Froin's syndrome is characterized by marked cerebrospinal fluid CSF xanthochromia yellow discoloration of the CSF and hypercoagulability due to increased protein content. The cause of the high protein content of the spinal fluid is meningeal irritation and inflammation. Pseudo-Froin's syndrome has been described as stagnation of the CSF distal to a spinal block due to spinal disc bulging or tumors [ 1 ]. A year-old man with paraplegia was admitted to the urology department of our institution for follow-up of a bladder wall malignancy.
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The analysis of the protein level in cerebrospinal fluid CSF is an important tool for evaluating a patient's condition. Mild elevations can indicate subtle disruption to the blood-brain barrier and the presence of inflammatory cells and microorganisms [ 1 - 3 ]. Elderly immobile patients, viral encephalitis, and multiple sclerosis are among some disease processes that can contribute to this clinical finding [ 1 - 3 ].
This phenomenon was first described by Georges Froin in upon performing a lumbar puncture on a patient with a known spinal cord tumor [ 5 ]. Active tissue, whether malignant or infectious, can accelerate this process, however, cases have been reported where no evidence of infection or malignancy was noted [ 5 ].
In this case, we discussed a patient with underlying acquired immunodeficiency syndrome AIDS and Varicella zoster virus VZV encephalitis who presented to a regional trauma center with signs of acute encephalopathy and evolving fever.
The patient was also found to have underlying chronic cervical spinal stenosis exacerbated acutely by trauma. A year-old male with an unknown past medical history was transferred by an emergency medical services EMS unit as a trauma patient to the closest designated regional trauma center after being involved in a motor vehicle collision.
The patient was found crawling on the ground outside of a vehicle, with major passenger space intrusion that was involved in a collision with multiple other vehicles at freeway speeds. The patient was disoriented and unable to communicate to the EMS team, therefore, it was uncertain if he has been restrained with or if he experienced a loss of consciousness.
He was thin, with significant temporal and extremity muscle wasting. At this time, the trauma team observed no obvious signs of penetrating trauma. Imaging studies were obtained, which included a computerized tomography CT scan of the brain and cervical, thoracic and lumbar spines without contrast. In addition, CT scans of the chest, abdomen, and pelvis with intravenous contrast were performed.
Overall, the imaging studies did not reveal any acute traumatic pathology. A trauma laboratory panel, which included complete blood count with differential CBC with diff , prothrombin time, international normalized ratio, basic metabolic panel, urinalysis, urine drug screen, and blood alcohol level, were also unremarkable. As the patient remained altered, he was subsequently admitted by the trauma service with concern for possible traumatic brain injury TBI.
He became increasingly agitated and tachycardic with his HR increasing from the 70s to the high 90s. Because of a high index of suspicion for infectious etiology, the patient was treated empirically with vancomycin, rocephin, decadron, and acyclovir. Subsequently, the patient underwent CT angiogram of the brain and cervical vessels, magnetic resonance imaging MRI of the brain and cervical spine without contrast, as well as a lumbar puncture.
Neither angiogram demonstrated any vascular findings. While CSF results were pending, the decision was made to admit the patient to the medical intensive care unit MICU for further management, with the trauma service staying on as a consultant.
The patient also became febrile with his temperature rising to He developed rigors and continued to be agitated despite sedation with a titratable propofol drip. Upon admission to the MICU, repeat laboratory studies were performed due to the evolving clinical picture. The comprehensive metabolic panel did not demonstrate any severe electrolyte abnormalities.
Additionally, cardiac enzymes, thyroid hormone levels, Tylenol and salicylate levels, blood alcohol level, and urine drug screen were all within normal limits.
Based on the information obtained from the medical records, the patient was not on a highly active antiretroviral therapy HAART regimen at the time of the accident. On hospital day four, CSF studies indicated the presence of Varicella zoster virus with multiple restriction bands corresponding to the same result obtained from his serum. Thus, the origin of the gammaglobulins could not be differentiated as systemic versus intracerebral.
Blood and urine cultures did not demonstrate any growth after five days. The patient had a prolonged hospitalization and experienced numerous complications due to his immunocompromised state and natural disease progression. His mentation continued to wax and wane. Late in the hospital course, the patient developed hypoxia and hypotension despite being on maximal oxygen settings, vasopressor therapies, and broad antibiotic coverage.
At this point in the hospital course, the family elected for hospice care and comfort measures. The patient expired on day 60 of his hospitalization. We noted an extraordinary level of CSF proteinosis in this case, one that should raise suspicion for obstruction of CSF flow. This patient was presumed to have Varicella encephalitis superimposed with the traumatic exacerbation of cervical stenosis. The significance of these findings is that CSF proteinosis can clue the clinician to evaluate leptomeningeal anatomy further.
Previous case series have described an increased signal intensity of CSF that is proximal to an obstruction when compared to distal [ 10 ]. This case report was associated with CNS vasculitis found on postmortem analysis [ 1 - 2 ]. Our case is the first in the published literature that is associated with isolated CSF proteinosis without significant pleocytosis.
Though our patient exhibited radiographic evidence of leukoaraiosis with deep matter changes caused by small vessel disease, we cannot confirm for certain that the patient had a similar presentation. It is important to consider a broad differential diagnosis for patients who present with altered mental status in the setting of a traumatic injury. Cureus is not responsible for the scientific accuracy or reliability of data or conclusions published herein.
All content published within Cureus is intended only for educational, research and reference purposes. Additionally, articles published within Cureus should not be deemed a suitable substitute for the advice of a qualified health care professional. Do not disregard or avoid professional medical advice due to content published within Cureus. The authors have declared that no competing interests exist. Consent was obtained by all participants in this study. Arrowhead Regional Medical Center issued approval The approval is National Center for Biotechnology Information , U.
Journal List Cureus v. Published online Dec 6. Author information Article notes Copyright and License information Disclaimer. Corresponding author. Michael Neeki moc. Received Nov 20; Accepted Dec 5. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Introduction The analysis of the protein level in cerebrospinal fluid CSF is an important tool for evaluating a patient's condition. Case presentation A year-old male with an unknown past medical history was transferred by an emergency medical services EMS unit as a trauma patient to the closest designated regional trauma center after being involved in a motor vehicle collision.
Open in a separate window. Figure 1. Magnetic resonance imaging of the brain without contrast demonstrating periventricular white matter signal abnormality white arrows consistent with chronic ischemic white matter disease versus demyelinating disease. Figure 2. Discussion We noted an extraordinary level of CSF proteinosis in this case, one that should raise suspicion for obstruction of CSF flow.
Human Ethics Consent was obtained by all participants in this study. References 1. Guidelines on routine cerebrospinal fluid analysis.
Report from an EFNS task force. European journal of neurology. Cerebrospinal fluid as a diagnostic body fluid. Am J Med. Cerebrospinal fluid in diseases of the nervous system.
Fishman RA. WB Saunders Company. Govindarajan R, Khan T. Eur Spine J. Profound cerebrospinal fluid pleocytosis and Froin's syndrome secondary to widespread necrotizing vasculitis in an HIV-positive patient with varicella zoster virus encephalomyelitis.
J Neurol Sci. An unusual cause of raised CSF protein. Pseudo-Froin's syndrome, xanthochromia with high protein level of cerebrospinal fluid. Korean J Anesthesiol. Varicella zoster virus encephalitis with extreme CSF lactate and protein unmasking Alzheimer's disease. Heckmann J. Clin Neurol Neurosurg. Froin's syndrome revisited, years on. Pseudo-Froin's syndrome on MRI. Clin Radiol. Meningitis, encephalitis, brain abscess, and empyema. Articles from Cureus are provided here courtesy of Cureus Inc.
Pseudo-Froin's syndrome, xanthochromia with high protein level of cerebrospinal fluid
Froin's syndrome — coexistence of xanthochromia , high protein level and marked coagulation of cerebrospinal fluid CSF. It is caused by meningeal irritation e. A clinical test formerly used for evaluation of spinal stenosis is Queckenstedt's maneuver. Nowadays, a magnetic resonance imaging is used for identification of CSF flow obstruction.
Froin’s Syndrome Secondary to Traumatic and Infectious Etiology