Humans ; Cranial Sinuses/surgery* ; Intracranial Hypertension/etiology*

In order to better understand the clinical manifestation of systemic lupus erythematosus (SLE) with intracranial hypertension syndrome (IHS), we analyzed the clinical features and treatment of a typical SLE patient with IHS. SLE is one of the most unpredictable autoimmune diseases involving multiple organ systems that is defined clinically and associated with antibodies directed against cell nuclei. IHS is an uncommon manifestation of neuropsychiatric SLE (NPSLE) and is characterized by an elevated intracranial pressure, papilledema, and headache with occasional abducens nerve paresis, absence of a space-occupying lesion or ventricular enlargement, and normal cerebrospinal fluid chemical and hematological constituents. IHS has been reported in a few sporadic cases in patients with SLE worldwide, but rarely has been reported in China. In this study, a 34-year-old female SLE patient with IHS was reported and pertinent literature reviewed. The clinical presentation, image logical features, and investigatory findings were discussed.
Diagnosis, Differential ; Intracranial Hypertension/diagnosis ; Intracranial Hypertension/*etiology ; Lupus Erythematosus, Systemic/*complications ; Lupus Erythematosus, Systemic/diagnosis

Intracranial infections are one of the most common neurological diseases in children and are associated with high mortality and morbidity. Intracranial hypertension and hydrocephalus are the common, fatal complications of intracranial infections, so early diagnosis and timely treatment are the keys to saving patients' lives and reducing neurological sequelae. This paper introduces the progress in the etiology, diagnosis, and treatment of intracranial hypertension and hydrocephalus in children with intracranial infections.
Central Nervous System Infections ; complications ; Child ; Humans ; Hydrocephalus ; diagnosis ; etiology ; therapy ; Intracranial Hypertension ; diagnosis ; etiology ; therapy

To determine the etiologies and risk factors of intracerebral hemorrhage in young people.
 Methods: A total of 401 young patients with intracerebral hemorrhage were enrolled, and they were assigned into a 20-29 , a 30-39, and a 40-45 age group. The differences of various etiologies and risk factors among the three groups were analyzed.
 Results: There were 273 men and 128 women in the 401 young patients. The etiologies of 294 patients (73.32%) were identified while 107 patients (26.68%) were unknown. Among those with identified etiology, 226 patients (56.36%) suffered from hypertension, 41 patients (10.22%) congenital cerebrovascular malformation (including 25 patients with cerebral arteriovenous malformation, 8 intracranial cavernous hemangioma, and 8 intracranial aneurysm), and 27 other etiologies (including 9 patients with moyamoya disease, 6 cerebral venous sinus thrombosis, 4 drug abuse, 3 hemorrhagic brain tumor, 2 intracranial infection, 1 systemic lupus erythematosus, 1 drug-induced, and 1 eclampsia). Risk factors included hypertension (237 cases, 59.10%), smoking (123 cases, 30.67%), alcohol consumption (74 cases, 18.45%), and others (19 cases, 4.74%; including 8 cases of pregnancy or in the puerperium, 8 family history of intracerebral hemorrhage, and 3 taking anti-platelet aggregation/anticoagulation agents). The rate of hypertension induced hemorrhage significantly increased with age (P<0.01); the rate of vascular malformations in 20-29 age group was obviously higher than other groups (P<0.01); the rate of unknown cause in the 40-45 age group was significantly lower than other groups (P<0.01) and the rate of other etiologies showed no significant difference in the 3 groups. The rate of hypertension was significantly elevated with the age (P<0.01), while smoking, alcohol consumption, and other risk factors showed no significant difference in the 3 groups.
 Conclusion: The rate of intracerebral hemorrhage in young people increases with the increasing of age and hemorrhage affects men more than women; hypertension may be the main cause and congenital cerebrovascular malformation is the second cause, which may be more common in younger patients. Hypertension, smoking, and alcohol consumption may be the major controllable risk factors in intracerebral hemorrhage in young people.
Adult ; Cerebral Hemorrhage ; etiology ; Female ; Humans ; Hypertension ; complications ; Intracranial Aneurysm ; complications ; Intracranial Arteriovenous Malformations ; complications ; Male ; Middle Aged ; Pregnancy ; Risk Factors ; Young Adult

OBJECTIVETo investigate the role of hypertension in the pathogenesis of cerebral aneurysms in rats.

METHODSTwenty spontaneous hypertensive rats (SHR) and 10 Wistar-Kyoto rats (WKY) were included in this observational study. Animals were fed with normal diet and drinking water. No experimental modifications were undertaken in either group. They were sacrificed at one year of age, the bifurcations of the circle of Willis were dissected and longitudinal serial sections were prepared for light microscopic and transmission electron microscopic study.

RESULTSIn the SHR group, 2 of the 20 rats formed an aneurysm respectively at the bifurcations of the basilar artery. As revealed by electron microscopy, injury at the bifurcation of the artery first occurred on the steeper side of the intimal pad. Furthermore, loss of endothelial cells, small depressions on the intima, disruptive internal elastic lamina and lymphocytes or red blood cells infiltration were noted at the steeper side of the intimal pad. No significant changes were observed in WKY group.

CONCLUSIONSCerebral aneurysms can form spontaneously in SHR without ligation of the common carotid artery and without a diet containing beta-aminoproprionitrile. Long-standing systemic arterial hypertension is one of the etiological factors that contributes to aneurysm formation in SHR rats.

Animals ; Cerebral Arteries ; pathology ; Hypertension ; complications ; Intracranial Aneurysm ; etiology ; pathology ; Male ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY

OBJECTIVETo determine the relationship between DNP level after human severe brain injury and hyponatremia as well as isorrhea.

METHODSThe peripheral venous plasma as control was collected from 8 volunteers. The peripheral venous plasma from 14 severe brain injury patients were collected in the 1, 3, 7 days after injury. Radioimmunoassay was used to detect the DNP concentration. Meanwhile, daily plasma and urine electrolytes, osmotic pressure as well as 24 h liquid intake and output volume were detected.

RESULTSThe normal adult human plasma DNP level was 62.46 pg/ml+/-27.56 pg/ml. In the experimental group, the plasma DNP levels were higher from day 1 to day 3 in 8 of the 14 patients than those in the control group (P(1)=0.05, P(3)=0.03). Negative fluid balance occurred in 8 patients and hyponatremia in 7 patients. The increase of plasma DNP level was significantly correlated with the development of a negative fluid balance (r =-0.69, P<0.01) and hyponatremia (chi(2) =4.38, P<0.05).

CONCLUSIONSThe increase of plasma DNP level is accompanied by the enhancement of natriuretic and diuretic responses in severe brain-injured patients, which is associated with the development of a negative fluid balance and hyponatremia after brain injury.

Adult ; Brain Injuries ; blood ; complications ; Elapid Venoms ; blood ; Female ; Humans ; Hyponatremia ; etiology ; Intracranial Hypertension ; blood ; etiology ; Male ; Middle Aged ; Peptides ; blood ; Reagent Kits, Diagnostic ; Water-Electrolyte Imbalance ; blood

Acute Disease ; Bacterial Infections ; prevention & control ; Brain Edema ; drug therapy ; etiology ; Critical Care ; Hepatic Encephalopathy ; etiology ; therapy ; Humans ; Intracranial Hypertension ; etiology ; therapy ; Liver Failure, Acute ; etiology ; nursing ; therapy ; Liver Transplantation ; nursing ; standards

PURPOSE: Hypertonic fluids such as mannitol and half-molar sodium lactate are given to treat intracranial hypertension in patients with severe traumatic brain injury (TBI). In this study, sodium lactate was compared to mannitol in patients with TBI to investigate the efficacy in reducing intracranial pressure (ICP). METHODS: This study was a systematic review with literature research on articles published in any year in the databases of PubMed, ScienceDirect, Asian Journal of Neurosurgery, and Cochrane Central Register of Controlled Trials. The keywords were "half-molar sodium lactate", "mannitol", "cerebral edema or brain swelling", and "severe traumatic brain injury". The inclusion criteria were (1) studies published in English, (2) randomized control trials or retrospective/prospective studies on TBI patients, and (3) therapies including half-molar sodium lactate and mannitol and (4) sufficient data such as mean difference (MD) and risk ratio (RR). Data analysis was conducted using Review Manager 5.3. RESULTS: From 1499 studies, a total of 8 studies were eligible. Mannitol group reduced ICP of 0.65 times (MD 0.65; p = 0.64) and improved cerebral perfusion pressure of 0.61 times (MD 0.61; p = 0.88), better than the half-molar group of sodium lactate. But the half-molar group of sodium lactate maintained the mean arterial pressure level of 0.86 times, better than the mannitol group (MD 0.86; p = 0.09). CONCLUSION Half-molar sodium lactate is as effective as mannitol in reducing ICP in the early phase of brain injury, superior over mannitol in an extended period. It is able to prevent intracranial hypertension and give better brain tissue perfusion as well as more stable hemodynamics. Blood osmolarity is a concern as it increases serum sodium.
Brain Edema ; Brain Injuries, Traumatic/drug therapy* ; Diuretics, Osmotic/therapeutic use* ; Humans ; Intracranial Hypertension/etiology* ; Intracranial Pressure ; Mannitol/therapeutic use* ; Prospective Studies ; Retrospective Studies ; Saline Solution, Hypertonic ; Sodium Lactate

A 26-year-old male presented with a 6-day history of paroxysmal headache which was worsen with nausea and vomiting for 1 day. Head CT on admission revealed left chronic subdural hematoma with midline shift. An emergency Burr hole drainage for hematoma was performed. Headache recurred 6 days later. MRI of the brain revealed a diffuse thickening and a gadolinium-enhancement of the falx, cranial dura mater and tentorium cerebelli on the left side with pia mater involved. Lumber puncture showed increased intracranial pressure and elevated IgG level in cerebrospinal fluid. Histological examination of the biopsy specimen showed thickened, fibrotic dura with a sterile chronic inflammation. According to pathological examination, idiopathic hypertrophic cranial pachymeningitis was considered as the final diagnosis. Symptoms were improved with steroid pulse therapy.
Adult ; Biopsy ; Brain ; pathology ; Drainage ; Dura Mater ; pathology ; Hematoma, Subdural, Chronic ; etiology ; surgery ; Humans ; Hypertrophy ; diagnosis ; Immunoglobulin G ; cerebrospinal fluid ; Intracranial Hypertension ; etiology ; Magnetic Resonance Imaging ; Male ; Meningitis ; diagnosis ; Steroids ; administration & dosage ; therapeutic use ; Tomography, X-Ray Computed

OBJECTIVETo study the correlation between brain edema, elevated intracranial pressure (ICP) and cell apoptosis in traumatic brain injury (TBI).

METHODSIn this study, totally 42 rabbits in 7 groups were studied. Six of the animals were identified as a control group, and the remaining 36 animals were equally divided into 6 TBI groups. TBI models were produced by the modified method of Feeney. After the impact, ICP of each subject was recorded continuously by an ICP monitor until the animal was sacrificed at scheduled time. The apoptotic brain cells were detected by an terminal deoxynucleotide-transferase-mediated dUTP-digoxigenin nick end labeling (TUNEL) assay. Cerebral water content (CWC) was measured with a drying method and calculated according to the Elliott formula. Then, an analysis was conducted to determine the correlation between the count of apoptotic cells and the clinical pathological changes of the brain.

RESULTSApoptotic cell count began to increase 2 h after the impact, and reached its maximum about 3 days after the impact. The peak value of CWC and ICP appeared 1 day and 3 days after the impact, respectively. Apoptotic cell count had a positive correlation with CWC and ICP.

CONCLUSIONSIn TBI, occurrence of brain edema and ICP increase might lead to apoptosis of brain cells. Any therapy which can relieve brain edema and/or decrease ICP would be able to reduce neuron apoptosis, thereby to attenuate the secondary brain damage.

Animals ; Apoptosis ; Brain Edema ; etiology ; metabolism ; pathology ; Brain Injuries ; complications ; pathology ; physiopathology ; Cell Count ; Disease Models, Animal ; In Situ Nick-End Labeling ; Intracranial Hypertension ; etiology ; pathology ; physiopathology ; Male ; Necrosis ; genetics ; pathology ; Rabbits ; Reference Values ; Telencephalon ; metabolism ; Water ; metabolism