Transient Obstructive Hydrocephalus in Patients With Intracerebral Hemorrhage: Report of Two Cases

Jergović, Ilija; Budinčević, Hrvoje; Planjar-Prvan, Miljenka; Bielen, Ivan

doi:10.20471/acc.2016.55.03.21

Cited by 6 publications

(5 citation statements)

References 9 publications

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“…To the best of our knowledge, this article describes only the second case reported. [5] Even in acute TOH cases due to other causes of spontaneous intracranial hemorrhage (SIH), there are only sporadic reports [6][7][8][9][10] in the literature. Acute OH frequently occurs in the early stages of SIH.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies noted that the reasons for rapid OH remission mainly include the following 2 aspects: acute OH resulting from a clot obstructing the aqueduct resolves when the CSF circulation is restored after clot dissolution [6][7][8] ; OH resulting from a clot blocking the aqueduct can cause an increase in ICP. [9,12] The increased ICP will force the clot migration.…”

Section: Discussionmentioning

confidence: 99%

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Delayed transient obstructive hydrocephalus after cerebral aneurysm rupture

Lai

Wang

et al. 2021

Medicine

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Rationale: Obstructive hydrocephalus (OH) frequently occurs in patients with a ruptured cerebral aneurysm (CA), and it may lead to severe neurological deficits, including life-threatening brain herniation. OH generally occurs in the early stage of CA rupture, rather than in the late stage, and rarely resolves without therapy. Patient concerns: A 64-year-old woman with a ruptured anterior communicating artery aneurysm was treated with coil embolization. Nineteen days after her CA rupture, because of the delayed transient OH, she experienced a dramatic cycle in consciousness over 9 hours: wakefulness–drowsiness–coma–drowsiness–wakefulness. Diagnosis: The patient was diagnosed with delayed transient obstructive hydrocephalus, which is a very rare condition. Interventions: Mannitol was administered to reduce intracranial pressure. Outcomes: The patient was discharged from the hospital 30 days after admission, with a final GCS score of 15 and without weaknesses. At follow-up 2 months after discharge, brain CT revealed non-recurrence of hydrocephalus. Lessons: A blood clot of any size in the ventricle is likely to lead to obstructive hydrocephalus. Prolonged bed rest for IVH patients may help to reduce the incidence of delayed OH.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Delayed transient obstructive hydrocephalus after cerebral aneurysm rupture

Lai

Wang

et al. 2021

Medicine

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“…Increased intracranial pressure is reported as a symptom or complication in several CNS pathologies like hydrocephalus [2, 107], IIH [108–110], TBI [111], intracerebral haemorrhage (ICH) [112], subarachnoid haemorrhage (SAH) [26, 113, 114], and ischaemic stroke [115, 116]. A comprehensive review of altered CSF dynamics in each of these CNS disorders would be beneficial; however, the depth required is outside the scope of this review.…”

Section: Reviewmentioning

confidence: 99%

“…Hydrocephalus is caused by disruptions to CSF secretion, flow, or drainage, which lead to increased ICP [2]. Around 95% of hydrocephalus is thought to be caused by disruptions to CSF flow, commonly caused by tumours throughout the ventricular system, and there is some evidence of transient obstructive hydrocephalus as a complication of intraventricular haemorrhage [107]. Hydrocephalus may also be non-obstructive, in which CSF flow within the ventricular system is not impaired but there is decreased absorption.…”

Section: Reviewmentioning

confidence: 99%

Cerebrospinal fluid dynamics and intracranial pressure elevation in neurological diseases

Bothwell

Janigro

Patabendige

2019

Fluids Barriers CNS

193

181

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The fine balance between the secretion, composition, volume and turnover of cerebrospinal fluid (CSF) is strictly regulated. However, during certain neurological diseases, this balance can be disrupted. A significant disruption to the normal CSF circulation can be life threatening, leading to increased intracranial pressure (ICP), and is implicated in hydrocephalus, idiopathic intracranial hypertension, brain trauma, brain tumours and stroke. Yet, the exact cellular, molecular and physiological mechanisms that contribute to altered hydrodynamic pathways in these diseases are poorly defined or hotly debated. The traditional views and concepts of CSF secretion, flow and drainage have been challenged, also due to recent findings suggesting more complex mechanisms of brain fluid dynamics than previously proposed. This review evaluates and summarises current hypotheses of CSF dynamics and presents evidence for the role of impaired CSF dynamics in elevated ICP, alongside discussion of the proteins that are potentially involved in altered CSF physiology during neurological disease. Undoubtedly CSF secretion, absorption and drainage are important aspects of brain fluid homeostasis in maintaining a stable ICP. Traditionally, pharmacological interventions or CSF drainage have been used to reduce ICP elevation due to over production of CSF. However, these drugs are used only as a temporary solution due to their undesirable side effects. Emerging evidence suggests that pharmacological targeting of aquaporins, transient receptor potential vanilloid type 4 (TRPV4), and the Na + –K + –2Cl − cotransporter (NKCC1) merit further investigation as potential targets in neurological diseases involving impaired brain fluid dynamics and elevated ICP.

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“…Intracranial pressure (ICP) elevation is reported in several neurological conditions including hydrocephalus [1,2], idiopathic intracranial hypertension [3], traumatic brain injury [4][5][6], subarachnoid haemorrhage [7][8][9], and stroke [10][11][12][13][14][15]. Elevated ICP can cause secondary brain injury and death, so should be monitored and managed as a priority for patients with neurological disease or injury [16,17].…”

Section: Introductionmentioning

confidence: 99%

CSF Secretion Is Not Altered by NKCC1 Nor TRPV4 Antagonism in Healthy Rats

et al. 2021

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Background: Cerebrospinal fluid (CSF) secretion can be targeted to reduce elevated intracranial pressure (ICP). Sodium-potassium-chloride cotransporter 1 (NKCC1) antagonism is used clinically. However, supporting evidence is limited. The transient receptor potential vanilloid-4 (TRPV4) channel may also regulate CSF secretion and ICP elevation. We investigated whether antagonism of these proteins reduces CSF secretion. Methods: We quantified CSF secretion rates in male Wistar rats. The cerebral aqueduct was blocked with viscous mineral oil, and a lateral ventricle was cannulated. Secretion rate was measured at baseline and after antagonist administration. Acetazolamide was administered as a positive control to confirm changes in CSF secretion rates. Results: Neither NKCC1, nor TRPV4 antagonism altered CSF secretion rate from baseline, n = 3, t(2) = 1.14, p = 0.37, and n = 4, t(3) = 0.58, p = 0.6, respectively. Acetazolamide reduced CSF secretion by ~50% across all groups, n = 7, t(6) = 4.294, p = 0.005. Conclusions: Acute antagonism of NKCC1 and TRPV4 proteins at the choroid plexus does not reduce CSF secretion in healthy rats. Further investigation of protein changes and antagonism should be explored in neurological disease where increased CSF secretion and ICP are observed before discounting the therapeutic potential of protein antagonism at these sites.

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Transient Obstructive Hydrocephalus in Patients With Intracerebral Hemorrhage: Report of Two Cases

Cited by 6 publications

References 9 publications

Delayed transient obstructive hydrocephalus after cerebral aneurysm rupture

Delayed transient obstructive hydrocephalus after cerebral aneurysm rupture

Cerebrospinal fluid dynamics and intracranial pressure elevation in neurological diseases

CSF Secretion Is Not Altered by NKCC1 Nor TRPV4 Antagonism in Healthy Rats

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