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Hebrew Bible. See more words from the same year. Accessed 11 Nov. Nglish: Translation of incremental for Spanish Speakers. Subscribe to America's largest dictionary and get thousands more definitions and advanced search—ad free! Log in Sign Up. Save Word. Definition of incremental. Examples of incremental in a Sentence the incremental evolution of the collection from a specialized gallery into a comprehensive art museum the incremental total for my collection of baseball cards. Recent Examples on the Web Sustaining these habits is about making minor adjustments and incremental change.
First Known Use of incremental , in the meaning defined above. Seizure Mild edema In Of them, complete or nearly complete resolution of edematous lesions was noted in Table 2. PRES is commonly described as a neuroradiological disease entity characterized by reversible vasogenic edema in the subcortical white matter of bilateral posterior parieto-occipital region with a rapid onset of neurological deficits including seizures, headache, visual disturbances, and altered mental state 2 , 4.
The precise pathophysiology underlying PRES is not entirely established. Two contradictory hypotheses are commonly cited 2 , 5. This concept is primarily supported by the common presence of significant elevation of blood pressure in patients with PRES. This theory is supported by recent vessel imaging and perfusion imaging studies, which have demonstrated diffuse or focal cerebral vasoconstriction, and cerebral hypoperfusion in lesional areas Our case had no stigmata of pre-eclampsia or eclampsia, and the blood pressure maintained normal before and during delivery.
Did hypertension lead to PRES? Our patient complained postural headache before the changes in blood pressure, and the development of hypertension was following the deterioration of headache.
On the other hand, the patient only had a slight elevation of averaged MAP. Even the maximum blood pressure didn't exceed the upper MAP limits of autoregulation. In our review, only 16 patients had hypertension 11 — 14 , 17 , 18 , 23 , 25 — 29 , 31 , 32 , 34 , 37 , while only one patient had systolic blood pressure more than mmHg Some patients even experienced hypotension during the development of the disease 11 , So, patients with CSF hypovolemia have a different pathophysiological process other than hypertension.
CSF hypovolemia is characterized by orthostatic headaches which almost relive after lying down 6. CSF hypovolemia was proposed to replace the definition of IH 7.
The neuroradiological features include pachymeningeal enhancement, brain sagging, subdural fluid collections, pituitary hyperemia, and venous distension sign Although the intracranial pressure was not measured in our case, CSF hypovolemia was well-established on clinical and neuroradiological evidence.
Grelat et al. Interestingly, the patient underwent another episode of PRES following emergency ventriculoperitoneal shunt placement. Similarly, Karakis et al. Both of them had no other trigger factors. So, it is not surprising that CSF hypovolemia plays a key role in the development of PRES via a different pathophysiology independent of hypertension. In our patient, the ASL imaging provided the evidence of cerebral hyperperfusion in basal ganglion and occipital regions.
Depends on the cerebral auto-regulation system, CPP varies from 60 to 80 mmHg. When the CPP overwhelms the limits of the cerebral auto-regulation system, cerebral hyperperfusion occurs. Therefore, on the base of CSF hypovolemia, either slightly elevated MAP or normal MAP can lead to cerebral hyperperfusion, endothelial dysfunction, and vasogenic edema 13 , 15 , On the other hand, the cerebral auto-regulation system ensures a steady ICP in the encephalic space as long as possible. In accordance with the Monro—Kellie doctrine, cerebral blood flow and perfusion in cerebral arteries will firstly increase to maintain normal ICP when CSF leak.
If the increased cerebral blood flow and perfusion failed to compensate for the loss of CSF completely, dural sinuses, and veins would engorge for increasing the cerebral blood volume which will lead to capillary and venous hypertension.
As a result, fluids extravasated into the interstitial space and vasogenic edema occur. In addition, the brain sagging can result in mechanical traction on the vessels, particularly on the veins of Galen and straight sinus 10 , Therefore, it impairs the deep venous drainage, induces venous hypertension in the deep venous system, and leads to vasogenic edema dominating in the basal ganglia and occipital regions. To summarize, a combination of arterial hyperperfusion and venous dysfunction may be the pathophysiological link between PRES and CSF hypovolemia.
Some authors hypothesized that reversible cerebral vasoconstriction syndrome RCVS secondary to the mechanical stimuli of the sagging of the brain and its affiliations would trigger PRES 11 , 16 , They share similar triggers, including postpartum, drugs, autoimmune disease, and transplantation.
The activation of the adrenergic system is presumed to be key of the development of both diseases In a MR-angiography study of a series of 56 patients with IH, only one patient was reported to show segmental stenosis of cerebral arteries There was no evidence of RCVS in our case. In general, PRES is regarded as a benign disease with favorable outcomes 2 , Early identification and rational treatments are crucial to reduce morbidity and mortality.
The diagnosis of PRES was usually delayed in patients with CSF hypovolemia until the patients presented with epilepsy and encephalopathy. The most common initial clinical presentations of PRES in patients with CSF hypovolemia is headache which usually misleads to a diagnosis of postdural puncture headache, intracranial hypotension, or pain-related headache.
In this regard, the symptom of headache was found to be not of value in the diagnosis of PRES in a retrospective study Only the symptoms of visual disturbances, epilepsy, and encephalopathy are the reasonable predictor of PRES. So, in patients with substantial risk factors of CSF hypovolemia including dural puncture, lumbar puncture, lumboperitoneal shunt, ventriculoperitoneal shunt, and spinal surgery, PRES should be early considered when the clinical manifestations e.
Clinical managements of PRES are based on the elimination of underlying trigger factors and immediate control of epilepsy. Due to the differences in pathogenesis, the treatment strategy for patients with CSF hypovolemia may differ from those with other etiology.
We found that seven patients experienced PRES within 1 day. On the other hand, a marked increase in blood pressure may contribute to the development of PRES. Patients who experienced a systolic blood pressure more than mmHg had a shorter interval of PRES onset. Base on the evidence from the reviewed reports, we propose the following recommendations: First, a precipitous reduction of CSF volume or ICP should be avoided. A graded reduction of ICP is strongly recommended in patients with intracranial hypertension, especially in patients with extremely high CSF pressures.
Second, in patients with CSF hypovolemia, the treatment of CSF hypovolemia should be initiated at the early stage of the disease CSF hypovolemia often recovered spontaneously. Conservative medical management could be processed, including strict supine positioning, ample hydration, analgesia, and non-steroidal drugs. When the conservative measures failed to bring alleviation of the symptoms or in patients who present moderate and severe CSF hypovolemia, epidural blood patching is recommended as the mainstay of first-line treatment 49 , Surgical repair should be considered for patients with clearly identified leak sites and no response to non-surgical treatment and EBPs PRES should be early considered in patients with a high risk of CSF hypovolemia when the clinical manifestations can not be explained by CSF hypovolemia or other conditions alone.
Precipitous reduction of CSF should be avoided, while appropriate treatments of CSF hypovolemia should be initiated early. The blood pressure should be strictly controlled in patients with CSF hypovolemia to prevent the development of PRES and improve the clinical outcome. The raw data supporting the conclusions of this article will be made available by the authors, without undue reservation, to any qualified researcher.
FF designed the study. YZ and XW collected clinical data and wrote the manuscript. YC and YL searched the literature and edited the pictures. GZ revised the manuscript. All authors contributed to the manuscript revision and approved the submitted version. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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