CSF & ICP Flashcards
How is CSF produced?
From arterial blood by the choroid plexus of the lateral and 4th ventricles
Combined process of diffusion, pinocytosis and active transfer
Small amount also produced by ependymal cells
What is CSF volume? How much is produced and at what rate?
Adult ~140ml with about 25ml in ventricles
Produced at rate of 0.2-0.7ml/min (600-700ml daily).
How is CSF circulated and absorbed?
Circulation aided by pulsations of choroid plexus and by motion of the cilia of ependymal cells
Absorbed across the arachnoid villi into the venous circulation. The foramina in the 4th ventricle connect to the subarachnoid space around the spinal cord
Name some of the functions of the CNS
9 listed in the book
- Buoyancy (brain weight reduced >95% - reduces shearing / tearing forces on neural tissue)
- Adjustment of intracranial volume (Monro-Kellie doctrine)
- Micronutrient transport (e.g. nucleosides, pyramidines, vitamin C): choroid plexus → CSF → brain cells
- Protein & peptide supply (macromolecules e.g. transthyretin, insulin-like growth factor, thyroxine)
- Buffer reservoir: if brain interstitial tissue fluid concs of H+, K+, glucose altered - ventricular fluid can buffer extracellular fluid changes
- Sink / drainage: Clears anion metabolites of NTs, protein products of catabolism / tissue breakdown + xenobiotic substances from CNS (active transporters in choroid plexus, or by bulk CSF drainage to venous blood / lymphatics)
- Immune mediation (cells adjacent to ventricles have antigen presenting capabilities - some CSF proteins drain into cervical lymphatics with potential for inducing antibody reactions)
- Information transfer: NT agents (e.g. amino acids, peptides) may be transported over distances to bind receptors in the parasynaptic mode)
- Drug delivery: some do not readily cross BBB but can be transported into CSF by endogenous proteins in choroid plexus epithelial membranes
What are the normal characteristics of CSF you would expect to see in clinical testing?
Crystal clear
Opening pressure of 80-180 mmH2O
Up to 5 mononuclear cells, 0-5 red blood cells
Glucose 60-70% of plasma values
Protein <500mg/dl and lower in ventricles
What can cause abnormalities in CSF pressure / volume?
Hydrocephalus
Idiopathic intracranial hypertension
Space occupying lesions / cerebral oedema / haemorrhage
Dural venous sinus thrombosis
CSF hypotension
Name six possible abnormalities in CSF constituents
- Raised white cells (meningitis, encephalitis, reactive to neoplastic involvement, autoimmune disorders, sarcoidosis)
- Raised red cells (traumatic tap, SAH)
- Low glucose (hypoglycaemia, meningitis, mumps and lymphocytic choriomeningitis infections, SAH, sarcoidosis)
- Raised protein (inflammatory conditions, infection, CSF block, neoplasms)
- Neoplastic cells (primary or metastatic, up to 3 attempts at lumbar puncture may be required to detect the abnormal cells)
- Oligoclonal bands (CNS myelination, not specific)
Name some SPECIFIC diagnostic tests that can be performed on CSF
TPPA (syphilis)
14-3-3 protein and S100 (sporadic or variant CJD)
Positive viral PCR (meningitis)
Positive Borrelia serology (Lyme)
Positive JC virus PCR (progressive multifocal leukoencephalopathy - PML)
Lumbar puncture is indicated if patients have symptoms consistent with which diseases?
- CNS infections (meningitis or encephalitis secondary to bacterial / TB, viral, fungal, protozoal and helminthic pathogens)
- SAH
- Inflammatory / Demyelinating CNS diseases: MS, sarcoidosis
- Inflammatory neuropathies (GBS, chronic inflammatory demyelinating polyneuropathy - CIDP)
- Idiopathic intracranial hypertension
- Unexplained pyrexia with neurological symptoms (particularly children)
- Malignant infiltration of meninges: leukaemia, metastatic melanoma
- Certain metabolic or degenerative diseases of the brain or spinal cord, inborn errors of metabolism
In what situations in brain imaging indicated prior to performing a lumbar puncture?
Symptoms (e.g. reduced consciousness) or signs (e.g. optic disc swelling) of significantly increased intracranial pressure, or focal neurological findings
In addition to diagnosis, what other indications are there for lumbar puncture?
Management of idiopathic intracranial hypertension
Administering intrathecal chemotherapeutic agents / antibiotic therapy
Measurement of pressure or lumbar infusion testing in hydrocephalus
Monitoring CSF pressure in patients with dural venous sinus thrombosis
When is LP contraindicated?
Evidence of raised intracranial pressure or focal neurological findings unless the risk of brain herniation has been excluded by cerebral imaging (note: all focal lesions do NOT automatically contraindicate lumbar pressure)
Soft tissue infection over lumbar spine area
Coagulopathy (INR >1.5) or thrombocytopenia (platelets <50,000/mm³)
(Info about performing lumbar puncture)
(Consider adding this - skip for now)
horizontal lateral decubitus position, perpendicular to be, apex of pelvic bone indentified - visualise direct to spine,
cord ends at L1-2, puncture spaces between posterior elements of 3-4 or 4-5.
What are the three main volumes within the skull?
CSF 150ml
Blood 150ml
Brain 1200ml
According to the Monroe-Kellie doctrine, what is compensation?
Brain can compensate for: expanding mass (tumour, abscess, haematoma). increased CSF (hydrocephalus), increased blood (outflow obstruction), or increased brain (oedema), by:
- Reducing CSF volume
- Then blood volume (initially venous then arterial)
- To some extent brain volume (reduced ECF)
According to the Monroe-Kellie doctrine, what is DECOMPENSATION?
Eventually, further small increments in volume produce larger and larger increments in intracranial pressure
How is cerebral blood flow calculated?
How is cerebral perfusion pressure calculated?
CBF = CPP (perfusion pressure) / CVR (vascular resistance)
CPP = MAP - ICP
Physiological range of CPP is 60-160mmHg
As ICP rises, how is cerebral blood flow maintained?
CPP is controlled by ICP + MAP
CVR is controlled by autoregulation + chemoregulation
How does autoregulation occur?
Cerebral perfusion pressure increases → arterial wall tension increases → detected by vascular smooth muscle which contracts → vessel diameter reduced → cerebral vascular resistance increases → blood flow reduced
If BP drops the opposite occurs (ensures CBF constant over physiological range of CPP - 60-160mmHg)
How does chemoregulation occur? Why can this be problematic?
Mainly by pCO₂ - also pH, metabolic waste products and pO₂ (only if <50kPa i.e. periarrest)
Physiological response can lead to problems, as all are markers of hypoxia and hence increase vessel diameter with intention of increasing blood flow - however also causes increased ICP which can be detrimental
How does chemoregulation affect clinical approach to raised ICP?
Clinically, can decrease pCO2 (which will reduce vessel diameter) and reduce the ICP, however this will increase CVR and therefore reduce CBF.
Ultimately: can have good ICP or good CBF - NOT both
Optimal pCO2 currently considered 4.5kPa in patient with raised ICP
What are signs + symptoms of raised ICP?
Headache: mornings, lying flat, coughing, stooping
Vomiting
Papilloedema: takes time to establish and to disappear
Reduced GCS
Cushings response (↑BP ↓HR) - limited use as late sign and always already comatose!
What are the 4 main herniation syndromes?
- SUBFALCINE: occurs early with unilateral SOLs. Rarely produces any clinical effects, although ipsilateral ACA occlusion has been recorded.
- LATERAL TENTORIAL (UNCAL): medial temporal lobe herniates under tentorium cerebelli (through the tentorial hiatus):
- CENTRAL TENTORIAL: progression from lateral tentorial herniation as ICP continues to rise. Midline lesion or diffuse swelling of hemispehres causes vertical displacement of midbrain and diencephalon through tentorial hiatus. Damage to these structures due to mechanical distortion or ischaemia secondary to stretching of perforating vessels.
- TONSILLAR: cerebellar tonsils through foramen magnum (caused by subtentorial expanding mass - degree of upward herniation through hiatus may also occur). Clinical effects difficult to distinguish from direct brainstem / midbrain compression.
Which structures can be affected in a lateral tentorial (uncal) herniation?
- Cerebral peduncle (against Kernohan’s notch: weakness, false localising signs)
- Occulomotor nerve (ipsilateral fixed and dilated pupil, ptosis and impaired eye movement, but in coma)
- PCA (homonymous hemianopia)
