From the Guidelines
Albuminocytologic dissociation occurs due to the increased permeability of the blood-CSF barrier to proteins, without a significant cellular immune response, typically seen in conditions like Guillain-Barré syndrome. This phenomenon is characterized by elevated protein levels in cerebrospinal fluid (CSF) without a corresponding increase in white blood cell count. According to a study published in Nature Reviews Neurology in 2019 1, the classic finding in Guillain-Barré syndrome (GBS) is the combination of an elevated CSF protein level and a normal CSF cell count, known as albumino-cytological dissociation.
The underlying mechanism involves damage to nerve roots or peripheral nerves without direct inflammation of the meninges, leading to increased protein leakage into the CSF. Conditions associated with albuminocytologic dissociation include:
- Guillain-Barré syndrome, where autoimmune attack on peripheral nerves leads to increased protein leakage into the CSF
- Chronic inflammatory demyelinating polyneuropathy (CIDP)
- Some spinal cord tumors
- Diabetic polyradiculopathy
The physiological explanation, as supported by the study 1, involves disruption of the blood-nerve barrier at the level of the nerve roots, allowing plasma proteins to leak into the CSF while the intact blood-brain barrier prevents cellular infiltration. This finding is diagnostically valuable as it helps distinguish peripheral nerve disorders from infectious or inflammatory central nervous system conditions, which typically show increases in both protein and cell counts. Notably, the study 1 highlights that normal CSF protein levels do not rule out a diagnosis of GBS, and marked pleocytosis suggests other pathologies.
From the Research
Albuminocytologic Dissociation
Albuminocytologic dissociation is a diagnostic hallmark of Guillain-Barré syndrome (GBS) characterized by elevated cerebrospinal fluid (CSF) protein levels with a relatively low cell count 2, 3, 4. This condition is also known as cytoalbuminologic dissociation.
Causes of Albuminocytologic Dissociation
The exact cause of albuminocytologic dissociation in GBS is not fully understood, but it is thought to be related to the disruption of the blood-nerve barrier, leading to the increased passage of proteins from the blood into the CSF 2, 4.
Factors Influencing Albuminocytologic Dissociation
Several factors can influence the presence and severity of albuminocytologic dissociation in GBS, including:
- Time from symptom onset to lumbar puncture: Earlier lumbar puncture may result in lower CSF protein levels and reduced albuminocytologic dissociation 2, 5, 6.
- Age: Older patients may have higher CSF protein levels and more pronounced albuminocytologic dissociation 3.
- Disease severity: More severe disease may be associated with higher CSF protein levels and greater albuminocytologic dissociation 3.
- Electrophysiological variants: Different electrophysiological variants of GBS, such as acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN), may have different associations with albuminocytologic dissociation 5.
Diagnostic Implications
Albuminocytologic dissociation is an important diagnostic feature of GBS, but its absence does not exclude the diagnosis 3, 4. The use of age-adjusted CSF protein levels may improve the specificity of albuminocytologic dissociation for diagnosing GBS, but may also reduce its sensitivity 3.
Key Findings
- Albuminocytologic dissociation is a common finding in GBS, but its presence and severity can vary depending on several factors 2, 3, 5, 4, 6.
- The diagnostic yield of albuminocytologic dissociation can be influenced by the timing of lumbar puncture, age, and disease severity 2, 3, 5, 6.
- Albuminocytologic dissociation is not a specific marker for GBS and can be found in other conditions, such as chronic inflammatory demyelinating polyneuropathy 4.