed.     

Cerebrospinal fluid neurohypophysial peptides in benign intracranial hypertension.

The cerebrospinal fluid (CSF) concentrations of arginine vasopressin (AVP) and oxytocin (OT) were investigated both in patients with benign intracranial hypertension and in age and sex matched controls. Twenty eight lumbar punctures were performed on 15 patients with benign intracranial hypertension as part of their routine investigation and therapy. All patients had raised intracranial pressure (27.4, SE 1.7 cm.CSF). CSF AVP levels were significantly elevated in benign intracranial hypertension (2.1, SE 0.3 pmol/l) compared with controls (0.7, SE 0.1 pmol/l, p less than 0.001) but CSF OT concentrations were similar in both groups. CSF osmolality and plasma AVP and osmolality were identical in patients and controls. There was no correlation between CSF AVP concentration and intracranial pressure. The selective elevation of AVP in CSF may be of importance in the pathogenesis of raised intracranial pressure in benign intracranial hypertension.     

CSF imaging in benign intracranial hypertension

The cisternographic images in 10 patients with benign intracranial hypertension were reviewed. Nine were normal. Transfer of labelled tracer from the subarachnoid space was measured in five patients and was found to be abnormal in only two. The relation of these findings to the proposed pathophysiological alterations is discussed.     

Increased intracranial volume in Parkinson's disease

BACKGROUND: Parkinson's disease (PD) and multiple system atrophy (MSA) are neurodegenerative diseases that can be difficult to diagnose and distinguish from each other. STUDY AIMS AND METHODS: Patients with PD and MSA and controls were studied with magnetic resonance imaging (MRI) using tissue segmentation and outlining of regions in order to identify regional volume changes that might be useful in the diagnosis of the two diseases. RESULTS: Patients with PD had significantly larger intracranial volumes (ICVs) and significantly smaller putaminal and sustantia nigra volumes than controls. MSA patients had significantly smaller substantia nigra and caudate volumes than controls but normal intracranial volume. In both patient groups there was a further trend towards smaller amygdala volumes. DISCUSSION: Increased ICV in PD patients is a new finding that may be explained by genetic factors or compensatory responses to early CNS damage. Atrophy of the amygdala in MSA patients has not been demonstrated with MR before. It might explain why these patients can have hyposmia. The putaminal atrophy found in the PD group may be a trait of the later stages of PD. Segmentation of the substantia nigra can be a useful aid in the diagnosis of PD and MSA.     

Potentially prothrombotic abnormalities of coagulation in benign intracranial hypertension.

OBJECTIVE: Benign intracranial hypertension (BIH) may be caused by intracranial venous sinus thrombosis. Cerebral angiograms may, however, be normal in patients with BIH that are associated with conditions with an increased risk of venous thrombosis. This raises the possibility that unrecognised non-occlusive venous thrombus might impede CSF drainage. This study therefore examined the strength of the association between risk factors for thrombosis and BIH. METHODS: The incidence of prothrombotic abnormalities among a mixed prospectively and retrospectively investigated cohort of 38 patients with BIH, was compared with healthy obese subjects, and patients with other neurological diseases. Prothrombotic abnormalities investigated included anticardiolipin antibodies, lupus anticoagulant, antithrombin III, proteins C and S, plasma fibrinogen, kaolin cephalin clotting time, prothrombin time, and full blood counts. RESULTS: Evidence for the presence of an antiphospholipid antibody was found in 32% of cases. Cases of familial deficiency of antithrombin III, thrombocytosis, and polycythaemia were also noted. Additionally, an increased concentration of plasma fibrinogen was found in 26%. A coagulation abnormality was more often detectable in those subjects with normal or low body mass index and in those tested within six months of onset. CONCLUSION: There is a thrombotic pathogenesis in some cases of BIH.     

Neurosarcoidosis presenting as benign intracranial hypertension

A patient who on presentation fulfilled diagnostic criteria for benign intracranial hypertension subsequently developed a lymphocytic meningitis. A final diagnosis of neurosarcoidosis was made and the patient responded well to oral steroids.     

Serial ventricular volume measurements: further insights into the aetiology and pathogenesis of benign intracranial hypertension.

Ventricular volumes have been measured from CT scans of patients with benign intracranial hypertension both at initial presentation and at a later date. Volumes initially were smaller than normal, but at review five patients showed a significant increase in ventricular size. Persisting small ventricular volume correlated with persisting symptoms and signs and with persisting obesity. This supports the view that patients with benign intracranial hypertension have brain swelling and that obesity may be implicated in the pathogenesis, perhaps via a neuroendocrine disturbance. It is suggested that weight reduction may be an important component of treatment.