Intracranial hypotension

Rebound Intracranial Hypertension: A Complication of Epidural Blood Patching for Intracranial Hypotension

Authors: Kranz PG, Amrhein TJ, Gray L.

Rebound intracranial hypertension is a complication of epidural blood patching for treatment of intracranial hypotension characterized by increased intracranial pressure, resulting in potentially severe headache, nausea, and vomiting. Because the symptoms of rebound intracranial hypertension may bear some similarity to those of intracranial hypotension and literature reports of rebound intracranial hypertension are limited, it may be mistaken for refractory intracranial hypotension, leading to inappropriate management. This clinical report of 9 patients with confirmed rebound intracranial hypertension reviews the clinical characteristics of patients with this condition, emphasizing factors that can be helpful in discriminating rebound intracranial hypertension from refractory spontaneous intracranial hypotension, and discusses treatment.

Intracranial hypotension syndrome in a patient due to suboccipital craniectomy secondary to Chiari type malformation

Authors: Dora B, Nikolaos B, Stylianos G, Damianos S.

Intracranial hypotension syndrome (IHS) is a rare disorder characterized by a decrease in cerebrospinal fluid pressure to less than 60 mm H2O. The syndrome is associated with occipital headache radiating to the frontal and temporal zones. The current clinical case describes the manifestation of IHS in a twenty-five year old female with a history of suboccipital craniectomy due to Chiari I malformation nine years earlier. The patient was admitted to the hospital complaining about postural, mainly occipital, headache during the last three months, aggravated by being in an upright position. The magnetic resonance imaging (MRI) revealed engorgement of the dural venous sinuses, significant enlargement of the pituitary gland and download displacement or sagging of the brain with effacement of the perichiasmatic cisterns and the prepontine cistern, while the spinal T2W MRI revealed a 7 mm × 2.5 mm dural defect with an extradural cerebrospinal fluid collection at the dorsal soft tissues of the cervical spine. The previous imaging did not reveal subdural effusions.

Deep venous structures distortion in spontaneous intracranial hypotension as an explanation for altered level of consciousness

Authors: Ajlan AM, Al-Jehani H, Torres C, Marcoux J.

Spontaneous intracranial hypotension (SIH) is a syndrome of low pressure headache associated with low CSF pressure. The condition is generally considered benign but extreme cases of SIH can lead to changes in the level of consciousness. We describe a case in which alteration in the level of consciousness was prolonged and severe, and could not be explained solely by the presence of subdural collections. MRI of the brain showed evidence of impaired venous flow secondary to brain sagging causing distortion of deep venous structures.

Deep venous structures distortion in spontaneous intracranial hypotension as an explanation for altered level of consciousness

Authors: Ajlan AM, Al-Jehani H, Torres C, Marcoux J.

Spontaneous intracranial hypotension (SIH) is a syndrome of low pressure headache associated with low CSF pressure. The condition is generally considered benign but extreme cases of SIH can lead to changes in the level of consciousness. We describe a case in which alteration in the level of consciousness was prolonged and severe, and could not be explained solely by the presence of subdural collections. MRI of the brain showed evidence of impaired venous flow secondary to brain sagging causing distortion of deep venous structures.

Intracranial hypotension masquerading as nonconvulsive status epilepticus

Authors: Hedna VS, Kumar A, Miller B, Bidari S, Salardini A, Waters MF, Hella M, Valenstein E, Eisenschenk S.

Intracranial hypotension (IH) has been a known entity in neurocritical care since 1938. Even though many cases are spontaneous, the incidence of intracranial hypotension in the neurocritical care setting is increasing by virtue of the increased number of neurosurgical interventions. Whether spontaneous or secondary in etiology, diagnosis of IH usually requires the presence of orthostatic symptoms, including headaches and nausea with low opening CSF pressure. However, typical clinical features in the appropriate clinical context and imaging, even with normal CSF pressure, can indicate IH. In the neurocritical care setting, challenges for accurate semiology include altered sensorium and reduced levels of responsiveness for which many etiologies may exist, including metabolic dysfunction, traumatic brain injury, IH, or nonconvulsive status epilepticus (NCSE). The authors describe 3 patients whose clinical picture and electroencephalography (EEG) findings initially suggested NCSE but who did not respond to treatment with antiepileptic drugs alone. Neuroimaging suggested IH, and subsequent treatment of IH successfully improved the patient's clinical status. To the authors' knowledge this paper is the first in the literature that reports a correlation of IH with electrographic findings similar to NCSE as cause and effect. The authors' hypothesis is that thalamocortical dysfunction causes EEG findings that appear to be similar to those in NCSE but that these conditions do not coexist. The EEG activity is not epileptogenic, and IH results in blocking network pathways producing thalamocortical dysfunction. The authors discuss the hypothesis and pathophysiology of these epileptiform changes in relation to IH.

Intracranial hypotension with a sixth cranial nerve palsy subsequent to massive thoracic CSF hygroma: a rare complication of thoracic disc excision

Authors: Khurana A, Brousil J, Russo A, Evans A, Quraishi NA, Boszczyk BM.

BACKGROUND: Thoracic cerebrospinal fluid (CSF) hygroma is a rare and potentially devastating complication of the anterior thoracic approach to the spine. We present two cases in which this complication resulted in acute cranial nerve palsy and discuss the pathoanatomy and management options in this scenario.
CASE REPORTS: Two male patients presented to our department with neurological deterioration due to a giant herniated thoracic disc. The extruded disc fragment was noted pre-operatively to be calcified in both patients. A durotomy was performed at primary disc prolapse resection in the first patient, whereas an incidental durotomy during the procedure caused complication in the second patient. These were repaired primarily or sealed with Tachosil®. Both patients re-presented with acute diplopia. Imaging of both patients confirmed a massive thoracic cerebrospinal fluid hygroma and evidence of intracranial changes in keeping with intracranial hypotension, but no obvious brain stem shift. The hemithorax was re-explored and the dural repair was revised. The first patient made a full recovery within 3 months. The second patient was managed conservatively and took 5 months for improvement in his ophthalmic symptoms.
CONCLUSIONS: The risk of CSF leakage post-dural repair into the thoracic cavity is raised due to local factors related to the chest cavity. Dural repairs can fail in the presence of an acute increase in CSF pressure, for example whilst sneezing. Intracranial hypotension can result in subsequent hygroma and possibly haematoma formation. The resultant cranial nerve palsy may be managed expectantly except in the setting of symptomatic subdural haematoma or compressive pneumocephaly.

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